Long-term results after ablation for long-standing atrial fibrillation concomitant to surgery for organic heart disease: is microwave energy reliable?

OBJECTIVE: Microwave ablation has been reported as efficient for the surgical treatment of long-standing atrial fibrillation. However, the influence of ablation lesions on long-term results is not known. METHODS: From August of 2000 to November of 2003, 41 patients underwent a left atrial endocardial microwave ablation procedure after a Cox-Maze-like lesion set for long-standing atrial fibrillation concomitant to surgery for valvular or coronary artery disease. Mitral valve surgery alone or combined was performed in 31 cases (75.6%). The mean diameter of the left atrium was 7.19 +/- 1.44 cm. The mean duration of preoperative atrial fibrillation was 4.7 +/- 3.6 years. Patient follow-up was conducted by means of direct clinical examination, electrocardiography, and transthoracic echocardiography. The mean follow-up was 5.37 +/- 0.91 years. RESULTS: Patient follow-up was achieved in 82% of cases (n = 28). Seven patients (17%) died during follow-up. Stroke was the cause of death in 1 patient with persistence of atrial fibrillation. Major complications occurred in 4 (14.3%) of the patients that were related to the persistence of atrial fibrillation. At 5 years follow-up, 39.3% of patients (11/28) were in sinus rhythm. Seventeen patients (60.7%) were in New York Heart Association classes I and II, and 11 patients (39.3%) were in New York Heart Association class III at the time of follow-up. CONCLUSION: In our experience, left atrial endocardial microwave ablation for long-standing atrial fibrillation after a Cox-Maze-like ablation lesion set during surgery for organic heart disease is not a reliable method of achieving long-term conversion to sinus rhythm.

Impact of coronary endothelial dysfunction on adverse long-term outcome after heart transplantation.

BACKGROUND: Coronary vasomotor dysfunction is a common finding in cardiac transplant recipients and is an early marker for the development of graft atherosclerosis. The present prospective study tested whether endothelial dysfunction independently predicts cardiovascular-related events and death after heart transplantation (HTx). METHODS: Functional and structural coronary changes were evaluated in 185 consecutive patients 25+/-33 months after HTx. The following potential risk factors for graft survival were assessed at baseline: hypertension, diabetes, dyslipidemia, donor and recipient characteristics (age, gender, cytomegalovirus-infection, human leukocyte antigen-mismatch), pretransplantation diagnosis, ischemic time, treated rejection episodes, immunosuppressive regimens, and medication.The prespecified prospectively defined endpoints were cardiovascular-related events with progressive heart failure, acute myocardial infarction, coronary revascularization, retransplantation, and death. Patients were followed-up for 60+/-17 months. RESULTS: Event-free survival for the entire group was 73% (25 cardiovascular-related events, 25 deaths). Using multivariate analysis, epicardial endothelial dysfunction (relative risk [RR] 1.97; P=0.028), angiographic cardiac allograft vasculopathy (RR 2.11; P=0.023), diabetes (RR 2.32; P=0.022), high serum levels of CyA (RR 3.54; P=0.006) and Tac (RR 6.82; P=0.002), uncommon reasons for transplantation (RR 4.69; P=0.002), and the absence of statin therapy (RR 0.33; P=0.025) were detected as independent predictors of cardiovascular-related events and death. CONCLUSION: This is the first study showing that epicardial endothelial dysfunction independently predicts outcome in HTx patients providing functional and prognostic information that complete angiographic risk factor assessment.

Graft-infiltrating dendritic cells and coronary endothelial dysfunction after human heart transplantation.

BACKGROUND: Indirect allorecognition is involved in chronic transplant rejection. We prospectively characterized graft-infiltrating dendritic cells (DCs) in sequential myocardial biopsies (n = 64; 1 to 24 months after transplantation) from 16 patients after heart transplantation (HTx) and analyzed the relation between graft immune activation and structural and functional coronary changes during follow-up. METHODS: DC invasion (immunostaining) in the human myocardium was detectable early after HTx, increased further during the first year, and decreased constantly thereafter. Also, graft-infiltrating DCs expressed markers of immaturity and maturity and were time-dependently clustered with CD3-positive T cells. RESULTS: Both epicardial and microvascular endothelial dysfunction were associated with elevated CD209-positive DCs at 12 months. CD209 positivity early after HTx was an independent marker for coronary endothelial dysfunction during follow-up. Intimal hyperplasia or angiographic disease during follow-up was not associated with myocardial DC infiltration. CONCLUSIONS: DCs frequently infiltrate the cardiac allograft with a peak during the first post-operative year and time-dependently cluster with T cells. Migratory active graft-infiltrating DCs may serve as a predictor for allograft coronary endothelial dysfunction.

Cardiac sarcoidosis concealed by arrhythmogenic right ventricular dysplasia/cardiomyopathy.

BACKGROUND: A 37-year-old male with a history of palpitations and ventricular tachycardia was diagnosed with arrhythmogenic right ventricular dysplasia/cardiomyopathy on the basis of clinical assessment, electrocardiography and echocardiography. Over the following 3 years the patient progressed to end-stage heart failure and eventually underwent heart transplantation. Histological analysis of the explanted heart revealed the presence of numerous noncaseating granulomas. INVESTIGATIONS: Electrocardiography, echocardiography, 24 h Holter monitoring, cardiac MRI, coronary angiography, endomyocardial biopsy, exercise testing, electrophysiological study, laboratory examinations and histological examination of the explanted heart. DIAGNOSIS: Cardiac sarcoidosis. MANAGEMENT: Immunosupressive and corticosteroid therapy. Routine endomyocardial biopsy is planned.

Coronary endothelial vasomotor function and vascular remodeling in heart transplant recipients randomized for tacrolimus or cyclosporine immunosuppression.

OBJECTIVES: This study aimed to compare changes in coronary endothelial function, systemic endothelin-1 (ET-1) levels, and vascular remodeling in heart transplant recipients randomized to cyclosporin A (CyA) or tacrolimus (Tac) immunosuppression. BACKGROUND: Functional endothelial abnormalities and intimal thickening are sensitive measures of early cardiac allograft vasculopathy (CAV). METHODS: The randomized, prospective study was performed in two groups of 22 patients, maintained on Tac or CyA and mycophenolate mofetil immunosuppression, 1 and 12 months after heart transplantation. We investigated epicardial luminal diameter, coronary blood flow velocity, and ET-1 plasma levels at 1 and 12 months after transplantation. Structural coronary alterations were determined using intravascular ultrasound. RESULTS: Epicardial vasomotor function at baseline and during follow-up was comparable between the groups. Deterioration of microvascular endothelial function during follow-up was significantly enhanced in the CyA versus Tac group (p < 0.05). Circulating ET-1 concentration increased in the CyA group but significantly decreased over time in the Tac group (CyA +17% vs. Tac -25%; p < 0.05). The time-dependent increase in mean intimal area was significantly enhanced in the CyA versus Tac group, whereas the vessel area significantly increased during follow-up in the Tac compared with the CyA group. CONCLUSIONS: Epicardial endothelial function is comparable between CyA- and Tac-treated patients. Microvascular endothelial function deteriorates more in CyA-treated patients, a finding that correlates with enhanced ET-1 concentration and an increased intimal area during follow-up. The mean vessel area in the Tac group increased over time, indicating positive vascular remodeling. Tac is superior to CyA with respect to microvascular endothelial function, intimal thickening, and vascular remodeling.

Vasospastic angina pectoris associated with Churg-Strauss syndrome.

BACKGROUND: A 50-year-old woman presented with recurrent episodes of unstable angina pectoris refractory to vasodilator treatment. Relevant coronary stenoses were excluded by coronary angiography and intravascular ultrasonography. Intracoronary infusion of acetylcholine revealed diffuse coronary vasospasms associated with clinical signs of myocardial ischemia and ST-segment elevation. Symptoms of bronchial asthma, polyneuropathy, nasal polyps, allergic rhinitis, gastritis and eosinophilia led to a diagnosis of Churg-Strauss syndrome. INVESTIGATIONS: Serum chemistry, coronary angiography, left-heart catheterization, intravascular ultrasonography and coronary vasospasm provocation with acetylcholine. DIAGNOSIS: Vasospastic angina pectoris associated with Churg-Strauss syndrome. MANAGEMENT: Treatment with systemic corticosteroids and cyclophosphamide.

Cytomegalovirus infection in heart transplant recipients is associated with impaired endothelial function.

BACKGROUND: Cardiac allograft vasculopathy (CAV) is initiated by allograft endothelial injury. We hypothesized that a major mechanism by which cytomegalovirus (CMV) could contribute to CAV is by dysregulation of the endothelial vasomotor response. METHODS: Coronary endothelial vasomotor function was determined in 183 consecutive patients (24+/-33 months after transplantation), and was correlated with recipient and donor CMV serological status before transplantation and with documented CMV infection episodes (CMVpp65Ag+). Serial endothelial function measurements were performed in a subgroup of 53 transplant recipients (1 month and 12 months after transplantation). The composite endpoint of cardiovascular related events and death during a follow-up of 66+/-41 months was analyzed based on the CMV serological status before transplantation. RESULTS: The medium event-free time for CMV-negative recipients of CMV-positive hearts was 8.1 years compared with 13.3 years for the other groups (P<0.05). Distal epicardial but not microvascular endothelial function was significantly impaired in CMV seronegative recipients of seropositive donor hearts (n=48) compared with all other groups (P<0.01 versus seronegative recipient/seronegative donor; P<0.05 versus seropositive recipient/seronegative donor; P<0.05 versus seropositive recipient/seropositive donor). Distal epicardial endothelial dysfunction was more pronounced in heart transplant recipients with a history of documented CMV infection compared with patients without any documented CMV infection (P<0.01). In a longitudinal subgroup analysis, distal epicardial and microcirculatory endothelial vasomotor response deteriorated significantly in recipients with documented CMV infection (P<0.05 versus baseline) but not in patients without previous CMV infection. CONCLUSIONS: Documented CMV infection episodes in heart transplant recipients are associated with impaired coronary endothelial function. CMV-negative recipients of CMV-positive donor hearts have an impaired distal epicardial endothelial function and an increased incidence of cardiovascular-related events and death during follow-up. CMV infection may contribute to allograft failure by accelerating coronary endothelial dysfunction.