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Seventy-nine patients with angiographically documented coronary artery disease were studied with exercise ECG and Holter ECG for ischaemic ST segment changes. Fifty-four patients (68.3%) had ischaemia on exercise, 48 patients (62.0%) had ischaemic ST segment depression during Holter monitoring. Twenty-four (30%) of the patients with a positive exercise test and 30 (61%) with a positive Holter ECG were asymptomatic during the test, 83.7% of the total count of 456 episodes of spontaneous ischemia during Holter monitoring were silent. Forty-four patients (55.7%) had ischaemic ECG changes during exercise and Holter ECG, 20 patients (25.3%) were negative on both tests. Ten (12.7%) had only a positive exercise test and five (6.3%) only a positive Holter ECG. The sensitivity of Holter monitoring for the detection of ischaemia in patients with coronary artery disease is comparable to the sensitivity of the exercise ECG.

The analysis of ST segment changes during Holter monitoring is one important diagnostic method for detection and diagnosis of silent myocardial ischaemia. To assess the specificity and sensitivity of ST segment alterations as a diagnostic tool, 106 healthy medical students (43 females, 57 males, aged 18-36 years, mean age 26 +/- 4 years) and 26 children (14 females, 12 males, aged 12-17 years, mean 14 +/- 3 years) with no history of heart disease and normal findings during physical examination were studied by exercise stress test and Holter monitoring. Criteria for exclusion were a history of hypertension, diabetes mellitus and ST segment alterations during conventional 12-lead ECG. Due to these criteria, eight volunteers had to be excluded from the study. The exercise stress test (maximum work load protocol) revealed no pathological ST segment depressions. During Holter monitoring seven episodes of ST segment depressions (greater than or equal to 1.0 mm planar or downsloping, duration greater than or equal to 1.0 min) were found. Typical ST segment depressions detected by Holter monitoring may be found in healthy subjects. Therefore this finding has to be considered cautiously as a diagnostic tool for evaluation of patients with suspected coronary heart disease.

On the occasion of a routine medical check-up 256 out of 1100 individuals with an accumulation of coronary risk factors were screened for silent myocardial ischaemia by exercise testing and Holter monitoring. Of these individuals 5.5% had a pathological exercise test, 7.4% had ischaemia-like events on the Holter ECG, 11.3% had at least one pathological test, but only 1.6% had ischaemic signs in both ECG tests. The outcome of the ECG tests appears to be independent of the type and the total number of risk factors. To date, 13 of the 29 individuals with a positive test have undergone thallium myocardial imaging: only three individuals had signs of ischaemia. Holter monitoring and exercise ECG show comparable results in this population. The pathological ECG findings were only partly confirmed by the thallium test. The follow-up will show the prognostic significance of the ECG changes.

Ventricular late potentials are regarded as an expression of delayed impulse conduction in an area of myocardial ischemia and, accordingly, indicative of a preformed reentry circuit. Late potentials can be detected in chronic, stable coronary artery disease and their presence correlates closely with impairment of ventricular function and with the probability of future occurrence of tachyarrhythmic events or sudden cardiac death. While repetitive ventricular arrhythmias in the chronic stage of coronary artery disease result almost invariably from circling intraventricular wavefronts, tachyarrhythmias associated with acute myocardial infarction appear attributable to differing pathomechanisms. According to experimental studies, in acute myocardial infarction, three phases of arrhythmogenesis can be differentiated: phase 1 encompasses the first hours after vessel occlusion which generally corresponds with the prehospital phase. Due to the difference in potential of up to 25 mV between ischemic and nonischemic cardiac muscle areas, an injury current is called into existence which leads to depolarization of normal cardiac muscle tissue. The ectopic impulses so precipitated, the conduction of which is supported by the functional inhomogeneity of the infarcted region, are capable of initiating reentry tachycardia. During phase 2, a few hours to days after the ischemic event, only the subendocardial Purkinje fibers in the infarcted region exhibit focal arrhythmogenicity. In contrast to the working myocardial cells, the latter survive due to their immediate proximity to the cardiac chamber and show, ischemia-induced, a propensity to high-frequency impulse formation in terms of abnormal automaticity. Similar to the experimental findings, the cause of the frequently-observed ventricular arrhythmias in the early hospital phase appears predominantly attributable to a focal arrhythmia mechanism. During phase 3, several days to weeks after the acute myocardial ischemic event, reentry mechanisms again are in the foreground in which the electrophysiologic changes in the Purkinje fibers, in terms of increasing desynchronization, together with conduction barriers arising through the infarct scar, pave the way for reentry phenomenon. After abrupt restoration of patency of a previously occluded vessel the very frequent "reperfusion arrhythmias" are also attributable primarily to reentry mechanisms due to inhomogeneous improvement of the conduction properties in the region of the reperfused myocardium. Ventricular late potentials can be registered both invasively by means of epi- or endocardial leads as well as noninvasively from the body surface.(ABSTRACT TRUNCATED AT 400 WORDS)

To evaluate spontaneous variability of ST-segment changes within the Holter ECG, in 20 patients with documented coronary heart disease (CHD) long-term ambulatory ECG recordings were performed over 3 consecutive days, when the patients were only receiving short-acting nitrates. ST-segment alterations per day were measured as the area beneath the baseline (mV x min), and were compared day-to-day intraindividually. The intra-day variations of ST-segment area alterations were a factor of about 10, when compared with the baseline values. Following administrations of 120 mg ISDN ret. at the beginning of day 4, the number of anginal attacks was reduced, as was the acute medication with short-acting nitrates. There was also a trend to reduction of ischemic ST-segment changes, but these reductions could not be confirmed statistically. In studies on the course and therapeutic interventions of patients with CHD, the phenomenon of spontaneous variability of ST-segment alterations must be taken into account--as applies also to the arrhythmia analysis within the Holter ECG--and the recording period must probably be prolonged beyond the 24-h limit presently used.

100 healthy medical students were studied with 24-h Holter monitoring for ST-segment evaluation. Six recordings (1.8% of males and 11.6% of females) contained at least one episode of horizontal or downsloping ST-segment depression of at least 0.1 mV or more and 1 min duration in the V-5-like lead. Since ST-segment elevations (in 73% of the recordings in the V-5-like lead, and in 40% in the V-2-like lead) and discordant (negative) T-waves associated with ST-segment depressions (in 31% of the recordings in the V-2-like lead) were commonly seen, these ECG findings have to be considered as nonspecific. During exercise tests using a protocol of maximal work load, not one of these healthy individuals displayed typical ST-segment depressions indicative of myocardial ischemia. Therefore, typical documented ST-segment alterations in Holter-ECG recordings should be used with caution when observed in individuals with suspected coronary heart disease, particularly when they are female.

In 70 patients (3 females and 67 males), aged 16-72 years (mean: 51 +/- 9 years), the low noise ECG was recorded from body surface by the signal averaging and the high resolution beat-to-beat techniques. We found 61 patients were suffering from coronary heart disease, 4 had atypical coronary heart disease (syndrome X), 4 had dilatative cardiomyopathy, and one had the long QT syndrome (Romano-Ward syndrome). We found the following recovery rates for ventricular late potentials within the ST segment with the averaging technique: clearcut in 13/53 patients, doubtful in 16/53 patients, and late potentials absent in 26/53 patients. With the beat-to-beat technique the following recovery rates were found: clearcut late potentials in 27/70 patients, doubtful in 23/70 patients, none in 20/70 patients, and intermittently occurring late potentials in 18/70 patients (categorized as doubtful late potentials). When comparing the detection of late potentials with both methods in individual patients, we found concordant results in 39/53 patients studied (positive with both methods in 24/53 patients, negative with both methods in 15/53 patients), and discordant results in 14/53 patients (positive with the beat-to-beat technique and negative with the averaging technique in 12 individuals, negative with the beat-to-beat technique and positive with the averaging technique in the remaining 2 patients). The correlation between the incidence of late potentials and the presence of exercise-induced myocardial ischemia (submaximal bicycle exercise) was higher when using the high resolution beat-to-beat technique, as holds also true for the correlation to complex ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)