Yochai Birnbaum

Prediction of the level of left anterior descending coronary artery obstruction during anterior wall acute myocardial infarction by the admission electrocardiogram

T he ability to predict the exact site of the occlusion of the infarct-related artery by a noninvasive method shortly after admission to the hospital may help the clinician in estimating the myocardial area at risk and planning therapeutic interventions. This is important especially for anterior wall acute myocardial infarction (M), because proximal left anterior descending (LAD) coronary artery disease has a poor prognosis.‘” The electrocardiogram is quite reliable in detecting anterior wall AMF9 or infarction caused by LAD coronary artery obstruction. l”,ll Based on the electrocardiogram, several subtypes of anterior wall AMI are recognized (anteroseptal, anterolateral, apical, and so forth)12; however, correlation of the various electrocardiographic patterns with the exact anatomic location of the infarct as determined by autopsy is poor.7,8,12 This study assesses the value of ST changes in the various electrocardiographic leads during evolving anterior wall AMI in predicting the location of the LAD coronary artery obstruction in relation to the origin of the tirst diagonal branch. All patients admitted to the coronary care unit with AM from July 1988 to November I992 were evaluated retrospectively. Patients who underwent coronary angi-

Prognostic significance of maximal precordial St-segment depression in right (V1 to V3) versus left (V4 to V6) leads in patients with inferior wall acute myocardial infarction

This study examines whether patients with inferior wall acute myocardial infarction (AMI) and maximal ST-segment depression in left precordial leads are at higher risk for in-hospital mortality. The charts of patients (n = 213) with inferior wall AMI and an initial electrocardiogram that displayed peaked, tall T waves or ST-segment elevation with upright T waves in inferior leads were reviewed, after excluding patients with inverted T waves in inferior leads (n = 75). ST-segment deviation from baseline was measured for all leads. Patients were classified into 3 types: I = no precordial ST-segment depression; II = 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; and III = maximal precordial ST-segment depression in leads V4 to V6. Thirty-six patients (17%) died in the hospital. In-hospital mortality rates for patients with types I and II were 12% and 10%, respectively, compared with 41% for those with type III (p < 0.0001). Mortality rates in surviving patients were similar for all types up to 1 year after infarction. Multivariate logistic regression models for in-hospital mortality by ST-segment depression type adjusted for age, previous AMI, diabetes mellitus, and thrombolytic therapy revealed that type III pattern was a strong predictive factor for in-hospital mortality (odds ratio = 4.9, p = 0.0008, 95% confidence interval 1.93 to 12.26). Thus, patients with inferior wall AMI and maximal precordial ST-segment depression in leads V4 to V6 are at high risk for in-hospital mortality.

Polymorphous ventricular tachycardia early after acute myocardial infarction

Abstract Ventricular tachyarrhythmias are a major cause of cardiac death within the early hours of an evolving acute myocardial infarction. Diverse cytochemical and metabolic alterations develop in the ischemic and periischemic zones after coronary artery occlusion and subsequent reperfusion. 1,2 These alterations change rapidly over time and may cause various morphologically distinct ventricular arrhythmias in the different stages of an acute myocardial infarction. 1,3 One type of malignant ventricular tachyarrhythmia that appears during an acute myocardial infarction is polymorphous ventricular tachycardia (VT). 3,4 The electrophysiologic mechanism and the therapy differ from those of other forms of VT. 5,6 The occurrence of polymorphous VT in the early stages of an acute myocardial infarction has been infrequently reported, 4 although an incidence of 1.2 to 2% during overall hospitalization for acute myocardial infarction had been reported. 4 This report describes the clinical and electrocardiographic features of patients with polymorphous VT in the early stages of an evolving acute myocardial infarction.

Acute myocardial infarction entailing ST-segment elevation in lead aVL: Electrocardiographic differentiation among occlusion of the left anterior descending, first diagonal, and first obtuse marginal coronary arteries

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%).

Plasma homocysteine, methylenetetrahydrofolate reductase genotypes, and age at onset of symptoms of myocardial ischemia

Elevated fasting plasma homocysteine is a graded risk factor of coronary artery disease (CAD) and may accelerate onset of CAD. Homozygosity for the C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is commonly but inconsistently associated with hyperhomocysteinemia. In the present study we examined the possible relation between levels of fasting plasma homocysteine and age at CAD onset in different MTHFR genotypes. We studied 182 patients with CAD, 74 patients with early onset CAD (aged < or = 45 years), and 108 patients with later onset CAD (aged 46 to 65 years). Plasma homocysteine levels in 90 subjects without CAD were used for control. Fasting plasma homocysteine levels in T/T homozygotes with early onset CAD (20.2 +/-12.5 micromol/L) was markedly higher than in T/T homozygotes with later onset CAD (13.4 +/- 6.8 micromol/L) and in patients with early onset CAD who were not T/T homozygotes (11.9 +/- 3.7 micromol/L; p = 0.034 and p = 0.0001, respectively). CAD developed earlier in T/T homozygotes who were hyperhomocysteinemic (>15 micromol/L) than in the T/T homozygotes who were not (p = 0.036). Plasma homocysteine levels had no effect on age at onset of CAD in patients who were non-T/T genotypes. Homocysteine levels in control subjects and in patients who were non-T/T genotypes were comparable and were not influenced by age. The results reveal an inverse relation between the level of fasting plasma homocysteine and age at onset of CAD in T/T homozygotes as opposed to no association in patients who were non-T/T genotypes. Additionally, these results show that hyperhomocysteinemia and the T/T genotype have a stronger effect on the pathogenesis of CAD when they are combined, and that a marked increase (>15 micromol/L) in fasting plasma homocysteine in T/T homozygotes is a risk factor for early onset of CAD.

Clinical significance and predisposing factors to symptomatic bradycardia and hypotension after percutaneous transluminal coronary angioplasty

Of 180 consecutive patients who underwent uneventful percutaneous transluminal coronary angioplasty (PTCA), 25 (13.9%) had at least 1 episode of symptomatic bradycardia and hypotension during the early postprocedure period. Symptomatic bradycardia and hypotension occurred 1 to 10 hours (mean 4 +/- 2) after PTCA. A higher incidence of symptomatic bradycardia and hypotension was found in patients receiving regular treatment with beta blockers (26% vs 10% in patients without beta blockers in their regimen, p < 0.01), diltiazem or verapamil (20% vs 9%, p < 0.025), or both a beta blocker and diltiazem or verapamil (64% vs 11%, p < 0.001). A higher incidence was also associated with angioplasty of the left anterior descending coronary artery compared with angioplasty of the other coronary arteries (22% vs 8%, p < 0.01). It is concluded that symptomatic bradycardia and hypotension is a common occurrence after PTCA. The incidence is higher after PTCA to the left anterior descending coronary artery and in patients receiving diltiazem, verapamil, and beta-blocking agents; it is particularly high in patients receiving a combination of a beta-blocking agent and either diltiazem or verapamil.

Maximal precordial ST-segment depression in leads V4–V6 in patients with inferior wall acute myocardial infarction indicates coronary artery disease involving the left anterior descending coronary artery system

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.

Electrocardiographic Q-Waves Inconstancy during Thrombolysis in Acute Anterior Wall Myocardial Infarction

It is the purpose of this paper to describe the electrocardiographic inconstancy of Q-waves during administration of thrombolytic therapy. This was documented in four patients given streptokinase early in the course of anterior wall myocardial infarction. Understanding the pathogenesis of sequential dynamic variations of Q-waves in this setting may offer important insights into coronary physiology and management of acute coronary events. We discuss the possible explanations for such changes with respect to tissue viability, dynamic vascular changes and electrophysiological properties of the reperfused infarcted myocardium.

Predicting postinfarction left ventricular dysfunction based on the configuration of the QRS complex and ST segment in the initial ECG of patients with a first anterior wall myocardial infarction.

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 of > 1 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: ST > 1 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 (LVEF < 40%) 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; p < 0.05). In conclusion, patients with anterior wall AMI and pattern B in the initial ECG are at high risk of post-AMILVD.

Spontaneous hemarthrosis following thrombolytic therapy for acute myocardial infarction

We describe a 45-year-old man who developed a spontaneous hemarthrosis of his right knee following thrombolytic therapy with streptokinase and rtPA for acute myocardial infarction. Surprisingly, despite the wide use of thrombolytic therapy, only four cases of spontaneous hemarthrosis following thrombolysis have been previously reported. Prompt aspiration of the joint, after stopping anticoagulant therapy, and splinting will provide early diagnosis and may prevent further damage to the joint.