Mitral annular calcification predicts cardiovascular morbidity and mortality in middle-aged patients with atrial fibrillation: the Belgrade Atrial Fibrillation Study.

BACKGROUND: Mitral annular calcification (MAC) has been suggested as a reliable, time-averaged marker of atherosclerosis and is associated with coronary artery disease, heart failure, ischemic stroke, and increased mortality. Data on the relationship between MAC and cardiovascular morbidity and mortality in atrial fibrillation (AF) are sparse, with the exception of the relationship between MAC and stroke. We investigated the association of MAC with cardiovascular morbidity, stroke, cardiovascular mortality, and all-cause death in a cohort of middle-aged patients with AF with a mean 10-year follow-up. METHODS: This was an observational study of patients with nonvalvular AF between 1992 and 2007. RESULTS: Of 1,056 patients, 33 (3.1%) had MAC; they were more likely to be older and female and to have a dilated left atrium, reduced left ventricular ejection fraction, permanent AF, hypertension, and/or diabetes mellitus (all P < .05). Total follow-up was 10,418.5 years (mean, 9.9 ± 5.9 years), and the mean age was 52.7 ± 12.2 years. In univariate analysis, MAC was associated with all-cause death, cardiovascular death, stroke, new cardiac morbidity (all P < .05), and the composite end point of ischemic stroke, myocardial infarction (MI), and all-cause death (P < .001). In multivariate analyses, MAC was related to all-cause death (hazard ratio [HR], 4.3; 95% CI, 1.8-10.0; P < .001), cardiovascular death (HR, 3.5; 95% CI, 1.2-10.4; P = .025), the composite end point (HR, 2.1; 95% CI, 1.0-4.3; P = .048), and new cardiac morbidity (HR, 2.4; 95% CI, 1.3-4.5; P = .005). There was no significant relationship between MAC and stroke or MI in the multivariate analyses. CONCLUSIONS: MAC is associated with increased cardiovascular morbidity, cardiovascular mortality, and all-cause mortality of patients with AF. MAC should be acknowledged as a marker of increased cardiovascular risk in middle-aged patients with AF.

The long-term risk of stroke in patients with acute myocardial infarction complicated with new-onset atrial fibrillation.

BACKGROUND: The long-term risk of stroke after acute myocardial infarction (AMI) complicated with new-onset atrial fibrillation (AF) remains unclear. The aim of this study was to determine the long-term risk of AF and stroke in patients with AMI complicated with new-onset AF. METHODS: Patients with AMI complicated with new-onset AF (n = 260) and those without new-onset AF (n = 292) were followed for a mean of 7 years. All patients had sinus rhythm at hospital discharge. RESULTS: During the follow-up, AMI patients with new-onset AF had more frequent AF than those without new-onset AF (10.4% vs 2.7%, respectively; P < 0.0001). New-onset AF during AMI was a significant predictor of subsequent AF occurrence (the time elapsing between 2 consecutive R waves [RR] = 3.15, P = 0.004); but AF recurrence in follow-up (RR = 5.08, P = 0.001) and non-anticoagulation at discharge (RR = 0.29, P = 0.008) were independent predictors of stroke (Cox regression analysis). A period of 3.5 hours of AF within the first 48 hours of AMI was the high sensitivity cut-off level for the prediction of low long-term risk of stroke obtained by receiver operating characteristic analysis. Among patients who did not receive anticoagulants at discharge, the patients with short AF did not experience stroke and AF recurrence during follow-up, while those in the other group developed it (10.8%, P = 0.038 and 13.5%, P = 0.019, respectively). CONCLUSION: New-onset AF during AMI identifies the patients at long-term risk for stroke who may potentially benefit from anticoagulant therapy. Atrial fibrillation recurrence in follow-up was independently related to the development of stroke. However, for low-risk patients with AF (those with short AF occurring early in AMI) long-term anticoagulants might not be required.

Carvedilol increases copper-zinc superoxide dismutase activity in patients with acute myocardial infarction.

Balanced and coordinated antioxidant defence enzyme activities are of utmost importance for correct physiological function and for shielding against unwelcome pathological conditions. We determined the activities of copper-zinc superoxide dismutase (CuZnSOD), catalase, glutathione peroxidase and glutathione reductase in erythrocytes isolated from patients receiving different therapy (streptokinase alone or in combination with metoprolol or with carvedilol) for up to 168 hr after starting treatment for acute myocardial infarction. We observed increased CuZnSOD activity in erythrocytes isolated from patients treated with streptokinase-carvedilol (after 6, 24 and 168 hr) and in erythrocytes isolated from patients treated with streptokinase-metoprolol (after 24 hr). In addition, positive correlation between CuZnSOD and catalase activities was found in erythrocytes isolated from patients that received streptokinase-carvedilol after 168 hr. As metoprolol does not react directly with hydrogen peroxide, it would appear that combined streptokinase-metoprolol therapy exerted its effects primarily via by beta-blockade whereas combined streptokinase-carvedilol therapy appeared to function via both beta-blockade and direct antioxidant mechanisms.