Jennifer H. Hamilton

Improvement in depressed cardiac function in hypertensive patients during pindolol treatment

To assess changes in left ventricular function during antihypertensive treatment using pindolol, a beta-adrenocepter blocking drug with potent intrinsic sympathomimetic activity, serial echocardiographic measurements were obtained in 70 hypertensive patients before and during 15 weeks of treatment with pindolol. For analysis, the patients were separated into three groups on the basis of their baseline left ventricular fractional shortening (Group I, 35 patients with normal fractional shortening of 28 percent or more; Group II, 16 patients with abnormal fractional shortening of 21 to 27 percent; and Group III, 19 patients with markedly abnormal fractional shortening of 20 percent or less). More than half of the patients in Group I and Group II had decreases in mean blood pressure of 10 percent or more in response to pindolol, but only one fourth of Group III patients had similar responses (p less than 0.05). Patients with normal pretreatment fractional shortening had a mild decrease in fractional shortening during pindolol treatment, whereas patients with either abnormal or markedly abnormal fractional shortening had an increase in fractional shortening. This increase in fractional shortening suggests the possibility that the partial agonist or intrinsic sympathomimetic activity of pindolol may play a role in preserving left ventricular function in patients with borderline or impaired function.

Cardiac arrhythmias after abrupt clonidine withdrawal.

Abrupt clonidine withdrawal may be associated with sharp marked increases in catecholamine levels, heart rate, and blood pressure, which may induce nausea, vomiting, and palpitations. Relatively little information is available on the incidence of cardiac arrhythmias in this setting. With continuous ambulatory ECG recordings, we determined the incidence of arrhythmias in seven male hypertensive patients (without active heart disease) after abrupt clonidine withdrawal. Serious ventricular arrhythmias, including brief ventricular tachycardia, developed in two patients who had greater increases in mean systolic blood pressure (28 ± 3 vs 10 ± 8 mm Hg) and double product (552 ± 681 vs 333 ± 195) than the others. The differences were not significant. Ventricular arrhythmias were not related to age, dose, withdrawal symptoms, initial blood pressure, urinary norepinephrine levels, or ECG abnormalities. We conclude that serious ventricular arrhythmias may be relatively common but unpredictable during clonidine withdrawal, even in patients with no clinically apparent heart disease. The triggering of ventricular arrhythmias should be added to the list of components of clonidine withdrawal syndrome.

Pindolol in the Treatment of Hypertension: Systolic Time Intervals as a Predictor of Response to Beta Receptor Blockade

Seventy-two hypertensive patients were treated with pindolol, a beta adrenergic blocking drug with intrinsic sympathomimetic activity. Serial measurements of systolic time intervals were utilized (1) to determine whether the therapeutic response to pindolol was predictable from pretreatment measurements, and (2) to assess changes in cardiac function during a 15 week treatment period. Patients with an abnormal pretreatment ratio of preejection period to left ventricular ejection time (PEP/LVET) of greater than 0.42 were less likely to respond with a decrease in mean blood pressure of greater than 10 percent (8 of 22) than were patients with a normal (0.42 or less) pretreatment PEP/LVET ratio (33 of 50) (p

Withdrawal phenomena in subjects with essential hypertension on clonidine or tiamenidine

The incidence and pathogenesis of withdrawal phenomena with the centrally acting drugs clonidine (CLON) and tiamenidine (TIAM) were evaluated. Thirty subjects with hypertension on hydrochlorothiazide (HCTZ) were randomized to TIAM or CLON. Blood pressure and integrated plasma catecholamine levels fell equally in response to both drugs. On withdrawal, blood pressure and pulse rose in both groups with no difference between them. Three subjects had symptoms of withdrawal, four had blood pressure overshoot above pretreatment levels of 10 mm Hg or more, and eight had a rise in blood pressure of 30 mm Hg systolic or 20 mm Hg diastolic. There was no difference between TIAM and CLON in these effects. There was a direct correlation between blood pressure rise and increase in integrated plasma norepinephrine levels. We conclude that the incidence of withdrawal phenomena in subjects on TIAM or CLON is infrequent and that there is a direct relationship between the rise in blood pressure and the loss of suppression of catecholamines by these drugs.