TY - JOUR
T1 - Effects of short-term administration of verapamil on left ventricular relaxation and filling dynamics measured by a combined hemodynamic-ultrasonic technique in patients with hypertrophic cardiomyopathy
AU - TenCate, F. J.
AU - Serruys, P. W.
AU - Mey, S.
AU - Roelandt, J.
PY - 1983
Y1 - 1983
N2 - The effects of short-term administration of verapamil on left ventricular isovolumetric relaxation and early and late diastolic filling dynamics were studied in 10 patients with hypertrophic cardiomyopathy by a combined hemodynamic-ultrasonic technique. Left ventricular pressures (recorded with high-fidelity micromanometers) were determined simultaneously with M mode echocardiography. After 10 mg of verapamil was given intravenously (2 mg/min), left ventricular contractility and systolic pressure dropped significantly (p < .05). Left ventricular dP/dt fell from 1947 ± 544 to 1489 ± 334 mm Hg/sec, maximal velocity of the contractile element at zero load fell from 50 ± 17 to 42 ± 15 l/sec, peak velocity contraction of the contractile element fell from 37 ± 10 l/sec to 29 ± 10 l/sec (p < .05), and left ventricular systolic pressure fell from 149 ± 30 to 127 ± 22 mm Hg. Left ventricular negative dP/dt increased from 1770 ± 479 to 1477 ± 377 mm Hg/sec (p < .05), and the time constant of isovolumetric pressure decay was prolonged from 48 ± 9 to 64 ± 15 msec (p < .05). Left ventricular end-diastolic pressure rose from 21 ± 7 to 23 ± 6 mm Hg (p < .05). The time constant of isovolumetric pressure decay was calculated in three different ways, but none of these measurements was influenced by verapamil. Time of isovolumetric relaxation, duration of rapid ventricular filling, and peak rate of left ventricular lengthening were not significantly influenced by verapamil and remained highly abnormal. In contrast, peak rate of left ventricular posterior wall thinning declined further after verapamil from 2.9 ± 1.2 to 2.4 ± 1.4 l/sec (p < .05). The constructed pressure-dimension loops did not show any change after verapamil. Plasma levels of verapamil in 8 of the 10 patients were in the therapeutic range (m: 90 to 180 ng/ml); heart rate did not change. Our data indicate that abnormal relaxation and disturbed filling dynamics of the left ventricle persisted after short-term administration of verapamil. Further studies in well-defined subgroups of patients after long-term oral treatment with verapamil are needed to establish the merits of medical treatment of hypertrophic cardiomyopathy.
AB - The effects of short-term administration of verapamil on left ventricular isovolumetric relaxation and early and late diastolic filling dynamics were studied in 10 patients with hypertrophic cardiomyopathy by a combined hemodynamic-ultrasonic technique. Left ventricular pressures (recorded with high-fidelity micromanometers) were determined simultaneously with M mode echocardiography. After 10 mg of verapamil was given intravenously (2 mg/min), left ventricular contractility and systolic pressure dropped significantly (p < .05). Left ventricular dP/dt fell from 1947 ± 544 to 1489 ± 334 mm Hg/sec, maximal velocity of the contractile element at zero load fell from 50 ± 17 to 42 ± 15 l/sec, peak velocity contraction of the contractile element fell from 37 ± 10 l/sec to 29 ± 10 l/sec (p < .05), and left ventricular systolic pressure fell from 149 ± 30 to 127 ± 22 mm Hg. Left ventricular negative dP/dt increased from 1770 ± 479 to 1477 ± 377 mm Hg/sec (p < .05), and the time constant of isovolumetric pressure decay was prolonged from 48 ± 9 to 64 ± 15 msec (p < .05). Left ventricular end-diastolic pressure rose from 21 ± 7 to 23 ± 6 mm Hg (p < .05). The time constant of isovolumetric pressure decay was calculated in three different ways, but none of these measurements was influenced by verapamil. Time of isovolumetric relaxation, duration of rapid ventricular filling, and peak rate of left ventricular lengthening were not significantly influenced by verapamil and remained highly abnormal. In contrast, peak rate of left ventricular posterior wall thinning declined further after verapamil from 2.9 ± 1.2 to 2.4 ± 1.4 l/sec (p < .05). The constructed pressure-dimension loops did not show any change after verapamil. Plasma levels of verapamil in 8 of the 10 patients were in the therapeutic range (m: 90 to 180 ng/ml); heart rate did not change. Our data indicate that abnormal relaxation and disturbed filling dynamics of the left ventricle persisted after short-term administration of verapamil. Further studies in well-defined subgroups of patients after long-term oral treatment with verapamil are needed to establish the merits of medical treatment of hypertrophic cardiomyopathy.
UR - http://www.scopus.com/inward/record.url?scp=0021079245&partnerID=8YFLogxK
U2 - 10.1161/01.CIR.68.6.1274
DO - 10.1161/01.CIR.68.6.1274
M3 - Article
C2 - 6685582
AN - SCOPUS:0021079245
SN - 0009-7322
VL - 68
SP - 1274
EP - 1279
JO - Circulation
JF - Circulation
IS - 6
ER -