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Biomedical subjects

G Hufnagel

Publications and source records attributed to G Hufnagel.

At least 19 recordsLinked to original sources
PubMed2001

[Prevention of atrial arrhythmias by pacing].

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.

Algorithms↗
PubMed2001

[Sclerosing peritonitis].

The case presented in this study illustrates the peritoneal changes observed in long-term peritoneal dialysis (PD) patients. This male patient was on peritoneal dialysis (CAPD) for seven months before and 86 months after renal transplantation. Two episodes of peritonitis occurred during that time. The patient developed symptoms (ascites, gastro-intestinal disturbances, deteriorating general condition, inflammatory syndrome) four months after starting hemodialysis, one month after ablation of the PD catheter. Other potential causes (infection, malignancy, hepatitis, etc.) of these symptoms were ruled out following an exhaustive etiological work-up. A final diagnosis of sclerosing peritonitis was made, and the patient was started on corticosteroid therapy. Both morphological and functional alterations of the peritoneal membrane associated with long term PD and the detection of such alterations in everyday practice are reviewed here, along with possible etiological factors and therapeutic measures discussed in the literature. A better understanding of the pathophysiological mecHanisms underlying these alterations would make it possible to develop preventive measures, such as more biocompatible dialysates.

Adrenal Cortex Hormones↗
PubMed2000

Arrhythmias in acute pericarditis. An endomyocardial biopsy study.

It is still controversial whether the arrhythmias in acute pericarditis are of myocardial or pericardial origin. The aim of the present study was to investigate the occurrence of arrhythmias and conduction disorders in patients with acute pericarditis with no endomyocardial biopsy evidence of myocarditis (group 1: 40 patients, 65% males, mean age 45.6 +/- 15.7 years, mean heart rate [HR] 98.7 +/- 22.2 beats per minute) in comparison to endomyocardial biopsy proven acute myocarditis/perimyocarditis (group 2: 10 patients, 3/10 with perimyocarditis, 70% males, mean age 46.1 +/- 15.8 years, mean heart rate 76.7 +/- 33.1 beats per minute). At the initial assessment all patients underwent comprehensive clinical work-up including echocardiography, cardiac catheterization, and endomyocardial biopsy. In all patients biventricular endomyocardial biopsy was performed using standard femoral approach and Schikumed 7 F or 8 F bioptomes. Tissue samples were stained by H & E, v. Gieson and independently reviewed by two cardiac pathologists. In addition immunohistochemistry and immunocytochemistry were performed, and only patients fulfilling Dallas and World Heart Federation criteria were selected for group 2. Comparative analysis of electrocardiograms and 24-hour Holter recordings at initial presentation revealed in group 1 vs group 2 significantly less frequent paroxysmal supraventricular tachyarrhythmias (5% vs 40%), and ventricular fibrillation (0 vs 20%), in contrast to atrial fibrillation that occurred more often (20% vs 0) (all p < 0.05). Furthermore, in the group 2 one patient died due to VF and two patients underwent ICD implantation. Low voltage (40% vs 30%) and ST/T wave changes (47.5% vs 30%), as well as the incidence of the II degree AV block (5% vs 0) and complete AV block (2.5% vs 10%) were not significantly different between the groups. In conclusion, patients with pericarditis and no endomyocardial biopsy indications of myocarditis had significantly less often life threatening rhythm disorders in contrast to patients with endomyocardial biopsy proven acute myocarditis/perimyocarditis. On the contrary, incidence of transitory atrial fibrillation was higher in acute pericarditis, than in myocarditis.

Acute Disease↗
PubMed2000

Cytokine activation in pericardial fluids in different forms of pericarditis.

There are many causes of pericardial effusion and it is useful to classify them etiologically, since this disorder is the most common pathologic process involving the pericardium. This report details our experience with pericardioscopy and epicardial biopsy in 101 patients with pericardial effusions in whom pericardioscopy was performed. By means of clinical data and polymerase chain reaction we tried to elucidate the etiology of the pericardial effusion which were classified as follows: we found 41 effusions to be induced by primary malignant tumors or tumors metastatic to the pericardium. Specific diagnosis of viral and bacterial pericarditis was established in 17 patients by examination of the pericardial effusion with PCR, where we found 3 patients positive for adenovirus, 5 patients positive for cytomegalovirus, 2 patients positive for enterovirus-RNA and 5 patients positive for borrelia Burgdorferi-DNA. Additionally, idiopathic effusions (lymphocytic and autoreactive) were seen in 35 patients. In summary immunological and molecular biology investigations seem to provide an additional tool in the diagnostic of pericardial effusion with unknown etiology. If we focus on the ELISA results, there is some evidence, that the demonstration [table: see text] of activation markers and soluble mediators of inflammation such as Il-6, Il-8 and IFN-gamma in pericardial effusion and the simultaneously lack of these mediators in sera of the patients first may be helpful in the discrimination of autoreactive and lymphocytic effusion. Second, this cytokine pattern or distribution indicates a possible local inflammatory process, where these cytokines were all released from activated T lymphocytes present in lymphocytic effusion. In the future, this may have therapeutic implications.

Bacterial Infections↗
PubMed2000

Definition of inflammatory cardiomyopathy (myocarditis): on the way to consensus. A status report.

This article reviews the current state of consensus reached for the diagnosis of myocarditis and dilated cardiomyopathy on the basis of conventional histopathological and immunohistochemical methods for inflammatory infiltrates in addition to molecular biological methods for persistence of viral genome in endomyocardial biopsies. Additionally, a brief overview is presented stating the current knowledge on effector mechanisms of the immune system in myocarditis and dilated cardiomyopathy.

Autoantibodies↗
PubMed2000

Prevalence of viral genome in endomyocardial biopsies from patients with inflammatory heart muscle disease.

In the report of the 1995 World Health Federation/International Society and Federation of Cardiology (WHF/ISFC) Task Force on the Definition and Classification of Cardiomyopathies, the definition of heart muscle diseases was updated. Idiopathic, autoimmune, and infectious forms of inflammatory cardiomyopathy are now recognized in this definition. Enteroviruses, adenoviruses and cytomegaloviruses are considered as main etiopathological factors in the pathogenesis of inflammatory heart disease. A wide range of different assays have been and are currently being used, either alone or in combination, to assay for the presence of enteroviral RNA and/or DNA of cytomegalo- and adenoviruses in endomyocardial biopsy and explanted heart samples. The prevalence of cardiotropic viruses in endomyocardial biopsies of patients with clinically suspected inflammatory cardiomyopathy varies widely: enteroviral genome was detected in endomyocardial biopsies of 3 to 53% of patients, cytomegaloviral DNA was detected in 3 to 40% of patients with inflammatory heart disease and adenoviruses in 3 to 23% of the patients. This report summarizes the methods that have been used and the results of molecular biological investigation with polymerase chain reaction, which were reported by several groups over the last years. Taking this together it seems to be clear that the improvement of molecular biological techniques and the experience of people working with these methods will lead to more reliable results on prevalence, persistence and the diagnostic value of these investigations. These findings have to be taken into account in future diagnostic and therapeutic studies in the field of cardiomyopathies.

Adenovirus Infections, Human↗
PubMed2000

The European Study of Epidemiology and Treatment of Cardiac Inflammatory Diseases (ESETCID). First epidemiological results.

By including immunohistochemical parameters the WHF Task Force for the Definition of Acute and Chronic Myocarditis expanded the light microscopical Dallas criteria of myocarditis. The rapid development of new molecular biological techniques such as polymerase chain reaction (PCR) and in-situ hybridization has improved our understanding of the underlying etiological and pathophysiological mechanisms in inflammatory heart disease. Treatment of dilated cardiomyopathy with inflammation is still controversial, however. The American Myocarditis Treatment Trial could not demonstrate a significant difference in the improvement of ejection fraction between patients with active myocarditis in the cyclosporine/prednisolone treated group when compared to placebo. In the European Study of Epidemiology and Treatment of Inflammatory Heart Disease (ESETCID) patients with acute or chronic myocarditis are treated specifically according to the etiology of the disease. Patients are screened not only for infiltrating cells, but also for the presence of persisting viral genome (enterovirus, cytomegalovirus and adenovirus). By investigating endomyocardial biopsies of 3,055 patients ongoing inflammatory processes in the heart could be found in 17.2%. Only 182 showed a reduced ejection fraction below 45% fulfilling the entrance criteria for the ESETCID trial. These data imply that in symptomatic patients inflammatory heart muscle disease has to be considered regardless of left ventricular function and that endomyocardial biopsy can be an important tool for diagnosis. Virus could be detected in 11.8% (enterovirus 2.2%, cytomegalovirus 5.4%, adenovirus 4.2%). These first epidemiological results of this prospective randomized study demonstrate that viral persistence may contribute to the pathogenesis of inflammatory heart muscle disease, and that in chronic myocarditis viral persistence occurs in a smaller percentage of patients compared to previously published studies which were performed on highly selected patients.

Cardiomyopathies↗
PubMed2000

Arrhythmia risk stratification in idiopathic dilated cardiomyopathy based on echocardiography and 12-lead, signal-averaged, and 24-hour holter electrocardiography.

BACKGROUND: To date, considerable controversy exists regarding noninvasive arrhythmia risk stratification in idiopathic dilated cardiomyopathy (IDC). Methods and Results Between 1992 and 1997, 202 patients with IDC without a history of sustained ventricular tachycardia (VT) underwent echocardiography, signal-averaged electrocardiogram (ECG), and 24-hour Holter ECG in the absence of antiarrhythmic drugs. During 32 +/- 15 months of prospective follow-up, major arrhythmic events, including sustained VT, ventricular fibrillation, or sudden death, occurred in 32 (16%) of 202 patients. After adjusting for baseline medical therapy and antiarrhythmic therapy during follow-up, multivariate Cox regression analysis identified a left ventricular (LV) end-diastolic diameter >/=70 mm and nonsustained VT on Holter as the only independent arrhythmia risk predictors. The combination of an LV end-diastolic diameter >/=70 mm and nonsustained VT was associated with a 14. 3-fold risk for future arrhythmic events (95% confidence interval 2. 3-90). To further elucidate the prognostic value of LV ejection fraction, multivariate Cox analysis was repeated with ejection fraction forced to remain in the model. In the latter model, an ejection fraction </=30% combined with nonsustained VT on Holter was found to be a significant arrhythmia risk predictor with a relative risk of 14.6 (95% confidence interval 2.2-97). CONCLUSIONS: The combination of an LV end-diastolic diameter >/=70 mm and nonsustained VT on Holter, and the combination of LV ejection fraction </=30% and nonsustained VT on Holter, identify a subgroup of patients with IDC with a 14-fold risk for subsequent arrhythmic events. These findings have important implications for the design of future studies evaluating the role of prophylactic defibrillator therapy in patients with IDC.

Adolescent↗
PubMed2000

Effects of atorvastatin on dyslipidaemia in uraemic patients on peritoneal dialysis.

BACKGROUND: Our purpose was to evaluate the efficacy and safety of atorvastatin, a potent cholesterol- and triglyceride-lowering agent, in peritoneal dialysis patients with dyslipidaemia. METHODS: Peritoneal dialysis patients with hypercholesterolaemia were treated for 4 months with atorvastatin at a starting dose of 10 mg. The dose could be increased to 20 or 40 mg in order to achieve the following targets: plasma LDL-cholesterol of 130 mg/dl for primary prevention of coronary heart disease, plasma LDL cholesterol of 100 mg/dl for secondary prevention, and plasma triglycerides of 200 mg/dl. Plasma lipid profile and liver and muscle enzyme levels were assessed at baseline and then monthly during treatment. RESULTS: Thirty-one patients with hypercholesterolaemia were included (16 males and 15 females; mean age 57+/-16 years; mean duration of peritoneal dialysis 27+/-17 months). Nineteen of the patients also had hypertriglyceridaemia and seven had diabetes. Twenty patients had no coronary history (primary prevention), whereas nine had experienced a coronary event (secondary prevention). In the primary and the secondary prevention patients, mean LDL-cholesterol levels (mg/dl) decreased significantly by 42 and 46% from 204+/-23 to 119+/-27 (P<0. 001) and 198+/-37 to 104+/-21 (P<0.001), and mean triglyceride levels (mg/dl) decreased by 37 and 26% from 289+/-132 to 186+/-92 (P<0.001) and 201+/-62 to 150+/-54 (P<0.001 respectively). Nineteen primary prevention and seven secondary prevention patients achieved the LDL-cholesterol target. The triglyceride target was achieved by 15 of the 19 hypertriglyceridaemic patients. Two patients stopped treatment (one because of gastrointestinal disturbances, the other because of an allergic skin reaction). After 4 months, there were no changes in enzyme levels. CONCLUSION: Atorvastatin is an effective and safe lipid-lowering agent for peritoneal dialysis patients with mixed dyslipidaemia.

Adult↗
PubMed1999

Intrapericardial treatment of inflammatory and neoplastic pericarditis guided by pericardioscopy and epicardial biopsy--results from a pilot study.

From a registry of 136 patients undergoing pericardiocentesis, 14 patients with autoimmune and 15 patients with neoplastic effusions were selected. All underwent pericardioscopy, epicardial and pericardial biopsy with histologic, immunohistologic, and polymerase chain reaction/or in situ hybridization analysis for microbial DNAs and RNA. Pericardioscopy identified neoplastic effusions by the high occurrence of protrusions. Fibrin threads and layers and neovascularization were found in both groups. For identification of the inflammatory and neoplastic process, the combined analysis of the cytology of the effusion and epicardial biopsy evaluation proved to be most important. Epicardial biopsy demonstrated a slightly higher sensitivity for identifying neoplastic disorders in the pericardium than cytology alone. Pericardial biopsy was inconclusive. Intrapericardial administration of 1 g of crystalloid triamcinolone in autoreactive pericarditis prevented recurrence in 13 of the 14 cases after 3 months and in 12 of the 14 cases after 1 year. In neoplastic effusion, intrapericardial administration of 50 mg cis-platin for 24 h prevented recurrence of a hemodynamically relevant effusion after 3 months in all, and after 6-12 months in 14 of 15 patients. Mortality in neoplastic effusion due to noncardiac tumor progression was 47 and 80%, respectively, after 3 and 6 months, as can be expected in endstage neoplastic disease. This pilot study demonstrates that local drug application is feasible, life-saving, and well tolerated by the patients. It opens perspectives for local drug application in other cardiac disorders as well.

Adolescent↗
PubMed1999

[Cell death in inflammatory heart muscle diseases--apoptosis or necrosis?].

Cell death can be induced by 2 different mechanisms: necrosis and apoptosis. Necrosis, on the one hand, is usually caused by unphysiological stress factors such as hyperthermia or hypoxia, apoptosis, on the other hand, is part of the normal organ development and controls for example immune responses. Morphologically, necrosis is characterized by swelling of cells and their organelles leading to the disruption of the cell membrane, which in turn causes an inflammatory reaction in the surrounding tissue. Morphological and biochemical criteria (Figure 1, Table 1) of apoptosis are the condensation of chromatin leading to the development of apoptotic bodies or membrane-enclosed vesicles containing oligonucleosomal DNA fragments. Important diagnostic tools of cell death (Table 2), such as the TUNEL test (Figure 2) or gel electrophoresis of extracted DNA (Figure 3) are based on the above mentioned biochemical characteristics, but a reliable differentiation of apoptotic versus necrotic processes is not always possible. Experimental studies in animals and studies in various diseases of the cardiovascular system were able to show that apoptosis in myocytes can be induced, an issue that has long been discussed controversially. Ischemia, reperfusion, and myocardial infarction were also shown to lead to apoptosis in cardiomyocytes, whereas cell destruction was caused mainly by necrosis. Several authors (Table 3) demonstrated apoptotic indices in cardiomyocytes of patients with dilatated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and patients with acute infarction from 0.25 to 35% by the use of the TUNEL test. Others were able to demonstrate an elevated expression of Fas-receptor in cells of atheroslerotic plaques in patients with atherosclerosis and high indices of apoptotic cardiomyocytes in patients with chronic heart failure. We investigated endomyocardial biopsies of patients with inflammatory cardiomyopathy, DCM without inflammatory reaction but the presence of adenoviral or cytomegaloviral genome and idiopathic DCM using the TUNEL test. The percentage of apoptotic cardiomyocytes in biopsies of patients with DCMi was 1.03 and in biopsies of patients with adenoviral genome 0.25, whereas in all other groups no apoptosis was found. If apoptosis plays a major role in myocardial diseases such as heart failure, arrhythmia and others, blocking this mechanism will have to be considered as a therapeutical strategy. Therefore, studies on the extent of apoptotic processes in diseased versus healthy cardiac tissue are of great importance.

Animals↗
PubMed1999

[Prospective evaluation of effect of carvedilol therapy on heart rate variability in patients with dilated cardiomyopathy].

The aim of the present study was to assess the effects of carvedilol therapy in addition to conventional heart failure therapy on heart rate variability (HRV) and on left ventricular function in 14 patients with mild to moderate heart failure due to idiopathic dilated cardiomyopathy (IDC). After a 3- to 4-week titration period, carvedilol was titrated up to 50mg daily, or the highest dose tolerated (at least 25mg daily). Maintenance treatment was then continued for 8 weeks. Digital 24-hour Holter recordings were obtained at baseline and after 8 weeks of carvedilol therapy. HRV for the entire 24-hour period was computed in the time domain using the Oxford Medilog Excel 2 analysis system. Measures of HRV included the mean of all coupling intervals between normal beats (RRm), the standard deviation of all normal RR intervals (SDNN), the square root of the mean of the squared differences between adjacent normal RR intervals (rMSSD), and the proportion of adjacent normal RR intervals differing >50 ms (pNN50). Additional treatment with carvedilol induced a significant increase in HRV: SDNN increased from 77+/-21 ms to 110+/-22 ms (p=0.001), rMSSD from 19+/-7 ms to 26+/-7 ms (p=0.02), and mean pNN50-value increased from 1.7+/-1.3% to 5.5+/-4.5% (p<0.01) under therapy with carvedilol. Mean heart rate on carvedilol calculated over 24 hours was 13 beats less than at baseline (75 bpm versus 88 bpm, p<0.01). After 2 months of additional treatment with carvedilol, both hemodynamic and clinical parameters improved: left ventricular ejection fraction increased from 24+/-7% to 30+/-10% (p<0.05), and New York Heart Association class decreased from 2.5+/-0.8 to 1.8+/-0.7 (p<0.05). In summary, eight weeks of additional carvedilol therapy induced a significant increase in HRV parameters related to parasympathetic activity in patients with IDC. Whether increased vagal tone may contribute to the protective effect of carvedilol has to be evaluated by further studies.

Adrenergic beta-Antagonists↗
PubMed1999

The influence of automated peritoneal dialysis on the decrease in residual renal function.

BACKGROUND: Automated peritoneal dialysis (APD) has been increasingly used in recent years. Our purpose was to investigate whether the good preservation of residual renal function (RRF) that has been reported in patients on continuous ambulatory peritoneal dialysis (CAPD) is also observed in APD. METHODS: RRF was determined and compared prospectively over 1 year in two groups of peritoneal dialysis (PD) patients: 18 consecutive new patients starting on APD (12 continuous cyclic peritoneal dialysis (CCPD) patients and six nightly intermittent peritoneal dialysis (NIPD) patients) and 18 selected patients who had started on CAPD at the same time and were matched for baseline characteristics. RRF was assessed on normalized creatinine clearance (ml/min/1.73 m2) measured before the start of PD, at 6 months, and at 1 year. Wilcoxon's rank sum test was used to compare differences between the two groups. RESULTS: Creatinine clearance (ClCr) was 6.1 ml/min in the APD group and 6 ml/min in the CAPD group at the start of PD. The monthly rate of ClCr decrease was significantly higher in the APD group: -0.28 ml/min vs -0.1 ml/min (P = 0.04) at 6 months and -0.26 ml/min vs -0.13 ml/min (P = 0.005) at 1 year. RRF decreased at the same rate in patients treated with NIPD or CCPD. The daily instilled volume of 3.86% glucose dialysis solution (l/day) was higher in APD patients than in CAPD patients: 2.5 vs 0 at 6 months and 1 year but there was no significant difference in ultrafiltration rate (l/day) between APD and CAPD patients at these timepoints: 0.53 vs 0.6 and 0.88 vs 0.7 respectively. There was no difference between the two groups in body weight and blood pressure, which remained stable in both groups throughout the study period. CONCLUSIONS: RRF declined rapidly in APD patients whereas it was well preserved in CAPD patients. This may be explained by the less stable fluid and osmotic load together with the intermittent nature of APD and the larger use of hypertonic dialysate. RRF should be closely monitored in APD patients in order to adjust PD prescriptions and maintain adequacy.

Creatinine↗
PubMed1998

[Cardiotropic DNA viruses and bacteria in the pathogenesis of dilated cardiomyopathy with or without inflammation].

In the report of the 1995 WHO/ISFC task force on the definition and classification of cardiomyopathies a new entity within the dilated cardiomyopathies was introduced as "inflammatory cardiomyopathy". It is defined as myocarditis associated with cardiac dysfunction. Idiopathic, autoimmune and infectious forms of inflammatory cardiomyopathy are now recognized through this definition. Dilated cardiomyopathy with inflammation (DCMi, chronic myocarditis) was also defined by a recent ISFC task force as > 14 lymphocytes/macrophages/mm3. Enteroviruses, adenoviruses and cytomegaloviruses are considered as main etiopathogenetic factors in the pathogenesis of inflammatory heart disease and have been demonstrated as important trigger for inflammatory cardiac disease. They may also cause dilated cardiomyopathy by viral persistence or secondary immunopathogenesis due to antigenic or molecular mimicry. For the detection of viral persistence the investigation of endomyocardial biopsies in patients with cardiomyopathy by the use of polymerase chain reaction and southern blot analysis is an important step for the standardization of diagnostic criteria on virally induced inflammatory cardiomyopathy. Present studies indicate an incidence of cytomegalovirus-DNA in patients with inflammatory cardiomyopathy in 10%, adenoviral-DNA in 17% and borreliosis only in rare cases (< 1%). In dilated cardiomyopathy without inflammation the respective incidences were for cytomegalovirus 12%, 15% for adenovirus and only 0.5% of cases for borreliosis. In addition the results of immunohistochemical analysis and molecular biological investigations of endomyocardial biopsies may have implications for future therapeutic studies. Depending on the etiology of the disease, immunosuppression may have benefit for patients with virus-negative cardiomyopathy with inflammation in contrast to patients with cytomegalo-, adenovirus-DNA or enteroviral persistence, in whom immunomodulation with hyperimmunoglobulins or immunoglobulins may be a feasible therapeutic option. Patients with a positive PCR for Borrelia burgdorferi should be treated with 3rd generation cephalosporines and/or sublactam.

Biopsy↗
PubMed1998

[Therapy of dilated cardiomyopathies with and without inflammation].

Diagnosis of inflammatory dilated cardiomyopathy relies on the histological and immunohistological examination of endomyocardial biopsies. Only with the demonstration of the etiological agents in the myocardium specific therapy can be attempted. Whereas the spontaneous course of endemic myocarditis with little hemodynamic impairment is fair, the prognosis of symptomatic myocarditis and dilated cardiomyopathy is poor, with complete restitution in 35% and a 10-year survival rate of 30%. Restriction of physical activity is a validated form of therapy with normalization of the heart size in 40 to 60%. Symptomatic medical therapy consists of digitalis, diuretics, ACE-inhibitors and vasodilators and betablocker therapy, where a reduction of mortality was demonstrated in clinical (sub)studies up to 60%. Specific forms of therapy in inflammatory cardiomyopathy rely on the demonstration or lack of viral persistence or signs of autoreactivity in the myocardial tissue. Immunosuppressive therapy in autoimmune forms improved cardiac function in up to 60% of the patients in controlled trials, when compared to controls (40%). The double-blind randomized myocarditis treatment trial, which unfortunately did not distinguish viral from autoimmune myocarditis could not demonstrate such a benefit, however. Depending on the etiology of the disease, immunomodulation with immunoglobulins or interferon or antiviral therapy with hyperimmunoglobulins are presently tested in clinical treatment trials (ESETCID) in patients with enterovirus-positive or cytomegalovirus-positive and adenovirus-positive chronic myocarditis. Specific therapies are aimed to avoid the progression of the disease which may ultimately lead to heart failure with a cardiac assist device or heart transplantation as ultimate therapeutic option.

Adjuvants, Immunologic↗
PubMed1998

[Cytomegalovirus and herpes simplex virus in pathogenesis and progression of native arteriosclerosis and recurrent stenosis after intervention].

An increasing number of clinical and experimental studies point to a contribution of various infectious organisms like chlamydia pneumoniae or herpesviruses to atherosclerosis in man. Cytomegalovirus induces atherosclerotic lesions in animals. In vitro studies reveal functional changes of endothelial cells after infection with cytomegalovirus. Infection with this virus renders endothelial cells immunogenic for cellular and humoral immune reactions. In man a significant association of infections with herpesviruses and atherosclerosis could be established in several studies. Cytomegalovirus infection has been incriminated as an independent risk factor in restenosis after coronary angioplasty.

Angioplasty, Balloon, Coronary↗