Transient myocardial ischemia detected by Holter monitoring during the early post-infarction period.

BACKGROUND: On the basis of extensive studies concerning the prognostic value of Holter monitoring in patients with angina, we evaluated the clinical outcome of patients with transient ischemic episodes soon after myocardial infarction. METHODS: The incidence and clinical significance of myocardial ischemia, detected in the acute phase of myocardial infarction, were evaluated in 87 patients. Twenty-four-hour Holter recordings were obtained on the 2nd, 4th, 6th, and 12th hospital day. RESULTS: Myocardial ischemia was detected during at least one of the four recording periods in 28 patients (32%). A total of 157 ischemic episodes were documented. The proportion of recordings that showed transient myocardial ischemia progressively declined from 20% on the 2nd day to 5% on the 12th post-infarction day. Of the 157 ischemic episodes, 132 (84%) were silent and 25 (16%) were symptomatic. Transient ST-segment elevation was present in 99 of the 157 episodes (63%), while transient ST-segment depression occurred in the remaining 58 of the 157 cases (37%). One or more in-hospital cardiac events (reinfarction, acute pulmonary edema, ventricular tachycardia or fibrillation, cardiac death) were more frequent in patients with (group I) than in those without (group II) transient myocardial ischemia [nine out of 28 (32%) versus six out of 59 (10%); P < 0.03]. At follow-up (mean 11.5 +/- 2 months) the incidence of cardiac events (angina, reinfarction, heart failure, ventricular tachycardia or fibrillation, revascularization procedures, cardiac death, sudden death) was comparable in the two groups [four out of 24 (17%) versus 10 out of 49 (20%); NS]. Predischarge exercise testing, performed in 64 patients (74%), showed myocardial ischemia in 50%; the percentage did not vary significantly between group I and group II patients. Moreover, a positive exercise test was not predictive of major cardiac events at follow-up. CONCLUSION: Transient myocardial ischemia, frequently silent, is not uncommon in the acute phase of myocardial infarction and progressively decreases during the in-hospital stay. Its recognition in the subacute phase of myocardial infarction may lead to the identification of a subset of patients at the highest risk of early major complications, who may benefit from aggressive diagnostic and therapeutic strategies.

Combined gallopamil and isosorbide-5-mononitrate in "mixed" angina pectoris.

The efficacy of combining gallopamil and isosorbide-5-mononitrate (IS-5-MN) was evaluated in 15 patients with "mixed" angina and documented coronary artery disease who participated in a 4-week, double-blind, double-dummy, crossover, placebo-controlled trial. After the first week of the placebo phase (single-blinded), all patients received in three different weeks IS-5-MN 20 mg three times daily, gallopamil 50 mg three times daily, and the same dosages of IS-5-MN and gallopamil three times daily. Exercise tolerance, and peak values of heart rate, systolic blood pressure, double product (DP/100), and ST-segment were evaluated with a treadmill test at the end of each phase. The improvement in exercise tolerance obtained by the combination of the two drugs was significantly greater (p < 0.01) than that achieved by IS-5-MN but not that by gallopamil monotherapy (NS). This effect was accompanied by significant (p < 0.05) reduction (-61%) in ST-segment and significant (p < 0.05) increment (+8%) in peak heart rate only after administration of the combination of the two drugs. The number of ST-depression (ST-) > 1 mm or ST-elevation (ST+) episodes on 24-h Holter monitoring lasting > or = 1 min were also noted in all patients at the end of each phase of the trial.(ABSTRACT TRUNCATED AT 250 WORDS)

The signal-averaged electrocardiogram and ventricular arrhythmias after thrombolysis for acute myocardial infarction.

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.

Lack of correlation between transient myocardial ischemia and late potentials on the signal-averaged electrocardiogram.

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.

Prevalence, time course and malignancy of ventricular arrhythmia during spontaneous ischemic ST-segment depression.

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.