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1
Shriki, J. E., K. Surti, A. Farvid, J. S. Shinbane, and P. M. Colletti. "Quantitative Evaluation of the Amount of Delayed Myocardial Enhancement as a Predictor of Systolic Dysfunction." Open Cardiovascular Medicine Journal 3, no. 1 (May 18, 2009): 35–38. http://dx.doi.org/10.2174/1874192400903010035.
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30 patients with delayed contrast enhancement in patterns suggestive of myocardial infarctions were reviewed. Infarct mass was quantitatively measured using short axis images obtained in the delayed phase of gadopentetate administration. Left ventricular mass and ejection fraction were measured using short axis, steady state free precession images. A relationship is drawn between increased mass of infarction and decreased left ventricular ejection fraction. For each gram of infarct, there is a 0.5 % reduction in ejection fraction (EF = 50 - (0.48 x gm infarcted myocardium); r2= 0.49). For each % increase of infarcted myocardium, there is a 0.67 % reduction in ejection fraction (EF = 50 - (0.67 x percent of infarcted myocardium); r2= 0.39). Left ventricular ejection fraction correlates inversely with the mass of myocardium with delayed enhancement on cardiac MRI.
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O'Regan, Declan P., Rizwan Ahmed, Clare Neuwirth, Yvonne Tan, Giuliana Durighel, Joseph V. Hajnal, Imad Nadra, Simon J. Corbett, and Stuart A. Cook. "Cardiac MRI of myocardial salvage at the peri-infarct border zones after primary coronary intervention." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 1 (July 2009): H340—H346. http://dx.doi.org/10.1152/ajpheart.00011.2009.
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The purpose of this study was to use cardiac MRI to define the morphology of the reversibly injured peri-infarct border zone in patients treated with primary percutaneous coronary intervention (PPCI) for acute ST elevation myocardial infarction. In 15 patients, T2-weighted myocardial edema imaging was used to identify the ischemic bed or area at risk (AAR), and late gadolinium enhancement imaging was used to measure infarct size. Images were coregistered, and the boundaries of edema and necrosis were defined using an edge-detection methodology. We observed that infarction always involved the subendocardium but showed variable transmural extension within the AAR. The mean infarct size was 22 ± 19% (range: 8–48%), and the mean AAR was 34 ± 12% (range: 20–57%). The infarcted myocardium was always smaller than the ischemic AAR and involved between 34% and 99% (mean 72 ± 21%) of the ischemic bed primarily due to variation in transmural infarct extension. Although a lateral border zone of potentially viable myocardium was often present, its extent was limited (range: 0–11 mm, mean: 5 ± 4 mm). As a result of this, infarcts occupied the majority (range: 70–100%, mean: 82 ± 13%) of the width of the AAR. The mean fractional wall thickening in the infarcted, peri-infarcted, and remote myocardium was 3.6 ± 16.0%, 40.5 ± 26.4%, and 88.2 ± 39.3%, respectively. These findings demonstrate that myocardial salvage is largely determined by epicardial limitation of the infarct within the ischemic AAR after PPCI. The lateral boundaries of necrosis approximate to the lateral extent of the ischemic bed and systolic wall motion abnormalities extend well beyond the infarct border zone.
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Carlsson, M., P. C. Ursell, D. Saloner, and M. Saeed. "Multidetector computed tomography for characterization of calcium deposits in reperfused myocardial infarction." Acta Radiologica 50, no. 4 (May 2009): 396–405. http://dx.doi.org/10.1080/02841850902756540.
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Background: Calcium overload is a major cause of reperfusion myocardial injury. Multidetector computed tomography (MDCT) has been previously used in visualizing coronary artery calcium, but not calcium deposits in reperfused infarction. Purpose: To assess the ability of MDCT to 1) noninvasively visualize and characterize calcium deposits in reperfused infarcts, and 2) monitor regional wall swelling, regional systolic wall thickening, and infarct resorption. Material and Methods: Reperfused myocardial infarcts were created in seven pigs by 2-hour occlusion of the left anterior descending coronary artery (LAD) after coronary catheterization. A 64-slice MDCT scanner was used for non-contrast images to depict calcium deposits. Furthermore, cine and delayed contrast-enhanced (DE) MDCT imaging were acquired to assess the chronological changes (2–4 hours, 1 week, and 8 weeks) in regional wall swelling, systolic wall thickening, and infarct size. Results: Non-contrast MDCT images depicted calcium deposits as “hot-spots.” Attenuation of calcium deposits was greater (89±6 Hounsfield units [HU]) than remote myocardium (36±3 HU; P<0.05). Calcium deposits were not evident at 2–4 hours and were substantially smaller at 8 weeks compared to 1 week. Correlations were found between the extent of calcium deposits, ejection fraction ( R=0.81), and infarction size ( R=0.70). Cine MCDT images demonstrated transient wall swelling (edema formation and resorption) at 2–4 hours and differences in regional systolic wall thickening among infarcted, peri-infarcted, and remote myocardium. Calcium-specific von Kossa stain confirmed the presence of calcium deposits in infarcted myocardium. Conclusion: 64-slice MDCT has the potential to demonstrate the progression and regression of calcium deposits, interstitial edema, and infarction. The presence of calcium deposits was transient and associated with reperfused recent infarction. The extent of calcium deposits was positively correlated with infarction size and negatively with global left-ventricular function.
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Nilsson, S., G. Wikström, A. Ericsson, M. Wikström, A. Waldenström, and A. Hemmingsson. "MR Imaging of Gadolinium-DTPA-BMA-Enhanced Reperfused and Nonreperfused Porcine Myocardial Infarction." Acta Radiologica 36, no. 4-6 (July 1995): 633–40. http://dx.doi.org/10.1177/028418519503600465.
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To investigate whether Gd-DTPA-BMA-enhanced MR imaging permits differentiation between reperfused and nonreperfused myocardial infarction, myocardial infarction was induced in 12 domestic pigs. In 6 pigs, Gd-DTPA-BMA, 0.3 mmol/kg b.w. was administered i.v. 60 min after the occlusion. In 6 other pigs, the infarctions were reperfused 80 min after the occlusion, followed by injection of Gd-DTPA-BMA after 20 min of reperfusion. Radiolabeled microspheres were used to confirm zero-flow during the occlusion period and reperfusion in the infarcted myocardium. All pigs were killed 20 min after injection of contrast medium, and the hearts were excised and imaged with MR. The Gd concentration was measured in infarcted and nonischemic myocardium by ICPAES. In the reperfused hearts, the infarctions were strongly highlighted, corresponding to a 5-fold higher Gd concentration in infarcted vis-à-vis nonischemic myocardium. In the hearts subjected to occlusion without reperfusion, there was only a rim of enhancement in the peripheral part of the infarctions.
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Ristic-Andjelkov, Andjelka, Branislav Baskot, Milorad Damjanovic, and Sasa Rafajlovski. "Ischemic preconditioning." Vojnosanitetski pregled 62, no. 1 (2005): 73–77. http://dx.doi.org/10.2298/vsp0501073r.
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Background. Ischemic preconditioning is a phenomenon during which myocardium, subjected to brief episodes of ischemia followed by reperfusion, tolerates better the subsequent, more prolonged episode of this ischemia, thus reducing the infarction size substantially. Case report. Two patients with acute left anterior descendent artery occlusion received fibrinolytic therapy (alteplase) within 6 hours of the onset of chest pain, but developed myocardial infarctions of different sizes. The first patient, without the history of preinfarction angina, developed large anterior infarct, because there was no time either for ischemic preconditioning or for the coronary collateral vessels development. In the second patient, with 4-day history of preinfarction angina, the more favorable outcome was seen he developed smaller apical necrosis, with the great degree of myocardial viability in the infarct-related area. Conclusion. Ischemic preconditioning in patients with acute myocardal infarction results in the reduction of mortality, infarction size, as well as in the frequency of malignant arrhythmias.
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Spath, Nick B., Trisha Singh, Giorgos Papanastasiou, Andrew Baker, Rob J. Janiczek, Gerry P. McCann, Marc R. Dweck, Lucy Kershaw, David E. Newby, and Scott Semple. "Assessment of stunned and viable myocardium using manganese-enhanced MRI." Open Heart 8, no. 1 (June 2021): e001646. http://dx.doi.org/10.1136/openhrt-2021-001646.
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ObjectiveIn a proof-of-concept study, to quantify myocardial viability in patients with acute myocardial infarction using manganese-enhanced MRI (MEMRI), a measure of intracellular calcium handling.MethodsHealthy volunteers (n=20) and patients with ST-elevation myocardial infarction (n=20) underwent late gadolinium enhancement (LGE) using gadobutrol and MEMRI using manganese dipyridoxyl diphosphate. Patients were scanned ≤7 days after reperfusion and rescanned after 3 months. Differential manganese uptake was described using a two-compartment model.ResultsAfter manganese administration, healthy control and remote non-infarcted myocardium showed a sustained 25% reduction in T1 values (mean reductions, 288±34 and 281±12 ms). Infarcted myocardium demonstrated less T1 shortening than healthy control or remote myocardium (1157±74 vs 859±36 and 835±28 ms; both p<0.0001) with intermediate T1 values (1007±31 ms) in peri-infarct regions. Compared with LGE, MEMRI was more sensitive in detecting dysfunctional myocardium (dysfunctional fraction 40.5±11.9 vs 34.9%±13.9%; p=0.02) and tracked more closely with abnormal wall motion (r2=0.72 vs 0.55; p<0.0001). Kinetic modelling showed reduced myocardial manganese influx between remote, peri-infarct and infarct regions, enabling absolute discrimination of infarcted myocardium. After 3 months, manganese uptake increased in peri-infarct regions (16.5±3.5 vs 22.8±3.5 mL/100 g/min, p<0.0001), but not the remote (23.3±2.8 vs 23.0±3.2 mL/100 g/min, p=0.8) or infarcted (11.5±3.7 vs 14.0±1.2 mL/100 g/min, p>0.1) myocardium.ConclusionsThrough visualisation of intracellular calcium handling, MEMRI accurately differentiates infarcted, stunned and viable myocardium, and correlates with myocardial dysfunction better than LGE. MEMRI holds major promise in directly assessing myocardial viability, function and calcium handling across a range of cardiac diseases.Trial registration numbersNCT03607669; EudraCT number 2016-003782-25.
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Song, Yi-Sun, Hyun-Woo Joo, In-Hwa Park, Guang-Yin Shen, Yonggu Lee, Jeong Hun Shin, Hyuck Kim, Il-Seob Shin, and Kyung-Soo Kim. "Transplanted Human Amniotic Epithelial Cells Secrete Paracrine Proangiogenic Cytokines in Rat Model of Myocardial Infarctio." Cell Transplantation 24, no. 10 (October 2015): 2055–64. http://dx.doi.org/10.3727/096368914x685609.
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Jin, Jiyang, Min Chen, Yongjun Li, YaLing Wang, Shijun Zhang, Zhen Wang, Lin Wang, and Shenghong Ju. "Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers." Texas Heart Institute Journal 43, no. 5 (October 1, 2016): 383–91. http://dx.doi.org/10.14503/thij-15-5462.
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We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (<4 hr) after acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) (P=0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction—identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers.
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Bo, Yang, and Li Min. "GW24-e0030 A multi-nationality study on gender differences in anxiety early after acute myocardial infarctio." Heart 99, Suppl 3 (August 2013): A259.2—A259. http://dx.doi.org/10.1136/heartjnl-2013-304613.730.
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PETTERSEN, K. I. "When Time is Precious--Time Lags as Indicators of Quality of Care in Acute Myocardial Infarctio." International Journal for Quality in Health Care 7, no. 1 (March 1, 1995): 3–10. http://dx.doi.org/10.1093/intqhc/7.1.3.
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Nilsson, Stefan, Mats Wikström, Anders Ericsson, Gerhard Wikström, Anders Waldenström, Audun Øksendal, and Anders Hemmingsson. "MR Imaging of Double-Contrast Enhanced Porcine Myocardial Infarction." Acta Radiologica 36, no. 4-6 (July 1995): 346–52. http://dx.doi.org/10.1177/028418519503600404.
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MR imaging was performed to investigate whether Gd-DTPA-BMA-induced contrast enhancement of myocardial infarction is counteracted by Dy-DTPA-BMA. Myocardial infarction was induced in 5 pigs. Microdialysate probes were inserted in ischemic and nonischemic myocardium. Gd-DTPA-BMA (0.3 mmol/kg b.w.) and Dy-DTPA-BMA (1.0 mmol/kg b.w.) were administered i.v. 4 hours post occlusion. The microdialysate was collected every 10 min and measured for Gd and Dy using inductively coupled plasma atomic emission spectrometry. The pigs were sacrificed 2 hours after administration of contrast media. The concentration of both contrast agents was 3 times higher in infarcted myocardium than in nonischemic myocardium. The infarctions displayed high signal intensity in spin-echo sequences ex vivo. This lack of detectable susceptibility effects from Dy may be caused by loss of cell membrane integrity in infarcted tissue as shown by our microdialysate and biopsy data.
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Hirsch, Alan T., John A. Opsahl, Mary M. Lunzer, and Stephen A. Katz. "Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1818—H1826. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1818.
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The renin-angiotensin system promotes cardiac hypertrophy after myocardial infarction. The purpose of this study was to measure renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Infarction involving 45 ± 4% of left ventricular circumference with accompanying hypertrophy was induced in rats ( n = 14). Plasma and myocardial renin were increased after infarction compared with sham controls ( n = 8) (27.4 ± 3.2 vs. 7.5 ± 1.8 ng ANG I ⋅ ml plasma ⋅ h−1, P < 0.0002; and 8.8 ± 1.6 vs. 2.5 ± 0.1 ng ANG I ⋅ g myocardium−1 ⋅ h−1, P < 0.008, respectively). After infarction, myocardial renin was correlated with infarct size ( r = 0.62, P < 0.02) and plasma renin ( r = 0.55, P < 0.04). Plasma angiotensinogen decreased in infarct animals, but myocardial angiotensinogen was not different from shams (1.1 ± 0.08 vs. 2.03 ± 0.06 nM/ml plasma, P < 0.002; and 0.081 ± 0.008 vs. 0.070 ± 0.004 nM/g myocardium, respectively). In conclusion, myocardial renin increased after infarction in proportion to plasma renin and infarct size, and myocardial angiotensinogen was maintained after infarction despite decreased plasma angiotensinogen and increased levels of myocardial renin.
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Thukkani, Arun K., Bradley D. Martinson, Carolyn J. Albert, George A. Vogler, and David A. Ford. "Neutrophil-mediated accumulation of 2-ClHDA during myocardial infarction: 2-ClHDA-mediated myocardial injury." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (June 2005): H2955—H2964. http://dx.doi.org/10.1152/ajpheart.00834.2004.
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The pathophysiological sequelae of myocardial infarction include neutrophil infiltration into the infarct zone that contributes to additional damage to viable tissue and removal of cellular debris from necrosed tissue. Reactive chlorinating species produced by myeloperoxidase amplify the oxidant capacity of activated neutrophils. Plasmalogens are a major phospholipid subclass of both endothelial cells and cardiac myocytes. Recent studies have shown that plasmalogens are targeted by neutrophil-derived reactive chlorinating species that lead to the production of α-chloro fatty aldehydes. Results herein demonstrate that the α-chloro fatty aldehyde 2-chlorohexadecanal (2-ClHDA) accumulates in rat hearts subjected to left anterior descending coronary artery occlusion. Myocardia from rats subjected to surgical infarction had increased 2-ClHDA and neutrophil infiltration levels compared with myocardia from rats subjected to sham surgery. Additionally, infarcted myocardia from rats rendered neutropenic by treatments with an anti-neutrophil antibody had diminished 2-ClHDA and neutrophil infiltration levels compared with infarcted myocardia from normopenic rats; 2-ClHDA was shown to elicit myocardial damage as determined by lactate dehydrogenase release in isolated perfused rat hearts. Additionally, 2-ClHDA treatment of hearts resulted in decreased heart rate and ventricular performance. Taken together, the present results demonstrate a novel neutrophil-dependent myeloperoxidase-based mechanism that results in 2-ClHDA production in response to regional myocardial infarction that may also contribute to cardiac dysfunction.
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Gosselin, H., X. Qi, and J. L. Rouleau. "Correlation between cardiac remodelling, function, and myocardial contractility in rat hearts 5 weeks after myocardial infarction." Canadian Journal of Physiology and Pharmacology 76, no. 1 (January 1, 1998): 53–62. http://dx.doi.org/10.1139/y97-175.
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Early after infarction, ventricular dysfunction occurs as a result of loss of myocardial tissue. Although papillary muscle studies suggest that reduced myocardial contractility contributes to this ventricular dysfunction, in vivo studies indicate that at rest, cardiac output is normal or near normal, suggesting that contractility of the remaining viable myocardium of the ventricular wall is preserved. However, this has never been verified. To explore this further, 100 rats with various-sized myocardial infarctions had ventricular function assessed by Langendorff preparation or by isolated papillary muscle studies 5 weeks after infarction. Morphologic studies were also done. Rats with large infarctions (54%) had marked ventricular dilatation (dilatation index from 0.23 to 0.75, p << 0.01) and papillary muscle dysfunction (total tension from 6.7 to 3.2 g/mm2, p << 0.01) but only moderate left ventricular dysfunction (maximum developed tension from 206 to 151 mmHg (1 mmHg = 133.3 Pa), p << 0.01), a decrease less than one would expect with an infarct size of 54%. The contractility of the remaining viable myocardium of the ventricle was also moderately depressed (peak systolic midwall stress 91 to 60 mmHg, p << 0.01). Rats with moderate infarctions (32%) had less marked but still moderate ventricular dilatation (dilatation index 0.37, p << 0.001) and moderate papillary muscle dysfunction (total tension 4.2 g/mm2, p << 0.01). However, their decrease in ventricular function was only mild (maximum developed pressure 178 mmHg, p << 0.01) and less than one would expect with an infarct size of 32%. The remaining viable myocardium of the ventricular wall appeared to have normal contractility (peak systolic midwall stress = 86 mmHg, ns). We conclude that in this postinfarction model, in large myocardial infarctions, a loss of contractility of the remaining viable myocardium of the ventricular wall occurs as early as 5 weeks after infarction and that papillary muscle studies slightly overestimate the degree of ventricular dysfunction. In moderate infarctions, the remaining viable myocardium of the ventricular wall has preserved contractility while papillary muscle function is depressed. In this relatively early postinfarction phase, ventricular remodelling appears to help maintain left ventricular function in both moderate and large infarctions. Key words: postinfarction, contractility, ventricular function, ventricular remodelling.
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Berg, J., R. Jablonowski, D. Nordlund, S. Kopic, S. Bidhult, C. G. Xanthis, M. Saeed, K. Solem, H. Arheden, and M. Carlsson. "Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in stroke volume." Journal of Applied Physiology 128, no. 2 (February 1, 2020): 252–63. http://dx.doi.org/10.1152/japplphysiol.00480.2019.
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Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1–2 h after AMI in a microembolization model ( n = 12) and an ischemia-reperfusion model ( n = 14). A subset of pigs ( n = 7) were additionally imaged at 24 h and at 7 days. Cine and late gadolinium enhancement images were analyzed for cardiac function, AVPD measurements and infarct size estimation, respectively. AVPD decreased ( P < 0.05) in all myocardial regions after AMI, with a concomitant SV decrease ( P < 0.001). The ischemia-reperfusion model affected SV to a higher degree and had a larger AVPD decrease than the microembolization model (−29 ± 14% vs. −15 ± 18%; P < 0.05). Wall thickening decreased in infarcted areas ( P < 0.001), and A-wave AVPD remained unchanged ( P = 0.93) whereas E-wave AVPD decreased ( P < 0.001) after AMI. We conclude that AVPD is coupled to SV independent of infarct type but likely to a greater degree in ischemia-reperfusion infarcts compared with microembolization infarcts. AMI reduces diastolic early filling AVPD but not AVPD from atrial contraction. These findings shed light on the physiological significance of atrioventricular plane motion when assessing acute and subacute myocardial infarction. NEW & NOTEWORTHY The link between cardiac longitudinal motion, measured as atrioventricular plane displacement (AVPD), and stroke volume (SV) is investigated in swine after acute myocardial infarction (AMI). This cardiac magnetic resonance study demonstrates a close coupling between AVPD and SV before and after AMI in an experimental setting and demonstrates that this connection is present in ischemia-reperfusion and microembolization infarcts, acutely and during the first week. Furthermore, AVPD is equally and persistently depressed in infarcted and remote myocardium after AMI.
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Soepriatna, Arvin H., A. Kevin Yeh, Abigail D. Clifford, Semih E. Bezci, Grace D. O'Connell, and Craig J. Goergen. "Three-dimensional myocardial strain correlates with murine left ventricular remodelling severity post-infarction." Journal of The Royal Society Interface 16, no. 160 (November 2019): 20190570. http://dx.doi.org/10.1098/rsif.2019.0570.
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Heart failure continues to be a common and deadly sequela of myocardial infarction (MI). Despite strong evidence suggesting the importance of myocardial mechanics in cardiac remodelling, many MI studies still rely on two-dimensional analyses to estimate global left ventricular (LV) function. Here, we integrated four-dimensional ultrasound with three-dimensional strain mapping to longitudinally characterize LV mechanics within and around infarcts in order to study the post-MI remodelling process. To induce infarcts with varying severities, we separated 15 mice into three equal-sized groups: (i) sham, (ii) 30 min ischaemia–reperfusion, and (iii) permanent ligation of the left coronary artery. Four-dimensional ultrasound from a high-frequency small animal system was used to monitor changes in LV geometry, function and strain over 28 days. We reconstructed three-dimensional myocardial strain maps and showed that strain profiles at the infarct border followed a sigmoidal behaviour. We also identified that mice with mild remodelling had significantly higher strains in the infarcted myocardium than those with severe injury. Finally, we developed a new approach to non-invasively estimate infarct size from strain maps, which correlated well with histological results. Taken together, the presented work provides a thorough approach to quantify regional strain, an important component when assessing post-MI remodelling.
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Sawall, Stefan, Danielle Franke, Anne Kirchherr, Jan Beckendorf, Jan Kuntz, Joscha Maier, Alexander Kraupner, Johannes Backs, Andreas Briel, and Marc Kachelrieß. "In Vivo Quantification of Myocardial Infarction in Mice Using Micro-CT and a Novel Blood Pool Agent." Contrast Media & Molecular Imaging 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/2617047.
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We herein developed a micro-CT method using the innovative contrast agent ExiTron™ MyoC 8000 to longitudinally monitor cardiac processes in vivo in small animals. Experiments were performed on healthy mice and mice with myocardial infarction inflicted by ligation of the left anterior descending artery. Time-dependent signal enhancement in different tissues of healthy mice was measured and various contrast agent doses were investigated so as to determine the minimum required dose for imaging of the myocardium. Due to its ability to be taken up by healthy myocardium but not by infarct tissue, ExiTron MyoC 8000 enables detection of myocardial infarction even at a very low dose. The signal enhancement in the myocardium of infarcted mice after contrast agent injection was exploited for quantification of infarct size. The values of infarct size obtained from the imaging method were compared with those obtained from histology and showed a significant correlation (R2=0.98). Thus, the developed micro-CT method allows for monitoring of a variety of processes such as cardiac remodeling in longitudinal studies.
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Niccoli, Giampaolo, Rocco A. Montone, Borja Ibanez, Holger Thiele, Filippo Crea, Gerd Heusch, Heerajnarain Bulluck, et al. "Optimized Treatment of ST-Elevation Myocardial Infarction." Circulation Research 125, no. 2 (July 5, 2019): 245–58. http://dx.doi.org/10.1161/circresaha.119.315344.
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Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infarct size, has long been known to be an independent predictor for major adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction. Previous cardioprotection studies were mainly aimed at protecting cardiomyocytes and reducing infarct size. However, several clinical and preclinical studies have reported that the presence and extent of MVO represent another important independent predictor of adverse left ventricular remodeling, and recent evidences support the notion that MVO may be more predictive of major adverse cardiovascular events than infarct size itself. Although timely and complete reperfusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective therapeutic strategies into improved clinical outcomes has been largely disappointing. Of importance, despite the presence of a large number of studies focused on infarct size, only few cardioprotection studies addressed MVO as a therapeutic target. In this review, we provide a detailed summary of MVO including underlying causes, diagnostic techniques, and current therapeutic approaches. Furthermore, we discuss the hypothesis that simultaneously addressing infarct size and MVO may help to translate cardioprotective strategies into improved clinical outcome following ST-segment–elevation myocardial infarction.
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Širmenis, Raimondas, Antanas Kraniauskas, Rasa Jarašienė, Daiva Baltriukienė, Audronė Kalvelytė, and Virginija Bukelskienė. "Recovery of Infarcted Myocardium in an In Vivo Experiment." Medicina 47, no. 11 (December 4, 2011): 88. http://dx.doi.org/10.3390/medicina47110088.
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Acute myocardial infarction leads to the loss of functional cardiomyocytes and structural integrity. The adult heart cannot repair the damaged tissue due to inability of mature cardiomyocytes to divide and lack of stem cells. The aim of this study was to evaluate the efficiency of introduced autologous skeletal musclederived stem cells to recover the function of acutely infarcted rabbit heart in the early postoperative period. Material and Methods. As a model for myocardium restoration in vivo, experimental rabbit heart infarct was used. Autologic adult myogenic stem cells were isolated from skeletal muscle and propagated in culture. Before transplantation, the cells were labeled with 4´,6-diamidino-2-phenylindole and then, during heart surgery, introduced into the rabbit acutely infarcted myocardium. Postoperative cardiac function was monitored by recording electrocardiograms and echocardiograms. At the end of the experiment, the efficiency of cell integration was evaluated histologically. Results. Rabbit cardiac function recovered after 1 month after the induction of experimental infarction both in the control and experimental groups. Therefore, the first month after the infarction was the most significant for the assessment of cell transplantation efficacy. Transplanted cell integration into infarcted myocardium was time- and individual-dependent. Evaluation of changes in left ventricular ejection fraction after the induction of myocardial infarction revealed better recovery in the experimental group; however, the difference among animals in the experimental and control groups varied and was not significant. Conclusions. Autologous myogenic stem cells repopulated infarcted myocardium with different efficiency in each individual. This variability may account for the observed difference in postoperative cardiac recovery in a rabbit model.
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Li, Jianqiang, Danghui Sun, and Yue Li. "Novel Findings and Therapeutic Targets on Cardioprotection of Ischemia/ Reperfusion Injury in STEMI." Current Pharmaceutical Design 25, no. 35 (December 11, 2019): 3726–39. http://dx.doi.org/10.2174/1381612825666191105103417.
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Acute ST-segment elevation myocardial infarction (STEMI) remains a leading cause of morbidity and mortality around the world. A large number of STEMI patients after the infarction gradually develop heart failure due to the infarcted myocardium. Timely reperfusion is essential to salvage ischemic myocardium from the infarction, but the restoration of coronary blood flow in the infarct-related artery itself induces myocardial injury and cardiomyocyte death, known as ischemia/reperfusion injury (IRI). The factors contributing to IRI in STEMI are complex, and microvascular obstruction, inflammation, release of reactive oxygen species, myocardial stunning, and activation of myocardial cell death are involved. Therefore, additional cardioprotection is required to prevent the heart from IRI. Although many mechanical conditioning procedures and pharmacological agents have been identified as effective cardioprotective approaches in animal studies, their translation into the clinical practice has been relatively disappointing due to a variety of reasons. With new emerging data on cardioprotection in STEMI over the past few years, it is mandatory to reevaluate the effectiveness of “old” cardioprotective interventions and highlight the novel therapeutic targets and new treatment strategies of cardioprotection.
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Spath, N. B., D. M. L. Lilburn, G. A. Gray, L. M. Le Page, G. Papanastasiou, R. J. Lennen, R. L. Janiczek, et al. "Manganese-Enhanced T1 Mapping in the Myocardium of Normal and Infarcted Hearts." Contrast Media & Molecular Imaging 2018 (October 25, 2018): 1–13. http://dx.doi.org/10.1155/2018/9641527.
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Background. Manganese-enhanced MRI (MEMRI) has the potential to identify viable myocardium and quantify calcium influx and handling. Two distinct manganese contrast media have been developed for clinical application, mangafodipir and EVP1001-1, employing different strategies to mitigate against adverse effects resulting from calcium-channel agonism. Mangafodipir delivers manganese ions as a chelate, and EVP1001-1 coadministers calcium gluconate. Using myocardial T1 mapping, we aimed to explore chelated and nonchelated manganese contrast agents, their mechanism of myocardial uptake, and their application to infarcted hearts. Methods. T1 mapping was performed in healthy adult male Sprague-Dawley rats using a 7T MRI scanner before and after nonchelated (EVP1001-1 or MnCl2 (22 μmol/kg)) or chelated (mangafodipir (22–44 μmol/kg)) manganese-based contrast media in the presence of calcium channel blockade (diltiazem (100–200 μmol/kg/min)) or sodium chloride (0.9%). A second cohort of rats underwent surgery to induce anterior myocardial infarction by permanent coronary artery ligation or sham surgery. Infarcted rats were imaged with standard gadolinium delayed enhancement MRI (DEMRI) with inversion recovery techniques (DEMRI inversion recovery) as well as DEMRI T1 mapping. A subsequent MEMRI scan was performed 48 h later using either nonchelated or chelated manganese and T1 mapping. Finally, animals were culled at 12 weeks, and infarct size was quantified histologically with Masson’s trichrome (MTC). Results. Both manganese agents induced concentration-dependent shortening of myocardial T1 values. This was greatest with nonchelated manganese, and could be inhibited by 30–43% with calcium-channel blockade. Manganese imaging successfully delineated the area of myocardial infarction. Indeed, irrespective of the manganese agent, there was good agreement between infarct size on MEMRI T1 mapping and histology (bias 1.4%, 95% CI −14.8 to 17.1 P>0.05). In contrast, DEMRI inversion recovery overestimated infarct size (bias 11.4%, 95% CI −9.1 to 31.8 P=0.002), as did DEMRI T1 mapping (bias 8.2%, 95% CI −10.7 to 27.2 P=0.008). Increased manganese uptake was also observed in the remote myocardium, with remote myocardial ∆T1 inversely correlating with left ventricular ejection fraction after myocardial infarction (r=−0.61, P=0.022). Conclusions. MEMRI causes concentration and calcium channel-dependent myocardial T1 shortening. MEMRI with T1 mapping provides an accurate assessment of infarct size and can also identify changes in calcium handling in the remote myocardium. This technique has potential applications for the assessment of myocardial viability, remodelling, and regeneration.
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Nilsson, Stefan, Mats Wikström, Hans J. Martinussen, Anders Ericsson, Gerhard Wikström, Anders Waldenström, Audun N. Øksendal, and Anders Hemmingsson. "Dy-DTPA-BMA as an Indicator of Tissue Viability in MR Imaging." Acta Radiologica 36, no. 4-6 (July 1995): 338–45. http://dx.doi.org/10.1177/028418519503600403.
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The aim of this study was to investigate whether dysprosium (Dy) induced signal intensity (SI) loss in infarcted tissue in MR imaging. Myocardial infarction was induced in 12 pigs and Dy-DTPA-BMA (1.0 mmol/kg b.w.) was administered i.v. to 6 pigs 4 hours after occlusion and allowed to accumulate in the infarctions for 2 hours. Dy was analysed by inductively coupled plasma atomic emission spectrometry in infarcted and non-ischaemic tissue samples. The remaining 6 pigs, not administered contrast medium, served as controls. The infarctions demonstrated a high SI in the proton density- and T2-weighted sequences in both groups ( ex vivo), although the Dy-DTPA-BMA group demonstrated a 3-fold greater concentration of Dy in infarcted compared with non-ischaemic myocardium. The lack of SI loss after Dy accumulation indicates that susceptibility effects are minor or absent in infarcted myocardium.
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Jiang, Yi, Jianwen Bai, Lunxian Tang, Pei Zhang, and Jun Pu. "Anti-CCL21 Antibody Attenuates Infarct Size and Improves Cardiac Remodeling After Myocardial Infarction." Cellular Physiology and Biochemistry 37, no. 3 (2015): 979–90. http://dx.doi.org/10.1159/000430224.
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Background/Aims: Over-activation of cellular inflammatory effectors adversely affects myocardial function after acute myocardial infarction (AMI). The CC-chemokine CCL21 is, via its receptor CCR7, one of the key regulators of inflammation and immune cell recruitment, participates in various inflammatory disorders, including cardiovascular ones. This study explored the therapeutic effect of an anti-CCL21 antibody in cardiac remodeling after myocardial infarction. Methods and Results: An animal model of AMI generated by left anterior descending coronary artery ligation in C57BL/6 mice resulted in higher levels of circulating CCL21 and cardiac CCR7. Neutralization of CCL21 by intravenous injection of anti-CCL21 monoclonal antibody reduced infarct size after AMI, decreased serum levels of neutrophil and monocyte chemo attractants post AMI, diminished neutrophil and macrophage recruitment in infarcted myocardium, and suppressed MMP-9 and total collagen content in myocardium. Anti-CCL21 treatment also limited cardiac enlargement and improved left ventricular function. Conclusions: Our study indicated that CCL21 was involved in cardiac remodeling post infarction and anti-CCL21 strategies might be useful in the treatment of AMI.
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Li, Yingxu, Bing Li, Xuechun Wang, Yan Meng, Lu Bai, and Yuanyuan Zheng. "Safe and efficient magnetic resonance imaging of acute myocardial infarction with gadolinium-doped carbon dots." Nanomedicine 15, no. 24 (October 2020): 2385–98. http://dx.doi.org/10.2217/nnm-2020-0160.
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Aim: The magneto-fluorescent gadolinium-doped carbon dots (Gd-CDs) were developed as a cardiac MR imaging contrast agent to detect the infarcted myocardium on a myocardial ischemia/reperfusion (I/R) mice model. Materials & methods: The chemophysical features, cardiac MR imaging effect, biodistribution and biocompatibility of Gd-CDs were studied. Results: The ultrasmall size and good aqueous dispersibility endows Gd-CDs with high longitudinal relaxivity, intense fluorescence, excellent physiological stability and superior biocompatibility. More importantly, Gd-CDs preferentially target the infarcts as determined by the confocal microscopy and MR imaging on the I/R mice at the acute stage of myocardial infarction. Conclusion: Gd-CDs manifest great potential for development as an MR imaging contrast agent to facilitate accurate visualization and image-guided therapy of acute myocardial infarction.
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Nilsson, S., G. Wikström, A. Ericsson, M. Wikström, A. Øksendal, A. Waldenström, and A. Hemmingsson. "Myocardial Cell Death in Reperfused and Nonreperfused Myocardial Infarctions." Acta Radiologica 37, no. 1P1 (January 1996): 18–26. http://dx.doi.org/10.1177/02841851960371p105.
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Purpose: To investigate whether Dy-DTPA-BMA-enhanced MR imaging would permit identification of myocardial cell death, myocardial infarction was induced in 12 domestic pigs. Material and Methods: In 6 pigs with irreversible cell damage, Dy-DTPA-BMA (1.0 mmol/kg b.w.) was administered i.v. 70 min after coronary occlusion. In 6 other pigs, the infarctions were reperfused 80 min after the occlusion, followed by injection of Dy-DTPA-BMA after 30 min of reperfusion. In 4 additional pigs, the hearts were reperfused after 2 min of occlusion. All 16 pigs were sacrificed 10 min after the injection of Dy-DTPA-BMA. The hearts were excised and imaged with MR. Results: Reversibly injured myocardium could not be distinguished from adjacent nonischaemic myocardium after the administration of Dy-DTPA-BMA. Reperfused, infarcted myocardium demonstrated a high signal intensity in the proton-density- and T2-weighted sequences, despite a 5-fold higher Dy concentration compared with both nonreperfused infarcted and nonischaemic myocardium. Conclusion: This lack of susceptibility effect in infarcted myocardium, due to a homogeneous distribution of Dy, indicates the usefulness of Dy as a marker of tissue viability.
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Kalinowski, Leszek, Lawrence W. Dobrucki, David F. Meoli, Donald P. Dione, Mehran M. Sadeghi, Joseph A. Madri, and Albert J. Sinusas. "Targeted imaging of hypoxia-induced integrin activation in myocardium early after infarction." Journal of Applied Physiology 104, no. 5 (May 2008): 1504–12. http://dx.doi.org/10.1152/japplphysiol.00861.2007.
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The αvβ3-integrin is expressed in angiogenic vessels in response to hypoxia and represents a potential novel target for imaging myocardial angiogenesis. This study evaluated the feasibility of noninvasively tracking hypoxia-induced αvβ3-integrin activation within the myocardium as a marker of angiogenesis early after myocardial infarction. Acute myocardial infarction was produced by coronary artery occlusion in rodent and canine studies. A novel 111In-labeled radiotracer targeted at the αvβ3-integrin (111In-RP748) was used to localize regions of hypoxia-induced angiogenesis early after infarction. In rodent studies, the specificity of 111In-RP748 for αvβ3-integrin was confirmed with a negative control compound (111In-RP790), and regional uptake of these compounds correlated with 201Tl perfusion and a 99mTc-labeled nitroimidazole (BRU59-21), which was used as a quantitative marker of myocardial hypoxia. The ex vivo analysis demonstrated that only 111In-RP748 was selectively retained in infarcted regions with reduced 201Tl perfusion and correlated with uptake of BRU59-21. In canine studies, myocardial uptake of 111In-RP748 was assessed using in vivo single-photon-emission computed tomography (SPECT), ex vivo planar imaging, and gamma well counting of myocardial tissue and correlated with 99mTc-labeled 2-methoxy-2-methyl-propyl-isonitrile (99mTc-sestamibi) perfusion. Dual-radiotracer in vivo SPECT imaging of 111In-RP748 and 99mTc-sestamibi provided visualization of 111In-RP748 uptake within the infarct region, which was confirmed by ex vivo planar imaging of excised myocardial slices. Myocardial 111In-RP748 retention was associated with histological evidence of αvβ3-integrin expression/activation in the infarct region. 111In-RP748 imaging provides a novel noninvasive approach for evaluation of hypoxia-induced αvβ3-integrin activation in myocardium early after infarction and may prove useful for directing and evaluating angiogenic therapies in patients with ischemic heart disease.
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Chilukoti, Ravi K., Josefine Lendeckel, Katrin Darm, Alicja Bukowska, Andreas Goette, Marc Sühling, Kirsten Utpatel, et al. "Integration of “omics” techniques: Dronedarone affects cardiac remodeling in the infarction border zone." Experimental Biology and Medicine 243, no. 11 (July 2018): 895–910. http://dx.doi.org/10.1177/1535370218788517.
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Dronedarone improves microvascular flow during atrial fibrillation and reduces the infarct size in acute models of myocardial infarction. However, dronedarone might be harmful in patients with recent decompensated heart failure and increases mortality in patients with permanent atrial fibrillation. A pathophysiological explanation for these discrepant data is lacking. This study investigated the effects of dronedarone on gene and protein expression in the infarcted area and border zone in pigs subjected to anterior ischemia/reperfusion myocardial infarction. The ischemia/reperfusion myocardial infarction was induced in 16 pigs. Eight pigs were treated with dronedarone for 28 days after myocardial infarction, the remaining pigs served as control. Microarray-based transcriptome profiling and 2D-DIGE-based proteome analysis were used to assess the effects of dronedarone on left ventricular gene expression in healthy (LV), infarcted (MI), and border zone tissue. Selected targets were validated by RT-qPCR or immunoblot analyses, with special emphasize given to the transcriptome/proteome overlap. Combined “omics” analysis was performed to identify most significant disease and function charts affected by dronedarone and to establish an integrated network. The levels of 879 (BZ) or 7 (MI) transcripts and 51 (LV) or 15 (BZ) proteins were significantly altered by dronedarone, pointing to a substantial efficacy of dronedarone in the border zone. Transcriptome and proteome data indicate that dronedarone influences post-infarction remodeling processes and identify matricellular proteins as major targets of dronedarone in this setting. This finding is fully supported by the disease and function charts as well as by the integrated network established by combined “omics”. Dronedarone therapy alters myocardial gene expression after acute myocardial infarction with pronounced effects in the border zone. Dronedarone promotes infarct healing via regulation of periostin and might contribute to the limitation of its expansion as well as cardiac rupture. Thus, there are no experimental hints that dronedarone per se has direct harmful effects after MI in ventricular tissue. Impact statement Dronedarone reduced the infarct size in models of acute myocardial infarction (MI). Here, we show that dronedarone attenuates many of the substantial changes in gene expression that are provoked by acute myocardial infarction (AMI) in pigs. Dronedarone modifies the expression of gene panels related to post-infarction cardiac healing and remodeling processes and, most remarkably, this occurs predominantly in the infarction border-zone and much less so in the vital or infarcted myocardium. Combined “omics” identified matricellular proteins and ECM as major dronedarone-regulated targets and emphasizes their relevance for Disease Charts and Tox Function Charts associated with tissue remodeling and cellular movement. The results demonstrate dronedarone’s capability of regulating cardiac repair and remodeling processes specifically in the infarction border zone and identify underlying mechanisms and pathways that might be employed in future therapeutic strategies to improve long-term cardiac tissue function and stability.
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Henning, Robert J., Jose D. Burgos, Mark Vasko, Felipe Alvarado, Cyndy D. Sanberg, Paul R. Sanberg, and Michael B. Morgan. "Human Cord Blood Cells and Myocardial Infarction: Effect of Dose and Route of Administration on Infarct Size." Cell Transplantation 16, no. 9 (October 2007): 907–17. http://dx.doi.org/10.3727/096368907783338299.
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There is no consensus regarding the optimal dose of stem cells or the optimal route of administration for the treatment of acute myocardial infarction. Bone marrow cells, containing hematopoietic and mesenchymal stem cells, in doses of 0.5 × 106 to >30 × 106 have been directly injected into the myocardium or into coronary arteries or infused intravenously in subjects with myocardial infarctions to reduce infarct size and improve heart function. Therefore, we determined the specific effects of different doses of human umbilical cord blood mononuclear cells (HUCBC), which contain hematopoietic and mesenchymal stem cells, on infarct size. In order to determine the optimal technique for stem cell administration, HUCBC were injected directly into the myocardium (IM), or into the LV cavity with the ascending aorta transiently clamped to facilitate coronary artery perfusion (IA), or injected intravenously (IV) in rats 1–2 h after the left anterior coronary artery was permanently ligated. Immune suppressive therapy was not given to any rat. One month later, the infarct size in control rat hearts treated with only Isolyte averaged 23.7 ± 1.7% of the LV muscle area. Intramyocardial injection of HUCBC reduced the infarct size by 71% with 0.5 × 106 HUCBC and by 93% with 4 × 106 HUCBC in comparison with the controls (p < 0. 001). Intracoronary injection reduced the infarction size by 47% with 0.5 × 106 HUCBC and by 80% with 4 × 106 HUCBC (p < 0. 001), and IV HUCBC reduced infarct size by 51% with 0.5 × 106 and by 75–77% with 16–32 million HUCBC (p < 0. 001) in comparison with control hearts. With 4 × 106 HUCBC, infarction size was 65% smaller with IM HUCBC than with IA HUCBC and 78% smaller than with IV HUCBC (p < 0. 05). Nevertheless, IM, IA, and IV HUCBC all produced significant reductions in infarct size in comparison with Isolyte-treated infarcted hearts without requirements for host immune suppression. The present experiments demonstrate that the optimal dose of HUCBC for reduction of infarct size in the rat is 4 × 106 IM, 4 × 106 IA, and 16 × 106 IV, and that the IM injection of HUCBC is the most effective technique for reduction in infarct size.
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Helle-Valle, Thomas, Espen W. Remme, Erik Lyseggen, Eirik Pettersen, Trond Vartdal, Anders Opdahl, Hans-Jørgen Smith, et al. "Clinical assessment of left ventricular rotation and strain: a novel approach for quantification of function in infarcted myocardium and its border zones." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 1 (July 2009): H257—H267. http://dx.doi.org/10.1152/ajpheart.01116.2008.
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Left ventricular (LV) circumferential strain and rotation have been introduced as clinical markers of myocardial function. This study investigates how regional LV apical rotation and strain can be used in combination to assess function in the infarcted ventricle. In healthy subjects ( n = 15) and patients with myocardial infarction ( n = 23), LV apical segmental rotation and strain were measured from apical short-axis recordings by speckle tracking echocardiography (STE) and MRI tagging. Infarct extent was determined by late gadolinium enhancement MRI. To investigate mechanisms of changes in strain and rotation, we used a mathematical finite element simulation model of the LV. Mean apical rotation and strain by STE were lower in patients than in healthy subjects (9.0 ± 4.9 vs. 12.9 ± 3.5° and −13.9 ± 10.7 vs. −23.8 ± 2.3%, respectively, P < 0.05). In patients, regional strain was reduced in proportion to segmental infarct extent ( r = 0.80, P < 0.0001). Regional rotation, however, was similar in the center of the infarct and in remote viable myocardium. Minimum and maximum rotations were found at the infarct borders: minimum rotation at the border zone opposite to the direction of apical rotation, and maximum rotation at the border zone in the direction of rotation. The simulation model reproduced the clinical findings and indicated that the dissociation between rotation and strain was caused by mechanical interactions between infarcted and viable myocardium. Systolic strain reflects regional myocardial function and infarct extent, whereas systolic rotation defines infarct borders in the LV apical region. Regional rotation, however, has limited ability to quantify regional myocardial dysfunction.
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Grothusen, Christina, Angelika Hagemann, Tim Attmann, Jan Braesen, Ole Broch, Jochen Cremer, and Jan Schoettler. "Impact of an Interleukin-1 Receptor Antagonist and Erythropoietin on Experimental Myocardial Ischemia/Reperfusion Injury." Scientific World Journal 2012 (2012): 1–6. http://dx.doi.org/10.1100/2012/737585.
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Background. Revascularization of infarcted myocardium results in release of inflammatory cytokines mediating myocardial reperfusion injury and heart failure. Blockage of inflammatory pathways dampens myocardial injury and reduces infarct size. We compared the impact of the interleukin-1 receptor antagonist Anakinra and erythropoietin on myocardial ischemia/reperfusion injury. In contrast to others, we hypothesized that drug administration prior to reperfusion reduces myocardial damage.Methods and Results. 12–15 week-old Lewis rats were subjected to myocardial ischemia by a 1 hr occlusion of the left anterior descending coronary artery. After 15 min of ischemia, a single shot of Anakinra (2 mg/kg body weight (bw)) or erythropoietin (5000 IE/kg bw) was administered intravenously. In contrast to erythropoietin, Anakinra decreased infarct size (P<0.05,N=4/group) and troponin T levels (P<0.05,N=4/group).Conclusion. One-time intravenous administration of Anakinra prior to myocardial reperfusion reduces infarct size in experimental ischemia/reperfusion injury. Thus, Anakinra may represent a treatment option in myocardial infarction prior to revascularization.
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Buttrick, P., C. Perla, A. Malhotra, D. Geenen, M. Lahorra, and J. Scheuer. "Effects of chronic dobutamine on cardiac mechanics and biochemistry after myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 2 (February 1, 1991): H473—H479. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h473.
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After myocardial infarction in rats, muscle performance in the remaining hypertrophied myocardium deteriorates and is associated with a decrease in myosin adenosinetriphosphatase (ATPase) activity and a shift to the V3 myosin heavy-chain isoform. We have previously shown in another model of hypertrophy, secondary to renovascular hypertension, that chronic intermittent adrenergic stimulation with dobutamine (Db) can prevent this biochemical adaptation. The present study was undertaken to assess the effects of chronic Db treatment on cardiac mass, function, metabolism, and myosin biochemistry in animals subjected to chronic myocardial infarction. Four groups of rats were studied: controls, animals treated with Db (2 mg/kg 2X daily for 4 wk), animals subjected to myocardial infarction and killed after 4 wk (MI), and MI animals concurrently treated with Db for 4 wk (MI-Db). The two MI groups were subdivided into those with and without congestive heart failure (CHF). Heart weight was increased by 13% with Db, unchanged in the infarct groups without CHF, and increased by 9 and 22% in the infarct groups with CHF. Db did not have any additional effect on heart weight in these later groups. Infarct weight was greatest in the animals with CHF, and viable myocardium was equivalent in all infarct groups suggesting that CHF was associated with a greater degree of hypertrophy. Ventricular performance, as assessed in an isovolumic heart apparatus, was markedly depressed in both infarct groups with CHF and was not affected by Db. Db increased myosin ATPase activity in control and infarcted animals both with and without congestive heart failure. Myosin oxygen consumption and lactate production were not adversely affected by Db.
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Liu, Chunping, Zhijin Fan, Dongyue He, Huiqi Chen, Shihui Zhang, Sien Guo, Bojun Zheng, et al. "Designer Functional Nanomedicine for Myocardial Repair by Regulating the Inflammatory Microenvironment." Pharmaceutics 14, no. 4 (March 31, 2022): 758. http://dx.doi.org/10.3390/pharmaceutics14040758.
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Acute myocardial infarction is a major global health problem, and the repair of damaged myocardium is still a major challenge. Myocardial injury triggers an inflammatory response: immune cells infiltrate into the myocardium while activating myofibroblasts and vascular endothelial cells, promoting tissue repair and scar formation. Fragments released by cardiomyocytes become endogenous “danger signals”, which are recognized by cardiac pattern recognition receptors, activate resident cardiac immune cells, release thrombin factors and inflammatory mediators, and trigger severe inflammatory responses. Inflammatory signaling plays an important role in the dilation and fibrosis remodeling of the infarcted heart, and is a key event driving the pathogenesis of post-infarct heart failure. At present, there is no effective way to reverse the inflammatory microenvironment in injured myocardium, so it is urgent to find new therapeutic and diagnostic strategies. Nanomedicine, the application of nanoparticles for the prevention, treatment, and imaging of disease, has produced a number of promising applications. This review discusses the treatment and challenges of myocardial injury and describes the advantages of functional nanoparticles in regulating the myocardial inflammatory microenvironment and overcoming side effects. In addition, the role of inflammatory signals in regulating the repair and remodeling of infarcted hearts is discussed, and specific therapeutic targets are identified to provide new therapeutic ideas for the treatment of myocardial injury.
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Berry, Mark F., Adam J. Engler, Y. Joseph Woo, Timothy J. Pirolli, Lawrence T. Bish, Vasant Jayasankar, Kevin J. Morine, Timothy J. Gardner, Dennis E. Discher, and H. Lee Sweeney. "Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (June 2006): H2196—H2203. http://dx.doi.org/10.1152/ajpheart.01017.2005.
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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSCs) into the acutely ischemic myocardium. Two weeks postinfarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were twofold stiffer than myocardium from noninfarcted animals but softer than myocardium from vehicle-treated infarcted animals. After 8 wk, the following variables were evaluated: MSC engraftment and left ventricular geometry by histological methods, cardiac function with a pressure-volume conductance catheter, myocardial fibrosis by Masson Trichrome staining, vascularity by immunohistochemistry, and apoptosis by TdT-mediated dUTP nick-end labeling assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated postinfarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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Vasudevan, Praveen, Ralf Gaebel, Piet Doering, Paula Mueller, Heiko Lemcke, Jan Stenzel, Tobias Lindner, et al. "18F-FDG PET-Based Imaging of Myocardial Inflammation Predicts a Functional Outcome Following Transplantation of mESC-Derived Cardiac Induced Cells in a Mouse Model of Myocardial Infarction." Cells 8, no. 12 (December 11, 2019): 1613. http://dx.doi.org/10.3390/cells8121613.
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Cellular inflammation following acute myocardial infarction has gained increasing importance as a target mechanism for therapeutic approaches. We sought to investigate the effect of syngeneic cardiac induced cells (CiC) on myocardial inflammation using 18F-FDG PET (Positron emission tomography)-based imaging and the resulting effect on cardiac pump function using cardiac magnetic resonance (CMR) imaging in a mouse model of myocardial infarction. Mice underwent permanent left anterior descending coronary artery (LAD) ligation inducing an acute inflammatory response. The therapy group received an intramyocardial injection of 106 CiC into the border zone of the infarction. Five days after myocardial infarction, 18F-FDG PET was performed under anaesthesia with ketamine and xylazine (KX) to image the inflammatory response in the heart. Flow cytometry of the mononuclear cells in the heart was performed to analyze the inflammatory response. The effect of CiC therapy on cardiac function was determined after three weeks by CMR. The 18F-FDG PET imaging of the heart five days after myocardial infarction (MI) revealed high focal tracer accumulation in the border zone of the infarcted myocardium, whereas no difference was observed in the tracer uptake between infarct and remote myocardium. The CiC transplantation induced a shift in 18F-FDG uptake pattern, leading to significantly higher 18F-FDG uptake in the whole heart, as well as the remote area of the heart. Correspondingly, high numbers of CD11+ cells could be measured by flow cytometry in this region. The CiC transplantation significantly improved the left ventricular ejection function (LVEF) three weeks after myocardial infarction. The CiC transplantation after myocardial infarction leads to an improvement in pump function through modulation of the cellular inflammatory response five days after myocardial infarction. By combining CiC transplantation and the cardiac glucose uptake suppression protocol with KX in a mouse model, we show for the first time, that imaging of cellular inflammation after myocardial infarction using 18F-FDG PET can be used as an early prognostic tool for assessing the efficacy of cardiac stem cell therapies.
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Janes, R. D., D. E. Johnstone, and J. A. Armour. "Functional integrity of intrinsic cardiac nerves located over an acute transmural myocardial infarction." Canadian Journal of Physiology and Pharmacology 65, no. 1 (January 1, 1987): 64–69. http://dx.doi.org/10.1139/y87-012.
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Acute transmural myocardial infarction has been reported to functionally denervate the normal myocardium distal to the infarcted zone by interrupting neurotransmission in axons coursing in the subepicardial region of the myocardial necrosis. To directly investigate the viability of such neurotransmission, the effects of acute transmural myocardial infarction on conduction in the intrinsic cardiac nerves overlying and distal to an experimentally induced acute transmural myocardial infarction were studied. In eight dogs, during control states electrical stimulation of the epicardium adjacent to a coronary artery produced compound action potentials in the more cranially located cardiopulmonary nerves. Thereafter, in four dogs an acute transmural myocardial infarction was produced by injecting rapidly hardening latex into a major diagonal branch of the left anterior descending coronary artery. Epicardial stimulation over the infarct, as well as proximal or distal to it, produced compound action potentials that conducted at normal velocities for at least 12 h postinfarction. The transmural extent of the infarct was verified with tetrazolium blue staining at the end of the experiment. In the other four dogs, compound action potentials were generated in cardiopulmonary nerves as described above and then ventricular fibrillation was produced to assess the effects of global anoxia on the function of axons coursing in cardiac nerves. Following the onset of ventricular fibrillation, compound action potentials were generated in these nerves in C fibers for up to 2 h, in B fibers for up to 4 h, and in A fibers for at least 12 h. However, the conduction velocities of these axons was gradually reduced over these periods of time, indicating that, in contrast to the function of axons coursing over a transmural myocardial infarction, their function gradually deteriorated. Thus, by directly assessing the function of axons coursing over a transmural infarction, it is concluded that an acute transmural myocardial infarction does not significantly modify the function of intrinsic cardiac nerves coursing over such an infarct.
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Hiesinger, William, Sergei A. Vinogradov, Pavan Atluri, J. Raymond Fitzpatrick, John R. Frederick, Rebecca D. Levit, Ryan C. McCormick, et al. "Oxygen-dependent quenching of phosphorescence used to characterize improved myocardial oxygenation resulting from vasculogenic cytokine therapy." Journal of Applied Physiology 110, no. 5 (May 2011): 1460–65. http://dx.doi.org/10.1152/japplphysiol.01138.2010.
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This study evaluates a therapy for infarct modulation and acute myocardial rescue and utilizes a novel technique to measure local myocardial oxygenation in vivo. Bone marrow-derived endothelial progenitor cells (EPCs) were targeted to the heart with peri-infarct intramyocardial injection of the potent EPC chemokine stromal cell-derived factor 1α (SDF). Myocardial oxygen pressure was assessed using a noninvasive, real-time optical technique for measuring oxygen pressures within microvasculature based on the oxygen-dependent quenching of the phosphorescence of Oxyphor G3. Myocardial infarction was induced in male Wistar rats ( n = 15) through left anterior descending coronary artery ligation. At the time of infarction, animals were randomized into two groups: saline control ( n = 8) and treatment with SDF ( n = 7). After 48 h, the animals underwent repeat thoracotomy and 20 μl of the phosphor Oxyphor G3 was injected into three areas (peri-infarct myocardium, myocardial scar, and remote left hindlimb muscle). Measurements of the oxygen distribution within the tissue were then made in vivo by applying the end of a light guide to the beating heart. Compared with controls, animals in the SDF group exhibited a significantly decreased percentage of hypoxic (defined as oxygen pressure ≤ 15.0 Torr) peri-infarct myocardium (9.7 ± 6.7% vs. 21.8 ± 11.9%, P = 0.017). The peak oxygen pressures in the peri-infarct region of the animals in the SDF group were significantly higher than the saline controls (39.5 ± 36.7 vs. 9.2 ± 8.6 Torr, P = 0.02). This strategy for targeting EPCs to vulnerable peri-infarct myocardium via the potent chemokine SDF-1α significantly decreased the degree of hypoxia in peri-infarct myocardium as measured in vivo by phosphorescence quenching. This effect could potentially mitigate the vicious cycle of myocyte death, myocardial fibrosis, progressive ventricular dilatation, and eventual heart failure seen after acute myocardial infarction.
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Zheng, Wei, Robert M. Weiss, Xinguo Wang, Ruifeng Zhou, Angie M. Arlen, Li Lei, Eric Lazartigues, and Robert J. Tomanek. "DITPA stimulates arteriolar growth and modifies myocardial postinfarction remodeling." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (May 2004): H1994—H2000. http://dx.doi.org/10.1152/ajpheart.00991.2003.
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Myocardial infarction (MI) is characterized by ventricular remodeling, hypertrophy of the surviving myocardium, and an insufficient angiogenic response. Thyroxine is a powerful stimulus for myocardial angiogenesis. Male rats that underwent coronary artery ligation and subsequent MI were given 3,5-diiodothyropropionic acid (DITPA; MI+DITPA group) during a 3-wk period. We evaluated ventricular remodeling using echocardiography and histology and myocardial vessel growth using image analysis. Protein expression was assessed using Western blotting and immunohistochemistry. This study tested the hypothesis that the thyroxine analog DITPA facilitates angiogenesis and influences postinfarction remodeling in the surviving hypertrophic myocardium. The increase in the region of akinesis (infarct expansion) was blunted in the MI+DITPA rats compared with the MI group (3 vs. 21%); the treated rats had smaller percent increases in the left ventricular (LV) volume (64 ± 14 vs. 95 ± 12) and the LV volume-to-mass ratio (47 ± 13 vs. 84 ± 10) as well as a blunted decrease in ejection fraction (–9 ± 8 vs. –30 ± 7%). Arteriolar length density was higher after treatment in the largest (>50% of the free wall) infarcts (64 ± 3 vs. 43 ± 7). Angiogenic growth factors [vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF)] and the angiopoietin receptor tyrosine kinase with immunoglobulin and epidermal growth factor homology domains (Tie-2) values were elevated during the first week after infarction. DITPA did not cause additional increases in VEGF or Tie-2 values but did induce an increase in bFGF value after 3 days of treatment. This study provides the first evidence for an anatomical basis, i.e., attenuated ventricular remodeling and arteriolar growth, for improved function attributed to DITPA therapy of the infarcted heart. The favorable influences of DITPA on LV remodeling after large infarction are principally due to border zone preservation.
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Mochizuki, Teruhito, Kenya Murase, Hiroshi Higashino, Masao Miyagawa, Yoshifumi Sugawara, Takanori Kikuchi, and Junpei Ikezoe. "Ischemic “memory image” in acute myocardial infarctio of123I-BMIPP after reperfusion therapy: A comparison with99mTc-pyrophosphate and201Tl dual-isotope SPECT." Annals of Nuclear Medicine 16, no. 8 (December 2002): 563–68. http://dx.doi.org/10.1007/bf02988634.
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Akhmedov, Alexander, Fabrizio Montecucco, Sarah Costantino, Daria Vdovenko, Ariane Schaub Clerigué, Daniel S. Gaul, Fabienne Burger, et al. "Cardiomyocyte-Specific JunD Overexpression Increases Infarct Size following Ischemia/Reperfusion Cardiac Injury by Downregulating Sirt3." Thrombosis and Haemostasis 120, no. 01 (December 13, 2019): 168–80. http://dx.doi.org/10.1055/s-0039-3400299.
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AbstractIschemia/reperfusion (I/R) injury in acute myocardial infarction activates several deleterious molecular mechanisms. The transcription factor JunD regulates pathways involved in oxidative stress as well as in cellular proliferation, differentiation, and death. The present study investigated the potential role of JunD as a modulator of myocardial injury pathways in a mouse model of cardiac I/R injury. Infarct size, systemic and local inflammation, and production of reactive oxygen species, as well as cytosolic and mitochondrial apoptotic pathways were investigated in adult males after myocardial I/R. In wild-type (WT) mice, 30 minutes after ischemia and up to 24 hours following reperfusion, cardiac JunD messenger ribonucleic acid expression was reduced while JunB increased. Cardiac-specific JunD overexpressing mice (JunDTg/0 ) displayed larger infarcts compared with WT. However, postischemic inflammatory or oxidative responses did not differ. JunD overexpression reduced Sirt3 transcription by binding to its promoter, thus leading to mitochondrial dysfunction, myocardial cell death, and increased infarct size. On the other hand, JunD silencing reduced, while Sirt3 silencing increased infarct size. In human myocardial autopsy specimens, JunD-positive areas within the infarcted left ventricle staining corresponded to undetectable Sirt3 areas in consecutive sections of the same heart. Cardiac-specific JunD overexpression increases myocardial infarct size following I/R. These effects are mediated via Sirt3 transcriptional repression, mitochondrial swelling, and increased apoptosis, suggesting that JunD is a key regulator of myocardial I/R injury. The present data set the stage for further investigation of the potential role of Sirt3 activation as a novel target for the treatment of acute myocardial infarction.
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Feldman, Dorothy, Gary Cavallo, and Lois Rosenberger. "Electron microscopic study of rat myocardial infarcts induced by a free radical generator system." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 876–77. http://dx.doi.org/10.1017/s0424820100128663.
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The role of oxygen free radicals in the development of tissue injury and necrosis, including myocardial ischemic damage, is well documented. In this investigation, application of a free radical generator system (FRG) to rat myocardium resulted in ECG alterations typical of myocardial infarction; 24 hours after treatment, plasma lactate dehydrogenase (LDH) levels were elevated and 20% of the left ventricle was infarcted. In order to characterize the type of cellular damage and the ultrastructural changes in the affected cells, myocardial infarcts and myocardium from control rats were examined in the electron microscope.Six spontaneously hypertensive rats were lightly anesthetized with sodium pentobarbital and infused for 10 minutes through a carotid cannula near the ostium of the coronary artery. Three rats were infused with a FRG consisting of purine (2.3 mM), xanthine oxidase (0.02 μ/ml), and Fe -loaded transferrin (0.06 μM), and 3 sham-operated rats served as controls.
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Saito, Takayuki, Ian W. Rodger, Hani Shennib, Fu Hu, Lara Tayara, and Adel Giaid. "Cyclooxygenase-2 (COX-2) in acute myocardial infarction: cellular expression and use of selective COX-2 inhibitor." Canadian Journal of Physiology and Pharmacology 81, no. 2 (February 1, 2003): 114–19. http://dx.doi.org/10.1139/y03-023.
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Our previous work has shown strong expression of COX-2 in the myocardium of patients with end-stage ischemic heart failure. The purpose of this study was to determine the cellular expression of this enzyme in the setting of acute myocardial infarction (AMI) and determine the role of COX-2 in experimental animals using a selective COX-2 inhibitor. Experimental AMI was induced in rats by ligating the left coronary artery. Animals were either treated with a selective COX-2 inhibitor (5 mg·kg1·day1) or vehicle. Three days after ligation, cardiac function was assessed and infarct size was determined. Myocardial specimens were immunostained with antiserum to COX-2. Plasma concentration of prostanoids was measured by enzyme immunoassay. There was strong expression of COX-2 in the myocytes, endocardium, vascular endothelial cells, and macrophages in the infarcted zone of the myocardium. In contrast, little expression was seen in the myocardium of control rats. Animals treated with the COX-2 inhibitor showed a significant improvement in left ventricular (LV) end-diastolic pressure (P < 0.05) and LV systolic pressure (P < 0.01), and a reduction in infarct size (P < 0.05). Inhibition of COX-2 significantly decreased plasma concentration of thromboxane B2 (P < 0.05); however, it did not affect 6-keto-prostaglandin F1α. Induction of COX-2 during AMI appears to contribute to myocardial injury, and treatment with the specific inhibitor of the enzyme ameliorated the course of the disease.Key words: cyclooxygenase-2, inhibitor, acute myocardial infarction.
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Watanabe, Eiichi, Duane M. Smith, Joseph B. Delcarpio, Jian Sun, Frank W. Smart, Clifford H. Van Meter, and William C. Claycomb. "Cardiomyocyte Transplantation in a Porcine Myocardial Infarction Model." Cell Transplantation 7, no. 3 (May 1998): 239–46. http://dx.doi.org/10.1177/096368979800700302.
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Transplantation of cardiomyocytes into the heart is a potential treatment for replacing damaged cardiac muscle. To investigate the feasibility and efficiency of this technique, either a cardiac-derived cell line (HL-1 cells), or normal fetal or neonatal pig cardiomyocytes were grafted into a porcine model of myocardial infarction. The myocardial infarction was created by the placement of an embolization coil in the distal portion of the left anterior descending artery in Yorkshire pigs (n = 9). Four to 5 wk after creation of an infarct, the three preparations of cardiomyocytes were grafted, at 1 × 106 cells/20 μL into normal and into the middle of the infarcted myocardium. The hearts were harvested and processed for histologic examinations 4 to 5 wk after the cell grafts. Histologic evaluation of the graft sites demonstrated that HL-1 cells and fetal pig cardiomyocytes formed stable grafts within the normal myocardium without any detrimental effect including arrhythmia. In addition, a marked increase in angiogenesis was observed both within the grafts and adjacent host myocardium. Electron microscopy studies demonstrated that fetal pig cardiomyocytes and the host myocardial cells were coupled with adherens-type junctions and gap junctions. Histologic examination of graft sites from infarct tissue failed to show the presence of grafted HL-1 cells, fetal, or neonatal pig cardiomyocytes. Cardiomyocyte transplantation may provide the potential means for cell-mediated gene therapy for introduction of therapeutic molecules into the heart.
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Kuhn, Donald E., Sashwati Roy, Jared Radtke, Savita Khanna, and Chandan K. Sen. "Laser microdissection and capture of pure cardiomyocytes and fibroblasts from infarcted heart regions: perceived hyperoxia induces p21 in peri-infarct myocytes." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 3 (March 2007): H1245—H1253. http://dx.doi.org/10.1152/ajpheart.01069.2006.
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Myocardial infarction caused by ischemia-reperfusion in the coronary vasculature is a focal event characterized by an infarct-core, bordering peri-infarct zone and remote noninfarct zone. Recently, we have reported the first technique, based on laser microdissection pressure catapulting (LMPC), enabling the dissection of infarction-induced biological responses in multicellular regions of the heart. Molecular mechanisms in play at the peri-infarct zone are central to myocardial healing. At the infarct site, myocytes are more sensitive to insult than robust fibroblasts. Understanding of cell-specific responses in the said zones is therefore critical. In this work, we describe the first technique to collect the myocardial tissue with a single-cell resolution. The infarcted myocardium was identified by using a truncated hematoxylin-eosin stain. Cell elements from the infarct, peri-infarct, and noninfarct zones were collected in a chaotropic RNA lysis solution with micron-level surgical precision. Isolated RNA was analyzed for quality by employing microfluidics technology and reverse transcribed to generate cDNA. Purity of the collected specimen was established by real-time PCR analyses of cell-specific genes. Previously, we have reported that the oxygen-sensitive induction of p21/Cip1/Waf1/Sdi1 in cardiac fibroblasts in the peri-infarct zone plays a vital role in myocardial remodeling. Using the novel LMPC technique developed herein, we confirmed that finding and report for the first time that the induction of p21 in the peri-infarct zone is not limited to fibroblasts but is also evident in myocytes. This work presents the first account of an analytical technique that applies the LMPC technology to study myocardial remodeling with a cell-type specific resolution.
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Bohl, Steffen, Craig A. Lygate, Hannah Barnes, Debra Medway, Lee-Anne Stork, Jeanette Schulz-Menger, Stefan Neubauer, and Jurgen E. Schneider. "Advanced methods for quantification of infarct size in mice using three-dimensional high-field late gadolinium enhancement MRI." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (April 2009): H1200—H1208. http://dx.doi.org/10.1152/ajpheart.01294.2008.
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Conventional methods to quantify infarct size after myocardial infarction in mice are not ideal, requiring either tissue destruction for histology or relying on nondirect measurements such as wall motion. We therefore implemented a fast, high-resolution method to directly measure infarct size in vivo using three-dimensional (3D) late gadolinium enhancement MRI (3D-LGE). Myocardial T1 relaxation was quantified at 9.4 Tesla in five mice, and reproducibility was tested by repeat imaging after 5 days. In a separate set of healthy and infarcted mice ( n = 8 of each), continuous T1 measurements were made following intravenous or intraperitoneal injection of a contrast agent (0.5 μmol/g gadolinium-diethylenetriamine pentaacetic acid). The time course of T1 contrast development between viable and nonviable myocardium was thereby determined, with optimal postinjection imaging windows and inversion times identified. Infarct sizes were quantified using 3D-LGE and compared with triphenyltetrazolium chloride histology on day 1 after infarction ( n = 8). Baseline myocardial T1 was highly reproducible: the mean value was 952 ± 41 ms. T1 contrast peaked earlier after intravenous injection than with intraperitoneal injection; however, contrast between viable and nonviable myocardium was comparable for both routes ( P = 0.31), with adequate contrast remaining for at least 60 min postinjection. Excellent correlation was obtained between infarct sizes derived from 3D-LGE and histology ( r = 0.91, P = 0.002), and Bland-Altman analysis indicated good agreement free from systematic bias. We have validated an improved 3D MRI method to noninvasively quantify infarct size in mice with unsurpassed spatial resolution and tissue contrast. This method is particularly suited to studies requiring early quantification of initial infarct size, for example, to measure damage before intervention with stem cells.
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Teng, Xiaomei, Lei Chen, Weiqian Chen, Junjie Yang, Ziying Yang, and Zhenya Shen. "Mesenchymal Stem Cell-Derived Exosomes Improve the Microenvironment of Infarcted Myocardium Contributing to Angiogenesis and Anti-Inflammation." Cellular Physiology and Biochemistry 37, no. 6 (2015): 2415–24. http://dx.doi.org/10.1159/000438594.
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Background/Aims: Bone marrow mesenchymal stem cells (MSCs) widely applied for treating myocardial infarction face survival challenges in the inflammatory and ischemia microenvironment of acute myocardial infarction. The study hypothesized that MSC-derived exosomes play a significant role in improving microenvironment after acute myocardial infarction and aimed to investigate the paracrine effects of exosomes on angiogenesis and anti-inflammatory activity. Methods: MSCs were cultured in DMEM/F12 supplemented with 10% exosome-depleted fetal bovine serum and 1% penicillin-streptomycin for 48 h. MSC-derived exosomes were isolated using ExoQuick-TC. Tube formation and T-cell proliferation assays were performed to assess the angiogenic potency of MSC-derived exosomes. Acute myocardial infarction was induced in Sprague-Dawley rats, and myocardium bordering the infarcted zone was injected at four different sites with phosphate-buffered saline (PBS, control), MSC-derived exosomes, and exosome-depleted MSC culture medium. Results: MSC-derived exosomes significantly enhanced the tube formation of human umbilical vein endothelial cells, impaired T-cell function by inhibiting cell proliferation in vitro, reduced infarct size, and preserved cardiac systolic and diastolic performance compared with PBS markedly enhancing the density of new functional capillary and hence blood flow recovery in rat myocardial infarction model. Conclusions: Exosomes stimulate neovascularization and restrain the inflammation response, thus improving heart function after ischemic injury.
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Carlsson, Marcus, Nael F. Osman, Philip C. Ursell, Alastair J. Martin, and Maythem Saeed. "Quantitative MR measurements of regional and global left ventricular function and strain after intramyocardial transfer of VM202 into infarcted swine myocardium." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 2 (August 2008): H522—H532. http://dx.doi.org/10.1152/ajpheart.00280.2008.
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Previous studies have shown the beneficial effects of the hepatocyte growth factor (HGF) gene on myocardial perfusion and infarction size but not on the regional strain in relationship to global left ventricular function. A noninvasive magnetic resonance (MR) study was performed to determine the effect of a new HGF gene, VM202, expressing two isoforms of HGF, on regional and global left ventricular function. Pigs (8/group) were divided into three groups: 1) controls without infarction; 2) reperfused, infarcted controls; and 3) infarcted, treated (1 h after reperfusion) with VM202 injected at eight sites. Cine, tagging, and delayed enhancement MR images were acquired at 3 and 50 ± 3 days after infarction. At 50 days, ejection fraction in infarcted, treated animals increased (38 ± 1% to 47 ± 2%, P < 0.01) to the level of controls without infarction (52 ± 1%, P = 0.16) but decreased in infarcted controls (41 ± 1% to 37 ± 1%, P < 0.05). Two-dimensional strain improved in remote, peri-infarcted, and infarcted myocardium. Furthermore, the infarction size was smaller in infarcted, treated animals (7.0 ± 0.5%) compared with infarcted controls (13.2 ± 1.6%, P < 0.05). Histopathology showed a lack of hypertrophy in myocytes in peri-infarcted and remote myocardium and the formation of islands/peninsulas of myocytes in infarcted, treated animals but not in infarcted controls. In conclusion, the plasmid HGF gene caused a near complete recovery of ejection fraction and improved the radial and circumferential strain of remote, peri-infarcted, and infarcted regions within 50 days. These beneficial effects may be explained by the combined effects of a speedy and significant infarct resorption and island/peninsulas of hypertrophied myocytes within the infarcted territory but not by compensatory hypertrophy. The combined use of cine and tagging MR imaging provides valuable information on the efficacy of gene therapy.
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Li, Ming, Cheuk Man Yu, Lei Cheng, Mei Wang, Xuemei Gu, Ka Ho Lee, Tian Wang, Yn Tz Sung, and John E. Sanderson. "Repair of Infarcted Myocardium by an Extract of Geum japonicum with Dual Effects on Angiogenesis and Myogenesis." Clinical Chemistry 52, no. 8 (August 1, 2006): 1460–68. http://dx.doi.org/10.1373/clinchem.2006.068247.
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Abstract Background: It has become apparent recently that cardiac myocytes can divide after myocardial infarction, a circumstance that challenges the orthodox view that myocytes may be terminally differentiated. Replacement of the necrosed heart tissue by newly regenerated functional myocardium is a therapeutic ideal, but attempts to reconstitute functional myocardia and coronary vessels have been less successful. Methods: We isolated a fraction containing 5 compounds from the Chinese herb Geum japonicum, which stimulates the processes of angiogenesis and cardiomyogenesis. We investigated these dual properties in both ex vivo and in vivo systems. Results: We observed that this bioactive fraction displayed favorable dual actions on early angiogenesis and cardiomyogenesis in acute myocardial infarction in an animal model. Our results demonstrated that application of this bioactive fraction showed pronounced effects on limiting infarct size by 35%–45%, stimulating early development of new blood vessels in 24 h, and regenerating myocardium, replacing ∼49% of the total infarction volume after 2 weeks. Echocardiographic studies demonstrated marked improvement of left ventricular function within 2 days after infarction, and the improvement was sustained for >1 month. Conclusions: The properties of this bioactive fraction appear to be entirely novel and represent a new approach for the treatment of ischemic heart disease.
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Sciahbasi, Alessandro, Eugenia De Marco, Attilio Maseri, and Felicita Andreotti. "Preinfarction Angina and Improved Reperfusion of the Infarct-related Artery." Thrombosis and Haemostasis 82, S 01 (1999): 68–72. http://dx.doi.org/10.1055/s-0037-1615557.
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SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.
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Eitel, Ingo, Juan Wang, Thomas Stiermaier, Georg Fuernau, Hans-Josef Feistritzer, Alexander Joost, Alexander Jobs, et al. "Impact of Morphine Treatment on Infarct Size and Reperfusion Injury in Acute Reperfused ST-Elevation Myocardial Infarction." Journal of Clinical Medicine 9, no. 3 (March 9, 2020): 735. http://dx.doi.org/10.3390/jcm9030735.
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Current evidence regarding the effect of intravenous morphine administration on reperfusion injury and/or cardioprotection in patients with myocardial infarction is conflicting. The aim of this study was to evaluate the impact of morphine administration, on infarct size and reperfusion injury assessed by cardiac magnetic resonance imaging (CMR) in a large multicenter ST-elevation myocardial infarction (STEMI) population. In total, 734 STEMI patients reperfused by primary percutaneous coronary intervention <12 h after symptom onset underwent CMR imaging at eight centers for assessment of myocardial damage. Intravenous morphine administration was recorded in all patients. CMR was completed within one week after infarction using a standardized protocol. The clinical endpoint of the study was the occurrence of major adverse cardiac events (MACE) within 12 months after infarction. Intravenous morphine was administered in 61.8% (n = 454) of all patients. There were no differences in infarct size (17%LV, interquartile range [IQR] 8–25%LV versus 16%LV, IQR 8–26%LV, p = 0.67) and microvascular obstruction (p = 0.92) in patients with versus without morphine administration. In the subgroup of patients with early reperfusion within 120 min and reduced flow of the infarcted vessel (TIMI-flow ≤2 before PCI) morphine administration resulted in significantly smaller infarcts (12%LV, IQR 12–19 versus 19%LV, IQR 10–29, p = 0.035) and reduced microvascular obstruction (p = 0.003). Morphine administration had no effect on hard clinical endpoints (log-rank test p = 0.74) and was not an independent predictor of clinical outcome in Cox regression analysis. In our large multicenter CMR study, morphine administration did not have a negative effect on myocardial damage or clinical prognosis in acute reperfused STEMI. In patients, presenting early ( ≤120 min) morphine may have a cardioprotective effect as reflected by smaller infarcts; but this finding has to be assessed in further well-designed clinical studies
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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of scar structure, mechanics, and ventricular function after myocardial infarction in the rat." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (January 2010): H221—H228. http://dx.doi.org/10.1152/ajpheart.00495.2009.
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The mechanical properties of the healing scar are an important determinant of heart function following myocardial infarction. Yet the relationship between scar structure, scar mechanics, and ventricular function remains poorly understood, in part because no published study has tracked all of these factors simultaneously in any animal model. We therefore studied the temporal evolution of scar structure, scar mechanics, and left ventricular (LV) function in large anterior myocardial infarcts in rats. At 1, 2, 3, and 6 wk after left anterior descending coronary ligation, we examined LV function using sonomicrometry, infarct mechanical properties using biaxial mechanical testing, infarct structure using polarized light microscopy, and scar collagen content and cross-linking using biochemical assays. Healing infarcts in the rat were structurally and mechanically isotropic at all time points. Collagen content increased with time and was the primary determinant of scar mechanical properties. The presence of healing infarcts influenced systolic LV function through a rightward shift of the end-systolic pressure-volume relationship (ESPVR) that depended on infarct size, infarct collagen content, and LV dilation. We conclude that in sharp contrast to previous reports in large animal models, healing infarcts are structurally and mechanically isotropic in the standard rat model of myocardial infarction. On the basis of the regional strain patterns we observed in healing rat infarcts in this study and in healing pig infarcts in previous studies, we hypothesize that the local pattern of stretching determines collagen alignment in healing myocardial infarct scars.