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:IntroductionIt is not clear whether patients with sinus rhythm and reduced left ventricular function should be treated with anticoagulation therapy during or after treatment for heart failure.Case presentationA 67-year-old Japanese man was hospitalized at our institution with heart failure due to dilated cardiomyopathy. On day after discharge, he developed cerebral infarction and showed persistence of multiple left ventricular thrombi. His paralysis completely improved at 2 days after edaravone and heparin administration; however, his left visual field defect persisted.ConclusionPatients in sinus rhythm with reduced left ventricular function might benefit from anticoagulation therapy during treatment for heart failure.
Project description:The majority of acute coronary syndromes are caused by coronary artery thrombotic occlusions secondary to atherosclerotic plaque erosion or rupture. Coronary embolism is an important yet forgotten underlying cause of acute coronary syndrome. We present a case of a young patient who presented with ST elevation myocardial infarction suspected to be secondary to coronary embolization originating from a left ventricular thrombus.
Project description:ObjectiveTo highlight detection of left ventricular thrombi on cardiac magnetic resonance (CMR) viability studies.MethodThis retrospective observational study was conducted in the Radiology Department at our Hospital in Dhahran, from April 2015-2019. All recently re-perfused (post-percutaneous coronary intervention/PCI) patients with ST-segment elevation myocardial infarctions (STEMI), having low ejection fractions (<40%), impaired LV functions or abnormal wall motions on transthoracic echocardiographies (TTEs), who underwent cardiac magnetic resonance (CMR) imaging viability studies were included. Patients with incomplete or limited studies (due to artifacts), previous coronary artery bypass graft (CABG), those who lost follow-ups, and those who were contraindicated or unfit for MRIs were excluded. An area of low signal intensity with no late gadolinium enhancement (LGE) was defined as thrombus on MR imaging, and two radiologists reached consensus report for the diagnoses. Patients with anterior or non-anterior wall MI were documented, and their ejection fractions were recorded. Percentage estimation of LV thrombi as detected on CMR studies was made. Any complications (like MI, stroke or death) that occurred within one year of diagnoses were documented. A Chi-square was used to determine association.ResultsOf the 125 patients, most were men (71.2%) with a mean age of 56.78 years. Eleven patients had left ventricular thrombi (8.8%), and most of these were anterior wall infarctions with low ejection fractions (<40%). Three out of 11 patients with LV thrombi developed complications versus 3 out of 114 without LV thrombi (P- value, .0005).ConclusionLeft ventricular thrombi can be detected on cardiac viability studies in recently re-perfused STEMI patients and may possibly predict the risk of complications.
Project description:Left ventricular (LV) thrombus formation is a well-known complication of acute myocardial infarction (AMI) and is reported to occur in 5-8% of patients who have anterior or apical myocardial infarction. However, right ventricular (RV) thrombus has not previously been reported after AMI. We describe a 54-year-old woman who presented with an ST-elevation myocardial infarction due to occlusion of the distal left anterior descending artery, which wrapped around the apex and led to simultaneous LV and RV apical thrombi. <Learning objective: This case emphasizes the following: (1) in patients who have a long left anterior descending artery (LAD) that wraps around the apex, even distal LAD occlusion can cause a large infarct area including the apex, inferior wall, and right ventricular apex, as well as serious complications such as cardiac arrest and left ventricular and right ventricular (RV) thrombus. (2) Cardiac magnetic resonance imaging is useful for detecting apical thrombus especially in the RV.>.
Project description:The length of anticoagulation for thrombotic events related to COVID-19 is unknown. We present a patient with COVID-19 complicated by a thrombotic anterior STEMI and multiple left ventricular (LV) thrombi that resolved after 8 weeks of anticoagulation. We suggest a shorter length of anticoagulation with COVID-19-related LV thrombus.
Project description:ImportanceLeft ventricular (LV) thrombi can arise in patients with ischemic and nonischemic cardiomyopathies. Anticoagulation is thought to reduce the risk of stroke or systemic embolism (SSE), but there are no high-quality data on the effectiveness of direct oral anticoagulants (DOACs) for this indication.ObjectiveTo compare the outcomes associated with DOAC use and warfarin use for the treatment of LV thrombi.Design, setting, and participantsA cohort study was performed at 3 tertiary care academic medical centers among 514 eligible patients with echocardiographically diagnosed LV thrombi between October 1, 2013, and March 31, 2019. Follow-up was performed through the end of the study period.ExposuresType and duration of anticoagulant use.Main outcomes and measuresClinically apparent SSE.ResultsA total of 514 patients (379 men; mean [SD] age, 58.4 [14.8] years) with LV thrombi were identified, including 300 who received warfarin and 185 who received a DOAC (64 patients switched treatment between these groups). The median follow-up across the patient cohort was 351 days (interquartile range, 51-866 days). On unadjusted analysis, DOAC treatment vs warfarin use (hazard ratio [HR], 2.71; 95% CI, 1.31-5.57; P = .01) and prior SSE (HR, 2.13; 95% CI, 1.22-3.72; P = .01) were associated with SSE. On multivariable analysis, anticoagulation with DOAC vs warfarin (HR, 2.64; 95% CI, 1.28-5.43; P = .01) and prior SSE (HR, 2.07; 95% CI, 1.17-3.66; P = .01) remained significantly associated with SSE.Conclusions and relevanceIn this multicenter cohort study of anticoagulation strategies for LV thrombi, DOAC treatment was associated with a higher risk of SSE compared with warfarin use, even after adjustment for other factors. These results challenge the assumption of DOAC equivalence with warfarin for LV thrombi and highlight the need for prospective randomized clinical trials to determine the most effective treatment strategies for LV thrombi.
Project description:Left ventricular (LV) abnormalities have been reported in cystic fibrosis (CF); however, it remains unclear if loss of cystic fibrosis transmembrane conductance regulator (CFTR) function causes heart defects independent of lung disease.Using gut-corrected F508del CFTR mutant mice (?F508), which do not develop human lung disease, we examined in vivo heart and aortic function via 2D transthoracic echocardiography and LV catheterization.?F508 mouse hearts showed LV concentric remodeling along with enhanced inotropy (increased +dP/dt, fractional shortening, decreased isovolumetric contraction time) and greater lusitropy (-dP/dt, Tau). Aortas displayed increased stiffness and altered diastolic flow. ?-adrenergic stimulation revealed diminished cardiac reserve (attenuated +dP/dt,-dP/dt, LV pressure).In a mouse model of CF, CFTR mutation leads to LV remodeling with alteration of cardiac and aortic functions in the absence of lung disease. As CF patients live longer, more active lives, their risk for cardiovascular disease should be considered.
Project description:Left ventricular non-compaction (LVNC) is a congenital cardiomyopathy characterized by deep ventricular trabeculations thought to be due to an arrest of myocardial morphogenesis. Integration of various cardiac imaging modalities such as echocardiography, cardiac computed tomography and cardiac magnetic resonance imaging help in the diagnosis of this rare clinical entity. We describe a child with rare variant of LVNC with predominant involvement of interventricular septum resulting in multiple ventricular septal defects.