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Echocardiographic investigations on patients with hypertrophic cardiomyopathy with obstruction have been detailed and compared with the changes found in sixty patients with chronic Chagas' 'cardiomyopathy'. These changes are similar to those encountered in congestive cardiomyopathy. Endomyocardial fibrosis is rare in Venezuela, but six patients have been found in that country and the echocardiographic changes in one of these patients has been included in this study. [ABSTRACT FROM PUBLISHER]

An electrocardiographic recording method with an associated reading guide, designed for epidemiological studies on Chagas' disease, was tested to assess its diagnostic reproducibility. Six cardiologists from five countries each read 100 electrocardiographic (ECG) tracings, including 30 from chronic chagasic patients, then reread them after an interval of 6 months. The readings were blind, with the tracings numbered randomly for the first reading and renumbered randomly for the second reading. The physicians, all experienced in interpreting ECGs from chagasic patients, followed printed instructions for reading the tracings. Reproducibility of the readings was evaluated using the kappa (kappa) index for concordance. The results showed a high degree of interobserver concordance with respect to the diagnosis of normal vs. abnormal tracings (kappa = 0.66; SE 0.02). While the interpretations of some categories of ECG abnormalities were highly reproducible, others, especially those having a low prevalence, showed lower levels of concordance. Intraobserver concordance was uniformly higher than interobserver concordance. The findings of this study justify the use by specialists of the recording of readings method proposed for epidemiological studies on Chagas' disease, but warrant caution in the interpretation of some categories of electrocardiographic alterations.

Immersion of the hand into ice water (cold-pressor test) in nine hypertensive subjects induced elevation of mean blood pressure, increase of vascular resistance in the extremities, decrease of blood flow in the extremities, and increase in heart rate. The preejection phase of systole was not altered. Indoramin and propranolol, each alone and together, attenuated the pressor and other cardiovascular responses. Submaximal exercise increased heart rate during placebo treatment, a response only partially attenuated by indoramin, propranolol, and their combination, but it did not induce changes in mean blood pressure during any of the treatments.

Eight out-patients with essential hypertension participated in a comparative, placebo-controlled study with a cross-over design. Pindolol and propranolol were administered orally in doses of 20.0 +/- 3.13 mg/d (mean +/- SEM) and 125.0 +/- 19.17 mg/d respectively. Pindolol reduced mean blood pressure by 11.9 mmHg; pre-ejection period index by 8.1 msec; total peripheral resistance by 3.1 mmHg min/L; and limb vascular resistance by 3.28 mmHg min 100 g/ml. Heart rate, cardiac output, plasma renin activity and urinary norepinephrine excretion rate were not altered by pindolol. Propranolol reduced mean blood pressure by 14.0 mmHg; heart rate by 9.1 beats/min; cardiac output by 0.57 L/min; limb blood flow by 1.06 ml/100 g.min; and plasma renin activity by 1.44 ng/ml/h; and increased pre-ejection period index by 8.7 msec. Total peripheral resistance, limb vascular resistance and urinary norepinephrine excretion rate were not altered by propranolol. It was concluded that: (1) the drugs, pindolol and propranolol, are equally effective as antihypertensive agents; (2) heart function and plasma renin activity are decreased by propranolol and unaltered by pindolol; (3) total peripheral resistance is decreased by pindolol and unaltered by propranolol; and (4) these findings may be explained by the intrinsic sympathomimetic activity exhibited by pindolol only.

Nineteen patients with essential hypertension (EH) were studied as outpatients. After administration of chlorthalidone, 50 mg/day for 4 weeks, prazosin 1-4 mg/day (1.82 +/- 0.33 mg/day) was added for a period of 12 weeks. Prazosin lowered supine blood pressure from 149.7 +/- 2.85/102.0 +/- 2.75 mm Hg to 128.2 +/- 3.0/86.1 +/- 1.04 mm Hg (p less than 0.001). Prazosin did not alter heart rate significantly. Prazosin increased the thyroid stimulating hormone (TSH) from 3.63 +/- 0.33 microunits/ml to 4.83 +/- 0.45 microunits/ml (p less than 0.025), thyroxine (T4) from 10.03 +/- 0.29 micrograms/ml to 10.85 +/- 0.42 micrograms/ml (p less than 0.005), and decreased triiodothyronine (T3) from 36.65 +/- 0.62% to 35.42 +/- 0.56%, which was not significant. The free thyroxine index (FTI) increased slightly from 3.67 +/- 0.12 to 3.83 +/- 0.14 (p less than 0.025). However, all values remained within the normal range for the laboratory. Serum cholesterol increased insignificantly. Triglycerides decreased significantly from 223.4 +/- 50.6 mg/dl to 161.7 +/- 29.0 mg/dl (p less than 0.05). High density lipoproteins (HDL) increased significantly from 30.1 +/- 2.1% to 36.0 +/- 3.06 (p less than 0.025). Low density lipoproteins (LDL) decreased insignificantly and very low density lipoproteins (VLDL) decreased from 20.9 +/- 3.44 to 16.3 +/- 2.85 (p less than 0.005). The cholesterol ratio increased from 45.51 +/- 4.3 to 64.71 +/- 10.7 (+42.1%). These results indicate that, in patients with essential hypertension, prazosin is an effective antihypertensive agent and that it significantly increases HDL, decreases VLDL, and improves the cholesterol ratio.

Prazosin and propranolol were compared in an open, crossover study to determine their effects on plasma lipids and lipoproteins. After a four-week placebo period, 10 hypertensive patients were randomly assigned to prazosin treatment (Group I) and another 10 to propranolol treatment (Group II) for eight weeks. After a second four-week placebo period, treatment in each group was switched to the alternative drug for eight weeks. The mean blood pressure was reduced to normal levels (diastolic blood pressure less than or equal to 90 mm Hg) by both drugs--prazosin (1 to 8 mg per day) and propranolol (40 to 240 mg per day). The results of the study indicate that prazosin decreases serum cholesterol levels. In contrast, propranolol not only increases serum triglyceride levels and very-low-density lipoprotein cholesterol, but decreases total high-density lipoprotein cholesterol, high-density lipoprotein2 cholesterol, high-density lipoprotein2, and apoprotein A-I. The data suggest that propranolol may induce significant, potentially atherogenic changes in lipid metabolism, whereas prazosin may represent an advantageous alternative as an antihypertensive agent, especially in subjects with an already atherogenic lipoprotein profile.

1 The effect of propranolol was examined on a) blood pressure and heart rate responses due to i.v. hydrallazine b) modification of these cardiovascular parameters during cold pressor test c) urinary catecholamine excretion rate. 2 Intravenous hydrallazine reduced significantly mean blood pressure by 15.2 mm Hg and increased heart rate by 24.9 beats/min. Propranolol reduced significantly mean blood pressure by 19.0 mm Hg and heart rate by 14.1 beats/min. Hydrallazine plus propranolol caused a significant reduction of mean blood pressure (by 37.7 mm Hg) but this was not accompanied by a significant fall in heart rate (by 3.3 beats/min). 3 During the control period, cold pressor test increased mean blood pressure by 16.0 mm Hg. Heart rate was increased by 12.5 beats/min in four patients. However, there was a reduction in heart rate (5.5 beats/min) in two other patients. During the propranolol period, cold pressor test-induced increase of mean blood pressure was not reduced but propranolol blocked the increase of heart rate. 4 Urinary catecholamine excretion rate was increased during hydrallazine administration. This excretion was not modified by propranolol.