Viral Cardiomyopathy Research Articles

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Enteroviral infections of the heart are among the most commonly identified causes of acute myocarditis in children and adults and have been implicated in dilated cardiomyopathy. Although there is considerable information regarding the cellular immune response in myocarditis, little is known about innate signaling mechanisms within the infected cardiac myocyte that contribute to the host defense against viral infection. Here we show the essential role of Janus kinase (JAK) signaling in cardiac myocyte antiviral defense and a negative role of an intrinsic JAK inhibitor, the suppressor of cytokine signaling (SOCS), in the early disease process. Cardiac myocyte–specific transgenic expression of SOCS1 inhibited enterovirus-induced signaling of JAK and the signal transducers and activators of transcription (STAT), with accompanying increases in viral replication, cardiomyopathy, and mortality in coxsackievirus-infected mice. Furthermore, the inhibition of SOCS in the cardiac myocyte through adeno-associated virus–mediated (AAV-mediated) expression of a dominant-negative SOCS1 increased the myocyte resistance to the acute cardiac injury caused by enteroviral infection. These results indicate that strategies directed at inhibition of SOCS in the heart and perhaps other organs can augment the host-cell antiviral system, thus preventing viral-mediated end-organ damage during the early stages of infection.

The suppressor of cytokine signaling-1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury.

Enteroviral infections of the heart are among the most commonly identified causes of acute myocarditis in children and adults and have been implicated in dilated cardiomyopathy. Although there is considerable information regarding the cellular immune response in myocarditis, little is known about innate signaling mechanisms within the infected cardiac myocyte that contribute to the host defense against viral infection. Here we show the essential role of Janus kinase (JAK) signaling in cardiac myocyte antiviral defense and a negative role of an intrinsic JAK inhibitor, the suppressor of cytokine signaling (SOCS), in the early disease process. Cardiac myocyte-specific transgenic expression of SOCS1 inhibited enterovirus-induced signaling of JAK and the signal transducers and activators of transcription (STAT), with accompanying increases in viral replication, cardiomyopathy, and mortality in coxsackievirus-infected mice. Furthermore, the inhibition of SOCS in the cardiac myocyte through adeno-associated virus-mediated (AAV-mediated) expression of a dominant-negative SOCS1 increased the myocyte resistance to the acute cardiac injury caused by enteroviral infection. These results indicate that strategies directed at inhibition of SOCS in the heart and perhaps other organs can augment the host-cell antiviral system, thus preventing viral-mediated end-organ damage during the early stages of infection.

Human viral cardiomyopathy.

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

Diagnosis and treatment of patients with virus induced inflammatory cardiomyopathy

Chronic viral induced inflammatory cardiomyopathy causes progression of left ventricular dysfunction and is an important cause of dilated cardiomyopathy. Despite of the progress made in heart failure therapy, mortality of dilated cardiomyopathy is still 10% per year. Current heart failure therapy is symptomatic and does not impact on the specific underlying pathogenic mechanisms. Thus, specific treatment strategies that are directed against the underlying pathogenetic causes are required if myocarditis and its sequela, namely inflammatory cardiomyopathy, are to be successfully treated. Because histological and, especially, clinical diagnosis is fraught with numerous problems, an aetiological classification based on histology, immunohistochemistry and molecular biology is favourable, particularly in view of the improvements in methods made in recent years. The combination of these diagnostic techni-ques allows a new classification of dilated cardiomyo-pathy by differentiating the disease entity in subgroups of virus positive and virus negative patients with or without cardiac inflammation. This may not only contribute toward improving our understanding of underlying pathological mechanisms, but ultimately may also assist in developing specific immunomodulatory treatments. Preliminary results from ongoing treatment trials suggest that specific antiviral or anti-inflammatory treatment strategies are successful in patients who have been carefully selected and characterized according to biopsy-based diagnostic criteria.

The immune pathophysiology of fibromyalgia and somatoform disorders

Viral diseases are one of the main problems and risk factors in aquaculture. At present diseases are diagnosed by detection of pathogens and clinical symptoms. Identification of genes involved in early responses to viruses is important for better knowledge of antiviral defence and development of diagnostic tools. The aim of this study was to search for gene markers common for viral infections in Atlantic salmon based on microarray analyses of a wide range of samples. Gene expression profiles from fish and cell cultures infected with different viruses and treated with the synthetic double-stranded RNA poly(I:C) were compared in order to identify virus responsive genes (VRG). The list of VRG defined in this study contained 117 genes with known or unidentified functions. Several genes, including the most highly ranked one (receptor transporting protein), had not been previously reported to be involved in antiviral defence. VRG were characterized by a rapid induction and low tissue specificity, and their expression levels were related to the viral load. Immunofluorescence analyses of proteins encoded by VRG in cardiac tissue of salmon with the viral disease cardiomyopathy syndrome (CMS) revealed a common expression pattern. In head kidney leukocytes VRG showed comparable or equal responses to CpG and poly(I:C), which mimic respectively bacterial DNA and viral RNA. Most VRG showed highly correlated expression with interferon-a (IFNa). Sequence comparison of salmon VRG with those from other species gave an understanding of the evolution of these genes, which showed a remarkably rapid sequence divergence in comparison with the entire proteome. VRG emerged both before and after separation of teleosts and tetrapods, and among genes found exclusively in fish species there were members of several multigene families: tripartite motif proteins, gig1- and gig2-like proteins. Several VRG, including genes with unknown functions and orthologs to mammalian RNA helicase RIG-I and chemokine C-X-C type 10, were present in cyprinid and salmonid fish but not in the phylogenetically advanced orders, suggesting that they have been lost in the evolution of Teleostei. Apparently, a number of genes involved in antiviral responses in salmon have acquired different functional roles in higher vertebrates.

Dilated cardiomyopathies as a cause of congestive heart failure.

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

USE OF MULTISYSTEM MONITORING AND MULTIDRUG THERAPY IN PEDIATRIC PATIENTS IMPLANTED WITH VENTRICULAR ASSIST DEVICES

We have previously reported on the use of multi-system monitoring (MSM) coupled with multi-drug therapy (MDT) in adult patients implanted with the CardioWest total artificial heart. Use of MSM plus MDT results in a low incidence of CVA's in this patient population. The purpose of this study is to report the use of MSM plus MDT in pediatric patients implanted with ventricular assist devices (VADs). Between July 1998 and July 2000 four patients (3 males, 1 female) with a mean age of 10 ± 3.5 years (range: 7 to 13 years old) underwent implantation with Thoratec LVAD (1 male), Thoratec BiVADS (1 male and 1 female) or Berlin BiVADs (1 male). Indications for LVADs were viral cardiomyopathy (2 patients), idiopathic dilated cardiomyopathy (1 patient) and restrictive cardiomyopathy (1 patient). MSM consisting of thrombelastography (TEG), complete blood count (CBC), platelet count, platelet aggregation studies (CTAG), prothrombin time (PT), international normalized ratio (INR), partial thromboplastin time (PTT), bleeding time (BT), renal and liver function studies, was used to individualize and monitor MDT, which consisted of unfractionated heparin, aspirin, dipyridamole, pentoxifylline and warfarin. Implant time averaged 40 ± 12.1 days (range: 23 to 50 days). All patients were successfully bridged to heart transplantation and have remained alive a total of 4 years (range: 2 months to 2.2 years) post-transplant. One of the patients experienced a right middle cerebral CVA while implanted with a Thoratec LVAD 14 days post-implant. At this time the patient was hypercoaguable by TEG, the INR had abruptly fallen from 2.7 to 1.8 and the BT was normal (8 minutes). The event did not preclude transplantation and the patient has exhibited a near-full recovery with only mild residual left-hand weakness. In conclusion, use of MSM plus MDT facilitates a high success rate of bridge to heart transplantation and post-transplant survival in pediatric patients implanted with VADs.

Bridge to transplantation with a thoratec left ventricular assist device in a 17-kg child

A Thoratec left ventricular assist device (LVAD) was used to support a 7-year-old 17-kg boy with viral cardiomyopathy for 23 days before heart transplantation. The boy is still living more than 1 year posttransplant, and functional except for some spastic paresis of the left hand, a residual from a stroke during device support. He is the smallest person to be supported with this device. We discuss techniques for using the Thoratec in children.

The differential metabolic impact of tacrolimus and cyclosporine immunosuppression in black heart transplant recipients: hyperlipidemia, hypertension and hyperglycemia

disease in 10, viral cardiomyopathy in 9, hypertrophic cardiomyopathy in 7, congenital heart disease in 6, and others in 14. The follow-up was 3.863.1 years (minimum 2 days, maximum 10.2 years, median 3.1 years). Thirty-day-mortality rate was 5.5%. The 1, 5, and 10-year actuarial survivals were 86%, 75%, and 54%, respectively. Cause of death for the entire group (total 69) were infection in 18(26% of deaths), graft coronary disease in 12(17%), acute rejection in 8(11.6%), stroke in 6(8.7%), malignancy in 4(5.8 %), primary graft failure in 4(5.8%), other causes in 13(18.8%), and unknown in 4(5.8%). Actuarial freedom from acute rejection at 1, 3 months, 1, 5, and 10 years was 64.4%, 54.1%, 43.7%, 40.1%, and 40.1%, respectively. Actuarial freedom from acute rejection-related death at 3 months, 1, 5, and 10 years was 98.2%, 97.7%, 95.4%, and 95.4%, respectively. Actuarial freedom from infection at 1, 3 months, 1, 5, and 10 years was 91.4%, 81.6%, 69.4%, 58.8%, and 54.2%, respectively. Actuarial freedom from infection-related death at 3 months, 1, 5, and 10 years was 96.8%, 93.3%, 91.2%, and 91.2%, respectively. Actuarial freedom from graft coronary artery disease at 1, 5, and 10 years was 95.7%, 72.4%, and 53.0%, respectively. Actuarial freedom from graft coronary artery disease-related death or retransplantation at 1, 5, and 10 years were 99.5%, 93.7%, and 85.3%, respectively. CONCLUSION: These data suggested satisfactory long-term results of adult cardiac transplantation utilizing FK506.

Progress toward vaccines against viruses that cause heart disease.

Of the numerous viruses that have been implicated as causes of viral inflammatory cardiomyopathy, only the 6 serotypes of the group B coxsackieviruses (CVB 1-6) and adenovirus type 2 (Ad 2) have been regularly linked to heart disease on the basis of both clinical investigations as well as animal models (in the case of the coxsackieviruses). Of these, only the coxsackieviruses offer a truly well-characterized system for not only investigations using a small animal disease model (myocarditis in mice) but for studies of the virus at the molecular level and in cell culture systems. The pending worldwide eradication of the related enteroviruses, the polioviruses, will further emphasize the importance of the coxsackieviruses in years to come. Studies using poliovirus have shown that enteroviruses can be attenuated for disease to create highly successful and safe human vaccines. Furthermore, using recombinant DNA approaches, strains of polioviruses have been created that demonstrate a human enterovirus can express small proteins as well as foreign antigenic epitopes, thus creating multivalent chimeric vaccine strains of virus. Our laboratory has been exploring coxsackievirus 3-based vectors as models for both multivalent chimeric vaccines as well as expression vectors. The coxsackievirus can be successfully attenuated using both point mutations as well as chimeric genome technology. The coxsackievirus can also express intact small proteins in biologically active form as well as antigenic epitopes. Although it is doubtful that the marketplace will support the development of antiviral vaccines to combat human heart disease at present, the technology exists to make such vaccines a reality.

Molecular Screening by Polymerase Chain Reaction Detects Panleukopenia Virus DNA in Formalin-Fixed Hearts from Cats with Idiopathic Cardiomyopathy and Myocarditis

Viral myocarditis has been suggested as an etiology for cardiomyopathy in several mammalian species. Myocarditis and idiopathic cardiomyopathy have been reported in the domestic cat, although a viral etiology has not been demonstrated. Because of the continuing interest in the potential relationship between viral myocarditis and cardiomyopathy, we evaluated hearts from cats with spontaneous, idiopathic cardiomyopathy for viral genomic material within myocytes by polymerase chain reaction, and for the presence of myocarditis by light microscopy. Thirty-one (31) formalin-fixed hearts from domestic cats who died of idiopathic cardiomyopathy were randomly selected from pathology archives. Seventeen (17) formalin-fixed hearts from healthy cats were similarly selected as normal controls. The polymerase chain reaction (PCR) was used to evaluate myocardial tissue for the presence of viral genome from feline panleukopenia virus, herpes virus, calici virus, and corona virus. Hearts were examined using light microscopy for histologic evidence of myocarditis according to the Dallas criteria. Panleukopenia virus was identified by PCR in 10 of 31 cats with cardiomyopathy but in none of the controls. Neither cardiomyopathic or control cats tested positive by PCR for herpes virus, calici virus, and corona virus. Myocarditis was detected by histologic examination in 18 of 31 cardiomyopathic cats and in none of 17 control cats. Myocarditis and or feline panleukopenia virus genome was detected in felines with idiopathic hypertrophic, dilated, and restrictive cardiomyopathy, suggesting a possible role of viral infection and inflammation in the pathogenesis of cardiomyopathy in this species.

Enteroviral genome in native hearts may influence outcome of patients who undergo cardiac transplantation.

The Enterovirus may be the most common agent responsible for viral myocarditis and cardiomyopathy. Very little of the literature is available concerning the follow-up of patients who underwent transplantation with enteroviral positivity in native hearts. In the present study, 45 explanted hearts from patients who underwent orthotopic heart transplant at University of Padova were studied by reverse transcriptase (RT)-polymerase chain reaction (PCR): 27 patients had dilated cardiomyopathy (DC), 12 had ischemic cardiopathy (IC), 2 had valvular disease (VD), 2 had arrhythmogenic right ventricular cardiomyopathy (ARVC), 1 had giant cell myocarditis (GCM), and 1 had lymphocytic myocarditis (LM). Two sets of PCR primers from the highly conserved region of Enterovirus and Rhinovirus were used. Samples of both ventricles and septum were analyzed in every patients. The RT-PCR and nucleotide sequencing of amplicons were also performed on all post-transplantation follow-up biopsies in patients with Enterovirus positivity in the native heart. The viral genome was detectable in only 1 of 27 patients with DC (3%) and in 1 patient with LM. Nucleotide sequence analysis of the amplified product showed differences in nucleotide sequence of PCR samples compared with the sequence of the coxsackievirus B3 used in the current study. The patient with Enterovirus-positive DC showed a higher index of severe rejection (>3A) in the first 6 months, compared with the other patients tested. The patient with Enterovirus-positive LM died of disease recurrence 2 months after transplantation. The present study reveals a scarce presence of Enterovirus in the myocardium of patients with chronic myocardial disease. Because Enterovirus infection was predictive of a poor prognosis in these two patients, molecular studies are useful in excluding viral involvement in native hearts of transplanted patients.

Dynamic Cardiomyoplasty: First Successful Case in Korea

Dynamic cardiomyoplasty occupies an important place among recent advances in treatment of heart failure. We report the first clinical dynamic cardiomyoplasty case in Korea. The patient was a 25-year-old male with viral cardiomyopathy and chronic active hepatitis. The preoperative echocardiogram showed a left ventricular ejection fraction of 30% and grade 2 mitral and tricuspid regurgitation with dilated left and right atria. The left latissimus dorsi muscle was mobilized to wrap the heart and a myocardial stimulator was connected and placed in the abdominal pocket. After a 10-week training period, the stimulation ratio was set at 1:4 and the stimulator functioned well. At the 8-month follow-up the left ventricular ejection fraction ranged between 30% and 35% and the patient was feeling much better with slightly increased activity.

Unexplained Transient Postoperative Myocardial Dysfunction in a Previously Healthy Child

Unexplained Transient Postoperative Myocardial Dysfunction in a Previously Healthy Child

P-304 Clinical findings of blood and progress of opthalmic lesions during interferon therapy for chronic hepatitis C

Viral diseases are one of the main problems and risk factors in aquaculture. At present diseases are diagnosed by detection of pathogens and clinical symptoms. Identification of genes involved in early responses to viruses is important for better knowledge of antiviral defence and development of diagnostic tools. The aim of this study was to search for gene markers common for viral infections in Atlantic salmon based on microarray analyses of a wide range of samples. Gene expression profiles from fish and cell cultures infected with different viruses and treated with the synthetic double-stranded RNA poly(I:C) were compared in order to identify virus responsive genes (VRG). The list of VRG defined in this study contained 117 genes with known or unidentified functions. Several genes, including the most highly ranked one (receptor transporting protein), had not been previously reported to be involved in antiviral defence. VRG were characterized by a rapid induction and low tissue specificity, and their expression levels were related to the viral load. Immunofluorescence analyses of proteins encoded by VRG in cardiac tissue of salmon with the viral disease cardiomyopathy syndrome (CMS) revealed a common expression pattern. In head kidney leukocytes VRG showed comparable or equal responses to CpG and poly(I:C), which mimic respectively bacterial DNA and viral RNA. Most VRG showed highly correlated expression with interferon-a (IFNa). Sequence comparison of salmon VRG with those from other species gave an understanding of the evolution of these genes, which showed a remarkably rapid sequence divergence in comparison with the entire proteome. VRG emerged both before and after separation of teleosts and tetrapods, and among genes found exclusively in fish species there were members of several multigene families: tripartite motif proteins, gig1- and gig2-like proteins. Several VRG, including genes with unknown functions and orthologs to mammalian RNA helicase RIG-I and chemokine C-X-C type 10, were present in cyprinid and salmonid fish but not in the phylogenetically advanced orders, suggesting that they have been lost in the evolution of Teleostei. Apparently, a number of genes involved in antiviral responses in salmon have acquired different functional roles in higher vertebrates.

Advances in acquired pediatric heart disease

Acquired heart disease in children may result in significant morbidity and mortality. Advances continue to be made in understanding Kawasaki disease, acute and chronic rheumatic heart disease, infective endocarditis, myocarditis, and dilated cardiomyopathy. The role of superantigens, particularly bacterial toxins, in the pathogenesis of Kawasaki disease continues to be defined. Intravascular ultrasound promises to improve the assessment of coronary arteries in Kawasaki disease. Current recommendations for the long-term management of Kawasaki disease are discussed. Significant changes in the epidemiology of acute rheumatic fever and endocarditis are noted. Updates on the role of echocardiography as well as current therapeutic issues in these diseases are addressed. The application of immunologic and molecular biologic techniques have implicated genetic and immune factors in the pathogenesis of myocarditis and cardiomyopathy. The relationship between viral infection and subsequent dilated cardiomyopathy, as well as the role of autoimmune mechanisms in the pathogenesis of these disorders, remains controversial.

Phenotype analysis of mononuclear cells in endomyocardial biopsy specimens from patients with viral myocarditis and dilated cardiomyopathy.

This study investigated the distribution and phenotype of mononuclear cells in endomyocardial biopsy (EMB) specimens from patients with viral myocarditis (VMC, 25 cases) and dilated cardiomyopathy (DCM, 10 cases). T lymphocytes, including Th/i cells in VMC and Tc/s cells in DCM, predominated in the infiltrating mononuclear cells in these specimens. The morphological relationship between infiltration of T lymphocytes and pathological changes of myocardia was also observed and neither macrophages nor B lymphocytes were found.

Cardiac transplantation: The Stanford experience in the cyclosporine era

We analyzed our experience with 496 patients who underwent primary cardiac transplantation since the introduction of cyclosporine immunosuppression (Dec. 16, 1980, to Jan. 7, 1993). There were 388 male and 108 female patients. Mean recipient age was 40 ± 16 years (range 0.1 to 70 years, median 44 years). Recipient diagnoses included coronary disease in 188, idiopathic cardiomyopathy in 196, viral cardiomyopathy in 35, and congenital heart disease in 28 patients. Donor age was 25 ± 10 years (range 1 to 53 years, median 24 years). Graft ischemic time was 148 ± 57 minutes (range 38 to 495 minutes, median 149 minutes). Operative mortality (hospital death) rate was 7.9% ± 1.3% (70% confidence intervals). Multivariate logistic regression analysis revealed that (higher) pulmonary vascular resistance and gender (female) were the only independent predictors of hospital death ( p < 0.05). Actuarial survival estimates for all patients at 1, 5, and 10 years are 82% ± 1.7% (83% ± 1.8% adult, 77% ± 5.2% pediatric), 61% ± 2.5% (65% ± 2.5% adult, 64% ± 6.6% pediatric), and 41% ± 3.7% (40% ± 4% adult, 54% ± 8.6% pediatric), respectively. For 232 patients treated with triple-drug immunosuppression and induction with OKT3 since 1987, survival estimates at 1 and 5 years are 82% ± 2.6% and 67% ± 3.7%, respectively. Causes of death for the entire group were rejection in 29 (14% of deaths), infection in 69 (34%), graft coronary disease in 36 (18%), nonspecific graft failure in 6 (3%), malignancy in 19 (10%), stroke in 6 (3%), pulmonary hypertension in 6 (3%), and other causes in 30 (15%) patients. Actuarial freedom from rejection at 3 months, 1 year, and 5 years was 21% ± 1.9%, 14% ± 1.7%, and 7.2% ± 1.5%, respectively (±1 standard error of the mean). Estimates of freedom from rejection-related death at 1, 5, and 10 years were 96% ± 1%, 93% ± 1.4%, and 93% ± 1.4%, respectively. Actuarial freedom from any infection at 3 months and at 1 and 5 years was 40% ± 2.3%, 27% ± 2.1%, and 15% ± 2.0% and from infection-related death, 95% ± 1.0%, 93% ± 1.2%, and 85% ± 1.9%, respectively. Actuarial freedom from (angiographic or autopsy proved) graft coronary artery disease at 1, 5, and 10 years was 95% ± 1.2%, 73% ± 2.7%, and 65% ± 3.6% and from coronary disease–related death or retransplantation 98% ± 0.7%, 84% ± 2.2%, and 66% ± 4.3%, respectively. Multivariate (Cox model) proportional hazard regression analysis revealed that (older) recipient age and race (nonwhite) were independent predictors of late (as opposed to hospital) death ( p < 0.05). Immunosuppressive protocol was an independent predictor ( p < 0.05) of freedom from rejection (but not from late death or from rejection-related death). These data demonstrate satisfactory long-term results of cardiac transplantation for treatment of patients with end-stage heart disease. (J T HORAC C ARDIOVASC S URG 1994;108:240-52)

Abdominal aortic aneurysm in the patient undergoing cardiac transplantation

In the past 3 years at our institution 130 patients have undergone cardiac transplantation for ischemic cardiomyopathy in 49 (38%), idiopathic cardiomyopathy in 42 (32%), viral cardiomyopathy in 9 (6.9%), pulmonary hypertension in 8 (6%), and graft atherosclerosis in 2 (1.5%). Routine preoperative abdominal ultrasonography was performed on 98 (75%) of these patients with specific visualization of the abdominal aorta in 93 (95%). Abdominal aortic aneurysms (all infrarenal) were found before operation in four patients and only in the subgroup undergoing transplantation for ischemic heart disease (10.5%). They measured 3.4, 4.5, 3.6, and 3.8 cm before transplantation. Periodic evaluation by ultrasonography was carried out after transplantation during the 3-year period of this study. One aneurysm that was initially 3.6 cm increased to 4.0 cm and ruptured 2 months after transplantation. The patient died despite emergent surgery. Aneurysms in three patients who demonstrated rapid aneurysm expansion after transplantation were successfully repaired at 5, 20, and 33 months after transplantation when the lesions reached 5.5, 5.9, and 4.8 cm. A fifth patient with an initially normal (1.5 cm) aorta developed a symptomatic aneurysm of 4.1 cm, which was repaired uneventfully. The average expansion rate of these aneurysms after transplantation was 0.74 ± 0.15 cm/year. This experience suggests that aneurysms are limited to patients undergoing transplantation for ischemic heart disease. Ultrasound examination may be appropriate for preoperative screening. Careful aortic surveillance after transplantation is important in patients having transplantation for ischemic cardiomyopathy because of the apparent rapid expansion rate compared to aneurysms in the population not receiving transplants.

Abdominal aortic aneurysm in the patient undergoing cardiac transplantation

In the past 3 years at our institution 130 patients have undergone cardiac transplantation for ischemic cardiomyopathy in 49 (38%), idiopathic cardiomyopathy in 42 (32%), viral cardiomyopathy in 9 (6.9%), pulmonary hypertension in 8 (6%), and graft atherosclerosis in 2 (1.5%). Routine preoperative abdominal ultrasonography was performed on 98 (75%) of these patients with specific visualization of the abdominal aorta in 93 (95%). Abdominal aortic aneurysms (all infrarenal) were found before operation in four patients and only in the subgroup undergoing transplantation for ischemic heart disease (10.5%). They measured 3.4, 4.5, 3.6, and 3.8 cm before transplantation. Periodic evaluation by ultrasonography was carried out after transplantation during the 3-year period of this study. One aneurysm that was initially 3.6 cm increased to 4.0 cm and ruptured 2 months after transplantation. The patient died despite emergent surgery. Aneurysms in three patients who demonstrated rapid aneurysm expansion after transplantation were successfully repaired at 5, 20, and 33 months after transplantation when the lesions reached 5.5, 5.9, and 4.8 cm. A fifth patient with an initially normal (1.5 cm) aorta developed a symptomatic aneurysm of 4.1 cm, which was repaired uneventfully. The average expansion rate of these aneurysms after transplantation was 0.74 +/- 0.15 cm/year. This experience suggests that aneurysms are limited to patients undergoing transplantation for ischemic heart disease. Ultrasound examination may be appropriate for preoperative screening. Careful aortic surveillance after transplantation is important in patients having transplantation for ischemic cardiomyopathy because of the apparent rapid expansion rate compared to aneurysms in the population not receiving transplants.