Abstract | OBJECTIVES: BACKGROUND: METHODS: RESULTS: In patients with outflow obstruction, pressure gradient at the outflow tract decreased from a mean +/- SD of 100 +/- 45 to 26 +/- 33 mm Hg (p < 0.01). Although systolic function was similarly impaired in both groups, the time constant of left ventricular pressure decay (tau) shortened from 56 +/- 10 to 44 +/- 8 ms (p < 0.01) and the constant of left ventricular chamber stiffness (kc) decreased from 0.049 +/- 0.017 to 0.038 +/- 0.014 m2/ml (p < 0.01) only in patients with outflow obstruction. Shortening in tau correlated best with decrease in left ventricular systolic pressure (r = 0.84, p < 0.01). In contrast, tau was prolonged from 52 +/- 10 to 64 +/- 11 ms (p < 0.01) and kc was unchanged in patients without outflow obstruction. CONCLUSIONS: The primary effects of disopyramide on the hypertrophied left ventricle were negative inotropic and negative lusitropic. However, left ventricular diastolic properties in patients with outflow obstruction were improved with a decrease in outflow pressure gradient. Relief of clinical symptoms in hypertrophic obstructive cardiomyopathy with disopyramide might be due in part to improvement of diastolic function, which appears secondary to the reduction in ventricular afterload.
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Authors | H Matsubara, S Nakatani, S Nagata, F Ishikura, Y Katagiri, T Ohe, K Miyatake |
Journal | Journal of the American College of Cardiology
(J Am Coll Cardiol)
Vol. 26
Issue 3
Pg. 768-75
(Sep 1995)
ISSN: 0735-1097 [Print] United States |
PMID | 7642872
(Publication Type: Clinical Trial, Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
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Topics |
- Adult
- Aged
- Analysis of Variance
- Blood Pressure
(drug effects)
- Cardiac Catheterization
- Cardiomyopathy, Hypertrophic
(complications, drug therapy, physiopathology)
- Diastole
(drug effects)
- Disopyramide
(pharmacology, therapeutic use)
- Female
- Humans
- Male
- Middle Aged
- Systole
(drug effects)
- Ventricular Function, Left
(drug effects)
- Ventricular Outflow Obstruction
(drug therapy, etiology, physiopathology)
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