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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary spasm was first demonstrated by Gensini in 1962, and the diagnostic value of spontaneous spasm during coronary angiography is now generally accepted. In its absence, provocation tests with ergonovine or its derivatives form part of routine hemodynamic investigation for confirming the spastic nature of atypical chest pain or pain suggestive of Prinzmetal angina. The coronary spasm so induced gives rise to reduced coronary flow, an increase in coronary resistance and myocardial ischemia as shown by an increased lactate extraction in coronary sinus blood; therefore, once it is documented, it must be treated in order to avoid myocardial necrosis or ventricular arrhythmias. Three groups of drugs of drugs are used to counteract spontaneous or provoked spasm: alpha-blockers, especially phentolamine, nitrate derivatives, trinitroglycerine or isosorbide dinitrate, and calcium inhibitors nifedipine or diltiazem, which have a direct antispastic effect. The hemodynamic and pharmacological actions of these three groups of drugs depend on whether they are given orally, intravenously or by intracoronary injection. Twenty six coronary spasms were observed in 23 patients out of a total of 780 coronary angiographies (3,3 per cent) performed between June 1980 and June 1981: 12 spasms were spontaneous (1,5 per cent), 6 provoked by the catheter (0,8 per cent) and 8 by methylergometrine. There were no complications. Five coronary spasms were also observed during 70 coronary angioplasties (7,1 per cent). The spasm was relieved in all cases by intravenous injection of 1,5 to 3 mg of trinitrin (Lenitral). Calcium inhibitors, especially nifedipine, have been used successfully by Hugenholtz and Bertrand who consider that nifedipine has a slower action and the coronary dilatation obtained is never as great with the nitrate derivatives. Trinitrin remains the treatment of choice for the rapid relief of provoked spasm.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Treatment of coronary artery vasospasm during coronary arteriography]. 640 34

Sixty patients without organic heart disease presenting with chest pain suggestive of angina pectoris and angiographically normal coronary arteries underwent clinical, hemodynamic and metabolic investigation. The study of myocardial lactate metabolism during atrial pacing (168 +/- 14 bpm) allowed identification of two groups: --40 patients with a normal coefficient of lactate extraction (K greater than or equal to 9 per cent); --20 patients with a pathologically low coefficient of lactate extraction (K less than 9 per cent) reflecting myocardial ischemia. In the first group, chest pain was often atypical (75 per cent of cases). Hemodynamic investigation showed minor abnormalities of the left ventricle in 48 per cent of cases. The diagnosis of angina was rejected in these patients. In the second group, the majority of patients developed chest pain (85 per cent of cases) at the maximal heart rate with significant ST depression (80 per cent of cases). The chest pain was typical of angina pectoris in 50 per cent of cases. Hemodynamic and angiographic investigation of the left ventricle was completely normal in nearly all cases. Only these patients with clinical, electrocardiographic and metabolic signs of myocardial ischemia can be considered as having angina with normal coronary arteries. Although studies of myocardial lactate metabolism and other signs of myocardial ischemia distinguish clearly between these two groups of patients, the coronary hemodynamics were similar. Resting coronary flow, its increase for the same myocardial oxygen demands and coronary resistances were comparable in both groups, and not significantly different from the values obtained in a control group of patients without coronary artery disease or chest pain. These results confirm that about 30 per cent of patients investigated for chest pain suggestive of angina pectoris who have angiographically normal coronary arteries, develop signs of myocardial ischemia during atrial pacing. The physiopathological explanation remains unclear as coronary hemodynamics have been found to be normal.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Angina pectoris with normal coronary arteries: clinical, hemodynamic and metabolic study]. 640 43

Ischemic heart disease is a major public health problem in all countries with high living standards. In France, in 1978, myocardial infarction was responsible for a quarter of cardiovascular deaths, which themselves represent 37% of all deaths. The economic burden of coronary artery disease may be assessed quantitatively in terms of hospital admission to departments of cardiology and cardiac surgery, and qualitatively, in terms of incapacity or invalidity, the socio-professional effects of which are considerable. This naturally incites cardiologists to examine closely the true context of their investigatory procedures, their comparative value and their ethical and financial consequences. Several factors must be taken into consideration: --increasing the availability of new techniques, which necessitates their critical evaluations; --specialisation within the medical team may affect relationships; --the efficacity and increasing risks of diagnostic evaluation and medical and surgical therapy. The evolution of cardiac treatment may be used to assess decisions taken during hospital admissions and so help avoid duplication of complementary investigations, unnecessary hospital admission and investigations. This research based on audits should help the cardiologist realise the true contribution of non-invasive investigations in the diagnosis of cardiac disease. By underlying the importance of his attitude, adapted to the patients' real needs, the cardiologist will abandon an often too subjective appreciation in favour of better management from the scientific, ethical and eventually, economical points of view. However, this type of assessment has its limits. It would be a worthless task to make all medical procedures generally available to all cardiologists in France. Local, epidemiological or scientific specificities would be disregarded. Similarly, excessive normalisation is incompatible with clinical research which implies high level, costly, scientific activity. But is this not one of the fundamental objectives of teaching hospitals?
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Evaluation of care in the ischemic cardiopathies. Advantages and limits]. 640 49

Evaluating the cost of coronary artery disease is difficult because it must take into account not only the cost of the disease process itself, but also that of prevention and research. 1. The cost of the disease process itself may be assessed by: a) an analytical study of the real cost of diagnostic and therapeutic procedures; b) a synthetic study of the procedures according to the clinical forms of the disease. Although this task is simple for a given patient, extrapolation of the results to a whole group of patients is more aleatory; c) an epidemiological study of the different forms of coronary artery disease: although global data is available the absence of a coronary artery disease register makes this a difficult problem; d) an evaluation of the socio-professional repercussions of coronary artery disease with integration of the cost and loss in gross national product. 2 The cost of prevention can be assessed by taking the following factors into consideration: a) cost of individual primary prevention which poses the problems of check-up examinations; b) cost of community primary prevention; c) cost of research including fundamental research on the atheromatous process and myocardial ischemia plus clinical research such as secondary prevention enquiries. In conclusion, it appears that: --it is difficult to determine the cost of coronary artery disease without a specialist register; --the cost of coronary artery disease should be considered from positive (source of economic activity) and negative points of view (socio-professional repercussions); --a reduction in the cost of coronary artery disease requires a deeper understanding of the disease, better prophylaxis and socio-professional rehabilitation, and improved organisation of exciting health structures.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Difficulties and limits in the evaluation of the cost of coronary disease in France]. 640 50

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53

Sixty four children with isolated congenital aortic stenosis (39 valvular, 16 fixed subvalvular, 4 supravalvular and 5 multiple) were operated at a mean age of 11,5 years. Valve repair was possible in all but three patients who had to undergo valvular replacement. Myotomy was associated in 18 cases (28 p. 100). The mean systolic pressure gradient was 79,9 mmHg (+/- 17,8); there was associated aortic regurgitation in 21 patients but this was minimal except in one case. Twenty children (31 p. 100) had symptoms on effort and the basal ECG showed ST-T wave changes in the left precordial leads in 30 cases (47 p. 100). Several preoperative exercise ECGs were performed in 29 patients without ST-T changes on the resting ECG. The exercise ECG was positive in 15 patients, providing one of the arguments for surgery; a poor blood pressure response to exercise was observed in 12 patients with a negative test. Out of the 28 patients with a positive preoperative exercise ECG, 7 (25 p. 100) went on having a positive result after surgery (p less than 0,05). The maximal heart rate was not significantly higher after surgery but the total work was significantly greater (p less than 0,01) and the increase in systolic blood pressure was even more significant (p less than 0,001). Out of 14 patients undergoing repeat catheterisation for a continuing positive exercise ECG or for ST-T wave changes on the resting ECG, there were 6 residual severe stenoses, 3 severe aortic regurgitations, 3 hypertrophic cardiomyopathies which were obstructive in 2 cases. The exercise ECG is a means of appreciating the consequences of the stenosis which are the cause of the complications (myocardial ischemia and poor blood pressure adaptation). This justifies its use in assessing the surgical indications and for the follow-up of the surgical result. A persistantly positive exercise ECG and continuing ST-T wave changes on the resting ECG are signs of a poor surgical result and hemodynamic revaluation should be considered; besides severe postoperative aortic regurgitation, residual or recurrent stenosis and, above all, asymmetric septal hypertrophy, obstructive or not, are the main causes of poor postoperative results.
Arch Mal Coeur Vaiss 1983 Jul
PMID:[Importance of the exercise test in the follow-up of surgically treated congenital aortic stenoses]. 641 51

The effects of aorto-coronary bypass surgery on myocardial lactate, free fatty acid and certain amino acid metabolism were studied in 30 coronary patients presenting with unstable, invalidating angina resistant to medical therapy. These patients had electrical signs of anterior wall ischemia without necrosis, significant proximal stenosis of the left anterior descending artery with good distal run-off, and underwent bypass surgery on this artery without signs of postoperative myocardial infarction. This study involved pre- and postoperative hemodynamic investigation with a Swan-Ganz catheter and a metabolic study of the coronary arteriovenous lactate (n = 30), free fatty acid, alanine and glutamate (n = 12) levels under basal conditions and after atrial pacing. These results were compared with those in 10 non-coronary control patients, operated for monovascular replacements. The increase of the pulmonary capillary pressure associated with a fall in systolic index at the 6th postoperative hour showed a reduction in left ventricular performance which tended to correct itself at the 24th hour. In the coronary patients, myocardial lactate production increased, alanine production increased and the uptake of free fatty acids fell during atrial pacing after surgery. These metabolic changes reflect the stimulation of anaerobic glycolysis secondary to myocardial ischemia which disappeared after surgery to compare with the control subjects. Therefore, effective myocardial revascularisation in patients with coronary artery disease is accompanied by the regression of the metabolic stigmata of myocardial ischemia.
Arch Mal Coeur Vaiss 1983 Jun
PMID:[Metabolic myocardial modifications following surgical revascularization]. 641 7

We have studied a series of 330 Holter recordings (HR) (including 5 double observations) 189 men and 136 women, mean age 58,4 years Old. The analysis of this series shows that: --105 HR were performed on patients with focal ischemia attacks of suputed embolic origin; the HRT was positive in 35 patients (33 p. 100) with 25 supraventricular arrhythmias (SVA) 16 ventricular arrhythmias, associated in 9 cases, and 3 conduction blocks second degrees type 2. These arrhythmias are rare in patients under 40, increasing with age, and reaching 53 p. 100 in patients greater than 70 years. --86 HR were performed in ischemic heart disease (IHD): 52 HR for ST segment analysis, positive in 5 cases, and coexisting with chest pain in 4 cases; 34 HR for detecting arrhythmias in IHD, positive in 18 cases with 14 VA and 4 SVA. In 83 p. 100 the arrhythmias occur without IHD. They were positive in 70 cases, with 49 SVA, 34 VA, associated in 17 cases, and 4 blocks second degrees type 2. --10 cardiomyopathies were recorded; the HR was positive in 6, with 4 SVA, 3 VA associated in 1 case. --8 mitral valve prolapses were recorded with 5 VA and 1 SVA. In conclusion, the HR was positive in 45 p. 100 of the cases, and show especially the great incidence of asymptomatic VA in patients with IHD.
Arch Mal Coeur Vaiss 1983 Jun
PMID:[Retrospective analysis of a series of 330 Holter recordings. Diagnostic value of the method and correlation with symptomology]. 641 10

Between 1976 and 1981, 173 patients with severe symptomatic mitral incompetence were referred for preoperative assessment. The etiological diagnosis was based on echocardiography, catheterisation, angiography, and, in the 71 patients operated on, the surgical findings. Rheumatic valvular disease was demonstrated in 40 cases (23,1 p. 100), bacterial endocarditis in II cases (6,3 p. 100), myocardial disease in 30 cases (17,3 p. 100) including 19 cases of mitral incompetence during cardiomyopathy with dilatation, and II cases of mitral incompetence during hypertrophic obstructive cardiomyopathy: ischemic heart disease was the underlying cause in 27 patients (15,6 p. 100), congenital heart disease in 9 patients (5,3 p. 100); dystrophic valvular disease (mitral valve prolapse with or without chordal rupture) was detected in 56 cases (32,3 p. 100). These results show a continuing reduction in the incidence of rheumatic fever and an increase in the number of cases of dystrophic mitral valve disease in patients of 50 to 70 years of age, a condition often rapidly progressive with hemodynamic characteristics very similar to those of mitral incompetence observed in ischemic heart diseases.
Arch Mal Coeur Vaiss 1983 Sep
PMID:[Current etiology of organic mitral insufficiency in adults]. 641 10

The authors report their clinical experience with flecainide, a new Class I antiarrhythmic drug, in 44 patients classified into three groups. The first group (7 cases) comprised patients with a wide range of arrhythmias sensitive to the usual antiarrhythmic agents. The second (17 cases) were atrial arrhythmias resistant to the usual antiarrhythmic agents and were mainly vagal atrial arrhythmias. The last group (20 cases) comprised patients with resistant VT, 14 of whom had underlying cardiac disease (8 chronic infarcts). The results obtained were analysed by a score test because of the wide range of arrhythmias and the wide variations in their spontaneous recurrent rate. The antiarrhythmic effect was checked by repeated Holter monitoring correlated with the results of interrogation. Provocative pacing studies were performed in 5 cases of inducible VT under therapy. The results with flecainide were compared with those obtained with reference Class I antiarrhythmics: quinidine, 700 to 1100 mg/day or disopyramide, 600 mg/day. Amiodarone was often associated with each Class I antiarrhythmic because of the resistant nature of these arrhythmias. In group I the results with flecainide were equivalent to those of quinidine. In the other two groups the results were significantly better than those of the reference antiarrhythmic: mean scores: group II 3,20 +/- 0,5 compared to 1,9 +/- 0,4 (p less than 0,01); group III 3,70 +/- 0,37 compared to 1,85 +/- 0,22 (p less than 0,001). Tolerance was good apart from neurosensory side effects (loss of accomodation, vertigo) which were dose dependent and which led to the withdrawal of therapy in only 4 cases. Four types of cardiac side effects were observed: aggravation of existing sinoatrial block (1 case); aggravation of existing intraventricular block (2 cases); aggravation of contractile function which was very poor before therapy (2 cases); and sudden death during therapy in patients with ischemic heart disease in cardiac failure and with incessant resistant VT (2 cases). In these instances the role of the drug cannot be confirmed. These complications were observed with doses of more than 5 mg/kg/day and in patients with cardiac failure. Two of these patients had serum flecainide levels which were very high. It may therefore be possible to reduce the incidence of these complications by adapting dosage to the patient's clinical state and to the serum drug levels.(ABSTRACT TRUNCATED AT 400 WORDS)
Arch Mal Coeur Vaiss 1983 Oct
PMID:[Flecainide: a new antiarrhythmic agent]. 641


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