Radiofrequency catheter ablation of ventricular tachycardia guided by nonsurgical epicardial mapping in chronic Chagasic heart disease.

We report a case of a 63-year-old women with Chagas' disease and recurrent, syncopal VT treated by RF catheter ablation in whom endocardial application of RF energy was guided by nonsurgical epicardial mapping. The procedure was undertaken in the electrophysiology laboratory under deep anesthesia. VT was interrupted after 2.4 seconds of application and rendered noninducible afterwards. Two weeks after the procedure, a distinct morphology VT was induced by programmed ventricular stimulation, and the patient was started on amiodarone, remaining asymptomatic 12 months after the procedure.

A new technique to perform epicardial mapping in the electrophysiology laboratory.

INTRODUCTION: A possible epicardial site of origin may be the reason for unsuccessful endocardial application of radiofrequency energy to control recurrent ventricular tachycardia. This study tests the feasibility and safety of a new epicardial mapping technique in patients with Chagas' disease and recurrent ventricular tachycardia. METHODS AND RESULTS: Epicardial mapping was performed through a pericardial puncture as an epidural introducer needle was advanced into the pericardial space under fluoroscopic guidance. Medium contrast was injected to demonstrate the position of the needle tip, and a guidewire was introduced until its tip lay within the pericardial space. A 8-French Hemaquet was advanced and 4-mm deflectable tip catheter introduced into the pericardial sac to map the right and left ventricular epicardium. Transthoracic echocardiographic monitoring was performed on the day of the procedure and on the day of hospital discharge. The pericardial space was reached in all patients with no complications. Electrophysiologic data suggesting the existence of an epicardial circuit was found in one patient. No complications occurred during the hospitalization period. CONCLUSION: Epicardial mapping can be safely performed through a pericardial puncture in the electrophysiology laboratory.

Autoimmunity in Chagas disease cardiopathy: biological relevance of a cardiac myosin-specific epitope crossreactive to an immunodominant Trypanosoma cruzi antigen.

Heart tissue destruction in chronic Chagas disease cardiopathy (CCC) may be caused by autoimmune recognition of heart tissue by a mononuclear cell infiltrate decades after Trypanosoma cruzi infection. Indirect evidence suggests that there is antigenic crossreactivity between T. cruzi and heart tissue. As there is evidence for immune recognition of cardiac myosin in CCC, we searched for a putative myosin-crossreactive T. cruzi antigen. T. cruzi lysate immunoblots were probed with anti-cardiac myosin heavy chain IgG antibodies (AMA) affinity-purified from CCC or asymptomatic Chagas disease patient-seropositive sera. A 140/116-kDa doublet was predominantly recognized by AMA from CCC sera. Further, recombinant T. cruzi protein B13--whose native protein is also a 140- and 116-kDa double band--was identified by crossreactive AMA. Among 28 sera tested in a dot-blot assay, AMA from 100% of CCC sera but only 14% of the asymptomatic Chagas disease sera recognized B13 protein (P = 2.3 x 10(-6)). Sequence homology to B13 protein was found at positions 8-13 and 1442-1447 of human cardiac myosin heavy chain. Competitive ELISA assays that used the correspondent myosin synthetic peptides to inhibit serum antibody binding to B13 protein identified the heart-specific AAALDK (1442-1447) sequence of human cardiac myosin heavy chain and the homologous AAAGDK B13 sequence as the respective crossreactive epitopes. The recognition of a heart-specific T. cruzi crossreactive epitope, in strong association with the presence of chronic heart lesions, suggests the involvement of crossreactivity between cardiac myosin and B13 in the pathogenesis of CCC.

Arrhythmias and sudden death after dynamic cardiomyoplasty.

BACKGROUND: The main causes of death in patients with severe cardiomyopathy are progressive heart failure and sudden death. The influence of cardiomyoplasty on the incidence of sudden death and arrhythmias in patients with cardiomyopathy remains unclear. The aim of this study was to investigate the occurrence of arrhythmias and sudden death after cardiomyoplasty. METHODS AND RESULTS: We studied 32 patients (26 male, 6 female; mean age, 48 +/- 12 years) who submitted to cardiomyoplasty for treatment of heart failure in New York Heart Association (NYHA) class III (n = 24) or class IV (n = 8). The etiology was idiopathic dilated cardiomyopathy in 27 patients, ischemic heart disease in 3 patients, and Chagas' heart disease in 2 patients. Patients were routinely studied before and every 6 months after cardiomyoplasty by means of radioisotopic angiography and 24-hour Holter monitor recordings. There were no operative or immediate postoperative deaths. During the postoperative period, 5 patients presented with acute atrial fibrillation and 1 had an episode of sustained ventricular tachycardia. All episodes were successfully treated with intravenous antiarrhythmic drugs or cardioversion. During follow-up (from 2 to 66 months), 15 patients died from sudden death (n = 5) or progressive heart failure (n = 10). Survival rates at 1, 2, and 4 years were 79.9 +/- 7%, 62.5 +/- 9.7% and 35 +/- 12.1%, respectively. At 6-month follow-up, NYHA functional class improved from 3.2 +/- 0.4 to 1.7 +/- 0.6 (P = .001) and left ventricular ejection fraction increased from 19.8 +/- 3.3% to 24 +/- 8.2% (P = .004). The mean values per day of premature ventricular complexes (PVCs) and episodes of nonsustained ventricular tachycardia (NSVT) did not change statistically. The mean number of PVCs per 24 hours before and at 6, 12, 24, 36, and 48 months after surgery were 126 +/- 44, 96 +/- 33, 90 +/- 29, 81 +/- 35, 71 +/- 35, and 59 +/- 48. The mean number of episodes of NSVT per 24 hours before and at 6, 12, 24, 36, and 48 months after surgery were 3.3 +/- 1.3, 1.9 +/- 0.5, 1.3 +/- 0.5, 1 +/- 0.5, 1.5 +/- 1.1, and 0.6 +/- 0.5, respectively. With respect to analysis of the idiopathic dilated cardiomyopathy subgroup, there also were no significant differences in the incidences of pre- and postoperative arrhythmias. CONCLUSIONS: Despite NYHA functional class and left ventricular function improvements observed after cardiomyoplasty, the incidence of arrhythmias did not change, and sudden death was an important finding mainly in late follow-up. The problem of sudden death after cardiomyoplasty, the mechanism that produces it, and the means to prevent it remain critical areas for future research.

Quality of life after cardiomyoplasty.

Cardiomyoplasty has recently been used as a surgical treatment for refractory heart failure, but its results have not been well described in quality-of-life patterns. We studied the quality of life of 14 patients (13 men, with a mean age of 43.3 +/- 7.4 years) submitted to this procedure for treatment of dilated or ischemic cardiomyopathies. They were approached by personal, structured interviews before and 13 +/- 9 months after the procedure, focusing on the following areas: physical activity, food and sleep patterns, working status, social activity, sexual activity, psychologic state, and perceptions and expectations about the treatment. The presence of limitation descriptors (discomfort, disability, and dissatisfaction) was recorded for all patients. The results showed an important decrease in limitation of physical activity, sleep pattern, social activity, and perceptions and expectations about the treatment. These findings suggest that cardiomyoplasty may improve the quality of life of a selected group of patients.

Homologous dura mater cardiac valves. Study of 533 surgical cases.

A group of 533 patients had cardiac valves replaced with homologous dura mater valves. The dura mater was preserved in a solution of 98 per cent glycerol and antibiotics for a period of 12 days before used. The leaflets were mounted in a stainless steel ring covered by Dacron velour. Two hundred forty-five patients had mitral valve replacement; 205 patients, aortic valve replacement; 17 patients, tricuspid valve replacement; and 2 patients, pulmonary valve replacement. Sixty-four patients were subjected to multivalvular replacements. The patients were followed for a period of 1 to 40 months after surgery with satisfactory clinical and hemodynamic results. Because 2 patients developed endocarditis produced by fungii, fungicidal drugs were added to the preservative solution. No bacterial endocarditis has been observed. No pressure gradient through the valve has been noted at rest. Anticoagulant drugs have not been used in the postoperative period.