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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite widespread clinical application of propranolol (P) in angina pectoris, convincing evidence of its efficacy has been incomplete, thereby resulting in continued controversy. Its antianginal effectivess was investigated in 20 patients with documented coronary heart disease in a 44-wk study incorporating a prolonged 12-wk lead-in period, individualization of P dosage in a 6-wk dose-finding period, and a 24-wk doule-blind crossover phase. On double-blind placebo, patients had 10.5 +/- 2.1 anginal attacks and consumed 12.8 +/- 3.0 nitroglycerin tablets (NTG) each week compared to 6.6 +/- 1.5 anginal episodes (- 37%, p less than 0.001) and 8.0 +/- 1.7 NTG (-38%, p less than 0.001) when on P. No patient experienced more angina with P than with placebo. In addition, time to onset of chest pain during treadmill exercise was prolonged by P from 190 +/- 16 to 248 +/- 22 sec (+31%, p less than 0.02) and ST depression was reduced from 1.7 +/- 0.21 to 0.99 +/- 0.18 mm (-42%, p less than 0.05). There was correlation (r = 0.64 p less than 0.01) between per cent declines in anginal frequency and resting double product with P. Thus, propranolol favorably altered several indices of myocardial ischemia in severe coronary heart disease. This investigation clearly documents the clinical efficacy of optimal beta adrenergic blockade in coronary disease and provides objective justification for the judicious application of propranolol in treatment of angina pectoris.
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PMID:Efficacy of beta adrenergic blockade in coronary heart disease: propranolol in angina pectoris. 81 Feb 95

The long-term efficacy of lidoflazine was investigated in 40 patients with a longer history of angina pectoris and well-documented ischemic heart disease over a whole range of 18 months in double-blind technique. Significant improvement occurs to frequency and severity of angina pectoris, related to reduction in consumption of nitro-compounds and in the extent of ST-segmental depression under resting and cycloergometric test conditions. Increase in cardiac work capacity is evident. There are no changes in heart rate, blood pressure and AV-interval in the ECG. The mode of action of lidoflazine may be an increase in the formation of coronary collaterals, whereas its acute vasodilating properties, experimentally verified in the dog, does not play any important part in the treatment of human coronary insufficiency. The introduction of lidoflazine in the treatment of coronary heart disease appears to be justified as an additive medication.
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PMID:[Efficacy of lidoflazine in angina pectoris. A long-term double-blind study]. 81 96

The effects of an intravenous infusion of nitroglycerin were studied in 20 acutely hypertensive patients during coronary-artery surgery. Eight patients had histories of essential hypertension and six had been treated for it. They were anesthetized with morphine, diazepam, N2O, O2, pancuronium, and enflurane. Control measurements were obtained after sternotomy. Nitroglycerin was then administered until the blood pressure returned to normal, and the measurements then repeated. The mean dose of nitroglycerin was 80.0 +/- 4.7 mug/min, or 0.96 mug/kg/min. This produced significant decreases (P less than .05) in systolic, diastolic, and mean arterial blood pressures, central venous pressure, pulmonary capillary wedge pressure, systemic vascular resistance, and left ventricular stroke work index. Cardiac index, stroke index, and heart rate were unchanged. Two indices of myocardial oxygen demand (rate-pressure product and tension-time index) were significantly decreased by nitroglycerin (P less than .005). Fifty per cent of the patients had improvement in ST-segment depression on the electrocardiogram. These findings demonstrate that nitroglycerin can be safely administered intravenously during operation, and suggest that nitroglycerin decreases myocardial oxygen demand and relieves myocardial ischemia.
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PMID:Nitroglycerin infusion during coronary-artery surgery. 82 Feb 17

A man with known coronary heart disease underwent treadmill exercise testing to determine his functional capacity. The test was negative for ischemia. Ventricular ectopic activity was noted at rest and in the recovery period. On the same day, while viewing a sporting event at home, the patient died suddenly. An ambulatory electrocardiographic recording documented ventricular fibrillations as the terminal mechanism. Ventricular ectopic activity and heart rate increased in the two hours prior to death, and ischemic ST-segment depression was noted at the time of the terminal arrhythmia. It is postulated that myocardial ischemia and catecholamine response lowered the threshold to ventricular fibrillation, thus facilitating the emergence of the fatal arrhythmia.
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PMID:Sudden death during ambulatory monitoring. Clinical and electrocardiographic correlations. Report of a case. 83 Feb 11

To clarify the influence of propranolol-and particularly its heart-rate effects-on myocardial ischemia, coronary hemodynamics and metabolism were studied in 15 patients utilizing a protocol to control heart rate. Ten patients had significant coronary narrowing (CAD) and 5 were normal. Systemic pressure, coronary sinus blood flow (CSBF), left ventricular oxygen utilization (LVVO2), ST Segment depression, and myocardial lactate extraction were measured before and after propranolol (10 mg IV), at rest, during pacing-induced tachycardia stress. Propranolol-related reduction in CSBF and LVVO2 at rest was reversed when heart rate was controlled in both patient groups. Propranolol failed to alter heart-rate threshold, tension-time index (TTI), CSBF, or LVVO2 at angina in the CAD patients. Likewise, ischemic-type ST depression, decreases in lactate extraction, and coronary resistance were unchanged compared to values observed during tachycardia stress before propranolol. In normal coronary patients, propranolol also produced no significant change in LVVO2 or coronary resistance when its heart rate effects were controlled. These data imply that a major coronary and metabolic influence of propranolol relates to changes occurring secondary to its influence on heart rate. Furthermore, this agent's anti-ischemic effect is not prominent during tachycardia stress suggesting that this stress test may be clinically useful in patients taking propranolol.
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PMID:Effects of propranolol on coronary hemodynamic and metabolic responses to tachycardia stress in patients with and without coronary disease. 83 33

The cardiac response to volume loading was evaluated in fifty severely septic patients. After a rapid infusion of albumin or whole blood the cardiac index (CI) and left ventricular stroke work index (LVSWI) were recorded as the pulmonary arterial wedge pressure (PAWP) increased. Initial values of PAWP, CI, and LVSWI were similar in both the nineteen surviving and thirty-one nonsurviving patients. Surviving patients, however, demonstrated greater increases in CI and LVSWI as PAWP rose. Nearly half of both patient groups developed decreases in CI and LVSWI as the PAWP continued to increase. These downslopes occurred at relatively low PAWP and are taken as evidence of an abnormality of myocardial function in both survivors and nonsurvivors. The lower upslope of the performance curves in nonsurvivors indicates myocardial depression or a negative inotropic effect. Cardiac ischemia, acute respiratory failure, and high affinity red cells were found to diminish the cardiac response to volume loading, whereas hepatic and renal failure were associated with a good CI and LVSWI response.
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PMID:Myocardial depression during sepsis. 84 86

ST-T wave changes in the electrocardiogram detected during routine examination and aggravated by erect posture, hyperventilation, and exercise in apparently healthy young individuals have been termed vasoregulatory abnormalities. No evidence of ischaemic heart disease has been found in such subjects. Ten young healthy air crew with vasoregulatory abnormalities were subjected to maximal exercise on treadmill and procedure repeated after 120 mg propranolol daily for 3 days. After one week, they were subjected to a stress of positive acceleration (+gz) in a human centrifuge at 2-5 g and 3-5 g for 15 seconds each at a constant rate of rise of 0-1 g/s and the electrocardiogram was monitored during and in the post-acceleration phase. The procedure was repeated after propranolol 120 mg daily for 3 days. The stress of positive acceleration resulted in pronounced prominence of P waves and inversion of T waves (as has been reported in normal subjects) with minimal ST depression in the electrocardiogram. ST segment depression during exercise, at heart rates corresponding to those achieved during peak centrifuge runs, was significantly more pronounced. The ST, P, and T wave changes were returned to normal after propranolol. It is concluded that minimal ST segment depression after stress of positive acceleration as compared with conspicuous ST segment depression during exercise at corresponding heart rates, and their normalisation after propranolol, rules out ischaemia as an aetiological factor in subjects with vasoregulatory abnormalities.
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PMID:Effect of positive acceleration (+gz) on electrocardiogram of subjects with vasoregulatory abnormality. 84 93

Stress testing is by no means perfect as far diagnosing coronary artery disease, but at this time it is the single best noninvasive method for establishing the presence of ischemic heart disease. From the data shown here, one can see that it adds some important prognostic features as well. The American Heart Association has published a "Coronary Risk Handbook" which can be used to predict the likelihood of a future coronary event by means of accepted risk factors such as hypertension, cholesterol level, and smoking. If we include a positive stress test as a risk factor and compare it to the others, it is clear that a positive stress test has a much higher correlation with future coronary events than any of the other risk factors alone or in combination (Figure 12). Physicians should pay close attention to all of the mentioned factors while carrying out a stress test rather than just looking for ST depression alone. The occurrence of anginal pain, the time of onset, the degree of ST depression, and the patient's pulse and blood pressure response are all useful in assessing the degree of coronary involvement and in predicting an individual's chances of suffering some form of coronary event.
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PMID:Stress testing in the prognosis and management of ischemic heart disease. 86 78

The effects of coronary occlusion and of subsequent propranolol administration were examined in 18 conscious dogs. Overall left ventricular (LV) function was assessed by measurements of LV pressure and dP/dt, and regional myocardial function was assessed by measurements of segment length (SL), velocity of SL shortening and regional myocardial "work", i.e., pressure-length loops in normal, moderately, and severely ischemic zones. Regional intra-myocardial electrograms were measured from the same sites along with regional myocardial blood flow as determined by the radioactive microsphere technique. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones with graded flow reduction and graded elevation of the ST segment. Propranolol depressed overall LV function, function in the normal zone (work fell by 17+/-4%), and in the majority of moderately ischemic segments (work fell by 7+/-3%). In severely ischemic segments the extent of paradoxical motion and post-systolic shortening was reduced by propranolol. After propranolol regional myocardial blood flow fell in the normal zone (11+/-2%) and rose in the moderately (15+/-4%) and severely (63+/-10%) ischemic zones. Thus, in the conscious dog with regional myocardial ischemia, propranolol induces a redistribution of myocardial blood flow, with flow falling in normal zones and rising in moderately and severely ischemic zones. The improvement in perfusion of ischemic tissue was associated with slight but significant depression of shortening, velocity, and work in the moderately ischemic zones and of paradoxical bulging and post-systolic shortening in the severely ischemic zone.
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PMID:Effects of propranolol on regional myocardial function, electrograms, and blood flow in conscious dogs with myocardial ischemia. 87 96

A group of 215 men and 272 women aged 62 to 90 forming a randomly-selected sample of the older population was studied by cardiovascular survey methods and followed for 5 years. The 5-year mortality of 28 per cent was related to age and was higher in men. Ischaemic heart disease was the certified cause of 28 per cent of the deaths. Mortality was greater in those with systolic hypertension. Among electrocardiographic features ST depression, T inversion, and atrial fibrillation increased overall and ischaemic heart disease mortality independently of their association with age. A positive response to an angina and infarct questionnaire was poorly related to subsequent mortality. Re-examination of 72 per cent of 5-year survivors was possible. Systolic and diastolic blood pressures were significantly lower and the frequency of electrocardiographic abnormalities, particularly left axis deviation, left ventricular hypertrophy, and ST and T wave changes, was increased.
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PMID:Longitudinal survey of ischaemic heart disease in randomly selected sample of older population. 90 84


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