Pathophysiology of heart disease

Our laboratory is examining the following areas: pathophysiology and prognostic implications of hypertensive cardiac and arterial involvement; etiology, pathophysiology, and prognosis of mitral valve prolapse and the Marfan syndrome; improved methods to detect left ventricular (LV) hypertrophy and dysfunction; effects of obesity, diabetes and renal dysfunction on cardiac structure and function; cardiac effects of antihypertensive and other treatments; physiologic effects of cardiac resynchronization therapy; relations of cardiac and peripheral arterial disease; and three-dimensional echocardiography.

The principal aims of our group's research are to examine critically the above topics using various modalities of ultrasound in combination with other methodologies in clinical and epidemiologic human population samples and in experimental models. On-going projects include:

1. Relations of non-invasively determined arterial structure, stiffness, and atherosclerosis to pathophysiologic variables and cardiac status.
2. Testing the hypothesis that treatment of blood pressure and LDL cholesterol to lower targets than embodied in current guidelines will have beneficial effect on carotid ultrasound measures of atherosclerosis and echocardiographic measures of heart disease, in the Stop Atherosclerosis in Native DiabeticS (SANDS) study. 3. Influence of gender on cardiac and arterial function in clinical and epidemiological populations.
4. Complications and predictors thereof in patients with valvular heart diseases, including mitral valve prolapse.
5. Marfan aortic involvement and the comparative ability of traditional beta-blocker based vs. newer treatment to reduce its progression.
6. Procedures to improve non-invasive determination of LV hypertrophy.
7. Prevalence of cardiac and arterial disease across ethnic groups and the cardiovascular effects of body composition, diabetes and indices of early renal dysfunction.
8. Refining methods for three-dimensional echocardiographic assessment of the mitral valve and left ventricle.
9. Phenotypic inheritance and genetic linkage of cardiac and arterial hypertrophy and dysfunction as well as of discrete atherosclerosic plaques.