Heart Transplantation in Systemic Sclerosis: New Impulses for Conventional Scleroderma Transplantation Regimen and Scleroderma Diagnostic Monitoring: 2 Case Reports.

BACKGROUND: Although low (but increasing) rates of lung/lung-heart transplantations of scleroderma (systemic sclerosis [SSc]) patients have been reported, exclusive heart transplantation is a rare approach for treatment of heart failure due to SSc. CASES: We report on 2 cases of SSc patients receiving a heart transplantation (HTx) due to severe and progressive right heart failure without pulmonary artery hypertension. One patient received a hepatitis C virus (HCV)-positive donor heart and recovered excellently from viral transmission after administration of a direct-acting antiviral (DAA) regimen. This is the first published case of an SSc patient who underwent HTx using an HCV-positive donor heart. The clinical course of both patients was monitored by different serum SSc biomarkers. Only xylosyltransferase activity proved to be a promising biomarker for disease stage determination and therapeutic monitoring, precisely reflecting fibrotic remodeling and successful organ recovery. CONCLUSIONS: Successful implementation of the 2 cases described here demonstrates that HTx is a safe and effective therapeutic option for defined SSc sub-patient groups despite the progressive character of the underlying disease. In the future, xylosyltransferase activity might be conducive to simplify the identification of patients with low systemic involvement but a strong indication for single heart transplantation. Finally, we demonstrate that treatment of HCV viral transmission from HCV-positive donor to organ recipient using DAA gives us new opportunities to consider HCV-positive donor organs for HTx and might reveal new possibilities to ease the lack of donor organs.

["Catecholamine refractory" cardiogenic shock? "Bridging-to-recovery" by implantation of a percutaneous cardiac assist device]. / "Therapierefraktärer" kardiogener Schock? "Bridging-to-recovery" mittels Implantation eines perkutanen Assistdevices.

HISTORY AND ADMISSION FINDINGS: A 27-year-old man presented with acute dyspnea and a previous respiratory tract infection with progressive dyspnoea and chest pain over 2 weeks. Clinical findings revealed severe cardiac failure with development of cardiogenic shock and need for adrenergic drug therapy for circulatory support. INVESTIGATIONS: The electrocardiogram showed a sinus tachycardia with unspecific T-wave-inversions, the echocardiogram revealed a dilated left ventricle and severely reduced systolic LV-function. An acute coronary syndrome could be excluded by coronary angiogram. TREATMENT AND COURSE: A myocardial biopsy was taken to exclude giant cell myocarditis. The immediate initiation of a mechanical circulatory support by an Extracorporal Membrane Oxygenator (ECMO) facilitated rapid hemodynamic stabilization and recovery of organ function. CONCLUSIONS: A drug-only circulatory support very often does not enable stabilization of a patient in progressive cardiogenic shock and cannot prevent multiorgan dysfunction. Therefore implantation of an assist device facilitates a "bridging-to-recovery" or a "bridging-to transplant" concept in critically ill patients presenting with cardiogenic shock. The bridging also allows for reviewing etiology and evaluation of further treatment options. In case of recovery continuous care in a specialized Heart Failure Clinic can help to maintain the clinical status and offer frequent reevaluation of cardiac status and therapeutic concepts.

An unusual presentation of a common infection.

A 40-year-old Ghanaian woman presented with fever and exanthema. She had anemia, leukopenia, increased erythrocyte sedimentation rate (ESR), creatinin kinase, lactate dehydrogenase (LDH), and liver enzymes. She was diagnosed with schistosomiasis and was cured with praziquantel. During the following years, she developed polymyositis, chronic nephritis, and life-threatening perimyocarditis. High numbers of Epstein-Barr virus (EBV)-encoded RNA copies were demonstrated in CD8+ T-lymphocytes from endomyocardial biopsies. There was no evidence of any underlying immunosuppression or an EBV-related malignancy. Chronic active EBV infection was diagnosed, a clinical picture not described in an adult African previously. Interestingly, among all therapy attempts, only rituximab was effective at stabilizing the disease.

Initial white blood cell count is an independent risk factor for survival in patients with dilated cardiomyopathy.

BACKGROUND: The impact of white blood cell count (WBCc) on the outcome of patients with non-ischemic left ventricular (LV) dysfunction is unknown. In the present study we investigated the influence of WBCc on mortality and cardiac inflammation in patients with reduced LV systolic function in the absence of ischemic or valvular etiology. METHODS AND RESULTS: We included 381 patients with reduced left ventricular (LV) ejection fraction (LVEF ≤ 45%) quantified by two-dimensional echocardiography. Coronary artery disease and valvular diseases were excluded by angiography and echo, respectively, in all patients. WBCc was quantified routinely upon first hospital admission. In 291 patients, endomyocardial biopsies from the right ventricle were performed upon first hospital admission for assessment of cardiac inflammation. Follow-up was up to 5.5 years (median 2.93 [1.7;4.0]). Information on vital status of patients was obtained from official resident data files. WBCc >11 Gpt/l was associated with significantly increased mortality in patients with severe LV dilation (end-diastolic diameter (LVEDD) >70 mm quantified by echocardiography) in comparison to patients showing WBCc ≤ 11 Gpt/l (41.7% vs 13.6%, p=0.02). Multivariable Cox regression analysis showed that WBCc predicts mortality independently of other cardiovascular risk factors and LVEF (hazard ratio 1.14; p=0.04). Doses of heart failure medication did not differ significantly in patients with LVEDD >70 mm and WBCc >11 Gpt/l when compared to LVEDD >70 mm and WBCc ≤ 11 Gpt/l (percent of maximum doses: ß-blockers p=0.51, ACE inhibitors p=0.56, AT1 antagonists p=0.77, aldosterone antagonists p=0.35). WBCc including its subpopulations (monocytes, lymphocytes and granulocytes) did not show a significant correlation with cardiac amounts of CD3(+)-lymphocytes (r=0.02, p=0.78) or CD68(+)-macrophages (r=1.0, p=0.09) (n=291). CONCLUSION: WBCc at first hospital admission predicts long term-mortality in patients with dilated cardiomyopathy independently of cardiovascular risk factors.

Cell volume, the serum and glucocorticoid inducible kinase 1 and the liver.

In virtually all cells including hepatocytes cell volume regulation is accomplished during cell swelling by cellular ion release (activation of K (+) channels and/or anion channels, KCl-cotransport, parallel activation of K (+)/H (+) exchange and Cl (-)/HCO (3)(-) exchange) and following cell shrinkage by cellular ion uptake (activation of Na (+), K (+), 2Cl (-) cotransport, Na (+)/H (+) exchange in parallel to Cl (-)/HCO (3)(-) exchange and Na (+)-channels). Moreover, cell shrinkage triggers the cellular accumulation of organic osmolytes (e. g., myoinositol, betaine, phosphorylcholine, taurine). Cell volume is a powerful regulator of hepatic metabolism. Cell shrinkage stimulates and cell swelling inhibits proteolysis and glycogenolysis. Moreover, cell volume influences the generation of and sensitivity to oxidants. Cell volume regulatory mechanisms furthermore do play a role in fibrosing disease. Kinases stimulating cell volume regulatory mechanisms include the serum and glucocorticoid inducible kinase SGK1, which is expressed in the liver, is genomically up-regulated by cell shrinkage, stimulates a wide variety of channels and transporters including Na (+), K (+), 2Cl (-) cotransport and Na (+)/H (+) exchange and is known to participate in the stimulation of fibrosis. Accordingly, excessive SGK1 expression is observed in liver cirrhosis. The case is made that SGK1 participates in the regulation of liver cell volume and thus in the regulation of hepatic metabolism.

[Immunsuppressive therapy in virus-negative eosinophilic inflammatory cardiomyopathy]. / Immunsuppressive Therapie bei Virus-negativer eosinophiler inflammatorischer Kardiomyopathie.

HISTORY AND ADMISSION FINDINGS: A 52 year-old women presented with long-standing dyspnoea at exercise as a symptom of heart failure. A coronary heart disease had been excluded by coronary angiography a year before. The symptoms had persisted despite application of guideline-based anticongestive medication. INVESTIGATIONS: Electrocardiography showed sinus rhythm with decreased anterior wall amplitudes without acute ischemic signs. The white blood count revealed elevated leucocytes with high numbers of eosinophilic granulocytes. Echocardiography demonstrated severe left ventricular dysfunction with an ejection fraction of 30 % and a left ventricular end-diastolic diameter of 75 mm. Magnetic resonance imaging showed a pathologic late enhancement in the left ventricular wall. Six myocardial biopsies were obtained and revealed virus-negative eosinophilic inflammatory cardiomyopathy with focal fibrotic scarring. DIAGNOSIS, TREATMENT AND COURSE: The patient was treated according to a previously published study on virus-negative inflammatory heart disease with prednisone 1 mg/kg daily for 4 weeks followed by 0.33 mg/kg daily for 5 month and azathioprine 2 mg/kg daily for 6 month. The echocardiography of the left ventricular function showed an increase from 30 to 45 % and the clinical symptoms of the heart failure resolved to NYHA II. CONCLUSION: In patients with virus-negative eosinophilic inflammatory cardiomyopathy standardized therapy with prednisone and azathioprine can improve LV function and clinical symptoms.

[Diagnosis of myocarditis]. / Myokarditis-Diagnostik.

The diagnosis of myocarditis is still a major challenge in clinical cardiology due to the variety of infectious and non-infectious disease entities. The present review summarizes from the point of view of cardiopathology and infectious medicine morphological and molecular pathological findings in myocardial biopsies of patients with infectious myocarditis, most commonly induced by viral infections, in addition to non-infectious myocarditis mediated by immune processes. A clinical relevant diagnosis of myocarditis is achieved only by integration of clinical, histological, immunohistological and molecular biological findings.

Glycogen synthase kinase-3ß is a crucial mediator of signal-induced RelB degradation.

The immediate early transcription factor nuclear factor (IκBs) kappa B (NF-κB) is crucially involved in the regulation of numerous physiological or pathophysiological processes such as inflammation and tumourigenesis. Therefore, the control of NF-κB activity, which is mainly regulated by signal-induced degradation of cytoplasmic inhibitors of NF-κB (IκBs), is of high relevance. One known alternative pathway of NF-κB regulation is the stimulus-induced proteasomal degradation of RelB, a component of the NF-κB dimer. Here, we identified the serine/threonine protein kinase glycogen synthase kinase-3ß (GSK-3ß) as a critical signalling component leading to RelB degradation. In Jurkat leukaemic T cells as well as in primary human T cells, tetradecanoylphorbolacetate/ionomycin- and CD3/CD28-induced RelB degradation were impaired by a GSK-3ß-specific pharmacological inhibitor, an ectopically expressed dominant-negative GSK-3ß mutant and by small-interfering RNA-mediated silencing of GSK-3ß expression. Furthermore, a physical interaction between RelB and GSK-3ß was shown by co-immunoprecipitation, which was already notable in unstimulated cells. Most importantly, as demonstrated by in vitro kinase assays, human RelB is inducibly phosphorylated by GSK-3ß, indicating a direct substrate-enzyme relationship. The serine residue 552 is a target of GSK-3ß-mediated phosphorylation in vitro and in vivo. We conclude that GSK-3ß is a crucial regulator of RelB degradation, stressing the relevant linkage between the NF-κB system and GSK-3ß.

[Risk stratification in non ischemic cardiomyopathy: a case report--Case 5/2010]. / Risikostratifizierung bei nichtischämischer Kardiomyopathie: Eine Kasuistik - Fall 5/2010.

HISTORY AND ADMISSION FINDINGS: A 65-year-old male patient with rapid increasing shortness of breath and newly diagnosed atrial fibrillation was admitted to our hospital. INVESTIGATIONS: The ECG revealed atrial fibrillation. Echocardiography showed severe decreased left ventricular function. The magnetic resonance imaging (MRI) scan confirmed the severe reduced left ventricular function with a two graded mitral regurgitation as well as a pronounced late enhancement in the posterobasal area of the interventricular septum. Cardiac catheterisation showed mild diffuse atherosclerosis of the coronary arteries without stenotic lesions. Multiple myocardial biopsies of the right ventricle revealed extensive remodelling processes with focal fibrosis in presence of mononuclear cell infiltrates, T-wave alternans and the heart rate variability were positive. DIAGNOSIS, TREATMENT AND COURSE: Nonischaemic cardiomyopathy (NICM) with severe reduced left ventriucular function was diagnosed. After successful electrical cardioversion and initiation of a sufficient heart failure treatment, the clinical symptoms as well as left ventricular function improved significantly. CONCLUSION: Risk stratification of sudden cardiac death remains a clinical challenge especially in NICM. Significantly predictors in ischaemic cardiomyopathy, such as heart rate turbulance (HRT) and T-wave alternans, are not useful or have no importance in NICM. However, the prognosis does not correlate with restricted left ventricular function in NICM. Cardiac MRI or marker of autonomic dysfunction could be helpful in risk stratification. How far late enhancement is a surrogate parameter or the real substrate for life threatening arrhythmias is still unclear. Non-invasive risk stratification could be helpful in borderline decisions, however, it should not be taken mandatory. Close-meshed control intervals of the clinical status under optimal medication are recommended, followed by a implantation of an implantable cardioverter-defibrillator (ICD) if needed. ICD implantation is superior to medical treatment in persistent depressed left ventricular function. The ideal time for ICD implantation in newly diagnosed NICM remains unclear at the moment.

Fcgamma-receptor IIa polymorphism and the role of immunoadsorption in cardiac dysfunction in patients with dilated cardiomyopathy.

In patients with dilated cardiomyopathy (DCM), cardiac autoantibodies are able to bind with their Fab fragment to epitopes on cardiomyocytes, but thereafter they crosslink through their Fc fragment to cardiac Fc(gamma)-receptor IIa. Polymorphic variability of the Fc(gamma)-receptor IIa is associated with modified affinity of immunoglobin G (IgG) binding and may influence therapeutic effects. In this study, 103 consecutive DCM patients were treated with immunoadsorption (IA) therapy with subsequent IgG substitution (IA/IgG). Echocardiography was performed at baseline and again at 3 and 6 months after IA/IgG. Fc(gamma)-receptor IIa polymorphism R/H131 was genotyped using a nested sequence-specific primer polymerase chain reaction (PCR). Patients with the Fc(gamma)-receptor IIa genotype R/R131 showed significantly greater improvement in left ventricular (LV) function than patients with the R/H131 or H/H131 genotypes did. Irrespective of the Fc(gamma)-receptor polymorphism, patients with shorter disease duration and a more impaired LV function responded with a greater increase in LV ejection fraction (LVEF). Therefore, the Fc(gamma)-receptor polymorphism influences the efficacy of immunomodulatory therapy involving IA/IgG.

Cardiomyopathies--misdiagnosed as Sudden Infant Death Syndrome (SIDS).

Cardiomyopathies are an important and heterogenous group of diseases. With the identification of several new disease entities over the past decade, advances in diagnosis and precise causation, some disease definitions have become outdated. The past decade has witnessed a rapid evolution of molecular genetics in cardiology, e.g. myocardial diseases (Hypertrophic cardiomyopathy-HCM, Arrhythmogenic right ventricular cardiomyopathy-ARVCM) and channelopathies (Long QT syndrome-LQTS, Brugada syndrome-BrS, Catecholaminergic Polymorphic Ventricular Tachycardia-CPVT and Short QT syndrome-SQTS) as diseases predisposing to potentially lethal ventricular tachyarrhythmias. Beside the detection of mutations in several genes, histological and immunohistochemical findings can point to a cardiomyopathy as underlying disease. Therefore, previous microscopical investigations of different parts of the myocardium can help to select those cases of suspected Sudden Infant Death Syndrome (SIDS), where a search for genetic mutations can lead to a diagnosis explaining the sudden and unexpected death.

The German Transregional Collaborative Research Centre 'Inflammatory Cardiomyopathy--Molecular Pathogenesis and Therapy'. Methods and baseline results from a 3-centre clinical study.

OBJECTIVES: This report focuses on the design and methods of the 3-centre clinical study of the Transregional Collaborative Research Centre 'Inflammatory Cardiomyopathy--Molecular Pathogenesis and Therapy', which aims to establish a comprehensive research registry on the diagnostics, therapy and disease outcomes of patients with inflammatory cardiomyopathy (CMi). The study goals are to investigate specific disease sub-entities and to develop standardised strategies for diagnostics and treatment. METHODS: All consecutive patients with clinically suspected CMi, post-myocarditic cardiomyopathy and acute myocarditis are included in the research registry. Cardiopulmonary functional tests, clinical and patient data are obtained at baseline and subsequent readmission appointments and are linked to allow for prospective follow-up. Co-morbidities, quality of life, health- related behaviour and sociodemographic variables are ascertained using uniform self-administered questionnaires. PRESENT STATUS: By May 2008, 2,061 cases had been included in the research registry (1,300 data-sets completed). At registration, 335 patients were diagnosed with CMi. The mean age was 50 +/- 13 years and the mean ejection fraction was 39.9 +/- 15.8%. CONCLUSIONS: The broad range of the acquired molecular-biological, histological, immunohistological, clinical and patient data makes this the most comprehensive research registry on patients with CMi to date.

[Molecular mechanisms and consequences of cardiac viral infections]. / Molekulare Mechanismen und Konsequenzen kardialer Virusinfektionen.

Molecular biological methods have confirmed the pathogenetic role of enteroviruses, primarily coxsackieviruses of group B (CVB), in the induction and maintenance of inflammatory cardiomyopathy. More recently, adenoviruses, various herpes viruses, and increasingly parvovirus B19 (B19) have been identified as potential cardiotropic agents. While cardiac myocytes are target cells for enterovirus and adenovirus infections with virus-induced cytolysis, B19-associated inflammatory cardiomyopathy is characterized by infection of intracardiac endothelial cells of small arterioles and veins, which may be associated with endothelial dysfunction, impairment of myocardial microcirculation, penetration of inflammatory cells, and secondary myocyte necrosis. Recent observations showed that B19 is involved in intracellular calcium regulation by the viral phospholipase. B19-induced caspase activation can lead to proinflammatory/proapoptotic processes through dysregulation of STAT signaling. These cellular interactions may contribute to mechanisms by which B19 establishes persistent infection in endothelial cells and play a critical role in viral pathogenesis of inflammatory cardiomyopathy.

Coronary vasospasm as the underlying cause for chest pain in patients with PVB19 myocarditis.

OBJECTIVE: To evaluate the incidence of coronary vasospasm as a possible pathophysiological mechanism causing chest pain symptoms in patients with clinically suspected myocarditis. DESIGN AND SETTING: Prospective study in a teaching hospital. PATIENTS: 85 patients who presented at hospital with atypical chest pain and demonstrated clinical signs suggestive of myocarditis. MAIN OUTCOME MEASURES: Incidence of coronary vasospasm demonstrated by intracoronary acetylcholine (ACh) testing. METHODS: The combined procedure of intracoronary ACh testing and endomyocardial biopsy (EMB) was performed after ruling out significant coronary artery disease (CAD). EMBs were analysed for myocardial inflammation by immunohistological methods and for virus genome persistence. RESULTS: Pathological biopsy results, including myocardial inflammation or detection of viral genomes, or both, were found in 55 (64.7%) patients while 30 (35.3%) patients showed neither cardiac inflammation nor viral genomes and were defined as the control group. Coronary vasospasm was demonstrated in 39/55 (70.9%) patients with pathological results compared with only 12/30 (40.0%) with normal biopsy results (p = 0.01). Patients with isolated PVB19 infection (n = 22) demonstrated a significantly higher incidence of coronary vasospasm than both those with isolated HHV6 infection (86.4% vs 46.7%; p = 0.025) and those with normal biopsy results (86.4% vs 40.0%; p<0.001). Univariate and multivariate logistic regression analysis showed that only PVB19 infection was independently correlated with coronary vasospasm (OR = 4.9, 95% CI 1.56 to 15.28, p = 0.006). CONCLUSIONS: Coronary vasospasm is one of the main reasons for atypical chest pain in patients with clinical signs of myocarditis and biopsy-proven PVB19 myocarditis in the absence of significant CAD.

[Acute thrombo-embolic elevated ST infarct in a patient with essential thrombocytosis]. / Akuter thrombembolischer ST-Hebungs-Infarkt bei einem Patienten mit essenzieller Thrombozytose.

A 48-year-old man presented with acute chest pain and a greatly increased platelet count. Emergency coronary angiographic revealed thrombotic occlusion of the right coronary artery. Coronary angioplasty and stenting were successfully combined with intracoronary abciximab administration. Due to inadequate postinterventional platelet inhibition an intensified dual antiplatelet therapy with acetylsalicylic acid (ASS) and clopidogrel was applied to prevent stent thrombosis. Due to the thrombo-embolic complication and a platelet count over 1 million/microl a cytoreductive treatment with hydroxyurea was initiated.

[Cardiologic findings in Hauptmann-Thannhauser muscular dystrophy (autosomal dominant Emery-Dreifuss muscular dystrophy)]. / Kardiologische Befunde bei Hauptmann-Thannhauser-Muskeldystrophie (autosomal dominante Emery-Dreifuss-Muskeldystrophie).

HISTORY: A 19-year-old man with congestive heart failure reported recent onset of exercise-induced dyspnea and pitting edema of the face. He also developed increasing muscular weakness. Three years before the diagnosis of autosomal-dominant Emery-Dreifuss muscular dystrophy (EDMD) had been made. FINDINGS: Cardiac and lung auscultation were unremarkable. The heart rate was 102 /min, and the blood pressure 100/70 mmHg. Aspartate aminotransferase (62 U/l) and lactate dehydrogensase (361 U/l) were elevated. The electrocardiogram during telemetric monitoring showed a 2 AV block, Mobitz type II. Echocardiography showed an ejection fraction of 20%. Coronary atherosclerosis was excluded by coronary angiography. A raised pulmonary wedge pressure at rest was recorded through an indwelling Swan-Ganz catheter, but cardiac output was normal. Histopathology revealed findings typical for dilated cardiomyopathy. THERAPY AND COURSE: The patient was already on diuretics when admitted; other medication included an ACE inhibitor, beta-blocker, aldosterone antagonist and digitalis. A cardioverter-defibrillator was implanted prophylactically. Congestive heart failure developed during the subsequent months. Two years later the patient underwent orthotopic heart transplantation. CONCLUSION: In patients with genetically determined neuromuscular diseases it is prognostically important early to recognize cardiomyopathy and cardiac arrhythmias. Subsequent cardiac transplantation may be life-saving.

Simplified detection of microsatellite instability in colorectal cancer without the need for corresponding germline DNA analysis.

A panel of five quasimonomorphic mononucleotide repeats that dispenses with the need to analyse corresponding germline DNA was proposed by Suraweera et al for the detection of high-frequency microsatellite instability (MSI) in colorectal cancer. Using this panel, a simplified and a more sensitive (compared with the original) algorithm (p<0.05) was developed to define the instability of each repeat by assessing the morphological shape of its plot and not its absolute length. 103 cases of colorectal tumours were investigated and the results compared with those obtained by the analysis of five consensus microsatellites (Bethesda reference panel). By the proposed method, a higher specificity, but no loss of sensitivity, was found. Thus, the use of the five mononucleotide repeats in combination with the modified assessment technique simplifies the assessment of MSI, while retaining the sensitivity of the Bethesda panel for the detection of high-frequency MSI.

[Recurrent transient ischaemic attacks in a patient with pansinusitis]. / Rezidivierende transitorische ischämische Attacken bei einer Patientin mit Pansinusitis.

A 31-year-old woman presented with neurological deficits after an operation for sinusitis. The cranial MRI revealed multiple ischaemic lesions. Laboratory results showed a hypereosinophilia as well as elevated creatine kinase and troponin levels. The ECG implied ST elevations, the left ventricular ejection fraction was highly reduced and the cardiac MRI was suspicious for endomyocarditis. The cardiac biopsy demonstrated the findings of Loeffler's endocarditis. In conclusion the diagnosis of hypereosinophilic syndrome was made and identified as the cause of the neurological deficits.

Comparison between recombinant baculo- and adenoviral-vectors as transfer system in cardiovascular cells.

The development of effective gene-therapeutic applications for cardiovascular disorders is in part limited by the lack of appropriate delivery systems. In an attempt to overcome this deficiency, we investigated the ability of baculoviral vectors to transduce human cardiovascular cells, for which data are missing in literature. Additionally, baculovirus ability to transduce target cells was compared to that of an adenoviral vector, a well characterized and widely used viral vector. Transduction experiments, performed using baculo/adenoviral vectors expressing the enhanced green fluorescence protein, revealed that, under the experimental condition considered, baculoviruses but not adenoviruses efficiently transduce human coronary smooth muscle cells (hCSMC); an opposite behavior was noticed for human coronary endothelial cells (hCEC). Thus, baculoviral vectors are potentially indicated as transfer system in the treatment of coronary restenosis, where growth inhibitory genes should reach hCSMC but not hCEC. When used to transduce human cardiomyocytes and fibroblasts, both vectors behaved similarly. Finally, studies on cellular DNA replication revealed a more prolonged and pronounced negative effect on cells transduced by adenoviral compared to baculoviral vectors. Our data indicate that baculoviruses represent an attractive alternative to adenoviruses as transfer vectors in cardiovascular cells and that baculovirus have the potential to be used as gene transfer system in cardiovascular diseases such as restenosis.

Human parvovirus B19: a new emerging pathogen of inflammatory cardiomyopathy.

The human parvovirus B19 (PVB19), an erythrovirus causing diverse clinical manifestations ranging from asymptomatic or mild to more severe outcomes such as hydrops fetalis, is the only known human pathogenic parvovirus so far. Although enteroviruses have long been considered the most common cause of inflammatory cardiomyopathy, PVB19 is emerging as a important candidate. Recent studies have indicated an association of PVB19 with paediatric and adult inflammatory cardiac disease. However, whether or not PVB19 has an impact on inflammatory cardiomyopathy in adult patients is still unclear. The first hints for a possible aetiopathogenetic role of the PVB19-infection and the development of cardiac dysfunction were demonstrated by molecular biology utilizing in situ hybridization (ISH) and polymerase chain reaction (PCR). According to available evidence, PVB19-associated inflammatory cardiomyopathy is characterized by infection of endothelial cells of small intracardiac arterioles and venules, which may be associated with endothelial dysfunction, impairment of myocardial microcirculation, and penetration of inflammatory cells into the myocardium.