Background: Cardiovascular complications are common in patients with obstructive sleep apnea (OSA). Blood rheology is a major determent of coagulation and an established risk factor for cardiovascular events. Since nocturnal hypoxemia could influence parameters of blood rheology, we hypothesized that OSA alters blood rheology independent of other cardiovascular risk factors. Methods: One hundred and ten consecutive patients admitted to the sleep laboratory were included. The association of plasma fibrinogen and viscosity (as parameters of blood rheology) with OSA was evaluated. Results: One hundred and ten patients aged 61.4 ± 10.1 years (body mass index 28.4 ± 4.1 kg/m²) were included. OSA was confirmed in 63 patients (57.2%) with an apnea-hypopnea index (AHI) of 28.7 ± 14.9 events/hour. Patients with OSA showed higher levels of plasma viscosity (1.36 ± 0.09 vs. 1.31 ± 0.08 mPas, p = 0.005). Nevertheless, hypertensive apneics have even higher levels of plasma viscosity than nonapneics (1.38 ± 0.091 vs. 1.32 ± 0.028 mPas, p = 0.018). Similar results were found in patients with coronary artery disease, where OSA was associated with elevated plasma viscosity (1.36 ± 0.076 vs. 1.31 ± 0.081 mPas, p = 0.007). Plasma fibrinogen was correlated with nocturnal minimal oxygen saturation (r = –0275, p = 0.0036) and AHI (r = 0.297, p = 0.001). OSA was associated with higher plasma fibrinogen (353 ± 83 vs. 317 ± 62 mg/dl, p = 0.015). These differences persist with control for cardiovascular risk factors. Conclusions: Patients with OSA have elevated morning fibrinogen levels and a higher plasma viscosity, which correlate positively with indices of sleep apnea severity. These changes in blood rheology are independent of cardiovascular risk factors, and therefore, might be specific mechanisms of OSA. This supports the pathophysiological concept that sleep apnea is a cardiovascular risk factor.

No abstract

PURPOSE AND DATA IDENTIFICATION: One of the main clinical problems of patients with arterial hypertension is the presence of arrhythmias, especially if left ventricular hypertrophy exists. Recent results from our group and all data available via Med-Line-search have been analysed. The analysis was focused on atrial and ventricular arrhythmias and arrhythmic risk prediction, using non-invasive markers. RESULTS OF ANALYSIS AND CONCLUSION: Arterial hypertension is a major cause of non-rheumatic atrial fibrillation and other supraventricular arrhythmias. The prevalence of ventricular arrhythmias is increased in hypertensive patients without left ventricular hypertrophy, compared to normotensives. If left ventricular hypertrophy is present, the risk for ventricular tachycardias is quadrupled. The presence of left ventricular hypertrophy is associated with an increase in all-cause mortality by a factor of seven in men and nine in women. In particular, patients with hypertrophy, increased rate of ventricular extrasystoles up to non-sustained ventricular tachycardia and ST-depression in long-term ECG are threatened by sudden cardiac death. At present, it is not possible to safely identify patients with increased risk. Regression of hypertrophy exists along with a decreased rate of ventricular extrasystoles. We hypothesize that by the regression of hypertrophy, the prevalence of sustained ventricular tachycardia decreases and therefore the prognosis of those patients can be improved, although controlled studies are not yet available.

Intensive care unit (ICU) support following allogeneic peripheral blood stem cell transplantation (PBSCT) is controversial due to the limited prognosis of these patients in case of secondary critical illness. In this retrospective single centre study, we looked for factors predicting survival in patients who needed ICU support after myeloablative (MAC) or non-myeloablative conditioning (non-MAC) therapy and allogeneic PBSCT. Between 1999 and 2006, 64 out of 319 patients following allogeneic PBSCT were admitted to the ICU (24 female and 40 male patients, median age 47 years, range 17-65 years; MAC 49 patients, non-MAC 15 patients). All 64 patients required mechanical ventilation. We looked for variables defining the Sepsis-related Organ Failure Assessment (SOFA) score as well as for baseline characteristics and transplant-associated parameters on the day of ICU admission possibly predictive for poor or good survival prognosis. Nineteen of 49 patients who had received MAC therapy survived the ICU stay for a median time of 9 months (range 2-29 months) and three of 15 patients who had received non-MAC therapy could be discharged from the ICU with a survival time of 4, 5 and 12 months. After univariate and multivariate analysis the SOFA score discriminated survivors and non-survivors of the ICU stay. We conclude that the SOFA score is predictive for survival when applied on the day of ICU admission.

The incidence of post-operative AF among high-risk patients was significantly reduced by a prophylactic amiodarone treatment resulting in a shorter time of intensive care unit and hospital stay. Our data supports the prophylactic use of amiodarone in peri-operative period in patients at high risk for AF after CABG.

Inappropriate sinus tachycardia is a disease which is relatively rarely found and sometimes difficult to treat. Up to now it has been mostly treated with a β-blocker or verapamil. If this did not work sinus node modulation was considered. Since the relatively new selective IF-stream blocker ivabradine has been approved for the therapy of chronic stable angina pectoris, a new therapeutic option is available. As ivabradine is well tolerated and only few side effects are known, it may become a new therapeutic step between medication and the invasive sinus node modulation. We report the case of a young female patient with inappropriate sinus tachycardia where a sustained therapeutic success was achieved with ivabradine medication as an alternative therapeutic trial after various ineffective medications.

No abstract

Our results show that a P-SAECG, an analysis of CHRS, and left atrial enlargement are clinical predictors of a progression from PAF to PEAF.