Association between activity at onset of symptoms and outcome of acute myocardial infarction.

OBJECTIVES: This study sought to compare the clinical features and outcome of a first myocardial infarction with onset of symptoms during or within 30 min of exercise, at rest and in bed. BACKGROUND: It is not known whether activity at onset influences outcome of acute myocardial infarction. METHODS: Information collected using a standard questionnaire was used to relate activity at the onset of symptoms to in-hospital outcome in 2,468 consecutive patients admitted to a coronary care unit with a first myocardial infarction between 1975 and 1993. RESULTS: Patients with exercise-related onset were more likely to be younger and male. Those with onset in bed were more likely to be older and have a history of stable or unstable angina. Compared with patients whose symptoms began at rest, those with exercise-related onset had a lower in-hospital mortality rate after adjusting for age, gender and year of admission (odds ratio [OR] 0.60, 95% confidence interval [CI] 0.40 to 0.89), and patients with onset in bed had a higher mortality rate (OR 1.38, 95% CI 1.03 to 1.85). The incidence of cardiac failure requiring diuretic therapy was also lower for exercise-related onset (OR 0.83, 95% CI 0.67 to 1.04) and higher when onset was in bed (OR 1.36, 95% CI 1.11 to 1.66). CONCLUSIONS: There is an association between activity at onset and outcome of acute myocardial infarction. Differences in pathophysiology or in the population at risk could explain this observation.

Myocardial infarction in young people with normal coronary arteries.

Myocardial infarction occurring in young people with angiographically normal coronary arteries is well described but the pathophysiology of this condition remains unknown. Coronary artery spasm in association with thrombus formation and minimal atheromatous disease or spontaneous coronary artery dissection are possible causes. Two young men presented with severe chest pain after acute alcohol intoxication and each sustained an extensive anterior myocardial infarction. Investigations including intravascular ultrasound showed no evidence of atherosclerotic coronary artery disease. Coronary artery spasm associated with acute alcohol intoxication as well as prothrombotic state and endothelial damage related to cigarette smoking may be mechanisms leading to acute myocardial infarction in these cases. Acute myocardial infarction occurs in young persons with normal coronary arteries and the diagnosis should be considered in young patients presenting with severe chest pain, particularly those abusing cocaine or alcohol, so that reperfusion therapy can be initiated promptly.

Family history, cigarette smoking and other risk factors in patients with myocardial infarction.

All patients entering a coronary care unit had data collected and stored prospectively on a computer file. Family history and risk factor data have been abstracted for those with confirmed myocardial infarction. These data are compared between those aged less than 50 years and those aged between 50 and 70 years. Cigarette smoking habits are compared with age matched data from the 1976 census population study of cigarette smoking habits. The risk factors of hypercholesteolaemia, obesity, diabetes, hypertension and cigarette smoking greater than 20 per day, do not separate the two age groups although cigarette smoking is more prevalent in the patient groups compared with the census population. Age of fathers' death is not different between the two age groups but death from myocardial infarction, presence of ischaemic heart disease during life in fathers and fewer nonsmokers in the younger age group clearly separate them from older age group patients. This study serves to emphasise that in order to prevent the development of myocardial infarction special attempts sould be made to prevent cigarette smoking in those whose fathers have died of a myocardial infarction or have symptoms of ischaemic heart disease.

Improved coronary artery flow after coronary angioplasty in patients with unstable angina.

BACKGROUND: Coronary artery flow is impaired after myocardial infarction but there is limited information regarding coronary flow in unstable angina. AIM: To assess baseline coronary artery flow and the effects of coronary angioplasty on coronary flow in patients with unstable angina. METHODS: Twenty-one patients with unstable angina with a culprit lesion suitable for coronary angioplasty were enrolled in the study. Coronary flow was assessed with the Thrombolysis In Myocardial Infarction (TIMI) grade and the Corrected TIMI Frame Count (CTFC) pre and post angioplasty. RESULTS: Baseline flow was impaired in the culprit artery compared to the non culprit artery (42.0+/-28.1 vs 25.3+/-7.0 frames, p<0.02). Pre angioplasty coronary flow was TIMI grade 2 in 52% and TIMI grade 3 in 48% of patients. Post angioplasty flow improved with TIMI grade 2 flow in 5% and TIMI grade 3 in 95%. After angioplasty coronary flow improved from 42.0+/-28.1 frames to 21.6+/-16.3 (p=0.0001). The culprit coronary stenosis decreased from 74+/-9% pre angioplasty to 28+/-12% after intervention (p=0.0001). CONCLUSIONS: Angioplasty and stenting of the culprit vessel restores normal coronary flow in most patients with unstable angina. This suggests that impaired flow in unstable angina is predominantly related to the culprit lesion residual stenosis.

Long stenting in native coronary arteries: relation between vessel size and outcome.

Procedural and 6-mo clinical outcomes were evaluated in 34 consecutive patients who had stenting (<40 mm) of a long segment of coronary artery. Procedural success was achieved in 32 (96%) patients. Before stenting, 32 (96%) patients had Canadian Cardiovascular Society Class 3 or 4 angina compared to 7 (21%) at 6-mo follow-up (P<0.001). Eleven patients (32%) suffered either acute/subacute stent thrombosis (n=4) or restenosis (n=7). On logistic regression distal reference diameter <2.5 mm (odds ratio 26, P<0.01) and previous cardiac intervention (odds ratio 9.0, P<0.01) were independent predictors of a major adverse event during follow-up. There was no significant association between outcome and indication for stenting, type of stent, or use of ticlopidine and aspirin. These results indicate that distal vessel diameter <2.5 mm is a powerful predictor of subacute thrombosis or restenosis after long coronary artery stenting.

IDL composition and angiographically determined progression of atherosclerotic lesions during simvastatin therapy.

Some patients with coronary artery disease experience continued progression of one or more coronary lesions despite treatment with drugs that inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and markedly lower plasma cholesterol levels. We examined relationships between the progression of coronary artery lesions and plasma lipoproteins, in particular intermediate density lipoprotein (IDL) and its composition, in 38 patients with coronary artery disease who had been treated with simvastatin for 2 years. Patients were given lipid-lowering dietary advice; 3 months later they were started on simvastatin therapy (10 mg/d) for 1 month, and after review of their plasma cholesterol levels, the dose was increased to 20 mg/d and later to 40 mg/d if the target level of plasma cholesterol had not been attained. Progression of lesions was determined by serial quantitative coronary angiography (variability of 5.5%) and was defined as an increase in percent diameter stenosis (%S)> or =10%; regression was defined as a decrease in %S > or =10%. The proportions of cholesteryl esters (CEs) and free cholesterol decreased significantly (P<.001), and proportions of protein and triglycerides increased significantly (P<.001) in IDL during simvastatin therapy. The CE content of IDL decreased significantly (-7.2 weight [wt]%, n=20, P<.001) in nonprogressors (patients who did not show progression of any lesions) and did not change significantly (-1.8 wt%, n=14, P=.36) in progressors (patients who showed progression of one or more lesions without regression of any lesion). This decrease in IDL CE content in nonprogressors was significantly (P=.01) different compared with the corresponding change in patients classified as progressors. Mean plasma cholesterol concentration tended to increase in progressors (0.47 mmol/L) and tended to decrease in nonprogressors (-0.39 mmol/L) during the initial 3-month diet period, and these changes were significantly different (P=.02). Furthermore, this change in plasma cholesterol level during the initial diet period was correlated significantly with the change in IDL CE content during the entire study (r=.348, n=38, P=.03). These data suggest that IDL CE content may be a determinant of progression of coronary lesions and may be influenced by compliance with or metabolic response to lipid-lowering dietary advice in patients with coronary artery disease during simvastatin treatment.