ABSTRACT
In a pilot study, a computerized precordial mapping system monitored ischaemia on-line in 50 patients (40 with acute myocardial infarction and 10 with unstable angina, class IV (Canadian Cardiovascular Society). All had ST-segment depression or elevation greater than or equal to 0.2 mV in one or more precordial leads when they were admitted to our coronary care unit. After preliminary precordial mapping with 48 electrodes to localize the area of ischemia, 5 to 8 electrodes were placed in and around the centre of the ST-segment changes. The patients were monitored between 24 and 48 h (mean 35.5 h). To minimize problems caused by artifacts, ECG signal quality was improved by the averaging technique. Thereafter, the ECG was evaluated with respect to Q and R wave amplitudes and ST-segment changes. At 3 min intervals, Q and R wave amplitudes and ST segment elevations or depressions, summed for all leads were plotted as a histogram. ECG signal quality was excellent and there were no problems with the attachment of the electrodes. All patients were treated with nitroglycerine intravenously and high doses of heparin and, in several cases, nifedipine as well. Some patients received thrombolytic therapy with streptokinase. Despite therapy, 21 ischaemic attacks were documented in five patients. Seventeen attacks were seen in patients with acute infarction but who were not treated with streptokinase. All attacks were accompanied by chest pain. The duration of ischaemia ranged from 18 to 87 min. Several attacks were stopped immediately by therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Coronary Disease/diagnosis , Electrocardiography/methods , Monitoring, Physiologic/methods , Online Systems , Angina, Unstable/diagnosis , Coronary Care Units , Coronary Disease/drug therapy , Female , Heparin/therapeutic use , Humans , Male , Middle Aged , Myocardial Infarction/diagnosis , Nitroglycerin/therapeutic use , Pilot Projects , Recurrence , Streptokinase/therapeutic useABSTRACT
Exercise electrocardiograms were registered in 50 patients with significant coronary artery stenosis (lumen narrowing greater than or equal to 70%) and in 20 controls without cardiac disease using automated registration (mapping). All patients had a normal ECG at rest and typical angina. ST-segment depression of more than 0.1 mV 60 ms after the J-point in three adjoining leads and in three consecutive registrations could be shown in 46 of the 50 patients (sensitivity 92%) with coronary artery disease, however in no proband of the control group. The sum of the R-amplitudes in the precardiac leads (sigma R) was calculated before and during maximal exercise and six minutes after. Diminution of R-wave amplitudes during exercise was seen in both groups. Six minutes after exercise initial values had been nearly regained. Differentiation of both groups using R-wave amplitudes after exercise thus was impossible. Even using only leads with ST-segment lowering during exercise, a slight increase of R-amplitudes could be measured in only one case. In all other patients R-wave amplitudes diminished also in the ischaemic area with increasing ST-segment depression. RS-inversion was shifted towards the cardiac apex. Thus an increase of R-wave amplitudes indicating coronary arterial disease does not occur in unipolar chest leads in patients with significant coronary artery stenosis and ST-segment lowering during exercise.
