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The clinically available IIb/IIIa antagonists have been studied in small angiographic trials of patients who receive these adjuncts combined with reduced doses of fibrinolytics for the purpose of evaluating their impact on infarct artery patency restoration in acute myocardial infarction. Larger clinical endpoint trials have then looked at some of these combinations, particularly with abciximab, to characterize mortality, morbidity and adverse event frequencies when compared with more traditional full dose fibrinolytic therapy. Similarly these agents have been evaluated (without fibrinolytics) for their potential to improve the results of mechanical reperfusion techniques. This article will summarize these experiences in terms of benefits and adverse events. The value of these drugs in STEMI seems modest at best.

Background: The grade of ischemia, as detected by the relation between the QRS complex and ST segment on the admission electrocardiogram, is associated with larger infarct size and increased mortality rates in acute myocardial infarction., Methods: We assessed the correlation between left ventricular function and the admission electrocardiogram in 151 patients with first anterior acute myocardial infarction who received thrombolytic therapy and underwent cardiac catheterization at 90 minutes and before hospital discharge. The number of leads with ST elevation, sum of ST elevation, maximal Selvester score, and the presence of severe (grade 3) ischemia were determined in each electrocardiogram. Left ventricular ejection fraction, the number of chords with wall motion abnormalities, and the severity of dysfunction (SD/chord) were determined., Results: At 90 minutes, the 39 ischemia grade 3 patients had lower ejection fraction than the 112 grade 2 patients. Both at 90 minutes and at hospital discharge, the grade 3 group had more chords with wall motion abnormalities and more severe regional dysfunction (SD/chord). However, the number of leads with ST elevation, sum of ST elevation, and maximal Selvester score had no correlation with ejection fraction at 90 minutes and only mild correlation with the extent of dysfunction (number of chords) at 90 minutes. There was no correlation between either the number of leads with ST elevation or the sum of ST elevation and the severity of regional dysfunction., Conclusions: The number of leads with ST elevation, sum of ST elevation, and maximal Selvester score had only mild correlation with the extent of myocardial dysfunction but not with the severity of dysfunction. Grade 3 ischemia is predictive of more extensive myocardial involvement and greater severity of regional dysfunction.

This study assessed whether differences in the underlying mechanisms for various patterns of precordial ST-segment depression with inferior acute myocardial infarction (AMI) are associated with poorer prognoses. We studied 1,155 patients with inferior AMI who underwent thrombolysis in the Global Utilization of Streptokinase and TPA for Occluded arteries (GUSTO-I) angiographic substudy: those without precordial ST depression (n = 412; 35.7%), those with maximum ST depression in leads V1 to V3 (n = 547; 47.4%), and those with maximum ST depression in leads V4 to V6 (n = 196; 17.0%) on admission electrocardiogram. We compared the infarct-related artery, presence of left anterior descending or multivessel coronary artery disease, and left ventricular function among groups. Patients with maximum ST depression in leads V4 to V6 more often had 3-vessel disease (26.0%) than those without precordial ST depression (13.5%) or those with ST depression in leads V1 to V3 (15.7%; p = 0.002), and they had a lower ejection fraction (median 54% vs 60% and 55%, respectively; p <0.001). Patients with maximum ST depression in leads V1 to V3 less often had AMIs due to proximal right coronary artery obstruction (23.9%) than patients without precordial ST depression (35.2%) or those with ST depression in leads V4 to V6 (40.0%; p = 0.001) and had larger AMIs as estimated by peak creatine kinase. Different patterns of precordial ST depression are associated with distinctive coronary anatomy. ST depression in leads V4 to V6, but not V1 to V3, confers a greater likelihood of multivessel coronary artery disease.

Signal-averaged electrocardiograms were performed in 225 patients with serologic evidence of human immunodeficiency virus infection as part of a prospective longitudinal study of patients with HIV-associated heart disease and 12 seronegative control subjects. The duration of signal-averaged QRS vector, root-mean-square voltage of the terminal 40 ms of the vector magnitude and the duration of the low-amplitude (less than 40 microV) signal were determined during serial visits at 4-month intervals. One or more of these variables was abnormal on initial visit in 59 of patients (26%); QRS duration was greater than 114 ms in 9 patients (4%), root-mean-square voltage less than 20 microV in 55 patients (24%) and low-amplitude signal duration greater than 39 ms in 43 (19%). In contrast, none of the seronegative control subjects had any abnormal variables (p less than 0.03). During follow-up (mean 10 +/- 8 months), 26 patients with initially normal studies developed abnormal variables and 24 with abnormal signal-averaged electrocardiograms reverted to normal. Left ventricular contractility was assessed by echocardiography using the rate-corrected velocity of fiber shortening-end-diastolic wall stress relation. Late potentials were not related to contractile abnormalities. Clinical arrhythmias were rare and did not appear more frequent among patients with late potentials. Thus, late potentials were both common and evanescent in patients infected with human immunodeficiency virus.

The long-term prognostic implications of the electrocardiographic location of a myocardial infarction and the subsequent retention or disappearance of diagnostic Q waves were examined in patients enrolled in the Aspirin Myocardial Infarction Study (AMIS). The 4524 participants, ages 30-69 years, had sustained a myocardial infarction 8 weeks to 60 months before randomization to aspirin and placebo groups. Subjects were followed for at least 3 years (average 38.2 months). Using the Minnesota Code, myocardial infarctions were classified according to three electrocardiographic locations: lateral, inferior and anterior, with further subdivision into major, moderate and minor criteria based on Q-wave duration and Q/R rations. Total mortality was not significantly different among patients with single infarct sites: lateral 11.8%, inferior 8.0% and anterior 9.4%. Patients with multiple electrocardiographic infarct locations had a significantly higher mortality (14.6%, p less than 0.0002). Participants with Minnesota Code major criteria of infarction also had a significantly higher mortality (10.6%) than those with moderate (7.2%) or minor (7.4%) criteria (p less than 0.01). Loss of a previously documented diagnostic Q wave occurred in 14.2% of participants. Mortality among patients who lost Q waves (6.5%) was not significantly different from that among those with persistent Q waves in a single infarct location (8.7%). No long-term prognostic significance can be attributed to the site of infarction or loss of Q wave on the resting ECG. However, major Q-wave criteria and extent of infarction based on multiple coded sites are associated with a higher 3-year mortality.

We evaluated the recently proposed concern that ECG anterior ST segment depression in patients with acute inferior wall myocardial infarction represents an additional area of ischemia and therefore implies worsened prognosis. We studied patients enrolled in the Aspirin Myocardial Infarction Study (AMIS), ages 30 to 69 years, who sustained an inferior myocardial infarction within 6 months from the start of the study. Two hundred nineteen patients who met those criteria were followed for an average of 38.2 months. One hundred ten patients had significant anterior lead ST depression (greater than or equal to 0.1 mV) during their acute inferior infarction and their 3-year mortality rate was 9.1%. One hundred nine patients had no anterior ST abnormality and a mortality rate of 10.1% (p = ns). Only one patient with significant depression had a subsequent anterior wall myocardial infarction. Anterior ST depression correlated closely with the magnitude of inferior ST segment elevation. Since ST depression does not alter long-term mortality but relates to magnitude of ST elevation, it probably represents a reciprocal change.

Sinoventricular rhythm implies preserved sinus node function with conduction of impulses to the A-V junction without generalized atrial excitation. Impulse propagation in such cases is presumably via specialized internodal tracts. In this present case, synchronized but localized activation from an area of the right atrium preceded each QRS, without generalized atrial depolarization. These recordings are offered as further evidence for the clinical occurrence of sinoventricular rhythm in humans.