[Rehabilitation standards for follow-up treatment and rehabilitation of patients with ventricular assist device (VAD)]. / Rehabilitationsstandards für die Anschlussheilbehandlung und allgemeine Rehabilitation von Patienten mit einem Herzunterstützungssystem (VAD - ventricular assist device).

The increasing use of ventricular assist devices (VADs) in terminal heart failure patients provides new challenges to cardiac rehabilitation physicians. Structured cardiac rehabilitation strategies are still poorly implemented for this special patient group. Clear guidance and more evidence for optimal modalities are needed. Thereby, attention has to be paid to specific aspects, such as psychological and social support and education (e.g., device management, INR self-management, drive-line care, and medication).In Germany, the post-implant treatment and rehabilitation of VAD Patients working group was founded in 2012. This working group has developed clear recommendations for the rehabilitation of VAD patients according to the available literature. All facets of VAD patients' rehabilitation are covered. The present paper is unique in Europe and represents a milestone to overcome the heterogeneity of VAD patient rehabilitation.

[Benefit of cardiac examination in competitive sports]. / Nutzen von kardiologischen Vorsorgeuntersuchungen beim Leistungssport.

The sudden and unexpected death in young athletes is always a tragic event. At the age < 35 years distinct structural cardiac disorders such as hypertrophic cardiomyopathy, inflammatory disorders, coronary artery anomalies, as well as conditions without structural cardiac abnormalities such as primary electrical diseases (Brugada's syndrome, long QT, short QT syndrome and catcholaminergic polymorphic ventricular tachycardia) are important causes of sudden death. At the age > 35 years coronary artery disease is the most common cause of cardiac death in athletes. In this review we give an overview about actual evaluation of competitive athletes and prevention of sudden cardiac death.

[Competitive karate and the risk of HIV infection--review, risk analysis and risk minimizing strategies]. / Wettkampfkarate und die Gefahr einer HIV-Infektion--Ubersicht, Risikoanalyse und Strategien zur Risikominimierung.

Bleeding facial injuries are not uncommon in competitive karate. Nevertheless, the risk of an infection with HIV is extremely low. Guidelines about the prevention of HIV infections are presented. Especially in contact sports and martial arts the athletes, judges and staff have to recognize and employ these recommendations. Bleeding wounds of the hands due to contact with the opponents teeth can be minimized by fist padding.

[Impairment of ventilatory parameters and exercise capacity in patients with pulmonary hypertension and chronic heart insufficiency]. / Einschränkung der Ventilationsparameter und Belastbarkeit durch pulmonale Hypertonie bei chronischer Herzinsuffizienz.

BACKGROUND AND OBJECTIVE: Chronic heart failure often coincides with secondary pulmonary hypertension. In this study the influence of pulmonary hypertension on exercise capacity and ventilatory parameters in patients with chronic heart failure was examined. PATIENTS AND METHODS: 21 patients with chronic heart failure (six women, 15 men, mean age 55 +/- 10 years) and a left ventricular ejection fraction of 25 % +/- 5 % were studied by right heart catheterization, bodyplethysmography including carbonmonoxide diffusion testing and spiroergometry. Seven patients suffered from ischemic and 14 patients from dilative cardiomyopathy. Pulmonary hypertension (defined as pulmonary artery mean pressure > 25 mmHg) was found in ten patients. RESULTS: Patients with pulmonary hypertension showed a reduced vital capacity (75 % +/- 20 % of normal values vs. 93 % +/- 14 % of normal values, p < 0.001), a lower forced expiratory volume in one second (FEV1 68 % +/- 21 % of normal values vs. 91 % +/- 15 % of normal values, p < 0.001), and a reduced carbonmonoxide-diffusing capacity (58 % +/- 21 % vs. 77 % +/- 21 %, p < 0.001) compared to patients without pulmonary hypertension. Mean expiratory flow at 25 % and 75 % of the exspiration time was lower in patients with pulmonary hypertension (30 % +/- 13 % vs. 50 % +/- 29 % and 62 % +/- 25 % vs. 81 % +/- 20 %, each p < 0.05). In patients with pulmonary hypertension, the flow-volume diagram characteristically showed signs of "small airway disease". Spiroergometry revealed a significantly lower maximum oxygen-uptake (12.5 +/- 2.1 vs. 15.2 +/- 4.1 ml/min/kg, p < 0.05), oxygen-uptake at the anaerobic threshold (9.7 +/- 1.6 vs. 12.0 +/- 3.0 ml/min/kg, p < 0.05), carbon dioxide ventilatory efficiency (EqCO2 38 +/- 9 vs. 31 +/- 3, p < 0.05) and ventilatory reserve (39 % +/- 22 % vs 51 % +/- 21 %, p < 0.05) in patients with pulmonary hypertension. CONCLUSION: In patients with chronic heart failure the presence of pulmonary hypertension leads to a reduction of exercise capacity and impaired ventilatory parameters. Lung functional testing reveals bronchial obstruction, "small airway disease" and a reduced ventilatory efficiency.

Activation of ATP-sensitive potassium channels in hypoxic cardiac failure is not mediated by adenosine-1 receptors in the isolated rat heart.

BACKGROUND: Hypoxic cardiac failure is accompanied by action potential shortening, which in part might be a consequence of opening of cardiac ATP-sensitive potassium channels (K(ATP) channels). Coupling of the adenosine-1 receptor (A-1 receptor) to these channels has been described; however, the interaction of A-1-receptors and K(ATP) channels in different models of ischemia is still under debate. The hypothesis as to whether A-1 receptors are involved in hypoxic K(ATP) channel-activation in the saline-perfused rat heart was tested. METHODS AND RESULTS: Pharmacologic modulation of the K(ATP) channel by Glibenclamide (inhibitor) and Rimalkalim (activator) and of the A-1 receptor by R(-)-N6-(1-methyl-2-phenylethyl)-adenosine (R(-)-PIA, agonist) and 1,3-diethyl-3,7-dihydro-8-phenyl-purine-2,6-dione (DPX, antagonist) at different oxygen tensions (95% O2 and 20% O2) was performed in isolated Langendorff-rat hearts. Peak systolic pressure (PSP, intraventricular balloon), duration of monophasic action potential (epicardial suction electrode, time to 67% of repolarization: MAP(67%)), coronary flow, and heart rate (HR) were registered. Hypoxic perfusion resulted in a significant reduction of PSP (from 106 +/-11 to 56 +/-8 mmHg, P < 0.005) and shortening of MAP(67%) (from 37 +/-3 to 25 +/-4 ms, P < 0.005). With application of 1 microM Glibenclamide, MAP(67%) returned to normoxic values and PSP increased to 78 +/-9 mmHg (P < 0.005 vs hypoxia). In normoxia, 2 microM Rimalkalin resulted in reduction of MAP(67%) and PSP, which was reversed by Glibenclamide. Application of 0.1 microM R(-)-PIA in normoxia resulted in a decrease of HR (from 235 +/-36/min to 75 +/-41/min, P < 0.005), which was accompanied by an increase of PSP from 96 +/-7 to 126 +/-9 mmHg (P < 0.05) without changes in MAP(67%). These effects were reversible by 1 microM DPX and remained unaffected by application of 1 microM Glibenclamide. Application of 1 microM DPX in hypoxia had no effect on the measured parameters. CONCLUSION: In isolated rat hearts, the K(ATP) channel-system is activated in hypoxic cardiac failure and contributes to action potential shortening and reduced contractile performance. These effects seem to be independent of the A-1 receptor in this model.

[Remission of nocturnal pathological respiratory patterns after orthotopic heart transplantation. A case report and overview of current status of therapy]. / Sistieren nächtlicher pathologischer Atmungsmuster nach orthotoper Herztransplantation. Ein Fallbericht sowie eine Ubersicht über den aktuellen Stand der Therapie.

BACKGROUND: Cheyne-Stokes respiration is characterized by recurrent phases of central apneas during sleep alternating with a crescendo-decrescendo hyperventilation. This abnormal respiratory pattern is often observed in patients with severe congestive heart failure and associated with fragmentation of sleep, excessive daytime sleepiness, and a relatively high mortality. Increased peripheral and central chemosensitivity, prolonged circulation time, and reduced blood gas buffering capacity are the major factors contributing to the pathology. However, the exact pathophysiologic mechanisms are not clear yet. Respiratory stimulants, oxygen and continuous or bilevel positive airway pressure (CPAP or BiPAP) might reduce the severity of Cheyne-Stokes respiration but have little effect on daytime sleepiness and cardiac function. There is only limited data supporting the assumption that intensive heart failure therapy has an effect on Cheyne-Stokes respiration. CASE REPORT: A 55-year-old male patient with dilative cardiomyopathy (NYHA IV) suffered excessive daytime sleepiness (Epworth Sleepiness Scale: 24 points). The patient was a heavy snorer with a normal body mass index. Treatment was initiated including ACE-inhibitors, beta-receptor blockers, diuretics and digoxin. The patient underwent sleep analysis with a Somno-Check system which demonstrated Cheyne-Stokes breathing (Respiratory Disturbance Index RDI: 40/h, lowest desaturation 76%) and body position dependent snoring. Oxygen therapy (21/min) had no effect on daytime sleepiness. Due to the cardiac condition, the patient was accepted for heart transplantation. Three weeks after transplantation sleep analysis was repeated and demonstrated a lack of evidence for periodic breathing (RDI 1/h, no desaturations below 90%), while snoring remained unchanged. Daytime sleepiness improved significantly (Epworth Sleepiness Scale: 6 points). Three weeks after normalizing left ventricular function a complete recovery from severe Cheyne-Stokes respiration was observed. CONCLUSION: Adequate therapy of the underlying cause of Cheyne-Stokes breathing such as end-stage congestive heart failure might sufficiently abolish any breathing abnormalities.

Relation between enzyme release and irreversible cell injury of the heart under the influence of cytoskeleton modulating agents.

The effects of agents modulating the cytoskeleton, taxol (microtubuli stabilizing), vinblastine (microtubuli destabilizing) and cytochalasin D (actin destabilizing) (10(-6) M each) on enzyme and ATP release as well as on irreversible cell injury were investigated in isolated perfused hypoxic and reoxygenated rat hearts. Enzyme (creatine kinase (CK)) and ATP concentration were assayed in the interstitial transudate and venous effluent. Irreversible cell injury was determined from trypan blue uptake and nuclear staining (NS) of cardiomyocytes in histologic sections. ATP release from nonneuronal cells was only detectable in the interstitial transudate and was not significantly altered by the agents. In controls total CK release (about 4% of total CK) exceeded the percentage of irreversibly injured cells by a factor of 8. Taxol and cytochalasin D abolished the hypoxia/reoxygenation induced interstitial CK release and reduced total CK release to a highly significant extent. The percentage of irreversible injured cells was even more diminished by these agents resulting in a ratio of CK/NS of 40. The effect of cytochalasin D apparently is the consequence of decreased contractile performance as shown by analogous depression by butonedione monoxine (BDM), whereas contractile activity was not altered by taxol. Vinblastine had no influence on CK release but increased the number of irreversibly injured cells significantly. In conclusion, cytoskeletal elements apparently participate in the hypoxia/reoxygenation induced process of release of cytosolic enzymes (CK) and irreversible injury in a different way and extent. Taxol exhibits a cytoprotective effect in isolated perfused rat hearts as evaluated by the extent of enzyme release and irreversible cell injury.