Early and Late Mortality Predictors in Patients with Acute Aortic Dissection Type B.

Background/Aim: Despite technological advances in diagnosis and treatment, in-hospital mortality with acute aortic dissection type B is still about 11%. The purpose of this study was to assess the risk factors for early and long-term adverse outcomes in patients with acute aortic dissection type B treated medically or with conventional open surgery. Methods: The present study included 104 consecutive patients with acute aortic dissection type B treated in our Center from January 1st, 1998 to January 1st, 2007. Patient demographic and clinical characteristics as well as in-hospital complications were reviewed. Univariate and multivariate testing was performed to identify the predictors of in-hospital (30-day) and late (within 9 years) mortality. Results: 92 (88.5%) patients were treated medically, while 12 (11.5%) patients with complicated acute aortic dissection type B were treated by open surgical repair. In-hospital complications occurred in 35.7% patients, the most often being acute renal failure (28%), hypotension/shock (24%), mesenteric ischemia (12%), and limb ischemia (8%). The in-hospital mortality rate was 15.7% and the 9-year mortality rate was 51.9%. Independent predictors of early mortality in patients with acute aortic dissection type B were uncontrolled hypertension (HR-20.69) and a dissecting aorta diameter >4.75 cm (HR-6.30). Independent predictors of late mortality were relapsing pain (HR-7.93), uncontrolled hypertension (HR-7.25), and a pathologic difference in arterial blood pressure (>20 mmHg) (HR-5.33). Conclusion: Knowledge of key risk factors may help with a better choice of treatment and mortality reduction in acute aortic dissection type B patients.

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.