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Background QT dispersion has been proposed as a simple, noninvasive measure for identifying patients at risk of postinfarction arrhythmia. It is assumed to reflect nonuniform ventricular repolarization, which, in turn, may result from regional differences in repolarization time as well as from localized activation delay. The aim of this study was to examine the relation between QT dispersion and intraventricular conduction abnormalities in patients with acute anterior wall myocardial infarction. Methods and Results Standard 12-lead electrocardiographic and 12-lead signal-averaged electrocardiographic recordings were performed in 25 patients with a first Q-wave anterior wall myocardial infarction. Measures calculated by using the 6 precordial (V 1 through V 6 ) leads for QT dispersion were (1) difference between maximum and minimum QT and QTc intervals and (2) standard deviation of QT and QTc intervals. Measures calculated from the signal-averaged electrocardiogram were (1) maximum filtered QRS duration; (2) mean; and (3) standard deviation of filtered QRS duration. No relation was found between any measure of filtered QRS duration and that of QT dispersion by using linear correlation analysis. Similarly, no significant association was demonstrated between the filtered QRS duration and corresponding QT interval measurements (total 131 leads). Conclusions The lack of correlation between signal-averaged electrocardiogram indexes of slow intraventricular conduction and electrocardiogram variables of QT dispersion suggests an independent predictive value for the 2 methods in identifying patients at risk of postinfarction arrhythmia. This suggestion is further supported by the finding that altered activation sequence is an unlikely mechanism of QT dispersion in patients with acute myocardial infarction, as indicated by the lack of association between the filtered QRS duration and corresponding QT interval measurements. (Am Heart J 1999;137:104-8.)

Acute myocardial infarction with ST elevation in lead aVL may represent involvement of the first diagonal or the first obtuse marginal branch. This study assesses the correlation among different electrocardiographic patterns of acute myocardial infarction with ST elevation in aVL and the site of the infarct-related artery occlusion. Patients who underwent coronary angiography within 14 days of infarction with an unequivocal culprit lesion were included. Fifty-seven patients were evaluated. The culprit lesion was in the left anterior descending coronary artery proximal to the first diagonal, first diagonal, and first obtuse marginal branches, in 38, 8, and 11 patients, respectively. ST elevation in aVL and V2 through V5 signifies left anterior descending artery occlusion proximal to the first diagonal branch (positive predictive value [PPV] and negative predictive value [NPV] of 95% and 94%, respectively). ST elevation in aVL and V2, not accompanied by ST elevation in V3 through V5, favors occlusion of the first diagonal branch (PPV, 89%; NPV, 100%). ST elevation in aVL accompanied by ST depression in V2 predicts obstruction of the first obtuse marginal branch (PPV, 100%; NPV, 98%).

This study assesses the significance of inferior ST-segment depression during anterior acute myocardial infarction (AMI) by investigating the relationship between inferior ST-segment depression and (1) the site of the left anterior descending (LAD) coronary artery lesion and (2) ST-segment deviation in the various anterior and lateral leads. We studied 126 patients with anterior AMI who underwent coronary angiography within 21 days of hospitalization. The admission 12-lead electrocardiograms were evaluated for ST-segment amplitude in each lead at 0.08 second after the J-point. Coronary angiography was evaluated for the site and severity of luminal narrowing of the coronary arteries. The site of the culprit lesion in the LAD artery, relative to the origin of the first septal and diagonal branches, was determined. In four patients no lesion was identified in the LAD artery. Of the remaining 122 patients, 40 and 53 patients had a LAD artery lesion proximal to the first septal and first diagonal branches, respectively. Additional luminal narrowing (≥70% of diameter) was found in the circumflex and the right coronary arteries in 27 and 37 patients, respectively. ST-segment depression of >1 mm in leads II, III, and aVF was noted in 24, 29, and 24 patients, respectively. The prevalence of a LAD artery preseptal and prediagonal lesion was higher in patients with inferior ST-segment depression. The positive predictive values of ST-segment depression >1 mm in leads II, III, and aVF for a lesion proximal to the first septal branch were 58.3%, 65.5%, and 75%, respectively, and those for a prediagonal lesion were 70.8%, 79.3%, and 87.5%. The corresponding specificities were 88%, 88%, and 93% for a preseptal lesion, and 90%, 91%, and 96% for a prediagonal lesion. No differences were observed between the groups with interior ST-segment depression in the distribution of single-vessel or three-vessel disease or significant right or circumflex coronary artery narrowing. Univariate linear regression models revealed that the magnitude of the ST amplitude in leads III and aVF is mainly affected by the ST amplitude in leads I and aVL (coefficient of the regression −0.75 and −0.80, R 2 = 43% and 68%, for lead III, respectively; coefficient of the regression −0.57, and −0.66, R 2 = 32% and 58%, for lead aVF, respectively). The magnitude of the ST deviation in the precordial leads has only a minor impact on the inferior ST-segment deviation. Multivariate regression models confirmed that the ST deviation in leads III and aVF is mainly influenced by the ST levels in aVL. It is concluded that ST-segment depression in the inferior leads during anterior AMI represents reciprocal changes to the high anterolateral region, shown by ST-segment elevation in leads I and aVL. ST depression in the inferior leads predicts a culprit lesion proximal to the origin of the first diagonal branch. No relationship was found between the magnitude of ST-segment depression in leads II, III, and aVF and the occurrence of right coronary or left circumflex artery narrowing or three-vessel disease.

T-lymphocyte levels may adversely affect the clinical course and outcome of patients with acute myocardial infarction (AMI). To characterize the T-lymphocyte profile during AMI and to explore whether these cells play a detrimental role in the extent of myocardial insult, levels of T-lymphocyte subpopulations, free soluble interleukin-2 receptor (sIL-2R), and interleukin-1 beta (IL-1 beta), were measured during the first week of AMI. Results were correlated with left ventricular ejection fraction (LVEF), age, sex, survival rate, thrombolytic therapy, and the occurrence of reinfarction. Thirty-nine patients, 20 men and 19 women aged 30 to 80 years, with first AMI were included. Patients were divided into two groups. Group A (13 patients) experienced reinfarction; group B (26 patients) did not. T-helper and-suppressor cells were measured by the indirect immunofluorescence method and sIL-2R and IL-1 serum levels by enzyme-linked immunosorbent assay (ELISA) methods on days 1, 4, and 7 after AMI. A low count of T-helper cells (CD4) was found on the first day after AMI in both AMI groups; however, the count returned to normal in group B but not in group A. A significant correlation (r = 0.63) was found between T-helper cell count on day 4 of AMI and LVEF assessed by radionuclide ventriculography, and between the CD4/CD8 ratio on day 1 and the creatine phosphokinase level (r = -0.6950). High sIL-2R levels were found in groups A and B of the AMI patients as compared with the control group (p < or = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The atrial arrhythmia profile during inferior wall acute myocardial infarction (AMI) has not been systematically examined with respect to right ventricular (RV) involvement. To this end, 62 consecutive patients with first inferior wall AMI and no other conditions known to increase susceptibility for rhythm disturbances were studied by 24-hour Holter monitoring during the first and tenth day of infarction. Based on radionuclear ventriculography performed on day 2 of infarction, patients were allocated to two groups: group A--36 patients (58%) with right ventricular ejection fraction (RVEF) less than 40% (mean +/- SD, 31 +/- 6%) and group B--26 patients (42%) with normal (greater than 40%) RVEF (mean +/- SD, 47 +/- 5%). There were no significant differences between the two groups with respect to age, sex, or left ventricular (LV) function. In the group as a whole, ectopic activity in the different categories of atrial arrhythmias was significantly higher during the first day than on the tenth day of infarction. Comparing the two groups, 33 patients (92%) in group A had a mean hourly frequency of one or more atrial premature contractions (APCs) during the first day of infarction compared with 18 patients (69%) in group B (p less than 0.001). Atrial and supraventricular tachycardia were recorded more frequently in group A patients (16 of 36 [44%] versus 8 of 26 [31%]) as well as atrial fibrillation (AF) (7 of 36 [19%] versus 1 of 26 [4%]). Quantitative analysis showed a similar trend for a higher rate of ectopic events in group A patients. Ectopic activity was neither influenced by LVEF nor by age or sex.(ABSTRACT TRUNCATED AT 250 WORDS)

Background: This study assessed the ability of clinical and electrocardiographic variables routinely obtained on admission to identify patients with acute myocardial infarction treated with thrombolytic therapy at risk of early reinfarction. Methods and Results: The study included 2602 patients who received thrombolytic therapy for acute myocardial infarction. Baseline demographic variables and admission clinical and electrocardiographic variables were compared between patients with and without reinfarction. Multivariable logistic regression technique was used and included recurrent infarction as the dependent variable, and baseline demographic, clinical, and electrocardiographic variables as independent variables. History of hypertension (odds ratio [OR] 1.52, 95% confidence interval [CI] 1.00 to 2.31) and diabetes mellitus (OR 1.59, 95% CI 1.00 to 2.53) were associated with a higher risk, and current smoking was associated with a lower risk (OR [no versus yes] 1.64, 95% CI 1.05 to 2.58) of early hospital reinfarction. Distortion of the terminal portion of the QRS complex (OR 1.86, 95% CI 1.20 to 2.87) and absence of abnormal Q waves on admission (OR 1.54, 95% CI 0.98 to 2.43) were associated with increased risk of early reinfarction. Conclusions: A simple electrocardiographic sign is a reliable predictor of early reinfarction among patients who receive thrombolytic therapy for acute myocardial infarction. (Am Heart J 1998;135:805-12.)

Objective The objective of this study was to evaluate the efficacy, tolerability, and safety of mibefradil, a new selective T-type calcium channel blocker, in patients with chronic stable angina pectoris receiving concomitant β-blocker therapy. Design This was a multicenter, double-blind, placebo-controlled study. Methods Ninety-five patients receiving a stable dose of β-blockers, which was not changed for the purpose of the study, were administered either 50 mg mibefradil once daily for 2 weeks, then 100 mg once daily for 2 weeks, or matching placebo. Efficacy was evaluated by treadmill exercise tolerance testing 24 hours after dose and by diary registration of anginal episodes and nitroglycerin consumption. Results Two weeks of treatment with 50 mg mibefradil resulted in a significant increase in symptom-limited exercise duration and a significant delay in the onset of persistent 1 mm ST-segment depression (placebo-corrected treatment effect: 23.2 and 51.7 seconds, respectively). Treatment with the 100 mg dose for 2 additional weeks resulted in a larger improvement in treadmill exercise tolerance testing duration and onset of ischemia (placebo-corrected treatment effect: 52.7 and 75.8 seconds, respectively). In addition, a significant decrease in weekly anginal episodes was observed with the 100 mg dose of mibefradil compared with the effect in the placebo group (-53% vs -12%, p = 0.037). Conclusions The combined treatment of mibefradil and β-blockers was well tolerated, and the overall incidence of adverse events was no different from that with β-blockers alone. The results indicate that adding mibefradil to chronic β-blocker treatment is associated with significant improvement in efficacy, which is not achieved at the expense of tolerability. (Am Heart J 1998;135:272-80.)

in the event of myocardial ischemia, SACE increases markedly at maximum effort as well as during recovery. Our data on SACE activity in nonischemic subjects support similar results obtained by Milledge and Catley,” who found SACE to remain unchanged during extended stress testing (up to 60 minutes) in normal healthy subjects. In light of our findings, we propose that SACE elevation could reflect acute endothelial vascular damage (both in general and in particular in the cardiac vasculature) in subjects with clinical and ECG signs of myocardial ischemia during stress testing (regardless of the duration of exercise).

In this study of 14 patients hospitalized with a first event of myocardial infarction, maximal ST segment depression in precordial leads V2 and V3 was the sole ECG finding during chest pain in the first 24 hours of evolving posterolateral infarction, based upon further two-dimensional echocardiographic examination and cardionuclear imaging. Other ECG findings compatible with posterolateral infarction such as the appearance of Q waves in leads V5 and V6, increased R/S ratio in leads V1 and V2, and a diminution of R wave amplitude in leads 1, aVL, V5, and V6 were relatively delayed manifestations in the majority of patients. The clinical course of all patients was benign. It therefore seems reasonable to conclude that ST segment depression in leads V2 and V3 in the absence of reciprocal ECG changes may represent the initial ECG finding of posterolateral infarction in the suitable clinical context of an acute coronary event.

Forty patients with recurrent syncopal episodes of uncertain etiology were evaluated with a 60-degree head-up tilt table test for 60 minutes. There were 21 men and 19 women, with a mean age of 36 ± 19 years, a mean of 7.6 syncopal episodes per patient, and a mean duration of symptoms of 4.2 ± 6 years. Twelve patients had evidence of organic heart disease. Ten control subjects with no history of syncope were studied similarly. Syncope did not occur in any of these controls. Syncope occurred in 15 patients (37.5%) after a mean standing time of 42 ± 12 minutes. Syncope was due to a typical vasovagal reaction in 11 patients and to hyperventilation in three patients. One last patient fainted without changes in heart rate or blood pressure. In each case, symptoms during the test resembled those prevlously experienced.

We have reviewed all available noninvasive diagnostic studies for the evaluation of syncope of suspected cardiovascular origin. This eight-step diagnostic approach covers the majority of available syncopal etiologies. In patients evaluated for syncope, we believe a complete noninvasive evaluation should be performed (if clinically indicated) before performing invasive electrophysiologic studies.

Thirty-two consecutive patients who initially had horizontal or downward-sloping ST segment depression confined to the precordial leads were studied. Patients were divided into two groups: group A included 21 patients with horizontal or downward-sloping ST depression with peaked positive T waves, and group B comprised 11 patients with peaked negative T waves and downward or horizontal ST depression. The incidence of acute myocardial infarction (AMI) was similar (group A 38.1% vs group B 36.4%; p greater than 0.05). In-hospital mortality was much more significant in group B (p = 0.03). Coronary arteriography was performed in 31 patients. Of the 10 patients in group B who were catheterized, seven (70%) had left main occlusion. Of the 21 patients in group A, none had a significant left main lesion (p = 0.001), although eight (38.1%) had single-vessel disease (p = 0.05). Thus the ECG pattern of horizontal or downward-sloping ST depression passing into a peaked negative T wave identifies a subgroup of high-risk patients in whom the prognosis is poor once AMI occurs. Early catheterization is recommended when this ischemic pattern is apparent on the ECG.

Seventy-six patients with acute inferior acute myocardial infarction (AMI) and advanced atrioventricular (AV) block are described. According to pre-established ECG criteria and time of appearance of the advanced AV block, patients were divided into two groups. The early block group consisted of 31 patients who developed advanced AV block during the hyperacute ECG stage of AMI. Advanced AV block in these patients was characterized by early appearance, short duration, third-degree type block, poor response to atropine, and increased need for pacemaker therapy. The late block group consisted of 45 patients who developed advanced AV block during subsequent ECG stages of AMI. Advanced AV block in these patients was characterized by late appearance, longer duration, second-degree type block, positive response to atropine, and diminished need for pacemaker therapy. Morbidity and mortality also differed between both groups. Patients with early block had more syncope (32% vs 2%, p less than 0.0001), more left heart failure (36 vs 7%, p less than 0.005), and more cardiogenic shock (39% vs 2%, p less than 0.001) than patients with late block. The mortality rate in the early block group was high (23%) and similar to that reported in the literature, whereas the mortality rate in the late block group was low (7%, p less than 0.05) and similar to the mortality rate reported for acute inferior AMI without advanced AV block. These data identify a subgroup of patients with acute inferior AMI and advanced AV block, which accounts for the high mortality rate reported in this group of patients.

We evaluated 46 patients with unstable angina (UA), who showed no significant changes in heart rate, blood pressure, and double product (as evidence of increased oxygen demand) during episodes of chest pain. Coronary angiography was performed in all patients during the same hospitalization. Of 26 patients with UA and ST depression (group A), 10 had left main coronary artery disease (CAD) and eight had left main equivalent CAD. Of 20 patients with UA and ST elevation (group B), only one had left main CAD and one had left main equivalent CAD. All patients in group A had ST depression in leads V4 and V5, and all patients in group B had ST elevation in leads V2 and V3. The presence of ST depression in leads V4 and V5 in UA patients without evidence of increased oxygen demand may be suggestive of significant left main or left main equivalent CAD. Therefore, coronary angiography is recommended during the same hospitalization.

We retrospectively evaluated 32 patients with unstable angina (UA) and no evidence of increased oxygen demand during episodes of chest pain (no significant changes in heart rate and blood pressure), who developed an acute myocardial infarction (AMI) during the same hospitalization. Based on the type of ST changes during anginal pain, two groups were defined: Group A included 19 patients who developed ST elevation during AMI; 15 of these 19 patients (79%) were in Killip class I, two were in class II, and there was one patient each in classes III and IV, respectively. Only one of the 19 patients died. Group B included 13 patients who developed ST depression during AMI; nine of these 13 patients were in Killip class IV and the remaining four patients died before they could be evaluated. Ten patients died (77%) (p less than 0.01), seven in electromechanical dissociation and three in cardiogenic shock. Postmortem examination, performed in four patients, revealed total obstruction of the left main coronary artery. It is concluded that patients with UA who, during attacks of chest pain, develop ST depression and no evidence of increased oxygen demand may have a poor prognosis when they develop an AMI. This selected group of high-risk patients appears to need immediate intensive medical care and most probably early surgical treatment.

We prospectively evaluated 19 patients with prolonged chest pain not evolving to myocardial infarction and accompanied with reversible ST-T changes and tachycardia (heart rate greater than 100 beats/min) in order to correlate heart rate reduction with ischemic electrocardiographic (ECG) changes. Fourteen patients (74%) received previous long-term combined treatment with nifedipine and nitrates. Continuous ECG monitoring was carried out until heart rate reduction and at least one of the following occurred: (1) relief of pain or (2) resolution of ischemic ECG changes. the study protocol consisted of carotid massage in three patients (16%), intravenous propranolol in seven patients (37%), slow intravenous amiodarone infusion in two patients (10%), and intravenous verapamil in four patients (21%) with atrial fibrillation. In three patients (16%) we observed a spontaneous heart rate reduction on admission. Patients responded with heart rate reduction from a mean of 125 +/- 10.4 beats/min to 84 +/- 7.5 beats/min (p less than 0.005) and an ST segment shift of 4.3 +/- 2.13 mm to 0.89 +/- 0.74 mm (p less than 0.005) within a mean interval of 13.2 +/- 12.7 minutes. Fifteen (79%) had complete response and the other four (21%) had partial relief of pain. A significant direct correlation was observed for heart rate reduction and ST segment deviation (depression or elevation) (r = 0.7527 and 0.8739, respectively). These patients represent a unique subgroup of unstable angina, in which the mechanism responsible for ischemia is excessive increase in heart rate. Conventional vasodilator therapy may be deleterious, and heart rate reduction in mandatory.

In search of a simple method for potential evaluation of leukocyte aggregation in states of infarction, we compared the leukergy test, which consists of leukocyte aggregation visualized in a peripheral blood test, to the neutrophil aggregation activity (NAA) test, which consists of in vitro aggregation of neutrophils from normal donors by a patient's plasma. Seventy-five patients participated in the study; 20 with ischemic heart disease and no infarction, 41 with relatively small myocardial infarctions, and 14 with large myocardial infarctions, the respective values of leukergy being 6.9 ± 3.2, 10.8 ± 4.6, and 20.5 ± 14%. On the other hand, neutrophil aggregation activity was the same in a group of 10 patients without myocardial infarction and 10 with myocardial infarction. In these two groups, which showed no difference in the NAA test, the respective leukergy values were 4 ± 1.5 and 21.7 ± 10.6%. Thus leukergy correlates better with the clinical picture than does the NAA test.