Biomedical subjects

Guido Gerken

Publications and source records attributed to Guido Gerken.

At least 55 records · Page 3Linked to original sources

PubMed2005

Development and functional consequences of LPS tolerance in sinusoidal endothelial cells of the liver.

Kupffer cells and liver sinusoidal endothelial cells (LSEC) clear portal venous blood from gut-derived bacterial degradation products such as lipopolysaccharide (LPS) without inducing a local inflammatory reaction. LPS tolerance was reported for Kupffer cells, but little is known whether sensitivity of LSEC toward LPS is dynamically regulated. Here, we demonstrate that LSEC react to LPS directly as a function of constitutive Toll-like receptor 4 (TLR4)/CD14 expression but gain a LPS-refractory state upon repetitive stimulation without loss of scavenger activity. LPS tolerance in LSEC is characterized by reduced nuclear localization of nuclear factor-kappaB upon LPS rechallenge. In contrast to monocytes, however, TLR4 surface expression of LSEC is not altered by LPS stimulation and thus does not account for LPS tolerance. Mechanistically, LPS tolerance in LSEC is linked to prostanoid production and may account for cross-tolerance of LPS-treated LSEC to interferon-gamma stimulation. Functionally, LPS tolerance in LSEC results in reduced leukocyte adhesion following LPS rechallenge as a consequence of decreased CD54 surface expression. Furthermore, LPS tolerance is operative in vivo, as we observed by intravital microscopy-reduced leukocyte adhesion to LSEC and improved sinusoidal microcirculation in the liver after repetitive LPS challenges. Our results support the notion that LPS tolerance in organ-resident scavenger LSEC contributes to local hepatic control of inflammation.

Animals↗

PubMed2005

Apoptosis and fibrosis in non-alcoholic fatty liver disease.

Nonalcoholic fatty liver disease is becoming an increasingly common medical problem in the developed countries which, unfortunately, still is associated with the lack of any effective treatment. However, recent data favor a model in which a pathologically increased rate of hepatocytic apoptosis and the subsequent induction and upregulation of inflammation and fibrosis in the liver provide both a rationale for the pathogenesis of nonalcoholic fatty liver disease, as well as a clue for designing first effective therapeutic strategies. In order to illuminate this context, this article focuses on the pathogenesis and possible new therapeutic options in nonalcoholic fatty liver disease.

Animals↗

PubMed2004

Increased levels of interleukin-10 in serum from patients with hepatocellular carcinoma correlate with profound numerical deficiencies and immature phenotype of circulating dendritic cell subsets.

Increased levels of interleukin (IL)-10 have been described as a negative prognostic indicator for survival in patients with various types of cancer. IL-10 exerts tolerogenic and immunosuppressive effects on dendritic cells, which are crucial for the induction of an antitumor immune response. Blood dendritic cell antigen (BDCA)-2 and BDCA-4 are specifically expressed by CD123(bright) CD11c- plasmacytoid dendritic cells; whereas BDCA-1 and BDCA-3 define 2 distinct subsets of CD11c+ myeloid dendritic cells. In this study, the T-helper cell (Th)1/Th2 cytokine serum profile of 65 hepatocellular carcinoma patients was assessed. We found that serum levels of IL-10 were substantially increased in hepatocellular carcinoma patients as compared with controls. Peripheral blood mononuclear cells from healthy volunteers were exposed to recombinant human (rh)IL-10 in vitro to additionally characterize its impact on distinct blood dendritic cell subsets. A dramatic decrease of all myeloid dendritic cell (MDC) and plasmacytoid dendritic cell (PDC) subsets was detectable after 24 hours of continuous rhIL-10 exposure. Moreover, the expression of HLA-DR, CD80 and CD86, was significantly reduced on rhIL-10-treated dendritic cell subsets. Direct ex vivo flow cytometric analysis of various dendritic cell subpopulations in peripheral blood from hepatocellular carcinoma patients revealed an immature phenotype and a substantial reduction of circulating dendritic cells that was associated with increased IL-10 concentrations in serum and with tumor progression. These findings confirm a predominantly immunosuppressive role of IL-10 for circulating dendritic cells in patients with hepatocellular carcinoma and, thus, may indicate novel aspects of tumor immune evasion.

Adult↗

PubMed2004

[Hepatic encephalopathy].

Hepatic encephalopathy (HE) may develop within the course of acute or chronic liver failure and is characterized by a complex of psychomotor symptoms. In addition, HE can be induced by portocaval shunting even in the absence of any apparent liver disease. HE is caused by substances, which are either reabsorbed from the gut or are a product of the body metabolism. Normally, these substances are effectively eliminated during their first passage through the liver. However, a decreasing number of functional hepatocytes or the presence of portocaval collaterals in liver disease may significantly impair hepatic detoxification. Ammonia seems to take a central position in the pathogenesis of HE, although the exact cerebral effects of this metabolite are still not known in detail. The actual pathogenetic hypotheses are subject of this review. Depending on the underlying liver disease, HE is divided into an acute and a chronic form. Chronic HE may be present as a persistent or an episodic form, the latter being usually induced by defined precipitating factors, such as diet failures, infection and gastrointestinal-bleeding. With regard to the psychomotor symptoms and the coma depth, the clinical picture is classified into five grades (West Haven criteria). Diagnosis is made by clinical examination of the mental status after relevant differential diagnoses have been excluded. The only causal therapeutic option in the presence of acute or chronic liver failure is liver transplantation. Therefore, the indication for transplantation has to be evaluated in all forms of HE. Symptomatic treatment has three principal aims: (1) stabilization of circulation, oxygen supply, blood sugar and nutrition; (2) identification of the precipitating factor and its removal; (3) reduction of ammonia and other potential toxins in the circulation. In the case of acute HE, these therapeutic aims are complemented by an effective prophylaxis or therapy of brain edema.

Animals↗

PubMed2004

Combined small and large bowel MR imaging in patients with Crohn's disease: a feasibility study.

MRI of the small bowel is a new method for the assessment of inflammatory bowel diseases. However, inflammatory bowel disease can affect both the small and large bowel. Therefore, our goal was to assess the feasibility of displaying the small bowel and colon simultaneously by MR imaging. Eighteen patients with inflammatory bowel disease were studied. For small bowel distension, patients ingested a solution containing mannitol and locust bean gum. Furthermore, the colon was rectally filled with water. MR examinations were performed on a 1.5-T system. Before and after intravenous gadolinium administration, a T1w data set was collected. All patients underwent conventional colonoscopy as a standard of reference. The oral ingestion and the rectal application of water allowed an assessment of the small bowel and colon in all patients. By means of MRI (endoscopy), 19 (13) inflamed bowel segments in the colon and terminal ileum were detected. Furthermore, eight additional inflammatory lesions in the jejunum and proximal ileum that had not been endoscopically accessible were found by MRI. The simultaneous display of the small and large bowel by MRI is feasible. Major advantages of the proposed MR concept are related to its non-invasive character as well as to the potential to visualize parts of the small bowel that cannot be reached by endoscopy.

Adult↗

PubMed2004

Proapoptotic function of protein kinase CK2alpha" is mediated by a JNK signaling cascade.

Protein kinase CK2 (formerly casein kinase II) is a tetrameric enzyme constitutively expressed in all eurakyotic tissues that plays a significant role in the regulation of cell proliferation, malignant transformation, and apoptosis. The catalytic alpha-subunit of the enzyme is known to exist in three isoforms CK2alpha, CK2alpha' and CK2alpha". CK2alpha" is highly expressed in liver compared with other tissues and is required for the normal trafficking of several hepatocellular membrane proteins. Initial studies of dengue virus infection indicated that the CK2alpha"-deficient membrane trafficking mutant cell line (Trf1) was resistant to virus-induced cell death compared with the parental human hepatoma (HuH)-7 hepatoma line. Expression of recombinant CK2alpha" in Trf1 was capable of reverting this resistant phenotype. This study was extended to TNF-alpha in addition to other stimuli of cell death in an attempt to uncover common death pathways that might be modulated by CK2alpha". Evaluation of different pathways involved in death signaling suggest that the regulation of a critical proapoptotic step in HuH-7 cells by CK2alpha" is mediated by a JNK signaling cascade.

Apoptosis↗

PubMed2004

Asialoglycoprotein receptor facilitates hemolysis in patients with alcoholic liver cirrhosis.

Hemolysis in patients with advanced alcoholic liver disease is a common clinical problem and indicates an unfavorable prognosis. In many cases, the etiology of the hemolysis remains unknown. We observed three patients with alcoholic liver disease, suffering from severe hemolytic anemia, requiring multiple blood transfusions. Steroid therapy was ineffective and two of the patients died. All patients had a soluble variant of the human asialoglycoprotein receptor (s-ASGP-R) in their serum, as well as high titers of autoantibodies against this receptor (anti-ASGP-R). Consecutively, examination of 60 patients with alcoholic liver disease revealed a high incidence for s-ASGP-R (36%) and anti-ASGP-R (27%) in patients with alcoholic liver cirrhosis (ALC) compared to patients with cirrhosis due to viral hepatitis. The potential etiology of hemolysis was studied in vitro on erythrocytes from patients with ALC and from healthy donors. Isolated ASGP-R but not anti-ASGP-R bound to the surface of erythrocytes preferentially of blood group A1 and caused dose-dependent agglutination and hemolysis, while this phenomenon was much lower using erythrocytes of the blood group B and almost absent with blood group O-erythrocytes. Furthermore, agglutination and hemolysis only occurred in erythrocytes from ALC-patients or after the pre-treatment of cells with neuraminidase. ASGP-R induced agglutination and hemolysis was blocked by the competitive ASGP-R inhibitor asialofetuin. In conclusion, our results indicate a new, non-immunological mechanism for hemolysis in patients with alcoholic liver disease, mediated through agglutination by a soluble variant of the human asialoglycoprotein receptor and mechanical shear stress.

Agglutination Tests↗

PubMed2004

Volumetric and functional recovery of the liver after right hepatectomy for living donation.

Our objective was to study the kinetics of recovery of the liver volume and liver function after right hepatectomy (RH) for living donation, comparing conventional and quantitative liver function tests, i.e., galactose elimination capacity (GEC). A total of 27 donors underwent RH averaging 61% of the whole liver volume. The conventional and quantitative liver function tests, as well as magnetic resonance imaging volumetric studies, were performed preoperatively at postoperative day (POD) 10, 90, 180, and 360. Mean residual volume increased by 88% within 10 days from RH and thereafter did not show any significant variation. After 1 year, only 83% of the original volume was reached. GEC per milliliter of liver volume expressed in percent of initial value (GEC/mL) showed a decrease of 25% at POD10, an increase up to 125% at POD 180, and returned to normal values at POD 360. Liver biochemistries, International Normalized Ratio (INR), and bilirubin returned to normal in 10 days. Cholinesterase showed a similar course like GEC. In conclusion, within 10 days of 61% loss of its initial volume, the liver is capable of regenerating a volume necessary to its function, although it corresponds to only 74% of the initial one. It takes only 10 days to normalize liver biochemistries, while cholinesterase and albumin recover over 90 days. However, a direct measure of the cytosolic liver function obtained by GEC shows that functional recovery occurs much more gradually than the recovery of volume and liver biochemistries.

Adult↗

PubMed2004

Experience after the evaluation of 700 potential donors for living donor liver transplantation in a single center.

Adequate selection of donors is a major prerequisite for living donor liver transplantation (LDLT). Few centers report on the entire number of potential donors considered or rejected for living donation. From April 1998 to July 2003, a total of 111 living donor liver transplantations were performed at our institution, with 622 potential donors for 297 adult recipients and 78 potential donors for 52 pediatric recipients evaluated. In the adult group, only 89 (14%) potential donors were considered suitable, with a total of 533 (86%) potential donors rejected. Of these, 67% were excluded either at initial screening or during the first and second steps of the evaluation procedure. In 31% of all cases, the evaluation of donors was canceled because of recipient issues. In the pediatric group, 22 (28%) donors were selected, with the other 56 (72%) rejected. Costs of the complete evaluation process accounted for 4,589 Euro (Euro) per donor. The evaluation of a potential living donor is a complex and expensive process. We present the results on the evaluation of the largest group of potential donors for adults reported in the literature. Only 14% of potential donors in our series were considered suitable candidates. It has not yet been established who should cover the expenses of the evaluation of all rejected donors. In conclusion, all efforts should be made in order to develop an effective screening protocol for the evaluation of donors with the aim of saving time and resources for a liver transplantation program.

Adolescent↗

PubMed2004

Toll-like receptor 2 enhances ZO-1-associated intestinal epithelial barrier integrity via protein kinase C.

BACKGROUND & AIMS: Protein kinase C (PKC) has been implicated in regulation of intestinal epithelial integrity in response to lumenal bacteria. Intestinal epithelial cells (IECs) constitutively express Toll-like receptor (TLR)2, which contains multiple potential PKC binding sites. The aim of this study was to determine whether TLR2 may activate PKC in response to specific ligands, thus potentially modulating barrier function in IECs. METHODS: TLR2 agonist (synthetic bacterial lipopeptide Pam(3)CysSK4, peptidoglycan)-induced activation of PKC-related signaling cascades were assessed by immunoprecipitation, Western blotting, immunofluorescence, and kinase assays-combined with functional transfection studies in the human model IEC lines HT-29 and Caco-2. Transepithelial electrical resistance characterized intestinal epithelial barrier function. RESULTS: Stimulation with TLR2 ligands led to activation (phosphorylation, enzymatic activity, translocation) of specific PKC isoforms (PKCalpha and PKCdelta). Phosphorylation of PKC by TLR2 ligands was blocked specifically by transfection with a TLR2 deletion mutant. Ligand-induced activation of TLR2 greatly enhanced transepithelial resistance in IECs, which was prevented by pretreatment with PKC-selective antagonists. This effect correlated with apical tightening and sealing of tight junction (TJ)-associated ZO-1, which was mediated via PKC in response to TLR2 ligands, whereas morphologic changes of occludin, claudin-1, or actin cytoskeleton were not evident. Downstream the endogenous PKC substrate myristoylated alanine-rich C kinase substrate (MARCKS), but not transcriptional factor activator protein-1 (AP-1), was activated significantly on stimulation. CONCLUSIONS: The present study provides evidence that PKC is an essential component of the TLR2 signaling pathway with the physiologic consequence of directly enhancing intestinal epithelial integrity through translocation of ZO-1 on activation.

Caco-2 Cells↗

PubMed2004

Which patients benefit from hemodialysis therapy in hepatorenal syndrome?

BACKGROUND AND AIM: Hepatorenal syndrome (HRS) occurs in patients with advanced liver cirrhosis and has a poor outcome. The aim of the present study was to investigate which patients with HRS are likely to benefit from hemodialysis. METHODS: Data were collected prospectively from 30 patients with Child-Pugh C liver cirrhosis and HRS. Patients were either treated with continuous veno-venous hemodialysis (CVVHD) if they were mechanically ventilated, or with intermittent hemodialysis (HD) if they were not mechanically ventilated. Prognosis was assessed by the Child-Pugh and by the Model for End-Stage Liver Disease (MELD) score. The primary aim of the study was the analysis of overall and 30-day patient survival during hemodialysis therapy. To identify predictive factors of survival, variables obtained before the initiation of dialysis therapy were evaluated. RESULTS: Patients' 30-day survival was 8/30 (median survival time 21 days). Among patients treated with mechanical ventilation, 30-day survival time was 0/15 while 8/15 patients without mechanical ventilation survived more than 30 days (P < 0.001). Using a multivariate model, the relative hazards for serum albumin, international normalized ratio (INR) and catecholamine therapy were not different from one another (P > 0.05), indicating that these parameters were not independent predictors of survival. Mechanical ventilation was an independent risk factor for 30-day (relative hazard 6.6 [1.6-27.7], P < 0.001) and overall survival (relative hazard 6.3 [1.5-26.5], P = 0.01). Child-Pugh (P < 0.01) and the MELD (P < 0.01) score were predictive for overall survival independent of mechanical ventilation. CONCLUSIONS: Patients with HRS without mechanical ventilation may benefit from hemodialysis, whereas hemodialysis seems to be futile in patients with mechanical ventilation.

Adult↗

PubMed2004

Presence of markers for liver progenitor cells in human-derived intrahepatic biliary epithelial cells.

AIMS: Rodent intrahepatic bile duct may harbor bipotential liver progenitor cells. In this study, human-derived intrahepatic biliary epithelial cells (BECs) were investigated in terms of whether they have the character of liver progenitor cells. METHODS: Ten liver tissue specimens were obtained after partial hepatectomy or liver explantation. Intrahepatic BECs were isolated by density-gradient centrifugation and immunomagnetic separation using anti-human epithelial antigen and cultured in medium containing epidermal growth factor and hepatocyte growth factor. The isolated and cultured cells were characterized by immunostaining and reverse transcription polymerase chain reaction with a variety of markers for fetal hepatocytes and liver progenitor cells. RESULTS: These cells had proliferated for up to 18 weeks in vitro. They continuously expressed epithelial markers (cytokeratin (CK) 8 and CK 18) as well as biliary markers (CK 7 and CK 19). Remarkably, some isolated and cultured cells also expressed markers for fetal hepatocytes and liver progenitor cells, including albumin, alpha-fetoprotein, alpha1-antitrypsin, c-kit and chromogranin-A. CONCLUSION: Some human-derived intrahepatic BECs coexpressed markers for liver progenitor cells. This finding further supports the hypothesis that the human biliary tree may also consist of liver progenitor cells.

Adult↗

PubMed2004

Aortoesophageal fistula secondary to stent-graft repair of the thoracic aorta.

PURPOSE: To report the incidence and management of aortoesophageal fistula (AEF) secondary to endovascular stent-graft repair of the descending thoracic aorta. METHODS: A retrospective review was conducted of patients treated at our facility between July 1999 and June 2003. During this interval, 60 patients (46 men; average age 66+/-10 years) underwent thoracic aortic stent-graft placement for a variety of pathologies. RESULTS: AEF occurred in 3 (5%) patients. One 62-year-old man presented with recurrent back pain and fever and died suddenly due to fatal exsanguination; the AEF was revealed at necropsy. The other 2 patients (both women) presented with hematemesis after endovascular repair of thoracic aortic aneurysms. AEF was detected by esophagogastroduodenoscopy. Both patients were treated conservatively, as open surgical repair was refused because of their general condition. Both patients developed severe mediastinitis and died after 5 weeks and 10 months, respectively. CONCLUSIONS: Aortoesophageal fistula is, in our experience, a catastrophic complication of endovascular stent-graft placement. Treatment options are very limited, as these patients are usually not candidates for open surgery. Outcome under conservative management is, however, almost invariably fatal.

Aged↗

PubMed2003

Serum ferritin and survival of renal transplant recipients: a prospective 10-year cohort study.

Increased serum ferritin is frequent in renal transplant recipients. This reflects iron overload due to blood transfusions given to treat renal anaemia. Previous studies suggested excess mortality in non-renal transplant recipients with iron overload. We hypothesized that serum ferritin levels above 1100 ng/ml may be associated with increased long-term mortality in renal transplant recipients. Twenty consecutive renal transplant recipients with high levels of serum ferritin and 20 renal transplant recipients with normal serum ferritin levels, matched for age and gender, were prospectively studied for 10 years. Nine patients (45%) with increased serum ferritin died during follow-up, compared to four controls (20%). Univariate and multivariate analysis identified multiple blood transfusions (>40 units) prior to transplantation as being associated with higher mortality in renal transplant recipients (risk ratio (RR): 3.1, confidence interval (CI): 1.1-9.2; P=0.03). These data suggest that serum ferritin levels above 1100 ng/ml due to multiple blood transfusions causing iron overload is a relevant factor that increases mortality.

Adult↗

PubMed2003

Efficacy of combined lamivudine and adefovir dipivoxil treatment for severe HBV graft reinfection after living donor liver transplantation.

Resistance to lamivudine and hyperimmune globulin (HBIG) may cause severe graft reinfection with progression to fulminant hepatic failure in liver transplant recipients. In this report, we describe the clinical course of a patient with perinatally acquired chronic hepatitis B virus (HBV) infection and hepatocellular carcinoma who developed severe fibrosing cholestatic hepatitis after living donor liver transplantation because of the emergence of lamivudine and HBIG-resistant chronic hepatitis B. Immunohistochemistry demonstrated that more than 30% of hepatocytes stained positively for hepatitis B core antigen. Hepatitis B virus sequence analysis revealed several mutations in the polymerase gene (L528M, M552I, M552V) as well as in the surface gene region encoding the immunogenic major hydrophilic loop of the small surface protein (G130N, M133T, D144G). The amino acid exchange at codon 144 has already been described to escape neutralization by HBIG. Combined treatment with lamivudine and adefovir dipivoxil (ADV) was associated with a dramatic biochemical, virological and clinical response with resolution of jaundice, ascites, peripheral edema and pleural effusions. Serum bilirubin normalized, HBV DNA levels significantly decreased and liver biopsy was remarkable for the absence of viral protein. These results indicate that ADV may provide a sustained rescue treatment for aggressive courses of HBV graft reinfection in liver transplant recipients.

Adenine↗

PubMed2003

Hepatitis B virus-induced defect of monocyte-derived dendritic cells leads to impaired T helper type 1 response in vitro: mechanisms for viral immune escape.

Dendritic cells (DC) are the most potent antigen-presenting cells and play a central role in the induction of antiviral immune responses. Recently, we have shown that monocyte-derived DC (MoDC) from patients with chronic hepatitis B virus (HBV) infection are functionally impaired. In our present study MoDC from healthy subjects were propagated in vitro and inoculated with HBV particles to investigate the precise mechanisms that underly MoDC dysfunction. T-cell proliferation assays revealed an impaired allostimulatory capacity of HBV-inoculated MoDC (HBV-MoDC) as well as a lower potential of stimulating autologous T cells against a recall antigen in comparison to control-MoDC. Interleukin-2, tumour necrosis factor-alpha and interferon-gamma production by T cells in proliferation assays with HBV-MoDC was significantly lower than with control-MoDC and correlated with lower IL-12 production in HBV-MoDC cultures. The presence of the nucleoside analogue lamivudine (3TC), an inhibitor of HBV replication, restored impaired allostimulatory function of HBV-MoDC and up-regulated major histocompatibility complex class II expression. These results show that HBV infection compromises the antigen-presenting function of MoDC with concomitant impairment of T helper cell type 1 responses. This may play an important role for viral immune escape leading to chronic HBV infection. However, 3TC treatment can overcome HBV-MoDC-related T-cell hyporeactivity and this underscores its important role in enhanced immune responses to HBV.

Adult↗

PubMed2003

Right living donor liver transplantation: an option for adult patients: single institution experience with 74 patients.

OBJECTIVE: To present an institutional experience with the use of right liver grafts in adult patients and to assess the practicability and efficacy of this procedure by analyzing the results. SUMMARY BACKGROUND DATA: Living donor liver transplantation (LDLT) for the pediatric population has gained worldwide acceptance. In the past few years, LDLT has also become feasible for adult patients due to technical evolution in hepatobiliary surgery and increased experience with reduced-size and split-liver transplants. Nevertheless, some graft losses remain unexplained and are possibly due to unrecognized venous outflow problems. METHODS: From April 1998 to September 2002, we performed 74 right LDLTs (segments 5-8). The 74 donors were selected from 474 candidates according to standard protocol. The median age of the donors was 35 years (range 18-58 years) and 51 years (range 18-64 years) in recipients. Standard and extended indications for transplantation were considered. Over the period reported, technical modifications in the bile duct anastomosis (duct-to-duct, end-to-end, or end-to-side) and a new graft implantation technique that provides maximized venous outflow, leading to outcome improvement, were developed. RESULTS: 64.9% of patients had liver cirrhosis and 35.1% had malignancy. While 44 donors (59.5%) presented an uneventful postoperative course, 27% minor (pleural effusion, pneumonia, venous thrombosis, wound infection, incisional hernia) and 13.5% major (biliary leakage, death of a donor due to unrecognized hereditary liver disease, and consecutive liver insufficiency) complications were documented. In recipients, 23% biliary complications and 6.8% hepatic artery thrombosis occurred. The overall patient and graft survival rate after 1 year was 79.4% and 75.3%, respectively. In cases with extended indication, the patient survival rate was 74% and the graft survival rate 68% at 12 months. Using technical modifications in the last 10 recipients, including 2 critically decompensated cirrhotics, the survival rate was 100% at a median follow-up of 3.5 months. CONCLUSIONS: In our transplant program, living donor liver transplantation has become a standard option in the adult patient population. The critical issue of this procedure is donor morbidity. Technical improvements in the harvesting and implantation of right grafts can also offer hope to patients with challenging forms of end-stage liver disease or malignant liver tumors.

Adolescent↗

PubMed2002

[Cardiac manifestations in HIV-infected individual].

The human immunodeficiency virus (HIV) does not only affect the immune system. Other organs including the cardiovascular system are influenced by the HIV as well. Most common HIV-associated cardiac manifestations are pericardial effusion and chronic active, focal or diffuse myocarditis. In addition to peri- and myocardial disease, endocardiac manifestations occur as infective endocarditis and nonbacterial thrombotic endocarditis in HIV-infected patients. Although most of the cardiac manifestations associated with HIV-infection exhibit a slow progression, rapid courses may lead to fatal complications. Early screening of HIV-infected patients will identify the potentially fatal complications of HIV disease and permit efficient treatment. The use of highly active antiretroviral therapy (HAART) significantly reduced the mortality and morbidity of HIV-infected patients. However, the impact that HAART will have on the incidence and prevalence of cardiac complications in HIV-infected patients is still unknown. It can be predicted, that the long-term viral infection and the increase of cardiovascular risk factors by HAART will probably lead to an increased prevalence of HIV-infected individuals with cardiac complications in the next decade. The present review describes the most frequent HIV-associated cardiac manifestations including diagnostic and therapeutic perspectives.

Adult↗