TY - JOUR
T1 - Pindolol and systolic time intervals in patients with hypertension
AU - Hammond, Jeremy J.
AU - Kirkendall, Walter M.
AU - Jacks-Nagle, Verne L.
AU - Plotnick, Gary D.
AU - Fisher, Michael L.
AU - Hamilton, Jennifer H.
AU - Robinson, Michael
AU - Carliner, Nathan H.
AU - Janoski, Alphonso H.
AU - Hamilton, Bruce P.
N1 - Funding Information:
From the Department of Medicine, University of Texas Medical School at Houston, and the Department of Medicine, Cardiology and Endocrine Section, Veterans Administration Medical Center, University of Maryland School of Medicine. Supported by a grant from the Veterans Administration, MD. Reprint requests: Walter M. Kirkendall, M.D., Department of Medicine, University of Texas Medical School at Houston, PO Box 20708, Houston, TX 77025.
PY - 1982/8
Y1 - 1982/8
N2 - Two studies of systolic time intervals (STIs) in patients with mild to moderate hypertension (HBP) revealed that no mean change in systolic intervals occurred with pindolol therapy, although some patients had significant alterations in their STIs. Pindolol responders with normal pretreatment preejection period to left ventricular ejection time ( PEP LVET) ratios had a significant increase in this ratio following pindolol therapy, whereas those with abnormal pretreatment PEP LVET ratios had improvement in this ratio on administration of the drug. Patients on propranolol showed no change in PEP LVET ratio. Propranolol administration slowed heart rate and lengthened Q-S2, S1-S2, and LVET, however, without altering the Q-S2 and LVET index, indicating that the changes were caused by the effect of propranolol on the heart rate alone. Chlorthalidone in high doses significantly reduced the Q-S2 index and the S1-S2 index, indicating that these changes were not caused by alteration of the heart rate. The second study suggests that STIs may provide a predictive clue for clinical response to pindolol. Patients with normal cardiac function (group I) are more likely to respond to pindolol than are those with abnormal cardiac function (group II). Directionally opposite changes in STIs in the two subgroups suggest different mechanisms for changing cardiac function. Pindolol's dual role as a beta-blocking agent with intrinsic sympathomimetic activity is proposed as a possible explanation, beta-blocking effects predominating in group I and sympathomimetic activity balancing the beta effect in group II.
AB - Two studies of systolic time intervals (STIs) in patients with mild to moderate hypertension (HBP) revealed that no mean change in systolic intervals occurred with pindolol therapy, although some patients had significant alterations in their STIs. Pindolol responders with normal pretreatment preejection period to left ventricular ejection time ( PEP LVET) ratios had a significant increase in this ratio following pindolol therapy, whereas those with abnormal pretreatment PEP LVET ratios had improvement in this ratio on administration of the drug. Patients on propranolol showed no change in PEP LVET ratio. Propranolol administration slowed heart rate and lengthened Q-S2, S1-S2, and LVET, however, without altering the Q-S2 and LVET index, indicating that the changes were caused by the effect of propranolol on the heart rate alone. Chlorthalidone in high doses significantly reduced the Q-S2 index and the S1-S2 index, indicating that these changes were not caused by alteration of the heart rate. The second study suggests that STIs may provide a predictive clue for clinical response to pindolol. Patients with normal cardiac function (group I) are more likely to respond to pindolol than are those with abnormal cardiac function (group II). Directionally opposite changes in STIs in the two subgroups suggest different mechanisms for changing cardiac function. Pindolol's dual role as a beta-blocking agent with intrinsic sympathomimetic activity is proposed as a possible explanation, beta-blocking effects predominating in group I and sympathomimetic activity balancing the beta effect in group II.
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U2 - 10.1016/0002-8703(82)90140-5
DO - 10.1016/0002-8703(82)90140-5
M3 - Article
C2 - 7102532
AN - SCOPUS:0020359629
SN - 0002-8703
VL - 104
SP - 456
EP - 464
JO - American heart journal
JF - American heart journal
IS - 2 PART 2
ER -