A case of recurrent constrictive pericarditis induced by pericardial substitution with an expanded polytetrafluoroethylene membrane.

A 72-year-old man presented with recurrent constrictive pericarditis, which developed 6 months after pericardiectomy, and pericardial substitution with an expanded polytetrafluoroethylene membrane. Re-pericardiectomy was performed. A new thick membranous structure had grown under the expanded polytetrafluoroethylene membrane anterior to the right ventricle, and was firmly adhered to the epicardium. This new structure exhibited collagenous fiber-based fibrotic thickening, and resembled a foreign body reaction. It was surmised that recurrence of constrictive pericarditis may have been induced by the expanded polytetrafluoroethylene membrane. Heart failure resolved after the operation; however, the patient died of respiratory failure on postoperative day 6.

Outcome of surgical management for active mitral native valve infective endocarditis: a collective review of 57 patients.

OBJECTIVE: At our institutions, mitral valve vegetation with a high risk for embolism is surgically treated as soon as possible to maintain the quality of life of patients, and valve repair has been actively performed. We reviewed the surgical outcome for active mitral infective endocarditis (AMIE) following this treatment policy. METHODS: Fifty-seven patients underwent surgery for native AMIE between April 1999 and December 2012 (repair 36, replacement 21). We retrospectively investigated the risk factors for in-hospital death, the prognosis of patients with cerebral infarction, and the short- and long-term outcomes of valve repair and replacement. RESULTS: The preoperative conditions and the intraoperative findings in the replacement group were more complicated. But, no significant differences were observed in in-hospital mortality, 4-year survival, or 4-year reoperation-free rate between the groups (repair 8, 88.2, and 92.4%; replacement 9, 90.5, and 94.7%, respectively). The incidence of postoperative cardiac-related events including heart failure, thromboembolism, and major bleeding was higher in the replacement group. Although our study failed to identify predictors of in-hospital mortality, uncontrolled and nosocomial infections were responsible for high in-hospital mortality of 17 and 33%, respectively. Nine patients with symptomatic non-hemorrhagic cerebral infarction underwent early surgery within 2 weeks of the onset of stroke (median maximum infarct diameter and volume: 18.2 mm and 0.72 cm(3), respectively). No patients had severe hemorrhagic conversion. CONCLUSION: Mitral valve repair is appropriate to prevent postoperative cardiac-related events. Reducing in-hospital mortality due to uncontrolled infection remains challenging. Early surgery may be reasonable for patients with small non-hemorrhagic infarction.

Video-assisted resection of papillary fibroelastoma arising from a miniature tendinous chord in the apex of the left ventricle.

We report a rare case of a papillary fibroelastoma (PFE) in the apex of the left ventricle.An 81-year-old woman with nonspecific symptoms was shown to have a mobile mass deep in the left ventricle. With videoscopic assistance, removal of the mass was accomplished through the mitral valve via a midline sternotomy under cardiopulmonary bypass. The tumor arose from a miniature tendinous chord in the apex, and histological examination revealed PFE. Videoscopy facilitated safe and effective removal of the lesion in this case.

Double patch technique for closing acute ventricular septal perforation.

PURPOSE: Ventricular septal perforation (VSP) is a rare but life-threatening complication of acute myocardial infarction (AMI). Even with assisted circulation heart failure often progresses quickly, and urgent surgical intervention is required to close the VSP. For several years, we have been performing a double patch closure technique using an equine pericardial patch. In this report, we present details of our patch closure technique and the VSP surgical results; we also examine the problems we encountered. METHODS: The present study was a review of nine patients who underwent our patch closure of VSP secondary to AMI. We used a large double-layered equine pericardial patch to close the VSP and did not exclude the infarction area from the left ventricular cavity. No necrotic myocardium was excised to avoid simultaneous excision of stunned myocardium. RESULTS: No patients died within 30 days of the surgery, and there were no in-hospital deaths. Over a mean clinical follow-up period of 4.5 years, no residual shunts were detected, and all patients were alive and had New York Heart Association functional class II. CONCLUSION: Our patch closure technique was effective for closing VSPs securely. The operating times and cardiopulmonary bypass times were short, and blood loss was minimal. Our patch closure technique may improve the prognosis of VSP.

Successful treatment of refractory cardiac tamponade due to rheumatoid arthritis using pericardial drainage.

Rheumatoid pericarditis occurs in patients with rheumatoid arthritis (RA). However, cardiac tamponade due to rheumatoid pericarditis is rare; we describe a case of a 72-year-old man with a 6-year history of rheumatoid arthritis who developed rheumatoid pericarditis with recurrent cardiac tamponade. The patient experienced relapse of the cardiac tamponade despite treatment with pericardiocentesis. Therefore, the patient underwent surgical pericardial drainage. The patient was also subsequently treated with increasing doses of corticosteroid, methotrexate and leukocytapheresis. These treatments resulted in a successful outcome without any complication. This case suggests that in addition to immunosuppressive therapy, pericardial drainage should be considered in the treatment of life-threatening refractory cardiac tamponade caused by rheumatoid arthritis.

A patient in whom survival was achieved by acute-stage surgery for infective endocarditis complicated by a cerebral hemorrhage.

We report a patient who underwent mitral valve replacement despite acute-stage cerebral hemorrhage related to a complication of infective endocarditis (IE) and rupture of intracerebral mycotic aneurysm, achieving survival. The patient was a 24-year-old female. She consulted our hospital because of a fever and was diagnosed with IE and a cerebral hemorrhage. A blood culture test on admission revealed methicillin-sensitive Staphylococcus aureus. Transthoracic echocardiography revealed giant vegetation in the left atrium. Besides the management of an acute-stage cerebral hemorrhage, medical therapy for IE was performed. However, a severe infection was refractory, and mitral-regurgitation-related heart failure deteriorated. Despite acute-stage cerebral hemorrhage, mitral valve replacement was performed 10 days after admission because advanced disseminated intravascular coagulation syndrome made conservative management difficult. After surgery, neither exacerbation of cerebral symptoms nor recurrent IE was noted, and the patient was discharged.

Primary pericardial malignant fibrous histiocytoma causing cardiac tamponade.

We describe herein an extremely rare case of a large primary pericardial malignant fibrous histiocytoma causing a cardiac tamponade that occurred in a 72-year-old woman. The clinical, radiographic, and pathologic features are reported here together with a brief review of the literature.

Acute dissecting thoracic aortic aneurysm in a patient with polymyalgia rheumatica.

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are closely related disorders found in older patients, and vasculitis has been proposed as a part of the pathogenesis of PMR. We describe a female patient with PMR plus aortitis, both of which were well controlled on maintenance steroid therapy. Six months after the onset of her condition, however, she suddenly presented with chest pain. A diagnosis of dissecting aortic aneurysm was confirmed, and the aorta was successfully resected. Histology revealed infiltration of mononuclear cells including giant cells around the vaso vasorum with disruption of elastic lamina of the resected aorta. PMR or GCA may indicate an increased risk for aortic dissection in patients with normal erythrocyte sedimentation rate or C-reactive protein, and prompt recognition and therapy, not only during the active disease but also after symptoms of PMR have resolved, are needed.

Stanford type A aortic dissection with Child B liver cirrhosis.

Cardiac surgery using cardiopulmonary bypass in patients with advanced liver cirrhosis has been infrequently performed, and reported to be too risky. Aortic dissection accompanied with liver cirrhosis is extremely rare. A 61-year-old woman who had aortic dissection and Child B liver cirrhosis underwent ascending aorta replacement. Liver protection during cardiopulmonary bypass was successfully accomplished by moderate hypothermia and use of an aortic occlusion balloon to maintain sufficient hepatic blood flow.

Bilateral subclavian steal associated with severe coarctation of the thoracic aorta and an aberrant right subclavian artery.

A 10-year-old girl having bilateral subclavian steal associated with severe coarctation of the thoracic aorta and an aberrant right subclavian artery was found, on admission, to have no difference between upper and lower extremity blood pressure, but echocardiography revealed severe thoracic aorta coarctation and systolic blood pressure in the carotid arteries exceeding 200 mmHg estimated by Doppler ultrasonography. Magnetic resonance imaging and angiography demonstrated bilateral subclavian steal without esophageal compression. We reconstructed the aortic arch using the left subclavian artery and a reversed Blalock-Park procedure, then repaired the coarctation with a 14 mm woven double velor vascular graft. The girl was symptom-free following uncomplicated recovery from surgery. Doppler ultrasonography 2 weeks after surgery showed the pressure gradient across the aortic arch had decreased from 180 mmHg to 60 mmHg. This residual gradient at the anastomosis between the ascending aorta and left subclavian artery may improve as native vessels grow.

Differential effects of the angiotensin-converting enzyme inhibitor lisinopril versus the beta-adrenergic receptor blocker atenolol on hemodynamics and left ventricular contractile function in experimental mitral regurgitation.

OBJECTIVES: The goal of this study was to determine the therapeutic efficacy of angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic receptor blockers in experimental chronic mitral regurgitation (MR), gaining knowledge using methods difficult to apply in humans. BACKGROUND: Both ACE inhibitors and beta-blockers are cornerstones in the treatment of human congestive heart failure. However, the roles of these treatments for chronic MR is unclear. METHODS: Mitral regurgitation was created in 11 closed-chest dogs. Three months after the creation, the ACE inhibitor lisinopril 20 mg was given orally daily. After three months of lisinopril therapy, the beta-blocker atenolol was added to lisinopril for another three months. Atenolol was begun at a dose of 12.5 mg daily and increased gradually to 100 mg daily. Hemodynamics and left ventricular (LV) function were assessed throughout the study. RESULTS: Regurgitant fraction was consistently >50% over the course of this study. Pulmonary capillary wedge pressure and LV end-diastolic pressure were significantly increased after three months of MR and decreased during both lisinopril and the combined therapy in which it was not different from baseline. Left ventricular contractility measured by the end-systolic stiffness constant was depressed from 3.66 +/- 0.20 to 2.65 +/- 0.12 (p < 0.05) at three months of MR and rose insignificantly after lisinopril treatment (2.99 +/- 0.17). When atenolol was added, it rose significantly and returned to normal (3.50 +/- 0.22, p < 0.05). CONCLUSIONS: Although lisinopril significantly reduced preload, its effect on LV contractility was insignificant in experimental MR. Conversely, atenolol, when added to lisinopril, achieved maximum hemodynamic benefit and also restored LV contractility.