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To evaluate the prevalence of type I silent myocardial ischemia and silent myocardial infarction, 4,842 men aged 40 to 59 years, identified in occupational samples in Florence and Rome, and free from major heart disease, severe illnesses and chest pain, underwent a 3-stage diagnostic procedure. The first stage included resting electrocardiogram, hyperventilation test, exercise electrocardiogram and 24-hour Holter electrocardiogram. The subjects who were suspected of having type 1 silent myocardial ischemia or previous silent infarction at the first stage (n = 439; 9.1%) were entered into the second stage, which included echocardiogram, thallium 201 scintigraphy in conjunction with exercise testing or dipyridamole test, exercise radionuclide ventriculography and ergonovine test. Three hundred eighty-seven men participated in the second stage; after the diagnostic procedures were performed, 104 men (2.1%) were still suspected of having type 1 silent myocardial ischemia or infarction on the basis of predefined criteria. Sixty-two men continued on into the third diagnostic workup including coronary angiography. The final diagnosis of type 1 silent myocardial ischemia or infarction was reached in 25 patients (prevalence 0.52%; adjusted estimate 0.89%). Of these 25, 19 had coronary atherosclerotic disease, 1 had Kawasaki disease, 1 had coronary anomaly, 1 had induced focal coronary spasm, and 2 had normal coronary arteriograms despite the presence of unquestionable old myocardial infarction. Altogether, 6 patients with silent myocardial infarction were identified.(ABSTRACT TRUNCATED AT 250 WORDS)

OBJECTIVE--A recent prospective study in patients with dilated cardiomyopathy has reported that the disease is familial in at least 20% of cases, but the pattern of inheritance could not be ascertained. The presence of an autosomal dominant pattern, such as seen in hypertrophic cardiomyopathy, could make it possible to search for single gene defects with linkage analysis, whereas polygenic inheritance would be consistent with the autoimmune hypothesis. To assess the pattern of inheritance, we retrospectively identified patients with familial disease and assessed their first degree relatives (parents, siblings and children) for dilated cardiomyopathy. DESIGN AND PATIENTS--The family history of 105 consecutive patients with dilated cardiomyopathy was reviewed and 14 who had at least one first degree relative with documented disease were identified as probands. Their healthy relatives (109) were studied by physical examination, electrocardiography, M mode and cross sectional echocardiography, and were classified as unequivocally normal or as potential carriers. The potential carriers had abnormal electrocardiography with either at least one echocardiographic measurement of left ventricular cavity dimension or percentage fractional shortening outside 2 SDs of normal values (based on age and body surface area). The potential carriers underwent 24 hour Holter monitoring and maximal treadmill exercise. RESULTS AND CONCLUSION--Twenty three relatives (21%) were classified as potential carriers: 12 had an increased left ventricular end diastolic dimension, with reduced percentage fractional shortening in three; 11 had an abnormal electrocardiogram and increased end diastolic dimension, with reduced percentage fractional shortening in five. Such abnormalities were very mild and follow up is necessary to find whether such changes represent early disease. Pedigree analysis was most consistent with polygenic inheritance.

The prevalence of an abnormal signal-averaged electrocardiogram (ECG) and ventricular arrhythmias on 24 h ambulatory electrocardiography was evaluated in 118 patients 13 +/- 2 days after acute myocardial infarction. Group 1 (46 patients) underwent intravenous thrombolysis within 6 h of the onset of symptoms, whereas Group 2 (72 patients) did not. An abnormal signal-averaged ECG was seen in 15% of patients in Group 1 and 21% of those in Group 2 (difference not significant). The number of ventricular premature complexes/h was lower in Group 1 than in Group 2: 2.58 +/- 1.63 versus 7.91 +/- 10.75 (p less than 0.01). However, complex arrhythmias (greater than or equal to 10 ventricular premature complexes/h or ventricular tachycardia) were equally common in Groups 1 and 2 (20% versus 22%, respectively). Their prevalence was similar in patients with or without an abnormal signal-averaged ECG (29% versus 18%, respectively, in Group 1 and 27% versus 21%, respectively, in Group 2). Comparison between patients with (n = 26) or without (n = 20) angiographic patency of the infarct-related coronary artery after thrombolysis showed no significant difference in the prevalence of an abnormal signal-averaged ECG (8% versus 25%, respectively) and complex ventricular arrhythmias (19% versus 20%, respectively). These data suggest that thrombolysis does not affect the prevalence of complex ventricular arrhythmias and an abnormal signal-averaged ECG or their relation after acute myocardial infarction.

The accuracy of sequential testing in the noninvasive diagnosis of coronary artery disease has been established in the symptomatic clinical populations, while little is known about its value when applied to low prevalence groups, such as totally asymptomatic men. To evaluate the accuracy of noninvasive sequential testing in the diagnosis of silent myocardial ischemia, data were collected from exercise electrocardiogram, 201Tl perfusion scintigraphy and radionuclide angiography for 62 totally asymptomatic middle-aged men who underwent coronary arteriography because they were positive for two or more markers of myocardial ischemia as determined by a diagnostic screening of a nonbiased population consisting of 4,842 presumably healthy men aged 40-59 years (the ECCIS Project). The predictive value of serial testing procedures for significant coronary artery obstruction was 35%. Predictive values of an abnormal electrocardiogram associated with either an abnormal 201Tl scintigram, an abnormal isotopic ventriculography, or both were 33, 38 and 31%, respectively. In asymptomatic middle-aged men, there is at least a 50% likelihood that an abnormal radionuclide test is a false-positive result, and the positive predictive value is not enhanced by the concordance of an abnormal 201Tl scintigraphy with an abnormal isotopic ventriculography. Thus, the application of noninvasive sequential testing in screening for asymptomatic coronary artery disease is limited by its low predictive value in accordance with the Bayesian probability theory.

An epidemiological study was conducted on 5163 men aged 40–59 years, made by occupational samples, from Florence and Rome to identify, by a three-stage procedure, subjects with asymptomatic silent ischemic heart disease (SIHD). This report describes some coronary risk factors. Men who are free from heart disease were compared with: (1) those having a low probability of SIHD (ECG signs only; n = 439); (2) those having a high probability of SIHD (ECG signs plus echographic signs, or positive markers of deficient perfusion, or altered radionuclide ventriculography; n = 104); (3) those having a definite SIHD (signs of the first two groups plus evidence from coronary angiography; n = 25). A clearcut increasing trend in the levels of major coronary risk factors, and in the multivariate estimated coronary risk for major events was found. The difference was not significant between highly probabile and definite cases of SIHD, due to the small numbers involved. Three multiple logistic models, with the three probability levels of silent ischemia as end-points, showed that four of 10 tested factors were associated with the presence of SIHD: age, systolic blood pressure, cigarette smoking and non-HDL serum cholesterol.

The relation between transient myocardial ischemia and late potentials was investigated in 100 patients with coronary artery disease who underwent serial recordings of the signal-averaged electrocardiogram before, during and after dipyridamole infusion. During this test, 47 patients (group 1) developed transient myocardial ischemia (with ST elevation in 14 cases and ST depression in 33), whereas 53 patients (group 2) did not. Baseline signal-averaged electrocardiogram was abnormal in 20 patients (20%): a QRS duration greater than 115 ms was seen in 6 patients, a late potential (root mean square voltage of last 40 ms of QRS [RMS40] less than 25 microV) in 9, both abnormalities in 5, with no significant differences between groups 1 and 2 (26 vs 15%, respectively). In both groups, comparison of recordings obtained before, during and after dipyridamole test revealed no significant changes in QRS duration and RMS40. Absence of significant differences was also observed when patients with transient ischemic ST elevation or ST depression were examined separately. During the test, 100% of abnormal basal recordings remained abnormal and 98% of normal recordings remained within normal limits. In only 2 patients (from group 1) RMS40, which showed borderline values at baseline, decreased to abnormal values during dipyridamole test. These data suggest that electrophysiologic abnormalities induced by transient myocardial ischemia may not bear any relation with the substrate for chronic reentrant ventricular tachyarrhythmias, as reflected by late potentials on the signal-averaged electrocardiogram.

Ventricular arrhythmias during transient myocardial ischemia were studied in 60 patients with spontaneous angina and greater than or equal to 1 ischemic attack with ST-segment depression during 24-hour ambulatory electrocardiography. The patients were divided into 2 groups: group 1, 10 patients (17%) who developed ventricular arrhythmias during 26 of 92 (28%) ischemic attacks; and group 2, 50 patients who did not show this phenomenon. Daily ischemic attacks, total ischemic time and the proportion of symptomatic ischemic attacks were significantly greater (p less than 0.01) in group 1 versus group 2. In group 1 patients, ischemic attacks were found to have twice the duration in the presence of arrhythmias than in their absence (20.4 +/- 11.9 vs 9.1 +/- 8.4 minutes, p less than 0.01); arrhythmias were more common during symptomatic than during silent ischemic attacks (39 vs 13%, p less than 0.02). Arrhythmias occurred at the onset or peak of ST-segment depression (ischemia phase) in 6 cases (60%), during the resolution of ST-segment depression (recovery phase) in 2 cases (20%) and during both phases of ischemic attacks in the remaining 2 (20%). When compared to recovery phase arrhythmias, ischemia phase arrhythmias were characterized by a later onset time (173 +/- 144 vs 58 +/- 54 seconds, p less than 0.01) and a longer duration (105 +/- 107 vs 41 +/- 22 seconds, p less than 0.01). During the ischemia phase, 16 of 353 ventricular premature complexes initiated ventricular tachycardia, while during the recovery phase only 1 of 161 ventricular premature complexes resulted in ventricular tachycardia (4.5 vs 0.6%, p less than 0.02). Thus, ventricular arrhythmias may accompany spontaneous ischemic ST-segment depression, when the latter is recurrent, prolonged and symptomatic; arrhythmias are characterized by a greater frequency, duration and malignancy during the ischemia phase than during the recovery phase of ischemic attacks.

The malignancy of ventricular premature complexes (VPCs) that have the R on T phenomenon has been extensively investigated in the animal model,1 as well as in the clinical settings of acute myocardial infarction2 and sudden death.3 Data are lacking relating the R on T phenomenon to the occurrence of ventricular tachyarrhythmias during episodes of transient myocardial ischemia in humans. We prospectively studied a group of patients with variant angina to establish the relation between the prematurity of VPCs during transient myocardial ischemic attacks and their malignancy.