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Disopyramide in hypertrophic cardiomyopathy. I. Hemodynamic assessment after intravenous administration
C Pollick1, B Kimball, M Henderson
1Department of Medicine, Toronto General Hospital, Ontario, Canada.
Insights
Intravenous disopyramide significantly reduced left ventricular outflow obstruction in hypertrophic cardiomyopathy patients. This drug effectively decreased pressure gradients, improving hemodynamic function in those with resting obstruction.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart muscle disease.
- Resting obstruction to left ventricular outflow is a common complication of HCM.
Purpose of the Study:
- To evaluate the hemodynamic effects of intravenous disopyramide in patients with HCM and resting obstruction.
Main Methods:
- 43 patients with HCM and resting obstruction received intravenous disopyramide.
- Hemodynamic parameters, including pressure gradients, left ventricular pressures, aortic pressures, and cardiac output, were measured.
Main Results:
- Disopyramide reduced the subaortic pressure gradient by a mean of 61 mm Hg, abolishing it in 35 patients.
- Left ventricular systolic pressure decreased, while aortic systolic pressure increased.
- Left ventricular ejection time and end-diastolic pressure were reduced.
- Cardiac output remained unchanged in a subgroup, despite decreased contractility, possibly due to reduced mitral regurgitation.
Conclusions:
- Intravenous disopyramide demonstrates favorable hemodynamic effects in patients with HCM and resting left ventricular outflow obstruction.
- Disopyramide may reduce mitral regurgitation by decreasing systolic anterior motion of the mitral valve.
Abstract:
The hemodynamic effects of intravenous disopyramide were determined in 43 patients with hypertrophic cardiomyopathy and pressure gradients at rest (resting obstruction). The basal subaortic pressure gradient decreased in all patients by a mean of 61 mm Hg (range 16 to 123); in 35 patients the gradient was abolished (less than 20 mm Hg). The reduction in pressure gradient was achieved through a decrease in left ventricular systolic pressure, from 178 to 135 mm Hg (p less than 0.0001), and a rise in aortic systolic pressure, from 105 to 123 mm Hg (p less than 0.0001). Left ventricular ejection time was reduced from 326 to 273 ms (p less than 0.0001). Left ventricular end-diastolic pressure decreased from 19 to 16 mm Hg (p less than 0.0001). In a subgroup of 13 patients, cardiac output was unchanged after disopyramide, despite a prolongation of the pre-ejection period from 104 to 137 ms (p less than 0.0001) indicating a decrease in contractility. The maintenance of cardiac output, despite a decrease in contractility, may reflect a decrease in mitral regurgitation resulting from the reduction of systolic anterior motion of the mitral valve by disopyramide. These results indicate that disopyramide produces predictably favorable hemodynamic effects in patients with hypertrophic cardiomyopathy and resting obstruction to left ventricular outflow.