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Bernhard Maisch

Publications and source records attributed to Bernhard Maisch.

At least 55 records · Page 3Linked to original sources
PubMed2005

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. Over 52 +/- 21 months of follow-up, MAE occurred in 38 patients (14%). SDNN at baseline 24-hour ambulatory ECG (106 +/- 46 vs 109 +/- 45, ns) and BRS (7.9 +/- 5.5 vs 7.7 +/- 5.3 ms/mmHg, ns) were both similar in patients with versus without MAE during follow-up. In contrast, left ventricular ejection fraction was significantly lower in patients with versus without MAE (24%+/- 7% vs 31%+/- 10%, P < 0.019. CONCLUSIONS: Neither HRV nor BRS predicted MAE in patients with IDC.

Arrhythmias, Cardiac↗
PubMed2005

Long runs of non-sustained ventricular tachycardia on 24-hour ambulatory electrocardiogram predict major arrhythmic events in patients with idiopathic dilated cardiomyopathy.

This study examined the prognostic significance of the rate and length of non-sustained (NS) ventricular tachycardia (VT) on 24-hour ambulatory electrocardiograms (ECG) recorded in 343 patients with idiopathic dilated cardiomyopathy (IDC) in the prospective Marburg Cardiomyopathy study. NSVT was defined as >/=3 consecutive ventricular premature beats at >120 bpm. During 52 +/- 21 months of follow-up, major arrhythmic events defined as sustained VT, VF, or sudden cardiac death occurred in 46 of 343 patients (13%). Patients with 3-4 beat runs of NSVT had a similar arrhythmia-free survival as patients without NSVT on baseline 24-hour ambulatory ECG. The incidence of major arrhythmic events during follow-up increased significantly from 2% per year in patients without NSVT, to 5% per year in patients with 5-9 beat runs of NSVT, to 10% per year in patients with >/=10 beat runs of NSVT (P < 0.05). Unlike the length, the rate of NSVT was similar in patients with versus without subsequent major arrhythmic events (163 +/- 23 vs 160 +/- 24 bpm). Thus, the length but not the rate of NSVT on 24-hour ambulatory ECG was a predictor of major arrhythmic events in patients with IDC. The presence of NSVT with >/=10 beat runs on ambulatory ECG was associated with a particularly high risk of major arrhythmic events.

Arrhythmias, Cardiac↗
PubMed2005

Marked improvement in left ventricular function and significant reverse left ventricular remodeling within 3 months of cardiac resynchronization therapy in patients with dilated cardiomyopathy.

We monitored reverse left ventricular (LV) remodeling and LV function during the first 6 months of cardiac resynchronization therapy (CRT) in 34 patients (mean age = 55.3 +/- 13.6 years, 28 men) with dilated cardiomyopathy (DCM), left bundle branch block, in stable New York Heart Association class III, and on fixed drug regimen who underwent implantation of CRT systems with or without cardioverter defibrillator back-up. QRS-complex duration was reduced from 169.69 +/- 19.6 ms (SD) to 144.1 +/- 23.4 ms during CRT. Parasternal M-mode and apical 2D-echocardiography was performed before and 3 and 6 months after device implantation. LV enddiastolic (EDD) and endsystolic (ESD) diameters were measured, and biplane LV enddiastolic (EDV), and endsystolic (ESV) volumes and ejection fractions (EF) were calculated using a modified Simpson formula. Significant decreases in LVEDD (P = 0.0064 at 3 months and P = 0.021 at 6 months), LVESD (P = 0.023 at 3 months, and P = 0.003 at 6 months), and LVESV (P = 0.006 resp. P = 0.007), and increases in LVEF (P = 0.003 at 3 months and P < 0.001 at 6 months) were observed. Mean LVEF increased from 23% at baseline to 39% at 6 months. CRT induced prominent reverse LV remodeling and significantly increased LVEF within a few months in patients with DCM.

Cardiac Pacing, Artificial↗
PubMed2005

Preoperative and perioperative care for patients with suspected or established aortic stenosis facing noncardiac surgery.

Current medicine has displayed a trend toward less interfering techniques but more invasive surgical approaches in older patients with more comorbidities. In this population, the prevalence of symptomatic cardiac disease including aortic stenosis is increased. More than 25 years have elapsed since severe aortic stenosis was identified as an independent, important risk factor for patients undergoing general anesthesia for noncardiac surgery. Despite impressive advances in anesthesiologic and surgical techniques, morbidity and mortality in patients with severe aortic stenosis remains high. Published study results clearly show that adverse perioperative risk in patients with aortic stenosis depends on the interaction of factors such as the severity of valve disease, concomitant coronary artery disease, and the severity and/or urgency of the surgical procedures. The mainstay of preoperative evaluation remains the obtaining of a comprehensive preoperative medical history and a physical examination, while transthoracic echocardiography is necessary to establish or exclude hemodynamically relevant aortic stenosis in selected patients. Perioperative care is established in patients with asymptomatic aortic stenosis and/or those undergoing low-risk surgery. However, further preoperative testing or aortic valve replacement prior to noncardiac surgery should be discussed individually with the patients awaiting urgent surgical procedures who are at medium or high risk. At this point, decisions should be made in an interdisciplinary manner, including the opinions/wishes of the patient and the patient's family.

Aortic Valve Stenosis↗
PubMed2005

Bacterial pericarditis: diagnosis and management.

Bacterial pericarditis occurs by direct infection during trauma, thoracic surgery, or catheter drainage, by spread from an intrathoracic, myocardial, or subdiaphragmatic focus, and by hematogenous dissemination. The frequent causes are Staphylococcus and Streptococcus (rheumatic pancarditis), Haemophilus, and M. tuberculosis. In AIDS pericarditis, the incidence of bacterial infection is much higher than in the general population, with a high proportion of Mycobacterium avium-intracellulare infection. Purulent pericarditis is the most serious manifestation of bacterial pericarditis, characterized by gross pus in the pericardium or microscopically purulent effusion. It is an acute, fulminant illness with fever in virtually all patients. Chest pain is uncommon. Purulent pericarditis is always fatal if untreated. The mortality rate in treated patients is 40%, and death is mostly due to cardiac tamponade, systemic toxicity, cardiac decompensation, and constriction. Tuberculous infection may present as acute pericarditis, cardiac tamponade, silent (often large) relapsing pericardial effusion, effusive-constrictive pericarditis, toxic symptoms with persistent fever, and acute, subacute, or chronic constriction. The mortality in untreated patients approaches 85%. Urgent pericardial drainage, combined with intravenous antibacterial therapy (e.g. vancomycin 1g twice daily, ceftriaxone 1-2g twice daily, and ciprofloxacin 400 mg/day) is mandatory in purulent pericarditis. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable. The initial treatment of tuberculous pericarditis should include isoniazid 300 mg/day, rifampin 600 mg/day, pyrazinamide 15-30 mg/kg/day, and ethambutol 15-25 mg/kg/day. Prednisone 1-2 mg/kg/day is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Pericardiectomy is reserved for recurrent effusions or continued elevation of central venous pressure after 4-6 weeks of antituberculous and corticosteroid therapy.

Anti-Bacterial Agents↗
PubMed2004

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. METHODS AND RESULTS: All 9 exons of the CYP2J2 gene and its proximal promoter were sequenced in 132 patients to identify potential variants. Functional consequence of a single nucleotide polymorphism (SNP) in the promoter of CYP2J2 was further evaluated by use of transcription factor-binding and reporter assays. A total of 17 polymorphisms were identified. One of the most relevant polymorphisms in terms of frequency and functional importance is located at -50 (G-50T) in the proximal promoter of CYP2J2. Screening of 289 patients with coronary artery disease and 255 control subjects revealed 77 individuals with the G-50T SNP (17.3% of coronary artery disease patients, 10.6% of control subjects; P=0.026). The association of the G-50T polymorphism remained significant after adjustment for age, gender, and conventional cardiovascular risk factors (OR, 2.23; 95% CI, 1.04 to 4.79). The G-50T mutation resulted in the loss of binding of the Sp1 transcription factor to the CYP2J2 promoter and resulted in a 48.1+/-2.4% decrease in CYP2J2 promoter activity (P<0.01). Plasma concentrations of stable EET metabolites were significantly lower in individuals with the G-50T SNP. CONCLUSIONS: A functionally relevant polymorphism of the CYP2J2 gene is independently associated with an increased risk of coronary artery disease.

3' Untranslated Regions↗
PubMed2004

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. A total of 458 sequence changes could be identified. These sequence changes were distributed among the whole mitochondrial DNA (mtDNA). An increased number of novel missense mutations could be detected nearly in all genes encoding for protein subunits in DCM patients. In genes coding for NADH dehydrogenase subunits the number of mtDNA mutations detected in patients with DCM was significantly increased (p < 0.05) compared with control subjects. Eight mutations were found to occur in conserved amino acids in the above species. The c.5973G > A (Ala-Trp) and the c.7042T > G (Val-Asp) mutations were located in highly conserved domains of the gene coding for cytochrome c oxidase subunit. Two tRNA mutations could be detected in the mtDNA of DCM patients alone. The T-C transition at nt 15,924 is connected with respiratory enzyme deficiency, mitochondrial myopathy, and cardiomyopathy. The c.16189T > C mutation in the D-loop region that is associated with susceptibility to DCM could be detected in 15.6% of patients as well as in 9.7% of controls. Thus, mutations altering the function of the enzyme subunits of the respiratory chain can be relevant for the pathogenesis of dilated cardiomyopathy.

Adult↗
PubMed2004

[Noninvasive methods in the diagnosis of macro- and microangiopathy of peripherial and carotid arteries].

PURPOSE: Indications and diagnostic value of the most important noninvasive procedures for the diagnosis of peripheral arterial disease and diseases of the supraaortic arteries are reviewed in this article with particular emphasis on cardiologic questions. PERIPHERAL ARTERIAL DISEASE: As compared to coronary artery disease, peripheral arterial disease has long been addressed as being negligible in number and importance, a view that had to be reassessed in recent years. The prevalence of claudication and critical leg ischemia has increased. Earlier diagnosis and specific therapeutic regimens will be able to prevent or at least slow progression of the disease and, thereby, major amputation. The patient's history and physical examination in addition to measurement of the ankle-brachial index (ABI; determined by dividing the systolic pressure measured by Doppler ultrasonography of the A. dorsalis pedis or A. tibialis posterior by that of the A. brachialis) usually allows for the diagnosis of peripheral arterial disease (ABI < 0.9). If in doubt (ABI > 0.9, but presence of typical claudication), a treadmill test or additional tests such as pressure-pulse recording (mechanical oscillography), toe pressure measurements, or duplex ultrasonography should be performed. When peripheral arterial disease has been diagnosed, duplex ultrasonography or treadmill testing aids in planning additional diagnostic procedures and the adequate therapeutic regimen. Transcutaneous oxymetry is of prognostic value in assessing the tendency of wound healing in distal limb ulceration and can distinguish between critical limb ischemia and complicated claudication. Thermography is used to document functional and organic peripheral arterial occlusions and capillaroscopy to directly view nail fold capillaries in order to distinguish between primary and secondary Raynaud's phenomenon. Noninvasive radiologic techniques in the diagnosis of peripheral arterial disease are also discussed in this journal. SUPRAAORTIC ARTERIES: Noninvasive diagnostic procedures in assessing disease of the supraaortic arteries include history-taking, physical examination, continuous-wave-(cw-)Doppler and color-coded ultrasonography. Cw-Doppler ultrasonography is still widely used and sufficient in diagnosing moderate to severe stenosis or occlusion of the carotid artery. B-mode and color-coded ultrasonography has several advantages over cw-Doppler ultrasonography through direct visualization of the vascular membrane, perivascular structures, and intravascular blood flow. Carotid stenosis < 50% and plaque morphology can be assessed, inflammatory processes, aneurysms, and dissections diagnosed. Increase in intima-media thickness and echolucent plaques are associated with cerebral ischemic events and can be diagnosed via duplex sonography. These findings have great implications in the consultation of patients with atherogenic risk factors.

Arterial Occlusive Diseases↗
PubMed2004

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. 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.

Arrhythmias, Cardiac↗
PubMed2004

[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. 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.

Cardiomyopathy, Dilated↗
PubMed2004

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). Since free acids of EPA and DHA are required for most of their biological effects, it appears essential not only to build up stores in the body for release of these fatty acids, but also to provide a sustained uptake of EPA and DHA in the form of ethyl esters. In contrast to rapidly absorbed triacylglycerols from fish, ethyl esters are taken up more slowly within 24 h. For the administration of 1 g/day highly purified EPA+DHA ethyl esters (Omacor) to healthy volunteers, it is shown that EPA is increased from 0.6% to 1.4% within 10 days, while DHA is increased from 2.9% to 4.3%. After withdrawal, EPA and DHA approach baseline values within 10 days. A gas chromatographic procedure was established which requires only 10 microl of whole blood for the identification of more than 35 fatty acids. Evidence is summarized strengthening the concept that a low "EPA+DHA level" presents a risk for sudden cardiac death and that the administration of 840 mg/day of EPA+DHA ethyl esters raises the "EPA+DHA level" to approximately 6% that is associated with a marked protection from sudden cardiac death. For reducing pro-inflammatory eicosanoids and cytokines, a higher "EPA+DHA level" is required which can be achieved with an intake of 2-4 g/day of 84% EPA+DHA ethyl esters. For assessing influences from pro-inflammatory eicosanoids and cytokines, the EPA/arachidonic acid ratio ("EPA/AA ratio") was identified as diagnostic parameter. To assess the dietary EPA+DHA intake, fatty acids were determined in fish dishes of the cafeteria of the Philipps University Hospital Marburg, Germany. The EPA+DHA content of the popular Alaska Pollock was 125 +/- 70 mg/100 g. A once daily fish dish can thus not provide the 840 mg/day EPA+DHA administered in the GISSI Prevention Study in the form of ethyl ester which markedly reduced the risk of sudden cardiac death in postmyocardial infarction patients. Nonetheless, at least two preferably oily fish meals per week should be consumed as preventive measure by persons without coronary artery disease. With documented coronary heart disease, it was advised to consume approximately 1 g/day of EPA+DHA.

Administration, Oral↗
PubMed2004

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. Accumulating data has revealed an important inflammatory component in the pathogenesis of dilated cardiomyopathy (DCM), and there is growing evidence, that myocarditis and DCM are closely related. Many faces of DCM coexist, while different phases of the disease progress simultaneously: phase 1 is dominated by viral infection itself, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation without an infectious agent and cardiac inflammation. Separation between the phases is not always distinct, they may overlap one another and phase 1 and 2 may recur after progression of DCM. Appropriate treatment during phase 1 includes eradication of virus and amelioration of injury caused by the virus. During phase 2, which is characterized by autoimmune processes, immunosuppression is the most appropriate therapy and warrants sophisticated diagnostic strategies including molecular biological and immunohistochemical techniques. Phase 3, DCM, although a result of viral and autoimmune injury, may then progress independently. The more attention given to serologic, molecular and immunologic factors to characterize and diagnose DCM lead to several changes in the terminology. The term cardiomyopathy is no longer reserved for the idiopathic forms but can be used interchangeably with the term heart muscle diseases including specific, secondary forms. Right ventricular cardiomyopathy (RVCM), valvular, hypertensive, ischemic, and inflammatory cardiomyopathy have been introduced. Idiopathic, autoimmune, and infectious forms of inflammatory cardiomyopathy were recognized. Viral cardiomyopathy is defined as viral persistence in a dilated heart. It may be accompanied by myocardial inflammation and is then termed inflammatory viral cardiomyopathy. Because of the overlap of pathophysiological stages in DCM, design of the appropriate therapy is important. It requires the immunohistochemical and molecular biological investigation of endomyocardial biopsies in parallel. In the modern molecular era the infective agent-immune system-host interaction has to be clarified leading to a better knowledge of the etiology of DCM. This may change the management of the disease in the future. One of the hopes is to discern the underlying dominant mechanism in a given patient to make a decision for the most promising therapy.

Animals↗
PubMed2004

Treatment of inflammatory dilated cardiomyopathy and (peri)myocarditis with immunosuppression and i.v. immunoglobulins.

OBJECTIVES: Treatment objectives in inflammatory dilated cardiomyopathy (DCMi), myocarditis (M) and peri(myo)carditis are 1) the elimination of inflammatory cells from the myocardium and pericardium, 2) the elimination or (second best) mitigation of B-cell products such as antibodies and immuncomplexes directed against cardiac epitopes such as sarcolemmal, fibrillary and mitochondrial epitopes, and 3) the eradication of the causative viral or microbial agent, if present. ANTIPHLOGISTIC TREATMENT: A "non-specific" anti-inflammatory treatment in peri(myo)carditis can be carried out with antiphlogistics (NSAIDs preferably colchicine 1-3 mg/d) independent from the presence of the infective agent. In larger virus and bacteria negative effusions we recommend intrapericardial instillation of cristalloid triamcinolon (Volon A) at a dose of 500 mg/m(2), which should be left in place to have a sustained effect over at least 4 weeks. This will effectively prevent recurrences particularly when colchicine is added over a period of at least 3-6 months. Taking into account the 2004 ESC task force recommendations on the management of pericardial diseases the treatment recommendation for NSAIDs and colchicine can be classified as level of evidence A, indication class I, for intrapericardial triamcinolon instillation as level of evidence B, indication class IIa. IMMUNOSUPPRESSION: In (immuno)histologically validated autoreactive (virus negative) myocarditis and DCMi double-blind randomized trials are lacking to demonstrate the superiority of immunosuppression over conventional heart failure management. The only published randomized and double-blind immunosuppression treatment trial (American Myocarditis Treatment Trial) was underpowered and did not distinguish viral from non-viral disease. It showed neither benefit nor harm of a combination of cyclosporin and prednisone. A number of retrospective analyses of immunosuppression in myocarditis showed some benefit of surrogate parameters (ejection fraction, exercise tolerance) but improvement under conventional heart failure treatment cannot be ruled out completely as the main cause for amelioration. ESETCID (European Study on the Epidemiology and Treatment of Cardiac Inflammatory Disease) is a double-blind, randomized, placebo-controled three-armed trial with prednisolone and azathioprine for autoreactive (virus negative) DCMi, interferon alpha for enterovirus positive DCMi, high-dose immunoglobulin for cytomegalovirus and intermediate dose for adeno- and Parvo B19 DCMi. It has now randomized more than 120 patients to the different treatment arms. Its final result has still to be awaited.-Patients not willing to randomize in the trial were included in a registry follow-up, which shows improvement of hemodynamic parameters and elimination of the inflammation in the majority of patients. This is in concordance with several non-randomized trials. Since evidence is conflicting (level of evidence C, indication class IIb; if negative viral etiology is taken into consideration class IIa) treatment with immunosuppression cannot be generally recommended but should be further evaluated in doubleblind randomized clinical trials or at least in controlled trials and registries. This also applies to treatment with interferon for enteroviral or other viral infections in the heart. IMMUNOADSORPTION: : The elimination of anticardiac antibodies, which have been associated with DCMi, is a currently discussed concept, which is supported by published registry data and a few very small controlled investigations but not by a randomized double-blind trial with clinical endpoints of relevance. In some studies immunoglobulins have been substituted, so that an additional immunomodulatory effect has to be taken into account. The current proof of concept can be ranked level of evidence C, indication class IIa only. An even more challenging and still more attractive hypothesis is that cardiac inflammation caused by specific circulating beta-adrenoceptor antibodies can be eradicated with the elimination of the beta-receptor antibody thus healing dilated cardiomyopathy. Application of this approach can be ranked level of evidence C, indication class IIb at present only. Therefore these two pathophysiologically attractive concepts have to await further validation by a double-blind, randomized clinical endpoint trial. IMMUNOGLOBULIN TREATMENT: It has been shown that immunoglobulins have both an antiviral and an anti-inflammatory effect. They may suppress proinflammatory cytokines and reduce oxidative stress. HIGH-DOSE I.V. IMMUNOGLOBULINS (IVIG): In biopsy proven CMVmyocarditis a controlled trial demonstrated eradication of inflammation and of the virus (level of evidence B, indication class IIa), which is in accordance with registry data and case reports. In suspected myocarditis (not biopsy proven, no viral etiology established or excluded) conflicting data exist with respect to the improvement of surrogate markers such as the ejection fraction under high-dose immunoglobulins. More evidence can be weighted in favour of a positive treatment effect (level of evidence B, indication class IIb). Importantly there were no detrimental effects of the ivIG reported in these trials. One has to consider the high costs of this treatment, however. A trial taking into account the different etiologies (different viruses assessed separately vs. non-viral/autoreactive vs. placebo) is still lacking. MODERATE-DOSE I.V. IMMUNOGLOBULINS: Registry data support a positive effect of 20 g i.v. pentaglobin (IgG and IgM) in adenovirus positive myocarditis for clinical improvement, eradication of both the inflammation and the virus. In Parvo B19 myocarditis our own registry data indicate that clinical improvement can be noted, but only inflammation is successfully eliminated, whereas Parvo B19 persistence remains a problem in the majority of patients. In Parvo B19 associated DCMi therefore dose finding studies and randomized trials are needed.

Cardiomyopathy, Dilated↗