Arrhythmia risk prediction in idiopathic dilated cardiomyopathy based on heart rate variability and baroreflex sensitivity.

Unlabelled: This study examined the relation between heart rate variability (HRV) and baroreflex sensitivity (BRS) and subsequent major arrhythmic events (MAE), defined as sustained VT, VF or sudden death, in 263 patients with idiopathic dilated cardiomyopathy (IDC) in sinus rhythm. The predefined measure of HRV was the standard deviation of all normal-to-normal RR intervals (SDNN) on baseline 24-hour ambulatory ECG. BRS was determined by the phenylephrine method.

Coronary artery spasm induced by 5-fluorouracil.

The frequently used chemotherapeutic drug 5-fluorouracil (5-FU) is known to cause angina pectoris and arrhythmias; myocardial infarction and sudden cardiac death could occur. Potential reasons for these phenomena range from toxic/metabolic disturbances to coronary artery spasms. This report shows angiographically proven spasmophilia of the coronary arteries and contributes to the understanding of angina pectoris occurring during treatment with 5-FU.

Inflammation in dilated cardiomyopathy.

Inflammation is an important component in the pathogenesis of many common cardiovascular diseases. In most cases, the role of inflammation is a natural response to injury, and an important mechanism for healing and tissue repair. However, the inflammatory response can be either inadequate or overwhelming, leading to direct injury or severe host disease.

Risk stratification by the "EPA+DHA level" and the "EPA/AA ratio" focus on anti-inflammatory and antiarrhythmogenic effects of long-chain omega-3 fatty acids.

The identification of risks associated with sudden cardiac death requires further investigations. The question was addressed whether parameters can be established which not only describe an increased risk for an enhanced electrical instability of the heart but also of inflammatory events underlying plaque rupture. Emphasis is placed on dose-dependent effects of the long-chain omega-(omega-)3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Long-term survival with acquired ventricular septal defect after myocardial infarction.

Acquired ventricular septal defects (VSD) are rare and devastating complications after myocardial infarction. The long-term prognosis with medical therapy is extremely poor. We report on a patient who developed progressive heart failure within 3 months after myocardial infarction due to an unknown VSD.

Risk of coronary artery disease associated with polymorphism of the cytochrome P450 epoxygenase CYP2J2.

Background: Cytochrome P450 (CYP) 2J2 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs). The EETs are potent endogenous vasodilators and inhibitors of vascular inflammation. However, it is not known whether genetic polymorphisms of CYP2J2 are associated with increased cardiovascular risks.

[Complicated course of Churg-Strauss syndrome with eosinophilic perimyocarditis and pericardial tamponade].

History: A 30-year-old patient suffered from a dry cough and increasing dyspnea since two years; he further complained about non radiating chest pain and weight loss of 15 kg in the past 8 weeks.

Examinations: Physical examination revealed pulsus paradoxus and distended neck veins. On chest x-ray, signs of cardiomegaly without infiltrations were found.

[Endomyocardial biopsy-guided diagnosis and treatment of inflammatory cardiomyopathies].

Background: Over 50 % of cases of inflammatory cardiomyopathy are caused by bacterial or viral infection, the latter frequently Parvovirus B19, enterovirus (Coxsackie B virus) or adenovirus. Regarding the pathogenesis of the disease, its early phase is dominated by the infectious pathogen, which directly damages the myocardium, while in the second phase an important role is played by activation of the immune system and the antiviral immune response with immunological processes.

History And Clinical Findings: A 24-year-old woman (height 175 cm, weight 88 kg) was admitted because of recurrent exertional dyspnea.

[Extracardiac causes of right ventricular insufficiency].

Evidence for manifest right ventricular dysfunction is considered a critical threshold in the development of a fatal event after acute pulmonary embolism. While the acute event impressively reflects the clinical significance of right ventricular function, various disorders such as idiopathic pulmonary arterial hypertension, secondary pulmonary hypertension in lung diseases, carcinoid heart disease, and portopulmonary hypertension can lead to chronic right ventricular failure. Adapted treatment makes it possible to alleviate the patients' distress and presumably also improve the prognosis.

Detection of anti-hsp70 immunoglobulin G antibodies indicates better outcome in coronary artery bypass grafting patients suffering from severe preoperative angina.

Background: Recent findings indicate that molecular chaperones actively participate in myocardial cytoprotection. Moreover, ischemic tolerance can be induced in humans by brief ischemic events. Therefore, we investigated patients with severe angina attacks before coronary artery bypass grafting.

Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis.

Vascular calcification may occur at different areas of the vessel wall, including the intima in atherosclerosis and the media in Mönckeberg's sclerosis. Medial calcification of arteries is common in patients with diabetes mellitus or chronic renal failure. Osteoprotegerin (OPG) and receptor activator of nuclear factor-kappaB ligand are essential modulators of bone homeostasis and may be involved in the process of vascular calcification.

Osteoprotegerin gene polymorphisms in men with coronary artery disease.

Osteoprotegerin (OPG) antagonizes receptor activator of nuclear factor-kappaB ligand (RANKL), the principal regulator of osteoclasts. Of note, OPG-deficient mice display osteoporosis and arterial calcification. Recently, OPG gene polymorphisms have been associated with osteoporosis and early predictors of cardiovascular disease.

Escape from cardiomyocyte apoptosis by enterovirus persistence due to elevated soluble Fas-receptors.

Background: Apoptosis causes loss of contractile cardiomyocytes in inflammatory heart disease. Despite recent examinations, the influence of virus infection on apoptosis remained ill-defined.

Methods: Apoptosis was assessed in left ventricular endomyocardial biopsies by the TUNEL method frompatients with chronic myocarditis and adeno-, cytomegalo- and enterovirus persistence.

[Physical activity and sports in heart failure due to myocarditis and dilated cardiomyopathy].

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.

[Premedication visits. Economizing at the cost of the patient?].

The older the patient, the higher the risk of perioperative cardiac complications. Therefore, patients at risk have to be identified and the appropriate diagnostic or therapeutic measures initiated. The most important factor in this context is whether a planned surgery can be postponed.

Arrhythmia risk stratification with regard to prophylactic implantable defibrillator therapy in patients with dilated cardiomyopathy. Results of MACAS, DEFINITE, and SCD-HeFT.

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.

A new but frequent mutation of apoB-100-apoB His3543Tyr.

ApolipoproteinB 100 (apoB-100) is an important component of atherogenic lipoproteins such as LDL and serves as a ligand for the LDL-receptor. Familial defective apolipoproteinB 100 (FDB) is caused by a R3500Q mutation of the apoB gene and results in decreased binding of LDL to the LDL-receptor. So far FDB is the most frequent and best studied alteration of apoB-100.

Novel point mutations in the mitochondrial DNA detected in patients with dilated cardiomyopathy by screening the whole mitochondrial genome.

Dilated cardiomyopathy (DCM) is widely accepted as a pluricausal or multifactorial disease. Because of the linkage between energy metabolism in the mitochondria and cardiac muscle contraction, it is reasonable to assume that mitochondrial abnormalities may be responsible for some forms of DCM. We analysed the whole mitochondrial genome in a series of 45 patients with DCM for alterations and compared the findings with those of 62 control subjects.