[Relations between pre- and post-infarction angina].
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Biomedical subjects
Publications and source records attributed to M T Larovere.
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Fifty male patients older than 65 years of age (mean 66.3) underwent a symptom-limited exercise test on an average of 34 days after acute myocardial infarction. After 4 weeks of supervised rehabilitation training and after one-year follow-up, the patients underwent controlled exercise tests. The ergometric parameters were compared with respective values in 10 healthy males (mean age 66.4, range 65-75). The rehabilitation training induced a substantial improvement in physical capacity (total work from 3149 +/- 1326 to 4791 +/- 1403 kg; P less than 0.001) with a better cardiovascular response: increased maximum oxygen pulse (from 8.97 +/- 2 to 10.7 +/- 2; P less than 0.001), decreased heart rate (from 120.5 +/- 16.1 to 111.3 +/- 14.7 beats min-1; P less than 0.05) and a decreased double product at a 75 W work load (from 22 866 +/- 4005 to 20 472 +/- 3982 beats min-1 mmHg; P less than 0.05). The recovery of physical capacity and cardiovascular tolerance in the physical exercise was nearly complete as compared with healthy subjects of the same age. During the training period one patient died from heart failure. In all the other patients the same improvement was still maintained one-year later. In conclusion, old age does not seem to be per se a contraindication to cardiac rehabilitation. Physiological beneficial effects from cardiac rehabilitation can also be received by patients older than 65 years of age.
To determine the incidence and the significance of anginal chest pain during abnormal exercise testing (S-T greater than or equal to 0.1 mV) in patients with recent myocardial infarction we reviewed a series of 353 patients who underwent maximal bicycle exercise stress 4-8 weeks following acute myocardial infarction. Of the 353 patients, 26 had ischemic ECG changes and chest pain (group A); 85 patients had ischemic ECG changes but no chest pain (group B). The two groups differ significantly only in the frequency of a history of typical angina pectoris more than 6 months prior to acute myocardial infarction (group A 42.3% vs. group B 15.2%, p less than 0.01). Typical chest pain is more frequent in anterior versus inferior myocardial infarction (50 vs. 14.4%, p less than 0.001). The patients were followed up for 28.8 +/- 8.7 months with clinical and exercise testing controls. The incidence of exertional angina during the follow-up was significantly more frequent in group A patients than in group B patients (80.7 vs. 24.7%, p less than 0.001). Unstable angina pectoris was more frequent in group A (34.6 vs. 11.8%, p less than 0.01). There was no statistically significant difference in mortality (group A 3.8% vs. group B 5.9%) and cardiac events (group A 3.8% vs. group B 5.9%) between the two groups. Thus, we concluded that the occurrence of anginal pain associated with S-T segment depression during exercise testing does not increase the prognostic risk.
UNLABELLED: Detection of post-infarction left ventricular aneurysm may have important clinical and therapeutic consequences. Differences in selection and in diagnostic criteria account for the wide range of incidence of left ventricular aneurysm in angiographic and autopsy series. To assess the incidence and related pathological features of ventricular aneurysm, 410 consecutive patients were studied by two-dimensional echocardiography 3 to 8 weeks after the onset of an acute myocardial infarction. In 395 patients (96.3%) technically adequate echograms were obtained: 42 patients (10.6%) had evidence of left ventricular aneurysm defined as a well demarcated bulge in diastole and in systole with a thinned, a-diskinetic walls. The incidence rate of left ventricular aneurysm was 17% in 188 anterior myocardial infarctions, 1.9% in 157 inferior ones, 25.9% in 27 anterior plus inferior infarctions; ventricular aneurysms were not found in any of 15 lateral and 8 posterior myocardial infarctions. Aneurysms were apical or apical-anterior in 25 patients (59.5%), apical-septal in 8 (19%), apical-diaphragmatic in 3 (7.1%), apical-septal-diaphragmatic in 3 (7.1%) and postero-basal in 3 (7.1%). Intraaneurysmal thrombi were detected in 24 patients (57.1%). In 12 cases echograms showed pericardial effusion; this was more frequent (28.6%) than in patients without an aneurysm (7.9%; p less than 0.001). Among patients with an aneurysm, heart failure was present in 19 (45.2%), mitral regurgitation in 3 (7.1%), of systemic emboly in 4 (9.5%), severe ventricular arrhythmias in 4 (9.5%) and angina in 5 (11.9%). IN CONCLUSION: left ventricular aneurysm is a frequent early complication of myocardial infarction. Two-dimensional echocardiography provides non-invasive direct information on localization, extent and related pathological features of ventricular aneurysm and thus appears to be a useful screening technique.
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Fifty-three calisthenics used in a cardiac rehabilitation program were evaluated in a group of patients who, 30-60 days after myocardial infarction, had undergone a multistage symptom-limited bicycle exercise test without S-T segment modifications or arrhythmias. The following measurements were made oxygen uptake (VO2), oxygen uptake/Kg (VO2/Kg), ventilation/m' (VE), heart rate/m' (HR), systolic blood pressure (sBP) and METS. A good correlation was observed during the physical exercises between HR and VO2 (r = 0.59; p less than 0.001) and between HR and VO2/Kg (r = 0.64; p less than 0.001). Such correlation was similar to that observed during bicycle ergometric test. Lower values were obtained for the correlations between sBP and both VO2 and VO2/Kg, but they were still statistically significant (p less than 0.001). Heart rate and sBP were lower during calisthenics than during bicycle exercise from a VO2 level of 600-800 ml up. It is therefore possible to tailor a safe training program based on calisthenics whose level of energy expenditure is known: HRxsBP reached during such physical exercises will be lower than during bicycle ergometric test, VO2 being equal.
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We have previously reported that labetalol infusion increases prolactin (PRL) secretion in hypertensive patients. In an attempt to investigate the site where labetalol stimulates PRL, the drug was infused intravenously (100 mg) into healthy subjects, both under basal conditions and after pretreatment with L-dopa plus carbidopa (250 mg and 25 mg respectively every 6 h for 1 day), since this regimen has been reported to blunt the PRL responses to centrally acting stimuli. The effects of oral labetalol administration (100 and 200 mg) on PRL was also evaluated. Serum PRL concentration did not change after oral labetalol, whereas it was increased by intravenous drug administration. This effect was completely abolished by pretreatment with L-dopa plus carbidopa. These findings, though they do not demonstrate the mechanism, suggest that the hyperprolactinaemia induced by labetalol is mediated inside the blood-brain barrier.
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Systolic time intervals (TS) were determined before and after intravenous injection of 400 mg of Potassium-Canrenoate (CK) in 33 patients 30 days after acute myocardial infarction, in order to evaluate the inotropic effect of this drug. It was observed a reduction of the pre-ejection period (I. PEP) and of the pre-ejection period/left ventricle ejection time (PEP/LVET) ratio without any significant changes in the electromechanical systole (I. Q-2), left ventricle ejection time (I. LVET) and isometric contraction time (ICT). These results do not allow to attribute positive inotropic effect to CK. In fact drugs which share this activity, like digitalis glycosides, shorten also I. Q-S2, I. LVET and ICT, with a reduction of I. PEP and PEP/LVET ratio by far greater than that determined by CK. TS determination, in 10 patients, 15, 30 and 45 min after the injection of CK yields results confirming these conclusions.
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