[Rehabilitation of cardiac patients. For whom? How?].
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Biomedical subjects
Publications and source records attributed to B Letac.
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In twenty patients with advanced heart disease with severe cardiac failure and the presence of conduction disturbances before digitalis therapy, but in whom such disturbances were worsened or revealed by the treatment, it was necessary to insert a permanent pacemaker in order to make effective long term digitalisation possible without the risk of excessive bradycardia or pauses due to worsening of atrioventricular block. Six patients died within a period of 9 days to 34 months after insertion of the pacemaker, two were lost from sight, and the other 12 were followed-up regularly for an average period of 20 months, their condition remaining stationary and, in general, satisfactory.
A very through ocular examination was made in 48 hypertensive patients treated for 18 months with acebutolol in a daily dose of between 400 and 2400 mg. Abnormal symptoms in the form of a prickling sensation were seen in two cases. Microscopic punctate lesions of the conjunctive were seen in 9 subjects, either with the Bengal Pink or fluorescein tests. These very slight microscopic lesions were found in general only in the region of the palpebral slits, a zone normaly exposed to microtrauma, which decreases the value of this finding. The results of a Schirmer test were considered to be abnormal in six patients. These ocular abnormalities were generally mild and it could not be shown conclusively that they were related to treatment with acebutolol. Ocular surveillance, with examinations repeated every six months, indicated the absence of any harmful effect on the eye of prolonged used of acebutolol in the treatment of hypertension.
CPK and its MB iso-enzymatic fraction were measured in 240 patients, 180 of whom suffered from myocardial infarction. MB iso-enzyme was expressed as a percentage of total CPK and a minimum figure of 4 per cent of MB isoenzyme was taken as indicative of a diagnosis of myocardial infarction. In the 180 patients with an infarction, the average MB level as a percentage of total CPK was 12.1 +/- 5.4 per cent. Five patients with a proven infarct had an MB iso-enzyme level of less than 4 per cent. Amongst the 60 patients without a myocardial infarction who were included in view of a pathological level of CPK, the average maximum level of MB was 1 +/- 2.5 per cent. Five of these 60 patients (false positives: 8.3%) had an MB iso-enzyme level of greater than 4 per cent. It is concluded that the estimation of MB iso-enzyme of CPK using a chromatographic technic is a highly valuable laboratory method for confirming or eliminating a diagnosis of myocardial infarction in the numerous clinical circumstances when such a diagnosis is difficult or even impossible on the basis of standard data.
We have studied 33 patients with a large ventricular aneurysm complicating an anterior myocardial infarction. The features of myocardial infarction progressing towards an aneurysm were no previous history of coronary disease, severe infarction as shown by the severity of pain and the presence of pericardial rub and heart failure, and large increase in serum levels of cardiac enzymes. A large aneurysm usually follows a large infarction resulting from the total or partial occlusion of the left anterior descending artery, which is involved alone in about half the patients and is associated with lesions of the circumflex and right coronary arteries in the other half. In most cases, standard radiography showed an abnormal cardiac configuration, but in 7 patients (21%) there was no radiological evidence of aneurysm. ST segment elevation (mean 2.7 mm) was reported in all subjects but one. Heart failure was present in most patients and was an indication for surgical treatment in one-third of the patients. A large aneurysm was not a contraindication to operation even when at angiography the aneurysm seemed to occupy almost all the left ventricle. Twenty-one patients were operated upon for resection of the aneurysm with a mortality rate of 14 per cent.
The various factors influencing the result of treatment have been studied in a series of 100 consecutive patients undergoing aorto-coronary bypass graft surgery. There were three operative deaths and twelve cases of post-operative infarction. Longterm, 85% of them were three year survivors, clinical improvement being maintained in 84% of them. Post-operative tests showed that 70% of patients have no pain on the maximal exercise test, but 48% had ischaemic depression of the ST segment. From among the 47 patients who had follow-up arteriography, 78% of the grafts were patent, but no improvement of the contractility of the left ventricle could be demonstrated (pre-operative ejection fraction 47 +/- 3%, post-operative 49+/- 3%). The pre-operative clinical features rarely give any indication of the prognosis. The same is true in the present series of the condition of the left ventricle, bearing in mind the fact that patients with grossly impaired ventricular contractility (ejection fraction below 30%) were routinely excluded from surgery. It is essentially the state of the coronary arterial network, as assessed by a score made up from the degree and number of stenoses, the quality of the distal bed, and the anatomical distribution, which will pick out those patients more at risk both from the surgery and from post-operative death and in whom the longterm result is likely to be disappointing with no improvement in function, with obstruction of the grafts, or with secondary death.
Fifteen subjects recovering from a myocardial infarction or suffering from angina were given a maximum effort test on a bicycle ergometer and hemodynamic and angiographic investigations before and after a period of physical training. The training program consisted of three sessions of 60 to 75 min each week for two months. Maximum effort tests showed that physical capacity had increased by 17% (P less than 0.02) and that for the same amount of effort the heart rate had decreased by 13% and the blood pressure by 7% (P less than 0.01). Hemodynamic and angiographic investigations showed no significant changes after training in the left ventricular end-diastolic pressure, ventricular volume, ejection fraction, VCF, percentage of shortening and segmental contractility, in the total group, in those patients whose contractility was considerably impaired, or in those who had large dyskinetic areas or widespread akinesia. It is concluded that training had no direct influence on the myocardium, either beneficial or detrimental.
A case is reported of gross lipomatosis of the heart which caused death by gross circulatory failure. The clinical, haemodynamic and angiographic diagnosis was Uhl's disease, and it was the post mortem examination which revealed the massive fatty infiltration of the heart; this involved mainly the right ventricle, but also affected the left ventricle to a major degree. Although fatty deposits in the heart have been recognised for some time, it is surprising to find that there have been extremely few publications on this subject during the last ten years; It is possible that a certain number of case reports of Uhl's disease in adults are really cases of lipomatosis of the heart which have not been recognised as such.
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A phonomechanographic study was carried out on 38 patients with recent myocardial infarction both during the initial phase of necrosis (between the 5th and 7th day) and at the end of the third week. The parameters studied were electromechanical systole (QB2), systolic ejection time corrected for heart rate (CET), the OBl interval, isometric contraction (IC), the pre-ejection periode (PEP), and the haemodynamic coefficient (PEP/ET). The results were compared with the values found in a similar control series. A tendency towards lengthening of the pre-ejection times and shortening of the corrected ejection time was noted. These changes were significant for the second measurement of CET, and for the ratio PEP/ET during the initial phase and on second measurement. The pre-ejection times were generally increased more markedly in the group of patients with left ventricular failure; the ejection time was also markedly shorter in this group, and the haemodynamic coefficient was larger. There was a tendency for the various measurements studied to return to normal by the third week.
In an attempt to improve the quality of information provided by measuring the systolic times, the effect of three thpes of sensitising test was studied: the test with venous tourniquets on the lower limbs, the test with methoxamine, and the test under isometric exercise. In none of these tests was there found to be a statistically significant difference between the controls and the patients with myocardial infarction, with or without left ventricular failure. Taken as a whole, however, the sensitising tests studied tended to accentuate the abnormalities in the systolic times established under basal conditions in patients with myocardial infarction more grossly than in controls.
A case of coronary artery aneurysm in the anterior descending artery of a young female is reported. It was complicated by myocardial infarction and ventricular aneurysm. The aetiology was probably bacterial. Surgical removal was undertaken because the ventricular aneurysm was so poorly tolerated.
Acebutolol, a cardioselective beta-blocker, was studied at doses of 600 to 800 mg in a double-blind trial against placebo in 33 patients with essential hypertension. A moderate reduction in the arterial pressure was seen with placebo, but the pressure was greatly reduced by treatment with acebutolol (p less than 0,01). The heart rate was unchanged after placebo and was reduced by about 10 p.cent by acebutolol. Similarly plasma renin activity, in both lying and standing subjects, was not changed by the placebo, but it was greatly reduced by acebutolol. In the 33 patients studied, the arterial pressure returned to normal in 13 cases (39 p.cent), an improvement was obtained in 12 cases (36 p.cent) but in 8 cases (24 p.cent) the hypertension was not modified by acebutolol. The tolerance to acebutolol was excellent in all cases. No relationship was found between the hypotensive effect of acebutolol and the heart rate or its augmentation induced by orthostatism nor with the levels of plasma renin activity.
50 consecutive cases of pericarditis were studied. Idiopathic and viral pericarditis made up 36 p. cent of all cases. The occurrence of tuberculous or rheumatic conditions was even lower than that reported in similar series in the literature. Amongst the clinical signs of these diseases, emphasis should be placed upon the frequency of chest pain which was increased by deep inspiration in only three out of four cases. Circulatory problems associated with the pericarditis were, on the whole, minimal. However, a fall in blood pressure was seen in 6 cases and true collapse in 3 more. The electrocardiogram showed, in addition to the classical signs, sagging of the PR interval in 36 p. cent and transient atrial fibrillation in 4 cases. As far as biological tests are concerned, it should be noted that elevation of creatine phospho-kinase to levels 4 times greater than normal may be seen, creating problems with the differential diagnosis from myocardial infarction. The course was in general favourable though two deaths occurred in this series (4 p. cent), one with tuberculous pericarditis and the other with idiopathic pericarditis.
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The haemodynamic effects of intravenous propranolol at low dosage (1 and 2 mg) have been evaluated on 14 patients in the acute stage of myocardial infarction. The first 1 mg propranolol was not followed by any significant variation in the variables measured. After the second 1 mg propranolol, the heart rate, cardiac index, and stroke index decreased significantly but moderately. Changes in pulmonary wedge pressure were not significant. It is concluded that intravenous propranolol in the small dosage of 1 or 2 mg, at which antiarrhythmic effect is still produced, has only a negligible depressant myocardial effect.
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MB iso-enzyme of creatine phosphokinase (CPK) was estimated after chromatography. The technique used, Mercer's technique, was simple and rapid. It required 1 ml of serum. The study carried out in 152 subjects showed that CPK was increased (N less than 90 mU/ml). In the group of 104 patients with myocardial infarction (average CPK levels = 829 mU/ml +/- 516), the MB iso-enzyme was found in the serum in significant levels (average level of the MB fraction = 10.9% +/- 5.4). On the other hand, in the control group of 44 patients with various diseases, (CPK = 672 mU/ml +/- 531) the MB iso-enzyme remained low (0.35% +/- 0.44). In two subjects with myocardial infarction, no MB fraction was found. On the other hand, in two patients who died, one from necrotic, prostatic adenocarcinoma, the other from necrotic epidermoid lung cancer, the MB iso-enzyme was significantly increased. The test proposed here, which is applicable in a routine laboratory, seems the most specific of all laboratory examinations available to the clinician for the diagnosis of myocardial infarction.