Regulation of coronary venular barrier function by blood borne inflammatory mediators and pharmacological tools: insights from novel microvascular wall models.

We hypothesized that postcapillary venules play a central role in the control of the tightness of the coronary system as a whole, particularly under inflammatory conditions. Sandwich cultures of endothelial cells and pericytes of precapillary arteriolar or postcapillary venular origin from human myocardium as models of the respective vascular walls (sandwich cultures of precapillary arteriolar or postcapillary venular origin) were exposed to thrombin and components of the acutely activatable inflammatory system, and their hydraulic conductivity (L(P)) was registered. L(P) of SC-PAO remained low under all conditions (3.24 ± 0.52·10(-8)cm·s(-1)·cmH(2)O(-1)). In contrast, in the venular wall model, PGE(2), platelet-activating factor (PAF), leukotriene B(4) (LTB(4)), IL-6, and IL-8 induced a prompt, concentration-dependent, up to 10-fold increase in L(P) with synergistic support when combined. PAF and LTB(4) released by metabolically cooperating platelets, and polymorphonuclear leucocytes (PMNs) caused selectively venular endothelial cells to contract and to open their clefts widely. This breakdown of the barrier function was preventable and even reversible within 6-8 h by the presence of 50 µM quercetin glucuronide (QG). LTB(4) synthesis was facilitated by biochemical involvement of erythrocytes. Platelets segregated in the arterioles and PMNs in the venules of blood-perfused human myocardium (histological studies on donor hearts refused for heart transplantation). Extrapolating these findings to the coronary microcirculation in vivo would imply that the latter's complex functionality after accumulation of blood borne inflammatory mediators can change rapidly due to selective breakdown of the postcapillary venular barrier. The resulting inflammatory edema and venulo-thrombosis will severely impair myocardial performance. The protection afforded by QG could be of particular relevance in the context of cardiosurgical intervention.

Homograft implantation for aortic valve replacement since 15 years: results and follow-up.

BACKGROUND: The use of homografts in aortic valve replacement is an alternative to other prostheses and has been established in our department for 15 years. METHODS: Since 1992, 360 homografts (HG) have been implanted in adult patients (mean age 51.6 years, 72.8% male). Prospective follow-up was done on an annual basis. RESULTS: Thirty-day mortality was 5.0% (n = 17); after 5, 10, and 15 years, survival was 88.3%, 84.6%, and 76.0%, respectively. Out of 39 late deaths, 11 were valve-related (10 HG infections, 1 aortic aneurysm). Freedom from reoperation was 99.4% 1 year after operation; after 5, 10, and 15 years it was 94.1%, 78.2%, and 67.3%, respectively. Indications for HG explantation were graft infections (n = 20), calcification (n = 16), regurgitation > grade II (n = 17), perforation (n = 8), and paravalvular leakage (n = 1). Eleven transitoric ischemic attacks, 2 strokes, and 1 cerebral bleeding event were recorded. In echocardiography, the transvalvular pressure gradient changed from 10.55 to 15.02 (P = .004), 19.9 mmHg (P = .056), and 37 mmHg (not applicable) after 5, 10, and 15 years, respectively. Mean HG regurgitation was grade 0.49 before discharge and increased to 1.0 (P < .001), 0.91, and 2.5 after 5, 10, and 15 years, respectively. Ejection fraction increased from 61.9% to 64% after 5 years and to 66% after 10 years (P = .021) and then decreased to 63.5% after 15 years. CONCLUSIONS: Comparing HG with other valve prostheses, survival and graft durability seem to be confirmed. They are vulnerable to infections. The hemodynamic performance is good, and hemorrhagic or thrombo-embolic events are rare.

Genomic analysis reveals poor separation of human cardiomyopathies of ischemic and nonischemic etiologies.

Clinically, the differentiation between ischemic (ICM) and nonischemic (NICM) human cardiomyopathies is highly relevant, because ICM and NICM differ with respect to prognosis and certain aspects of pharmacological therapy, despite a common final phenotype characterized by ventricular dilatation and reduced contractility. So far, it is unclear whether microarray-based signatures can be used to infer the etiology of heart failure. Using three different classification algorithms, we independently analyzed one cDNA and two publicly available high-density oligonucleotide microarray studies comprising a total of 279 end-stage human heart failure samples. When classifiers identified in a single study were applied to the remaining studies, misclassification rates >25% for ICM and NICM specimens were noted, indicating poor separation of both etiologies. However, data mining of 458 classifier genes that were concordantly identified in at least two of the three data sets points to different biological processes in ICM vs. NICM. Consistent with the underlying ischemia, cytokine signaling pathways and immediate-early response genes were overrepresented in ICM samples, whereas NICM samples displayed a deregulation of cytoskeletal transcripts, genes encoding for the major histocompatibility complex, and antigen processing and presentation pathways, potentially pointing to immunologic processes in NICM. Overall, our results suggest that ICM and NICM exhibit substantial heterogeneity at the transcriptomic level. Prospective studies are required to test whether etiology-specific gene expression patterns are present at earlier disease stages or in subsets of both etiologies.

Immunoglobulin G treatment of postcardiac surgery patients with score-identified severe systemic inflammatory response syndrome--the ESSICS study.

OBJECTIVE: A minority of patients develop severe systemic inflammatory response syndrome (SIRS) with high mortality following cardiopulmonary bypass-assisted cardiac surgery. We assessed whether intravenous immunoglobulin G (ivIgG) improves postoperative short-term (5-day) morbidity and reduces 28-day mortality in these patients. DESIGN: Randomized, double-blind, placebo-controlled, multicenter trial. SETTING: Intensive care units of 11 cardiothoracic centers. PATIENTS AND INTERVENTIONS: Of 6,984 patients screened, we identified 244 with severe SIRS (Acute Physiology and Chronic Health Evaluation II score > or = 28 on the first postoperative day). INTERVENTIONS: The 244 patients with severe SIRS were randomly assigned to receive an intravenous infusion of either albumin 0.1% (placebo group, 6 mL [6 mg]/kg of body weight on day 1 and 3 mL [3 mg]/kg of body weight on day 2) or immunoglobulin G 10% (ivIgG group, 6 mL [600 mg]/kg of body weight on day 1 and 3 mL [300 mg]/kg of body weight on day 2). MEASUREMENTS AND MAIN RESULTS: The prospectively defined primary end points were improvement in morbidity on day 5 and death from any cause assessed on day 28. A total of 218 patients received both doses of the study drug (placebo n = 108, ivIgG n = 110). Acute Physiology and Chronic Health Evaluation II scores in the placebo group decreased from 31.8 +/- 4.0 (day 1) to 25.8 +/- 9.3 (day 5) and in the ivIgG group from 31.8 +/- 3.4 (day 1) to 25.9 +/- 10.3 (day 5), with no significant difference between the groups (p = .56). The 28-day mortality rate was not significantly different between the groups (per protocol population, placebo group 31.5%, ivIgG group 39.1%; intent-to-treat population, placebo group 37.2%, ivIgG group: 44.7%). No effect of ivIgG on plasma levels of interleukin-6, tumor necrosis factor, and tumor necrosis factor receptor I/II was observed. Drug-related adverse events were rare in both groups. CONCLUSIONS: Patients undergoing cardiac surgery (involving cardiopulmonary bypass) who develop severe SIRS derive no improvement in short-term morbidity or 28-day mortality from ivIgG.

Outcome after aortic valve replacement: comparison of homografts with mechanical prostheses.

BACKGROUND AND AIM OF THE STUDY: Aortic valve replacement (AVR) in younger patients is conventionally performed using a mechanical prosthesis (MP), although homograft (HG) implantation is an accepted alternative. This study compares, retrospectively, the follow up of these two dissimilar prostheses. METHODS: Since 1990, a total of 147 Sorin Bicarbon MPs and 285 HGs have been implanted at the authors' institution, and compared statistically for survival, reoperation rate and valve-dependent complications. Only patients aged <70 years were included in the study. RESULTS: The demographic parameters of both patient groups differed with regards to gender, age at the time of implantation, and duration of follow up. Survival was superior in the HG group (log-rank, p = 0.01). Sixteen of 42 late deaths in the MP group were valve-related due to cerebral infarction (n = 7), ventricular arrhythmias (n = 3), or ventricular failure (n = 6). Six of 24 deaths after HG implantation were valve-related (all prosthesis infections). The choice of valve type and patient age were independent risk factors in the multivariate analysis. Freedom from reoperation was superior after MP implantation (log rank, p = 0.007); in six MP patients the indications for redo surgery were prosthesis infection (n = 2) and paravalvular leak (n = 4). In 20 HG patients, redo surgery was required due to prosthesis infection (n = 12), stenotic degeneration (n = 2), regurgitation > grade II (n = 4), or paravalvular leak (n = 2). Age at the time of implantation and valve type were independent risk factors. Thromboembolic complications were mainly seen in MP patients (log rank, p <0.001): there were five ischemic infarctions and 11 transient ischemic attacks (TIAs) compared to three TIAs among HG patients. Cerebral bleeding was found in only 18 cases after MP implantation, and in no cases after HG implantation. In the multivariate analysis, the type of prosthesis was an independent risk factor. CONCLUSION: As expected, these data confirm a longer time period without need for reoperation after MP implantation, but demonstrate a significantly higher survival and fewer complications after AVR with HG.

Surgical and endovascular treatment of symptomatic aberrant right subclavian artery (arteria lusoria).

Right aberrant subclavian artery, also called arteria lusoria, is one of the most common intrathoracic arterial anomalies. Although mostly asymptomatic, the retroesophageal and retrotracheal course of the lusorian artery might result in unspecific thoracic pain, dysphagia, dyspnea, arterioesophageal or arteriotracheal fistulae with hematemesis or hemoptysis, and aneurysmal formation with relevant risk of rupture. The purpose was to present our experience with six patients with a symptomatic aberrant right subclavian artery, two patients with dysphagia or dyspnea caused by a nonaneurysmal lusorian artery, and four patients with arteria lusoria aneurysms. The operative procedures performed are described and discussed in view of the data reported in the literature. According to the classification of the lusorian artery pathology, a combined intervention with right subclavian artery transposition, distal or proximal lusorian artery ligation or proximal endovascular occlusion for nonaneurysmal disease, or endovascular thoracic aortic stent graft implantation for lusorian artery aneurysms seems to be an additional and minimally invasive approach with promising midterm results.

Mediastinal pheochromocytoma with single coronary blood supply: a case report.

Primary pheochromocytomas located outside the adrenal glands account for only 10% of all pheochromocytomas. Mediastinal pheochromocytomas are even rarer and usually represent a therapeutic challenge as they often infiltrate adjacent structures. We report the case of a large primary mediastinal pheochromocytoma in a 65-year-old patient presenting with a sudden angina-like chest pain and dyspnea. Thoracic multislice computed tomography showed an 8 x 5 x 6-cm retrocardiac mass causing compression of both atria and infiltrating the left superior pulmonary vein. The tumor was highly vascularized and presented a blood supply derived from the circumflex artery. The mass was successfully removed by open heart surgery, and the patient was discharged 10 days postoperatively.

Identification of a common gene expression signature in dilated cardiomyopathy across independent microarray studies.

OBJECTIVES: This study was designed to identify a common gene expression signature in dilated cardiomyopathy (DCM) across different microarray studies. BACKGROUND: Dilated cardiomyopathy is a common cause of heart failure in Western countries. Although gene expression arrays have emerged as a powerful tool for delineating complex disease patterns, differences in platform technology, tissue heterogeneity, and small sample sizes obscure the underlying pathophysiologic events and hamper a comprehensive interpretation of different microarray studies in heart failure. METHODS: We accounted for tissue heterogeneity and technical aspects by performing 2 genome-wide expression studies based on cDNA and short-oligonucleotide microarray platforms which comprised independent septal and left ventricular tissue samples from nonfailing (NF) (n = 20) and DCM (n = 20) hearts. RESULTS: Concordant results emerged for major gene ontology classes between cDNA and oligonucleotide microarrays. Notably, immune response processes displayed the most pronounced down-regulation on both microarray types, linking this functional gene class to the pathogenesis of end-stage DCM. Furthermore, a robust set of 27 genes was identified that classified DCM and NF samples with >90% accuracy in a total of 108 myocardial samples from our cDNA and oligonucleotide microarray studies as well as 2 publicly available datasets. CONCLUSIONS: For the first time, independent microarray datasets pointed to significant involvement of immune response processes in end-stage DCM. Moreover, based on 4 independent microarray datasets, we present a robust gene expression signature of DCM, encouraging future prospective studies for the implementation of disease biomarkers in the management of patients with heart failure.

Endovascular treatment of a symptomatic suture aneurysm caused by an aortic isthmus restenosis.

After operative treatment of aortic isthmus stenoses, late complications, such as aneurysm formation or aortic restenosis, might occur, with relevant morbidity and mortality rates during open surgical reintervention. We report on the endovascular repair of a symptomatic suture aneurysm caused by an aortic isthmus restenosis by thoracic aortic stent graft implantation and additional intraoperative balloon dilatation. Based on our experience, endovascular repair of thoracic aortic aneuryms caused by native aortic isthmus stenosis or postcoarctation restenosis is a valuable treatment option, especially in symptomatic patients with an imminent risk of rupture or a difficult immediate transthoracic surgical approach. Long-term follow-up is required to assess the durability of the stent graft treatment.

Changes in myocardial vasoreactivity after drastic reduction of plasma fibrinogen and cholesterol: a clinical study in long-term heart transplant survivors using positron emission tomography.

BACKGROUND: Given the central importance of the microvasculature in heart transplant recipients, we investigated the possibility of increasing cardiac perfusion after reduction of low-density lipoprotein (LDL)-cholesterol, lipoprotein (a), C-reactive protein (CRP) and fibrinogen plasma levels after apheresis treatment in transplanted patients. METHODS: Ten long-term heart transplant recipients were examined with positron emission tomography (PET) to measure myocardial perfusion before and after a single heparin-mediated extracorporeal LDL/fibrinogen precipitation (HELP)-apheresis treatment. PET studies were performed the mornings before and after the apheresis treatment. Myocardial blood flow at rest and during adenosine-induced hyperemia was measured using (13)N-ammonia. RESULTS: HELP-apheresis reduced the plasma levels of LDL-cholesterol, lipoprotein (a) and C-reactive protein by 48% (p < 0.001), fibrinogen by 42% (p = 0.02), plasma viscosity by 14% (p = 0.004) and erythrocyte aggregation by 28% (p < 0.02). Osmolality (<1%) and hematocrit (<2%) remained stable. A single apheresis treatment increased median corrected rest flow by 17.5% (p = 0.007) and median hyperemic flow by 27% (p = 0.02). Median coronary flow reserve increased by 8.1% (p = 0.09). Hyperemic flow after adenosine infusion increased plasma vascular endothelial growth factor levels only before HELP-apheresis (+60%), indicating better ischemic tolerance after apheresis (p = 0.01). CONCLUSIONS: Myocardial perfusion in transplanted hearts increases significantly after single HELP-apheresis treatment. The present study is only a proof of concept, providing complementary evidence to clinical long-term studies showing that cholesterol reduction either with statins and/or apheresis improves heart transplant outcome.

Reprogramming of the human atrial transcriptome in permanent atrial fibrillation: expression of a ventricular-like genomic signature.

Atrial fibrillation is associated with increased expression of ventricular myosin isoforms in atrial myocardium, regarded as part of a dedifferentiation process. Whether reexpression of ventricular isoforms in atrial fibrillation is restricted to transcripts encoding for contractile proteins is unknown. Therefore, this study compares atrial mRNA expression in patients with permanent atrial fibrillation to atrial mRNA expression in patients with sinus rhythm and to ventricular gene expression using Affymetrix U133 arrays. In atrial myocardium, we identified 1434 genes deregulated in atrial fibrillation, the majority of which, including key elements of calcium-dependent signaling pathways, displayed downregulation. Functional classification based on Gene Ontology provided the specific gene sets of the interdependent processes of structural, contractile, and electrophysiological remodeling. In addition, we demonstrate for the first time a prominent upregulation of transcripts involved in metabolic activities, suggesting an adaptive response to increased metabolic demand in fibrillating atrial myocardium. Ventricular-predominant genes were 5 times more likely to be upregulated in atrial fibrillation (174 genes upregulated, 35 genes downregulated), whereas atrial-specific transcripts were predominantly downregulated (56 genes upregulated, 564 genes downregulated). Overall, in fibrillating atrial myocardium, functional classes of genes characteristic of ventricular myocardium were found to be upregulated (eg, metabolic processes), whereas functional classes predominantly expressed in atrial myocardium were downregulated (eg, signal transduction and cell communication). Therefore, dedifferentiation with adoption of a ventricular-like signature is a general feature of the fibrillating atrium.

Ten years' experience in aortic valve replacement with homografts in 389 cases.

BACKGROUND AND AIM OF THE STUDY: Aortic valve replacement using homografts is an accepted alternative to the use of other replacement devices, and has been established at the authors' institution for more than 10 years. METHODS: Since 1992, a total of 389 homografts was implanted, and 332 patients (mean age 54 years, 72% males) were followed up. The initial patients (n = 75) had subcoronary implantation, all subsequent patients had root replacement. Both aortic grafts (AG) and pulmonary grafts (PG) were used. Follow up was conducted with regard to the factors 'graft origin', 'implantation technique' and 'gender', and included clinical examination, ECG and transthoracic echocardiography on an annual basis. RESULTS: Overall 30-day mortality was 5.4% (AG patients 3.9%, PG patients 13.5%; p = 0.09). Among late deaths (n = 22), six were valve-related (all prosthetic infection). Four minor thrombembolic events were recorded due to amaurosis fugax and transient ischemic attacks (TIA). Freedom from reoperation was 86.5%. Indication for graft replacement was greater after subcoronary implantation than after root implantation (p = 0.04). Reoperation was necessary in 24 patients due to restenosis (n = 4), regurgitation grade >II (n = 5), paravalvular leak (n = 2) and prosthetic infection (n = 13). At the latest echocardiographic follow up, mean peak pressure gradient was 15.60 +/- 11.76 mmHg, homograft regurgitation grade was 0.82 +/- 0.66, left ventricular end-diastolic diameter (EDD) was 49.1 +/- 7.54 mm, and mean aortic root diameter was 30.54 +/- 5.48 mm. When comparing parameters at a mean of five years postoperatively, the pressure gradient increased from 10.26 to 15.02 mmHg, regurgitation grade increased from 0.53 to 0.81, and EDD decreased from 52.3 to 50.4 mm. Other variables showed no significant differences. CONCLUSION: The present results confirmed good midterm-results for aortic valve replacement with homografts. These prostheses are vulnerable to infection, and root replacement was superior to the subcoronary implantation technique.

Successful cardic surgery 24 hours after craniotomy in a patient with infective endocarditis and embolic cerebellar infarction: case report.

Follow up management in a patient already treated with decompressive craniotomy for a space-occupying endocarditic stroke is difficult. While immediate valve replacement eliminates the focus and therefore the high risk of re-embolization, a neurosurgical intervention is considered a contraindication to early cardiosurgery. Herein, the first report is presented of a critically ill patient with bacterial endocarditis and a space-occupying cerebellar infarction with imminent herniation, who successfully underwent mitral valve replacement only 24 h after decompressive craniotomy. To prevent rebleeding, maximal hemostasis was ensured during the neurosurgical intervention. For cardiosurgery, the patient was cooled to 21 degrees C, mildly hyperventilated, and maintained at an adequate perfusion pressure during cardiopulmonary bypass. A bioprosthesis was used to reduce the time of anticoagulation. The patient did not develop new infarcts after either intervention, and there was only a very small hemorrhagic transformation without a relevant mass effect. At five months after surgery the patient had minimal neurological abnormalities and was able to conduct his daily life without help.

Global gene expression in human myocardium-oligonucleotide microarray analysis of regional diversity and transcriptional regulation in heart failure.

To obtain region- and disease-specific transcription profiles of human myocardial tissue, we explored mRNA expression from all four chambers of eight explanted failing [idiopathic dilated cardiomyopathy (DCM), n=5; ischemic cardiomyopathy (ICM), n=3], and five non-failing hearts using high-density oligonucleotide arrays (Affymetrix U95Av2). We performed pair-wise comparisons of gene expression in the categories (1) atria versus ventricles, (2) disease-regulated genes in atria and (3) disease-regulated genes in ventricles. In the 51 heart samples examined, 549 genes showed divergent distribution between atria and ventricles (272 genes with higher expression in atria, 277 genes with higher expression in ventricles). Two hundred and eighty-eight genes were differentially expressed in failing myocardium compared to non-failing hearts (19 genes regulated in atria and ventricles, 172 regulated in atria only, 97 genes regulated in ventricles only). For disease-regulated genes, down-regulation was 4.5-times more common than up-regulation. Functional classification according to Gene Ontology identified specific biological patterns for differentially expressed genes. Eleven genes were validated by RT-PCR showing a good correlation with the microarray data. Our goal was to determine a gene expression fingerprint of the heart, accounting for region- and disease-specific aspects. Recognizing common gene expression patterns in heart failure will significantly contribute to the understanding of heart failure and may eventually lead to the development of pathway-specific therapies.

Risk factors for atherosclerosis and the degeneration of pericardial valves after aortic valve replacement.

BACKGROUND: Recent studies have demonstrated the influence of atherosclerotic risk factors on the progression of aortic stenosis. We hypothesized that risk factors for atherosclerosis might also be involved in the degeneration of pericardial heart valves and might lead to reoperation as a result of structural valve failure, especially in younger patients with high degeneration rates. METHODS: In 1984 and 1985, 161 patients (74% male; mean age, 54.4 +/- 1.0 years; age range, 17-76 years; median age, 56.5 years) survived isolated aortic (n = 137) or combined aortic and mitral (n = 25) valve replacement with a Hancock extracorporeal pericardial valve. Of these patients, 90 (56%) had reoperations as a result of tissue failure of the aortic valve 5.6 +/- 0.25 years postoperatively. RESULTS: The patient group was split in half at the median age. In patients aged 57 years or younger, diabetes mellitus, female sex, cigarette smoking, and high cholesterol and triglyceride levels were associated with accelerated valve failure. In a multivariate model sex (female, P =.001), smoking (P =.001), diabetes mellitus (P =.020), and cholesterol levels (P =.011) are risk factors for reoperation. Patients without risk factors had reoperation after a mean of 9.25 +/- 0.88 years compared with 4.05 +/- 0.43 years (P =.0002) in patients with 2 or 3 risk factors. CONCLUSIONS: Risk factors of atherosclerosis might play a substantial role in the degeneration of aortic bioprosthetic valves. Lowering of serum lipid levels, smoking cessation, therapy for diabetes, and careful patient selection could be new strategies to postpone degeneration. Younger patients could then possibly benefit from the advantages of bioprostheses.

Case reports on emergency treatment of cardiovascular syndromes through heparin-mediated low-density lipoprotein/fibrinogen precipitation: a new approach to augment cerebral and myocardial salvage.

We report the first experiences with HELP apheresis as an emergency treatment for acute cardiovascular syndromes; two patients who were not eligible for lysis therapy and catheter intervention were treated with HELP apheresis instead. Both patients had a most severe, generalized atherosclerosis and reached the hospital too late for conventional measures. In both cases, the use of the apheresis dramatically improved the clinical situation to such an extent that the possibilities of this apheresis system urge further investigation.

Is there an advantage in using homografts in patients with acute infective endocarditis of the aortic valve?

BACKGROUND AND AIM OF THE STUDY: Acute infective endocarditis is a surgical challenge, particularly when paravalvular abscesses and annular destruction are present. The choice of a homograft or mechanical valve prosthesis is an important issue in these patients. The study aim was to compare the outcome with homografts and mechanical valves in patients with acute infective endocarditis. METHODS: A total of 77 patients (mean age 49+/-9 years) operated on for acute endocarditis of the aortic valve was included in the study and analyzed retrospectively. The causative bacterium was isolated from blood cultures in 71 cases. Preoperatively, 21 patients required artificial ventilation and 24 had inotropic support due to hemodynamic instability. Aortic homografts were implanted in 43 patients, and mechanical valve prostheses in 34. The two patient groups were similar in terms of gender, age and preoperative inotropic support. In total, 31 patients (44%) had paravalvular abscesses, and a homograft was used significantly more often (77%, p <0.05) in these cases. Follow up examinations (clinical examination, ECG and transthoracic echocardiography) were performed six months postoperatively and continued on an annual basis. Endocarditis relapse was defined as persisting infection, whereas re-endocarditis indicated a new infection after an interval of at least six months. RESULTS: Perioperative mortality was 11.5% (5/43) in homograft patients. In the 38 survivors, follow up was complete and averaged 5.0+/-1.2 years. One patient had an endocarditis relapse three months after surgery. Re-endocarditis occurred in three patients after two or three years. One other patient had pseudoaneurysm formation without a need for intervention, and one had repeat aortic valve replacement due to dysfunction of the graft after four years. The other 33 patients had an uneventful follow up. Echocardiography revealed aortic insufficiency grade 1 in 12 cases (36%), with no progression during follow up. Perioperative mortality in mechanicat valve patients was 20.5% (n = 7) (p <0.05 versus homograft), and in those with paravalvular abscess, perioperative mortality was even higher than in homograft patients (4/7, 57.1% versus 3/24, 12.5%; p <0.05). When considering only patients without paravalvular abscess, there was no significant difference between groups (10.5% versus 12.5%). Three relapses occurred in mechanical valve patients (10.3%), but no endocarditis recurred during follow up. One late death (3.7%) occurred due to bleeding complicating long-term anticoagulation. CONCLUSION: The study results do not permit a general recommendation to be made for homograft use in patients with acute endocarditis. In cases with paravalvular abscesses, however, there was a trend towards improved outcome in the homograft group.