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Sabine Pankuweit

Publications and source records attributed to Sabine Pankuweit.

33 records · Page 2Linked to original sources
PubMed2004

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. We focused on appearance of anti-hsp70 antibodies as an immunologic response to heat shock protein induction by ischemia followed up by hemodynamic measurements perioperatively. We correlated these clinical findings with the presence of antibodies against hsp70 and the antioxidative capacity of patients' sera. METHODS: Thirty-five consecutive patients with coronary artery disease scheduled for coronary artery bypass grafting were included. Seventeen patients had severe angina, and 18 patients suffered from chronic stable angina preoperatively. In the patients' sera, antibodies against hsp70 were detected by enzyme-linked immunosorbent assay, and antioxidative capacity was detected using the chromogen assay. Cardiac output and pulmonary capillary wedge pressure were measured using a thermodilution catheter. We also evaluated C-reactive protein and creatine kinase MB isoenzyme, and performed a conventional leukocyte count. RESULTS: The sera of the 17 patients with severe angina attacks before surgery contained antibodies against hsp70 and a low antioxidative capacity. The interval between a severe angina attack and anti-hsp70 antibody titer are inversely correlated. These patients had better cardiac output and lower pulmonary capillary wedge pressure values after surgery. CONCLUSIONS: Severe angina before cardiac surgery coincided with an improved outcome as measured by hemodynamic variables as compared with chronic stable angina. This finding correlated significantly with a low antioxidative capacity and the presence of antibodies against hsp70. These pathophysiologic mechanisms might therefore play a role in myocardial protection.

Aged↗
PubMed2003

Human viral cardiomyopathy.

Viral infection of the heart is relatively common, usually asymptomatic and has a spontaneous and complete resolution. It can, however, in rare cases, lead to substantial cardiac damage, development of viral cardiomyopathy and congestive heart failure. Viral cardiomyopathy is defined as viral persistence in a dilated heart. It may be accompanied by myocardial inflammation and then termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). If no inflammation is observed in the biopsy of a dilated heart (<14 lymphocytes and macrophages/mm ) the term viral cardiomyopathy or viral persistence in dilated cardiomyopathy should be applied. The diagnosis of myocarditis and viral cardiomyopathy can be made only by endomyocardial biopsy, implementing the WHO/WHF criteria, and PCR techniques for identification of viral genome. The most frequent cardiotropic viruses detected by endomyocardial biopsy are Parvo B19, enteroviruses, adenoviruses, cytomegalovirus, and less frequently Epstein-Barr virus, and influenza virus.

Animals↗
PubMed2003

[Pregnancy and cardiomyopathies].

This overview on the topic of cardiomyopathy and gestation comprises the diagnostic and therapeutic options of patients with preexistent cardiomyopathies (dilated, hypertrophic, inflammatory, and others) and with cardiomyopathies which have been discovered during or in the 6 months following delivery. CARDIOMYOPATHIES PREEXISTENT BEFORE GESTATION: If cardiomyopathy is present before an intended gestation, the couple should be advised against pregnancy because of the high risk of deterioration both during gestation and peripartum. If pregnancy occurs, according to ESC (European Society of Cardiology) recommendations termination should be advised if the ejection fraction is < 50% and/or the LV dimensions are definitely above normal. If termination is refused, the patient must be checked regularly by both gynecologist and cardiologist, by the latter to perform regular echocardiograms. Termination is not recommended for the hypertrophic (nonobstructive) cardiomyopathies. If atrial fibrillation occurs, anticoagulation with low molecular weight heparin and digoxin and/or Betablockers are recommended for rhythm and rate control. PERIPARTUM CARDIOMYOPATHIES: In peripartum cardiomyopathies, which are discovered clinically postpartum, inflammation of the myocardium sometimes associated with pericarditis is frequently found. For those patients, we recommend heart catheterization with endomyocardial biopsy to allow for the exact diagnosis of the underlying cardiac process (inflammatory and/or viral vs autoreactive myocarditis or noninflammatory or nonviral [= idiopathic] forms). This diagnostic algorithm, which we recommend for any form of dilated cardiomyopathy, bears impact on treatment options beyond the mere heart failure therapy that should be instigated anyhow.

Abortion, Induced↗
PubMed2003

Pericardial disease in pregnancy.

BACKGROUND: There is no evidence that pregnancy affects susceptibility to pericardial disease. However, when such a condition occurs, its proper diagnosis and management may be crucial for the outcome of the pregnancy. INCIDENCE AND DIAGNOSIS: Hydropericardium is the most frequent form of pericardial involvement in pregnancy. It is typically a small, clinically silent pericardial effusion present in the third trimester in approximately 40% of healthy pregnant women. Small amounts of fetal pericardial fluid (< 2 mm in echocardiography, in diastole) can be detected after 20 weeks of gestation. Larger effusions should raise clinical concern for hydrops fetalis, Rh disease, hypoalbuminemia, and infectious or autoimmune disorder. Wide varieties of etiologic forms of pericardial diseases occur sporadically in pregnant women. Significant symptoms, electrocardiographic changes, or physiologic impairment warrant hospitalization. TREATMENT: Most pericardial disorders are managed during pregnancy as in nonpregnant patients (i.e., nonsteroidal antiinflammatory drugs for acute, antibiotics and drainage for purulent pericarditis, and corticosteroids for systemic autoimmune disorders). However, colchicine is contraindicated in pregnancy, and pericardiocentesis should be performed only for very large effusions causing clinical signs of cardiac tamponade or if presence of suppurative, tuberculous or neoplastic pericardial effusion is suspected. Echocardiographic guidance of pericardiocentesis is preferred to fluoroscopic guidance in order to avoid fetal X-ray exposure. Pericardiectomy should be reserved for significant pericardial constriction and resistant bacterial infections. Delivery of normal infants in term after pericardiocentesis or pericardiectomy is expected, whenever natural history of causative disease allows. Pericardiectomy itself is not a contraindication for subsequent successful pregnancies.

Colchicine↗
PubMed2003

Prognostic significance of morphometric endomyocardial biopsy analysis in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: To date, considerable controversy exists on the prognostic significance of morphometric endomyocardial biopsy findings in patients with idiopathic dilated cardiomyopathy (IDC). METHODS: Quantitative analyses of interstitial structured tissue, myofibril volume fraction, and myocytic fiber diameters of left ventricular endomyocardial biopsy specimens were performed in 124 patients with IDC. RESULTS: During 51 +/- 22 months follow-up after left ventricular endomyocardial biopsy, major arrhythmic events, defined as sustained ventricular tachycardia (VT), ventricular fibrillation (VF), or sudden cardiac death, were observed in 24 patients (19%). Death from any cause or heart transplant was observed in 39 patients (31%). The amount of interstitial structured tissue, myofibril volume fraction, and myocytic fiber diameters determined from left ventricular endomyocardial biopsy specimens did not differ significantly between patients with and patients without major arrhythmic events or between patients with and patients without transplant-free survival during follow-up. CONCLUSIONS: Quantitative analysis of the amount of interstitial structured tissue, myofibril volume fraction, and myocytic fiber diameters in left ventricular endomyocardial biopsy specimens does not appear to be useful for predicting arrhythmic events and transplant-free survival in IDC.

Adolescent↗
PubMed2003

Prevalence of the parvovirus B19 genome in endomyocardial biopsy specimens.

Although enteroviruses have long been considered the most common cause of inflammatory heart muscle diseases, parvovirus B19 (PVB19) is emerging as a new and important candidate for myocarditis and dilated cardiomyopathy with inflammation (DCMi) and without inflammation (DCM). We investigated left ventricular endomyocardial biopsy specimens from 110 patients with suspected inflammatory heart disease for the presence of PVB19, Coxsackie virus (CVB), and adenovirus (Ad2) genome by polymerase chain reaction. Diagnosis of myocarditis (36 patients), DCM (18 patients), DCMi (13 patients), and perimyocarditis (12 patients) was made by immunohistochemical and histopathological investigation of endomyocardial biopsy specimens. A control group consisting of patients with arterial hypertension was also investigated. Prevalence of the PVB19 genome in endomyocardial biopsy specimens was highest in patients with DCMi (3 of 13) and patients with myocarditis (7 of 36); in patients with DCM and perimyocarditis, prevalence was 3 of 13 and 2 of 12, respectively. In patients with resolved myocarditis, no PVB19 DNA was detected; in patients with no inflammation and controls, prevalence was only 4% and 7%, respectively. CVB-RNA was detected in endomyocardial biopsy specimens from 3 of 37 patients with myocarditis; Ad2-DNA was found in 1 patient with DCM and 1 patient with perimyocarditis. These findings suggest an association of the PVB19 genome in endomyocardial biopsy specimens of adults with the development of DCM, DCMi, and chronic myocarditis more frequently than previously expected. PVB19 should therefore be recognized as a potential cardiotropic pathogen in patients of all ages.

Adult↗
PubMed2003

Acute parvovirus B19 infection associated with myocarditis in an immunocompetent adult.

Inflammatory heart disease is causally linked with progressive left ventricular dysfunction and congestive heart failure. In childhood, infection with parvovirus B19 (PVB19) is usually benign, causing erythema infectiosum. However, severe fetal PVB19 infection may be associated with hydrops fetalis and fetal death caused by myocarditis. Here we report a PVB19-induced myocarditis in a previously healthy 37-year-old patient admitted to the hospital because of chest pain and dyspnea due to left ventricular dysfunction. Four weeks after the onset of symptoms, we found lymphocytic infiltrates and PVB19 genome in left ventricular endomyocardial biopsy specimens. Consistently, acute PVB19 infection was indicated serologically by elevated IgM titers and the presence of PVB19 genome in peripheral blood lymphocytes. In conclusion, PVB19 infection may be complicated by acute myocarditis in immunocompetent adults. Because PVB19 myocarditis may progress to chronic dilated cardiomyopathy, early diagnosis by endomyocardial biopsy is important to initiate anti-inflammatory treatment.

Acute Disease↗
PubMed2003

Cardiac sarcoidosis: cytokine patterns in the course of the disease.

Sarcoidosis is a chronic systemic disease of unknown etiology, which is characterized by noncaseating epitheloid granulomas usually in multiple organs. Here we describe changes in cytokine mRNA expression by peripheral blood mononuclear cells (PBMCs) and changes of cytokine protein levels in plasma over a time course of 12 months in a patient with sarcoidosis confined to the heart as diagnosed by endomyocardial biopsy. Mitogen-stimulated PBMCs exhibited a more T(H)1 cytokine profile at onset of symptoms before immunosuppressive therapy was initiated, with a change to a T(H)0 response in the course of the disease as evidenced by multiplex-polymerase chain reaction. In plasma, high levels of interleukin-6 could be detected by an enzyme-linked immunosorbent assay system, with rapid decline correlating with immunosuppression and improving clinical course. These changes may point to a role of T(H)1 and T(H)2 cytokines in the pathogenesis and the healing process of cardiac sarcoidosis.

Adult↗
PubMed2003

CD83+ dendritic cells in inflammatory infiltrates of Churg-Strauss myocarditis.

Churg-Strauss syndrome (CSS) is characterized by a granulomatous vasculitis of multiple organs with the cardiovascular system being commonly affected. The initiation of the disease is not well understood, but immunologic phenomena are thought to contribute at least partially to the syndrome. We have studied endomyocardial biopsy specimens from a patient with CSS and eosinophilic myocarditis for characterization of infiltrating immune cells by immunofluorescence staining techniques and found a major population to be composed of CD83+CD14-CD19-CD56-HLA-DR+ dendritic cells (DCs). Further phenotypic characterization of infiltrating CD83+ cells in CSS myocarditis showed a surface profile reminiscent of immature DCs. In the same patient, the cytokine expression pattern of mitogen-stimulated peripheral blood mononuclear cells revealed a TH0 response as evidenced by multiplex polymerase chain reaction, and interleukin-5 levels were elevated in plasma analyzed by enzyme-linked immunosorbent assay. Thus, in this case of CSS myocarditis, we found DC-like cells in myocardial lesions, which may suggest that DCs are involved in the inflammatory process possibly triggered or sustained by an imbalance of DCs and their failure to confer tolerance to self-antigens.

Antigens, CD↗
PubMed2002

Dilated cardiomyopathies as a cause of congestive heart failure.

DEFINITION AND CLASSIFICATION: Cardiomyopathies are disorders affecting the heart muscle that frequently result in congestive heart failure. Five major forms are recognized: dilated, hypertrophic, restrictive, right ventricular, and nonclassifiable cardiomyopathies with distinct hemodynamic properties. Furthermore, the new WHO/WHF definition also comprises inflammatory cardiomyopathy, defined as myocarditis in association with cardiac dysfunction. 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 then termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). If no inflammation is observed in the biopsy of a dilated heart (< 14 lymphocytes and macrophages/mm2), the term viral cardiomyopathy or viral persistence in dilated cardiomyopathy should be applied. DIAGNOSIS AND TREATMENT: In recent years, there have been breakthroughs in understanding the molecular and genetic mechanisms involved in this group of conditions, enabling improvement of diagnostic strategies and introduction of new therapies. Ongoing evaluation of antiviral, immunoglobulin, and immunosuppressive therapies including the European Study of Epidemiology and Treatment of Cardiac Inflammatory Diseases (ESETCID), removal of antibodies by immunoadsorption, anticytokine and gene therapy, as well as the mechanical support devices may provide new treatment options.

Cardiomyopathy, Dilated↗
PubMed2002

Pathophysiology of cardiac inflammation: molecular mechanisms.

BACKGROUND: Inflammatory processes induced by rival infection are believed to be one of the major pathogenetic mechanisms in inflammatory dilated cardiomyopathy. Although the reason for progression to myocardial failure is not fully understood, postulated mechanisms include persistent viral infection alone or in combination with autoimmune processes. PATHOPHYSIOLOGY: Murine models of myocarditis have provided insight into the mechanisms by which autoimmune responses to cardiac antigens, probably in response to viral infection of the myocardium, arise and cause tissue pathology. Organ-specificity, cross-reactivity between microbial agents and cardiac tissue, and induction of tolerance to self-antigen are issues still at stake. In addition, cytokines mediate activation and effector phase of innate and specific immunity, which are both important in controlling viral infection. The innate immune response not only has an important protective function but also serves to initiate and regulate subsequent specific immune responses. In man, on the one hand specific T cells and antibodies against different cardiac tissue components have been demonstrated in myocardium and sera of patients with inflammatory cardiomyopathy, and on the other hand viral genome has been identified in endomyocardial biopsies due to the rapid development of new molecular biological techniques such as polymerase chain reaction (PCR), southern blot analysis and in-situ hybridization. But it is still a mater of debate whether virus infection itself, the ensuing immune response, or both, contribute to the deterioration of left ventricular function. CONCLUSION: Taking these mechanisms into account, screening for viral genome by PCR and detection of inflammatory infiltrates by immunohistochemistry are considered crucial for the establishment of a definite diagnosis thereby allowing for the initiation of specific therapeutic strategies.

Adult↗
PubMed2002

Detection of Porphyromonas gingivalis DNA in aortic tissue by PCR.

BACKGROUND: Periodontopathogens may play a role in the etiology of cardiovascular disease. The aim of the present study was to investigate biopsies of aortic tissue for the presence of periodontopathogens. METHODS: Samples taken from the aortas of 26 patients connected to a heart-lung machine during open-heart surgery were analyzed in a gene-diagnostics laboratory by polymerase chain reaction. Immediately after biopsy, the samples were transferred into liquid nitrogen and stored at -80 degrees C. 16S rRNA gene-directed primers were used for general detection of bacterial cells, and specific primers for detection of Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans. Questionable amplificons were verified by Southern hybridization using DNA probes. RESULTS: Bacterial DNA was found in 23 of 26 (88.5%) samples, in most cases only in concentrations around the detection limit. Four samples were clearly positive for P. gingivalis; A. actinomycetemcomitans was not detected. CONCLUSION: These results might indicate a link between periodontopathogens entering the cardiovascular system and cardiovascular disease.

Aggregatibacter actinomycetemcomitans↗
PubMedDate not supplied

Pathophysiology of viral myocarditis: the role of humoral immune response.

The pathophysiology of viral myocarditis is still a matter of debate. Humoral autoimmunity in postviral heart disease remains an attractive but complex hypothesis. Antigenic mimicry with or without cytolytic antibody properties has been shown to play a role in the immunopathogenesis of myocarditis with respect to sarcolemmal/myolemmal epitopes (including the beta-receptor), myosin and some mitochondrial proteins including the antinucleotide translocator (ANT)-carrier and dihydrolipoamid dehydrogenase. Today, refined two-dimensional Western blots are able to identify receptors and enzymes that are target of a humoral immune response or the consequence of an "immunization process." A humoral immune response to an invading agent will most likely lead to immunodestruction first. After conversion to IgG, the continuing antibody response may indicate the healing or healed process and last for many years or life-long. This paper reviews our present knowledge on the humoral immune response in myocarditis and its interplay with the viral agents and the other components of the immune system.

Animals↗