Precordial Electrocardiographic Mapping Research Articles

Assessing the cause of T wave inversion in precordial leads with ECG mapping

Inversion of the T wave in precordial leads in patients with angina pectoris is a predictor of coronary disease; however, it may also be seen in normal adults. The aim of this study was to assess the cause of T wave inversion by carrying out precordial electrocardiographic (ECG) mapping in 51 patients, who also underwent echocardiography and coronary angiography. The 37 patients in group A had atypical symptoms. They included 11 patients who showed M pattern mapping, of whom 7 had noncoronary cardiac disease and 4 were normal. In 23 other group A patients, whose mappings were in the N pattern, the angiography was normal. In the remaining three patients of this group, mappings were in the I pattern, with angiography revealing coronary disease in two of them and no disease in the third. The 14 group B patients all had typical angina; mappings were in the I pattern in 8 of the patients and in the N pattern in the remaining 6. Angiography revealed coronary artery disease in all patients with the I pattern mapping, while all those with the N pattern were found to be normal. Sensitivity, specificity, and positive predictive value for detecting normal subjects were all 100% for N pattern mapping; for detecting coronary disease, they were 100%, 90%, and 90% for I pattern mapping, respectively. It is concluded that precordial ECG mapping is an accurate method for the assessment of T wave inversion in precordial leads.

The relationship between ST segment deviation projected to the front of the chest during exercise and simultaneous Holter monitoring.

Simultaneous two-channel Holter monitoring, with a direct recording system, and maximal exercise testing with a 12-lead precordial electrocardiographic mapping system were performed in 50 patients with chest pain (41 with documented coronary artery disease, 9 without). The exploring Holter leads were placed to correspond to CM5 and an aVF-like lead. In 36 patients, ST segment changes were found with both Holter and the 12-lead precordial electrocardiogram, while in 12 patients no ischaemic changes were detected by either method. Thus the results of the two methods concurred in 48 of 50 patient (96%). The magnitude of the ischaemic change was similar in 24 of 36 patients (67%), while the Holter system underestimated the ischaemic change by 0.5-2.0 mm in 12 patients. When the maximal ST segment deviation in V5 was compared with CM5, the deviations with both systems were identical in all but one patient in whom a difference of 0.5 mm was found. The use of a Holter lead resembling a VF identified maximal ST segment change on only one occasion, and in only four patients was an ST segment change of 1 mm noted. In conclusion, ambulatory monitoring utilizing only CM5 seems to detect most episodes with ST segment changes, but the use of a 12-lead precordial mapping system during exercise testing may expand the possibility of defining the optimal sites for the exploring Holter leads to detect maximal ST segment change.

Intravenous Clonidine Treatment in Acute Myocardial Infarction (with Comparison to a Nitroglycerin-Treated and Control Group)

This study describes the effects of intravenous clonidine treatment in a group of 24 patients with acute myocardial transmural anterior and/or lateral wall infarction. Clonidine was administered as a bolus injection of 1-2 µg/kg body weight and repeated every 1-3 h. The range of the time of administration varied from 20 min to 4 h, with the maximal range of doses from 37 to 150 µg, depending on the hemodynamic status. The effects were measured by precordial electrocardiographic mapping and compared with similar effects obtained in the nitroglycerin-treated group (30 patients) and a control group (12 patients). A large decrease in ST segment elevation was observed. The ST reduction after 24 h was 37% of initial value (compared with 52% in the nitroglycerin group, 140% in the control group); after 48 h there was a 30% reduction (compared with 55% in the nitroglycerin group and 120% in the control group). After 24 h there was a fall in NST of 45% (71% with nitroglycerin and 145% in the control group); after 48 h there was a 41% decrease (compared with 65% in the nitroglycerin group and 142% in the control group). New Q waves increased after 24 h to 135% of the initial value (compared with 122% in the nitroglycerin group and 156% in the control group); after 72 h this increased to 137% (128% in the nitroglycerin group and 167% in the control group). Detailed analysis revealed a correlation between the dosage and favorable dynamics of mapping parameters. Hemodynamic, antiarrhythmic, and, in particular, adrenolytic activity were noted. The clonidine treatment caused a distinct deterioration in daily adrenalinuria mean values to 5.99 µg in the first day (control 14.20) and even lower in the following days. A temporal association between diminished adrenalinuria and a clinical improvement and limitation of infarct size was also observed. Therapy with intravenous clonidine requires meticulous attention to the dosage depending on the individual patient's hemodynamic status.

Intravenous clonidine in acute myocardial infarction in men

We studied the effects of intravenous clonidine treatment in a group of 24 patients with acute myocardial transmural anterior and/or lateral wall infarction. Clonidine, known as an antihypertonic agent, was administered as a bolus of 1–2 μg/kg body weight and repeated every 2–3 hr. However, maximal range of the time interval was 20 min to 4 hr, maximal range of doses 37 to 150 μg, depending on the hemodynamic status. The effects were measured by precordial electrocardiographic mapping as well as serial creatine phosphokinase determinations. A big decrease in ST-segment elevation was observed: ΣST reduction after 24 hr was 37% of initial value (140% in control group), after 48 hr - 30% (120% - control). NST fall after 24 hr - 45% (145% - control), after 48 hr - 41% (142% - control). NQ increased after 24 hr to 135% of initial value (156% - control), after 72 hr to 137% (167% - control). Detailed analysis revealed undoubted correlation between the dosage and favourable dynamics of precordial mapping parameters. Hemodynamic, antiarrhythmic and above all adrenolytic activity were noted. The treatment caused a distinct deterioration in daily adrenalinuria mean values to 5.99 μg in the first day (14.20 - control) and lower in the following days. No side effects were observed but sudden discontinuation of the therapy caused an unfavorable reaction. A temporal association between diminished adrenalinuria and both clinical improvement and limitation of infarct size was observed. Therapy with intravenous clonidine requires meticulous individualization of clonidine dosage depending on the patient's initial hemodynamic status.

Precordial electrocardiographic mapping in the identification of patients with left main stem narrowing

This study was designed to determine if exercise testing using 16-lead precordial mapping can be used to identify patients with left main stem narrowing. In a group of 235 consecutive patients undergoing coronary angiography there were 35 patients with left main stem narrowing. The patients with left main stem disease differed from the others in that not only did they develop extensive S-T segment depression, but more specifically these changes occupied a characteristic position high on the precordium above the usual site of the precordial leads of the 12-lead electrocardiogram. This finding was then tested prospectively in a second group of 100 patients. Fourteen of the 100 patients had left main stem narrowing; the sensitivity and specificity of S-T segment changes high on the precordium in identifying patients with left main stem disease were 82 and 84% respectively. Thus precordial mapping and exercise testing is valuable in the diagnosis of patients with left main stem narrowing. The technique is simple and inexpensive and provides data not available using the conventional precordial leads of the 12-lead electrocardiogram.

Effect of metoprolol on indirect signs of the size and severity of acute myocardial infarction

In a double-blind randomized trial, 1,395 patients with suspected acute myocardial infarction (MI) were investigated to evaluate the possibility of limiting indirect signs of the size and severity of acute MI with the beta1-selective adrenoceptor antagonist metoprolol. Metoprolol (15 mg) was given intravenously and followed by oral administration for 3 months (200 mg daily). Placebo was given in the same way. The size of the MI was estimated by heat-stable lactate dehydrogenase (LD[EC 1.1.1.27]) analyses and precordial electrocardiographic mapping. Lower maximal enzyme activities compared with placebo were seen in the metoprolol group (11.1 ± 0.5 μkat · liter−1)when the patient was treated within 12 hours of the onset of pain (13.3 ± 0.6 μkat · liter−1; n = 936; p = 0.009). When treatment was started later than 12 hours, no difference was found between the 2 groups. Enzyme analyses were performed in all but 20 patients (n = 1,375). Precordial mapping with 24 chest electrodes was performed in patients with anterior wall MI. The final total R-wave amplitude was higher and the final total Q-wave amplitude lower in the metoprolol group than in the placebo group. Patients treated with metoprolol ≤12 hours also showed a decreased need for furosemide, a shortened hospital stay, and a significantly reduced 1-year mortality compared with the placebo group, whereas no difference was observed among patients treated later on. After 3 months, however, there was a similar reduction in mortality among patients in whom therapy was started ⩽12 hours and >12 hours after the onset of pain. The results support the hypothesis that intravenous metoprolol followed by oral treatment early in the course of suspected myocardial infarction can limit infarct size and improve longterm prognosis.

Significance of exercise induced ST segment elevation in patients with previous myocardial infarction.

In order to determine the significance of exercise induced ST segment elevation in patients with previous myocardial infarction, we have studied 156 patients, 26 months (mean) after myocardial infarction. Each patient underwent 16 lead precordial electrocardiographic mapping before, during, and after exercise and in addition coronary arteriography was performed. There was no significant difference in the extent of coronary disease or abnormalities of left ventricular function between patients with exercise induced ST segment elevation that was noted to occur in leads with Q waves and those with ST segment elevation plus depression or those with ST segment depression alone. Patients without exercise induced ST segment changes had fewer coronary arteries involved than those who developed ST segment changes. Nineteen patients with exercise induced ST segment elevation alone underwent coronary artery bypass surgery; in 11 this resulted in complete abolition of the exercise induced ST segment elevation and was associated with symptomatic relief and patent grafts without alteration of left ventricular function. Thus, exercise induced ST segment elevation in patients with previous myocardial infarction should be considered as important as ST segment depression in terms of underlying myocardial ischaemia, coronary anatomy, and left ventricular function.

Precordial electrocardiographic mapping in the identification of patients with left main stem disease

Precordial electrocardiographic mapping in the identification of patients with left main stem disease

The reappraisal fo ST segment elevation as an index of infarct size in patients with acute anterior myocardial infarction.

The clinical meaning or precordial ST segment mapping for assessment of infarct size was studied in 12 patients with acute anterior myocardial infarction. sigma ST39 (the sum of ST segment elevations in 39 precordial leads), sigma STV1--6 (the sum of ST segment elevations in the standard chest leads) and STMAX (the maximum of ST segment elevation in 39 precordial leads) were obtained serially after the onset from precordial electrocardiographic mapping records. The infarct size and the time (Tf) when the evolution of myocardial infarction finished were calculated by the total creatine phosphokinase released (sigma CPK) and serial changes in CPK releasing rate, respectively. sigma STV1--6 at Tf, as closely as sigma ST39 (r = 0.82, p less than 0.01), correlated with sigma CPK (r = 0.79, p less than 0.01). Even STMAX at the time of Tf significantly correlated with sigma CPK (r = 0.60, p less than 0.05), although the correlation coefficient was not so well as the former two. These results showed that sigma STV1--6 reflected infarct size as satisfactorily as sigma ST39 and could be useful for measuring infarct size.

Precordial electrocardiographic mapping after exercise in the diagnosis of coronary artery disease

A technique is described for recording the precordial electrocardiographic body surface map before and after exercise. The technique provides an extra dimension to the conventional exercise electrocardiogram because a measurement can be made of the area and severity of S-T segment changes that are projected onto the front of the chest. Sixteen lead isopotential surface maps were recorded before and after exercise in 109 patients with angina who subsequently underwent coronary arteriography. In addition, exercise electrocardiograms were obtained in 53 of these patients using three orthogonal leads and in all patients using a single chest unipolar chest lead. Precordial surface mapping after exercise was found to have a greater sensitivity (95 percent) than electrocardiography using either the orthogonal leads (68 percent) or a single chest lead (64 percent) ( P < 0.01). The specificity of the three techniques did not differ significantly ( P > 0.05). The technique of precordial surface mapping after exercise improves the ability to diagnose coronary artery disease and can easily be applied to clinical practice.

Precordial electrocardiographic mapping. A technique to assess the efficacy of interventions designed to limit infarct size.

Precordial electrocardiographic mapping. A technique to assess the efficacy of interventions designed to limit infarct size.

Evaluation of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemic injury.

Precordial electrocardiographic mapping has been proposed as a method for evaluating the extent of myocardial injury in patients with acute myocardial infarction. To assess the relationship between direct measures of myocardial cell damage and findings obtained by precordial mapping, the left anterior descending coronary artery (LAD) was occluded in dogs instrumented for simultaneous recording of epicardial and precordial electrocardiograms. The sum in millivolts of ST-segment elevation recorded from 30 electrodes placed in a Silastic grid sutured to the epicardium (EPIsigmaST) was compared to that recorded from 30 precordial electrodes (PresigmaST). While ischemic injury was: 1) maintained constant with a fixed occlusion; 2) reduced by partial reperfusion; 3) increased by addition of a second occlusion; or 4) increased repeatedly by intermittent infusions of isoproterenol, EPIsigmaST and PresigmaST were always closely correlated in each of the 16 dogs studied: r equal 0.92 plus or minus 0.01 (SEM). In seven control dogs, 30 minutes after coronary occlusion, PresigmaST had fallen to 77.4 plus or minus 6.6% of its value 15 minutes postocclusion. In seven experimental dogs, two branches of the LAD were occluded. Fifteen minutes after double occlusion, one occlusion was released; 30 min after the initial occlusion PresigmaST had fallen significantly more than control, to 43.1 plus or minus 13.1% of its value 15 minutes postocclusion. Simultaneously, epicardial sites in the reperfused area also showed normalization of ST segments and 24 hours later exhibited normal myocardial creatine phosphokinase activity and normal histologic appearance. During the same experiment, the mean precordial R wave voltage of sites with ST-segment elevations exceeding 0.15 mV 15 minutes following occlusion fell significantly (P less than 0.05) more in the control group (from 1.14 plus or minus 0.15 to 0.75 plus or minus 0.06 mV) than in the reperfused group (from 1.06 plus or minus 0.09 to 0.96 plus or minus 0.17 mV) during the ensuing 45 minutes. Thus, more rapid normalization of PresigmaST or preservation of precordial R wave voltage reflected the actual prevention of myocardial necrosis by reperfusion. These findings demonstrate the usefulness of precordial electrocardiographic mapping for evaluation changes in myocardial ischemic injury. Sites at which appearance of epicardial ST segment is not a reliable index of ischemic injury were associated with the development of intraventricular conduction blocks with Q to intrinsic deflection intervals exceeding 40 mesc or QRS durations exceeding 65 msec; these changes were associated with precordial RSR' configurations. Such sites, whether recorded from precordial or epicardial leads, should be excluded from ST-segment measurements used in the assessment of myocardial ischemia.

Myocardial necrosis from direct current countershock. Effect of paddle electrode size and time interval between discharges.

The effect of varying both paddle electrode size and the time interval between direct current countershock on myocardial necrosis was studied. Forty-two dogs were divided into seven groups of six dogs each. All dogs were given ten consecutive, 240 watt-second countershocks (delivered energy into a 50 ohm load). Three groups were shocked with paddle electrode diameters of 8.0 cm (standard electrodes), two groups with paddle electrode diameters of 12.8 cm (large electrodes), and two groups with paddle electrode diameters of 4.3 cm (small electrodes). The time intervals between discharges in the groups shocked with the standard electrodes were 15 seconds, one minute, and three minutes. The time interval between discharges in the groups shocked with small and large electrodes was 15 seconds and three minutes. Myocardial necrosis was quantitated by precordial electrocardiographic mapping recorded minutes after, and by gross and microscopic examination of the hearts four days after direct current countershock. When the time interval between discharges was shorter, myocardial necrosis was greater. When the time interval between discharges was constant, more necrosis was produced with smaller-sized paddle electrodes. It is concluded that large paddle electrodes should be used for delivering direct current countershocks, and that during elective cardioversion, consecutive discharges should be delivered at time intervals greater than three minutes.