TY - JOUR
T1 - Isovolumic relaxation period in hypertrophic cardiomyopathy
T2 - Assessment by radionuclide angiography
AU - Betocchi, S.
AU - Bonow, R. O.
AU - Bacharach, S. L.
AU - Rosing, D. R.
AU - Maron, B. J.
AU - Green, M. V.
N1 - Funding Information:
From the Cardiology Branch, National Heart, Lung, and Blood Insti• tute, Bethesda. Maryland and Department of Nuclear Medicine. Clinical Center. National Institutes of Health. Bethesda, Maryland. Dr. Betocchi is a recipient of Fellowship F05 TW03350 from the National Institutes of Health-Fogarty International Research, Bethesda, Maryland. His present address is Clinica Medica I, Facolta di Medicina. Naples. Italy. Manuscript received May 21. 1985; revised manuscript receIved July 23, 1985. accepted July 31. 1985. Address for reprints: Robert O. Bonow, MD, Building 10. Room 7B-15. National Institutes of Health, Bethesda. Maryland 20892.
PY - 1986
Y1 - 1986
N2 - Left ventricular isovolumic relaxation and the relation between relaxation and filling were studied in 90 patients with hypertrophic cardiomyopathy and 29 control subjects using radionuclide angiography. The isovolumic relaxation period was determined automatically on left ventricular time-activity curves as the interval between minimal volume and onset of rapid filling. In 17 patients, M-mode echocardiography performed simultaneously with radionuclide angiography demonstrated that onset of mitral valve opening correlated well with onset of rapid filling (r = 0.84, p < 0.001). The isovolumic relaxation period was longer in patients with hypertrophic cardiomyopathy than in cdntrol subjects (95 ± 44 versus 50 ± 23 ms, p < 0.01) and was longer in patients without an outflow tract gradient at rest than in patients with a gradient (109 ± 37 versus 86 ± 35 ms, p < 0.05). In these patients without obstruction, a weak linear relation between duration of the isovolumic period and peak filling rate was fodnd (r = 0.48, p < 0.02). Filling was impaired in patients with hypertrophic cardiomyopathy, as assessed by lower peak filling rate (3.2 ± 1.2 versus 3.5 ± 0.5 end-diastolic volume/s, p < 0.05) and prolonged time to peak filling rate (185 ± 44 versus 145 ± 20 ms, p < 0.01) compared with values in control subjects. The delay in time to peak filling rate was caused primarily by the prolonged isovolumic period, because the interval from onset of rapid filling to peak filling rate was similar in patients with hypertrophic cardiomyopathy and control subjects (87 ± 31 versus 95 ± 25 ms, NS). Studies were repeated in 43 patients after administration of oral verapamil (320 to 640 mg/day). Verapamil decreased the isovolumic relaxation period (from 95 ± 42 to 80 ± 31 ms, p < 0.05), associated with improved filling; peak filling rate increased and time to peak filling rate decreased. Thus, the delay in peak filling rate in patients with hypertrophic cardiomyopathy is caused by prolongation of the isovolumic period. Verapamil decreases the isovolumic relaxation period and improves subsequent diastolic filling. These data suggest that impaired relaxation is an important determinant of decreased left ventricular filling in patients with hypertrophic cardiomyopathy.
AB - Left ventricular isovolumic relaxation and the relation between relaxation and filling were studied in 90 patients with hypertrophic cardiomyopathy and 29 control subjects using radionuclide angiography. The isovolumic relaxation period was determined automatically on left ventricular time-activity curves as the interval between minimal volume and onset of rapid filling. In 17 patients, M-mode echocardiography performed simultaneously with radionuclide angiography demonstrated that onset of mitral valve opening correlated well with onset of rapid filling (r = 0.84, p < 0.001). The isovolumic relaxation period was longer in patients with hypertrophic cardiomyopathy than in cdntrol subjects (95 ± 44 versus 50 ± 23 ms, p < 0.01) and was longer in patients without an outflow tract gradient at rest than in patients with a gradient (109 ± 37 versus 86 ± 35 ms, p < 0.05). In these patients without obstruction, a weak linear relation between duration of the isovolumic period and peak filling rate was fodnd (r = 0.48, p < 0.02). Filling was impaired in patients with hypertrophic cardiomyopathy, as assessed by lower peak filling rate (3.2 ± 1.2 versus 3.5 ± 0.5 end-diastolic volume/s, p < 0.05) and prolonged time to peak filling rate (185 ± 44 versus 145 ± 20 ms, p < 0.01) compared with values in control subjects. The delay in time to peak filling rate was caused primarily by the prolonged isovolumic period, because the interval from onset of rapid filling to peak filling rate was similar in patients with hypertrophic cardiomyopathy and control subjects (87 ± 31 versus 95 ± 25 ms, NS). Studies were repeated in 43 patients after administration of oral verapamil (320 to 640 mg/day). Verapamil decreased the isovolumic relaxation period (from 95 ± 42 to 80 ± 31 ms, p < 0.05), associated with improved filling; peak filling rate increased and time to peak filling rate decreased. Thus, the delay in peak filling rate in patients with hypertrophic cardiomyopathy is caused by prolongation of the isovolumic period. Verapamil decreases the isovolumic relaxation period and improves subsequent diastolic filling. These data suggest that impaired relaxation is an important determinant of decreased left ventricular filling in patients with hypertrophic cardiomyopathy.
UR - http://www.scopus.com/inward/record.url?scp=0022575932&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0022575932&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(86)80262-5
DO - 10.1016/S0735-1097(86)80262-5
M3 - Article
C2 - 3941220
AN - SCOPUS:0022575932
SN - 0735-1097
VL - 7
SP - 74
EP - 81
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 1
ER -