Pulmonary autograft versus homograft replacement of the aortic valve: A prospective randomized trial

AbstractBackground: Pulmonary autografts offer many theoretical advantages. However, the operation is complex, may interfere with right ventricular and pulmonary outflow function, and requires a longer operative time than does the homograft operation. The effects of these potential disadvantages are unknown. Methods: To clarify these issues we randomized 70 patients undergoing aortic valve replacement to an aortic homograft group (group A = 37 patients; 53%; 34 male, 3 female) or a pulmonary autograft group (group B = 33 patients; 47%; 28 male, 5 female). Ages varied from 12 to 65 years (mean 39 ± 15 years) for group A and from 3 to 54 years (mean 29 ± 15 years) for group B (p = not significant). Eleven patients in group A (30%) and eight in group B (24%) had previous aortic valve surgery. All patients were operated on by the same surgeon. The mean cardiopulmonary bypass time was 113 ± 29 minutes (range 66 to 175 minutes) for group A and 151 ± 31 minutes (range 115 to 226 minutes) for group B (p < 0.002). Mean aortic crossclamp time was 85 ± 19 minutes (range 45 to 140 minutes) for group A and 109 ± 20 minutes (range 74 to 164 minutes) for group B (p = 0.02). In 32 patients (86.5%) the aortic homograft was implanted as a root with coronary reimplantation. All pulmonary autografts were implanted as a root. Results: No early or late deaths had occurred in this series at a mean follow-up time of 16 months (range 3 to 21 months). Two patients (one in each group) required reexploration for bleeding. No statistically significant differences were observed between the two groups with regard to ventilatory support (group A, mean 10 ± 8.5 hours; group B, mean 29 ± 85 hours), total blood loss (group A, mean 471 ± 347 ml; group B, mean 543 ± 404 ml), intensive care unit stay (group A, mean 1.2 ± 0.6 days; group B, mean 2 ± 3.7 days), and hospital stay (group A, mean 9.5 = 3.2 days; group B, mean 12 ± 6 days). Postoperatively, all patients are in New York Heart Association class I (93%) or II (7%) (p = not significant). Ejection fraction for the two groups did not change significantly over the follow-up period. Left ventricular mass and diastolic diameter showed progressive regression, with no apparent difference between the two treatment groups to date. Echocardiographic evalu- ation of aortic valve function at 6 months showed good valve function in all patients with no evidence of aortic regurgitation in 80% of both groups. In group B the right ventricular outflow gradient was below 15 mm Hg over the follow-up period. Holter monitoring, available only in 44 patients (63%), showed most of the arrhythmias to be grade 0 to 1 of the modified Lown grading system. Conclusion: Although the pulmonary autograft requires a significantly longer operating time, this does not seem to affect early and medium-term outcome when compared with results obtained with aortic homografts. Continued patient evaluation is warranted, particularly with regard to evidence of valve degeneration and right ventricular function and arrhythmias in the long term. (J Thorac Cardiovasc Surg 1997;113:894-900

Primary Cardiac Kaposiform Hemangioendothelioma: The Rare Adult-Onset. Review of the Literature

Hemangioendothelioma (HE) is the term used to name vascular neoplasms that show a borderline biological behaviour, intermediate between entirely benign hemangiomas and highly malignant angiosarcomas. The HE are classified in several types (papillary intralymphatic, kaposiform, epithelioid, retiform, pseudomyogenic and composite). Each of them have characteristic histo-pathological features and in the most of cases they present in childhood. The current scientific literature about HE is limited: infant and child case reports but lack of adult cases. In particularly no reported primary cardiac kaposiform HE has been described in the adult within nowadays. We analyzed all scientific literature and reported an outstanding and extremely rare case of primary cardiac kaposiform HE in the adult and make a comprehensive analysis of the scientific literature of this unusual interesting but not enough known issue

Surgical Treatment of Valvular Infective Endocarditis Complicated by An Abscess: A Single Center’s Experience

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Induction of mitochondrial biogenesis is a maladaptive mechanism in mitochondrial cardiomyopathies

Objectives The purpose of this study was to clarify the molecular mechanisms linking human mitochondrial deoxyribonucleic acid (mtDNA) dysfunction to cardiac remodeling. Background Defects of the mitochondrial genome cause a heterogeneous group of clinical disorders, including mitochondrial cardiomyopathies (MIC). The molecular events linking mtDNA defects to cardiac remodeling are unknown. Energy derangements and increase of mitochondrial-derived reactive oxygen species (ROS) could both play a role in the development of cardiac dysfunction in MIC. In addition, mitochondrial proliferation could interfere with sarcomere alignment and contraction. Methods We performed a detailed morphologic and molecular analysis on failing hearts from 3 patients with MIC, failing human hearts due to ischemic heart disease (IHD) or dilated cardiomyopathies (DCM), and nonfailing hearts. Results The MIC hearts showed marked mitochondrial proliferation with myofibril displacement. Consistent with morphologic features, increase in mtDNA content per cell and induction of genes involved in mitochondrial biogenesis, fatty acid metabolism, and glucose transport were observed. Down-regulation of these genes characterized DCM and IHD hearts. A pronounced increase in mitochondrial-derived ROS was observed in MIC hearts compared with failing hearts due to other causes. This was paralleled by up-regulation of genes encoding for uncoupling proteins and antioxidant enzymes. However, there was not a significant increase in antioxidant enzyme activity. Conclusions Our results suggest that besides energy deficiency, mitochondrial biogenesis per se is a maladaptive response in MIC and, possibly, in other metabolic cardiomyopathies