Project description:A 53-year-old male status post pacemaker placement three months prior for sinus bradycardia presented with worsening dyspnea, holosystolic murmur, and a ventricular-paced right bundle branch block on electrocardiogram. Transesophageal echocardiography demonstrated a pacer wire in the right atrium coursing into the left atrium and ventricle through an undiagnosed patent foramen ovale. The patient underwent surgical repair and repositioning of the pacemaker lead without complication. Although rare, it should be suspected after recent lead placement.
Project description:ObjectiveRestrictive leaflet tethering resulting from regional left ventricular (LV) contractile injury causes ischemic mitral regurgitation (MR). We hypothesized that 3-dimensional LV topographic mapping by MRI-based multiparametric strain analysis could characterize the regional contractile injury patterns that differentiate ischemic coronary artery disease patients who have ischemic MR from those who do not.MethodsMagnetic resonance imaging-based multiparametric strain data were calculated for 15,300 LV grid points in 100 normal volunteers. Strain parameters from ischemic MR (n = 10) and ischemic no-MR (n = 36) patients were then normalized to this normal human strain database with z score quantification of standard deviation from the normal mean. Mean multiparametric strain z scores were calculated for 18 LV subregions (basilar/mid/apical levels; 6 LV regions). Mean strain z scores for papillary muscle-related (basilar/mid levels of anterolateral, posterolateral, and posterior) and nonpapillary muscle-related (all other) subregions were compared between ischemic MR and ischemic no-MR groups.ResultsAcross all patients, contractile injury was greater in the papillary muscle-related regions compared with the nonpapillary regions (P = .007). In the papillary regions, contractile injury was greater in the ischemic MR group compared with the no-MR group (z scores, 1.91 ± 1.13 vs 1.20 ± 1.01, respectively; P < .001). Strain values in the nonpapillary muscle-related subregions were not different between the 2 groups (1.31 ± 1.04 vs 1.20 ± 1.03; P = .301).ConclusionsMultiparametric strain analysis demonstrated severe normalized contractile injury in the papillary muscle-related LV subregions in patients with ischemic MR. The mean degree of normalized injury approached 2 standard deviations and was significantly worse than the levels seen in ischemic no-MR patients.
Project description:The major clinical features of myocardial noncompaction are heart failure, arrhythmias, and thromboembolic events. Prominent myocardial trabeculae and deep recesses characteristic of myocardial noncompaction can cause stagnant blood flow and the formation of left ventricular clots. We describe the case of a 62-year-old woman who presented with symptoms of heart failure secondary to left ventricular noncompaction. Transthoracic and transesophageal echocardiography revealed multiple left ventricular thrombi, which had formed despite the patient's long-term therapy with aspirin. Anticoagulative therapy should be considered for patients with myocardial noncompaction who also have risk factors for thromboembolism, such as atrial fibrillation, a history of systemic embolism, or severe left ventricular systolic dysfunction. However, chronic antiplatelet therapy may not sufficiently prevent clot formation in patients who have myocardial noncompaction and severe left ventricular systolic dysfunction.
Project description:Dilated cardiomyopathy is a life-threatening syndrome that can arise from a myriad of causes, but predisposition toward this malady is inherited in many cases. A number of inherited forms of dilated cardiomyopathy arise from mutations in genes that encode proteins involved in linking the cytoskeleton to the extracellular matrix, and disruption of this link renders the cell membrane more susceptible to injury. Membrane repair is an important cellular mechanism that animal cells have developed to survive membrane disruption. We have previously shown that dysferlin deficiency leads to defective membrane resealing in skeletal muscle and muscle necrosis; however, the function of dysferlin in the heart remains to be determined. Here, we demonstrate that dysferlin is also involved in cardiomyocyte membrane repair and that dysferlin deficiency leads to cardiomyopathy. In particular, stress exercise disturbs left ventricular function in dysferlin-null mice and increases Evans blue dye uptake in dysferlin-deficient cardiomyocytes. Furthermore, a combined deficiency of dystrophin and dysferlin leads to early onset cardiomyopathy. Our results suggest that dysferlin-mediated membrane repair is important for maintaining membrane integrity of cardiomyocytes, particularly under conditions of mechanical stress. Thus, our study establishes what we believe is a novel mechanism underlying the cardiomyopathy that results from a defective membrane repair in the absence of dysferlin.
Project description:PurposeSARS-COV-2 infection can develop into a multi-organ disease. Although pathophysiological mechanisms of COVID-19-associated myocardial injury have been studied throughout the pandemic course in 2019, its morphological characterisation is still unclear. With this study, we aimed to characterise echocardiographic patterns of ventricular function in patients with COVID-19-associated myocardial injury.MethodsWe prospectively assessed 32 patients hospitalised with COVID-19 and presence or absence of elevated high sensitive troponin T (hsTNT+ vs. hsTNT-) by comprehensive three-dimensional (3D) and strain echocardiography.ResultsA minority (34.3%) of patients had normal ventricular function, whereas 65.7% had left and/or right ventricular dysfunction defined by impaired left and/or right ventricular ejection fraction and strain measurements. Concomitant biventricular dysfunction was common in hsTNT+ patients. We observed impaired left ventricular (LV) global longitudinal strain (GLS) in patients with myocardial injury (-13.9% vs. -17.7% for hsTNT+ vs. hsTNT-, p = 0.005) but preserved LV ejection fraction (52% vs. 59%, p = 0.074). Further, in these patients, right ventricular (RV) systolic function was impaired with lower RV ejection fraction (40% vs. 49%, p = 0.001) and reduced RV free wall strain (-18.5% vs. -28.3%, p = 0.003). Myocardial dysfunction partially recovered in hsTNT + patients after 52 days of follow-up. In particular, LV-GLS and RV-FWS significantly improved from baseline to follow-up (LV-GLS: -13.9% to -16.5%, p = 0.013; RV-FWS: -18.5% to -22.3%, p = 0.037).ConclusionIn patients with COVID-19-associated myocardial injury, comprehensive 3D and strain echocardiography revealed LV dysfunction by GLS and RV dysfunction, which partially resolved at 2-month follow-up.Trial registrationCOVID-19 Registry of the LMU University Hospital Munich (CORKUM), WHO trial ID DRKS00021225.
Project description:19 paired human left ventricular apex samples were harvested at the time of implant of a left ventricular assist device (PRE) and at the time of explant (POST). The cohort included patients that were clinically classified as "ischemic" (I) showing evidence of coronary artery disease, "non-ischemic" (N) no evidence of coronary artery disease or "acute Myocardial infarction" (IM) myocardial infarction within 10 days of the implant. Tissue was processed and hybridized to the Affymetrix HG-U133A chip. Keywords: other
Project description:An increased incidence of myocardial infarction (MI) has recently emerged as the cause of cardiovascular morbidity and mortality worldwide. In this study, cardiac function was investigated in a rat myocardial ischemia/reperfusion (I/R) model using echocardiography. Metformin administration significantly increased ejection fraction and fractional shortening values on Days 3 and 7 when MI occurred, indicating that metformin improved left ventricular systolic function. In the Sham + MET and MI + MET groups, the E' value was significantly different up to Day 3 but not at Day 7. This may mean that left ventricular diastolic function was effectively restored to some extent by Day 7 when metformin was administered. These results suggest that diastolic dysfunction, assessed by echocardiography, does not recover in the early phase of ischemic reperfusion injury in the rat myocardial I/R model. However, administering metformin resulted in recovery in the early phase of ischemic reperfusion injury in this model. Further gene expression profiling of left ventricle tissues revealed that the metformin-treated group had notably attenuated immune and inflammatory profiles. To sum up, a rat myocardial I/R injury model and ultrasound-based assessment of left ventricular systolic and diastolic function can be used in translational research and for the development of new heart failure-related drugs, in addition to evaluating the potential of metformin to improve left ventricular (LV) diastolic function.