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It is of fundamental importance to differentiate whether chronic hypoxia occurs intermittently or persistently. While chronic intermittent hypoxia (CIH) is found typically in patients with obstructive sleep apnea (OAS), chronic persistent hypoxia (CPH) is typically diagnosed in patients with chronic lung disease. Cardiovascular risk is markedly increased in patients with CIH compared to patients with CPH. The frequent change between oxygen desaturation and reoxygenation in patients with CIH is associated with increased hypoxic stress, increased systemic inflammation, and enhanced adrenergic activation followed by endothelial dysfunction and increased arteriosclerosis. The pathophysiologic consequences of CPH are less well understood. The relationship between CPH and the development of pulmonary hypertension, pulmonary heart disease as well as polycythemia has been established.

Acute decompensated heart failure (ADHF) has become the leading cause of hospitalization in patients > 65 years of age. Traditional drug therapy for ADHF has remained unchanged for many years including morphine, diuretics, nitrates and inotropic agents in addition to oxygen supplementation and mechanical ventilatory support, if necessary. In the year 2005, the European Society of Cardiology published new guidelines for diagnosis and treatment of ADHF. These guidelines emphasize that ADHF is not a disease entity but a complex syndrome with various etiologies and several distinct clinical conditions as a result of systolic and/or diastolic left and/or right ventricular dysfunction. This review article describes the current role of traditional drugs for ADHF as well as the role of newer concepts including vasodilators like the recombinant human brain peptide nesiritide, endothelin antagonists or vasopressin antagonists and newer inotropic agents like the calcium sensitizer levosimendan.

Obstructive sleep apnea is a common disorder and affects approximately 4% of middle-aged men and 2% of middle-aged women. Obstructive sleep apnea is clearly associated with obesity, with more than 50% of patients having a body mass index>30 kg/m2. Substantial evidence identified obstructive sleep apnea as risk factor not only for excessive daytime sleepiness and road traffic accidents, but also for increased cardiovascular morbidity and mortality. In addition, all kinds of arrhythmias have been observed in patients with sleep apnea ranging from asymptomatic sinus bradycardia to sudden cardiac death. Approximately 5-10% of patients with obstructive sleep apnea show marked apnea-related bradyarrhythmias due to enhanced vagal tone and pronounced hypoxia. Therapeutic options in obese patients with obstructive sleep apnea include consequent weight loss and nasal continuous positive airway pressure (CPAP) ventilation as the therapy of first choice. Weight reduction and effective nasal CPAP therapy significantly decrease cardiovascular morbidity and mortality and eliminate sleep-related bradyarrhythmias in 80-90% of patients obviating the need for pacemaker implantation in these patients.

Background: Cardiac myxomas are the most common type of cardiac tumors. About 75-85% of cardiac myxomas originate in the left atrium, 15-20% in the right atrium. Most myxomas arise from the interatrial septum adjacent to the fossa ovalis. Only 3-4% are found in the left and right ventricle each. Although myxomas are histologically benign, they may be fatal because of their strategic position., Case Study: The authors report on a 24-year-old patient with stabbing thoracic pain and dyspnea due to pulmonary thromboembolism that was caused by an atypically localized myxoma at the right ventricular apex originating from the interventricular septum. The diagnosis was based on cardiac magnetic resonance (CMR) imaging. Superior to echocardiography, CMR could strengthen the diagnostic accuracy by additional information on tissue characterization using different imaging sequences. Typically for cardiac myxomas, contrast enhancement was moderate and delayed enhancement was found in the outer circumferential tumor margins only., Conclusion: High spatial resolution and multiplane imaging combined with different acquisition patterns of CMR achieve a global view of the heart that seems to be useful for diagnosing cardiac tumorous masses.

Background: Sudden cardiac death of suspected healthy young athletes is a rare, but deeply moving event. Usually, the affected person has been completely free of symptoms. Commonly, unrecognized inflammatory, hypertrophic or dilated cardiomyopathies are the most frequent causes. All therapeutic principles of angiotensin-converting-enzyme (ACE) inhibition, beta-blockade, and diuretics in heart failure aim to unload the heart. During physical activity increased sympathetic tonus and loading conditions for the heart point into the opposite direction. This raises the question to what extent physical activity in patients with myocarditis, dilated cardiomyopathy or heart failure in general is tolerable., Synopsis: Several experimental studies revealed disadvantages of physical exercise during acute myocarditis leading to an increase in mortality. On the other hand, several small trials in men demonstrate an improvement of physical fitness and quality of life attributed to controlled supervised exercise training in patients with heart failure without assessment of mortality. Dilated cardiomyopathy was diagnosed in one third of these patients. There was no biopsy confirmation of these conditions. The other two thirds of patients suffered from ischemic heart diseases., Conclusion: Since the borderline between inflammatory heart disease and noninflammatory or postinflammatory dilated cardiomyopathy is difficult to determine, abstention from physical training during and shortly after inflammatory heart disease is recommended, because it is known that viral persistence or autoimmune processes could last for several months.

To date, generally accepted indications for prophylactic defibrillator implantation in patients with dilated cardiomyopathy do not exist. Recently, the Marburg Cardiomyopathy Study (MACAS) revealed left ventricular ejection fraction to be the only significant arrhythmia risk predictor in a relatively large patient population with dilated cardiomyopathy. Meanwhile, the preliminary results of two prospective randomized trials evaluating prophylactic defibrillator therapy in dilated cardiomyopathy have been reported. The Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation study (DEFINITE) randomized 458 patients with a history of symptomatic heart failure, a left ventricular ejection fraction < or = 35% and arrhythmias on Holter to an ICD versus no ICD. As a result, ICD therapy was associated with a significant reduction of arrhythmic deaths, which failed to result in a significant decrease in total mortality due to an insufficient number of patients in DEFINITE. The Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) was a three-arm study comparing placebo to amiodarone to prophylactic ICD therapy in a total of 2,521 patients with ischemic cardiomyopathy (51%) or nonischemic dilated cardiomyopathy (49%). All patients in SCD-HeFT had a left ventricular ejection fraction inverted exclamation mark U 35% despite optimized medical heart failure therapy. SCD-HeFT showed a significant reduction of total mortality in the ICD group, whereas amiodarone did not improve survival.

Background: Despite routine use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and spironolactone in patients with heart failure due to dilated cardiomyopathy (DCM), these patients still have a considerable annual mortality rate of 5-10%. Sudden unexpected death accounts for up to 50% of all deaths and is most often due to rapid ventricular tachycardia or ventricular fibrillation and less often due to bradyarrhythmias or asystole., Therapeutic Options: The use of beta-blockers in patients with heart failure has been shown to improve overall mortality considerably. This survival benefit has been demonstrated for bisoprolol, metoprolol and carvedilol. Therefore, one of these three beta-blocking agents should be administered routinely starting with low doses in all patients with New York Heart Association (NYHA) class II or III heart failure in addition to ACE inhibitors, unless there is a contraindication to beta-blocker use. In addition, NYHA class IV heart failure patients have been shown to benefit from carvedilol therapy, if tolerated. The conflicting results of GESICA and CHF-STAT studies do not support a strategy of "prophylactic" amiodarone therapy in patients with DCM in order to prevent sudden cardiac death. Despite growing evidence that implantable cardioverter defibrillator (ICD) therapy results in improved overall survival py preventing sudden cardiac death in patients at high risk for serious arrhythmic events, arrhythmia risk stratification with regard to prophylactic ICD implantation remains highly controversial in patients with DCM., Conclusion: This review describes potential arrhythmia mechanisms in DCM and summarizes the results of antiarrhythmic drug trials and of prophylactic ICD trials in patients with heart failure as well as our knowledge concerning arrhythmia risk stratification in patients with DCM.

Background: Once contraindicated, beta-blockers have become an established, evidence-based, recommended treatment concept in chronic heart failure during the last years., Pathophysiology: The increased activation of the adrenergic system in heart failure syndrome, which leads to transmission of several adverse biological signals to myocytes through adrenergic receptors, provides the rationale for the use of beta-blockers in patients with chronic heart failure. Long-term treatment with different types of beta-blockers addictive to an ACE-inhibitor and diuretics results in normalization of left ventricular shape, an improvement of left ventricular function, and a reduction of hospitalization rate for heart failure. Hemodynamic and clinical improvement is independent of etiology and severity of left ventricular dysfunction. THERAPEUTICAL RECOMMENDATIONS ACCORDINGS TO STUDIES: Adequately powered clinical trials (CIBIS II, MERIT-HF, COPERNICUS) testing different types of beta-blockers (bisoprolol, metoprolol, carvedilol) clearly demonstrated that total mortality and the incidence of sudden cardiac death were significantly reduced in heart failure patients by each of these agents. On the basis of all available evidence, all patients with chronic, stable heart failure (NYHA class II-IV) and with impaired left ventricular function (LVEF < 45%) should receive one of the three above mentioned beta-blockers. Protective effects of beta-blockers in heart failure comprise decrease in heart rate, a decrease of energy consumption, antifibrillatory effects, protection against adrenergic overactivation, and hence, inhibition of myocardial cell necrosis. Moreover, several beta-blockers induce an up-regulation of beta-receptors leading to an improvement of contractility during long-term treatment. It should be mentioned that even a low dosage of beta-blockers exert negative inotropic effects and may lead to a deterioration of hemodynamics and heart failure symptoms in patients with heart failure. The patients treated should be informed that the success of the "paradoxical intervention" will be obvious until 2-3 months after initiation of additional beta-blocker therapy. Beta-blocker treatment for heart failure should be started in stable patients with a very low initial dosage and then up-titrated to the maximal tolerated dosage and should be continued indefinitely. Mortality reduction by beta-blockade in heart failure is no class effect. So far, beneficial effects could only be demonstrated for lipophilic agents. Whether the non-selective beta-blocker carvedilol with additional properties has advantages over the beta-1-selective metoprolol is currently investigated in the COMET (Carvedilol or Metoprolol European Trial) study. Despite the impressive effects in terms of morbidity and mortality reduction, the transfer of these benefits to the clinical practice setting is difficult, with international data showing only 10% of patients with heart failure being treated.

Background: Atrial fibrillation is the most frequent arrhythmia. It can impair quality of life considerably. Due to thromboembolic complications it contributes to the patients' morbidity and mortality and to the costs for their medical treatment., Prevention: In chronic atrial fibrillation there is a need for adequate anticoagulation and heart rate control. In paroxysmal and intermittent atrial fibrillation it should be sought to prevent its progression to chronic atrial fibrillation. Since atrial fibrillation initiates negative processes of remodeling within the atrial myocardium, it has the tendency to perpetuate itself. From a theoretical point of view, it can be expected that all means which prevent episodes of atrial fibrillation or which terminate it immediately after its onset, are able to prevent or at least to delay the progression to chronic atrial fibrillation. Pharmacologic treatment is usually used to prevent recurrences of atrial fibrillation. Based on the actual data it can also be expected that pacemakers with special preventive pacing algorithms are able to reduce the atrial arrhythmic burden. Besides consequent overdrive pacing, more sophisticated algorithms like "suppression of premature atrial contractions", "post exercise response", "automatic rest rate" or "post mode-switch pacing" have been developed. They can be applied either alone or in combination with special lead positions (interatrial septal pacing or pacing of the triangle of Koch) or special stimulation configurations like dual site right atrial pacing or biatrial pacing. These pacing strategies cover the most relevant onset mechanisms of atrial fibrillation. Furthermore, there are algorithms to treat atrial tachyarrhythmias actively by antitachycardia pacing (ATP). First clinical results have shown that about 2/3 of the diagnosed atrial tachyarrhythmias could be terminated by these means immediately after their onset., Ongoing Trials: This article gives an overview over the principles of pacing in the management of atrial arrhythmias and ongoing clinical trials in this field. Before a definite judgement on the clinical relevance of these new preventive and therapeutic pacing strategies can be given, the results of these ongoing controlled clinical studies have to be analyzed.

The Marburg Cardiomyopathy Study (MACAS) is a prospective observational study designed to determine the value of the following potential non-invasive arrhythmia risk predictors in more than 200 patients with idiopathic dilated cardiomyopathy (IDC) over a 5-year follow-up period: New York Heart Association functional class, left ventricular end-diastolic diameter and ejection fraction, left bundle branch block and atrial fibrillation on ECG, QTc and JTc-dispersion on 12-lead ECG, abnormal time-domain analysis and spectral turbulence analysis of the signal-averaged ECG, ventricular arrhythmias and heart-rate variability on 24-hour Holter ECG, baroreflex sensitivity, and microvolt T wave alternans during exercise. This report describes the rationale of MACAS as well as the clinical characteristics of the first 236 patients enrolled between March 1996 and October 1999. The prognostic significance of the potential arrhythmia risk predictors in MACAS will be determined by multivariate Cox analysis at the end of 5-year follow-up. Primary endpoints are total mortality and major arrhythmic events defined as sustained ventricular tachycardia, ventricular fibrillation or sudden cardiac death. The results of MACAS will have important implications for the design of future studies evaluating the role of prophylactic defibrillator therapy in idiopathic dilated cardiomyopathy.

Artificial bradycardias due to tape-running alterations of old long-term ECG recorders were observed with increasing frequency in the last 2 years at our hospital. To document the extent of this problem, 115 consecutive 24-hour long-term ECG recordings of 10 still used tape recorders with an age of 12 +/- 4 years were examined. Analysis of the tapes with a new analysis system revealed artificial bradycardias with rates of 10 to 40/min in 22 of 115 long-term ECG recordings (19%). These artificial bradycardias were observed in 4 out of 10 examined tape recorders (40%). Three of 4 concerned recorders were 14 years old at the time of examination, and one recorder was only 5 years old. Artificial bradycardias were caused by extensive alterations of tape-running speed in all cases. Diagnostic proof of artificial bradycardias due to tape running alterations on long-term ECG are simultaneous with prolonged RR-intervals occurring increases in all ECG times including P-width. PQ-time, QRS-width and QT-duration with otherwise unchanged ECG morphology. To avoid prolonged hospital stays or therapeutic mistakes like unnecessary pacemaker implantation, especially older long-term ECG-tape recorders should be checked regularly and, if necessary, be replaced by new devices.

The association between alcohol use and rhythm disturbances, particularly supraventricular tachyarrhythmias in apparently healthy people is called "holiday heart syndrome". The syndrome was first described in persons with heavy alcohol consumption, who typically presented at weekends or after holidays, but it may also occur in patients who usually drink little or no alcohol. The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours. The incidence of the holiday heart syndrome depends on the drinking habits of the studied population. The holiday heart syndrome should be considered particularly as a diagnosis in patients without overt heart disease presenting with new onset atrial fibrillation. Though recurrences occur, the clinical course is benign and specific antiarrhythmic therapy is usually not warranted.