Journal articles on the topic 'Ventricular chambers expansion'
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Creswell, L. L., M. J. Moulton, S. G. Wyers, J. S. Pirolo, D. S. Fishman, W. H. Perman, K. W. Myers, et al. "An experimental method for evaluating constitutive models of myocardium in in vivo hearts." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (August 1, 1994): H853—H863. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h853.
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A new experimental method for the evaluation of myocardial constitutive models combines magnetic resonance (MR) radiofrequency (RF) tissue-tagging techniques with iterative two-dimensional (2-D) nonlinear finite element (FE) analysis. For demonstration, a nonlinear isotropic constitutive model for passive diastolic expansion in the in vivo canine heart is evaluated. A 2-D early diastolic FE mesh was constructed with loading parameters for the ventricular chambers taken from mean early diastolic-to-late diastolic pressure changes measured during MR imaging. FE solution was performed for regional, intramyocardial ventricular wall strains using small-strain, small-displacement theory. Corresponding regional ventricular wall strains were computed independently using MR images that incorporated RF tissue tagging. Two unknown parameters were determined for an exponential strain energy function that maximized agreement between observed (from MR) and predicted (from FE analysis) regional wall strains. Extension of this methodology will provide a framework in which to evaluate the quality of myocardial constitutive models of arbitrary complexity on a regional basis.
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Todo, Tomoki, Masaaki Usui, and Kintomo Takakura. "Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase." Journal of Neurosurgery 74, no. 1 (January 1991): 81–86. http://dx.doi.org/10.3171/jns.1991.74.1.0081.
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✓ Six patients with severe intraventricular hemorrhage were treated with direct intraventricular infusion of urokinase. In each case, hemorrhage extended into all ventricular chambers, and a cast formation and expansion of the third and fourth ventricles were found. Immediately after the therapy was started (within 7 days from onset of symptoms), reduction of intraventricular hematoma volume was observed on computerized tomography. On average, both the third and fourth ventricles became clear on the third day after hemorrhage; there was one exception, a case of ruptured aneurysm. Five of the six patients showed excellent or good outcome, although two developed delayed hydrocephalus. No infection or rebleeding was observed. The outcome in a retrospectively studied group of five patients not treated with urokinase is also reported. The authors conclude that this relatively easy method of treatment will greatly improve the prognosis of severe intraventricular hemorrhage.
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Sagitova, G. R., I. V. Tkachev, O. V. Antonova, and O. V. Davydova. "A clinical case of aortic coarctation in combination with a septal defect in a newborn child." Meditsinskiy sovet = Medical Council, no. 17 (November 2, 2023): 220–24. http://dx.doi.org/10.21518/ms2023-254.
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Coarctation of the aorta is a congenital malformation characterized by the presence of narrowing of the aorta, which can be localized in any part of it. In this publication, we present a clinical case of coarctation of the aorta before and after surgical correction in a newborn. The child was admitted to the cardiosurgical hospital at the age of 6 days. Congenital heart disease of a low category of complexity was diagnosed prenatally. After birth, the condition is satisfactory. After 3 hours, the negative dynamics due to the clinic of respiratory failure. According to echocardiography – hypoplasia of the aortic arch, coarctation of the aorta? Open ductus arteriosus, ventricular septal defect. On the 3rd day of life, a diagnosis of congenital pneumonia was made and the child was transferred to a cardiosurgical hospital. Upon admission to the FCSSH in Astrakhan, the condition was regarded as severe, due to heart and respiratory failure. The child is examined. On echocardiography – Pronounced preductal form of coarctation of the aorta. Hypoplasia of the proximal arch and isthmus. Open ductus arteriosus. Ventricular septal defect. biventricular hypertrophy. Severe dilatation of the right chambers of the heart. Relative hypoplasia of the left ventricle. Tricuspid regurgitation. On the 7th day of life, surgical correction of the defect was performed plasty of the arch and isthmus of the aorta, plasty of the VSD. The early postoperative period proceeded with a clinic of moderate respiratory and heart failure. Against the background of the expansion of the volume of feeding, chylothorax was detected, drainage of the right pleural cavity was prescribed. Enteral feeding has been replaced by parenteral nutrition. The child was extubated on the 4th postoperative day. However, oxygen dependence was noted. The pleural drainage was removed on the 11th day after the operation. On the 12th day, the newborn was transferred from the intensive care unit. Discharged from the hospital on the 20th day after surgical treatment. After 4 months the child was examined in the hospital. The general condition was regarded as satisfactory. This clinical example shows the complexity of prenatal diagnosis of obstructive pathology of the aortic arch and the rapid manifestation of clinical manifestations after birth against the background of an unfavorable combination with a large septal defect.
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Pfefferbaum, Adolf, Natalie M. Zahr, Dirk Mayer, Shara Vinco, Juan Orduna, Torsten Rohlfing, and Edith V. Sullivan. "Ventricular Expansion in Wild-Type Wistar Rats After Alcohol Exposure by Vapor Chamber." Alcoholism: Clinical and Experimental Research 32, no. 8 (August 2008): 1459–67. http://dx.doi.org/10.1111/j.1530-0277.2008.00721.x.
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Laurindo, F. R., R. E. Goldstein, N. J. Davenport, D. Ezra, and G. Z. Feuerstein. "Mechanisms of hypotension produced by platelet-activating factor." Journal of Applied Physiology 66, no. 6 (June 1, 1989): 2681–90. http://dx.doi.org/10.1152/jappl.1989.66.6.2681.
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Platelet-activating factor (PAF) is a phospholipid mediator that induces cardiovascular collapse and release of the secondary mediator thromboxane A2 (TxA2). To clarify mechanisms involved in this collapse and, specifically, the relative contribution of left ventricular and right ventricular dysfunction, we studied 12 open-chest pigs. PAF infusion (0.04–0.28 nmol.kg-1.min-1) induced a 5- to 120-fold increase in pulmonary vascular resistance, a 75–98% fall in cardiac output, and systemic arterial hypotension. Right ventricular failure was indicated by chamber enlargement, decreased shortening, and increased right atrial pressures. In contrast, left ventricular dysfunction was accompanied by decreases in chamber dimensions and filling pressures that were unresponsive to volume expansion. U 46619 (a stable TxA2 analogue) and mechanical pulmonary artery constriction induced changes similar to PAF. In 11 additional closed-chest pigs, TxA2 blockade with indomethacin attenuated the PAF-induced rise in pulmonary vascular resistance, right ventricular dysfunction, and systemic hypotension. A specific TxA2 synthase inhibitor, OKY-046, also diminished hemodynamic effects of PAF in six other pigs. Tachyphylaxis was not observed in five pigs repeatedly given PAF. We conclude that acute right ventricular failure as the result of severe increase in pulmonary vascular resistance is the primary mechanism early in the course of PAF-induced shock in the pig. PAF-induced release of TxA2 may contribute significantly to these events.
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Galli, Alessio, and Federico Lombardi. "Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure." Cardiology Research and Practice 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/2579832.
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Heart failure is a chronic disease with high morbidity and mortality, which represents a growing challenge in medicine. A major risk factor for heart failure with reduced ejection fraction is a history of myocardial infarction. The expansion of a large infarct scar and subsequent regional ventricular dilatation can cause postinfarct remodelling, leading to significant enlargement of the left ventricular chamber. It has a negative prognostic value, because it precedes the clinical manifestations of heart failure. The characteristics of the infarcted myocardium predicting postinfarct remodelling can be studied with cardiac magnetic resonance and experimental imaging modalities such as diffusion tensor imaging can identify the changes in the architecture of myocardial fibers. This review discusses all the aspects related to postinfarct left ventricular remodelling: definition, pathogenesis, diagnosis, consequences, and available therapies, together with experimental interventions that show promising results against postinfarct remodelling and heart failure.
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Micheletti, R., E. D. Di Paola, A. Schiavone, E. English, P. Benatti, J. M. Capasso, P. Anversa, and G. Bianchi. "Propionyl-L-carnitine limits chronic ventricular dilation after myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 4 (April 1, 1993): H1111—H1117. http://dx.doi.org/10.1152/ajpheart.1993.264.4.h1111.
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To determine whether propionyl-L-carnitine (PLC) administration ameliorates ventricular remodeling after myocardial infarction, we performed coronary occlusion in rats and examined the long-term effects of the drug 19-24 wk after surgery. In view of the well-established role of angiotensin-converting enzyme (ACE) inhibitors in the reduction of ventricular dilation after infarction, the therapeutic impact of oral PLC (60 mg/kg) was compared with that of enalapril (1 mg/kg). Infarct size measured planimetrically was found to be comparable in untreated, PLC-treated, and enalapril-treated rats, averaging 40-46% of the left ventricular free wall. Heart weight was increased 14, 16, and 11% with no treatment, with PLC, and with enalapril, respectively. The relationship between left ventricular filling pressure and chamber volume demonstrated that PLC and enalapril significantly prevented the expansion in cavitary size after infarction. These protective influences were observed throughout the range of filling pressures measured, from 0 to 30 mmHg. At a uniform reference point of filling pressure of 4 mmHg, untreated infarcted hearts showed an expansion in ventricular volume of 2.17-fold (P < 0.0001). Corresponding increases in this parameter after PLC and enalapril were 36 and 43%, respectively, both not statistically significant. Moreover, PLC was capable of reducing the alterations in myocardial compliance associated with myocardial infarction. In conclusion, PLC reduces the magnitude of decompensated eccentric hypertrophy produced by myocardial infarction in a manner similar to that found with ACE inhibition.
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Li, Baosheng, Qiong Li, Xiaowei Wang, Kumar P. Jana, Giorgio Redaelli, Jan Kajstura, and Piero Anversa. "Coronary constriction impairs cardiac function and induces myocardial damage and ventricular remodeling in mice." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 5 (November 1, 1997): H2508—H2519. http://dx.doi.org/10.1152/ajpheart.1997.273.5.h2508.
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To establish whether coronary artery narrowing (CAN) in mice was accompanied by depressed ventricular function, tissue injury, and modifications in cardiac anatomy, the left coronary artery was constricted in FVB/N mice and the animals were killed 7 days later. CAN consisted of a 53% reduction in luminal diameter, which resulted in a twofold increase in left ventricular end-diastolic pressure. Left ventricular systolic pressure and left ventricular + and −dP/d t decreased 15, 21, and 11%, respectively. Left ventricular weight-to-body weight ratio increased 33%. This hypertrophic adaptation was characterized by a 9 and 20% increase in the longitudinal and transverse cavitary diameters, which provoked a 1.5-fold expansion in chamber volume. In contrast, wall thickness decreased 15%. These anatomic and functional changes induced a threefold elevation in diastolic stress. Foci of reparative fibrosis were found in the endomyocardium and epimyocardium, involving 2–3% of the tissue. Finally, myocyte loss in the ventricle was 15%, and myocyte hypertrophy was 38%. Impaired ventricular function, diastolic Laplace overloading, myocyte loss, and decompensated eccentric hypertrophy in mice after CAN mimic the ischemic cardiomyopathic heart in humans.
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Lee, Da Young. "Obesity and heart failure with preserved ejection fraction: pathophysiology and clinical significance." Cardiovascular Prevention and Pharmacotherapy 4, no. 2 (April 30, 2022): 70–74. http://dx.doi.org/10.36011/cpp.2022.4.e10.
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Obesity is a risk factor for heart failure and cardiovascular disease. Of particular note, over 80% of patients with heart failure with a preserved ejection fraction (HFpEF) are overweight or obese. In this study, we aimed to review the association between obesity and HFpEF. Obese patients with HFpEF exhibit a distinct phenotype. In addition to impaired left ventricular (LV) diastolic function and high filling pressures, obese patients with HFpEF possess other factors that cause elevated LV filling pressure, such as a greater dependence on plasma volume expansion, aggravated pericardial restraint, and increased ventricular interaction. Obesity can contribute to HFpEF through hemodynamic, neurohormonal, inflammatory, and mechanical mechanisms. An increased amount of body fat can induce plasma volume expansion, resulting in chamber remodeling, pericardial restraint, and ultimately elevations in LV filling pressure. Obesity can mediate the activation of sympathetic nervous system signaling and the renin-angiotensin-aldosterone system. These unique pathophysiological characteristics of individuals with both obesity and HFpEF suggest that obesity with HFpEF can be considered a specific phenotype. Future research is expected to clarify effective treatment modalities for obesity-related HFpEF.
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Morton, Sarah U., Paul J. Scherz, Kimberly R. Cordes, Kathryn N. Ivey, Didier Y. R. Stainier, and Deepak Srivastava. "microRNA-138 modulates cardiac patterning during embryonic development." Proceedings of the National Academy of Sciences 105, no. 46 (November 12, 2008): 17830–35. http://dx.doi.org/10.1073/pnas.0804673105.
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Organ patterning during embryonic development requires precise temporal and spatial regulation of protein activity. microRNAs (miRNAs), small noncoding RNAs that typically inhibit protein expression, are broadly important for proper development, but their individual functions during organogenesis are largely unknown. We report that miR-138 is expressed in specific domains in the zebrafish heart and is required to establish appropriate chamber-specific gene expression patterns. Disruption of miR-138 function led to ventricular expansion of gene expression normally restricted to the atrio-ventricular valve region and, ultimately, to disrupted ventricular cardiomyocyte morphology and cardiac function. Temporal-specific knockdown of miR-138 by antagomiRs showed miR-138 function was required during a discrete developmental window, 24–34 h post-fertilization (hpf). miR-138 functioned partially by repressing the retinoic acid synthesis enzyme, aldehyde dehydrogenase-1a2, in the ventricle. This activity was complemented by miR-138-mediated ventricular repression of the gene encoding versican (cspg2), which was positively regulated by retinoic-acid signaling. Our findings demonstrate that miR-138 helps establish discrete domains of gene expression during cardiac morphogenesis by targeting multiple members of a common pathway, and also establish the use of antagomiRs in fish for temporal knockdown of miRNA function.
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Sharma, Rahul Kumar, Navneet Kaur, Ajay Singh Kushwah, Nisha Singh, and Shilpa Thakur. "A Comprehensive Review of Dilated Cardiomyopathy in Pre-clinical Animal Models in Addition to Herbal Treatment Options and Multi-modality Imaging Strategies." Cardiovascular & Hematological Disorders-Drug Targets 22, no. 4 (December 2022): 207–25. http://dx.doi.org/10.2174/1871529x23666230123122808.
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Abstract: Dilated cardiomyopathy (DCM) is distinguished by ventricular chamber expansion, systolic dysfunction, and normal left ventricular (LV) wall thickness, and is mainly caused due to genetic or environmental factors; however, its aetiology is undetermined in the majority of patients. The focus of this work is on pathogenesis, small animal models, as well as the herbal medicinal approach, and the most recent advances in imaging modalities for patients with dilated cardiomyopathy. Several small animal models have been proposed over the last few years to mimic various pathomechanisms that contribute to dilated cardiomyopathy. Surgical procedures, gene mutations, and drug therapies are all characteristic features of these models. The pros and cons, including heart failure stimulation of extensively established small animal models for dilated cardiomyopathy, are illustrated, as these models tend to procure key insights and contribute to the development of innovative treatment techniques for patients. Traditional medicinal plants used as treatment in these models are also discussed, along with contemporary developments in herbal therapies. In the last few decades, accurate diagnosis, proper recognition of the underlying disease, specific risk stratification, and forecasting of clinical outcome, have indeed improved the health of DCM patients. Cardiac magnetic resonance (CMR) is the bullion criterion for assessing ventricular volume and ejection fraction in a reliable and consistent direction. Other technologies, like strain analysis and 3D echocardiography, have enhanced this technique's predictive and therapeutic potential. Nuclear imaging potentially helps doctors pinpoint the causative factors of left ventricular dysfunction, as with cardiac sarcoidosis and amyloidosis.
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Wu, Mingfu, and Jingjing Li. "Numb family proteins: novel players in cardiac morphogenesis and cardiac progenitor cell differentiation." Biomolecular Concepts 6, no. 2 (April 1, 2015): 137–48. http://dx.doi.org/10.1515/bmc-2015-0003.
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AbstractVertebrate heart formation is a spatiotemporally regulated morphogenic process that initiates with bilaterally symmetric cardiac primordial cells migrating toward the midline to form a linear heart tube. The heart tube then elongates and undergoes a series of looping morphogenesis, followed by expansions of regions that are destined to become primitive heart chambers. During the cardiac morphogenesis, cells derived from the first heart field contribute to the primary heart tube, and cells from the secondary heart field, cardiac neural crest, and pro-epicardial organ are added to the heart tube in a precise spatiotemporal manner. The coordinated addition of these cells and the accompanying endocardial cushion morphogenesis yield the atrial, ventricular, and valvular septa, resulting in the formation of a four-chambered heart. Perturbation of progenitor cells’ deployment and differentiation leads to a spectrum of congenital heart diseases. Two of the genes that were recently discovered to be involved in cardiac morphogenesis are Numb and Numblike. Numb, an intracellular adaptor protein, distinguishes sibling cell fates by its asymmetric distribution between the two daughter cells and its ability to inhibit Notch signaling. Numb regulates cardiac progenitor cell differentiation in Drosophila and controls heart tube laterality in Zebrafish. In mice, Numb and Numblike, the Numb family proteins (NFPs), function redundantly and have been shown to be essential for epicardial development, cardiac progenitor cell differentiation, outflow tract alignment, atrioventricular septum morphogenesis, myocardial trabeculation, and compaction. In this review, we will summarize the functions of NFPs in cardiac development and discuss potential mechanisms of NFPs in the regulation of cardiac development.
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Tucci, Paulo José Ferreira, Neif Murad, Clever Land Rossi, Roberto Janzon Nogueira, and Orlando Santana. "Heart rate modulates the slow enhancement of contraction due to sudden left ventricular dilation." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 5 (May 1, 2001): H2136—H2143. http://dx.doi.org/10.1152/ajpheart.2001.280.5.h2136.
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In isovolumic blood-perfused dog hearts, left ventricular developed pressure (DP) was recorded while a sudden ventricular dilation was promoted at three heart rate (HR) levels: low (L: 52 ± 1.7 beats/min), intermediate (M: 82 ± 2.2 beats/min), and high (H: 117 ± 3.5 beats/min). DP increased instantaneously with chamber expansion (Δ1DP), and another continuous increase occurred for several minutes (Δ2DP). HR elevation did not alter Δ1DP (32.8 ± 1.6, 33.6 ± 1.5, and 34.3 ± 1.2 mmHg for L, M, and H, respectively), even though it intensified Δ2DP (17.3 ± 0.9, 20.7 ± 1.0, and 26.8 ± 1.2 mmHg for L, M, and H, respectively), meaning that the treppe phenomenon enhances the length dependence of the contraction component related to changes in intracellular Ca2+ concentration. Frequency increments reduced the half time of the slow response (82 ± 3.6, 67 ± 2.6, and 53 ± 2.0 s for L, M, and H, respectively), while the number of beats included in half time increased (72 ± 2.9, 95 ± 2.9, and 111 ± 3.2 beats for L, M, and H, respectively). HR modulation of the slow response suggests that L-type Ca2+ channel currents and/or the Na+/Ca2+ exchanger plays a relevant role in the stretch-triggered Ca2+ gain when HR increases in the canine heart.
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Yang, Yining, Yitong Ma, Wei Han, Jun Li, Yang Xiang, Fen Liu, Xiang Ma, et al. "Age-related differences in postinfarct left ventricular rupture and remodeling." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 4 (April 2008): H1815—H1822. http://dx.doi.org/10.1152/ajpheart.00831.2007.
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Cardiac rupture is more prevalent in elderly patients with first onset of acute myocardial infarct (MI), but the mechanism remains unexplored. We investigated the differences in the incidence of cardiac rupture and early left ventricular (LV) remodeling following coronary artery ligation between old (12-mo) and young (3-mo) C57Bl/6 male mice and explored responsible mechanisms. The incidence of rupture within 1 wk after MI was significantly higher in old than in young mice (40.7 vs. 18.3%, P = 0.013) despite a similar infarct size in both age groups. Old mice dying of rupture had more severe infarct expansion than young counterparts. Echocardiography and catheterization at day 7 revealed more profound LV chamber dilatation and dysfunction as well as higher blood pressures in aged mice. At day 3 after MI immediately before the peak of rupture occurrence, we observed significantly higher content of type I and III collagen, a greater density of macrophage and neutrophil, and markedly enhanced mRNA expression of inflammatory cytokines in the infarcted myocardium in old than in young mice. Furthermore, a more dramatic increment of matrix metalloproteinase (MMP)-9 activity was found in old than in young infarcted hearts, in keeping with enhanced inflammatory response. Collectively, these results revealed that old mice had a higher risk of post-MI cardiac rupture despite a higher level of collagen content and cross-linking. Enhanced inflammatory response and subsequent increase in MMP-9 activity together with higher blood pressure are important factors responsible for the higher risk of cardiac rupture and more severe LV remodeling in the aged heart following acute MI.
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Cheng-Baron, June, Kelvin Chow, Nee Scze Khoo, Ben T. Esch, Jessica M. Scott, Mark J. Haykowsky, John V. Tyberg, and Richard B. Thompson. "Measurements of changes in left ventricular volume, strain, and twist during isovolumic relaxation using MRI." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 6 (June 2010): H1908—H1918. http://dx.doi.org/10.1152/ajpheart.00131.2010.
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Left ventricular (LV) active relaxation begins before aortic valve closure and is largely completed during isovolumic relaxation (IVR), before mitral valve opening. During IVR, despite closed mitral and aortic valves, indirect assessments of LV volume have suggested volume increases during this period. The aim of this study is to measure LV volume throughout IVR and to determine the sources of any volume changes. For 10 healthy individuals (26.0 ± 3.8 yr), magnetic resonance imaging was used to measure time courses of LV volume, principal myocardial strains (circumferential, longitudinal, radial), and LV twist. Mitral leaflet motion was observed using echocardiography. During IVR, LV volume measurements showed an apparent increase of 4.6 ± 1.5 ml (5.0 ± 2.0% of the early filling volume change), the LV untwisted by 4.5 ± 1.9° (36.6 ± 18.0% of peak systolic twist), and changes in circumferential, longitudinal, and radial strains were +0.87 ± 0.64%, +0.93 ± 0.57%, and −1.46 ± 1.66% (4.2 ± 3.3%, 5.9 ± 3.3%, and 5.3 ± 7.5% of peak systolic strains), respectively. The apparent changes in volume correlated ( P < 0.01) with changes in circumferential, longitudinal, and radial strains ( r = 0.86, 0.69, and −0.37, respectively) and untwisting ( r = 0.83). The closed mitral valve leaflets were observed to descend into the LV throughout IVR in all subjects in apical four- and three-chamber and parasternal long-axis views by 6.0 ± 3.3, 5.1 ± 2.4, and 2.1 ± 5.0 mm, respectively. In conclusion, LV relaxation during IVR is associated with changes in principal strains and untwisting, which are all correlated with an apparent increase in LV volume. Since closed mitral and aortic valves ensure true isovolumic conditions, the apparent volume change likely reflects expansion of the LV myocardium and the inward bowing of the closed mitral leaflets toward the LV interior.
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Yang, Fang, Yun-He Liu, Xiao-Ping Yang, Jiang Xu, and Oscar A. Carretero. "Myocardial Infarct Evolution and Cardiac Remodeling in Mice." Hypertension 36, suppl_1 (October 2000): 704. http://dx.doi.org/10.1161/hyp.36.suppl_1.704-a.
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P62 A mouse model of myocardial infarction (MI) has been widely used since genetically engineered mice became available, which allows us to study gene regulation of cardiac phenotype, function, and pathophysiology of heart failure. However, some basic information, such as the healing process, infarct expansion and LV remodeling after MI in mice, is lacking. To clarify this process, 42 male C57B1/6J mice underwent coronary artery ligation and were killed at 1, 2, 4, or 7 days, or 2, 3, or 4 weeks after MI. Left ventricular (LV) morphology and function were evaluated by histopathology and echocardiography. We found that at the margin of the necrotic myocardium, infiltration by neutrophils was noticeable at 1 and 2 days. Marked infiltration by mononuclear cells occurred at day 4. Lymphocyte infiltration was apparent at 7 and 14 days. Massive proliferation of fibroblasts and fibrocytes and accumulation of collagen began at day 14 and scar formation was completed by day 21. The infarct expansion index increased gradually from 0.62 ± 0.12 at day 1 to 1.66 ± 0.35 at day 14, which reached a maximum, then decreased slightly to 1.51 ± 0.26 at day 28. In non-infarcted areas of the heart, myocyte cross-sectional area and collagen content increased from 161 ± 17 μm 2 and 5.7 ± 0.3% at day 1 to 252 ± 8 μm 2 and 10.8 ± 0.8% at day 21, respectively, and remained similar at day 28. Infarct size was 47%, 52% and 47% at day 1, 14 and 28 respectively. Increased LV diastolic chamber dimension and mass and decreased shortening fraction (SF) appeared as early as 2 weeks after MI and continued for 4 weeks (table). Thus this study provides important qualitative and quantitative information on the natural history of MI and validation of the mouse model.
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Togi, Kiyonori, Takahiro Kawamoto, Ryoko Yamauchi, Yoshinori Yoshida, Toru Kita, and Makoto Tanaka. "Role of Hand1/eHAND in the Dorso-Ventral Patterning and Interventricular Septum Formation in the Embryonic Heart." Molecular and Cellular Biology 24, no. 11 (June 1, 2004): 4627–35. http://dx.doi.org/10.1128/mcb.24.11.4627-4635.2004.
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ABSTRACT Molecular mechanisms for the dorso-ventral patterning and interventricular septum formation in the embryonic heart are unknown. To investigate a role of Hand1/eHAND in cardiac chamber formation, we generated Hand1/eHAND knock-in mice where Hand1/eHAND cDNA was placed under the control of the MLC2V promoter. In Hand1/eHAND knock-in mice, the outer curvature of the right and left ventricles expanded more markedly. Moreover, there was no interventricular groove or septum formation, although molecularly, Hand1/eHAND knock-in hearts had two ventricles. However, the morphology of the inner curvature of the ventricles, the atrioventricular canal, and the outflow tract was not affected by Hand1/eHAND expression. Furthermore, expression of Hand1/eHAND in the whole ventricles altered the expression patterns of Chisel, ANF, and Hand2/dHAND but did not affect Tbx5 expression. In contrast, the interventricular septum formed normally in transgenic embryos overexpressing Hand1/eHAND in the right ventricle but not in the boundary region. These results suggested that Hand1/eHAND is involved in expansion of the ventricular walls and that absence of Hand1/eHAND expression in the boundary region between the right and left ventricles may be critical in the proper formation of the interventricular groove and septum. Furthermore, Hand1/eHAND is not a master regulatory gene that specifies the left ventricle myocyte lineage but may control the dorso-ventral patterning in concert with additional genes.
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Weberruß, Heidi, Lisa Baumgartner, Frauke Mühlbauer, Nerejda Shehu, and Renate Oberhoffer-Fritz. "Training intensity influences left ventricular dimensions in young competitive athletes." Frontiers in Cardiovascular Medicine 9 (October 6, 2022). http://dx.doi.org/10.3389/fcvm.2022.961979.
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BackgroundIn young athletes, exercise causes changes in the heart that include growth in wall thickness and mass of the left ventricle and expansion of the heart’s chambers. The heart’s function is either preserved or enhanced, but this may change to the opposite over time.ObjectiveThis study aimed to assess structural and functional cardiac adaptations in relation to exercise training time, intensity, and performance in young competitive athletes.MethodsA total of 404 children and adolescents (14.23 ± 2.0 years, 97 females) were enrolled in the Munich Cardiovascular Adaptations in Young Athletes Study (MuCAYA-Study). Eighty-five participants were examined two times a year. Two-dimensional echocardiography was performed to assess left ventricular structure and function. Training time and intensity was measured with the MoMo physical activity questionnaire, maximum aerobic capacity by cardiopulmonary exercise testing, and strength with the handgrip strength test.ResultsMaximum aerobic capacity significantly influenced interventricular septal thickness in diastole. Training intensity significantly influenced left ventricular internal diameter in diastole and systole, and left ventricular mass indexed to body surface area. Within one year, interventricular wall thickness, relative wall thickness and left ventricular mass, indexed to body surface area and height, increased significantly. Training intensity and aerobic capacity contributed to cardiac adaptations in young competitive athletes, as represented by altered structural parameters but preserved cardiac function. Within a year, however, structural changes and a decline in diastolic performance were observed within the longitudinal sub-sample.ConclusionOur results confirm the hypothesis that cardiac adaptations to exercise occur at a young age. Cardiac adaptation in our cohort was influenced by exercise intensity and maximum aerobic capacity.
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Andresen, K., LG Klaeboe, ØH Lie, K. Broch, AB Kvaslerud, GS Bosse, E. Hopp, KH Haugaa, and T. Edvardsen. "No signs of diffuse myocardial fibrosis by T1 mapping in male elite endurance athletes." European Heart Journal - Cardiovascular Imaging 23, Supplement_1 (February 1, 2022). http://dx.doi.org/10.1093/ehjci/jeab289.423.
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Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Oslo University Hospital Rikshospitalet, Department of Cardiology, Oslo, Norway. Background/Introduction: Observational data indicating increased prevalence of focal myocardial fibrosis in endurance athletes have raised concerns regarding the potential detrimental cardiac consequences of long-term athleticism. Cumulative exercise and competitive exposure has been associated with focal myocardial fibrosis visualised as late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) imaging. Reports of higher extracellular volume (ECV) in the remote myocardium of athletes with LGE have suggested that this fibrotic process may affect the entire myocardium. However, detailed data on exercise exposure and possible associations with diffuse myocardial fibrosis in endurance athletes are scarce. Purpose Our aim was to investigate the association between cumulative exercise exposure and diffuse myocardial fibrosis in male elite endurance athletes. Methods In this cross-sectional observational study we evaluated 27 healthy adult male elite endurance athletes age 41 ± 9 years and 16 healthy controls age 41 ± 12 years. All subjects underwent 3 T CMR including LGE and T1 mapping. The athletes detailed their exercise history from 12 years of age in a structured interview. Results Athletes had lower resting heart rate, enlarged cardiac chambers and increased left ventricular mass compared to controls, in accordance with the athlete’s heart phenotype (table 1). In contrast to what would have been expected in diffuse myocardial fibrosis, athletes had shorter native T1 time than controls (1214 ± 24 vs. 1268 ± 48 ms, p < 0.001). The native T1 time fell with increasing yearly exercise dose, accumulated exercise duration and accumulated exercise dose (r=-0.46, -0.51 and -0.53, p < 0.05 for all). In a stepwise multiple linear regression model, only the accumulated exercise dose was independently associated with native T1 time as shown in figure 1 (r = 0.53, p = 0.01). There was no clear difference in ECV between athletes and controls (22.5 ± 3.1 vs. 23.8 ± 2.0 %, p = 0.16), indicating that increased left ventricular mass in the athletes was balanced without disproportionate extracellular expansion. There was no association between exercise exposure and ECV. LGE was observed in 5 (19 %) of the athletes and none of the controls (p = 0.14). There was no difference in native T1 time (1220 ± 4 vs. 1212 ± 27 ms, p = 0.56) or ECV (22.0 ± 1.2 vs. 22.7 ± 3.4 %, p = 0.69) between athletes with or without LGE. Conclusion(s): We did not observe signs of diffuse myocardial fibrosis in healthy elite endurance athletes. These results indicate that diffuse myocardial fibrosis is not highly prevalent in healthy athletes with extreme exercise exposure. Abstract Figure. Abstract Figure.
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Skidan, V. I., A. Y. Goda, A. B. Challa, C. Pislaru, V. T. Nkomo, W. L. Miller, and S. V. Pislaru. "Impact of plasma volume redistribution on outcomes in patients with heart failure with reduced ejection fraction." European Heart Journal - Cardiovascular Imaging 24, Supplement_1 (June 2023). http://dx.doi.org/10.1093/ehjci/jead119.260.
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Abstract Funding Acknowledgements Type of funding sources: None. Background The impact of capacitance and blood volume redistribution on outcomes of patients with chronic heart failure is incompletely understood. Quantitative plasma volume (PV) measurements together with echocardiographic evaluation allow a comprehensive assessment of the interplay between volumetric overload, cardiac chamber remodelling and myocardial function. Purpose We hypothesize that PV expansion is associated with myocardial and renal dysfunction, right ventricular-pulmonary arterial uncoupling and unfavorable outcomes in HF patients with reduced ejection fraction (HFrEF). Methods Patients hospitalized at Mayo Clinic with decompensated HF and who had PV by the indicator-dilution nuclear methodology (Daxor BVA100) were included. Patients were considered hypervolemic if BV was ≥25% over expected. The primary endpoint was the composite of all-cause mortality or heart transplantation. The closest TTE to the time of PV was used to measure various indexes of myocardial performance (standard echo parameters and global chamber-specific strain parameters). Event-free survival was estimated using the Kaplan-Meier method. The relationship between PV and various parameters was evaluated with correlation coefficient (r²). Results A total of 65 patients were enrolled in the study. Reduced LVEF was present in 53 (81.6%) patients. There were 44 events (32 deaths, 12 heart transplants) after a median follow-up of 43 months (IQR 14–65). Results in patients with HFrEF are presented in the Table. Our main findings were: 1) PV expansion was associated with an increased risk of adverse events (Figure 1); 2) Volume redistribution correlated with various indexes of cardiac chamber function, suggesting that volume overload and associated cardiac remodeling may be responsible for altered myocardial mechanics in patients with HFrEF (Figure 2); 3) right ventricular-pulmonary arterial uncoupling was triggered by the plasma volume expansion, that causes postcapillary pulmonary hypertension; 4) PV redistribution was also associated with renal dysfunction and increasing the level of the protein catabolism (Table 1). Conclusion Expansion of plasma volume in HFrEF patients is associated with left atrium dilatation, abnormal filling of both atria and right ventricular dilatation / dysfunction. Plasma volume redistributions apparently became a trigger of right ventricular-pulmonary arterial uncoupling and stimulated postcapillary pulmonary hypertension, renal dysfunction with increasing the level of protein catabolism and unfavorable outcomes.
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Challa, A. B., V. I. Skidan, A. Y. Goda, V. T. Nkomo, W. L. Miller, and S. V. Pislaru. "Relationship and outcomes between volume status, cardiac and renal dysfunction in patients with chronic heart failure." European Heart Journal 44, Supplement_1 (January 25, 2023). http://dx.doi.org/10.1093/eurheartj/ehac779.032.
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Abstract Funding Acknowledgements Type of funding sources: None. Background Right heart and renal dysfunction occurring due to volume fluid redistribution remain a front-line issue in the development of the syndrome of congestion in chronic heart failure (HF). Quantitative total blood volume (TBV) measurements and Speckle-tracking Echo (STE) provide complementary information on the myocardial function which allows for providing a more integrated assessment of clinical status and outcomes. Purpose We hypothesize adverse outcomes in patients with heart failure (HF) who have expansion of TBV, right ventricular (RV) and renal dysfunction. Methods This is a prospective study and a total of 66 participants NYHA class III&IV with chronic HF are enrolled from 2014-2022. TBV, right heart catheterization, TTE, TEE, and kidney function tests is performed. STE is calculated using TomTec software for all heart chambers. Patients is divided into 1-st group of the total participants, 2-nd group is patients adverse outcomes which are heart transplant (HT) or death, 3rd group is of alive patients. Simple, multivariable linear regression analyses is used to evaluate associations between TBV, cardiac and renal function. Statistical analyses is performed using JMP, BlueSky, and two-sided with P-values <0.05 considered to be statistically. Results Of 66 patients, the 1-st group has 66 patients, the 2nd group has 44 patients out of which deceased are 32 patients (48.4%), HT has 12 patients (18.1%), and the 3rd group has 22 patients (33.3%). In the 2nd group, out of the 44 patients, 35 (79.5%) patients have HFrEF, and 9 (20.4%) patients presented HFpEF. In the 3rd group out of 22 patients, 15 (68.2%) have HFrEF, and 7 (31.8%) patients have HFpEF. RV dimensions are significantly related to TBV in all groups of participants (Table 1). In the total patients, TBV is directly correlated to a moderate degree with EDSRV (r = 0.51, P < 0.001), ESSRV (r = 0.44, P < 0.001) and FAC (r = 0.40, P < 0.001). More significant moderate and strong relationships are observed in patients with adverse outcome between TVB and EDSRV (r = 0.54, P < 0.001), ESSRV (r = 0.65, P < 0.001) and FAC (r = 0.48, P < 0.001). In group 1, weak and direct association of TBV and RV GLS, FW LS, FW LSR, and RA reservoir strain. In the 2nd group, TBV directly correlated to a moderate degree with FW LS (r = 0.41, P = 0.005) and FW LSR (r = 0.43, P = 0.002). Similar relationships in the 2nd group are observed between TBV and renal function parameters (TBV and eGFR (r = 0.53, P < 0.001)). The direct and weak correlation obtained between TBV and BUN in both 1st and 2nd groups. In patients with adverse outcomes, TBV is directly proportional to LV Diastolic BP. Conclusion The association among intravascular volume and parameters of RV dilatation, myocardial and renal dysfunction in patients with chronic HF is associated with adverse outcomes. Understanding the impact of all these variables guide optimal and effective individualized HF management and therapy.
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Chianese, Salvatore, Valentina Capone, Andrea Salzano, Eduardo Bossone, and Rosangela Cocchia. "652 SUCCESSFUL SURGICAL REPAIR OF LEFT VENTRICULAR PSEUDOANEURYSM IN A PATIENT WITH SUBACUTE ST-ELEVATION MYOCARDIAL INFARCTION." European Heart Journal Supplements 24, Supplement_K (December 14, 2022). http://dx.doi.org/10.1093/eurheartjsupp/suac121.505.
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Abstract A 65-year-old man was admitted to the emergency department for abdominal pain begun 4 days before. Past medical history consisted of ischemic stroke and diabetes mellitus. Of note, he was not taking any medication. Vital signs: blood pressure 90/50 mmHg, heart rate 50/minute, respiratory rate 18/minute, body temperature 36.5°C; saturation oxygen level 93%. High-sensitivity cardiac troponin was mildly elevated (121 pg/mL). Electrocardiogram showed sinus bradycardia, Q waves with ST elevation in antero-lateral leads consistent with subacute STEMI. Transthoracic echocardiogram (TTE) revealed aneurysmatic expansion of apical left ventricular (LV) walls (ejection fraction 30%) with a large apical thrombus (35×15 mm). Coronary angiography showed complete occlusion of proximal left anterior descending artery and a critical stenosis of right coronary artery; percutaneous coronary intervention with stent implantation on right coronary artery was performed. He received triple antithrombotic therapy with aspirin, clopidogrel, intravenous heparin first and then oral anticoagulation with warfarin. During coronary care unit stay, the patient was asymptomatic and hemodynamically stable. However, a control TTE (day 6) in cardiology ward revealed the presence of pseudoaneurysm with an oval out-pouching (23 × 13 mm) from the apical aspect of LV septum, communicating with the LV chamber through a passage measuring 1.6 cm. Partially organized pericardial effusion was evident around right ventricular free wall (Figure 1). Thus, the patient was immediately transferred to the cardiac surgery department for urgent surgical repair. The LV anterior wall rupture with pseudoaneurysm was then treated with endoaneurysmectomy of the LV with dacron patch and freewall reconstruction with prolene sutures and teflon felt stripes. The patient was finally discharged 3 weeks after surgery with betablockers, ace- inhibitors, diuretics, statins and dual antiplatelet therapy with aspirin and clopidogrel. At one month follow-up visit, the patient was hemodynamically stable with acceptable functional capacity. Figure 1Modified five chamber view (a, b) and three chamber view (c, d) showing apical LV pseudoaneurysm (arrows) with moderate pericardial effusion (arrowhead); color Doppler through the passage (arrow) in 3 chamber view (d). LV, left ventricular.
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Viezelis, M., G. Neverauskaite-Piliponiene, A. Marcinkeviciene, E. Teleisyte, T. Kazakevicius, V. Zabiela, V. Sileikis, V. Kviesulaitis, and A. Puodziukynas. "Dual-chamber cardiac pacing effect on left and right atria morphometric parameters and function." European Heart Journal 42, Supplement_1 (October 1, 2021). http://dx.doi.org/10.1093/eurheartj/ehab724.0682.
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Abstract Background Dual-chamber pacemaker implantation is a standard interventional treatment strategy for atrioventricular block (AVB) and sick sinus syndrome (SSS). It has been proven that a high percentage of right ventricular pacing might have detrimental effects on cardiac function. However, there is a lack of data on atrial pacing effect on left (LA) and right (RA) atria function. Purpose To assess the impact atrial pacing on left and right atria morphologic and functional parameters in patients after dual-chamber pacemaker implantation. Methods We conducted a prospective study that included patients who received a dual-chamber pacemaker for an indication of AVB or SSS. After signing of the informed consent pacemaker was programmed for base rate of 40 bpm and no rate response in case of clear AVB indication or for base rate of 60 bpm and rate response if indication was SSS. An transthoracic echocardiography was done the next day after pacemaker implantation and after one month at follow up (FU). During the FU the atrial pacing (AP) and ventricular pacing (VP) percentage were captured. To exclude the impact of right ventricular pacing, patients with high VP percentage (>40%) were excluded from analysis. Patients were divided into two groups – group A with high AP (>50%), and group B – low AP (<50%). LA expansion fraction reflecting reservoir function, emptying – reflecting conduit, and active emptying reflecting “atrial kick” were analysed. To compare means the Mann Whitney U test, and for categorical variables – X2 test were used. Results A total of n=100 patients underwent dual-chamber implantation and signed informed consent. Due to significant structural heart disease or reduced ejection fraction (<50%) 11 patients were excluded. Out of those, n=30 were excluded due to a high VP percentage. Group consisted of n=28 and group B of – n=31 patients. Average AP in group A was 66.2% and 5.0% in group B. The mean age (group A 73.6 SD 8.8 years vs group B 79.2 SD 7.3 years, p=0.197), gender distribution (group A males 45.5% vs group B 50.0%, p=0.773), and mean BMI (group A 26.5 SD 4.7 kg/m2 vs group B 29.2 SD 3.3 kg/m2, p=0.191) did not differ significantly between the two groups. The baseline LA and RA morphometric and functional parameters presented in figure 1 and did not differ significantly between the two groups. The change in LA and RA functional parameters presented in figure 2. Even though it did not reach statistical significance, a tendency for lower LA expansion fraction, active emptying fraction and LA ejection fraction were observed in group A. RA morphometric parameters did not change significantly between the two groups at FU. Conclusion A higher percentage of atrial pacing in dual-chamber pacemaker population could lead to impaired LA function over time. Though, longer observational period is needed. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2
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Viezelis, M., G. Neverauskaite-Piliponiene, A. Marcinkeviciene, E. Teleisyte, T. Kazakevicius, V. Zabiela, V. Kviesulaitis, V. Sileikis, and A. Puodziukynas. "Dual-chamber cardiac pacing short-term effect on left and right atria morphometric parameters and function." European Heart Journal - Cardiovascular Imaging 23, Supplement_1 (February 1, 2022). http://dx.doi.org/10.1093/ehjci/jeab289.145.
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Abstract Funding Acknowledgements Type of funding sources: None. Background. Dual-chamber pacemaker implantation is a standard interventional treatment strategy for symptomatic sinus syndrome (SSS) or advanced atrioventricular block (AVB). It is already known that right ventricular pacing might have detrimental effects on cardiac function. However, knowledge about atrial pacing effect on left (LA) and right (RA) atria function is still lacking. Purpose. To assess the impact atrial pacing on left and right atria morphologic and functional parameters in patients after dual-chamber pacemaker implantation. Methods. We conducted a prospective study that included patients who received a dual-chamber pacemaker for an indication of AVB or SSS. A base rate of 40 bpm and no rate response in case of clear AVB indication or a base rate of 60 bpm and rate response if indication was SSS were chosen. A transthoracic echocardiography was done the next day after pacemaker implantation and after 1 and 3 months. To remove the impact of right ventricular pacing, patients with high VP percentage (>40%) were excluded from analysis. Patients were divided into two groups – group A with high AP (>50%), and group B – low AP (<50%). LA expansion fraction reflecting reservoir function, emptying - reflecting conduit, and active emptying reflecting "atrial kick" were analysed. To compare means the Mann Whitney U test, and for categorical variables – X² test were used. Results A total of n = 78 patients underwent dual-chamber implantation and signed informed consent. Due to significant structural heart disease or reduced ejection fraction (<50%) 7 patients were excluded from further analysis. Out of those, n = 21 were excluded due to a high VP percentage. Group A consisted of n = 26 and group B of – n = 24 patients. Average AP in group A was 63,5% and 68,3% at 1 and 3 months and 5,6% and 7,2% in group B respectively. The mean age (group A 74,5 SD 8,6 years vs group B 78,1 SD 8,0 years, p = 0,266), gender distribution (group A males 45,5% vs group B 48,4%, p = 0,774), and mean BMI (group A 26,4 SD 4,8 kg/m2 vs group B 29,5 SD 3,7 kg/m2, p = 0,202) did not differ significantly between the two groups. The mean left ventricular end diastolic diameter (LVEDD) and indexed LVEDD were not significantly different at baseline and did not change during the follow up period. The baseline LA and RA morphometric and functional parameters presented was not different at baseline between the two groups. The change in LA and RA functional parameters presented in figures. A tendency for a lower LA expansion fraction, active emptying fraction and LA ejection fraction were observed in group A. The trend was contant during 1 and 3 month follow-up periods. RA morphometric parameters did not change significantly between the two groups. Conclusion Impaired LA function in a higher percentage of atrial pacing is seen early after pacemaker implantation and could progress over time. Though, even longer observational period is needed. Abstract Figure. Abstract Figure.
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Ogawa, Emiyo, Kaoru Dohi, Katsuya Onishi, Takeshi Takamura, Hiroshi Nakajima, Masaki Tanabe, Satoshi Ota, et al. "Abstract 5779: Quantification of Right Ventricular Dyssynchrony in Acute Pulmonary Embolism and Right Ventricular Pressure Overload Using Speckle-Tracking Strain Imaging." Circulation 118, suppl_18 (October 28, 2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_100-b.
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Acute right ventricular (RV) pressure overload can alter RV systolic synchronicity associated with RV expansion and wall motion abnormalities in patinets with acute pulmonary thrombo-embolism (APTE). Twenty patients with massive or sub-massive APTE (mean age 57 ± 18 years, estimated peak systolic pulmonary pressure 51 ± 16mmHg) had echocardiography with speckle-tracking strain imaging on admission. RV dyssynchrony was defined as the time difference from earliest to latest peak strain among 6-sites (basal septum, mid septum, apical septum, apical free wall, mid free wall, basal free wall) form apical 4-chamber view using speckle-tracking longitudinal strain imaging. All intervals were corrected for heart rate (corrected interval = measured interval/(RR interval) 1/2 ). Twenty normal subjects (Control: mean age 58 ± 10 years) were also assessed RV function and synchronicity for comparison. APTE had significantly low RV fractional area change (29 ± 10%* vs. 50 ± 7%), low global RV strain (−13 ± 4%* vs. −25 ± 3%), and large RV dyssynchorny (220 ± 103msec* vs. 78 ± 39msec) compared with Control (*p<0.05 vs. Control). After hemodynamic recovery from acute RV pressure overload by primary thrombolysis and/or anticoagulation therapy, both global RV strain and dyssynchrony were improved (−18 ± 4%† and 130 ± 53msec†, †p<0.05 vs. APTE on admission, respectively). Acute RV pressure overload induced reversible RV systolic dyssynchrony associated with RV systolic dysfunction in patients with APTE.
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Sudo, Yuta, and Hiroshi Inagaki. "Rapid daily expansion of highly mobile intracardiac calcified tissue: a case report." European Heart Journal - Case Reports, May 31, 2023. http://dx.doi.org/10.1093/ehjcr/ytad265.
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Abstract Background A calcified amorphous tumour (CAT) is a nonneoplastic mass lesion arising within the cardiac chamber. CATs are rare but are a common cause of organ embolism. In the present study, we experienced a case of an intracardiac mass with calcification that, in contrast to a typical CAT, suddenly appeared and rapidly expanded without an inflammatory response based on pathological findings. Case Summary A 58-year-old Japanese man undergoing peritoneal haemodialysis had a high-echoic mobile mass (15 × 6 mm), which was not visible on the transthoracic echocardiography (TTE) approximately a month earlier, in the left ventricular outflow tract noted on TTE performed during a close examination for fever. Although multiple blood cultures were negative, ampicillin/sulbactam and ceftriaxone were initially administered because of suspected blood culture-negative endocarditis. The mass rapidly enlarged (22 × 5 mm) over the following days. A CAT was suspected and resected based on imaging findings with calcification; however, the pathological findings did not indicate inflammation and fibrin that are typically found in CATs. Echocardiography performed 12 months after the resection showed no recurrence. Discussion This intracardiac calcified tissue had several similar features to a CAT. However, the initial presentation, enlargement rate, and pathological features of the tissue differed from that of a typical CAT. Although it is unknown whether this mass is a subtype of CAT, when an intracardiac calcified tissue is detected using an imaging test, careful follow-up or early surgical resection should be considered given the possibility of rapid tissue enlargement and embolism caused by the mass.
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Tan, Joo Hor, Min Sen Yew, Wenjie Huang, and Kenny Tan. "Left ventricular systolic dysfunction with concomitant bradyarrhythmia in a patient with POEMS syndrome: a case report." European Heart Journal - Case Reports, January 4, 2021. http://dx.doi.org/10.1093/ehjcr/ytaa510.
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Abstract Background POEMS syndrome (PS) is a paraneoplastic disorder from plasma cell dyscrasia, characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes. Vascular endothelial growth factors (VEGFs)-driven fluid extracellular matrix expansion plays a key role in this condition. Associated cardiac involvement has been sparsely reported thus far. Case summary A 55-year-old woman with PS presented with a pleural effusion and respiratory failure requiring mechanical ventilation. Transthoracic echocardiogram revealed left ventricular (LV) systolic dysfunction with a moderate pericardial effusion. She developed intermittent complete heart block and ventricular standstill, requiring temporary transcutaneous pacing. Further evaluation revealed no significant coronary stenosis on coronary angiogram and cardiac magnetic resonance (CMR) showed elevated T1 and extracellular volume suggestive of myocardial oedema with possible early cardiac infiltration. She had a dual-chamber permanent pacemaker implanted in view of recurrent high-grade heart block. She was initiated on a daratumumab-based chemotherapy regimen prior to discharge. She recovered well subsequently with a promising clinical response to chemotherapy. Discussion We describe the first case of LV systolic dysfunction with concomitant significant bradyarrhythmia in a patient with PS. CMR revealed evidence suggestive of LV myocardial oedema and/or possible early infiltration. VEGF overexpression could explain oedema-related LV dysfunction which reversed with adequate diuresis, as well as damage to the conduction system. Early cardiac amyloidosis, which can be associated with PS, is an important differential diagnosis. Pacemaker implantation, adequate diuresis, and definitive chemotherapy are key to the management of concomitant ventricular myocardial and electrical dysfunction in such rare case.
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Onohara, Daisuke, Roberto Hernandez-Merlo, Daniella Corporan, Robert A. Guyton, and Muralidhar Padala. "Abstract 16795: A Trans-Ventricular Restraint to Reshape and Reduce the Left Ventricle Halts Chronic Adverse Remodeling in a Rodent Model of Ischemic Cardiomyopathy." Circulation 138, Suppl_1 (November 6, 2018). http://dx.doi.org/10.1161/circ.138.suppl_1.16795.
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Introduction: Elevated wall stress (WS) from chamber dilatation and wall thinning drive cause congestive heart failure(CHF) after a myocardial infarction(MI). Reducing WS by reshaping the left ventricle (LV) could decelerate or halt CHF progression, delaying need for ventricular assist devices or transplantation. In this study, we sought to investigate if a transventricular reshaping device (TRD - Fig 1A,B ) can preserve cardiac function and inhibit adverse remodeling in a rodent model of chronic ischemic cardiomyopathy. Hypothesis: Reducing left ventricular WS and sphericity index (SI) can preserve cardiac function and inhibit adverse remodeling in ischemic cardiomyopathy. Methods: Rats (n=18) were induced with an MI by left coronary artery ligation. 3 weeks post-MI, TRD was implanted on a beating heart in 9 rats (MI+TRD) ( Fig 2A-C ) and no surgery in others (MI only).TRD was tightened with echo, for 25% reduction in end-diastolic diameter and in WS. All rats were survived for another 3 weeks, with echo at 0, 2, 4, 6 weeks post-MI, and invasive hemodynamics at termination. Tissue was snap frozen for RNA-seq analysis. Results: Cardiac dysfunction were confirmed in both groups prior to TRD implantation (%EF in MI+TRD: 77.4±1.2vs. 59.6±2.1; p<0.0001; %EF in MI: 74.7±1.8 vs. 57.0±3.3; p=0.0002 ). TRD implantation and tightening, reduced LVEDD from 8.7±0.2mm to 6.7±0.2mm (23% change, p <0.0001), reduced sphericity index from 0.74±0.04 to 0.54±0.05 (27% reduction, p<0.0001), and WS from 19.9±2.0 to 14.5±1.7 (27% decrease, p=0.0662) ( Fig 3A-B ). At termination, EDV and ESV were significantly reduced in MI+TRD compared to MI alone (EDV: 647.5±39.0μl vs 500.1±14.4μl; p=0.0032; 317.5±16.9 μl vs 218.1±14.7 μl; p=0.0021), indicating halted adverse remodeling with TRD ( Fig 4A-B ). Infarct border zone wall thickness was preserved in MI+TRD, but significantly reduced/thinned in MI ( Fig 5A ), containing infarct expansion. Pre-load adjusted LV dp/dt(max), was significantly higher in MI+TRD compared to MI only ( Fig 5B ). Conclusions: Reshaping and reducing the ischemic LV with the transventricular restraint, improves cardiac contractility, preserves ventricular wall thickness and inhibits infarct expansion in this chronic rodent model of cardiomyopathy.
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Shati, Ayed A., Mohamed Samir A. Zaki, Youssef A. Alqahtani, Mohamed A. Haidara, Mohammed A. Alshehri, Amal F. Dawood, and Refaat A. Eid. "Intermittent Short-Duration Re-oxygenation Attenuates Cardiac Changes in Response to Hypoxia: Histological, Ultrastructural and Oxidant/Antioxidant Parameters." British Journal of Biomedical Science 79 (March 18, 2022). http://dx.doi.org/10.3389/bjbs.2022.10150.
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Context: Intermittent short-duration re-oxygenation attenuates cardiac changes in response to hypoxia.Objective: To see if intermittent short-duration re-oxygenation may protect the heart muscle from hypoxia damage.Materials and Methods: Eighteen albino rats were used to carry out the study. Rats divided into: (normoxia); rats exposed to room air as a control, second (hypoxic) group; rats subjected to a pressure of 405 mmHg in a hypobaric chamber to simulate hypoxia at 5,000 m, and third (intermittent short-duration re-oxygenation); rats exposed to room air three times per day. Experiments were all 14 days long.Results: Hypoxia enhanced the oxidative stress biomarker malondialdehyde while lowering the antioxidant superoxide dismutase . The levels of tumour necrosis factor (TNF-α) and interleukin-6 (IL-6) in the myocardium were elevated in hypoxic hearts. The hypoxic rats’ cardiac myofibrils showed disarray of muscle fibres, vacuolation of the sarcoplasm, pyknosis of the nucleus, and expansion of intercellular gaps on histological examination. In addition, cardiomyocytes showed degenerative defects in ventricular myocardial cells on ultrastructural analysis. Myofibril thinning and degenerative mitochondrial changes affected intercalated discs with fascia adherent, desmosomes, and gap junction. Intermittent short-duration re-oxygenation improve cardiac histological, ultrastructural and oxidant/antioxidant parameters changes during hypoxia.Conclusion: Hypoxia showed a substantial impact on myocardial architecture, as well as increased oxidative stress and pro-inflammatory cytokines. Intermittent short-duration re-oxygenation significantly decreases hypoxia-induced cardiac changes.
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Anupraiwan, Orawan, Sorin V. Pislaru, Patricia A. Pellikka, and Cristina Pislaru. "Abstract 16921: Noninvasive Quantification of Myocardial Elasticity in Patients With Hypertrophic Cardiomyopathy." Circulation 138, Suppl_1 (November 6, 2018). http://dx.doi.org/10.1161/circ.138.suppl_1.16921.
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Introduction: Hypertrophic cardiomyopathy (HCM) is associated with excessive left ventricular (LV) hypertrophy (LVH), myocyte disarray and expansion of interstitial collagen. These factors alter mechanical properties of the myocardial tissue. Intrinsic velocity propagation (iVP) of myocardial stretch is a new validated measure of myocardial elasticity. Hypothesis: iVP in left ventricular (LV) myocardium of patients with HCM will be increased compared to normal subjects. Methods: We studied prospectively 100 subjects: 42 with HCM (age 57 ± 14 years; 79% with asymmetric septal LVH) and 58 normal controls without cardiovascular disease (age 48 ± 13 years). Patients had comprehensive transthoracic echocardiography and cardiac magnetic resonance imaging (MRI; n=29). iVP was measured throughout the LV myocardium during late diastole using ultra-high frame rate tissue Doppler imaging (350-460 fps) (6 LV walls, 3 standard apical views). Chamber stiffness (CS) was evaluated from end-diastolic pressure-volume relationship (EDPVR) estimated noninvasively by the single-beat method (EDP=αV β ). End-diastolic pressure (EDP) was estimated from E/e’. Results: LV ejection fraction was normal in both groups (HCM: 68 ± 7%; Controls: 65 ± 5%). Myocardial stiffness by iVP was markedly higher in HCM vs. controls (Fig.A, left panel). This was confirmed by EDPVRs, which were steeper and shifted leftward (Fig. B, left). The slope (β, load-independent) of EDPVR and CS (dP/dV) were higher and LV capacitance (V 30 , estimated volume at 30 mmHg EDP) was lower in HCM (Fig. B, right) and correlated significantly, though weakly, with iVP (β: r = 0.41; CS dP/dV: r = 0.48; EDP: r = 0.61; p<0.002 for all). Patients with apical variant had lower levels of global iVP compared to patients with predominant septal LVH and diffuse concentric LVH (Fig. A, right). Conclusions: Myocardial stiffness measured noninvasively by the intrinsic wave method is highly abnormal in HCM. This novel approach allows mapping of myocardial elasticity of the entire left ventricle and shows promise to become a clinical tool for evaluation of patients with diastolic tissue abnormalities.
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Ahmet, Ismayil, Hyun-Jin Tae, Michael Brines, Anthony Cerami, Edward G. Lakatta, and Mark Talan. "Abstract 9927: Helix B Surface Peptide, a Small Non-erythropoietic Molecule Based on the Erythropoietin Structure, Effectively Ameliorates the Progression of Chronic Heart Failure in the Rat Post Myocardial Infarction Model." Circulation 126, suppl_21 (November 20, 2012). http://dx.doi.org/10.1161/circ.126.suppl_21.a9927.
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The cardioprotective properties of Erythropoietin (EPO) are well documented in pre-clinical studies. However, due to its erythropoietic and prothrombotic properties, the EPO treatment cannot be used in chronic heart failure (CHF), unless indicated by accompanied anemia. Helix B surface peptide (HBSP), a small peptide synthetized on the basis of EPO molecule (ARA290, Araim Pharmaceutical), does not stimulate erythropoiesis. We have reported similarly strong cardioprotective effects of HBSP and EPO in the rat model of myocardial infarction (MI). In this study, we tested the effect of long-term treatment with HBSP on mortality and cardiac remodeling in post-MI CHF in rats. For the 10 months, starting two weeks after left coronary artery ligation, rats received the i.p. injections of HBSP (60µg/kg; n=33) or saline (n=33) 2 times per week. Compared to saline-treated rats, HBSP treatment significantly reduced mortality (35% vs. 65%; p<0.05). Repeated Echocardiography demonstrated remarkable attenuation of left ventricular (LV) chamber dilatation (EDV: 41% vs. 86%; ESV: 44% vs. 135%; p<0.05), LV functional deterioration (EF: -4% vs. -63%; p<0.05) and MI expansion (3% vs. 38%; p<0.05) in HPSP-treated rats compared to saline-treated rats. Blood hematocrit level measured monthly was not affected by HBSP treatment. An invasive hemodynamic assessment at the end of 10-mo treatment showed better LV systolic function (PRSW: 63±5 vs. 40±4; p<0.05) and Arterio-ventricular coupling (Ea/Ees: 1.2±0.2 vs. 2.7±0.7; p<0.05) in HBSP-treated rats compared to saline-treated rats. Histological analysis revealed less apoptosis (0.6±0.1% vs. 0.9±0.1%; p<0.05), myocardial fibrosis (2.6±0.2% vs. 4.1±0.5%; p<0.05), and myocyte hypertrophy (cell diameter: 31±1µm vs. 37±1µm; p<0.05) in non-infarcted myocardium among HBSP-treated rats compared to saline-treated rats. Results suggest that HBSP could be considered as a safe alternative to EPO for a further clinical testing in the patients with chronic heart failure.
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Che, Chen, Kayla Dudick, and Robin Shoemaker. "Cardiac hypertrophy with obesity is augmented after pregnancy in C57BL/6 mice." Biology of Sex Differences 10, no. 1 (December 2019). http://dx.doi.org/10.1186/s13293-019-0269-z.
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Abstract Background Over a third of reproductive-age women in the USA are obese, and the prevalence of cardiovascular disease (CVD) is rising in premenopausal women. Cardiac hypertrophy is an independent predictor of CVD. In contrast to pregnancy, where transiently increased left ventricular (LV) mass is not associated with cardiac damage, obesity-mediated cardiac hypertrophy is pathological. There is a paucity of data describing the effect of obesity during pregnancy on maternal cardiovascular health. The purpose of this study was to determine the long-term effect of obesity during pregnancy on cardiac function and structure in mice. Methods Female C57BL/6 J mice were fed a high-fat (HF) or a low-fat (LF) diet for 20 weeks. After 4 weeks, LF- and HF-fed female mice were either crossed with males to become pregnant or remained non-pregnant controls. Following delivery, pups were euthanized, and females maintained on respective diets. After 20 weeks of diet feeding, cardiac function was quantified by echocardiography, and plasma leptin and adiponectin concentrations quantified in LF- and HF-fed postpartum and nulliparous females. mRNA abundance of genes regulating cardiac hypertrophy and remodeling was quantified from left ventricles using the NanoString nCounter Analysis System. Cardiac fibrosis was assessed from picrosirius red staining of left ventricles. Results HF-fed postpartum mice had markedly greater weight gain and fat mass expansion with obesity, associated with significantly increased LV mass, cardiac output, and stroke volume compared with HF-fed nulliparous mice. Plasma leptin, but not adiponectin, concentrations were correlated with LV mass in HF-fed females. HF feeding increased LV posterior wall thickness; however, LV chamber diameter was only increased in HF-fed postpartum females. Despite the marked increase in LV mass in HF-fed postpartum mice, mRNA abundance of genes regulating fibrosis and interstitial collagen content was similar between HF-fed nulliparous and postpartum mice. In contrast, only HF-fed postpartum mice exhibited altered expression of genes regulating the extracellular matrix. Conclusions These results suggest that the combined effects of pregnancy and obesity augment cardiac hypertrophy and promote remodeling. The rising prevalence of CVD in premenopausal women may be attributed to an increased prevalence of women entering pregnancy with an overweight or obese BMI.
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Larsen, A. I., N. Butt, P. Aukrust, P. S. Munk, J. M. Nilsen, S. Orn, and T. Ueland. "P826Peri-procedural treatment with high dose Rosuvastatin reduces soluble TNF receptor 1 in patients treated with primary percutaneous coronary intervention for ST elevation myocardial infarction." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz747.0425.
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Abstract Background The extent of cardiac injury in ST elevation myocardial infarction (STEMI) depends on the level of inflammation and subsequent immune cell recruitment. An inflammatory phase that is disproportionately prolonged, of excessive magnitude, or insufficiently suppressed, can lead to sustained tissue damage and improper healing, promoting infarct expansion, adverse remodelling and chamber dilatation. Soluble TNF receptor 1 (sTNFR-1) is believed to mirror systemic pan-inflammatory status more closely than a single cytokine antigenic level. sTNFR-1 levels might give prognostic information, independent from and, at the same time, additive with some well-recognized outcome predictors such as left ventricular ejection fraction. Purpose We hypothesised that sTNFR-1 and other inflammatory markers could be modulated by statins. Methods Plasma levels of inflammatory markers were measured at baseline, 2 days, 7 days and 2 months in consecutive patients with first time STEMI with single vessel disease. Twenty-five patients (treatment group (TG)) were treated with 80 mg Rosuvastatin daily with first dose before primary percutaneous coronary intervention (PCI) whereas the control group (CG) consisted of 34 patients in whom treatment with 20 mg simvastatin daily were initiated the day after PPCI. Results sTNFR1 increased during the first 48 hours following PCI and this increase was larger in the CG compared with the TG (0.22±0.30 ng/mL vs 0.08±0.19 ng/nmL, p=0.025). The difference in increase during one week was only borderline statistically significant (0.21±0.30 ng/mL vs 0.08±0.26 ng/mL, p=0.081). These differences in the kinetics of sTNRF-1 were mirrored by changes in Pentraxin 3 (PTX3) between groups from baseline to 1 week, CG vs TG. (0.28±0.70 μmol/l vs 0.10±0.05 ng/mL, p=0.014) and at 2 months (−0.42±0.56 ng/mL vs 0.08±0.60 μmol/l, p=0.032) Conclusion High dose Rosuvastatin therapy initiated peri-procedural during PPCI for STEMI reduces pan inflammation as reflected by sTNFR1 and is associated with a less abrupt fall in PTX3 at 1 week and 2 months supporting recent research suggesting that PTX3 plays a cardiovascular protective effect in cardiovascular disease and healing. Acknowledgement/Funding Western Norway Regional Health Authority
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Vijiiac, A. E., C. Acatrinei, C. Neagu, S. Onciul, D. Zamfir, R. Onut, M. Stoian, S. Iancovici, I. Petre, and M. Dorobantu. "P2598Left atrial mechanics in patients with acute pulmonary edema and preserved ejection fraction." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz748.0923.
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Abstract Background The left atrium (LA) is a highly dynamic chamber that has 3 mechanical functions (reservoir, conduit, booster pump), as well as additional endocrine and regulatory properties. It is a marker of both the severity and chronicity of diastolic dysfunction and its remodelling has been shown to be a reliable predictor of clinical outcome in patients with heart disease. While LA function has been extensively studied in chronic heart failure, information about LA mechanics in patients with acute heart failure and preserved left ventricular ejection fraction (EF) are scarce. Purpose We sought to assess LA mechanics in a cohort of patients with acute pulmonary edema and preserved EF and compare it with a normal reference group. Methods We included 50 consecutive patients (22 men) with acute pulmonary edema, preserved EF and sinus rhythm in our study. Patients with significant mitral or aortic valve disease were not considered eligible. The control group consisted of 30 subjects (18 men) with no previous cardiovascular disease. We performed conventional transthoracic echocardiography for all patients and we assessed various parameters of LA mechanics. To evaluate the reservoir function, we determined the total ejection volume (EV), the total EF, the LA expansion index (LAEI) and the LA function index (LAFI). To evaluate the conduit function, we determined the passive EV and passive EF. For the booster pump function, we determined the active EV, active EF, the atrial filling fraction, the ejection force and the LA kinetic energy (LAKE). We used T-test to compare the parameters between the two groups. Results The mean age in the study group was 72±14 years, while in the control group the mean age was 56±16 years (p=0.06). The total EV did not differ significantly between groups (p=0.44). The total LA ejection fraction was lower in the study group: 29±10% vs. 51±9% (p<0.001), as well as the LAEI (45.1±24.6 vs. 110.9±32.1, p<0.001) and the LAFI (0.17±0.12 vs. 0.58±0.20, p<0.001). Among parameters assessing LA conduit function, there were no differences in passive EV (p=0.64), but passive LA ejection fraction was significantly lower in the study group: 15±7% vs. 28±11%, p=0.003. The same trend was noted for active LA ejection fraction (16±10% vs. 31±13%, p=0.005). The ejection force was impaired in the study group: 39.1±30.6 kdynes vs. 15.2±12.3 kdynes, p<0.001. Other parameters evaluating LA booster pump function did not differ significantly between groups (p=0.12 for atrial filling fraction, p=0.74 for LAKE). Conclusion All three integrated phases of left atrial mechanics (reservoir, conduit, booster pump) are impaired in patients with acute pulmonary edema and preserved left ventricular EF. These findings highlight the importance of diastolic dysfunction in the pathogenesis of acute heart failure for these patients and they suggest that LA dysfunction might be a potential therapeutic target in this clinical setting. Acknowledgement/Funding This work was supported by CREDO Project - ID: 49182, financed through the SOP IEC-A2-0.2.2.1-2013-1 cofinanced by the ERDF
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Bhat, A., H. H. L. Chen, S. Khanna, C. H. Gan, R. Menzies, C. M. Nunes, R. MacIntyre, and T. C. Tan. "P2468Clinical and cardiac structural differences between paroxysmal and persistent/permanent non-valvular atrial fibrillation." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz748.0800.
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Abstract Background Atrial Fibrillation (AF) is a heterogeneous condition and is traditionally classified by duration (paroxysmal, persistent and permanent). There is a relationship between AF and left atrial (LA) remodeling, with increased likelihood of AF recurrence and maintenance with increasing LA volumes. Purpose To assess clinical and cardiac structural differences between the subtypes of AF. Methods We examined 1247 (68±13.4y; 50% men) consecutive admissions presenting to our institution with the primary diagnosis of AF. Repeat admissions (n=263) were excluded. Of remaining 984 subjects, a majority had diagnosed paroxysmal (72.2%), with lower numbers of persistent (23.4%) and permanent (4.4%) AF. Echo parameters of cardiac chamber size and function were examined in a subset of subjects with complete echo (n=646) performed during incident hospital admission. Results There were significantly higher rates of diabetes mellitus (p=0.03), ischaemic heart disease (IHD; p=0.04) and peripheral vascular disease (PVD; p=0.02) in those with persistent/permanent AF compared to paroxysmal AF. No significant differences in age (p=0.19), BMI (p=0.42), OSA (p=0.05), or hypertension (p=0.76) was noted. There were significant differences in left ventricular (LV) mass and systolic function, LA size and function between the two groups (Table 1). Receiver operator curve analysis revealed that LAEF was a discriminator for persistent/permanent AF with an area under the curve of 0.689 (95% CI, 0.646 to 0.732; p<0.001). Echo parameters in AF subtype Echocardiographic Parameters Paroxysmal AF (n=433) Persistent and Permanent AF (n=213) Significance (p value) LVEDD (cm) 4.8±3.0 5.0±0.9 0.29 LVESD (cm) 3.3±1.3 3.7±1.1 <0.01 IVS thickness (cm) 1.2±0.7 1.1±0.3 0.44 PW thickness (cm) 1.1±0.7 1.1±0.2 0.77 LV mass (g) 92.3±28.3 108.2±35.3 <0.01 LVEF (%) 56.1±14.1 47.4±16.8 <0.01 LA Expansion Index 89.4±69.1 53.4±40.3 <0.01 Min LA Volume indexed (ml/m2) 18.9±17.2 27.3±20.6 0.01 Max LA Volume indexed (ml/m2) 32.5±19.2 37.7±15.3 <0.01 LAEF (%) 41.8±16.4 31.5±13.6 <0.01 Conclusions Our results suggest diabetes, IHD and PVD are associated with persistent/permanent AF. Additionally, greater LA remodeling and reduced atrial function was noted in this group, suggestive of an association between duration of AF electrical burden and LA remodeling and function.
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Henry, J. A., I. Abdesselam, O. Deal, A. J. Lewis, J. Rayner, M. Bernard, A. Dutour, et al. "Changes in epicardial and visceral adipose tissue depots following bariatric surgery and their effect on cardiac geometry." Frontiers in Endocrinology 14 (January 25, 2023). http://dx.doi.org/10.3389/fendo.2023.1092777.
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IntroductionObesity affects cardiac geometry, causing both eccentric (due to increased cardiac output) and concentric (due to insulin resistance) remodelling. Following bariatric surgery, reversal of both processes should occur. Furthermore, epicardial adipose tissue loss following bariatric surgery may reduce pericardial restraint, allowing further chamber expansion. We investigated these changes in a serial imaging study of adipose depots and cardiac geometry following bariatric surgery.Methods62 patients underwent cardiac magnetic resonance (CMR) before and after bariatric surgery, including 36 with short-term (median 212 days), 37 medium-term (median 428 days) and 32 long-term (median 1030 days) follow-up. CMR was used to assess cardiac geometry (left atrial volume (LAV) and left ventricular end-diastolic volume (LVEDV)), LV mass (LVM) and LV eccentricity index (LVei – a marker of pericardial restraint). Abdominal visceral (VAT) and epicardial (EAT) adipose tissue were also measured.ResultsPatients on average had lost 21kg (38.9% excess weight loss, EWL) at 212 days and 36kg (64.7% EWL) at 1030 days following bariatric surgery. Most VAT and EAT loss (43% and 14%, p<0.0001) occurred within the first 212 days, with non-significant reductions thereafter. In the short-term LVM (7.4%), LVEDV (8.6%) and LAV (13%) all decreased (all p<0.0001), with change in cardiac output correlated with LVEDV (r=0.35,p=0.03) and LAV change (r=0.37,p=0.03). Whereas LVM continued to decrease with time (12% decrease relative to baseline at 1030 days, p<0.0001), both LAV and LVEDV had returned to baseline by 1030 days. LV mass:volume ratio (a marker of concentric hypertrophy) reached its nadir at the longest timepoint (p<0.001). At baseline, LVei correlated with baseline EAT (r=0.37,p=0.0040), and decreased significantly from 1.09 at baseline to a low of 1.04 at 428 days (p<0.0001). Furthermore, change in EAT following bariatric surgery correlated with change in LVei (r=0.43,p=0.0007).ConclusionsCardiac volumes show a biphasic response to weight loss, initially becoming smaller and then returning to pre-operative sizes by 1030 days. We propose this is due to an initial reversal of eccentric remodelling followed by reversal of concentric remodelling. Furthermore, we provide evidence for a role of EAT contributing to pericardial restraint, with EAT loss improving markers of pericardial restraint.
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Poleggi, Cristina, Davide Restelli, Alfredo Luongo, Olga La Cognata, Armando Lo Savio, Pasquale Crea, Antonio Micari, Gianluca Di Bella, and Giuseppe Dattilo. "230 ANOMALOUS ORIGIN OF LEFT CIRCUMFLEX ARTERY FROM RIGHT SINUS OF VALSALVA: A RARE CASE BUT WITH GREAT CLINICAL RELEVANCE." European Heart Journal Supplements 24, Supplement_K (December 14, 2022). http://dx.doi.org/10.1093/eurheartjsupp/suac121.274.
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Abstract Introduction The anomalous connection of the left circumflex artery (LCx) to the right coronary artery (RCA) or sinus is the most frequent coronary artery (CA) anomaly. Among them, only those with an interarterial course are regarded as hidden conditions at risk of myocardial ischemia (MI) and sudden cardiac death (SCD). We report an uncommon of anomalous origin of LCx from the right sinus of Valsalva and a retroaortic path causing MI. Case presentation A 61-year-old man presented to the emergency department complaining palpitations and chest discomfort for an hour. He only had history of hypertension. Physical examination was unremarkable. The ECG demonstrated atrial flutter with a 2:1 conduction ratio and a ventricular rate of 157 bpm and ST segment depression in leads V4-6. Transthoracic echocardiography did not reveal segmental kinetic anomalies but a five-chamber apical view showed a “RAC sign”, typical of anomalous retroaortic course of the left coronary artery. The patient was treated with intravenous infusion of amiodarone. He restored sinus rhythm and symptoms regressed completely, but the ECG taken after conversion showed flattened T waves in leads V5-6 and negative T waves in I and aVL. Cardiac enzymes had transient increase. After the acute episode ended the patient underwent cardiac computed tomography angiography (CTA) with evidence of anomalous origin of LCx from the right sinus with a retroaortic course. A coronary angiography excluded obstructive atherosclerotic coronary lesions. Nuclear myocardial perfusion imaging revealed reversible small subsegmental perfusion defects in mid inferolateral wall and apical lateral wall. We established a medical treatment with beta-blocker. Discussion Our patient had anomalous connection of the LCx branch to the right sinus of Valsalva with a retroaortic course. Although this anomaly is usually considered benign, cases of association with SCD and MI have been reported. The factor responsible for this pathogenicity could be high orifice, ostial stenosis, slit-like/fish-mouth-shaped orifice and acute-angle take-off. As cardiac CTA did not reveal any of these characteristics, we hypothesized that the increased cardiac output and expansion of the great vessels during tachycardia could cause compression of the retroaortic segment or angling at its origin and generate ischemia. Repolarization abnormalities at ECG are well documented during supraventricular tachycardia as a response to pacing-induced stress. These changes are usually diffused and disappear after conversion to sinus rhythm. In this case they appeared hours later, accompanied by cardiac enzyme buildup. As the epicardial coronary arteries did not show any pathology, we suggest that the patient had transient ischemia due to LCx anomaly. We confirmed it by myocardial perfusion imaging. As for the management of this anomaly in adults, surgery is recommended as class IC in patients with typical angina symptoms who present with evidence of stress-induced myocardial ischemia in a matching territory or high-risk anatomy. Our patient has never had clear manifestations of angina. All these elements together with the age of our patient motivated us to use a conservative approach. Conclusions We report a case of anomalous origin of LCx from right sinus of Valsalva causing transient myocardial ischemia in a patient that has always been asymptomatic. This anomaly has been and continues to be considered benign, nevertheless we suggest to judge the clinical significance of this kind of CA anomaly on a case-by-case integrated approach.