View clinical trials related to Diastolic Dysfunction.
Filter by:Metabolic syndrome (MS) is a cluster of risk factors for cardiovascular disease with increasing prevalence worldwide and insulin resistance is central to its pathophysiology and multi-organ deleterious effects. One of the most affected organs, the heart, undergoes a remodeling process with an increase in fibrous tissue that impairs global cardiac function. Considering that myocardial fibrosis increases myocardial stiffness, one important determinant of diastolic function, it probably contributes decisively to subclinical left ventricular diastolic dysfunction (DD) and heart failure with preserved ejection fraction in patients with MS. Since insulin resistance is a dominant player in the pathophysiology of MS, improvement of the metabolic profile of these patients with metformin might be associated with favorable remodeling of myocardial structure and an improvement in myocardial function. Metformin is a widely used drug to treat type 2 diabetes mellitus and is considered an option in the treatment of high-risk non-diabetic patients with MS, in addition to lifestyle counseling including a healthy diet and physical activity. In this way, we aim to: i) assess if treating non-diabetic patients with MS and DD with metformin in addition to lifestyle counseling decreases cardiac fibrosis and improves diastolic function and assess its impact in functional capacity and health-related quality of life (HRQoL); ii) evaluate if biomarkers of cardiac remodeling and inflammation are predictive factors of response to metformin treatment in these patients. This is a prospective, randomized, open-label, blinded-endpoint (PROBE) trial (scheduled follow-up of 24 months) with 2 arms: lifestyle counseling only and lifestyle counseling plus metformin (maximum dose of 1000mg twice daily). The primary endpoint will be change in change in mean of septal and lateral early diastolic mitral annular velocities (E') (at the end of the 24 months of follow-up). The secondary endpoints will include a composite of major cardiovascular events; diastolic function parameters at rest; plasma levels of insulin, glucose, insulin resistance index, NTproBNP, high-sensitivity C-reactive protein, tumor necrosis factor-α (TNFα), tissue inhibitor of matrix metalloproteinase type 1 (TIMP1) and growth differentiation factor-15 (GDF-15); functional capacity; epicardial, pericardial and abdominal adipose tissue volumes, and coronary calcium score; HRQoL.
Although half of the patients with HF has normal ejection fraction or slightly altered (HF-PEF) and the prognosis differs little from those with reduced ejection fraction, the pathophysiology of HF-PEF is still poorly understood. Sodium restriction is the most common measure of self-care oriented to HF patients for management of congestive episodes. The role of this orientation in the treatment of patients with preserved ejection fraction, however, is still unclear. The evaluation of the effects of sodium restriction on neurohormonal activation and episodes of decompensation in HF-PEF can promote a better understanding of the pathophysiological progression of this complex syndrome.
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the United States with older age being a primary risk factor. The number of adults greater than age 65 years will almost double to 70 million by 2030, therefore identifying therapeutic strategies for treating or preventing age-related disorders in humans is of major biomedical importance. Cardiovascular aging, defined as a reduction in vascular and cardiac functions with normal aging, occurs even in the absence of CVD risk factors and overt CVD. A key feature of cardiovascular aging is stiffening of the large elastic central arteries such as the aorta. This is important because aortic stiffness directly contributes to clinical problems such as increased blood pressure, reduced blood flow to the heart muscle, and thickening of the heart muscle. Therefore, these clinical consequences are hypothesized to mediate a substantial proportion of the increase in CVD risk in older adults. However, effective drug treatments for aortic stiffness are not currently available and the biological reasons (mechanisms) involved in causing aortic stiffening remain undefined. In addition, the inability of smaller blood vessels to relax, impairment of the heart to relax during the filling phase of the heart cycle (i.e., diastole), and increased blood pressure variability, have all been linked to aortic stiffness. Furthermore, chronic low-grade inflammation with advancing age has been proposed to be a common mechanistic link (i.e., biological reason) between these reductions in cardiovascular function in older adults. Therefore, the investigators propose that inflammation could be a novel therapeutic target to treat cardiovascular aging in older adults. Our central hypothesis is that inflammation mediates the age-related deterioration in cardiovascular functions observed with advancing age through the development of oxidative stress (i.e., imbalance between damaging oxygen free radicals vs. protective antioxidants). Our hypothesis predicts that chronic inhibition of inflammation with Salsalate, an FDA-approved anti-inflammatory drug similar to aspirin that is used to treat rheumatoid arthritis pain and known to inhibit the 'master' regulator of inflammation in the cell (i.e., nuclear factor kappa B), will improve cardiovascular function in older adults. In addition, the investigators hypothesize that the mechanism for the improvement in cardiovascular function during inhibition of inflammation will be by suppressing oxidative stress. To test our hypothesis, the investigators will randomize older healthy adults (age 50-79 years) to 3 g/day of salsalate or placebo (i.e., pill with inactive substance) pills for 4 weeks and have cardiovascular function measured at baseline and again after 4 weeks.
The most important cause of mortality amongst DM2 patients is cardiovascular disease. An early finding of cardiovascular disease in DM2 and obesity is diastolic dysfunction. Diastolic dysfunction is an independent predictor of mortality and has been shown to improve in patients on a low calorie diet. The improvement of diastolic function was associated with a reduction in triglyceride accumulation in the heart and liver. A relatively new widely prescribed therapeutic agent for DM2 patients is Liraglutide (Victoza®). Liraglutide is a Glucagon Like Peptide - 1 homologue that improves glucose homeostasis and reduces blood pressure and body weight. Next to the induction of weight loss, which is potentially beneficial for cardiac function, GLP-1 therapy might have a direct advantageous effect on the cardiovascular system. However, the effect of Liraglutide on cardiovascular function has not been investigated yet. The investigators hypothesize that treatment of DM2 patients with Liraglutide is associated with improvement of cardiovascular function and a reduction of triglyceride accumulation in end-organs.
The purpose of this study is to compare the effect of heart rate on cardiac index in patients with or without left ventricular hypertrophy. The study will be conducted in postoperative heart surgery patients with a pacemaker.
This is a clinical, randomised, double-blinded study in which patients eligible for aortic valve replacement are enrolled. Patients receive infusion of either levosimendan or placebo 4 hours prior to surgery and until the end of surgery.
Diastolic dysfunction (DD) is an increasingly frequent condition in hypertensive individuals whose treatment remains unclear. Its presence is related to higher morbidity and mortality independent of blood pressure levels. The aim of this study is to investigate the additive effect of simvastatin on enalapril on DD in hypertensive patients with average cholesterol levels. For this aim, hypertensive patients with DD and LDL-cholesterol <160 mg/dL will undergo a run-in phase to achieve a systolic blood pressure (SBP) <135 mmHg and diastolic blood pressure (DBP) <85 mmHg with enalapril. Hydrochlorothiazide could be added when need to achieve SBP or DBP control. Four weeks after reaching the optimum anti-hypertensive regimen patients will be randomized to receive 80 mg simvastatin or placebo for a period of 20 weeks. Echocardiograms will be performed before and after treatment with measurement of left atrial volume, conventional and tissue Doppler velocities in early diastole and late diastole. The evaluation of these will allow to identify changes of DD severity after treatment.
The heart becoming "stiff" due to increased fibrous tissue or decreased elasticity of the heart tissue is one of the earliest changes caused by heart failure. These changes can be detected by simple non-invasive echocardiogram techniques. However, these techniques usually detect the increased "stiffness" of the heart only after it has progressed to a significant extent. The investigators hypothesize that if they stress the heart using a Dobutamine infusion and measure the filling pressure using echocardiogram, it will provide them with tools to identify these changes earlier.
The project aims to investigate the effect of a regular exercise for 6 months on diastolic parameters in patients who present with shortness of breath and who have evidence of early diastolic dysfunction on echocardiography. Patients will be enrolled from the VA General Medicine and Cardiology Clinics, and will be screened for diastolic dysfunction. Once enrolled, they will be on an exercise regimen that involves aerobic exercise for 30-45 minutes five times a week at home. The participants will have an initial supervised exercise session with the VA Cardiac Rehabilitation team, and will have either every other week or monthly supervised sessions at the VA Cardiac Rehabilitation Center to monitor their progress. Clinical, biometric, laboratory and echocardiographic parameters will be obtained before and after the 6 month period.
Successful heart surgery requires the resumption of a strong beating heart prior to separation from the heart and lung machine. There are different ways to do this. At this hospital, the surgical team usually gives calcium to people when they come off of the heart and lung machine because some doctors believe that calcium can "jump start" the heart. Not every hospital does this. Some people think that calcium may have a side effect of making the heart more stiff. Stiff hearts do not beat as well or receive as much blood to tissues as non-stiff hearts. If calcium makes the heart stiff, then doctors may have to use other medicines to support the heart in the operating room and the intensive care unit. This may ultimately lead to poorer outcomes including a longer stay in the intensive care unit and in the hospital. This study is being performed to find out if calcium has the side effect of making the heart more stiff. This study compares calcium to placebo. The placebo looks exactly like the calcium, but it contains no calcium. During this study patients may receive placebo instead of calcium. Neither the doctor nor the study team will know which drug the subject will receive.