Cardiology
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beta-Adrenergic blockade represents a major pharmacologic advance. These drugs bind to membrane adrenergic receptors interfering with the effects of endogenous catecholamines. ⋯ The drugs have varying pharmacodynamic properties that may modify certain side effects: beta 1-selectivity, partial agonism, alpha-adrenergic blocking activity, membrane stabilization, and varying pharmacokinetic characteristics. The drugs have been shown to be relatively safe and useful for a wide variety of cardiovascular and noncardiovascular disease states, and their wide spectrum of therapeutic activity illustrates the importance of the sympathetic nervous system in the pathophysiology of medical illness.
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Randomized Controlled Trial Clinical Trial Controlled Clinical Trial
Effects of glucose-insulin-potassium infusion on the angina response during treadmill exercise.
The effects of glucose-insulin-potassium (GIK) and placebo normal saline (S) infusion on treadmill-walking time to angina, ST depression, heart rate (HR), systolic blood pressure (SBP), rate pressure product (RPP), blood glucose (G), lactate (L) and free fatty acids (FFA) were studied in 14 non diabetic patients with exertional angina. For the whole group, the post-GIK walking time to angina (393 +/- 33 sec, mean +/- SEM) was greater than the values during control GIK (319 +/- 20 sec, p less than 0.02) and post-S infusion (334 +/- sec, p less than 0.05), but circulatory and ST responses were similar in post-GIK and post-S studies. 7 of the 14 patients experienced significantly greater improvement in exercise tolerance following GIK (467 +/- 39 sec) in comparison to control GIK (313 +/- 29 sec, p less than 0.001) and post-S infusion (334 +/- 32 sec, p less than 0.005) and exercised to a higher HR, SBP and RPP after GIK than after S infusion. At the onset of angina these patients had similar ST-segment depression before and after GIK but when ST segments were assessed after GIK at the same exercise duration when angina had occurred during the control and post-S studies, there was significantly less ST depression (p less than 0.01). ⋯ Comparison of post-GUK and post-S values for G, L and FFA for the whole group showed significantly lower resting values of FFA and post-exercise values of G following GIK infusion. The differences in clinical and circulatory responses between patients who improved and those who did not improve following GIK were not related to the angiographically determined severity of coronary artery disease or to GIK-induced metabolic changes. Results suggest that some patients with angina pectoris do benefit from GIK infusion but the response in a given patient to this therapeutic modality is unpredictable.
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A triple human catheter was used for the determination of cardiac output during the acute phase of moycardial infarction in 23 patients. The correlation coefficient between thermodilution and the Fick method was 0.91. ⋯ Quadruplicate determinations allowed to detect variations of cardiac output in the range of 0.465 1/min. Variation between two successive determinations of more than 9.4% can probably be attributed to a technical error.
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Clinical Trial
Dihydroergotamine: an effective treatment for postural hypotension due to antihypertensive drugs (ganglion-blocking agents excepted).
In this study the effect of DHE on postural hypotension induced by major antihypertensive drugs was evaluated in 40 patients. 30 patients were treated with methyldopa, five with guanoxan sulphate and five with bethanidine sulphate. To obtain a more accurate picture of the effectiveness of DHE and to test the reproducibility of its effect, each patient was observed during five separate, successive periods: in the first period the antihypertensive agent was given alone; in the second period it was given along with placebo; in the third period it was given with DHE; in the fourth period the antihypertensive agent was given alone again; and in the fifth period it was again given with DHE. In the third and in the fifth period, DHE was administered at the same time as the antihypertensive agent in a dose of 9-15 mg/24 h (3-5 mg three times daily). ⋯ In these patients the standing arterial blood pressure showed a significant response (p less than 0.01). DHE did not interfere with the therapeutic effect of the antihypertensive agents. Furthermore, DHE did not affect the heart rate, nor did it give rise to any adverse reactions.