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Serum albumin (SA) level is a powerful cardiovascular prognostic marker, suggested to be involved in regulation of platelet function. High on-aspirin platelet reactivity (HAPR) is associated with increased risk for deleterious cardiovascular events. The aim of the present study was to evaluate the association between HAPR and albumin levels in patients with stable coronary artery disease (CAD) treated with aspirin. Patients with known stable CAD, who were taking aspirin (75 to 100 mg qd) regularly for at least 1 month, were screened for the present study. Exclusion criteria: cancer, sepsis or acute infection, active inflammatory/rheumatic disease, recent major surgery, chronic liver failure, the administration of other antiplatelet drugs, nonadherence with aspirin and thrombocytopenia. Blood was drawn from the participants and sent for SA level and platelet function test (VerifyNow). HAPR was defined as aspirin reaction units (ARU)550. Overall 116 patients were analyzed; age 69 ± 10, 28% women. Twenty (17%) were hypoalbuminemic (≤3.5 g/dl). Hypoalbuminemic patients had similar characteristics to the normal albumin group except mildly higher creatinine in the former. SA levels were significantly lower in the hypoalbuminemic group (3.2 ± 0.2 g/dl vs 4.2 ± 0.4 g/dl, respectively, p0.001) whereas mean ARU was significantly higher compared with the normal albumin group (548 ± 45 vs 444 ± 66 ARU, respectively, p0.001). A significant inverse association was observed between SA and ARU with (R

Recent studies have suggested that clopidogrel response may vary significantly with age. Limited data are available exploring the age dependency of ex vivo aspirin response in young and old patients with stable coronary artery disease. Patients with stable coronary artery disease (n = 583) who had been treated with aspirin 75 to 325 mg/day for ≥1 week were recruited from a general cardiology practice. The study cohort was divided into 2 groups: patients aged75 years (n = 438) and patients aged ≥75 years (n = 145). Aspirin response was determined using the VerifyNow Aspirin Test, and resistance was defined as ≥500 or 550 aspirin reaction units (ARU). The independent predictive value of age on VerifyNow score (as a continuous function) was determined using multivariate linear regression, adjusted for gender, body mass index, and diabetes mellitus. Younger and older patients had similar baseline clinical profiles, including relative doses of aspirin therapy. The mean VerifyNow Aspirin Test score was significantly higher in patients aged ≥75 years: 450 ± 54 versus 434 ± 53 ARU (p = 0.0007). After accounting for the primary covariates, age remained a predictor of VerifyNow score (p = 0.007). Aspirin resistance on the basis of the 500-ARU cutoff was higher in older patients (19% vs 11%, p = 0.009), but there was no difference when the 550-ARU cutoff was used (7% vs 5%, p = 0.40). In conclusion, aspirin response differs significantly by age in patients with stable CAD.

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.

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.

The feasibility of coronary stenting without predilation is demonstrated in 240 patients. In all, 249 stents were placed. Primary implantation was successful in 93% of cases. In 17 lesions the stents could not be advanced through the stenotic lesion. The unexpanded stents were removed through the guiding catheter, and stenting was performed after prediction. Minor complications (side branch compromise and intimal dissection), which were successfully treated, occurred in 26 patients (10.6%).

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.

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.

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.

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