Influence of intimal Chlamydophila pneumoniae persistence on cardiovascular complications after coronary intervention.

PURPOSE: Chlamydophila pneumoniae has been implicated in atherosclerosis/restenosis; however, clear evidence is missing. Therefore, the aim of our study was to examine the influence of intimal infection and systemic inflammation on cardiovascular complications after coronary intervention. METHODS: 45 atheroma specimens from patients with symptomatic coronary artery disease who underwent directional endatherectomy with stent implantation were analyzed by immunohistochemistry to detect chlamydial (c) and human (h) heat shock protein (HSP) 60. The antibodies used against cHSP60 and hHSP60 were characterized by specificity and lack of cross immunoreactivity. In addition, serum Ig antibodies against Chlamydophila pneumoniae and against mycobacterial (m) HSP65 as well as serum CRP levels were measured. At follow-up of 6 months, quantitative coronary angiography was performed and major adverse cardiac events (MACE) were assessed. RESULTS: Atheroma specimens of all 10 patients with MACE were positive for cHSP60 with overall higher cHSP60 tissue expressions (1.1 ± 0.4 %) and serum CRP levels (2.18 ± 0.85 mg/dl) compared to the remaining 35 patients without MACE (7 of 35 specimens positive for cHSP60, mean cHSP60 expression: 0.4 ± 0.1 %, CRP levels: 0.67 ± 0.16 mg/dl, p < 0.05). Colocalization of both HSP60 homologues was more frequent in the MACE group. Anti-mHSP65 serum titers were significantly higher in MACE (1:510) versus non-MACE patients (1:335) and correlated positively with plaque expressions of cHSP60 and hHSP60 (r = 0.54, p < 0.05; r = 0.46, p < 0.05; resp.). CONCLUSIONS: Intimal presence of cHSP60, systemic CRP and antibodies against mHSP65 are predictors for occurrence of MACE after coronary intervention.

Cerebral embolism with interventional closure of symptomatic patent foramen ovale: an MRI-based study using diffusion-weighted imaging.

Paradoxical embolism via patent foramen ovale (PFO) is an important cause of stroke, especially in younger patients. Transcatheter PFO closure is considered to bear a low risk and to be technically feasable with a high primary success rate. There are no data for the rate of procedure-associated silent embolic events. The present study sought to analyze the total number of cerebral ischemic complications with interventional PFO closure. Thirty-five symptomatic PFO patients (15 male, 26-71 years) with cerebral infarctions proven by magnetic resonance imaging (MRI) were examined by diffusion-weighted imaging (DWI) before and after PFO closure. In the MRI examinations following the intervention, new microembolic lesions were found in three of 35 (8.6%) patients. The lesions were located in the right and left thalamus and the left frontoparietal white matter respectively. Two of three infarcts were clinically inapparent, whereas the third patient suffered from a transient right-sided hemihypaesthesia for 12 h. If the prevention of recurrent cerebrovascular events associated with the presence of PFO is necessary, a low frequency of closure associated silent cerebral embolisms was documented after interventional PFO closure. The rate of microembolic events with neurological deficit was 1/35 (approximately 2.8%).

Could activated tissue remodeling be considered as early marker for progressive valve degeneration? Comparative analysis of checkpoint and ECM remodeling gene expression in native degenerating aortic valves and after bioprosthetic replacement.

OBJECTIVES: Aortic stenosis is the leading cause of heart valve disease in elderly. Little is known about molecular mechanisms leading to altered left ventricular geometry generally and, particularly, to remodeling of degenerating aortic valve. Alterations in native degenerating aortic valves and valvular tissue after replacement might result from a stage specific tissue remodeling protein core induced by stress responsible factors. Here we were looking for a possible stage specificity of tissue remodeling and stress responsive checkpoint gene activation in native degenerating human aortic valves and bioprosthetic valvular tissue after replacement. MATERIALS AND METHODS: Specimens of native degenerating aortic valves as well as bioprosthetic valves after replacement were tested for their morphological properties. Native degenerating valves were selected for two groups: non-calcified (7 samples) and calcified (5 samples) one; the third group (5 samples) was consisting of bioprosthetic valve samples after replacement. Individual mRNA-pools were isolated from each tissue sample, and semi-quantitative RT-PCR was performed. Target transcripts of p21(waf1/cip1), MT1-MMP, MMP-2, MMP-9 and TIMP-1 were measured. The specificity was controlled by restriction analysis of PCR products. RESULTS AND CONCLUSIONS: According to the abundant expression of p21(waf1/cip1), a highly activated stress response was found in non-calcified native degenerating aortic valves, whereas no stress response was monitored in valvular tissue after replacement. Whereas MT1-MMP expression was almost equally induced in all three groups investigated, MMP-9 was higher expressed in non-calcified versus calcified native valves, and was not expressed after replacement. An induced expression of MMP-2 was detected in non-calcified native degenerating aortic valves only. An abundant expression of tissue inhibitor of metalloproteinases TIMP-1 was observed in all three groups tested. Apparently, the ECM degradation potential is specifically enhanced in non-calcified native degenerating aortic valves e.g. at the early degeneration stages. In contrast, the replaced valves were found to be actively resorbing tissue with no detectable stress response, where both MT1-MMP and TIMP-1 might play the key role in geometry remodeling.

p21WAF1/CIP1 and 14-3-3 sigma gene expression in degenerated aortic valves: a link between cell cycle checkpoints and calcification.

The mechanisms underlying aortic valve degeneration are largely unknown. Cardiac tissue responds to a variety of stimuli by hypertrophic growth. Molecular mechanisms resulting in the hypertrophic response indicate similarity and overlap with those involved in both cell growth and death. We hypothesized cell cycle control to be the key event in progression regulation of heart valve degeneration followed by tissue mineralization. Human post-operative tissue samples of native non-rheumatic stenosed aortic valves were categorized according to absence (group 1) or presence of calcification (group 2). The samples were ex vivo examined for cell density and presence of macrophage (CD68), as well as expression of two checkpoint genes, p21WAF1/CIP1 and 14-3-3 sigma, arresting the G1 and G2 cell cycle phases, respectively. Expression rates were measured by "Real-Time"-PCR on transcriptional level. Target protein expression was measured and their co-localization in different kinds of valvular cells was tested using immunohistochemical analysis. Whereas macrophages were localized predominantly in sub-endothelial layer of valvular fibrosis, p21WAF1/CIP1 and 14-3-3 sigma expression was observed also in the valvular spongiosa co-localized with alpha-actin positive cells. Significantly higher cell density and inflammation grade were observed in group 2 versus group 1. Accordingly, p21WAF1/CIP1 and 14-3-3 sigma expression was several fold higher in group 1 versus group 2 on both transcription and translation levels. The present findings on degenerated aortic valves show that increased cell density accompanied with consequent calcification might be attributed to the down-regulation of both G1 and G2 checkpoint genes.

Tissue resident C reactive protein in degenerative aortic valves: correlation with serum C reactive protein concentrations and modification by statins.

OBJECTIVE: To assess aortic valve probes for valvar C reactive protein (CRP) presence, the relation between valvar and serum CRP, and a possible modification of CRP by statin medication. SETTING: Tertiary referral centre. PATIENTS AND DESIGN: End stage, degenerative valve tissue was taken from 81 patients, 57 with non-rheumatic aortic valve stenosis (AS) and 24 with degenerative aortic valve bioprosthesis (BP). Five non-stenosed valves served as controls. Tissue from four non-implanted bioprostheses was also examined. The presence and location of CRP was analysed by use of immunostaining and morphometry. Serum CRP concentrations were measured preoperatively. RESULTS: The majority of AS and BP valves exhibited CRP labelled cells, predominantly localised to the valvar fibrosa. The expression of CRP was much higher in BP than in AS (by a factor of 3.7, p = 0.03). Notably, non-stenosed aortic valves and non-implanted bioprostheses did not have CRP signalling. Serum CRP was also increased with BP (by a factor of 2.5, p = 0.02) and was significantly correlated with valvar CRP expression (r = 0.54, p < 0.001). The main finding in patients with (n = 26) and without statin treatment (n = 55) was that both valvar CRP expression (p = 0.02) and serum CRP concentrations (p = 0.04) were lower in the statin treated group. CONCLUSIONS: CRP was found in a large series of degenerative aortic valves, more often in bioprostheses than in native cusps. Serum CRP concentrations may reflect inflammatory processes within the aortic valve. The association of statin treatment with decreases in both valvar and serum CRP concentrations may explain known pleiotropic effects of statins in patients with aortic stenosis.

Fetoscopic and ultrasound-guided decompression of the fetal trachea in a human fetus with Fraser syndrome and congenital high airway obstruction syndrome (CHAOS) from laryngeal atresia.

Congenital high airway obstruction syndrome (CHAOS) from laryngeal atresia bears a poor prognosis for hydropic fetuses owing to cardiac failure. We attempted percutaneous fetoscopic and ultrasound-guided tracheal decompression in a hydropic human fetus with CHAOS associated with Fraser syndrome. Percutaneous fetoscopic and ultrasound-guided tracheal decompression was performed using three trocars under general materno-fetal anesthesia at 19 + 5 weeks of gestation. Abnormal fetoplacental blood flow normalized within hours as a result of the intervention. Furthermore, a normalization of lung : heart size and lung echogenicity was observed within days. Resolution of hydrops was complete within 3 weeks. Premature rupture of membranes and premature contractions prompted emergency delivery of the fetus by ex-utero intrapartum treatment (EXIT) at 28 + 2 weeks of gestation. Following delivery, the lungs could be ventilated at low pressures and ambient oxygen concentration. Weaning from ventilation was achieved at 18 days of postnatal life. Our experience indicated that percutaneous fetoscopic and ultrasound-guided decompression of the fetal trachea is feasible and may permit normalization of hemodynamics in hydropic human fetuses with CHAOS from laryngeal atresia. The procedure may also result in normalization of heart : lung size and provide the time needed to regain the function of the overstretched diaphragm in this grave fetal condition.

[Interventional catheter closure of persistent foramen ovale (PFO) in a patient with paradoxical embolism and Brugada's syndrome]. / Katheterinterventioneller PFO-Verschluss bei einem Patienten mit paradoxer Embolie und Brugada-Syndrom.

HISTORY AND ADMISSION FINDINGS: A 41-year-man was admitted because of acute bluish-grey skin discoloration in cold sensation in the right hand. His brother had suffered sudden cardiac death, aged 42 years. INVESTIGATIONS: Angiography demonstrated embolic occlusion of the digital artery of the right thumb. Transesophageal echocardiography showed a persistent foramen ovale (PFO) with an aneurysm of the atrial septum (ASA) with marked right-to-left shunt of contrast medium during a Valsalva maneuvre as well as two smaller septal fenestrations. There was no evidence of any other source of embolism. The resting electrocardiogram showed an incomplete right bundle branch block with ST elevations in V (1)-V (3), changes like those described in Brugada's syndrome. TREATMENT AND COURSE: Paradoxical embolism having been demonstrated, the PFO with ASA were closed with a percutaneously introduced Helex septum occluder. Later an implantable cardioverter-defibrillator (ICD) was introduced. CONCLUSIONS: A PFO, particularly if associated with an atrial aneurysm, is an important site of paradoxical embolism. In symptomatic patients percutaneous transcatheter septal occlusion should be considered preceding any ICD insertion thought necessary for concurrent Brugada's syndrome.

Transcatheter PFO closure with a prominent Eustachian valve.

We report the successful PFO closure in a 57-year old woman with complex atrial anatomy. To avoid the risk of interfering with the occluder device due to a prominent Eustachian valve, a Helex Septal Occluder was implanted. Differential therapeutic considerations and specific device characteristics are outlined.

[Prevalence of intimal pathogen burden in acute coronary syndromes]. / Prävalenz von intimalem Pathogen burden bei akutem Koronarsyndrom.

Increasing evidence supports a link between serological evidence of prior exposure to infectious pathogens, pathogen burden, and the risk for future myocardial infarction and death in patients with coronary artery disease. Based on this concept, we evaluated the intimal presence of four pathogens in human coronary atheroma, clinically associated with acute coronary syndromes (ACS) and stable angina (SA), and the effect of pathogen burden on the expression of human heatshock protein 60 (hHSP60), a key protein in (auto-)immune pathogenesis of atherosclerosis. Coronary atherectomy specimens retrieved from 53 primary target lesions of patients with ACS (n=33) or SA (n=20) were assessed immunohistochemically for the presence of Chlamydia pneumoniae (C. pn.), Helicobacter pylori (H.p.), Cytomegalovirus (CMV) and Epstein-Barr Virus (EBV), and for the expression of hHSP60. Chlamydia pneumoniae was present in 74%, Helicobacter pylori in 32%, CMV in 13% and EBV in 42%. Exclusively C.pn. revealed a prevalence in ACS (91%) vs SA (45%; p<0.001). Immunohistochemical analysis revealed 6 lesions without, 21 lesions with 1, 17 lesions with 2, 6 lesions with 3 and 3 lesions with 4 infectious agents. As an important finding, the mean value in ACS lesions was significantly increased compared to those in SA (1.9 vs 1.1; p<0.01). ACS-subgroup analysis revealed the highest mean value in patients with pain at rest within the last two days (Braunwald class III). In addition, expression of hHSP60 was significantly higher in ACS (8.7%) compared to SA (1.3%; p<0.001). Pathogen burden correlated highly significant (p<0.01) with the expression of hHSP60 (r=0.44).Our data demonstrate the impact of intimal pathogen burden in plaque instability, and suggest the presence of (auto-)immunoreactions against upregulated hHSP60 as an important pathomechanism that may contribute to acute coronary syndromes.

[Biventricular thrombi dissolution and antibody development with lepirudin therapy]. / Biventrikuläre Thrombenauflösung und Antikörper-Bildung unter Lepirudin-Therapie.

HISTORY AND ADMISSION FINDINGS: A 50-year-old patient presented with clinical symptoms of heart failure with orthopnoe and edema (NYHA IV). INVESTIGATIONS: Echocardiography revealed a dilated left ventricle with severely reduced left ventricular function and biventricular floating thrombi, due to dilatative cardiomyopathy. TREATMENT AND COURSE: With a heart failure medication clinical symptoms reduced and body weight decreased > 10 kg in 3 weeks. Due to the high-risk constellation, anticoagulation was performed with lepirudin and the biventricular thrombi were dissolved within 17 days. At this point in time, the patient suffered from petechial bleedings, hemoptysis and gross hematuria. Despite breaking anticoagulation and substitution of PPSB with not measurable fibrinogen, subarachnoid hemorrhage occurred leading to exitus letalis. CONCLUSION: Lepirudin is a highly effective anticoagulant, that can induce severe hemorrhagic side effects in individual cases. The present case report demonstrates an immunological reaction as a rare cause with activation of prothrombin and formation of fibrin.

[Chlamydial and human heat shock protein 60 homologues in acute coronary syndromes. (Auto-)immune reactions as a link between infection and atherosclerosis]. / Chlamydiales und humanes Hitzeschockprotein 60 bei akutem Koronarsyndrom. Antikörpervermittelte (Auto-)Immunreaktionen als Link zwischen Infektion und Arteriosklerose.

Recent studies provide evidence that infectious agents play a causal role in the pathogenesis of atherosclerosis. In this respect, a chronic persistent Chlamydia pneumoniae infection, indicated by the presence of chlamydial heat shock protein 60 (cHSP 60), is of central interest. Both cHSP60 and endogenous human (h) HSP60 are upregulated under stress conditions in intimal cells and serve as a target for cross-reactive cytotoxic HSP-serum-antibodies. Therefore, the present study evaluates the expressions of both HSP60 homologues in advanced human coronary lesions and a correlation between intimal tissuebound protein and serum antibodies (Ab) to HSP65. Coronary atherectomy specimens retrieved from 114 primary target lesions of patients with acute coronary syndrome (ACS; n=46) or stable angina (SA; n=68) were assessed immunohistochemically for the presence of cHSP60 and hHSP60. Chronic persistency of Chlamydia pneumoniae was additionally examined by transmission electron microscopy. Blood samples from30 patients were tested for anti-Chlamydia pneumoniae-IgG/IgA- and anti-HSP65-Ab titers and for serum CRP levels. Coronary plaques revealed immunoreactive cHSP60 in 47% and hHSP60 in 57% of the lesions colocalized within macrophages/foam cells. Chlamydia in foam cells most often presented ultrastructural patterns that pointed to the persistency of the pathogen. Intact, non-atherosclerotic vessels showed no signals. Mean expressions were 3.1% for cHSP60 and 3.3% for hHSP60. As a central finding, the expression of both HSP homologues was significantly (each p<0.001) higher in ACS lesions compared to SA lesions (cHSP60: 6.2 vs 1.0%, and hHSP60: 7.2 vs 0.7%). Moreover, we found positive correlations between both determinants in ACS and SA lesions (r=0.41, r=0.37; p<0.01). Most interestingly, cHSP60 revealed no relationship with anti-Chlamydia pneumoniae-IgG/IgA titers, whereas expression of cHSP60 as well as that of hHSP60 correlated with anti-HSP65-Ab titers (r=0.50, p<0.01, and r=0.42, p<0.05, respectively).cHSP60 and hHSP60 colocalize within coronary primary atheroma, most prevalent in lesions associated with ACS. For the first time, our data demonstrate a significant correlation between the intimal expression of these HSP60 homologues and serum HSP65 antibodies, thereby suggesting that humoral immune reactions to bacterial and human HSPs may play an important role in coronary atherosclerosis and plaque instability.

[Neointimal hyperplasia by luminal cell recruitment and not be transmural migration. The role of Bcl-2 and HSP47 after balloon angioplasty]. / Neointimale Hyperplasie durch luminale Zellrekrutierung und nicht durch transmurale Migration. Die Rolle von Bcl-2 und HSP47 nach Ballonangioplastie.

Restenosis post angioplasty remains the major limitation of several therapeutic interventions including stent implantation. This explains the ongoing interest in its basic pathogenic mechanisms and factors. The aim of the present study was to assess the localization and maximal expression of Bcl-2, a central antiapoptotic protooncogene, and of heat shock protein 47 (HSP47), a marker of early collagen synthesis, in the context with hyperplastic neointima formation as well as concomitant transmural remodeling processes following angioplasty. 0, 4, 24 and 48 hours, 4, 7 and 14 days post balloon traumatization by use of a rat carotid artery model, specific vascular wall compartments were evaluated concerning area, cell density as well as Bcl-2 and HSP47 expression by immunohistochemistry and morphometry, supplemented by electron microscopy (TEM). Neointimal cell accumulation was detected 4 days post angioplasty, characterized by luminal cells adherent to the internal elastic lamina, associated with maximal Bcl-2 and HSP47 expression amounting to 49% and 41%, respectively. With ongoing neointimal formation, a luminal prevalence of both key determinants and a decreasing expression in basal neointimal areas were found. In the media, a temporally reduced cell density was observed significant at 48 hours post trauma. Constitutive HSP47 expression of the media was constant during the entire observation period, whereas sparse Bcl-2 signalling was induced post angioplasty maximal on day 2 with 3% and on day 14 with 5%. The adventitia demonstrated a transient structural separation between day 4 and 7, exhibiting an inner layer with sparse cellularity and an outer layer with extremely high cell density as well as pronounced neovascularization. In this outer adventitia layer, a high frequency of signals for both Bcl-2 and HSP47 were observed amounting to 29% and 57%, respectively. Complementary TEM analysis gave no evidence of transmural migratory events propagated by adventitial cells and thereby supports early neointimal formation by luminal cell recruitment and marked co-expression of anti-apoptotic Bcl-2 and matrix-generating HSP47 as important survival factors. Clinical implications of these findings may be seen in the integration of proapoptotic substances with temporal efficacy in order to prevent restenosis, e.g., by use of coated stents.

[C-reactive protein in coronary plaques -- prevalence with acute coronary syndrome]. / C-reaktives Protein in koronarem Plaquegewebe -- Prävalenz bei akutem Koronarsyndrom.

Inflammatory mechanisms are central in human atherosclerosis. Although C-reactive protein (CRP) as a serum marker is highly predictive for cardiovascular events, the intimal expression of CRP in clinically relevant coronary lesions is unknown, in particular in acute coronary syndromes (ACS). Shown by reduced CRP serum values, statins have antiinflammatory and plaque-stabilizing effects. In the present study, the presence of CRP in coronary atheromas with ACS versus stable angina (SA) as well as its possible modification by chronic statin medication was assessed. Coronary atherectomy probes from 90 primary stenoses were immunohistochemically analyzed with regard to the presence and the localization of CRP. Intimal results of patients with ACS (n=36), categorized according to the Braunwald classification, were compared with those of patients with SA (n=54). In 40 of 90 lesions (44%), immunoreaction specific for CRP was observed demonstrating a mean CRP expression of 1.7%. CRP was focally localized in a maximum of 69% of all plaque cells, the most in macrophages/foam cells, infrequently in smooth muscle cells. CRP-positive plaques showed more thrombus than plaques without CRP (63% vs 41%). Intact non-atherosclerotic control tissue revealed no signaling. As a central finding, intimal presence and expression were higher (each p<0.001) with ACS (69% and 3.1%, respectively) compared to SA (28% and 0.8%, respective). Subgroup analysis of target lesions associated with ACS according to the clinical Braunwald classification showed an increase of intimal CRP with classes I-III. In the presence of statin medication, intimal CRP was significantly lower than that without statin therapy (29 and 1.3%, vs 61 and 2.6%, respectively; p<0.01), in particular in the subgroup of ACS patients. Intimal CRP is frequently found in coronary primary stenoses, very often with macrophages/foam cells, and shows a highly significant prevalence with ACS. In this subgroup of patients, statin therapy is associated with significantly reduced intimal CRP. Our in situ findings as shown might explain the well-known serum constellations with statin therapy.

[Association between progression of untreated coronary lesions and in-stent restenosis]. / Assoziation zwischen Progression unbehandelter Koronarstenosen und In-Stent-Restenosierung.

BACKGROUND AND OBJECTIVES: Progression of coronary artery disease is only incompletely understood regarding de-novo stenoses as well as in-stent restenoses (ISR) indicative of accelerated atherosclerosis. The objective of the present angiographic study was to prove an association between target lesion ISR and progression of primarily untreated coronary lesions. PATIENTS AND METHODS: A total of 179 high-grade native coronary stenoses (mean diameter stenosis 68+/-16 %) of 131 patients were treated by stent implantation. Additional 101 lesions remained untreated because of their moderate to intermediate diameter stenoses (>30 %). Quantitative coronary angiographic analysis was performed 6+/-2 months later to evaluate ISR (diameter stenosis > 50 %), coronary progression (>20 % increase in diameter stenosis) and regression (>20 % decrease), respectively. Angiographic, procedural and clinical characteristics were assessed for a possible association with ISR and/or coronary progression and regression, respectively. RESULTS: ISR was seen in 70 of 179 (39 %) stented target lesions. Presence of diabetes mellitus (p = 0.04) and cumulative duration of inflations (p = 0.01) as procedural determinant were predictive for ISR. Significant progression was found in ten of 101 (10 %) primarily untreated lesions. Progression of previously normal segments or regression were not seen. Progression of native plaques was associated with ISR presence in nine cases and with ISR absence in only one case (p = 0.01). Of note, smoking (p = 0.02) turned out to be predictive for plaque progression, whereas medication and procedural/angiographic parameters were not. CONCLUSIONS: The findings of the present pilot study demonstrate target lesion ISR associated with progression of other primarily untreated lesions and thereby suggest that both atherosclerosis types share common systemic pathogenetic mechanisms. With presence of ISR, coronary angiography should also include primarily untreated arteries, especially in case of preexisting plaques.

[Noncompaction of the left ventricular myocardium. Case report and review of the literature]. / Noncompaction des linksventrikulären Myokards. Fallbericht und Literaturübersicht.

Left ventricular non-compaction is an unclassified cardiomyopathy characterized by an excessively prominent trabecular meshwork due to an arrest in myocardial morphogenesis. We report on a 51-year-old female patient with abnormal myocardial trabeculations associated with a congenital mitral valve stenosis post commissurotomy at the age of 14. In the present case report, clinical manifestation of the disorder included impaired left ventricular systolic function and atrial fibrillation. Noncompaction was diagnosed by echocardiography and levocardiography. In addition, a review of the literature on this rare disorder is presented.

[Parvovirus B19 myocarditis in a young man with previous non-bacterial meningitis]. / Parvovirus B19-Myokarditis eines jungen Erwachsenen nach abakterieller Meningitis.

HISTORY AND CLINICAL FINDINGS: A 22-year old man presented with fatigue, dyspnea NYHA III and presyncopes that had persisted since a non-bacterial meningitis 3 months before. INVESTIGATIONS: Transthoracic echocardiography revealed a dilated left ventricle with an ejection fraction (EF) reduced to 35-40 % due to global hypokinesia. No pericardial effusion was seen; ECG and lung function test were normal. Serological, immunological and microbiological tests as well as nested PCR analysis of blood leucocytes for detection of cardiotropic pathogens were inconclusive. In endomyocardial biopsies retrieved from the left ventricular posterolateral wall, a chronic macro-phage-rich myocarditis was shown by histopathology and, in addition, Parvovirus B19 was identified as specific pathogen by use of nested PCR analysis. TREATMENT AND COURSE: At physical rest and with ACE inhibitor therapy (2.5 mg ramipril/day), heart failure decreased steadily. Follow-up echocardiography 1 month later revealed a left ventricle that was only slightly dilated with an EF of 50 %. 3 months later, the patient was markedly more load-bearing; the EF amounted to 55-60 %. CONCLUSIONS: Parvovirus B19 should be regarded as potential pathogen in case of suspected myocarditis in adulthood. Whether the previous non-bacterial meningitis was also attributable to this specific pathogen, remains open. Of note, however, the present case report by demonstrating a localized myocardial Parvovirus B19 infection without detectable systemic infection underscores the importance of molecular tests for diagnostic accuracy in manifest organ failure.