Related Experiment Videos
Effects of diltiazem on left ventricular systolic and diastolic function in hypertrophic cardiomyopathy
S Betocchi1, F Piscione, A Losi M
1Department of Cardiology and Cardiac Surgery, Federico II University School of Medicine, Naples, Italy.
Insights
Diltiazem improves diastolic function in hypertrophic cardiomyopathy (HC) patients by enhancing active relaxation and cardiac output. While generally safe, it may increase left ventricular outflow tract obstruction in some individuals.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Hypertrophic cardiomyopathy (HC) is marked by diastolic dysfunction and potential left ventricular (LV) outflow tract obstruction.
- Verapamil shows benefits for diastolic properties but carries risks.
Purpose of the Study:
- To evaluate the effects of diltiazem on hemodynamics and LV function in patients with HC.
- To assess diltiazem's impact on LV outflow tract obstruction.
Main Methods:
- Cardiac catheterization and radionuclide angiography were used in 16 HC patients.
- Measurements were taken at baseline and during intravenous diltiazem infusion under atrial pacing.
Main Results:
- Diltiazem induced systemic vasodilation, increasing cardiac index and decreasing systemic resistance.
- Active diastolic function improved, evidenced by increased peak filling rate and decreased relaxation time constant (tau).
- LV outflow tract gradient did not significantly change, but some patients experienced increased obstruction and elevated pulmonary artery wedge pressure.
Conclusions:
- Acute diltiazem administration improves active diastolic function in HC through direct and indirect hemodynamic effects.
- LV outflow tract obstruction did not worsen overall despite vasodilation, but individual responses vary.
- Passive diastolic function remained unaffected.
Abstract:
Hypertrophic cardiomyopathy (HC) is characterized by impaired diastolic function, and left ventricular (LV) outflow tract obstruction in about one-fourth of patients. Verapamil improves diastolic properties, but may have dangerous adverse effects. This study investigates the effects of diltiazem on hemodynamics and LV function in 16 patients with HC who were studied with cardiac catheterization and simultaneous radionuclide angiography. Studies were performed during atrial pacing (15 beats above spontaneous rhythm) at baseline and during intravenous diltiazem administration (0.25 mg x kg(-1) over 2 minutes, and 0.014 mg x kg(-1) x min(-1). Diltiazem induced a systemic vasodilation (cardiac index: 3.4 +/- 1.0 to 4.0 +/- 1.0 L x min(-1) x m(-2), p = 0.003; aortic systolic pressure: 116 +/- 16 to 107 +/- 19 mm Hg, p = 0.007; systemic resistance index: 676 +/- 235 to 532 +/- 193 dynes x s x cm(-5) x m(-2), p = 0.006), not associated with changes in the LV outflow tract gradient. The end-systolic pressure/volume ratio decreased (30 +/- 42 to 21 +/- 29 mm Hg x ml(-1) x m(-2); p = 0.044). Pulmonary artery wedge pressure (11 +/- 5 to 15 +/- 6 mm Hg, p = 0.006), and peak filling rate increased (4.1 +/- 1.3 to 6.0 +/- 2.4 stroke counts x s(-1), p = 0.004). The time constant of isovolumetric relaxation tau decreased (74 +/- 40 to 59 +/- 38 ms, p = 0.045). The constant of LV chamber stiffness did not change. Thus, active diastolic function is improved by the acute administration of diltiazem by both direct action and changes in hemodynamics and loading conditions. LV outflow tract gradient does not increase despite systemic vasodilation. In some patients, however, a marked increase in obstruction and a potentially harmful elevation in pulmonary artery wedge pressure do occur. Passive diastolic function is not affected.