Background— We investigated the association between 9 polymorphisms of genes encoding hemostasis factors and myocardial infarction in a large sample of young patients chosen because they have less coronary atherosclerosis than older patients, and thus their disease is more likely to be related to a genetic predisposition to a prothrombotic state. Methods and Results— This nationwide case-control study involved 1210 patients who had survived a first myocardial infarction at an age of <45 years who underwent coronary arteriography in 125 coronary care units and 1210 healthy subjects matched for age, sex, and geographical origin. None of the 9 polymorphisms of genes encoding proteins involved in coagulation (G-455A β-fibrinogen: OR, 1.0; CI, 0.8 to 1.2; G1691A factor V: OR, 1.1; CI, 0.6 to 2.1; G20210A factor II: OR, 1.0; CI, 0.5 to 1.9; and G10976A factor VII: OR, 1.0; CI, 0.8 to 1.3), platelet function (C807T glycoprotein Ia: OR, 1.1; CI, 0.9 to 1.3; and C1565T glycoprotein IIIa: OR, 0.9; CI, 0.8 to 1.2), fibrinolysis (G185T factor XIII: OR, 1.2; CI, 0.9 to 1.6; and 4G/5G plasminogen activator inhibitor type 1: OR, 0.9; CI, 0.7 to 1.2), or homocysteine metabolism (C677T methylenetetrahydrofolate reductase: OR, 0.9; CI, 0.8 to 1.1) were associated with an increased or decreased risk of myocardial infarction. Conclusions— This study provides no evidence supporting an association between 9 polymorphisms of genes encoding proteins involved in hemostasis and the occurrence of premature myocardial infarction or protection against it.

The demonstration of extensive coronary artery disease (CAD) after acute myocardial infarction (AMI) has important prognostic implications. Exercise-induced ST segment depression is commonly used for detecting the presence of CAD and evaluating its extension. However, even though there have been many attempts to increase its diagnostic yield, the accuracy of the electrocardiographic signal for identifying multivessel disease (MVD) is relatively low, particularly in post-MI patients. The aim of this study was to evaluate the ability of a simple index, combining information on the amount and kinetics of ST depression in the heart rate domain during exercise and recovery, to identify MVD after AMI. Seventy patients (mean age 53.4 years) underwent a bicycle, symptom-limited exercise stress test and coronary angiography 2-3 weeks and 6 weeks respectively, after uncomplicated AMI while cardioactive therapy was discontinued. After obtaining a computer-derived measurement of ST levels based on incremental averaging of normal complexes, the area subtended to baseline and limited by the ST trend against heart rate during both exercise (A1) and recovery (A2) was calculated. The difference (A1-A2) was defined as the 'Stress-Recovery Index' (SRI) and dichotomized, by means of receiver-operating characteristics curve analysis, at 5 mm x beats.min-1 to define an increased risk of MVD. The SRI of patients with MVD was significantly lower than that of patients with single vessel disease. The sensitivity of SRI < -5 mm x beats.min-1 (65%) for predicting MVD was significantly higher than that obtained by other conventional parameters, without appreciable loss of specificity (81%).(ABSTRACT TRUNCATED AT 250 WORDS)

Although previous studies have confirmed the safety of dobutamine stress echocardiography, complex ventricular arrhythmias have been reported. Our aim was (1) to identify the markers of increased arrhythmic risk during dobutamine stress echocardiography and (2) to assess whether the occurrence of major ventricular arrhythmias during the test may represent a clinically useful marker of electrical instability. Three hundred and seventy-seven consecutive survivors from acute myocardial infarction, off cardioactive therapy, underwent dobutamine stress echocardiography 11.4 days after the acute event. Holter monitoring with assessment of heart rate variability and echocardiographic determination of left ventricular ejection fraction. In addition, exercise stress testing, signal averaged ECG and coronary angiography were carried out, respectively, in 357, 150 and 273 patients. Ten subjects showed complex ventricular arrhythmias (eight non-sustained and one sustained ventricular tachycardia and one ventricular fibrillation) during dobutamine stress echocardiography (group A), whilst 366 did not (group B). Complex ventricular arrhythmias were detected by Holter monitoring in 8/10 patients in group A and 45/367 patients in group B (odds ratio 28.6, 95% CI 5.4-92.2) and by exercise testing in 4/10 patients in group A and 33/347 patients in group B (odds ratio 6.3, 95% CI 1.4-27.2). Ejection fraction < 40% was present in 3/10 patients in group A and 50/367 in group B (odds ratio 2.7, 95% CI 0.3-12.2), whilst multivessel disease was present, respectively, in 8/10 and 176/263 patients (odds ratio 1.9, 95% CI 0.3-25.5). Reduced heart rate variability and the presence of late potentials on signal averaged ECG were found in, respectively, 40/367 and 13/140 patients in group B, but none were found in group A. A total of 61 events (35 CABG, 15 PTCA, four cardiac deaths and seven non-fatal reinfarctions) occurred during the follow-up (11.4 months, range 6 to 20): four in group A and 57 in group B. No documented major arrhythmic event was reported. We conclude that (1) complex arrhythmias during dobutamine stress may occur in patients early after acute myocardial infarction; (2) the preexisting evidence of frequent, as well as repetitive, arrhythmias represents a potential marker of increased risk in this connection and, finally, (3) dobutamine-induced arrhythmias seem to represent an uncommon, even though potentially dangerous, event but not a useful new "window' on electrical instability of post-MI patients.

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