Role of glycoprotein IIb/IIIa inhibitors in unstable angina: current perspectives.
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Angina, Unstable↗
Biomedical subjects
D Hasdai
Publications and source records attributed to D Hasdai.
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.
Adult↗
Pathophysiology of precordial ST-segment depression in inferior wall acute myocardial infarction: an echocardiographic appraisal.
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, p < 0.05). 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.
Adult↗