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.

Impact on long-term mortality of access and non-access site bleeding after primary percutaneous coronary intervention.

OBJECTIVES: The influence of the bleeding site on long-term survival after the primary percutaneous coronary intervention (PCI) is poorly understood. This study sought to investigate the relationship between in-hospital access site versus non-access site bleeding and very late mortality in unselected patients treated with primary PCI. METHODS: Data of the 2715 consecutive patients with ST-segment elevation myocardial infarction treated with primary PCI, enrolled in a prospective registry of a high volume tertiary centre, were analysed. Bleeding events were assessed according to the Bleeding Academic Research Consortium (BARC) criteria. The primary outcome was 4-year mortality. RESULTS: The BARC type ≥2 bleeding occurred in 171 patients (6.3%). Access site bleeding occurred in 3.8%, and non-access site bleeding in 2.5% of patients. Four-year mortality was significantly higher for patients with bleeding (BARC type ≥2) than in patients without bleeding (BARC type 0+1), (36.3% vs 16.2%, p<0.001). Patients with non-access site bleeding had higher 4 year mortality (50.7% vs 26.5%, p=0.001). After multivariable adjustment, BARC type ≥2 bleeding was the independent predictor of 4 year mortality (HR 2.01; 95% CI 1.49 to 2.71, p<0.001). Patients with a non-access site bleeding were at 2-fold higher risk of very late mortality than patients with an access site bleeding (HR 2.62; 1.78 to 3.86, p<0.001 vs HR 1.57; 1.03 to 2.38, p=0.034). CONCLUSIONS: Both access and non-access site BARC type ≥2 bleeding is independently associated with a high risk of 4-year mortality after primary PCI. Patients with non-access site bleeding were at higher risk of late mortality than patients with access site bleeding.

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.

Temporal variations at the onset of spontaneous acute aortic dissection.

There have only been a few studies of the chronobiological occurrence of acute aortic dissection (AAD), and most were international and multicentered. The aim of the present study, conducted at only one center, was to determine the most frequent daily, monthly, and seasonal occurrences of AAD. The study population included 204 patients (66.5% male) treated at our institute between January 1, 1998 and January 1, 2004. A significantly higher frequency of AAD occurred from 6:00 AM to 12:00 noon, compared with other time periods (P < 0.001). The results showed a significant circadian variation in AAD (P < 0.001) with a peak between 9:00 AM and 10:00 AM. No significant variation was found for the day of the week; however, AAD occurred most frequently on Wednesday and Monday. The frequency of AAD was found to be significantly higher during winter versus other seasons (P < 0.001). The analysis of monthly variations of the onset of AAD confirmed a peak in February (12.9%) and in January (12.3%). Similar to other cardiovascular diseases, AAD exhibits significant circadian and seasonal/monthly variations. Our findings indicate that the prevention of AAD, especially during the aforementioned vulnerable periods, is possible by adequate tailoring of the treatment of hypertension, which is the main AAD predisposing factor.