Methods have and are being developed, evaluated and applied to more objectively determine and quantify abnormalities of extent and timing of left and right ventricular wall motion and extent of coronary artery stenoses from cineventriculograms and cinearteriograms. The centerline method, developed in this laboratory to quantify regional ventricular wall motion abnormalities, is being applied to determine the extent to which the human left ventricle can compensate by regional hypercontraction for regional hypofunction and maintain global function as determined by the ejection fraction. These methods are also being applied to determine: (1) the effect of thrombolytic therapy in improving regional and global left and right ventricular performance in myocardial infarction, (2) the effect of residual coronary stenosis on regional ventricular performance after thrombolytic therapy in myocardial infarction, (3) regional abnormalities of timing of motion during systole and diastole, the relationship of these abnormalities to global ventricular performance and to conduction defects in the electrocardiogram. Studies are also in progress to determine the prognostic significance for survival of regional contraction abnormalities. The quantitative coronary arteriographic method is being further developed and applied to determine vasomobility responses of coronary arteries and coronary artery stenoses to various drugs and also to reflexes, such as handgrip, which cause coronary artery constriction. The drug studies are providing new knowledge on the mechanism of action of drugs used to treat patients with angina pectoris. These methods are also being used to determine the natural history of coronary atherosclerotic lesions and the effect of serum lipid lowering with colestepol plus niacin or mevinolin and also cholestyramine on the rate of lesion progression. These quantitative techniques are also being used to determine the dynamics of clot lysis in the coronary arteries of patients with acute myocardial infarction who receive thrombolytic therapy. Factors influencing the rate of lysis and rethrombosis following thrombolytic therapy are being identified.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL019451-13
Application #
3335848
Study Section
Cardiovascular and Pulmonary Research B Study Section (CVB)
Project Start
1976-05-01
Project End
1991-04-30
Budget Start
1988-05-01
Budget End
1989-04-30
Support Year
13
Fiscal Year
1988
Total Cost
Indirect Cost
Name
University of Washington
Department
Type
Schools of Medicine
DUNS #
135646524
City
Seattle
State
WA
Country
United States
Zip Code
98195
Zambon, Alberto; Zhao, Xue-Qiao; Brown, B Greg et al. (2014) Effects of niacin combination therapy with statin or bile acid resin on lipoproteins and cardiovascular disease. Am J Cardiol 113:1494-8
Phan, Binh An P; Moore, Andrew B; Davis, Joseph et al. (2014) Prolonged combination lipid therapy is associated with reduced carotid intima-media thickness: a case-control study of the 20-year Familial Atherosclerosis Treatment - Observational Study (FATS-OS). J Clin Lipidol 8:489-93
Zhao, Xue-Qiao; Krasuski, Richard A; Baer, Jefferson et al. (2009) Effects of combination lipid therapy on coronary stenosis progression and clinical cardiovascular events in coronary disease patients with metabolic syndrome: a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), the HDL-Atherosclero Am J Cardiol 104:1457-64
Zhao, X Q; Yuan, C; Hatsukami, T S et al. (2001) Effects of prolonged intensive lipid-lowering therapy on the characteristics of carotid atherosclerotic plaques in vivo by MRI: a case-control study. Arterioscler Thromb Vasc Biol 21:1623-9
Hosokawa, H; Sheehan, F H; Suzuki, T (2000) Measurement of postsystolic shortening to assess viability and predict recovery of left ventricular function after acute myocardial infarction. J Am Coll Cardiol 35:1842-9
Brown, B G (1999) Assessment for subclinical ischemia: bridging the gap between primary and secondary prevention. Am J Med 107:28S-30S
Zambon, A; Hokanson, J E; Brown, B G et al. (1999) Evidence for a new pathophysiological mechanism for coronary artery disease regression: hepatic lipase-mediated changes in LDL density. Circulation 99:1959-64
Brown, B G; Zambon, A; Poulin, D et al. (1998) Use of niacin, statins, and resins in patients with combined hyperlipidemia. Am J Cardiol 81:52B-59B
Brown, B G; Zhao, X Q; Bardsley, J et al. (1997) Secondary prevention of heart disease amongst patients with lipid abnormalities: practice and trends in the United States. J Intern Med 241:283-94
Hosokawa, H; Sheehan, F H; Suzuki, T et al. (1997) Variability in frame by frame analysis of left ventricular wall motion from contrast angiograms. Int J Card Imaging 13:367-74; discussion 375-7

Showing the most recent 10 out of 50 publications