EFFECTS OF DILTIAZEM ON LEFT-VENTRICULAR SYSTOLIC AND DIASTOLIC FUNCTION IN HYPERTROPHIC CARDIOMYOPATHY

Hypertrophic cardiomyopathy (HC) is characterized by impaired diastoli c function, and left ventricular (LV) outflow tract obstruction in abo ut one-fourth of patients. Verapamil improves diastolic properties, bu t may have dangerous adverse effects. This study investigates the effe cts of diltiazem on hemodynamics and LV function in 16 patients with H C who were studied with cardiac catheterization and simultaneous radio nuclide angiography. Studies were performed during atrial pacing (15 b eats above spontaneous rhythm) at baseline and during intravenous dilt iazem administration (0.25 mg . kg(-1) over 2 minutes, and 0.014 mg . kg(-1). min(-1)). Diltiazem induced a systemic vasodilation (cardiac i ndex: 3.4 +/- 1.0 to 4.0 +/- 1.0 L . min(-1). m(-2), p = 0.003; aortic systolic pressure: 116 +/- 16 to 107 +/- 19 mm Hg, p = 0.007; systemi c resistance index: 676 +/- 235 to 532 +/- 193 dynes . s . cm(-5). m(- 2), p = 0.006), not associated with changes in the LV outflow tract gr adient. The end-systolic pressure/volume ratio decreased (30 +/- 42 to 21 +/- 29 mm Hg . ml(-1). m(-2); 0.044). Pulmonary artery wedge press ure (11 +/- 5 to 15 +/- 6 mm Hg, p = 0.006), and peak filling rate inc reased (4.1 +/- 1.3 to 6.0 +/- 2.4 stroke counts . 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 hemod ynamics and loading conditions. LV outflow tract gradient does not inc rease despite systemic vasodilation. In some patients, however, a mark ed increase in obstruction and a potentially harmful elevation in pulm onary artery wedge pressure do occur. Passive diastolic function is no t affected.