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Background: The cardiomyocyte cytoskeleton may be altered in chronic ischemia as well as in dilated cardiomyopathy. Carvedilol, a beta-blocking agent with alpha-blocking properties, is widely used for the treatment of heart failure. In addition to its beta-adrenergic and alpha-receptor blockade, additional cardioprotective, antioxidant and antiapoptotic effects have been demonstrated in experimental models. Whether carvedilol exhibits additional effects on the cytoskeleton in myocardial ischemia is unknown. We hypothesized that cytoskeleton stabilization is cardioprotective while cytoskeleton destabilization increases myocardial injury. Further, we hypothesized that carvedilol has a cytoskeleton stabilizing effect as one of its cardioprotective mechanisms.Methods: The effects of carvedilol, propranolol, and BM-91.0228 (a vascularly inactive metabolite of carvedilol), with and without cytoskeleton-modulating agents taxol (cytoskeleton stabilizer) and vinblastin (cytoskeleton destabilizer) were evaluated with regard to myocardial enzyme release (creatine kinase, CK) and cellular apoptosis (TUNEL method) during hypoxia in isolated perfused rat hearts in the following groups (n = 10 per group): group 1, controls (normoxia followed by hypoxia); group 2, carvedilol; group 3, propranolol; group 4, BM-91.0228; group 5, taxol; group 6, vinblastin; group 7, taxol plus carvedilol; group 8, vinblastin plus carvedilol; group 9, taxol plus propranolol; group 10, vinblastin plus propranolol; group 11, taxol plus BM-91.0228; group 12, vinblastin plus BM-91.0228.Results. Hypoxia-induced CK release was reduced by carvedilol (group 2, 4,817 +/- 968 mU/g wwt), propranolol (group 3, 4,513 +/- 464 mU/g wwt) and taxol (group 5, 2,860 +/- 1524 mU/g wwt; P < 0.05 versus controls), but not BM-91.0228, compared with controls (group 1, 16,747 +/- 3026; P < 0.05). Vinblastin (group 6) increased CK release during hypoxia (28,626 +/- 9700 mU/g wwt; P < 0.05 versus controls). Addition of carvedilol to vinblastin (group 8) ameliorated the increased CK release (8,353 +/- 2230 mU/g wwt; P < 0.05), whereas propranolol (group 10) and BM-91.0228 (group 12) added to vinblastin had no effect during hypoxia. Treatment with carvedilol (group 2), BM-91.0228 (group 4) and taxol (group 5) resulted in reduced apoptosis (up to 50%), whereas vinblastin (group 6) or propranolol (group 3) showed no effect compared with controls. Carvedilol and taxol in combination (group 7) resulted in significant reduced CK release and reduced apoptosis compared with controls (9%+/-2% vs. 59%+/-12%, P < 0.005).Conclusion: Modulating the stability of the cytoskeleton affects the degree of necrosis as defined by enzyme (CK) release. Carvedilol appears to exert a cytoskeleton stabilizing action, which may be involved in its cardioprotective effects. Both cytoskeleton stabilizing agents taxol and carvedilol also appear to demonstrate apoptosis sparing effects during hypoxia, which may be related to the beneficial effect on the cytoskeleton. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Patients with a wide variety of cardiovascular diseases, including arterial and pulmonary hypertension, arrhythmia, coronary artery disease and heart failure, are more likely to report impaired sleep with reduced sleep duration and quality, and also, sometimes, sleep interruptions because of paroxysmal nocturnal dyspnoea or arrhythmias. Overall, objective short sleep and bad sleep quality (non-restorative sleep) and subjective long sleep duration are clearly associated with major cardiovascular diseases and fatal cardiovascular outcomes. Sleep apnoea, either obstructive or central in origin, represents the most prevalent, but only one, of many sleep-related disorders in cardiovascular patients. However, observations suggest a bidirectional relationship between sleep and cardiovascular diseases that may go beyond what can be explained based on concomitant sleep-related disorders as confounding factors. This makes sleep itself a modifiable treatment target. Therefore, this article reviews the available literature on the association of sleep with cardiovascular diseases, and discusses potential pathophysiological mechanisms. In addition, important limitations of the current assessment, quantification and interpretation of sleep in patients with cardiovascular disease, along with a discussion of suitable study designs to address future research questions and clinical implications are highlighted. There are only a few randomised controlled interventional outcome trials in this field, and some of the largest studies have failed to demonstrate improved survival with treatment (with worse outcomes in some cases). In contrast, some recent pilot studies have shown a benefit of treatment in selected patients with underlying cardiovascular diseases., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)

Objective: This study aims to compare the informative value of a capacitively coupled electrocardiogram (cECG) to a conventional galvanic reference ECG (rECG) in patients after a major cardiac event under simulated driving conditions. Addressed research questions are the comparison and coherence of cECG and rECG by means of the signal quality, the artifact rate, the rate of assessable data for differential diagnosis, the visibility of characteristic ECG structures in cECG, the precision of ECG time intervals, and heart rate (in particular, despite possible waveform deformations due to the cardiac preconditions)., Methods: In a clinical trial, cECG and rECG data were recorded from ten patients after a major cardiac event. The cECG and rECG data were blindly evaluated by two cardiologists with regard to signal quality, artifacts, assessable data for differential diagnosis, visibility of ECG structures, and ECG time intervals. The results were statistically compared., Results: The cECG presented with more artifacts, an inferior signal quality, and less assessable data. However, when the data were assessable, determination of the ECG interval lengths was coherent to the one obtained from the rECG., Conclusion: When the signal quality is sufficient, the cECG yields the same informative value as the rECG., Significance: For certain scenarios, cECG might replace rECG systems. Hence, it is an important research question whether a similar amount of information can be obtained using a cECG system.

Introduction Home-based programmes for cardiac rehabilitation play a key role in the recovery of patients with coronary artery disease. However, their necessary educational and motivational components have been rarely implemented with the help of modern mobile technologies. We developed a mobile health system designed for motivating patients to adhere to their rehabilitation programme by providing exercise monitoring, guidance, motivational feedback, and educational content. Methods Our multi-disciplinary approach is based on mapping "desired behaviours" into specific system's specifications, borrowing concepts from Fogg's Persuasive Systems Design principles. A randomised controlled trial was conducted to compare mobile-based rehabilitation (55 patients) versus standard care (63 patients). Results Some technical issues related to connectivity, usability and exercise sessions interrupted by safety algorithms affected the trial. For those who completed the rehabilitation (19 of 55), results show high levels of both user acceptance and perceived usefulness. Adherence in terms of started exercise sessions was high, but not in terms of total time of performed exercise or drop-outs. Educational level about heart-related health improved more in the intervention group than the control. Exercise habits at 6 months follow-up also improved, although without statistical significance. Discussion Results indicate that the adopted design methodology is promising for creating applications that help improve education and foster better exercise habits, but further studies would be needed to confirm these indications.

Low adherence to cardiac rehabilitation (CR) might be improved by remote monitoring systems that can be used to motivate and supervise patients and tailor CR safely and effectively to their needs. The main objective of this study was to evaluate the feasibility of a smartphone-guided training system (GEX) and whether it could improve exercise capacity compared to CR delivered by conventional methods for patients with coronary artery disease (CAD). A prospective, randomized, international, multi-center study comparing CR delivered by conventional means (CG) or by remote monitoring (IG) using a new training steering/feedback tool (GEx System). This consisted of a sensor monitoring breathing rate and the electrocardiogram that transmitted information on training intensity, arrhythmias and adherence to training prescriptions, wirelessly via the internet, to a medical team that provided feedback and adjusted training prescriptions. Exercise capacity was evaluated prior to and 6 months after intervention. 118 patients (58 ± 10 years, 105 men) with CAD referred for CR were randomized (IG: n = 55, CG: n = 63). However, 15 patients (27 %) in the IG and 18 (29 %) in the CG withdrew participation and technical problems prevented a further 21 patients (38 %) in the IG from participating. No training-related complications occurred. For those who completed the study, peak VO 2 improved more (p = 0.005) in the IG (1.76 ± 4.1 ml/min/kg) compared to CG (-0.4 ± 2.7 ml/min/kg). A newly designed system for home-based CR appears feasible, safe and improves exercise capacity compared to national CR. Technical problems reflected the complexity of applying remote monitoring solutions at an international level.

Sleep disordered breathing (SDB) (obstructive sleep apnea, central sleep apnea/Cheyne-Stokes respiration or the combination of both) is highly prevalent in patients with a wide variety of cardiovascular diseases including hypertension, arrhythmia, coronary artery disease, myocardial infarction and stroke (reviewed previously in the September issue of this journal). Its close association with outcomes in chronic heart failure with reduced ejection fraction (HF-REF) suggests that it may be a potential treatment target. Herein, we provide an update on SDB and its treatment in HF-REF.

Aim: To determine the prevalence of, and the risk factors for, sleep apnoea in cardiac rehabilitation (CR) facilities in Germany., Methods: 1152 patients presenting for CR were screened for sleep-disordered breathing with 2-channel polygraphy (ApneaLink™; ResMed). Parameters recorded included the apnoea-hypopnoea index (AHI), number of desaturations per hour of recording (ODI), mean and minimum nocturnal oxygen saturation and number of snoring episodes. Patients rated subjective sleep quality on a scale from 1 (poor) to 10 (best) and completed the Epworth Sleepiness Scale (ESS)., Results: Clinically significant sleep apnoea (AHI ≥15/h) was documented in 33% of patients. Mean AHI was 14 ± 16/h (range 0-106/h). Sleep apnoea was defined as being of moderate severity in 18% of patients (AHI ≥15-29/h) and severe in 15% (AHI ≥30/h). There were small, but statistically significant, differences in ESS score and subjective sleep quality between patients with and without sleep apnoea. Logistic regression model analysis identified the following as risk factors for sleep apnoea in CR patients: age (per 10 years) (odds ratio (OR) 1.51; p<0.001), body mass index (per 5 units) (OR 1.31; p=0.001), male gender (OR 2.19; p<0.001), type 2 diabetes mellitus (OR 1.45; p=0.040), haemoglobin level (OR 0.91; p=0.012) and witnessed apnoeas (OR 1.99; p<0.001)., Conclusions: The findings of this study indicate that more than one-third of patients undergoing cardiac rehabilitation in Germany have sleep apnoea, with one-third having moderate-to-severe SDB that requires further evaluation or intervention. Inclusion of sleep apnoea screening as part of cardiac rehabilitation appears to be appropriate., (© The European Society of Cardiology 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)

Today, heart diseases are the most common cause of death in the U.S.. Due to improved healthcare, more and more patients survive a major cardiac event, e.g. a heart attack. However, participation in everyday activity (e.g. driving a car) can be impaired afterwards. Patients might benefit from heart activity monitoring while driving using a capacitive ECG (cECG). However, it is unknown whether cECG is an appropriate monitoring tool for such patients. In this work, first results from a study including 10 patients having survived at least one major cardiac event are presented. It is shown that cECG can be used to diagnose heart rhythm deviations and estimate beat-to-beat intervals similar to conventional ECG.

Background: Participation in phase-III cardiac rehabilitation (CR) remains low but adherence could potentially be improved with supervised home-based CR. New technological approaches are needed to provide sufficient supervision with respect to safety and performance of individual exercise programmes., Design: The newly designed closed-loop tool, HeartCycle's guided exercise (GEX) system, will support professionals and patients during exercise-based CR. Patients wear a dedicated shirt with incorporated wireless sensors, and ECG, heart rate (HR), breathing frequency (BF), and activity are monitored during exercise. This information is streamed live to a mobile device (PDA) that processes these parameters., Methods: A phase-I study was performed to evaluate feasibility, function, and reliability of this GEX device and compare it to conventional cardiac exercise testing (CPX, spiroergometry) in 50 patients (seven women, mean ± SD age 69 ± 9 years, body mass index 26 ± 3 kg/m(2), ejection fraction 58 ± 10%). ECG, HR, and BF were monitored using standard equipment and the GEX device simultaneously. Furthermore, HR recorded on the PDA was compared with CPX measurements., Results: The fit of the shirt and the sensor was good. No technical problems were encountered. All occurring arrhythmia were reliably detected. There was an acceptable comparability between HR on the GEX device vs. CPX, a good comparability between HR on the PDA vs. CPX, and a moderate comparability between BF on the GEX device vs., Cpx Conclusions: Comparability between CPX and the GEX device was acceptable for HR measurement and moderate for BF; arrhythmias were reliably detected. HR processing and display on the PDA was even better comparable. The whole system seems suitable for monitoring home-based CR. Further studies are now needed to implement training prescription to facilitate individual exercise., (© The Author(s) 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)

Background: Depression in cardiac patients has gained importance due to increased mortality. Although sleep disturbances are a core symptom of depression, the prevalence and patterns of sleep disturbances in heart disease have hardly been examined regarding depression., Purpose: This cross-sectional study aims to examine sleep disturbances and depressive symptoms in consecutively admitted cardiac patients and depressed patients., Methods: Two hundred four inpatients (113 male, 91 female) were examined: 94 cardiac inpatients (mean age 49.3 ± 14.3 years) with different heart diseases and 110 psychiatric inpatients (mean age 41.6 ± 13.0 years) with depressive disorders (DP). A depressive episode according to International Classification of Diseases (ICD)-10 was also diagnosed in 14 of the cardiac patients (DCP). The Pittsburgh Sleep Quality Index (PSQI) and the Beck Depression Inventory (BDI) were used to assess subjective sleep quality and severity of depressive symptoms., Results: Poor sleep quality (PSQI > 5) was reported in all comorbid DCP (PSQI 12.00 ± 3.53, BDI 17.86 ± 4.28), in 60% of the 80 non-DCP (PSQI 5.59 ± 3.73, BDI 4.47 ± 3.07), and in 86.4% of the DP (PSQI 11.76 ± 4.77, BDI 27.11 ± 10.54). The cardiac inpatients showed a significant correlation between increased depressive symptoms and the PSQI components subjective sleep quality (r = 0.40) and daytime dysfunction (r = 0.34). Both sleep components were significant predictors of self-rated depression (R² = 0.404)., Conclusions: Most cardiac patients experience poor sleep quality. Self-reported sleep disturbances in heart disease could serve as predictors of clinical or subclinical comorbid depression outside of a psychiatric setting in cardiology and other fields, and such patients should be referred to consultation-liaison psychiatry or polysomnography where sleep disorders like sleep apnea are suspected.

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., (© Georg Thieme Verlag KG Stuttgart · New York.)

Background: Early studies in different stress models have shown potential beneficial effects of exogenous zinc application with reduction in the rate of apoptotic cell death. This has not been shown in models of myocardial infarction., Methods: Rats were exposed to either brief episodes of acute ischemia followed by reperfusion (phase 1) or chronic coronary occlusion (phase 2). Animals were either treated with zinc or vehicle. Groups 1 and 3 received zinc-bis-(DL-hydrogenaspartate) 10 mg/kg body weight as a single 5-mL bolus administered intraperitoneally 24 hours prior to coronary occlusion, groups 2 and 4 received saline. The infarct sizes were determined by triphenyltetrazolium chloride staining and expressed at relative areas to areas of ischemia. Histological slices of the rat's myocardium at the border zones of the infarcts were stained with the TUNEL method to assess for apoptosis. Animals in groups 5, 7, and 9 received zinc, given once before and then repeated every 4 days after coronary occlusion, whereas groups 6, 8, and 10 received saline. Animals were observed for observation periods of 13 (groups 9 and 10), 16 (groups 7 and 8), or 19 weeks (groups 5 and 6), respectively. Two-dimensional echocardiography was performed to measure ejection fraction (EF) at baseline and at the end of the observation periods. TUNEL staining was used to detect and quantify apoptosis rate in the border zones of infarcts after the hearts were excised., Results: Infarct sizes were 49% + 22% in group 1 (zinc + 30 minutes ischemia + 30 minutes reperfusion); 48% + 10% in group 2 (vehicle + 30 minutes ischemia + 30 minutes reperfusion); 42% + 11% in group 3 (zinc + 60 minutes ischemia + 30 minutes reperfusion); and 41% + 23% in group 4 (vehicle + 60 minutes ischemia + 60 minutes reperfusion). In group 1, 11% + 6% of cells were apoptotic compared to 12% + 4% in group 2, 16% + 9% in group 3, and 17% + 7% in group 4 (P > .05). In phase 2, echocardiography revealed a significant reduction in EF in all groups after coronary occlusion. There were no significant differences in EF between the 5 groups at baseline and at follow-up. TUNEL staining did not reveal any significant apoptosis after 13 to 19 weeks., Conclusion: Application of zinc failed to result in reduction of infarct size after temporary coronary occlusion followed by reperfusion and did not demonstrate any reduction in apoptotic cell death. In chronic coronary occlusion, zinc also did not improve EF compared to controls in the presented model in rats. The mechanisms involved in antiapoptotic effects seem to be more complex and might not be inducible by simple zinc injections.

Purpose: To determine the maximum tolerated dose (MTD) of gemcitabine every 2 weeks to a concurrent radiotherapy administered during an aggressive program of sequential and simultaneous radio-/chemotherapy for locally advanced, unresectable non-small cell lung cancer (NSCLC)., Patients and Methods: Ten patients with histologically confirmed NSCLC were observed and treated in accordance with a combined radio-/chemotherapy protocol. This included two cycles of induction chemotherapy with gemcitabine (1,200 mg/m(2)) and vinorelbine (30 mg/m(2)) at days 1, 8 and 22, 29, followed by concurrent radiotherapy including [(18)F] fluorodeoxyglucose positron emission tomography-(FDG-PET-)based target volume definition (2.0 Gy/d; total dose 66.0 Gy) and chemotherapy with gemcitabine every 2 weeks at days 43, 57, and 71. The initial dose was 300 mg/m(2). The dose of gemcitabine was increased by 100 mg/m(2) until the MTD was realized. Three patients were enrolled for each dose level., Results: Dose-limiting toxicity (DLT) was identified for the patient group receiving gemcitabine 500 mg/m(2), due to grade 2 esophagitis (next to grade 3) in all patients. 6 weeks after the completion of radio-/chemotherapy, most patients still presented treatment-induced esophagitis. In accordance with expected complications, such as esophagitis, dysphagia and odynophagia, the MTD was defined at this dose level, although no DLT grade 3 was reached., Conclusion: After induction chemotherapy, the MTD and frequency of gemcitabine in locally advanced NSCLC is 500 mg/m(2) every 2 weeks during a maximum of 7 weeks of thoracic radiotherapy.

Background: Objective assessment of the cardiopulmonary capacity in patients with complex congenital cardiac disease often remains difficult in clinical practice. The cardiopulmonary exercise test and determination of the levels of brain natriuretic peptide in the plasma are established tests, but expensive. The 6-minute walk test is also validated, but has not often been used in patients with heart failure due to congenital heart disease, nor compared with other tests. We sought to compare its value with the results of cardiopulmonary exercise testing and measuring the levels of brain natriuretic peptide in the plasma., Methods: We carried out a standardized 6-minute walk test in 31 patients with complex congenital cardiac disease on the same day that they underwent cardiopulmonary exercise testing and determination of levels of brain natriuretic peptide in the plasma. Of the patients, 7 had functionally univentricular hearts, 9 had transposition, 9 had tetralogy of Fallot, 3 had common arterial trunk, and 3 had pulmonary atresia with intact interventricular septum. Uptakes of oxygen at peak exercise, and at the anaerobic threshold, were determined using cardiopulmonary exercise testing, and classified as suggested by Weber. The 6-minute walk test was performed according to a standard protocol., Results: There was a significant correlation between brain natriuretic peptide, oxygen uptakes at peak exercise and 6-minute walk. The correlation between the 6-minute walk test and oxygen uptakes at the anaerobic threshold, however, was not significant., Conclusions: The 6-minute walk test can be performed easily, is inexpensive, widely available, and correlates well with measurements of brain natriuretic peptide and cardiopulmonary exercise testing, even in patients with corrected or palliated congenital cardiac malformations. A cut-off value of 450 metres in the 6-minute walk test allows a semi-quantitative classification in analogy to the classification suggested by Weber for cardiopulmonary exercise testing, and to a level of brain natriuretic peptide in the plasma of less or more than 100 picograms per millilitre.

Background: Quality of life in patients with chronic heart failure (HF) is often severely compromised. Sleep-related breathing disorders (SRBD) like Cheyne-Stokes Respiration (CSR) or obstructive sleep apnea (OSAS) are often observed in patients with severe HF resulting in fragmentation of sleep, excessive daytime sleepiness and an increased mortality. While an apnea/hypopnea-index (AHI) >30/h represents an independent predictor of poor prognosis, clinical relevance of even minor SRBD with an AHI <30/h remains unclear with respect to quality of life, exercise capacity or depression rate., Methods: Sixty-nine consecutive ambulatory patients with stable HF (NYHA II-III, EF 25%) underwent two night polygraphies with a six-channel ambulatory recording. Spiroergometry was performed, and patients were examined for sleep quality (PSQI), depressed mood (BDI) and health-related quality of life (SF-36). The data were compared to 10 age-matched healthy controls and 11 patients with OSAS (AHI 14-29/h) not suffering from HF., Results: Fifty-one patients completed follow up. 52% were positively diagnosed for SRBD (AHI 16-30/h: 12 patients CSR, 5 patients OSAS, 9 patients mixed); 25 patients (48%) showed no relevant SRBD. Patients with HF and SRBD had lower quality of life than patients without SRBD and HF. The severity of SRBD as indicated by the AHI significantly correlated with quality of life measures: Bodily pain, physical functioning and social functioning showed largest impairment in patients with HF and SRBD. Furthermore, elevated depression rates in correlation to the AHI were only observed in patients with SRBD similar to patients with OSAS without HF., Conclusion: Even minor SRBD in patients with HF independently influence quality of life and correlate with estimation of depression and sleep disturbances.

Studies have demonstrated the feasibility of transplanting cardiomyocytes after myocardial infarction (MI). However, persistence and effects on left ventricular (LV) function have not been elucidated in long-term studies. Ventricular fetal cardiomyocytes from embryos of both sexes were injected into marginal regions of MI 4 weeks after suture occlusion of the left anterior descending artery in adult female rats. Two and 6 months after transplantation (Tx), engrafted cells were traced by immunohistochemical in situ hybridization for Y chromosomes or bromodeoxyuridine (BrdU) staining, LV dimensions and function were assessed by echocardiography, and LV pressure was assessed ex vivo in a Langendorff perfusion system. Immunohistochemistry for alpha-sarcomeric actin and Y chromosomes revealed the presence of transplanted cells in infarcted host myocardium at both 2 and 6 months. End-diastolic LV diameter markedly decreased after Tx and fractional shortening gradually increased after Tx (31.3 +/- 4.5% before Tx, 45.4 +/- 4.2% at 6 months; p<0.005). Wall area fraction and MI size were unaffected by Tx. In hearts with MI, but not in normal hearts, Tx led to the development of higher pressures (87 +/- 18 versus 38 +/- 8 mmHg, 6 months post-Tx versus nontreated). After catecholamine stimulation, both infarcted and normal hearts developed higher pressures after Tx (p<0.005), ultimately associated with reduced mortality after Tx versus nontreated. Transplanted cardiomyocyte-rich graft cells persist in host myocardium and mediate continuous improvement of LV function and survival in a rat model of MI even during long-term follow-up, possibly involving a catecholamine-sensitive mechanism.

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.

Tuberculosis (TB) increasingly appears in a multidrug-resistant form (MDR-TB) in Europe, too. Treatment remains difficult due to various side effects of the multi-drug-regimens. Ciprofloxacin is widely used as one of the few TB-second-line drugs. We report on the course of a ciprofloxacin-induced acute psychosis in a patient with MDR(isoniazid, streptomycin)-TB which resolved after cessation of ciprofloxacin treatment and introduction of a novel oxazolidone. Careful treatment considerations particularly in patients with additional predisposing factors to neuropsychiatric symptoms are recommended in the potentially dangerous MDR-TB, thus creating an enormous therapeutic challenge.

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.

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.