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Prasad, Megha, Michel T. Corban, Timothy D. Henry, Allan B. Dietz, Lilach O. Lerman, and Amir Lerman. "Promise of autologous CD34+ stem/progenitor cell therapy for treatment of cardiovascular disease." Cardiovascular Research 116, no. 8 (February 5, 2020): 1424–33. http://dx.doi.org/10.1093/cvr/cvaa027.
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Abstract CD34+ cells are haematopoietic stem cells used therapeutically in patients undergoing radiation or chemotherapy due to their regenerative potential and ability to restore the haematopoietic system. In animal models, CD34+ cells have been associated with therapeutic angiogenesis in response to ischaemia. Several trials have shown the potential safety and efficacy of CD34+ cell delivery in various cardiovascular diseases. Moreover, Phase III trials have now begun to explore the potential role of CD34+ cells in treatment of both myocardial and peripheral ischaemia. CD34+ cells have been shown to be safe and well-tolerated in the acute myocardial infarction (AMI), heart failure, and angina models. Several studies have suggested potential benefit of CD34+ cell therapy in patients with coronary microvascular disease as well. In this review, we will discuss the therapeutic potential of CD34+ cells, and describe the pertinent trials that have used autologous CD34+ cells in no-options refractory angina, AMI, and heart failure. Lastly, we will review the potential utility of autologous CD34+ cells in coronary endothelial and microvascular dysfunction.
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Morrow, Andrew J., Sabrina Nordin, Patrick O’Boyle, and Colin Berry. "‘Acute micro-coronary syndrome’: detailed coronary physiology in a patient with Takotsubo cardiomyopathy." BMJ Case Reports 12, no. 8 (August 2019): e229618. http://dx.doi.org/10.1136/bcr-2019-229618.
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Takotsubo cardiomyopathy (TC), otherwise known as stress cardiomyopathy, is characterised by acute, transient left ventricular systolic dysfunction with apical ballooning in the absence of obstructive epicardial coronary stenosis. The presentation of TC mimics that of acute myocardial infarction. More recently there has been a shift towards thinking of TC as a ‘microvascular acute coronary syndrome’. Our case is of an 82-year-old woman who presented with TC mimicking acute anterior ST elevation myocardial infarction in the context of sepsis. Slow flow noted in the left anterior descending artery prompted us to perform coronary physiology. Her fractional flow reserve was 0.91, with an index of myocardial resistance of 117 and a coronary flow reserve of 1.6. In combination these results are indicative of microvascular coronary dysfunction in the absence of significant epicardial stenosis.
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Beltrame, John F. "Coronary microvascular dysfunction in acute ST elevation myocardial infarction." Coronary Artery Disease 28, no. 1 (January 2017): 3–4. http://dx.doi.org/10.1097/mca.0000000000000443.
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Camici, Paolo G., Carsten Tschöpe, Marcelo F. Di Carli, Ornella Rimoldi, and Sophie Van Linthout. "Coronary microvascular dysfunction in hypertrophy and heart failure." Cardiovascular Research 116, no. 4 (January 30, 2020): 806–16. http://dx.doi.org/10.1093/cvr/cvaa023.
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Abstract Left ventricular (LV) hypertrophy (LVH) is a growth in left myocardial mass mainly caused by increased cardiomyocyte size. LVH can be a physiological adaptation to physical exercise or a pathological condition either primary, i.e. genetic, or secondary to LV overload. Patients with both primary and secondary LVH have evidence of coronary microvascular dysfunction (CMD). The latter is mainly due to capillary rarefaction and adverse remodelling of intramural coronary arterioles due to medial wall thickening with an increased wall/lumen ratio. An important feature of this phenomenon is the diffuse nature of this remodelling, which generally affects the coronary microvessels in the whole of the left ventricle. Patients with LVH secondary to arterial hypertension can develop both heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). These patients can develop HFrEF via a ‘direct pathway’ with an interval myocardial infarction and also in its absence. On the other hand, patients can develop HFpEF that can then progress to HFrEF with or without interval myocardial infarction. A similar evolution towards LV dysfunction and both HFpEF and HFrEF can occur in patients with hypertrophic cardiomyopathy, the most common genetic cardiomyopathy with a phenotype characterized by massive LVH. In this review article, we will discuss both the experimental and clinical studies explaining the mechanisms responsible for CMD in LVH as well as the evidence linking CMD with HFpEF and HFrEF.
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Konijnenberg, Lara S. F., Peter Damman, Dirk J. Duncker, Robert A. Kloner, Robin Nijveldt, Robert-Jan M. van Geuns, Colin Berry, Niels P. Riksen, Javier Escaned, and Niels van Royen. "Pathophysiology and diagnosis of coronary microvascular dysfunction in ST-elevation myocardial infarction." Cardiovascular Research 116, no. 4 (November 9, 2019): 787–805. http://dx.doi.org/10.1093/cvr/cvz301.
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Abstract Early mechanical reperfusion of the epicardial coronary artery by primary percutaneous coronary intervention (PCI) is the guideline-recommended treatment for ST-elevation myocardial infarction (STEMI). Successful restoration of epicardial coronary blood flow can be achieved in over 95% of PCI procedures. However, despite angiographically complete epicardial coronary artery patency, in about half of the patients perfusion to the distal coronary microvasculature is not fully restored, which is associated with increased morbidity and mortality. The exact pathophysiological mechanism of post-ischaemic coronary microvascular dysfunction (CMD) is still debated. Therefore, the current review discusses invasive and non-invasive techniques for the diagnosis and quantification of CMD in STEMI in the clinical setting as well as results from experimental in vitro and in vivo models focusing on ischaemic-, reperfusion-, and inflammatory damage to the coronary microvascular endothelial cells. Finally, we discuss future opportunities to prevent or treat CMD in STEMI patients.
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Varrichione, Giuseppe, Flavio Giuseppe Biccire’, Riccardo Di Pietro, Francesco Prati, and Paola Battisti. "The risk of acute coronary events in microvascular disease." European Heart Journal Supplements 24, Supplement_I (November 12, 2022): I127—I130. http://dx.doi.org/10.1093/eurheartjsupp/suac103.
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Abstract The microvascular disease represents a widespread clinical entity in the general population, especially among women. The dysfunction of the microcirculation is often responsible for myocardial ischaemia and angina in the absence of significant stenosis of the epicardial district, while in other cases it can represent a contributing cause of angina even in the presence of coronary artery disease, cardiomyopathies or heart failure. The cardiovascular risk factors of people with microvascular disease are similar to those who develop epicardial atherosclerotic disease. However, the prognostic significance of microvascular disease remains a matter of debate. An element to be clarified, in fact, is whether subjects with dysfunction of the microcirculation and coronary tree without significant stenoses present an increased risk of myocardial infarction and sudden death. In recent years, several studies seem to confirm an association between microvascular disease and progression of coronary epicardial atherosclerosis. The prognosis of microvascular disease would therefore not be benign as was previously believed, but associated with an increased risk of cardiovascular events including revascularization, heart attack, and cardiac death.
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Kang, Min Gyu, Bon-Kwon Koo, Udaya S. Tantry, Kyehwan Kim, Jong-Hwa Ahn, Hyun Woong Park, Jeong Rang Park, et al. "Association Between Thrombogenicity Indices and Coronary Microvascular Dysfunction in Patients With Acute Myocardial Infarction." JACC: Basic to Translational Science 6, no. 9-10 (September 2021): 749–61. http://dx.doi.org/10.1016/j.jacbts.2021.08.007.
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Safdar, Basmah, Gail D’Onofrio, James Dziura, Raymond R. Russell, Caitlin Johnson, and Albert J. Sinusas. "Prevalence and characteristics of coronary microvascular dysfunction among chest pain patients in the emergency department." European Heart Journal: Acute Cardiovascular Care 9, no. 1 (March 15, 2018): 5–13. http://dx.doi.org/10.1177/2048872618764418.
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Aims: Coronary microvascular dysfunction (CMD) is common in patients with non-obstructive coronary arteries but has not been described in low-risk symptomatic patients. We therefore assessed the prevalence and characteristics of CMD in low to moderate risk patients with chest pain in an emergency department. Methods and results: We used three-dimensional Rb82 cardiac positron emission tomography/computed tomography to diagnose coronary artery disease (known or new regional defect, any coronary calcification) and CMD (low coronary flow reserve without coronary artery disease) in chest pain patients after being ruled out for acute myocardial infarction. Exclusions included age 30 years or less, acute myocardial infarction, hemodynamic instability, heart failure and dialysis. Among 195 participants undergoing cardiac positron emission tomography/computed tomography, 42% had CMD, 36% had coronary artery disease and 22% had normal flows; 70% were women and 84% were obese. Patients with CMD and coronary artery disease had significantly lower coronary flow reserve than normal patients (mean coronary flow reserve 1.6 and 1.9 vs. 2.6, respectively, P<0.05). However, CMD patients were younger (mean age 51 vs. 61 years), and had fewer traditional cardiac risk factors ( P<0.05) than patients with coronary artery disease. Nearly one third (31%) of patients had a prior emergency department visit for chest pain within three years of index presentation. Women were four times as likely to have CMD as men (adjusted odds ratio 4.2; 95% confidence interval 1.8, 9.6) after controlling for age, race, hypertension, diabetes, smoking, dyslipidemia, obesity and family history of coronary artery disease. Conclusions: Despite their low-risk profile, nearly one half of symptomatic and mostly obese emergency department patients without evidence of myocardial infarction or coronary artery disease had CMD. The results could explain the high rates of return visits associated with chest pain, although their application to the general emergency department population require validation.
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Sachdev, Esha, C. Noel Bairey Merz, and Puja K. Mehta. "Takotsubo Cardiomyopathy." European Cardiology Review 10, no. 1 (2015): 25. http://dx.doi.org/10.15420/ecr.2015.10.01.25.
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Takotsubo cardiomyopathy (TTC) is an acute, stress-induced cardiomyopathy with an increased prevalence in post-menopausal women. The syndrome is most frequently precipitated by an acute emotional or physical stressor and mimics acute myocardial infarction with symptoms, electrocardiogram (ECG) changes and cardiac troponin elevation that are indistinguishable from those caused by plaque rupture or coronary thrombosis. Diagnosis of TTC is made when coronary angiography reveals no obstructive coronary artery disease and the left ventricle demonstrates apical ballooning and basal hypercontractility. Other ventricular patterns have also been described. An abnormal myocardial response to the catecholamine surge from an emotional or a physical stressor is implicated in the pathophysiology, but the reasons for the high prevalence of TTC presentations in post-menopausal women are unknown. Several mechanisms including multi-vessel coronary vasospasm, endothelial and coronary microvascular dysfunction and direct catecholamine toxicity have been proposed. No specific guidelines for treatment of TTC have been established, but treatment is based on the American Heart Association/ American College of Cardiology guidelines for acute coronary syndrome/acute myocardial infarction and heart failure guidelines. In this review article, we discuss the characteristic clinical presentation of TTC and the commonly proposed mechanisms.
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de Waard, Guus A., Gregor Fahrni, Douwe de Wit, Hironori Kitabata, Rupert Williams, Niket Patel, Paul F. Teunissen, et al. "Hyperaemic microvascular resistance predicts clinical outcome and microvascular injury after myocardial infarction." Heart 104, no. 2 (June 29, 2017): 127–34. http://dx.doi.org/10.1136/heartjnl-2017-311431.
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ObjectivesEarly detection of microvascular dysfunction after acute myocardial infarction (AMI) could identify patients at high risk of adverse clinical outcome, who may benefit from adjunctive treatment. Our objective was to compare invasively measured coronary flow reserve (CFR) and hyperaemic microvascular resistance (HMR) for their predictive power of long-term clinical outcome and cardiac magnetic resonance (CMR)-defined microvascular injury (MVI).MethodsSimultaneous intracoronary Doppler flow velocity and pressure measurements acquired immediately after revascularisation for AMI from five centres were pooled. Clinical follow-up was completed for 176 patients (mean age 60±10 years; 140(80%) male; ST-elevation myocardial infarction (STEMI) 130(74%) and non-ST-segment elevation myocardial infarction 46(26%)) with median follow-up time of 3.2 years. In 110 patients with STEMI, additional CMR was performed.ResultsThe composite end point of death and hospitalisation for heart failure occurred in 17 patients (10%). Optimal cut-off values to predict the composite end point were 1.5 for CFR and 3.0 mm Hg cm−1•s for HMR. CFR <1.5 was predictive for the composite end point (HR 3.5;95% CI 1.1 to 10.8), but not for its individual components. HMR ≥3.0 mm Hg cm−1 s was predictive for the composite end point (HR 7.0;95% CI 1.5 to 33.7) as well as both individual components. HMR had significantly greater area under the receiver operating characteristic curve for MVI than CFR. HMR remained an independent predictor of adverse clinical outcome and MVI, whereas CFR did not.ConclusionsHMR measured immediately following percutaneous coronary intervention for AMI with a cut-off value of 3.0 mm Hg cm−1 s, identifies patients with MVI who are at high risk of adverse clinical outcome. For this purpose, HMR is superior to CFR.
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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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Bularga, Anda, John Hung, Marwa Daghem, Stacey Stewart, Caelan Taggart, Ryan Wereski, Trisha Singh, et al. "Coronary Artery and Cardiac Disease in Patients With Type 2 Myocardial Infarction: A Prospective Cohort Study." Circulation 145, no. 16 (April 19, 2022): 1188–200. http://dx.doi.org/10.1161/circulationaha.121.058542.
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Background: Type 2 myocardial infarction is caused by myocardial oxygen supply-demand imbalance, and its diagnosis is increasingly common with the advent of high-sensitivity cardiac troponin assays. Although this diagnosis is associated with poor outcomes, widespread uncertainty and confusion remain among clinicians as to how to investigate and manage this heterogeneous group of patients with type 2 myocardial infarction. Methods: In a prospective cohort study, 8064 consecutive patients with increased cardiac troponin concentrations were screened to identify patients with type 2 myocardial infarction. We excluded patients with frailty or renal or hepatic failure. All study participants underwent coronary (invasive or computed tomography angiography) and cardiac (magnetic resonance or echocardiography) imaging, and the underlying causes of infarction were independently adjudicated. The primary outcome was the prevalence of coronary artery disease. Results: In 100 patients with a provisional diagnosis of type 2 myocardial infarction (median age, 65 years [interquartile range, 55–74 years]; 43% women), coronary and cardiac imaging reclassified the diagnosis in 7 patients: type 1 or 4b myocardial infarction in 5 and acute myocardial injury in 2 patients. In those with type 2 myocardial infarction, median cardiac troponin I concentrations were 195 ng/L (interquartile range, 62–760 ng/L) at presentation and 1165 ng/L (interquartile range, 277–3782 ng/L) on repeat testing. The prevalence of coronary artery disease was 68% (63 of 93), which was obstructive in 30% (28 of 93). Infarct-pattern late gadolinium enhancement or regional wall motion abnormalities were observed in 42% (39 of 93), and left ventricular systolic dysfunction was seen in 34% (32 of 93). Only 10 patients had both normal coronary and normal cardiac imaging. Coronary artery disease and left ventricular systolic dysfunction were previously unrecognized in 60% (38 of 63) and 84% (27 of 32), respectively, with only 33% (21 of 63) and 19% (6 of 32) on evidence-based treatments. Conclusions: Systematic coronary and cardiac imaging of patients with type 2 myocardial infarction identified coronary artery disease in two-thirds and left ventricular systolic dysfunction in one-third of patients. Unrecognized and untreated coronary or cardiac disease is seen in most patients with type 2 myocardial infarction, presenting opportunities for initiation of evidence-based treatments with major potential to improve clinical outcomes. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03338504.
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ABE, Y., M. KONDO, T. KUBOTA, R. MATSUOKA, M. ARAKI, K. DOYAMA, and H. TANIO. "Noninvasive assessment of coronary microvascular dysfunction using Tc-99m tetrofosmin SPECT in patients with acute myocardial infarction." Journal of Nuclear Cardiology 11, no. 5 (October 2004): 562–69. http://dx.doi.org/10.1016/j.nuclcard.2004.06.129.
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Turhan, Hasan, Yuksel Aksoy, Gulacan Ozgun Tekin, and Ertan Yetkin. "Cocaine-induced acute myocardial infarction in young individuals with otherwise normal coronary risk profile: Is coronary microvascular dysfunction one of the underlying mechanisms?" International Journal of Cardiology 114, no. 1 (January 2007): 106–7. http://dx.doi.org/10.1016/j.ijcard.2005.11.020.
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Lindsey, Merry L., Keith R. Brunt, Jonathan A. Kirk, Petra Kleinbongard, John W. Calvert, Lisandra E. de Castro Brás, Kristine Y. DeLeon-Pennell, et al. "Guidelines for in vivo mouse models of myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 321, no. 6 (December 1, 2021): H1056—H1073. http://dx.doi.org/10.1152/ajpheart.00459.2021.
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Despite significant improvements in reperfusion strategies, acute coronary syndromes all too often culminate in a myocardial infarction (MI). The consequent MI can, in turn, lead to remodeling of the left ventricle (LV), the development of LV dysfunction, and ultimately progression to heart failure (HF). Accordingly, an improved understanding of the underlying mechanisms of MI remodeling and progression to HF is necessary. One common approach to examine MI pathology is with murine models that recapitulate components of the clinical context of acute coronary syndrome and subsequent MI. We evaluated the different approaches used to produce MI in mouse models and identified opportunities to consolidate methods, recognizing that reperfused and nonreperfused MI yield different responses. The overall goal in compiling this consensus statement is to unify best practices regarding mouse MI models to improve interpretation and allow comparative examination across studies and laboratories. These guidelines will help to establish rigor and reproducibility and provide increased potential for clinical translation. Listen to another corresponding podcast at https://ajpheart.podbean.com/e/guidelines-for-in-vivo-mouse-models-of-myocardial-infarction/ .
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Sicard, Pierre, Timothée Jouitteau, Thales Andrade-Martins, Abdallah Massad, Glaucy Rodrigues de Araujo, Hélène David, Lucile Miquerol, Pascal Colson, and Sylvain Richard. "Right coronary artery ligation in mice: a novel method to investigate right ventricular dysfunction and biventricular interaction." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 3 (March 1, 2019): H684—H692. http://dx.doi.org/10.1152/ajpheart.00573.2018.
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Right ventricular (RV) dysfunction can lead to complications after acute inferior myocardial infarction (MI). However, it is unclear how RV failure after MI contributes to left-sided dysfunction. The aim of the present study was to investigate the consequences of right coronary artery (RCA) ligation in mice. RCA ligation was performed in C57BL/6JRj mice ( n = 38). The cardiac phenotypes were characterized using high-resolution echocardiography performed up to 4 wk post-RCA ligation. Infarct size was measured using 2,3,5-triphenyltetrazolium chloride staining 24 h post-RCA ligation, and the extent of the fibrotic area was determined 4 wk after MI. RV dysfunction was confirmed 24 h post-RCA ligation by a decrease in the tricuspid annular plane systolic excursion ( P < 0.001) and RV longitudinal strain analysis ( P < 0.001). Infarct size measured ex vivo represented 45.1 ± 9.1% of the RV free wall. RCA permanent ligation increased the RV-to-left ventricular (LV) area ratio ( P < 0.01). Septum hypertrophy ( P < 0.01) was associated with diastolic septal flattening. During the 4-wk post-RCA ligation, LV ejection fraction was preserved, yet it was associated with impaired LV diastolic parameters ( E/ E′, global strain rate during early diastole). Histological staining after 4 wk confirmed the remodeling process with a thin and fibrotic RV. This study validates that RCA ligation in mice is feasible and induces RV heart failure associated with the development of LV diastolic dysfunction. Our model offers a new opportunity to study mechanisms and treatments of RV/LV dysfunction after MI. NEW & NOTEWORTHY Right ventricular (RV) dysfunction frequently causes complications after acute inferior myocardial infarction. How RV failure contributes to left-sided dysfunction is elusive because of the lack of models to study molecular mechanisms. Here, we created a new model of myocardial infarction by permanently tying the right coronary artery in mice. This model offers a new opportunity to unravel mechanisms underlying RV/left ventricular dysfunction and evaluate drug therapy.
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Gosling, Rebecca C., Gareth Williams, Abdulaziz Al Baraikan, Samer Alabed, Eylem Levelt, Amrit Chowdhary, Peter P. Swoboda, et al. "Quantifying Myocardial Blood Flow and Resistance Using 4D-Flow Cardiac Magnetic Resonance Imaging." Cardiology Research and Practice 2023 (February 2, 2023): 1–7. http://dx.doi.org/10.1155/2023/3875924.
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Background. Ischaemia with nonobstructive coronary arteries is most commonly caused by coronary microvascular dysfunction but remains difficult to diagnose without invasive testing. Myocardial blood flow (MBF) can be quantified noninvasively on stress perfusion cardiac magnetic resonance (CMR) or positron emission tomography but neither is routinely used in clinical practice due to practical and technical constraints. Quantification of coronary sinus (CS) flow may represent a simpler method for CMR MBF quantification. 4D flow CMR offers comprehensive intracardiac and transvalvular flow quantification. However, it is feasibility to quantify MBF remains unknown. Methods. Patients with acute myocardial infarction (MI) and healthy volunteers underwent CMR. The CS contours were traced from the 2-chamber view. A reformatted phase contrast plane was generated through the CS, and flow was quantified using 4D flow CMR over the cardiac cycle and normalised for myocardial mass. MBF and resistance (MyoR) was determined in ten healthy volunteers, ten patients with myocardial infarction (MI) without microvascular obstruction (MVO), and ten with known MVO. Results. MBF was quantified in all 30 subjects. MBF was highest in healthy controls (123.8 ± 48.4 mL/min), significantly lower in those with MI (85.7 ± 30.5 mL/min), and even lower in those with MI and MVO (67.9 ± 29.2 mL/min/) ( P < 0.01 for both differences). Compared with healthy controls, MyoR was higher in those with MI and even higher in those with MI and MVO (0.79 (±0.35) versus 1.10 (±0.50) versus 1.50 (±0.69), P = 0.02 ). Conclusions. MBF and MyoR can be quantified from 4D flow CMR. Resting MBF was reduced in patients with MI and MVO.
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Nielsen, Natalie R., Krsna V. Rangarajan, Lan Mao, Howard A. Rockman, and Kathleen M. Caron. "A murine model of increased coronary sinus pressure induces myocardial edema with cardiac lymphatic dilation and fibrosis." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 4 (April 1, 2020): H895—H907. http://dx.doi.org/10.1152/ajpheart.00436.2019.
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Myocardial edema is a consequence of many cardiovascular stressors, including myocardial infarction, cardiac bypass surgery, and hypertension. The aim of this study was to establish a murine model of myocardial edema and elucidate the response of cardiac lymphatics and the myocardium. Myocardial edema without infarction was induced in mice by cauterizing the coronary sinus, increasing pressure in the coronary venous system, and inducing myocardial edema. In male mice, there was rapid development of edema 3 h following coronary sinus cauterization (CSC), with associated dilation of cardiac lymphatics. By 24 h, males displayed significant cardiovascular contractile dysfunction. In contrast, female mice exhibited a temporal delay in the formation of myocardial edema, with onset of cardiovascular dysfunction by 24 h. Furthermore, myocardial edema induced a ring of fibrosis around the epicardial surface of the left ventricle in both sexes that included fibroblasts, immune cells, and increased lymphatics. Interestingly, the pattern of fibrosis and the cells that make up the fibrotic epicardial ring differ between sexes. We conclude that a novel surgical model of myocardial edema without infarct was established in mice. Cardiac lymphatics compensated by exhibiting both an acute dilatory and chronic growth response. Transient myocardial edema was sufficient to induce a robust epicardial fibrotic and inflammatory response, with distinct sex differences, which underscores the sex-dependent differences that exist in cardiac vascular physiology. NEW & NOTEWORTHY Myocardial edema is a consequence of many cardiovascular stressors, including myocardial infarction, cardiac bypass surgery, and high blood pressure. Cardiac lymphatics regulate interstitial fluid balance and, in a myocardial infarction model, have been shown to be therapeutically targetable by increasing heart function. Cardiac lymphatics have only rarely been studied in a noninfarct setting in the heart, and so we characterized the first murine model of increased coronary sinus pressure to induce myocardial edema, demonstrating distinct sex differences in the response to myocardial edema. The temporal pattern of myocardial edema induction and resolution is different between males and females, underscoring sex-dependent differences in the response to myocardial edema. This model provides an important platform for future research in cardiovascular and lymphatic fields with the potential to develop therapeutic interventions for many common cardiovascular diseases.
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Scarsini, Roberto, Giovanni Luigi De Maria, Mayooran Shanmuganathan, Rafail A. Kotronias, Dimitrios Terentes-Printzios, Jeremy Langrish, Andrew J. Lucking, et al. "Pressure-bounded coronary flow reserve to assess the extent of microvascular dysfunction in patients with ST-elevation acute myocardial infarction." EuroIntervention 16, no. 17 (April 2021): 1434–43. http://dx.doi.org/10.4244/eij-d-19-00674.
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Orii, Makoto, Kumiko Hirata, Kazushi Takemoto, and Takashi Akasaka. "Effect of Erythropoietin Administration on Myocardial Viability and Coronary Microvascular Dysfunction in Anterior Acute Myocardial Infarction: Randomized Controlled Trial in the Japanese Population." Cardiology and Therapy 7, no. 2 (October 23, 2018): 151–62. http://dx.doi.org/10.1007/s40119-018-0122-1.
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Corban, Michel T., Takumi Toya, Diana Albers, Faten Sebaali, Bradley R. Lewis, John Bois, Rajiv Gulati, et al. "IMPROvE-CED Trial: Intracoronary Autologous CD34+ Cell Therapy for Treatment of Coronary Endothelial Dysfunction in Patients With Angina and Nonobstructive Coronary Arteries." Circulation Research 130, no. 3 (February 4, 2022): 326–38. http://dx.doi.org/10.1161/circresaha.121.319644.
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Background: Coronary endothelial dysfunction (CED) causes angina/ischemia in patients with nonobstructive coronary artery disease (NOCAD). Patients with CED have decreased number and function of CD34+ cells involved in normal vascular repair with microcirculatory regenerative potential and paracrine anti-inflammatory effects. We evaluated safety and potential efficacy of intracoronary autologous CD34+ cell therapy for CED. Methods: Twenty NOCAD patients with invasively diagnosed CED and persistent angina despite maximally tolerated medical therapy underwent baseline exercise stress test, GCSF (granulocyte colony stimulating factor)-mediated CD34+ cell mobilization, leukapheresis, and selective 1×10 5 CD34+ cells/kg infusion into left anterior descending. Invasive CED evaluation and exercise stress test were repeated 6 months after cell infusion. Primary end points were safety and effect of intracoronary autologous CD34+ cell therapy on CED at 6 months of follow-up. Secondary end points were change in Canadian Cardiovascular Society angina class, as-needed sublingual nitroglycerin use/day, Seattle Angina Questionnaire scores, and exercise time at 6 months. Change in CED was compared with that of 51 historic control NOCAD patients treated with maximally tolerated medical therapy alone. Results: Mean age was 52±13 years; 75% were women. No death, myocardial infarction, or stroke occurred. Intracoronary CD34+ cell infusion improved microvascular CED (%acetylcholine-mediated coronary blood flow increased from 7.2 [−18.0 to 32.4] to 57.6 [16.3–98.3]%; P =0.014), decreased Canadian Cardiovascular Society angina class (3.7±0.5 to 1.7±0.9, Wilcoxon signed-rank test, P =0.00018), and sublingual nitroglycerin use/day (1 [0.4–3.5] to 0 [0–1], Wilcoxon signed-rank test, P =0.00047), and improved all Seattle Angina Questionnaire scores with no significant change in exercise time at 6 months of follow-up. Historic control patients had no significant change in CED. Conclusions: A single intracoronary autologous CD34+ cell infusion was safe and may potentially be an effective disease-modifying therapy for microvascular CED in humans. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03471611.
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Montone, Rocco A., Leonarda Galiuto, Maria Chiara Meucci, Marco Giuseppe Del Buono, Federico Vergni, Massimiliano Camilli, Tommaso Sanna, et al. "Coronary slow flow is associated with a worse clinical outcome in patients with Takotsubo syndrome." Heart 106, no. 12 (January 10, 2020): 923–30. http://dx.doi.org/10.1136/heartjnl-2019-315909.
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ObjectivePatients with Takotsubo syndrome (TTS) present an acute microvascular dysfunction that leads to an impaired myocardial perfusion and, in more severe forms, an impaired epicardial flow. However, clinical relevance of a delayed coronary flow, the coronary slow flow (CSF), has never been investigated. We studied the prognostic value of CSF occurring in the acute phase of TTS.MethodsThis cohort study prospectively evaluated patients with a diagnosis of TTS. CSF was defined as angiographically non-obstructive coronary arteries with thrombolysis in myocardial infarction-2 flow. The incidence of overall mortality and major adverse cardiovascular events (MACEs), defined as the composite of TTS recurrence, cardiac rehospitalisation, cerebrovascular events and mortality, was assessed at follow-up.ResultsWe enrolled 101 patients (mean age 71.0±11.1 years, 86 (85.1%) female); CSF occurred in 18 (17.8%) patients. At admission, patients with CSF presented more frequently with Killip class III/IV, moderate-to-severe left ventricle systolic dysfunction and right ventricle dysfunction. During the index admission, patients with CSF had a higher rate of intrahospital complications (12 (66.7%) vs 28 (33.7%), p=0.01). At long-term follow-up, patients with CSF had a significantly higher occurrence of overall mortality (9 (50%) vs 19 (22.9%), p=0.011), mainly due to non-cardiac causes (89.3%), and a higher rate of MACE (10 (55.5%) vs 27 (32.5%), p=0.06). At multivariable Cox regression, CSF was independently associated with death from any causes.ConclusionsPatients with TTS presenting with CSF have a worse clinical presentation with a higher rate of intrahospital complications and a poor long-term clinical outcome.
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Noirclerc, N., S. Marliere, A. Bakhti, L. Mangin, E. Cassar, L. Belle, H. Bonnet, et al. "Impact of use stent with a polyethylene terephthalate micro-net covering on coronary microvascular dysfunction in patients with acute myocardial infarction." Archives of Cardiovascular Diseases Supplements 13, no. 1 (January 2021): 11. http://dx.doi.org/10.1016/j.acvdsp.2020.10.013.
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Leshnower, Bradley G., Hiroaki Sakamoto, Hirotsugu Hamamoto, Ahmad Zeeshan, Joseph H. Gorman, and Robert C. Gorman. "Progression of myocardial injury during coronary occlusion in the collateral-deficient heart: a non-wavefront phenomenon." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (September 2007): H1799—H1804. http://dx.doi.org/10.1152/ajpheart.00590.2007.
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It is widely accepted that, during acute coronary occlusion, ischemic cell death progresses from the subendocardium to the subepicardium in a wavefront fashion. This concept, which implies that the subendocardium is the most susceptible myocardial region to ischemic injury, was established using a canine model with an extensive system of subepicardial coronary collaterals. In humans, particularly in those with coronary artery disease, there is a wide range in the distribution and functional capacity of the collateral circulation, which may affect the pattern of infarct evolution. Using an ovine model with a limited system of preformed subendocardial coronary collaterals, we characterized the effect of increasing lengths of ischemia on regional blood flow and infarct size in three regions of the ventricular wall: subendocardium, midmyocardium, and subepicardium. Our results demonstrate that the myocardium and microvasculature in these three regions are equally susceptible to injury after 45 min of ischemia. When ischemic time is increased to 1 h, infarct size in the midmyocardium (90 ± 2%) is greater than in the subendocardium (76 ± 4%, P = 0.004) and subepicardium (84 ± 3%, P = 0.13). Microvascular dysfunction as assessed as a percentage of baseline flow is also greater in the midmyocardium (14 ± 5%) compared with the subendocardium (20 ± 3%, P = 0.23) and subepicardium (51 ± 9%, P = 0.007). These findings suggest that, in subjects with a limited system of coronary collateral circulation, the midmyocardium is the most susceptible myocardial region to ischemia and the subendocardium is the most resistant. Myocardial viability during coronary occlusion appears to be primarily determined by the distribution and functional capacity of the collateral circulation.
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Zhu, Peili, Li Lu, Ya Xu, Clifford Greyson, and Gregory G. Schwartz. "Glucose-insulin-potassium preserves systolic and diastolic function in ischemia and reperfusion in pigs." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (February 1, 2000): H595—H603. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h595.
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Clinical and experimental studies have suggested benefit of treatment with intravenous glucose-insulin-potassium (GIK) in acute myocardial infarction. However, patients hospitalized with acute coronary syndromes often experience recurrent myocardial ischemia without infarction that may cause progressive left ventricular (LV) dysfunction. This study tested the hypothesis that anticipatory treatment with GIK attenuates both systolic and diastolic LV dysfunction resulting from ischemia and reperfusion without infarction in vivo. Open-chest, anesthetized pigs underwent 90 min of moderate regional ischemia (mean subendocardial blood flow 0.3 ml ⋅ g−1 ⋅ min−1) and 90 min reperfusion. Eight pigs were treated with GIK (300 g/l glucose, 50 U/l insulin, and 80 meq/l KCl; infused at 2 ml ⋅ kg−1 ⋅ h−1) beginning 30 min before ischemia and continuing through reperfusion. Eight untreated pigs comprised the control group. Regional LV wall area was measured with orthogonal pairs of sonomicrometry crystals. GIK significantly increased myocardial glucose uptake and lactate release during ischemia. After reperfusion, indexes of regional systolic function (external work and fractional systolic wall area reduction), regional diastolic function (maximum rate of diastolic wall area expansion), and global LV function (LV positive and negative maximum rate of change in pressure with respect to time) recovered to a significantly greater extent in GIK-treated pigs than in control pigs (all P < 0.05). The findings suggest that the clinical utility of GIK may extend beyond treatment of acute myocardial infarction to anticipatory metabolic protection of myocardium in patients at risk for recurrent episodes of ischemia.
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Rademaker, Miriam T., Vicky A. Cameron, Christopher J. Charles, Eric A. Espiner, M. Gary Nicholls, Christopher J. Pemberton, and A. Mark Richards. "Neurohormones in an ovine model of compensated postinfarction left ventricular dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 3 (March 1, 2000): H731—H740. http://dx.doi.org/10.1152/ajpheart.2000.278.3.h731.
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Clinical heart failure, often the result of myocardial infarction, may be preceded by a period of compensated left ventricular impairment. There is substantial need for an experimental model that reflects this human condition. In sheep, coronary artery ligation produced consistent left ventricular anteroapical myocardial infarctions resulting in chronic (5 wk), stable hemodynamic changes compared with sham controls, including reductions in ejection fraction (51 ± 2 vs. 30 ± 5%, P < 0.001), cardiac output (6.3 ± 0.2 vs. 5.1 ± 0.2 l/min, P< 0.01), and arterial pressure (93 ± 2 vs. 79 ± 3 mmHg, P< 0.001), and increases in cardiac preload (left atrial pressure, 3.3 ± 0.1 vs. 8.3 ± 1.3 mmHg, P < 0.001). These changes were associated with acute and sustained increases in plasma concentrations of atrial natriuretic peptide (ANP; 5 wk, 11 ± 2 vs. 27 ± 5 pmol/l, P < 0.001), brain natriuretic peptide (BNP; 3 ± 0.2 vs. 11 ± 2 pmol/l, P < 0.001), and amino-terminal pro-brain natriuretic peptide (NT-BNP; 17 ± 3 vs. 42 ± 12 pmol/l, P < 0.001). Significant correlations were observed between plasma levels of the natriuretic peptides (ANP, day 7 to week 5 samples; BNP and NT-BNP, day 1 to week 5samples) and changes in left ventricular volumes and ejection fraction. In contrast, renin activity, aldosterone, catecholamines, and endothelin were not chronically elevated postinfarction and were not related to indexes of ventricular function. Coronary artery ligation in sheep produces the pathological, hemodynamic, and neurohormonal characteristics of compensated left ventricular impairment secondary to myocardial infarction. Plasma concentrations of the cardiac natriuretic peptides are sensitive markers of left ventricular dysfunction. This is a reproducible model that reflects the clinical condition and should prove suitable for investigating the pathophysiology of, and experimental therapies in, early left ventricular dysfunction.
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Nambirajan, J., Harshal Pamecha, and D. Chakkravarthi. "Analysis of Conventional and Nonconventional Risk Factors, Clinical Profile and Angiographic Correlation in Young Myocardial Infarction at Tertiary Care Centre." International Journal of Science and Healthcare Research 7, no. 3 (August 26, 2022): 211–16. http://dx.doi.org/10.52403/ijshr.20220730.
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Background: CAD in the young require special attention as the clinical profile, risk factors and prognosis are different from that in older patients. Method: The present study is an attempt to evaluate acute myocardial infarction in young individuals (<40 years of age) undergoing coronary angiography (CAG). A total of 290 patients aged 40 years or younger who underwent CAG in the Department of Cardiology, Coimbatore medical college hospital between December 2019 to February 2021 were included in this study. Demographic characteristics, risk factor profile, laboratory test results, ECG and echocardiographic findings, CAG findings, and in-hospital mortality were assessed. All subjects completed the Hospital Anxiety and Depression Scale (HADS) to assess anxiety levels or presence of depressive symptoms as a potential risk factor among young patients. Results: The mean patient age was 35.6 ± 4.4 years. Men made up 87.2% of the study sample. STEMI was present in 84 % of acute MI while remaining had NSTEMI. CHF (Killip class II or III) was present at hospital admission 14.4% patients. Angiographically normal coronary arteries were found in 4% of patients with the diagnosis of ACS. The most common location of significant atherosclerotic coronary lesions was the left anterior descending artery (60.1%) followed by the right coronary artery (32.4%). The most prevalent were conventional cardiovascular risk factors followed by anxiety/depression, a family history of CAD. The findings showed that 32% of the respondents had anxiety caseness and 40% had depression caseness. Conclusion: Significant risk of CHF on presentation and STEMI most common cases. Modifiable risk factors constitute primary etiology with less commonly evaluated cause as anxiety and depression need to be monitored regularly, provide regular counselling services. 4.0% revealing normal coronaries suggesting microvascular dysfunction important process other than atherosclerosis. Keywords: [young MI, nonconventional risk factors, STEMI, coronary angiogram]
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Zhao, Xiangmin, Wei Zhang, Dongqi Xing, Peng Li, Jinyan Fu, Kaizheng Gong, Fadi G. Hage, Suzanne Oparil, and Yiu-Fai Chen. "Endothelial cells overexpressing IL-8 receptor reduce cardiac remodeling and dysfunction following myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 4 (August 15, 2013): H590—H598. http://dx.doi.org/10.1152/ajpheart.00571.2012.
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The endothelium is a dynamic component of the cardiovascular system that plays an important role in health and disease. This study tested the hypothesis that targeted delivery of endothelial cells (ECs) overexpressing neutrophil membrane IL-8 receptors IL8RA and IL8RB reduces acute myocardial infarction (MI)-induced left ventricular (LV) remodeling and dysfunction and increases neovascularization in the area at risk surrounding the infarcted tissue. MI was created by ligating the left anterior descending coronary artery in 12-wk-old male Sprague-Dawley rats. Four groups of rats were studied: group 1: sham-operated rats without MI or EC transfusion; group 2: MI rats with intravenous vehicle; group 3: MI rats with transfused ECs transduced with empty adenoviral vector (Null-EC); and group 4: MI rats with transfused ECs overexpressing IL8RA/RB (1.5 × 106 cells post-MI). Two weeks after MI, LV function was assessed by echocardiography; infarct size was assessed by triphenyltetrazolium chloride (live tissue) and picrosirus red (collagen) staining, and capillary density and neutrophil infiltration in the area at risk were measured by CD31 and MPO immunohistochemical staining, respectively. When compared with the MI + vehicle and MI-Null-EC groups, transfusion of IL8RA/RB-ECs decreased neutrophil infiltration and pro-inflammatory cytokine expression and increased capillary density in the area at risk, decreased infarct size, and reduced MI-induced LV dysfunction. These findings provide proof of principle that targeted delivery of ECs is effective in repairing injured cardiac tissue. Targeted delivery of ECs to infarcted hearts provides a potential novel strategy for the treatment of acute MI in humans.
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Li, Yulin, Boya Chen, Xinying Yang, Congcong Zhang, Yao Jiao, Ping Li, Yan Liu, et al. "S100a8/a9 Signaling Causes Mitochondrial Dysfunction and Cardiomyocyte Death in Response to Ischemic/Reperfusion Injury." Circulation 140, no. 9 (August 27, 2019): 751–64. http://dx.doi.org/10.1161/circulationaha.118.039262.
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Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate MI/R injury. Methods: We used a dynamic transcriptome analysis of mouse heart exposed to various MI/R periods to identify S100a8/a9 as an early mediator. Using loss/gain-of-function approaches to understand the role of S100a8/a9 in MI/R injury, we explored the mechanisms through transcriptome and functional experiment. Dynamic serum S100a8/a9 levels were measured in patients with acute myocardial infarction before and after percutaneous coronary intervention. Patients were prospectively followed for the occurrence of major adverse cardiovascular events. Results: S100a8/a9 was identified as the most significantly upregulated gene during the early reperfusion stage. Knockout of S100a9 markedly decreased cardiomyocyte death and improved heart function, whereas hematopoietic overexpression of S100a9 exacerbated MI/R injury. Transcriptome/functional studies revealed that S100a8/a9 caused mitochondrial respiratory dysfunction in cardiomyocytes. Mechanistically, S100a8/a9 downregulated NDUF gene expression with subsequent mitochondrial complex I inhibition via Toll-like receptor 4/Erk–mediated Pparg coactivator 1 alpha/nuclear respiratory factor 1 signaling suppression. Administration of S100a9 neutralizing antibody significantly reduced MI/R injury and improved cardiac function. Finally, we demonstrated that serum S100a8/a9 levels were significantly increased 1 day after percutaneous coronary intervention in patients with acute myocardial infarction, and elevated S100a8/a9 levels were associated with the incidence of major adverse cardiovascular events. Conclusions: Our study identified S100a8/a9 as a master regulator causing cardiomyocyte death in the early stage of MI/R injury via the suppression of mitochondrial function. Targeting S100a8/a9-intiated signaling may represent a novel therapeutic intervention against MI/R injury. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03752515
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Leenen, Frans H. H., Baoxue Yuan, and Bing S. Huang. "Brain “ouabain” and angiotensin II contribute to cardiac dysfunction after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 5 (November 1, 1999): H1786—H1792. http://dx.doi.org/10.1152/ajpheart.1999.277.5.h1786.
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In chronic heart failure (CHF), sympathetic activity increases in parallel with the impairment of left ventricle (LV) function, and sympathetic hyperactivity has been postulated to contribute to the progression of heart failure. In the brain, compounds with ouabain-like activity (“ouabain,” for brevity) and the renin-angiotensin system contribute to sympathetic hyperactivity in rats with CHF after myocardial infarction (MI). In the present studies, we assessed whether, in rats, chronic blockade of brain “ouabain” or the brain renin-angiotensin system inhibits the post-MI LV dysfunction. In rats, an MI was induced by acute coronary artery ligation. At either 0.5 or 4 wk post-MI, chronic treatment with Fab fragments for blocking brain “ouabain” or with losartan for blocking brain AT1 receptors was started and continued until 8 wk post-MI using osmotic minipumps connected to intracerebroventricular cannulas. At 8 wk post-MI, in conscious rats, LV pressures were measured at rest and in response to volume and pressure overload, followed by LV passive pressure-volume curves in vitro. At 8 wk post-MI, control MI rats exhibited clear increases in LV end-diastolic pressure (LVEDP) at rest and in response to pressure and volume overload. LV pressure-volume curves in vitro showed a marked shift to the right. Intravenous administration of the Fab fragments or losartan at rates used for central blockade did not affect these parameters. In contrast, chronic central blockade with either Fab fragments or losartan significantly lowered LVEDP at rest (only in 0.5- to 8-wk groups) and particularly in response to pressure or volume overload. LV dilation, as assessed from LV pressure-volume curves, was also significantly inhibited. These results indicate that chronic blockade of brain “ouabain” or brain AT1 receptors substantially inhibits development of LV dilation and dysfunction in rats post-MI.
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Mohan, Iyyapu K., Mahmood Khan, Sheik Wisel, Karuppaiyah Selvendiran, Arun Sridhar, Cynthia A. Carnes, Balazs Bognar, Tamás Kálai, Kálmán Hideg, and Periannan Kuppusamy. "Cardioprotection by HO-4038, a novel verapamil derivative, targeted against ischemia and reperfusion-mediated acute myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 1 (January 2009): H140—H151. http://dx.doi.org/10.1152/ajpheart.00687.2008.
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Many cardiac interventional procedures, such as coronary angioplasty, stenting, and thrombolysis, attempt to reintroduce blood flow (reperfusion) to an ischemic region of myocardium. However, the reperfusion is accompanied by a complex cascade of cellular and molecular events resulting in oxidative damage, termed myocardial ischemia-reperfusion (I/R) injury. In this study, we evaluated the ability of HO-4038, an N-hydroxypiperidine derivative of verapamil, on the modulation of myocardial tissue oxygenation (Po2), I/R injury, and key signaling molecules involved in cardioprotection in an in vivo rat model of acute myocardial infarction (MI). MI was created in rats by ligating the left anterior descending coronary artery (LAD) for 30 min followed by 24 h of reperfusion. Verapamil or HO-4038 was infused through the jugular vein 10 min before the induction of ischemia. Myocardial Po2 and the free-radical scavenging ability of HO-4038 were measured using electron paramagnetic resonance spectroscopy. HO-4038 showed a significantly better scavenging ability of reactive oxygen radicals compared with verapamil. The cardiac contractile functions in the I/R hearts were significantly higher recovery in HO-4038 compared with the verapamil group. A significant decrease in the plasma levels of creatine kinase and lactate dehydrogenase was observed in the HO-4038 group compared with the verapamil or untreated I/R groups. The left ventricular infarct size was significantly less in the HO-4038 (23 ± 2%) compared with the untreated I/R (36 ± 4%) group. HO-4038 significantly attenuated the hyperoxygenation (36 ± 1 mmHg) during reperfusion compared with the untreated I/R group (44 ± 2 mmHg). The HO-4038-treated group also markedly attenuated superoxide production, increased nitric oxide generation, and enhanced Akt and Bcl-2 levels in the reperfused myocardium. Overall, the results demonstrated that HO-4038 significantly protected hearts against I/R-induced cardiac dysfunction and damage through the combined beneficial actions of calcium-channel blocking, antioxidant, and prosurvival signaling activities.
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Takahashi, Toshiyuki, Toshihisa Anzai, Hidehiro Kaneko, Yoshinori Mano, Atsushi Anzai, Toshiyuki Nagai, Takashi Kohno, et al. "Increased C-reactive protein expression exacerbates left ventricular dysfunction and remodeling after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 6 (December 2010): H1795—H1804. http://dx.doi.org/10.1152/ajpheart.00001.2010.
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We previously reported serum C-reactive protein (CRP) elevation after acute myocardial infarction (MI) to be associated with adverse outcomes including cardiac rupture, left ventricular (LV) remodeling, and cardiac death. Experimental studies have indicated that CRP per se has various biological actions including proinflammatory and proapoptotic effects, suggesting a pathogenic role of CRP in the post-MI remodeling process. We tested the hypothesis that increased CRP expression would exacerbate adverse LV remodeling after MI via deleterious effects of CRP. Transgenic mice with human CRP expression (CRP-Tg) and their transgene-negative littermates (control) underwent left coronary artery ligation. There was no apparent difference in phenotypic features between CRP-Tg and control mice before MI. Although mortality and infarct size were similar in the two groups, CRP-Tg mice showed more LV dilation and worse LV function with more prominent cardiomyocyte hypertrophy and fibrosis in the noninfarcted regions after MI than controls. Histological evaluation conducted 1 wk post-MI revealed a higher rate of apoptosis and more macrophage infiltration in the border zones of infarcted hearts from CRP-Tg mice in relation to increased monocyte chemotactic protein (MCP)-1 expression and matrix metalloproteinase (MMP)-9 activity. Increased CRP expression exacerbates LV dysfunction and promotes adverse LV remodeling after MI in mice. The deleterious effect of CRP on post-MI LV remodeling may be associated with increased apoptotic rates, macrophage infiltration, MCP-1 expression, and MMP-9 activity in the border zone.
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An, Yoshimori, Atsushi Yamamuro, Shuichiro Kaji, Makoto Kinoshita, Natsuhiko Ehara, Atsushi Kobori, Takeshi Kitai, et al. "MICROVASCULAR DYSFUNCTION ASSESSED BY CORONARY FLOW VELOCITY PATTERN AS A PREDICTOR OF LEFT VENTRICULAR REMODELING AND THROMBUS FORMATION IN PATIENTS WITH ANTERIOR ACUTE MYOCARDIAL INFARCTION." Journal of the American College of Cardiology 55, no. 10 (March 2010): A188.E1759. http://dx.doi.org/10.1016/s0735-1097(10)61760-3.
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Yamamuro, Atsushi, Takashi Akasaka, Shuichiro Kaji, Koichi Tamita, Minako Katayama, Makoto Kinoshita, Natsuhiko Ehara, et al. "Abstract 2513: Assessment of Both Coronary Microvascular Damage and Epicardial Flow Velocity Measurement Immediately after Successful Percutaneous Coronary Intervention for Acute Myocardial Infarction Predicts In-Hospital Complications and Survival." Circulation 118, suppl_18 (October 28, 2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_735-c.
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Quantitative measurement of post-reperfusion epicardial flow velocity by a Doppler guidewire can predict clinical cardiac events in patients with acute myocardial infarction (AMI). It has also been reported that the coronary flow velocity pattern in patients with microvascular dysfunction is characterized by the presence of early systolic retrograde flow and a rapid diastolic deceleration time (DDT). The purpose of this study was to examine the role of assessing both epicardial flow velocity and microvascular damage in the prediction of in-hospital complications and survival after percutaneous coronary intervention (PCI). Two hundred and eleven consecutive patients with first anterior AMI who underwent successful PCI were subjected to coronary flow measurement immediately after successful PCI with a Doppler guidewire. The coronary flow velocity spectrum provided the following parameters: time-averaged peak velocity (cm/s, APV), systolic peak velocity (cm/s) and DDT (ms). We defined the presence of microvascular dysfunction as DDT ≤600 ms and the presence of systolic flow reversal, and slow epicardial flow as resting APV ≤10cm/s. We classified the patients into three categories: without microvascular dysfunction (group 1, n=122), with microvascular dysfunction and normal epicardial flow (group 2, n= 54), with microvascular dysfunction and slow epicardial flow (group 3, n=35). The clinical event rate was compared among the 3 groups. The in-hospital event rates for congestive heart failure, cardiac rupture and death were highest in group 3 and lowest in group 1 (Table ). Assessment of both coronary microvascular damage and epicardial flow velocity can accurately predict in-hospital complications and survival in AMI patients who underwent successful reperfusion of the infarct-related coronary artery, identifying a subset of high risk patients. In-hospital event rates (%)
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Yamamuro, Atsushi, Takashi Akasaka, Shuichiro Kaji, Koichi Tamita, Minako Katayama, Makoto Kinoshita, Natsuhiko Ehara, et al. "Abstract 4206: Microvascular Dysfunction and Left Ventricular Chamber Stiffness after Successful Percutaneous Coronary Intervention Critically Determine Left Ventricular Remodeling in Patients with Acute Myocardial Infarction." Circulation 118, suppl_18 (October 28, 2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_843-a.
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In patients with acute myocardial infarction (AMI), the short deceleration time of left ventricular (LV) early filling by Doppler is a powerful independent predictor of LV remodeling. On the other hand, recent studies have shown that microvascular dysfunction in recanalized infarct-related coronary arteries may predict progressive LV dilation. The purpose of this study was to examine the effects of both microvascular dysfunction and LV chamber stiffness on LV remodeling after successful percutaneous coronary intervention (PCI) in AMI patients. Two hundred and one consecutive patients with first anterior AMI were studied following successful PCI. Microvascular injury was evaluated on the basis of coronary flow velocity patterns immediately after successful PCI using Doppler guidewires. We defined the presence of microvascular dysfunction as diastolic deceleration time ≤600 ms and the presence of systolic flow reversal. LV filling patterns were determined by mitral inflow pulsed-wave Doppler examination on day 3 after AMI. Deceleration time ≤130 ms was defined as restrictive. We classified the patients into three categories: without restrictive and microvascular dysfunction (group 1, n=116), with restrictive or microvascular dysfunction (group 2, n= 38), and with restrictive and microvascular dysfunction (group 3, n=47). Left ventriculograms were obtained immediately and 6 months after PCI. LV remodeling was defined as an increase in end-diastolic volume index ≥20%. Group 3 was at the highest risk of LV remodeling, while group 1 was at the lowest (Table ). Assessment of both microvascular dysfunction and LV chamber stiffness enable accurate prediction of LV remodeling in AMI patients after successful PCI. LV remodeling in each group
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Tamita, Koichi, Atsushi Yamamuro, Syuichiro Kaji, Minako Katayama, Tomoko Tani, Makoto Kinoshita, Natsuhiko Ehara, et al. "Abstract 901: Impact of Microvascular Dysfunction on Long-Term Cardiovascular Events after Primary Coronary Intervention for Acute Myocardial Infarction in Patients Achieving TIMI Grade 3 Reperfusion." Circulation 118, suppl_18 (October 28, 2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_628-b.
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It has been reported that even if TIMI 3 flow is achieved in epicardial coronary arteries after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI), microvascular dysfunction results in insufficient reperfusion. Recent studies have shown that microvascular injury can be assessed from coronary flow velocity (CFV) pattern. The aim of this prospective study was to examine whether the CFV pattern predicts the long-term cardiovascular outcomes in AMI patients who achieved TIMI grade 3 reperfusion. The study population consisted of 161 consecutive patients with a first anterior AMI successfully treated with primary PCI (≤50% residual stenosis with TIMI grade 3). We examined the CFV pattern immediately after PCI using a Doppler guidewire. We defined microvascular dysfunction as a diastolic deceleration time ≤600 ms and the presence of systolic flow reversal. Patients were divided into two groups: those without microvascular dysfunction (n=126; group 1) and those with micriovascular dysfunction (n=35; group 2). We evaluated the association between the microvascular dysfunction and the long-term major adverse cardiovascular event (MACE) rates. The Kaplan-Meier survival curves showed that group 2 was poorer than group 1 in prognosis (p=0.0014). Risk-adjusted data by multivariate analysis showed that the microvascular dysfunction was the strongest predictor for long-term MACE (hazard ratio: 3.37; 95% CI, 1.59–7.15; p=0.0015). The CFV pattern immediately after PCI is an accurate predictor of the long-term cardiovascular outcomes in patients with AMI who achieved TIMI grade 3 reperfusion.
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Kumar, Varun, Mukesh Singh, Lakshmi Gopalakrishnan, Daniela F. Kovacs, Daniel Benatar, Charles M. Gibson, and Sandeep Khosla. "Abstract 17488: Effect of Cocaine on Coronary Microvasculature." Circulation 130, suppl_2 (November 25, 2014). http://dx.doi.org/10.1161/circ.130.suppl_2.17488.
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Background: Presence of coronary microvascular dysfunction despite normal epicardial coronary arteries is known to significantly impact mortality and morbidity. With the increasing number of cocaine users among urban population, it is imperative to assess its effect on the coronary microvasculature. Method: In this blinded, retrospective study, microvascular dysfunction was assessed using corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (cTFC) and TIMI perfusion grade (TMPG), in an available consecutive series of 202 cocaine users in the absence of acute or recent MI, significant epicardial coronary artery disease (CAD) or vasospasm, among the 775 cocaine users who underwent coronary angiography at Mount Sinai Hospital, Chicago from 2005 to 2013. Applying the same criteria, the cTFCs and TMPGs were then compared with 210 randomly chosen non-cocaine users. Angiographers were blinded when determining the cTFC and TMPG. Results: The TMPG 0/1 for the left anterior descending (LAD), circumflex (LCx), and right coronary (RCA) arteries were statistically significant among cocaine users (LAD 22% versus 5%, p=<0.0001; LCx 25% versus 6%, p=<0.0001; RCA 42% versus 8%, p=<0.0001). For the cTFC, the LAD and LCx were significantly elevated among cocaine users (27.33 ± 10.9 versus 24.88 ± 10.05, p=0.03 and 41.11 ± 14.28 versus 38.23 ± 12.69, p=0.04; respectively). Additionally, there was a significant percentage of cocaine users with cTFC<14 (i.e. faster flow) observed in the RCA (9% versus 3%; p=0.008). Conclusion: Our study concludes that there is significant coronary microvascular dysfunction associated with cocaine use despite the absence of significant epicardial CAD. Additionally, reduced coronary filling time might be the reason for the observed higher frequency of hyperemic flow in the RCA among cocaine users, which is associated with poorer clinical outcomes, particularly in the context of impaired myocardial perfusion.
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Yamamuro, Atsushi, Takashi Akasaka, Shuichiro Kaji, Koichi Tamita, Minako Katayama, Makoto Kinoshita, Natsuhiko Ehara, et al. "Abstract 4473: Coronary Flow Velocity Pattern Immediately after Percutaneous Coronary Intervention Predicts True Left Ventricular Aneurysm in Patients with Acute Anterior Myocardial Infarction." Circulation 118, suppl_18 (October 28, 2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_895-b.
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Aggressive management of acute myocardial infarction (AMI), including prompt reperfusion, may diminish the incidence of true left ventricular (LV) aneurysm; however, it has been reported that even if successful reperfusion is achieved in epicardial coronary arteries, microvascular dysfunction causes insufficient reperfusion of the infracted myocardium, leading to LV dysfunction. Recent studies have shown that microvascular damage can be assessed quantitatively from coronary flow velocity (CFV) patterns immediately after successful reperfusion. The purpose of this study was to examine whether the CFV patterns may predict the risk of true LV aneurysm formation following successful percutaneous coronary intervention (PCI). Two hundred and one consecutive patients with first anterior AMI who underwent successful PCI were subjected to CFV measurement immediately after PCI with Doppler guidewires. The CFV spectrum provided systolic peak velocity (cm/s, SPV) and diastolic deceleration time (ms, DDT). Left ventriculogram obtained 6 months after the infarction was analyzed to measure the LV volume index. True LV aneurysm was defined as a deformity of the infarct segment that was apparent during diastole as well as during systole, and demonstrated diastolic contour abnormality. Patients were divided into the two groups: those subsequently complicated by true LV aneurysm (n=42; group 1) and those without true LV aneurysm (n=159; group 2) CFV analysis immediately after PCI showed significantly lower SPV (−29 ± 17 vs. 5 ± 22 cm/s; p<0.001) and shorter DDT (317 ± 156 vs. 665 ± 204 ms; p<0.001) in group 1 than in group 2. The optimal cutoff values to predict true LV aneurysm formation were −20 cm/s for SPV and 400 ms for DDT (sensitivity=0.83, specificity=0.82; and sensitivity=0.81, specificity=0.87, respectively). SPV and DDT correlated to the LV end-diastolic volume index obtained 6 months after AMI (r= −0.67; p<0.001 and r = −0.78; p<0.001, respectively). CFV pattern of infarct-related coronary artery immediately after PCI predicts true LV aneurysm formation, and enables accurate risk stratification in patients with anterior AMI.
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Chou, Annie Y., Graham C. Wong, Min S. Gao, Julie Park, Carolyn M. Taylor, and Krishnan Ramanathan. "Abstract 19842: Microvascular Dysfunction in Patients with ST-Elevation Myocardial Infarction after Primary Percutaneous Coronary Intervention: No Sex Disparity." Circulation 130, suppl_2 (November 25, 2014). http://dx.doi.org/10.1161/circ.130.suppl_2.19842.
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Background: Microvascular dysfunction is highly prevalent in women and presumed secondary to hormonal fluctuations, increased vascular tone, and endothelial dysfunction. Its contribution has never been examined in the acute setting. Patients with ST-elevation myocardial infarction (STEMI) with persistent ST-elevation (ST-E) post successful primary percutaneous coronary intervention (PPCI) are at risk of in-hospital cardiac events. We used ST-E recovery on ECGs pre and post PPCI to study potential sex differences in microvascular dysfunction, in conjunction with cardiac events in a STEMI population. Methods: Retrospective analysis was conducted on consecutive STEMI patients undergoing PPCI in Vancouver between May 2007 and September 2010 with evaluable ECGs pre and post PPCI. Patients with bundle branch block were excluded. Quantification of ST-E in each lead was done by electronic calipers by investigators blinded to clinical outcomes. Univariate analysis was performed by sex, for the association between ST-E recovery in the lead with maximal ST-E and the composite of in-hospital mortality, heart failure, cardiogenic shock, and reinfarction. Results: Of our 413 patients, 23% were women. In comparing baseline characteristics, age was significantly different (mean age of females = 72 vs. males = 61, p<0.001). More female than male patients had incomplete (<50%) ST-E recovery (20.6% vs. 12.7%, p=0.052). Women with incomplete recovery had an odds ratio of 2.3 for the primary outcome, compared with 1.4 in men, which was not statistically significant between sex. The primary outcome occurred more often in women (29.9% vs. 18.0%, p=0.012), but after adjusting for age, sex difference was no longer significant. Conclusions: Female STEMI patients are older, had more incomplete ST-E recovery after PPCI and had more in-hospital cardiac events, although significance was lost after adjusting for age. The higher prevalence of microvascular dysfunction in stable women may not be a large contributor of persistent ST-E in the acute setting. The higher incidence of incomplete ST-elevation in women may be attributable to the increasing prevalence of endothelial dysfunction with age. This novel interaction should be further examined with objective measures.
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Roumeliotis, Anastasios, Periklis Davlouros, Maria Anastasopoulou, Grigorios Tsigkas, Georgios Hahalis, and Nicholas G. Kounis. "Abstract 16404: Allergy Associated Myocardial Infarction: A Comprehensive Review of Clinical Presentation, Diagnosis and Management of Kounis Syndrome." Circulation 142, Suppl_3 (November 17, 2020). http://dx.doi.org/10.1161/circ.142.suppl_3.16404.
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Introduction: Kounis syndrome (KS) is defined as acute coronary syndrome (ACS) in the context of a hypersensitivity reaction. Patients may present with normal coronary arteries (Type I), established coronary artery disease (Type II) or in-stent thrombosis and restenosis (Type III). Hypothesis: We sought to investigate the clinical presentation, underlying pathophysiology, diagnosis and medical management of patients with KS. Methods: We searched PubMed until 1/1/2020 for case reports of KS. Patients with age <18 years, non-coronary vascular manifestations and without an established KS diagnosis were excluded. Information regarding patient demographics, medical history, clinical presentation, allergic reaction trigger, angiographic results as well as management were manually extracted from every report. All data were pulled in a combined data set and descriptive statistics were analyzed. Results: Out of the 269 unique patients with KS, 157 (58.4%) had Type I, 64 (23.8%) Type II and 18 (6.7%) Type III while 30 (11.2%) could not be classified. Their mean age was 54.1 years and 190 (70.6%) were male. The majority presented with a combination of cardiac and allergic symptoms [Panel A] and medication was the most commonly reported trigger [Panel B]. Electrocardiographically, 75.1% of cases had ST segment elevation with only 3.3% demonstrating no abnormalities. Coronary imaging was available in 228 (84.8%) patients showing occlusive lesions (32.5%), vascular spasm (16.2%), or normal coronary arteries (51.3%). Percutaneous coronary intervention or coronary artery bypass grafting was performed in 70 (29.4%) of the 238 patients with available information. Conclusions: Hypersensitivity induced ACS is most frequently triggered by medications, and the majority of patients have patent coronary arteries suggesting microvascular dysfunction. KS should be considered in the differential diagnosis of myocardial infarction with non-obstructive coronary arteries.
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Succar, Camil, Ali Zgheib, and Habib A. Dakik. "Coronary microvascular dysfunction post acute myocardial infarction." Journal of Nuclear Cardiology, May 14, 2020. http://dx.doi.org/10.1007/s12350-020-02175-4.
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Yildiz, Mehmet, Namrita Ashokprabhu, Aarushi Shewale, Madison Pico, Timothy D. Henry, and Odayme Quesada. "Myocardial infarction with non-obstructive coronary arteries (MINOCA)." Frontiers in Cardiovascular Medicine 9 (November 15, 2022). http://dx.doi.org/10.3389/fcvm.2022.1032436.
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Myocardial infarction with non-obstructive coronary arteries (MINOCA) is evident in up to 15% of all acute myocardial infarctions (AMI) and disproportionally affects females. Despite younger age, female predominance, and fewer cardiovascular risk factors, MINOCA patients have a worse prognosis than patients without cardiovascular disease and a similar prognosis compared to patients with MI and obstructive coronary artery disease (CAD). MINOCA is a syndrome with a broad differential diagnosis that includes both ischemic [coronary artery plaque disruption, coronary vasospasm, coronary microvascular dysfunction, spontaneous coronary artery dissection (SCAD), and coronary embolism/thrombosis] and non-ischemic mechanisms (Takotsubo cardiomyopathy, myocarditis, and non-ischemic cardiomyopathy)—the latter called MINOCA mimickers. Therefore, a standardized approach that includes multimodality imaging, such as coronary intravascular imaging, cardiac magnetic resonance, and in selected cases, coronary reactivity testing, including provocation testing for coronary vasospasm, is necessary to determine underlying etiology and direct treatment. Herein, we review the prevalence, characteristics, prognosis, diagnosis, and treatment of MINOCA -a syndrome often overlooked.
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Silva, Marta, Luis Paiva, Rogério Teixeira, Maria João Ferreira, and Lino Gonçalves. "Microcirculation function assessment in acute myocardial infarction: A systematic review of microcirculatory resistance indices." Frontiers in Cardiovascular Medicine 9 (November 11, 2022). http://dx.doi.org/10.3389/fcvm.2022.1041444.
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BackgroundUp to 50% of acute myocardial infarction (MI) patients present with microvascular dysfunction, after a successful percutaneous coronary intervention (PCI), which leads to worse clinical outcomes. The main purpose of this study is to provide a critical appraisal of the emerging role of invasive microvascular resistance indices in the MI setting, using the index of microcirculatory resistance (IMR), hyperemic microvascular resistance (HMR) and zero-flow pressure (Pzf).MethodsWe systematically explored relevant studies in the context of MI that correlated microcirculation resistance indices with microvascular dysfunction on cardiac magnetic resonance (CMR), microvascular dysfunction occurring in infarct related arteries (IRA) and non-IRA and its relation to clinical outcomes.ResultsThe microcirculation resistance indices correlated significantly with microvascular obstruction (MVO) and infarct size (IS) on CMR. Although HMR and Pzf seem to have better diagnostic accuracy for MVO and IS, IMR has more validation data. Although, both IMR and HMR were independent predictors of adverse cardiovascular events, HMR has no validated cut-off value and data is limited to small observational studies. The presence of microvascular dysfunction in non-IRA does not impact prognosis.ConclusionMicrovascular resistance indices are valuable means to evaluate microcirculation function following MI. Microvascular dysfunction relates to the extent of myocardial damage and clinical outcomes after MI.Systematic review registration[https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021228432], identifier [CRD42021228432].
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Locorotondo, Gabriella, Leonarda Galiuto, Italo Porto, Elisa Fedele, Lazzaro Paraggio, Antonio G. Rebuzzi, and Filippo Crea. "Coronary microvascular dysfunction beyond microvascular obstruction in ST‐elevation myocardial infarction: Functional and clinical correlates." Microcirculation 28, no. 5 (May 6, 2021). http://dx.doi.org/10.1111/micc.12696.
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Baghdasaryan, Patrick, Balaji Natarajan, Madlena Nalbandian, Padmini Varadarajan, and Ramdas G. Pai. "Myocardial Infarction with Nonobstructive Coronary Artery Disease—Definition, Etiopathogenesis, Diagnosis, and Management." International Journal of Angiology, March 3, 2021. http://dx.doi.org/10.1055/s-0041-1724040.
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AbstractMyocardial infarction with nonobstructive coronary arteries (MINOCA) is a complex clinical syndrome that is characterized by evidence of acute myocardial infarction in the absence of significant epicardial coronary artery disease on angiography. The term “MINOCA” encompasses a group of heterogeneous diseases with varying underlying mechanisms and each with its own pathophysiology. Overlooked plaque rupture or erosion and coronary vasospasm are the most common causes of MINOCA and can be diagnosed by routine intracoronary imaging and vasoreactivity testing, respectively. Coronary microvascular dysfunction is a less recognized, albeit an important cause of morbidity in patients presenting with MINOCA. Although MINOCA is a rare presentation of acute coronary syndrome, it is not a benign disorder and can have adverse consequences if untreated. In this article, we aim to review the pathogenesis, clinical characteristics, and finally propose a systematic approach in the diagnosis and management of patients with MINOCA.
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Schwartz, Robert S., Allen Burke, Andrew Farb, David Kaye, John R. Lesser, and Renu Virmani. "Abstract 3725: Myocardial Microvascular Obstruction in Sudden Death from Acute Myocardial Infarction Occurs more often in Coronary Plaque Erosion than in Plaque Rupture." Circulation 118, suppl_18 (October 28, 2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_475.
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Epicardial coronary artery thrombosis is associated with myocardial microvascular obstruction (MVO) and microemboli. Clinical consequences include acute myocardial infarction and sudden cardiac death from myocardial MVO and myocyte necrosis. We thus characterized myocardial histopathology and morphometry and related these findings to epicardial coronary artery plaque in patients dying from coronary artery occlusion. Hearts from patients with proven sudden coronary death from acute coronary artery occlusion underwent histopathologic characterization for MVO, cardiac microemboli, and epicardial coronary artery plaque. Immunohistochemistry was performed on microvascular thrombus to evaluate for platelet and fibrin content. Forty four cases were studied (mean age at death 51 ± 15 yrs). All emboli and MVO thrombus stained for both fibrin and platelets, and occurred in 54% of all patients, mean 4.5 microemboli/heart. Of all occluded microvessels, 89% were less than 120 um diameter (39% were < 30 um dia), and only 4% were greater than 200 um diameter. Microvascular obstruction and emboli occurred more often in epicardial plaque erosion (74% vs 40% of cases with MVO), and was most common in the LAD territory. Histopathologic epicardial coronary stenosis severity was (mean) 74% in those with emboli and 75% in those without (p=ns). Microemboli and microvascular obstruction are very common in patients dying of acute coronary artery thrombosis. Plaque erosion may be most likely to cause such emboli, with accumulation in sub-200 micron vessels. These emboli and microvessel obstruction have a prominent clinical role due to associated myonecrosis. Interventional strategies for eliminating MVO may be useful to limit myocardial damage and prevent long term sequelae.
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Konijnenberg, Lara S. F., Tom T. J. Luiken, Andor Veltien, Laween Uthman, Carolien T. A. Kuster, Laura Rodwell, Guus A. de Waard, et al. "Imatinib attenuates reperfusion injury in a rat model of acute myocardial infarction." Basic Research in Cardiology 118, no. 1 (January 13, 2023). http://dx.doi.org/10.1007/s00395-022-00974-z.
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AbstractFollowing an acute myocardial infarction, reperfusion of an occluded coronary artery is often accompanied by microvascular injury, leading to worse long-term prognosis. Experimental studies have revealed the potential of tyrosine-kinase inhibitor imatinib to reduce vascular leakage in various organs. Here, we examined the potential of imatinib to attenuate microvascular injury in a rat model of myocardial reperfusion injury. Isolated male Wistar rat hearts (n = 20) in a Langendorff system and male Wistar rats (n = 37) in an in vivo model were randomly assigned to imatinib or placebo and subjected to ischaemia and reperfusion. Evans-blue/Thioflavin-S/TTC staining and Cardiac Magnetic Resonance Imaging were performed to assess the extent of reperfusion injury. Subsequently, in vivo hearts were perfused ex vivo with a vascular leakage tracer and fluorescence and electron microscopy were performed. In isolated rat hearts, imatinib reduced global infarct size, improved end-diastolic pressure, and improved rate pressure product recovery compared to placebo. In vivo, imatinib reduced no-reflow and infarct size with no difference between imatinib and placebo for global cardiac function. In addition, imatinib showed lower vascular resistance, higher coronary flow, and less microvascular leakage in the affected myocardium. At the ultrastructural level, imatinib showed higher preserved microvascular integrity compared to placebo. We provide evidence that low-dose imatinib can reduce microvascular injury and accompanying myocardial infarct size in a rat model of acute myocardial infarction. These data warrant future work to examine the potential of imatinib to reduce reperfusion injury in patients with acute myocardial infarction.
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Banai, A., L. Lupu, A. Borohovitz, E. Levi, S. Banai, and M. Konigstein. "Microvascular dysfunction in patients with angina and non-obstructive coronary artery disease – preliminary data from a single center registry." European Heart Journal 42, Supplement_1 (October 1, 2021). http://dx.doi.org/10.1093/eurheartj/ehab724.2095.
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Abstract Introduction About 50% of patients referred for coronary angiography because of angina and/or myocardial ischemia are found to have non-obstructive coronary artery disease (CAD). The role of microvascular dysfunction as the cause of angina or ischemia is becoming increasingly recognized. Purpose Our aim was to describe coronary physiology and microvascular function in patients with angina and ischemia and non-obstructive CAD (ANOCA/INOCA). Methods Patients with angina, referred for coronary angiography and found to have non-obstructive CAD enter a prospective registry and undergo invasive coronary physiology evaluation. Fractional flow reserve (FFR), coronary flow reserve (CFR), index of myocardial resistance (IMR) and resistive reserve ratio (RRR) are recorded. Patients with obstructive CAD (≥50% diameter stenosis and/or FFR≤0.8), acute coronary syndrome and/or hemodynamic instability are excluded. Microvascular dysfunction is considered significant if either CFR<2.5, IMR≥25 and/or RRR≤3.5. Results 58 patients with ANOCA or INOCA were studied. Mean age was 64.8±10.4 and 65.5% were females. Hyperlipidemia, hypertension, and obesity were the most frequent cardiovascular risk factors (65.5%, 55.1% and 39%, respectively), and approximately 25% had known ischemic heart disease with a previous percutaneous coronary intervention. Microvascular dysfunction was found in 29 (52.7%) of the patients. 10 (18.2%) had CFR<2.5, 20 (34.5%), had IMR≥25, and 27 (50%) had RRR≤3.5. Among patients with IMR≥25, mean CFR and RRR were 2.1±0.5 and 2.4±6.8, respectively. Conclusion Microvascular dysfunction is present in approximately half of the patients with angina and/or ischemia referred for coronary angiography and found to have non-obstructive CAD. Funding Acknowledgement Type of funding sources: None.
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Sawch, Douglas, Benjamin Ruth, Sula Mazimba, Jamieson M. Bourque, Kenneth C. Bilchick, and Nishtha Sodhi. "Abstract 16233: Systemic Arterial Pulsatility Index is a Potential Metric for Microvascular Dysfunction." Circulation 142, Suppl_3 (November 17, 2020). http://dx.doi.org/10.1161/circ.142.suppl_3.16233.
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Introduction: Coronary microvascular dysfunction is associated with both atherosclerosis and heart failure (HF). We aimed to evaluate the prognostic value of global coronary flow reserve (CFR) and systemic arterial pulsatility index, a metric of ventricular-arterial coupling, (SAPi = [systemic systolic pressure-systemic diastolic pressure]/pulmonary capillary wedge pressure) in patients with known or suspected coronary artery disease. Methods: This was a retrospective analysis at an academic tertiary care center for patients who underwent right heart catheterization (RHC) and positron emission tomography (PET) imaging within a 6 month period. Global CFR was evaluated with PET imaging and SAPi was calculated using cardiac hemodynamics from RHC. Patients were evaluated for endpoints of non-fatal myocardial infarction, revascularization, and death. Cox proportional hazards regression modeling was used to examine the associations between CFR & SAPi with death and other adverse cardiovascular events. Results: Among 74 patients with complete imaging and hemodynamic data (mean age 64.23 ± 11.18 years, 54.67% female) the mean SAPi was 4.87 ± 3.09 and CFR was 52.95 ± 16.17. Increased SAPi as a continuous variable trended towards decreased mortality [HR: 0.814 (95% CI 0.663-1.016, chi square 3.31, p=.07).] Increased CFR as a continuous variable was significantly associated with decreased mortality [HR: 0.964 (95% CI 0.936-0.993, chi square 6.03, p<0.05). Neither were associated with non-fatal myocardial infarction or early revascularization. There was a weak trend toward correlation between SAPi and CFR (r=0.19, p=0.11). Conclusions: SAPi a hemodynamic marker of ventricular arterial coupling was weakly associated with CFR. On the other hand, CFR was significantly associated with death in patients with known or suspected coronary artery disease. Future work is needed to assess the correlation between SAPi and coronary microvascular dysfunction.
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Kang, M. G., K. H. Kim, J. S. Bae, J. H. Ahn, H. W. Park, Y. W. Park, S. J. Hwang, J. Y. Hwang, J. S. Koh, and Y. H. Jeong. "Association between hypercoagulability and microvascular dysfunction in patients with acute myocardial infarction." European Heart Journal 41, Supplement_2 (November 1, 2020). http://dx.doi.org/10.1093/ehjci/ehaa946.1529.
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Abstract Background Microvascular dysfunction (MVD) following percutaneous coronary intervention (PCI) can increase the risk of adverse clinical outcomes, which partly may be related with thromboembolic microvascular obstruction. This study was sought to determine whether hypercoagulability is linked with MVD post-PCI in patients with acute myocardial infarction (AMI). Methods Hypercoagulability was determined with thrombin-induced platelet-fibrin clot strength (maximal amplitude [MAthrombin] ≥68 mm evaluated by thromboelastography). Microvascular function was assessed by invasive physiological index after PCI (MVD: index of microcirculatory resistance [IMR] ≥40 U). Major adverse cardiovascular events (MACE) was defined as the incidence of death or rehospitalization for heart failure post-PCI. Results Among AMI patients (n=116), 46 patients (39.7%) met the criteria of hypercoagulability and 27 patients (23.3%) had a MVD. Level of IMR showed a significant correlation with MAthrombin value (r=0.313; p=0.001). Prevalence of MVD was increased proportionally according to the quartile scale of MAthrombin (3.6% vs. 21.9% vs. 25.9% vs. 41.4%; p for trend = 0.009). Hypercoagulability significantly increased the predictive value for MVD occurrence (odds ratio: 4.35; 95% confidence interval: 1.74 to 10.89; p=0.001). During the follow-up post-PCI of 40.9 months (IQR: 19.8 to 59.4 months), MVD and hypercoagulability were both associated with MACE (hazard ratio: 5.86 and 2.28 respectively). Patients with both MVD and hypercoagulability showed an increased risk for MACE compared with the others (18.2% vs. 5.3%; adjusted hazard ratio: 4.50; 95% confidence interval: 1.26 to 16.12; Log rank p=0.011) (Figure). Conclusion This is the first analysis to demonstrate that baseline hypercoagulability is an independent determinant of post-PCI MVD in AMI patients. Combining the measurements of hypercoagulability and MVD may enhance risk stratification and deserves further study. Long-term outcomes Funding Acknowledgement Type of funding source: None