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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.
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
December 1979,
Ceskoslovenska pediatrie,
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
July 1988,
Polski tygodnik lekarski (Warsaw, Poland : 1960),
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
July 1988,
Polski tygodnik lekarski (Warsaw, Poland : 1960),
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
March 1980,
The American journal of cardiology,
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
January 1976,
Australian and New Zealand journal of medicine,
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
July 1975,
Japanese circulation journal,
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
November 1979,
Archives des maladies du coeur et des vaisseaux,
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
April 1979,
European journal of cardiology,
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
February 1971,
Klinische Wochenschrift,
J J Hammond, and
W M Kirkendall, and
V L Jacks-Nagle, and
G D Plotnick, and
M L Fisher, and
J H Hamilton, and
M Robinson, and
N H Carliner, and
A H Janoski, and
B P Hamilton
January 1978,
Circulation,
