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purpose: The purpose of this study was to determine the effect of acute and old myocardial infarction (MI) sites on early (15 days) mortality in patients with a second MI. patients and methods: Data are derived from the SPRINT 2 study population that included 1,161 consecutive patients with acute MI, aged 50 to 79 years, recruited from 14 coronary care units in Israel between November 1985 and July 1986. Two hundred twenty-six of these patients (19.5%) had a previous MI prior to the index acute MI. Sixty-two patients were excluded from the analysis either because the MI site was not of anterior or inferior location, or because of incomplete data. In the 164 (73%) remaining patients, acute and old MI locations were determined to be either anterior or inferior and were accordingly divided into 4 groups: acute anterior-old anterior (Group 1–23 patients); acute anterior-old inferior (Group 2–86 patients); acute inferior-old anterior (Group 3–34 patients); acute inferior-old inferior (Group 4–21 patients). results: Significant differences in clinical parameters among the four groups included a higher proportion of Q-wave MI (p = 0.04), severe congestive heart failure during admission (p = 0.04), and markedly elevated serum lactate dehydrogenase levels (p = 0.05) in Group 3. High-degree atrioventricular block (p = 0.001) and cardiogenic shock (p = 0.05) also developed more often in this group during hospitalization. Twenty-three patients (14%) died within 15 days. Death rates in the acute anterior (Group 1 plus Group 2) and the acute inferior (Group 3 plus Group 4) groups were 11% versus 20%, respectively (NS). However, death rate variability across the four groups was statistically significant (p = 0.018), with the highest mortality observed in Group 3 (old anterior-acute inferior MI—29%). Multivariate analysis identified acute inferior MI following old anterior MI as a strong independent predictor of early death (relative odds vis-a-vis other combinations 5.0, 95% confidence interval 1.5 to 16.6). conclusion: This study identifies a subgroup of patients with acute inferior MI at high risk for early mortality. It is possible that such patients would benefit from early reperfusion therapy.

Right and left circumflex coronary artery occlusions cause inferior myocardial infarction. To improve the targeting of diagnostic and therapeutic measures individually, factors interfering with identification of the culprit artery by the electrocardiogram (ECG) were explored.Patients with inferior preinfarction syndrome (n = 266) were included to the Danish Trial in Acute Myocardial Infarction-2 substudy. The culprit vessel was predicted by the ECG, and findings were correlated with angiography. Factors associated with false identification of the culprit artery by the ECG were examined.Electrocardiogram criteria for right coronary artery occlusion to predict coronary angiography findings had sensitivity, specificity, and positive and negative predictive values of 95%, 52%, 84%, and 81%. For left circumflex coronary artery occlusion, the corresponding values were 51%, 93%, 70%, and 85%, respectively. False ECG identification of the culprit artery was independently associated with left coronary dominance (P.001; odds ratio [OR], 22.0; 95% confidence interval [CI], 7.2-67.0), multivessel disease (P = .035; OR, 2.2; 95% CI, 1.1-4.7), and absence of proximal occlusion pattern in the ECG (P = .003; OR, 4.0; 95% CI, 1.6-9.8).Left coronary artery dominance, multivessel disease, and absence of ECG signs of proximal culprit lesion are associated with failure to predict the culprit artery of inferior myocardial infarction by the 12-lead ECG.

We examined the prevalence and prognostic impact of poor R-wave progression (PRWP) in a standard electrocardiogram (ECG) in a general population.Data and standard resting ECG recording were collected from a large nationally representative (random sample) health examination survey conducted in Finland in 2000-2001. The final study population consisted of 5613 individuals.The prevalence of PRWP (defined as RV3or = 3 mm and RV2or = RV3) was 7.0% in women and 2.7% in men (Por = 0.001 for difference). During follow-up of 70 +/- 9 months (mean +/- SD), 317 patients died (5.6%). Both all-cause and cardiovascular mortality was higher in the group with PRWP than in those without PRWP in both women and men. In Cox regression analysis after adjustment for age, hypertension, diabetes, previous myocardial infarction, and coronary heart disease, the relative risk for all-cause mortality for PRWP was 1.69 (95% CI 0.89-3.22, P=0.112) for men and 2.00 (95% CI 1.28-3.13, P=0.002) for women. For cardiovascular mortality the relative risk for individuals with PRWP was 1.85 (0.74-4.65, P=0.19) for men and 3.02 (1.54-5.93, P=0.001) for women.PRWP is a common ECG finding and predicts risk for total and cardiovascular mortality in women in a general population.

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)

Most series of patients with ventricular tachycardia (VT) of right bundle-branch block (RBBB)-left axis deviation (LAD) morphology include young individuals with no overt evidence of structural heart disease. In the present report, the clinical and electrophysiologic findings in two patients with verapamil-responsive VT and organic heart disease are described.

Right-sided chest leads (V3-V4R) were recorded in the early stages of first inferior wall acute myocardial infarction (AMI) in 100 consecutive patients. Nine patients (9%) presenting with S-T segment depression (greater than 1 mm) in these leads were subsequently studied by echocardiography and radionuclear angiography. In this group, there were 5 patients with intact right ventricular (RV) function and 4 other patients with clinical findings compatible with RV infarction. We suggest that one should not rule out RV involvement when S-T segment depression rather than elevation is seen in the right precordial leads in the presence of inferior wall AMI. An individual assessment for RV infarction is recommended when this pattern is apparent on the ECG.

From the electrocardiographic (ECG) point of view, the tako-tsubo cardiomyopathy (TTC) behaves like an acute subepicardial circumferential ischemic syndrome. The electrical manifestations are significantly different from those of acute transmural segmental ischemia, in which the ECG primarily expresses the electrophysiologic and metabolic changes occurring in the subepicardial layer. In comparison with transmural anterior ischemia and despite acute contraction impairment (circumferential middle and apical dyskinesis and basal hyperkinesis), in TTC there is typically only moderate ST elevation in the precordial leads. This paradox can be understood by taking into consideration the molecular biology and basic electrophysiology. In the senescent female with hypoestrogenemia, the subepicardium is almost totally unprotected against “adrenergic storm.” In the fertile female, estrogen plays the pivotal role of protecting the myocardium at many levels of the metabolic cascade, such as in the regulation of the presynaptic release of adrenergic substances and by increasing the release of adenosine. There is consequental increase of the adenosine triphosphate (ATP)–sensitive K+ channels, thus regulating the inward flow of Ca2+ toward the sarcoplasmic reticulum. The ATP-sensitive K+ channels hyperpolarize the subepicardial cells during extremely aggressive situations such as ischemia and adrenergic storm. The hyperpolarization of the subepicardium is manifested in the ECG by tall, peaked T waves, indicating an increase of the repolarization gradient between the subendocardial and subepicardial layers. In the absence of estrogen, there are severe decreases in the concentration of adenosine and in the density of the ATP-sensitive K+ channels. The subepicardial myocytes cannot be hyperpolarized, and the adrenergic storm is manifested by moderate ST-T elevation. Furthermore, the very rapid appearance and disappearance of a Q wave are “against the rules.” This is a classical example of electrical stunning, that disappears before mechanical stunning in which contraction is typically recovered only after 1 week.

Background: Atrial natriuretic peptide (ANP) is released from cardiac atrium secondary to increased atrial pressure. The plasma levels of ANP have been found to be related to short-and long-term prognosis after acute myocardial infarction (MI). The purpose of the present study was to investigate the plasma levels of ANP in three groups of patients with inferior wall acute MI classified according to ST-segment depression in the precordial leads. Methods: The study population consisted of 18 patients with inferior wall acute MI classified into three types: Type 1 = no precordial ST-segment depression (7 patients), Type 2 = sum of ST-segment depression in leads V1 to V3 equal to or more than the sum of ST-segment depression in leads V4 to V6 (4 patients), and Type 3 = maximal precordial ST-segment depression in leads V4 to V6 (7 patients). Results: Radioimmunoassay showed that plasma ANP levels were significantly higher in patients with Type 3 acute inferior wall myocardial infarction compared with those with Types 1 and 2 (313.1 ± 233, 73.0 ± 27.5), and 84 ± 32.7 pg/ml, respectively, p = 0.018). Conclusions: Plasma ANP levels are higher in patients with Type 3 acute inferior wall MI compared with patients with Types 1 and 2. These findings, together with earlier ones, may contribute to our understanding of the pathophysiology of the presence of ST-segment depression in the precordial leads in inferior wall acute MI.

The course of 357 balloon inflations performed during 38 angioplasties for single-vessel coronary artery disease was prospectively studied using continuous ECG recording. Ischemic ECG changes appeared during 91 percent of the inflations at a mean of 20 ± 8 seconds after inflation and resolved in 97 percent of those at a mean of 11 ± 5 seconds after deflation. Elevation of the plasma CPK level was found in six patients who had ischemic ECG changes for at least 7.8 minutes. The duration of ischemia did not exceed 5.4 minutes in any of the patients without CPK elevation. Resolution of the ischemic changes was delayed in patients with CPK elevation and in last vs initial inflations. We conclude that in patients with noninfarcted myocardium, ECG changes follow coronary occlusion and reflow very rapidly, detecting these coronary events with a high sensitivity. Lack of rapid regression predicts lack of reperfusion, and persistence of ischemia for more than 7.8 minutes is sufficient to cause myocardial necrosis.

As the establishment of science-based theories further elucidate our expanding technological knowledge, they become less vulnerable to refutation. In most sciences, theories that permit superior prediction are less likely to be replaced by mere conjecture. The report by Madias is an historical overview covering a 50-year-period that compares both the clinical and experimental approaches between 2 research groups investigating the electrocardiographic (ECG) patterns in myocardial ischemic syndromes. I will try to clarify the question raised about the developments of clinical electrocardiology in the light of modern invasive and noninvasive technology throughout the latter half of the 20th century. Such progress, together with advancement in the field of molecular biology, has contributed toward a more exact diagnosis that in turn can facilitate an improved pharmacological and/or mechanical therapeutic approach. In early 1979, while Director of the ICCU at the Beilinson Medical Center, I developed the hypothesis that the morphologic ECG recorded during the preinfarction stage is a unique method of providing clinical, anatomical, hemodynamic, and physiopathologic data for improved management of patients with an acute ischemic myocardial event. I reached this conclusion following 4 years of work with the legendary master Mauricio B. Rosenbaum. To convert this hypothesis into theory, I devised a protocol that included continuous ECG recordings during the initial 3to 4-hour period on all patients treated in the ICCU. It should be remembered that cardiac mortality was high during this period (the prethrombolytic era), and the gold standard to corroborate and correlate the ECG was the anatomical study of the heart at post mortem. From this protocol we learned much about the natural evolution of the ECG: (1) the numerous types of ischemic syndromes, (2) the prognostic differences between ischemic events with ST elevation vs ST depression, and (3) the different types of spontaneous reperfusion and nonreperfusion patterns. Serial ECG recordings plus echocardiographic and isotopic images were added to the protocol in the mid-seventies. By early 1989, we

Signal-averaged electrocardiograms were obtained in 53 consecutive patients with a first acute myocardial infarction (AMI) who survived the first 10 days of hospitalization. The recording was performed twice, at Day 1 and at Day 10 of hospitalization, in patients without bundle-branch block and who did not receive antiarrhythmic therapy. Signal-averaged ECGs were obtained with an instrument which analyzes the presence of late potentials (LP) in each individual precordial lead. There were 41 men and 12 women, mean age of 67 years. On Day 1, three patients had L.P (5.6%). On Day 10, LP was recorded in 11 patients (21%). In only one patient was LP transient. Patients who developed LP by Day 10 (absent in Day 1) had statistically significant lower root mean square (rms) voltage and higher QRS duration than patients who did not develop LP on Day 10. In conclusion, in patients with a first AMI who survive the initial hospitalization period and are not in need of antiarrhythmic therapy have an incidence of LP of 21%. A predischarge recording is preferable since this will maximize the chances of detecting LP.

Aims The aim of the study was to assess two distinct 12-lead electrocardiogram (ECG) patterns and their prognostic value with respect to reperfusion strategy. Methods and results In a DANAMI-2 substudy ( n = 1522), we defined the pre-infarction syndrome (PIS) as ST-elevation accompanied by positive T waves and evolving myocardial infarction (EMI) as pathological Q waves and/or negative T wave. We used a composite of death, clinical re-infarction, or disabling stroke at median 2.7 year follow-up. A higher overall event rate was observed in the EMI group compared with the PIS group [11.4 (9.4–13.9) and 6.9 (6.0–8.0) per 100 person-years, respectively, ratio of the rate (RR) 1.6, P < 0.001]. The EMI pattern was independently predictive of adverse outcome in multivariable analysis (hazard ratio 1.52, confidence interval 1.01–2.30, P = 0.04). The PIS pattern ( n = 952) was associated with lower overall event rate in patients treated with primary percutaneous coronary intervention (PCI) compared with fibrinolytic therapy (FT) [5.5 (4.4–6.9) and 8.5 (7.0–10.4) per 100 person-years, respectively, RR = 0.6, P = 0.004]. No significant difference in the outcome between treatment strategies was observed in the EMI group as a whole. However, in patients with anterior EMI without ECG signs of reperfusion, superiority of primary PCI was driven by a 51% reduction in the relative risk of composite endpoint ( P = 0.008). Conclusion More detailed ECG analysis, involving also Q- and T-wave morphology, is useful for rapid identification of high-risk patients in whom every effort should be made to transfer for primary PCI, or vice versa, for identifying low-risk patients in whom FT might be an alternative option.

Two readily obtainable measurements on the admission electrocardiogram-a higher ST-segment elevation in lead III than in lead II and a greater ST-segment depression in lead aVL than in lead I-can distinguish right coronary artery from left circumflex artery-related acute inferior wall myocardial infarction.

Of the 87 consecutive patients admitted with first inferior wall acute myocardial infarction, 17 had acute left anterior hemiblock. The appearance of left anterior hemiblock identified a specific group with more extensive coronary artery disease and suggests disease of the left anterior descending coronary artery.

Treatment of acute myocardial infarction has changed considerably during the last few years with the introduction of primary coronary angioplasty. In the acute phase risk stratification is largely based on simple clinical parameters, laboratory markers of myocardial injury and 12-lead electrocardiography. The electrocardiogram is of crucial importance especially during the first few hours after initiation of chest pain when important therapeutic decisions are made. Biochemical markers of myocardial injury are usually not elevated at that time point. Cases with inferior ST-elevation myocardial infarction from our hospital are presented to show how anatomical interpretation of ECG recorded during chest pain helps to risk stratify patients.

Trasodone, a second generation antidepressant, has been shown to equal standard tricyclics in clinical efficacy while causing significantly fewer cardiac side effects. Although clinical trials have demonstrated a relatively safe arrhythmogenic profile, trasodone has been implicated in the pathogenesis of ventricular arrhythmias. This report describes a patient in whom the administration of trasodone in addition to previously well-tolerated long-term amiodarone therapy was associated with a marked prolongation of the QT interval and polymorphous ventricular tachycardia. Caution in the concurrent use of trasodone and other medications known to cause QT prolongation and polymorphous ventricular tachycardia is recommended.

Patients with acute myocardial infarction who have terminal QRS distortion in addition to ST-segment elevation (grade III ischemia) on their presenting electrocardiogram have higher mortality and larger final infarct size than patients with ST-segment elevation without changes in the terminal portion of the QRS complex (grade II ischemia). This article discusses the data concerning the prognostic significance of the grades of ischemia on the presenting electrocardiogram and the possible underlying mechanism of terminal QRS distortion. Patients with grade III ischemia have more severe ischemia and faster progression of necrosis than patients with grade II ischemia. This might be related to less protection by "ischemic preconditioning" or presence of collateral circulation.

A 21-year-old man with aborted sudden death developed bundle-branch reentry tachycardia at electrophysiologic study. Ablation of the right bundle branch was performed in an attempt to eliminate the recurrence of ventricular arrhythmia. The clinical arrhythmia was no longer inducible; however, a second type of ventricular tachycardia of a different mechanism and origin was induced. Following a new clinical episode of ventricular tachycardia with hemodynamic deterioration, an automatic implantable cardioverter and defibrillator was implanted.

Four patients who developed acute myocardial infarction (AMI) in the setting of systemic febrile illness are described. They were all treated with anticoagulants or lytic agents (or both), demonstrating patient coronary arteries following infarction. We discuss the pathogenesis and therapeutic implications of AMI occurring in this setting.

OBJECTIVES We sought to evaluate the effectiveness and safety of thrombolytic therapy in stuck mitral bileaflet heart valves in the absence of high-risk thrombi. BACKGROUND Current recommendations for the thrombolytic treatment of stuck prosthetic mitral valves are partially based on older valve models and inclusion of patients in whom high-risk thrombi were either ignored or not sought for. The feasibility and safety of thrombolysis in bileaflet models may be affected by the predilection of thrombi to catch the leaflet hinge. METHODS We studied 12 consecutive patients (men/women = 5/7, age 58.8 ± 14.9 years) who experienced one or more episodes of stuck bileaflet mitral valve over a 33-month period and received thrombolytic therapy with streptokinase, urokinase or tissue-type plasminogen activator. Transesophageal echocardiography was performed in all patients. Patients with mobile or large (>5 mm) thrombi were excluded. Functional class at initial episode was I–II in 4 patients (33.3%) and III–IV in 8 patients (66.6%). RESULTS Patients receiving thrombolytic therapy achieved an overall 83.3% freedom from a repeat operation or major complications (95% confidence interval 51.6–97.9%). Minor bleeding occurred in three patients (25%) and allergic reaction in one (8.3%). Transient vague neurologic complaints, without subjective findings, occurred in four patients (33.3%). Three patients had one or more relapses within 5.2 ± 3.1 months from the previous episode, and readministration of thrombolytics was successful. CONCLUSIONS In clinically stable patients with stuck bileaflet mitral valves and no high-risk thrombi, thrombolysis is highly successful and safe, both in the primary episode and in recurrence. The best thrombolytic regimen is yet to be established.

In the prethrombolytic era it was found that infarct size and left ventricular ejection fraction could be predicted using the Selvester QRS score. We evaluated whether infarct size and left ventricular ejection fraction could be predicted by the predischarge QRS score in patients who had received reperfusion therapy and whether considering the configuration of the ST segments and T waves would increase the accuracy of these predictions. We evaluated 51 patients with first anterior wall myocardial infarction who had received reperfusion therapy and predischarge resting technetium-99m-sestamibi scan. The electrocardiograms recorded on the same day of the scan were analyzed for the QRS score and were divided into 3 groups: A, isoelectric ST and negative T waves; B, ST elevation (or =0.1 mV) and negative T waves; and C, ST elevation (or =0.1 mV) and positive T waves. Groups A, B, and C included 12, 23, and 16 patients, respectively. The myocardial perfusion defect extent increased from groups A to C (median 21%, 37%, and 43.5% in groups A, B, and C, respectively; p = 0.023). Similarly, left ventricular ejection fraction decreased (44%, 38%, and 34%, respectively; p = 0.042) from groups A to C. Overall, the correlation between the QRS score and the myocardial perfusion defect extent (rho 0.249; p = 0.08) and ejection fraction (rho -0.229; p = 0.11) was poor. A statistically significant correlation between myocardial perfusion defect size and QRS score was found only in group A (rho 0.599, p = 0.04). Among patients with anterior myocardial infarction who received reperfusion therapy, the predischarge QRS score was predictive of infarct size only in those in whom ST elevation resolved completely. In patients with residual ST elevation there was no correlation between QRS score and infarct size.

OBJECTIVESTo examine the relationship between the persistence of ST segment depression in leads V5–V6 after Q-wave anterior wall myocardial infarction (MI) and the filling pattern of the left ventricle (LV).BACKGROUNDPrecordial ST segment depression predominantly in leads V5–V6 is associated with increased in-hospital morbidity and mortality after acute myocardial ischemia, perhaps due to reduced diastolic distensibility of the LV.METHODSWe prospectively studied 19 patients after Q-wave anterior wall MI (>6 months). All patients underwent 12-lead ECG recording, symptom-limited treadmill exercise testing with single photon emission computed tomography thallium-201 imaging, transthoracic Doppler echocardiography, cardiac catheterization and measurement of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels. Patients were classified based on the presence of ST segment depression in leads V5–V6: Group I = ST segment depression

To the editor: Verouden et al 1 incorrectly report the ECG finding of ST-segment depression (measured at the J-point) and tall, positive symmetrical T waves as a “new” sign of proximal left anterior descending artery occlusion. In …

Summary: During three consecutive days of prazosin treatment in a patient with pheochromocytoma, urinary catecholamine metabolite levels were correlated with plasma renin activity. Suppression of renin plasma activity resulted in sustained hemodynamic and clinical improvement, while no remarkable changes were observed in urinary catecholamine metabolite levels. This suggests that prazosin may interrupt the vicious cycle of worsening hypertension provoked by further activation of the renin-angiotensin system mediated by excessive circulating catecholamines.

Ten patients, who were admitted to the Intensive Coronary Care Unit during a one year period with symptomatic bradycardia while on combination therapy with oral diltiazem and beta-blocker agents, are described. The important features of this adverse reaction to drug combination were that it appeared mainly in a relatively elderly age group and with presenting symptoms of lethargy, dizziness, syncope, chest pain, and (in one patient with poor left ventricular function) pulmonary edema. It was not dose dependent and occurred even in very low doses of each drug. Electrophysiologic abnormalities were localized to the sinus node in all 10 patients and the primary rhythm disorders were junctional escape rhythm, sinus bradycardia, and sinus pause. These rhythm abnormalities resolved within 24 h following withdrawal of the offending drugs. Temporary pacemaker insertion was necessary in four patients. The duration of drug combination used before the acute episode range from within hours to up to 2 years. In conclusion, although combination diltiazem/beta blocker therapy is very effective in ischemic syndrome, caution is advised when this combination is used especially in the elderly or in patients with left ventricular dysfunction or antecedent sinoatrial or atrioventricular conduction abnormality.

Two patterns of the QRS complex in the lateral lead aVL on the admission electrocardiograms of patients with inferior wall acute myocardial infarction (AMI) were correlated with the culprit artery. S/R wave ratioor =1/3 with ST depressionor =1 mm was found to be a sensitive and specific marker for left circumflex artery AMI, whereas S/R-wave ratio1/3 with ST-segment depression1 mm was suggestive of right coronary artery AMI.

We assessed whether there are differences among patients with inferior acute myocardial infarction and ST segment depression in leads V2–V3 between those with positive versus negative T waves on admission. We found no differences in the prevalence of concomitant significant left anterior descending coronary artery stenosis and anterior or posterior wall motion abnormalities on echocardiography between the two groups. Precordial ST segment depression with negative T wave may be the early electrocardiographic pattern of posterior infarction, reflecting ST segment elevation with positive T waves that would have been detected by leads facing the posterior wall.

This study assessed the ability of simple clinical and electrocardiographic (ECG) variables routinely obtained on admission to identify patients with inferior myocardial infarction who are at high risk of developing high-degree atrioventricular (AV) block within the first 24 h of hospitalization in 205 patients. The admission ECGs were classified into two patterns based on the J-point to R-wave amplitude ratio: pattern 1: those with J-point/R-wave ratio 1 (OR 2.33, CI 0.83–6.54; p = 0.1065) and thrombolytic therapy (OR 0.32, 95% CI 0.11–0.93; p = 0.037).

Background: Lead III ST-segment depression during acute anterior wall myocardial infarction (AMI) has been attributed to reciprocal changes. However, the value of the T-wave direction (positive or negative) in predicting the site of obstruction and type of the left anterior descending (LAD) artery is not clear and has not been studied before. Hypothesis: The aim of the study was to assess retrospectively the correlation between two patterns of lead III ST-segment depression, and type of LAD artery and its level of obstruction during first AMI. Methods: The study group consisted of 48 consecutive patients, admitted to the coronary care unit for first AMI, who showed ST-segment elevation in lead aVL and ST-segment depression in lead III on admission 12-lead electrocardiogram. The patients were divided by T-wave direction into Group 1 (n = 31), negative T wave, and Group 2 (n = 17), positive T wave. The coronary angiogram was evaluated for type of LAD (“wrapped”, i.e., surrounding the apex or not), site of obstruction (pre- or postdiagonal branch), and other significant coronary artery obstructions. Results: Mean lead III ST-segment depression was 1.99 ± 1.32 mm in Group 1 and 1.13 ± 0.74 mm in Group 2 (p = 0.004); mean ST-segment elevation in aVL was 1.35 ± 0.84 mm and 1.23 ± 0.5 mm, respectively (p = 0.5). A wrapped LAD was found in 12 patients (38.7%) in Group 1 and in 13 in Group 2 (76.4%) (p = 0.02). The sensitivity of lead III ST-segment depression with positive T wave to predict a wrapped LAD was 52%, and the specificity was 82% with a positive predictive value of 76%. On angiography, 25 patients (80%) in Group 1 and 13 (76%) in Group 2 had prediagonal occlusion of the LAD (p = 0.77 ). No significant difference between groups was found for right and circumflex coronary artery involvement or incidence of multivessel disease. Conclusions: The presence of lead III ST-segment depression with positive T wave associated with ST-segment elevation in aVL in the early course of AMI can serve as an early electrocardiographic marker of prediagonal occlusion of a “wrapped” LAD.

Background: The correlation between ST elevation in lead V1 during anterior wall acute myocardial infaction (AMI) and the culprit lesion site in the left anterior descending (LAD) coronary artery is poor. Hypothesis: The study was undertaken to assess the electrocardiographic (ECG) characteristics and angiographic significance of ST-segment elevation in lead V1 during anterior wall acute myocardial infarction (AMI). Methods: Data from 115 patients with anterior wall AMI, who underwent coronary angiography within 14 days of hospitalization, were studied. The admission 12-lead ECG was examined and the coronary angiogram was evaluated for the nature of the conal branch of the right coronary artery (RCA) and for the culprit lesion site in the left anterior descending (LAD) coronary artery. Results: Mean ST-segment deviation and the frequency of patients with ST-segment elevation > 0.1 mV were significantly lower in lead V i than in lead V2 (0.136 $$ 0.111 mV vs. 0.421 $$ 0.260 mV, and 37 vs. 96%, for leads Vi and Vi, respectively). A small conal branch not reaching the interventricular septum (IVS) was more prevalent among patients with ST-segnicni elevation >0.1 mV in lead Vi (67%), whereas a large conal branch was more prevalent in patients with ST-segment deviation (1 mV in that lead (83%, p

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.)

One hundred forty-one patients with first acute inferior wall myocardial infarction were examined. ST-segment elevation in precordial leads V5 to V6 was found in 34; 94% of them had "mega-artery" compared with 2% in those without ST-segment elevation in precordial leads V5 to V6.

The authors report the implantation of two wallstents in a patient by use of the transra dial artery approach. This approach for coronary wallstent implantation allows for intensive anticoagulation therapy with less risk of bleeding.

Precordial ST-segment depression (PSD) in inferior wall acute myocardial infarction (IAMI), especially when maximal in leads V4-V6, has been shown to portend a higher rate of heart failure and mortality. To better understand the pathophysiology behind this phenomenon, we evaluated patients with a first IAMI by echocardiography 48-72 h after the acute event, using segmental scoring (0 = normal to 3 = dyskinesia) of left ventricle wall motion, and a dichotomous assessment of right ventricle involvement. Patients were categorized into 3 groups: I = no PSD (n = 14); II = maximal PSD in leads V1-V3 (n = 28); III = maximal PSD in leads V4-V6 (n = 8). As compared with group I, patients in groups II-III had more severe wall motion abnormalities in inferior segments (1.36 +/- 0.97 vs. 2.19 +/- 1.74, p = 0.04), and a similar trend for posterior and lateral segments (1 +/- 1.75 vs. 2 +/- 2.41, p = 0.11), translating into a worse total left ventricle score (2.36 +/- 2.34 vs. 4.25 +/- 4.05, p0.05). Frequency of right ventricle involvement was similar in patients with and without PSD (6 (43%) vs. 9 (25%), p = 0.37). Segmental scores for groups I, II, and III, respectively, were not different for inferior (1.36 +/- 1, 2.25 +/- 1.82 and 2 +/- 1.51, p = 0.24), posterior and lateral (1 +/- 1.75, 1.96 +/- 2.32 and 2.13 +/- 2.9, p = 0.38), and septal, anteroseptal and anterior segments (0 +/- 0, 0.04 +/- 0.19 and 0.13 +/- 0.35, p = 0.28). Right ventricle abnormalities occurred in 43, 21 and 38% of patients in groups I, II and III, respectively, p = 0.3. Thus, IAMI with PSD is associated with worse left ventricle wall motion. However, since patients with maximal PSD in leads V4-V6 do not have greater wall motion abnormalities or higher rate of right ventricle involvement, their poorer prognosis cannot be explained by worse systolic dysfunction. We propose that maximal PSD in leads V4-V6 reflects transient diffuse ischemia and altered diastolic distensibility due to extensive coronary artery disease, causing increased left ventricle end-diastolic pressure.

Background: Q waves developed in the subacute and persisting into the chronic phase of myocardial infarction (MI) usually signify myocardial necrosis. However, the mechanism and significance of Q waves that appear very early in the course of acute MI (

Background: Being a potent promoter of endothelial and smooth muscle cell proliferation, basic fibroblast growth factor (bFGF) is presumed to play a key role in coronary collateral development and atherogenesis. Purpose: To characterize serum bFGF levels in patients with ischemic heart disease. Methods: The study population consisted of patients with angina (n=33) and after uncomplicated myocardial infarction (n=12). The number of significantly stenosed (≥50%) vessels and angiographic coronary collateral score were noted. Blood was drawn immediately prior to elective coronary angiography in study patients for bFGF levels. Twenty healthy, age-matched subjects served as control for serum bFGF. Results: Serum bFGF levels were undetectable in all 20 control subjects, but were detectable in 15/33 (45%) patients with angina and 3/12 (25%) post-infarction patients, respectively (P=0.002). Serum bFGF levels were detectable in 13/23 (57%) patients with 0- or 1-vessel disease, as compared with 5/22 (23%) patients with 2- or 3-vessel disease (P

Background : In inferior wall acute myocardial infarction, maximal ST-segment depression in left precordial leads (V4–V6) has been shown to be associated with increased in-hospital mortality, presumably due to coronary artery disease involving the left anterior descending coronary artery system. Methods : We measured ST-segment deviation from baseline in the initial electrocardiogram of patients with inferior wall acute myocardial infarction, who subsequently underwent coronary angiography during their in-hospital stay. Patients were divided into three groups: (I) No precordial ST-segment depression ( n =34). (II) Maximal precordial ST-segment depression in leads V1–V3 ( n =44). (III) Maximal precordial ST-segment depression in leads V4–V6 ( n =14). Results : The left anterior descending coronary artery or its diagonal branch were stenosed (>50%) in 32%, 41%, and 71% of patients in groups I, II, and III, respectively ( p =0.04), and severely stenosed (>70%) in 18%, 18% and 57% of patients in the respective groups ( p =0.007). Conclusion : In patients with inferior wall acute myocardial infarction, maximal precordial ST-segment depression in leads V4–V6 is suggestive of severe coronary artery disease involving the left anterior descending coronary artery or its diagonal branch.

Ethanol causes vasodilation, which might have an adverse effect, due to increased obstruction of the left ventricular outflow tract, in patients with hypertrophic obstructive cardiomyopathy. We assessed the hemodynamic effects of the ingestion of ethanol, in an amount commonly consumed socially, in patients with hypertrophic cardiomyopathy.We performed echocardiography in 36 patients before and several times after the ingestion of either 50 ml of 40 percent ethanol or an isocaloric placebo with the aroma of rum. Each patient received both ethanol and placebo, on different days. The patients, but not the physicians, were blinded to the content of the drink. We measured the sizes of the left atrium and left ventricle, the left-ventricular-wall thickness, blood pressure, heart rate, the degree of systolic anterior motion of the mitral valve, and the pressure gradient across the left ventricular outflow tract.The ingestion of ethanol regulated in a significant drop in the mean (+/- SD) systolic blood pressure (from 130.5 +/- 18.6 to 122.5 +/- 20.3 mm Hg, P0.001), a significant increase in systolic anterior motion of the mitral valve (from a grade of 2.1 to a grade of 2.5, P0.001), and a 63 percent increase in the mean gradient across the left ventricular outflow tract (from 38.1 +/- 26.5 to 62.2 +/- 42.4 mm Hg, P0.001). These changes, which were not associated with symptoms, did not occur after the ingestion of placebo.The ingestion of a small amount of ethanol caused an increase in the gradient across the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy, which could have and adverse clinical effect.

The objective of the study was to identify patients with anterior wall acute myocardial infarction (AMI) at high risk of postinfarction left ventricular dysfunction (LVD). This study population included all patients admitted with a diagnosis of anterior wall AMI (ST segment elevation of1 mm in 2 or more precordial leads) without history or ECG evidence of antecedent AMI,who underwent assessment of left ventricular ejection fraction (LVEF) during emergency hospitalization. ST segment deviation from baseline was measured manually 0.08 s after the J point in all leads. Patients (n = 81) were classified into two groups based on the configuration of the QRS complex and ST segment: ST1 mm with preserved (pattern A; n = 60) or distorted terminal QRS (emergence of the J point at a level above the lower half of the R wave or disappearance of the S wave in leads with an Rs configuration; pattern B; n = 21). LVD (LVEF40%) was significantly more prevalent in patients with pattern B than pattern A (48 vs. 12%; p = 0.002). There was no correlation between the number of leads with ST segment elevation and LVD (p = 0.47). The sum of ST segment elevation in involved leads correlated weakly, yet significantly with LVEF (R = -0.22; p0.05). In conclusion, patients with anterior wall AMI and pattern B in the initial ECG are at high risk of post-AMILVD.

Summary: The purpose of the study was to determine whether the initial electrocardiographic pattern is predictive of in-hospital mortality in inferior wall acute myocardial infarction. It is commonly perceived that patients with acute myocardial infarction presenting with greater ST elevation have a worse prognosis. The initial electrocardiogram of patients (n = 213) with inferior wall myocardial infarction was categorized based on the pattern of ST-segment elevation in inferior leads: (A) ST

A total of 140 consecutive patients with acute Q-wave myocardial infarction was evaluated to assess the relationship between different electrocardiographic patterns of evolution and the incidence of recurrent ischemia within 10 days of infarction. Patients were allocated to three groups according to the electrocardiogram at 12 h after admission: Group A: ST elevation of2 mm and negative T waves (75 patients); Group B: ST elevation of2 mm and negative T waves (35 patients); Group C: ST elevation of2 mm and positive T waves (30 patients). Patients in Group C had more anterior wall infarctions (82%) than Group A (40%) or Group B (58%) (p = 0.0001). Peak creatine kinase levels were lower in Group A (782 +/- 115 IU) than in Groups B (1415 +/- 257 IU) and C (1501 +/- 287 IU) (p0.0001). The occurrence of post-infarction recurrent ischemia was more frequent in Group A (79.2%) than in Groups B (33.3%) and C (14.8%) (p0.0001). Patients in Group A had relatively smaller infarctions and a higher incidence of recurrent ischemia, whereas patients in Group C had larger infarctions and a lower incidence of recurrent ischemia. The electrocardiographic pattern 12 h after admission for acute myocardial infarction is helpful in identifying a subgroup at high risk of recurrent ischemia.

Previous studies have shown that ST depression in the precordial leads in inferior wall acute myocardial infarction (lAMI) is associated with increased in hospital mortality. However, no distinction has been made between maximal ST depression in the right versus left precordial leads. This study assesses the correlation between the pattern of precordial ST depression in the admission ECG and 30-day mortality in 1321 pts with IAMI. All pts were admitted within 6 hours from onset of symptoms and received either STK or tPA intravenously. Only pts with ST elevation ≥ 0.1 mV and positive T waves in at least two of the inferior leads were included. Pts were allocated into 4 groups: group A-no precordial ST depression (n = 346); group B-sum of ST depression in right leads (VI-V3) greater than the sum in left leads (V4–V6) (n = 700); group C-surn of ST depression in right leads equal to the surn in left leads (n = 162); and group D-rnaximal ST depression in V4–V6(n = 113). A total of 48 pts (3.6%) died. The mortality for group A, B, C, and D were 10 (2.9%), 20 (2.8%), 7 (4.3%), and 11 (9.7%), respectively. Using logistic regression model, only the following parameters were found to be independent predictors for 30-days mortality; Odds Ratio 95% Confidence Interval Sex (Females vs. Males) 2.39 1.15-4.94 Age (years): (60-69 vs. l60) 3.42 0.89-13.1 ( ≥ 70 vs. l 60) 13.4 3.85-46.3 Previous Myocardial Infarction 2.33 1.11-4.89 Diabetes Mellitus 1.95 0.92-4.12 Killip on Admission ( g 1vs. 1) 2.99 1.48-6.04 Peak CK Level (per 1000 IU) 1.28 1.02-1.61 Group B versus Group A 0.85 0.32-2.27 Group Cversus Group A 1.72 0.55-5.37 Group D versus Group A 2.84 0.94-8.59 Conclusions pts with IAMI and maximal ST depression in left precordial leads in the admission ECG, are at high risk for 3D-day mortality, while ST depression in the right precordial leads (Vl–V3) is not associated with increased risk.

In previous studies we have shown good correlation between different patterns of the admission ECG's and outcome in acute myocardial infarction (AM I). The current study assesses the correlation between patterns of the admission ECG and occurrence of reinfarction within 30 days of admission in 2603 pts with AMI enrolled in 25 centers in Israel for the GUSTO trial. All pts were admitted within 6 hours from onset of symptoms and received either STK or tPA intravenously. Only pts with ST elevation and positive T waves were included. Pts were allocated into 2 groups based on the absence (group A; 1232 pts) or presence (group B; 1371 pts) of distortion of the terminal portion of the QRS on the admission ECG: i.e. emergence of the J point at a level above the lower half of the R wave in leads with qR configuration or disappearance of the S wave in leads with an Rs configuration. There were no differences between the groups in the prevalence of previous angina, AMI, diabetes mellitus, hypertension, current smoking, anterior infarction, or the time elapsed from onset of symptoms to therapy. Using logistic regression model, only the following parameters were found to be independent predictors for reinfarction: Odds Ratio 95% Confidence Interval Pvalue Initial ECG Pattern 2.59 1.31-5.13 0.006 O wave on admission 2.32 1.15-4.68 0.05 Hypertension 2.05 1.10-3.84 0.02 Diabetes Mellitus (yes vs. no) 1.95 0.99-3.82 0.05 Distortion of the terminal portion of the QRS on the admission ECG is associated with significantly higher risk for reinfarction in pts with AMI undergoing thrombolytic therapy.