Active clinical trials for "Cardiomyopathies"

To detect by Doppler echocardiography the incidence of cardiac abnormalities in HIV-positive patients in a prospective, longitudinal study.

Hypertrophic cardiomyopathy (HCM) is a genetically inherited heart disease. It causes thickening of heart muscle, especially the chamber responsible for pumping blood out of the heart, the left ventricle. Hypertrophic cardiomyopathy (HCM) is the most important cause of sudden death in apparently healthy young people. A genetic test called linkage analysis is used to locate genes causing inherited diseases like HCM. Linkage analysis requires large families to be evaluated clinically in order to identify the members with and without the disease. In this study researchers will collect samples of DNA from family members of patients with HCM. The diagnosis of the disease will be made by history and physical examination, electrocardiogram (12 lead ECG), and ultrasound of the heart (2-D echocardiogram). The ability of the researchers to locate the gene responsible for the disease improves with increases in the size of the family and members evaluated. In order to continue research on the genetic causes of heart disease, researchers intend on studying families with specific genetic mutations (beta-MHC) causing HCM. Researcher plan to also study families with HCM not linked to specific gene mutations (beta-MHC).

To determine normal T1 and T2 values of the liver, and to assess the impact of age and gender To determine the relation between markers of right heart decompensation and T1/T2 values of the liver in patients with pulmonary hypertension, patients with dilated cardiomyopathy, and patients with constrictive pericarditis (or constrictive physiology) To determine inter/intra-observer reproducibility for liver T1/T2 assessment To test/develop multi-feature texture analysis for T1/T2 analysis of the liver and implement machine learning to derive indicative features (MR-derived measures only vs combined with other clinical readouts)

Patients with Takotsubo cardiomiopathy (TTC) have over-inflammation and over-sympathetic tone. However, these conditions could cause higher rate of heart failure (HF) events and deaths at 2 years of follow-up. Conversely, hyperglycemia vs. normoglycemia could result in over expression of inflammatory markers and catecholamines thta could result in higher rate of HF and deaths at 2 years of follow-up in TTC patients.

A comparative study to follow subjects who received stem cell therapies three, five, seven, nine, and thirteen years after their follow-on visit. Subjects will be selected from a pool of previous Interdisciplinary Stem Cell Institute trial participants.

The aim of this project is to identify common genetic polymorphisms associated with the occurrence of rhythmic events in patients with severe cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a primitive myocardic disease and the first of genetic cardiac diseases. The definition of HCM is an increase of the myocardial thickness of the left ventricle (LV) wall without any other causes of hypertrophy. It's characterized by an important heterogeneity of prognosis and clinical expression going from a asymptomatic state until the devastating sudden death occurring in a young person.The diagnosis of HCM is definite by a myocardial thickness greater or equal to 15mm (or 13mm if there is a familial history).This hypertrophy is often accompanied by other abnormalities detected by echocardiography: dynamic left ventricular outflow obstruction at rest or stress, mitral regurgitation …Now, the current challenge is to determine the prognosis factors of the disease that could help to identify the patients with high risk of sudden death. Some prognosis factors are knowed and used in the calculation of a new risk score. This risk score allows to estimate the risk of sudden death at 5 years and propose depending on the result, the implantation of a defibrillator for primary prevention.The physiopathological mechanism of HCM is very complex and still misunderstood. Myocardial fibrosis could be a major mechanism of the disease evolution. Indeed, fibrosis is responsible of scar areas where ventricular tachycardia may develop. Moreover, if the fibrosis is very extensive, it can be the responsible of a systolic or diastolic dysfunction of the left ventricle leading to heart failure.Myocardial ischemia caused by a microvascular dysfunction is now recognized as an important mechanism of the disease evolution. Acute ischemic events could be a trigger of malignant arrhythmia whereas chronic ischemia leads to fibrosis.Left ventricle function is long time preserved in HCM. Segmentary hypokinesia corresponding to extensive fibrosis appears at a very advanced stage of the disease. Exercice stress echocardiography permits to detect myocardial ischemia caused by microvascular dysfunction in the HCM before the fibrosis apparition. Moreover the investigators suggest to study the deformation parameters by speckle tracking or 2D strain witness of a contractile LV dysfunction before the apparition of segmentary hypokinesia.Magnetic resonance imaging (MRI) is now recognized as the more sensible technique to identify focal myocardial fibrosis resulting in areas of late gadolinium enhancement (LGE). LGE is frequent in HCM and his extension is correlated with the severity of the hypertrophy and the risk of sudden death. Myocardial ischemia is detected by hypoperfused defects in the perfusion sequences and as LGE, is correlated with the degree of hypertrophy. Some studies using stress MRI with vasodilatator agent show inductible hypoperfused areas correlated to the degree of hypertrophy. T1 mapping is a new hopeful sequence of MRI permitting to detect the diffuse and early myocardial fibrosis. Some studies show that T1 mapping values are reduced in the areas of LGE in HCM but also in areas without LGE which reflects the presence of new fibrosis.The objective of study is to compare these two imagery techniques in order to detect ischemia and fibrosis. These techniques are usually used in the diagnosis or the monitoring of the disease. The investigators propose to realize an exercise stress echocardiography to study: the segmentary kinetic of the left ventricle and the 2D strain and a stress MRI to study the LGE, the stress perfusion and the T1 mapping.Actually the investigators consider that LGE is a risk factor of the disease (although not yet involved in the calculation of the risk of sudden death) and need to be study in each MRI realized for HCM. From the same way, the investigators suggest to follow patients to determine if the abnormalities detected by these two techniques and particularly 2D strain abnormalities, stress myocardial ischemia and T1 mapping abnormalities are prognosis factors of the disease and appear more precociously than LGE.

The goal is to determine how lifestyle and exercise impact the well-being of individuals with hypertrophic cardiomyopathy (HCM) and long QT syndrome (LQTS). Ancillary study Aim: To understand how the coronavirus epidemic is impacting psychological health and quality of life in the LIVE population

To establish if, in patients with new diagnosis of left ventricular dilatation without documentation at the coronary artery angiography of significant coronary artery lesions, there is a damage of the coronary microcirculation at the IMR (index of microcirculatory resistance) assessment

Myocardial fibrosis is the fundamental substrate for the development of heart failure. Cardiovascular magnetic resonance (CMR) allows non-invasive assessment of myocardial fibrosis based on late gadolinium enhancement (LGE) and T1 mapping. Patients: Prospective longitudinal observational multicenter study of consecutive patients with suspected or known non-ischemic cardiomyopathy. Imaging: Non-invasive measures of myocardial fibrosis: native T1, extracellular volume fraction (ECV) and LGE. Primary endpoints: all cause and cardiovascular mortality. Secondary endpoints: arrhythmic composite and HF composite endpoints.