Search PubMed⌕ Search

Biomedical subjects

G Thiene

Publications and source records attributed to G Thiene.

At least 91 records · Page 5Linked to original sources
PubMed1998

Cardiac transplantation in a Duchenne muscular dystrophy carrier.

We report here for the first time the case of a symptomatic DMD carrier, who had a heart transplant for a severe dilated cardiomyopathy. Dystrophin immunohistochemistry, western blot and analysis of X-chromosome inactivation on leucocytes, and skeletal and cardiac muscle biopsies on the explanted heart were performed. The patient was a heterozygote for exons 50-52 deletion in the dystrophin gene. The number of dystrophin-deficient fibres in the heart was much higher than in skeletal muscle. On the other hand, the explanted heart showed a non-skewed pattern of X-chromosome inactivation, as in leukocytes and skeletal muscle. The adverse cardiac course may be explained by the absence of regeneration among cardiomyocytes.

Adult↗
PubMed1998

HIV infection in the first heart transplantation in Italy: fatal outcome. Case report.

A 46-year-old man with alcoholic dilated cardiomyopathy underwent heart transplantation on November 14, 1985. It was the first cardiac transplant in Italy and at that time no HIV antibody screening test was available in this country. The patient remained in good health for 6 years postoperatively, with only one episode of rejection (type 3A). In June 1992 he died of fulminant complications of AIDS and severe chronic rejection. Neither the patient nor the organ donor belonged to any of the known risk groups for HIV infection; a retrospective analysis revealed that perioperative blood transfusions had been the vectors of transmission.

AIDS-Related Opportunistic Infections↗
PubMed1998

Novel heart diseases requiring transplantation.

Cardiac transplantation represents an extraordinary opportunity to study in vivo the pathology of native disease in the terminal phase. The experience cumulated at the University of Padua in 418 orthotopic cardiac transplant procedures allowed to come across previously unrecognized disease: idiopathic left ventricular aneurysm, non-compacted (spongy) myocardium, restrictive cardiomyopathy. A discrepancy between pre- and post-transplant diagnosis was found in 8% of cases. Endomyocardial biopsy and coronary arteriography should be carried out in each patient with apparently dilated cardiomyopathy before proceeding to heart removal, since alternative therapeutic procedures may be available.

Journal Article↗
PubMed1998

In vivo evidence of apoptosis in arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary heart muscle disease characterized by progressive atrophy of the right ventricular myocardium with fibro-fatty replacement and the risk of electrical instability and sudden death. The disease is often familial and the aetiopathogenesis is still unknown. Recently apoptosis (genetically determined cell death) was postulated to account for progressive loss of myocardium. To establish whether apoptosis is present in ARVC, right ventricular endomyocardial biopsies from 20 patients with clinical and histological diagnosis of ARVC were examined by electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling method (TUNEL). Apoptotic index was calculated as the percentage of positive nuclei in sections stained by TUNEL. Cell proliferation activity was also assessed by argyrophilic staining of the nucleolar organizer region (AgNOR) and MIB-1 antibody analysis. Twenty biopsies taken from patients during monitoring of cardiac transplantation (grade 0 rejection) served as control. Occurrence of apoptosis was correlated with clinical history duration and the presence of acute symptoms and signs like angina, pyrexia, erythrocyte sedimentation rate and creatine phosphokinase elevation, as well as ST segment elevation on basal electrocardiogram. Electron microscopy and TUNEL revealed presence of apoptotic myocytes in seven cases (35%) with a mean apoptotic index of 24.4+/-9.8. The remaining 13 patients and all of the 20 controls were negative both at the electron microscopy and TUNEL. Presence of apoptosis appeared to be significantly related to clinical history duration of less than 6 months (P < 0.001) and presence of acute symptoms and signs (P = 0.007). AgNOR staining and MIB-1 antibody analysis ruled out cell proliferation activity. In conclusion, apoptosis is present in endomyocardial biopsies of patients with ARVC, especially in the early symptomatic phase of disease. Myocardial destruction with replacement by fat may be episodic rather than gradual and continuous.

Adult↗
PubMed1998

[Clinicopathological conference: sudden coronary death in a 32-year old man].

A 32-year-old man without risk factors for coronary artery disease but moderate cigarette smoking died suddenly 5 years after a cardiological check-up for chest pain on effort. Autopsy investigation ruled out extracardiac causes of death and pointed to a multivessel coronary artery disease with organized and recanalized occlusive thrombosis, sometimes superimposed to smooth muscle cells proliferation, in the absence of peripheral vascular disease. Thromboangiitis obliterans of the coronary arteries or accelerated atherosclerosis complicated by thrombosis due to endothelial erosion are debated as possible etiopathogenetic mechanisms. The case is still open for achieving a final diagnosis.

Adult↗
PubMed1998

Pathology of the Pericarbon bovine pericardial xenograft implanted in humans.

BACKGROUND AND AIMS OF THE STUDY: Pericarbon is a new-generation bovine pericardial bioprosthesis designed to withstand mechanical wear. Following optimal in vitro testing and animal experiments, clinical trials were initiated in many European centers and explants sent to our department for pathological evaluation. This included gross, radiographic, histologic and ultrastructural investigations. METHODS: Between 1986 and 1996, 24 bioprostheses (eight aortic, 11 mitral, two mitro-aortic, one tricuspid) were collected from 22 patients (10 males and 12 females; mean age 57.0 +/- 18.9 years) either at autopsy (nine) or reoperation (15). RESULTS: Ten bioprostheses explanted < 2 months after surgery were either normal or failed because of surgical problems or non-structural causes. Among the other 14 bioprostheses (mean placement 41.9 +/- 23.6 months; range: 7 to 90 months), structural deterioration occurred in seven and was due to dystrophic calcification with stenosis in five (three aortic, two mitral), mixed lesion in one (mitral), and incompetence in one by calcium-related commissural tear (mitral). At the ultrastructural level, calcification was detected either on cell debris or upon collagen fibers. No bioprosthesis failed because of fibrous tissue overgrowth. Of the remaining seven bioprostheses, vegetative endocarditis occurred in two, thrombosis in one, and aseptic paravalvular leak in one; whereas three showed no signs of dysfunction. CONCLUSIONS: This pathologic experience with the Pericarbon valve showed calcification to be the main cause of late structural failure, causing mainly cusp stiffness and bioprosthesis stenosis. Tissue rupture or abrupt dysfunction never occurred. Thus, prevention of mineralization remains the main challenge.

Adult↗
PubMed1998

Detoxified glutaraldehyde cross-linked pericardium: tissue preservation and mineralization mitigation in a subcutaneous rat model.

BACKGROUND AND AIM OF THE STUDY: Glutaraldehyde is considered a promoter of calcification by the action of toxic aldehyde group residuals from cross-linking. Post-fixation treatment with homocysteic acid (HA), besides bonding aldehyde groups and neutralizing toxicity, should enhance biocompatibility due to the strongly electronegative sulfonic group. The aim of this investigation was to evaluate HA efficacy on tissue preservation and dystrophic calcification mitigation in glutaraldehyde cross-linked bovine pericardium (BP) using a subcutaneous rat model. METHODS: Four samples of BP, two with glutaraldehyde-HA and two with glutaraldehyde treatment, were implanted in each of 24 male Sprague-Dawley rats. Three rats were killed at 14 days, eight at 28 days, eight at 56 days and five at 84 days. Unimplanted glutaraldehyde-HA- and glutaraldehyde-treated samples served as controls. All samples were studied by gross examination, mammography, light transmission and scanning electron microscopy, and atomic absorption spectroscopy. The nature of mineralization was investigated by coupling techniques of scanning electron microscopy, electron microprobe analysis and X-ray powder diffraction. RESULTS: No histological and ultrastructural differences were found between glutaraldehyde-HA- and glutaraldehyde-treated BP, whether implanted or unimplanted. In both groups, calcification progressed with time, but significantly less after glutaraldehyde-HA treatment than after glutaraldehyde alone and at all time intervals (14.63 +/- 21.34 versus 43.17 +/- 15.99 at 28 days, p = 0.003; 56.42 +/- 40.20 versus 90.59 +/- 32.90 at 56 days, p = 0.008; 91.68 +/- 67.68 versus 156.23 +/- 17.85 at 84 days, p = 0.01). Differences were evident by mammography and histology (von Kossa stain). Electron microprobe analysis in both groups showed the composition of calcified nuclei to be calcium phosphate, stoichiometrically close to apatite (Ca5(PO4)3(OH)). The occurrence of crystallized apatite was supported by X-ray powder diffraction findings, the amount of crystallized apatite being higher in glutaraldehyde-treated samples. CONCLUSIONS: Post-fixation treatment with HA preserves BP structural properties and significantly mitigates mineralization of long-term subcutaneous implants.

Animals↗
PubMed1997

Spectrum of clinicopathologic manifestations of arrhythmogenic right ventricular cardiomyopathy/dysplasia: a multicenter study.

OBJECTIVES: The aim of the present investigation was to redefine the clinicopathologic profile of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC), with special reference to disease progression and left ventricular (LV) involvement. BACKGROUND: Long-term follow-up data from clinical studies indicate that ARVC is a progressive heart muscle disease that with time may lead to more diffuse right ventricular (RV) involvement and LV abnormalities and culminate in heart failure. METHODS: Forty-two patients (27 male, 15 female; 9 to 65 years old, mean [+/-SD] age 29.6 +/- 18) from six collaborative medical centers, with a pathologic diagnosis of ARVC at autopsy or heart transplantation, and with the whole heart available, were studied according to a specific clinicomorphologic protocol. RESULTS: Thirty-four patients died suddenly (16 during effort); 4 underwent heart transplantation; 2 died as a result of advanced heart failure; and 2 died of other causes. Sudden death was the first sign of disease in 12 patients; the other 30 had palpitations, with syncope in 11, heart failure in 8 and stroke in 3. Twenty-seven patients experienced ventricular arrhythmias (ventricular tachycardia in 17), and 5 received a pacemaker. Ten patients had isolated RV involvement (group A); the remaining 32 (76%) also had fibrofatty LV involvement that was observed histologically only in 15 (group B) and histologically and macroscopically in 17 (group C). Patients in group C were significantly older than those in groups A and B (39 +/- 15 years vs. 20 +/- 8.8 and 25 +/- 9.7 years, respectively), had significantly longer clinical follow-up (9.3 +/- 7.3 years vs. 1.2 +/- 2.1 and 3.4 +/- 2.2 years, respectively) and developed heart failure significantly more often (47% vs. 0 and 0, respectively). Patients in groups B and C had warning symptoms (80% and 87%, respectively, vs. 30%) and clinical ventricular arrhythmias (73% and 82%, respectively, vs. 20%) significantly more often than patients in group A. Hearts from patients in group C weighed significantly more than those from patients in groups A and B (500 +/- 150 g vs. 328 +/- 40 and 380 +/- 95 g, respectively), whereas hearts from both group B and C patients had severe RV thinning (87% and 71%, respectively, vs. 20%) and inflammatory infiltrates (73% and 88%, respectively, vs. 30%) significantly more often than those from group A patients. CONCLUSIONS: LV involvement was found in 76% of hearts with ARVC, was age dependent and was associated with clinical arrhythmic events, more severe cardiomegaly, inflammatory infiltrates and heart failure. ARVC can no longer be regarded as an isolated disease of the right ventricle.

Adolescent↗
PubMed1997

Cardiac lithomyxoma.

Among 102 consecutive cardiac myxomas, 10 (10%) showed heavy calcification both on gross inspection and on x-ray examination. Mineralization was partial in 6 patients (mean age 56.8 years) and massive stone-like in 4 (mean age 70 years); relevant histologic findings in patients with partial calcification were Gamma-Gandy bodies in 5, cartilaginous and bone metaplasia in 2, and aspecific calcium deposits in 1. All were incidental findings either at autopsy or during clinical investigation.

Calcinosis↗
PubMed1997

ARVD4, a new locus for arrhythmogenic right ventricular cardiomyopathy, maps to chromosome 2 long arm.

Autosomal dominant arrhythmogenic right ventricular dysplasia (ARVD; MIM 107970) is a genetically heterogeneous cardiomyopathy, which often causes sudden death in juveniles and athletes. Two disease loci were previously mapped respectively to 14q23-q24 (ARVD1) and to 1q42-q43 (ARVD2). A third possible locus was assigned to 14q12-q22. We report here on a linkage study performed on three independent families with recurrence of ARVD characterized by localized involvement of the left ventricle. In these families the disease appears to be transmitted with three polymorphic DNA markers of the chromosome 2 long arm, showing a maximum lod score of 3.46 at theta = 0 for the marker D2S152. The multipoint linkage analysis suggests that the novel ARVD locus, provisionally named ARVD4, maps to 2q32. 1-q32.3, within the chromosomal region including markers D2S152, D2S103, and D2S389.

Arrhythmogenic Right Ventricular Dysplasia↗
PubMed1997

Morphologic spectrum of primary restrictive cardiomyopathy.

A restrictive hemodynamic profile with left ventricular (LV) end-diastolic volume < 100 ml/m2 and LV end-diastolic pressure > 18 mm Hg, in the absence of endomyocardial, pericardial, and specific cardiomyopathy, is a peculiar feature of primary restrictive cardiomyopathy. From 1985 to 1994, 7 hearts of patients who met the above hemodynamic criteria and underwent endomyocardial biopsy because of heart failure, were studied through gross (5 cardiectomies and 2 autopsies), histologic, and electron microscopic investigations. Ages ranged from 9 to 48 years (mean age 29 +/- 13). Four patients (57%) had a positive family history: 2 for hypertrophic and 2 for restrictive cardiomyopathy. Three patterns were identified in the 7 hearts: (1) pure restrictive form in 4 cases with mass/volume ratio 1.2 +/- 0.5 g/ml, ejection fraction 58 +/- 5%, LV end-diastolic volume 67.5 +/- 12.6 ml/m2, LV end-diastolic pressure 26.7 +/- 3.5 mm Hg; (2) hypertrophic-restrictive form in 2 cases with mass/volume ratio 1.5 +/- 0.07 g/ml, ejection fraction 62 +/- 1%, LV end-diastolic volume 69 +/- 10 ml/m2, LV end-diastolic pressure 30 +/- 7 mm Hg; and (3) mildly dilated restrictive form in 1 case with mass/volume ratio 0.9 g/ml, ejection fraction 25%, LV end-diastolic volume 98 ml/m2, LV end-diastolic pressure 40 mm Hg. Histology and electron microscopy disclosed myocardial and myofibrillar disarray and endoperimysial interstitial fibrosis in each pattern. The familial forms suggest the presence of a genetic abnormality. Primary restrictive cardiomyopathy may present with or without hypertrophy and shares similar microscopic pictures with hypertrophic cardiomyopathy. The 2 entities may represent a different phenotypic expression of the same genetic disease.

Adolescent↗
PubMed1997

Angiographic and morphologic features of the left ventricle in Ebstein's malformation.

Quantitative and qualitative cineangiographic analysis of the left ventricle (LV) was performed in 26 patients with isolated Ebstein's malformation, having a mean age of 23 +/- 17 years. Nine autopsied hearts with isolated Ebstein's malformation were submitted to morphologic and morphometric analysis. In 4 of the cases, it was possible to make a direct correlation between the angiographic data obtained during life and the autopsy findings. On the basis of the LV end-diastolic volume we identified 3 groups of patients: 7 with volume <60 ml/m2, another 7 with volume between 60 and 80 ml/m2, and 12 with volume >80 ml/m2. The LV ejection fraction was reduced in 2 patients with normal LV end-diastolic volume and in 6 with increased LV end-diastolic volume. The ratio of ventricular mass to LV end-diastolic volume was always adequate, but a reduction of the ventricular contractive performance (end-systolic pressure to end-systolic volume ratio <3 mm Hg/ml/m2) was found only in patients with a dilated left ventricle. No correlation was demonstrated between the extent of the atrialized component of the right ventricle (mean value 67 +/- 31 cm2, range 13 to 133) and the LV dimensions. All but 2 patients showed a leftward diastolic displacement of the ventricular septum, but in only 1 did this produce an elongated shape of the left ventricle. Sixteen had anomalies of LV dynamics: 10 with hypokinesia (3 of the posterior wall, 4 of the apex, 1 of the inferior wall, 1 of the septum, and 1 global), 6 with dyskinesia (1 of the posterior wall, 2 of the apex, 1 of the posterior wall and apex, 1 of the superior part of the septum, and 1 of the anterior wall), and 8 with premature diastolic distension of the anterobasal wall. Morphometric analysis produced mean values for myocytes of 59 +/- 10%, for the interstitium of 21 +/- 4%, and for fibrous tissue of 20 +/- 9% (normal 4 +/- 1%). Five autopsied hearts had a prolapsing and/or dysplastic mitral valve.

Adolescent↗
PubMed1997

Arrhythmogenic right ventricular cardiomyopathy: a survey of the investigations at the University of Padua.

The purpose of this paper is to review the history of the clinico-pathologic investigations performed at the University of Padua on an old morbid entity ("parchment heart"), which, in the 1960s, led to the clinical description of the disease, in the 1980s to the revival of the scientific interest, and in the mid 1990s to the understanding of the genetic background. All the steps of the progressive knowledge are reviewed: necropsy of young people who died suddenly, in vivo diagnosis by ECG, echocardiography, angiocardiography, endomyocardial biopsy, nuclear magnetic resonance, and diagnostic criteria. Familial occurrence with autosomic dominant transmission and various penetrance was documented. Gene defects were recently mapped both to chromosome 14q23-q24 and 1q42-q43, thus providing evidence for genetic heterogeneity. The pathologic substrates of arrhythmogenic right ventricular cardiomyopathy pointed to an acquired progressive myocardial atrophy with fibro-fatty replacement of dying myocytes. Nowadays the disease is definitively regarded as a primary myocardial disorder and it has been included in the revised WHO classification of cardiomyopathies.

Arrhythmias, Cardiac↗
PubMed1997

The elongation of the internal carotid artery: early and long-term results of patients having surgery compared with unoperated controls.

The purposes of this study are to (1) demonstrate the association of elongations of the internal carotid artery (ICA), that is, kinking, coiling, tortuousity, and angulation, and the neurologic symptoms with high stroke risk; (2) compare the results of the surgical treatment versus the medical treatment alone; (3) contribute to the knowledge of the natural history of these anatomical particularities. From January 1992 to December 1994, 113 patients with ICA kinking, coiling, tortuousity, and angulation were randomized either to surgery (group I, n = 55) or not (group II, n = 58). Patients, who presented a carotid hemodynamically significant lesion (>60%) at the origin and associated distal elongation were excluded. The groups were comparable with regard to sex, age, risk factors for atherosclerosis, associated diseases, symptoms and anatomic feature of the contralateral ICA. Follow-up was obtained in all patients: it consisted of clinical evaluation and Duplex scan control at 3-month intervals during the follow-up period (6-36 months; average, 23). Histologic specimens were obtained in all surgically treated arteries. Early results were excellent: in group I, no patient died, no patient presented major or minor stroke. Only one patient had an immediate transient ischemic attack (TIA) which spontaneously recovered within 24 hours. All symptomatic patients examined the complete disappearance of clinical signs. There were no late deaths due to stroke and no late major or minor neurologic deficit occurred. All reconstructed ICAs were patent. In group II, three patients experienced a major stroke with hemiplegia due to ICA occlusion. Most of the symptomatic patients (37) of group II remained stable, while seven of them had worsening of symptoms and were referred for surgery. To conclude, all surgically treated patients had the complete relief of preoperative neurologic symptoms; none of the medically treated patients had an improvement. Although there was no statistically significant difference between the two groups with regard to stroke risk, three medically treated patients progressed to total occlusion. This suggests that kinking, coiling, tortuousity, and angulations of the ICA are not merely an anatomic curiosity but a potentially disabling, even fatal condition.

Adult↗
PubMed1997

Surgical pathology of primary cardiac and pericardial tumors.

OBJECTIVE: Retrospective study of surgical pathology experience on cardiac and pericardial tumors at the University of Padua in the era of immunohistochemistry and endomyocardial biopsy. METHODS: In the period 1970-1995, we studied 125 bioptic primary neoplasms: specimens were obtained from surgical resection in 116 cases, heart transplantation in 3, pericardiectomy in 3, endomyocardial biopsy in 2 and thoracoscopic biopsy in 1. Tumor histotype was established by light microscopy and more recently by immuno-histochemistry, using a large panel of antibodies, through avidin-biotin peroxidase method, against factor VIII-related antigen, ulex-europaeus, desmin, myoglobin, muscle-specific actin, smooth muscle-specific actin, vimentin, cytokeratins, leukocytic common antigen, neurofilaments and S100-protein. RESULTS: One hundred and thirteen were benign neoplasms: myxoma was the most frequent (87 cases) followed by pericardial cyst (8), endocardial papilloma (5), fibroma (3), rhabdomyoma (3), hematic cyst (2), teratoma (2), hemangioma (1), celothelioma (1) and lipoma (1). Malignancy was diagnosed in 12 cases, and consisted of pericardial mesothelioma (3), myxosarcoma (3), angiosarcoma (2), fibrosarcoma (2) and leiomyosarcoma (2); 4 of them were intracavitary atrial masses and were supposed to be atrial myxoma on the clinical ground. Differential diagnosis included endocardial thrombosis (10), metastasis of concealed extracardiac tumors (5), echinococcosis (3), and Loeffler's fibroplastic endocarditis (3). In 4 cases, cardiac mass histotype was defined without thoracotomy, through endomyocardial (3) and thoracoscopic (1) biopsy. CONCLUSIONS: A large spectrum of cardiac tumors is observed in the surgical pathology practice. Although the diagnosis of cardiac masses is easily attainable by routine imaging techniques, differential diagnosis between primary and secondary tumors, malignant and benign forms, and non neoplastic masses, is achievable only by a thorough microscopic study of surgical resections. The role of the cardiac pathologist is becoming crucial as in other fields of oncology.

Adolescent↗
PubMed1997

Autoimmunity in myocarditis and dilated cardiomyopathy: cardiac autoantibody frequency and clinical correlates in a patient series from Italy.

BACKGROUND: Organ- and disease-specific cardiac autoantibodies, detected by indirect immunofluorescence, represent markers of autoimmunity in a subgroup (25-35%) of patients with dilated cardiomyopathy or myocarditis from Northern Europe and the United States of America. Autoantibody frequencies, as well as associations between clinical and immunological features, may vary in patients from different countries, due to ethnically related differences in genetic susceptibility to autoimmune disease. METHODS: We assessed the frequency of cardiac autoantibodies in a series from Italy, including 91 subjects with idiopathic dilated cardiomyopathy (61 male, aged 49 +/- 11 years) and 11 with biopsy-proven (Dallas criteria) myocarditis (7 male, aged 23 +/- 16), including 2 cases of giant cell myocarditis. Controls were 160 patients with other cardiac disease, 141 with ischemic heart failure and 270 normals Cardiac antibody test was performed blindly by indirect immunofluorescence on normal human myocardium and skeletal muscle. RESULTS: The frequency of organ-specific cardiac autoantibodies was higher (p = 0.0001) in myocarditis (45%) and in dilated cardiomyopathy (20%) than in other cardiac disease (1%), in ischemic heart failure (1%), or in normals (2.5%). Cross-reactive antibodies were detected in similar proportions of study patients and controls. Both patients with giant cell myocarditis were antibody positive. Myocarditis patients with cardiac antibodies had shorter duration of symptoms compared to those who were antibody negative (0.4 +/- 0.3 vs 4 +/- 1 months, p = 0.004). In dilated cardiomyopathy, antibody status was not associated with any clinical or diagnostic feature. CONCLUSIONS: Autoimmunity is involved in a subset of patients with myocarditis and with dilated cardiomyopathy, regardless of their geographical origin or immunogenetic background. The antibody frequency in our dilated cardiomyopathy series from Italy tended to be lower than in other countries. This may reflect reduced antibody levels with disease progression and/or the recognised feature that Mediterranean populations are often less susceptible to autoimmune disease.

Acute Disease↗
PubMed1997

Retrospective risk analysis for early heart-related death after cardiomyoplasty. The Worldwide Cardiomyoplasty Group.

BACKGROUND: Dynamic cardiomyoplasty is an evolving treatment for heart failure that uses an electrically stimulated latissimus dorsi muscle wrapped around the heart to improve cardiac function. Preoperative patient characteristics and deaths after cardiomyoplasty have been recorded during the past 5 years in a cumulative database representing worldwide experience of 42 medical centers. METHODS: Statistical models of hazards (monthly death rates) were used to identify risk factors for transiently increased risk of cardiovascular mortality within 2 months after cardiomyoplasty. RESULTS: Actuarial survival (n = 261) was 88%, 80%, and 76% at 1, 3, and 6 months after cardiomyoplasty, respectively. The peak hazard of 6% dying per month occurred during the first month after the surgical procedure. Lower ejection fraction, increased number of major coronary arteries with > or = 70% stenotic lesions, and lower chronotropic responses during exercise were independent risk factors for the transient increase in early cardiovascular mortality. Early risk of cardiovascular mortality was significantly reduced as centers gained experience with more than 3 patients. CONCLUSION: Early survival after cardiomyoplasty has improved with experience and might be reduced further by preoperative assessments that identify patients at highest risk.

Actuarial Analysis↗