Sustained ventricular tachycardia after repair of tetralogy of Fallot: new electrophysiologic findings.

Ventricular arrhythmia originating from the outflow tract of the right ventricle is a presumed cause of late sudden death in patients after repair of tetralogy of Fallot. Exercise testing has been shown to enhance detection, and phenytoin has been shown to control ventricular arrhythmias in these patients. This study reports new findings in 3 patients who underwent electrophysiologic studies at postoperative cardiac catheterization; in each, sustained ventricular tachycardia was induced and found to originate from the inflow-septal area of the right ventricle. Using serial studies, the same sustained ventricular tachycardia was induced during therapeutic serum concentrations of phenytoin but not after propranolol. No patient had ventricular arrhythmia during a 24-hour electrocardiogram or during exercise. Although no patient had normal hemodynamic function, only 1 patient had right ventricular pressure greater than two-thirds systemic pressure. Each patient had undergone initial intracardiac repair at a relatively late age (3, 9, and 9 years).

Critical aortic coarctation: patch aortoplasty in infants less than age 3 months.

Twenty-three infants less than age 3 months (mean age 31 days) underwent patch aortoplasty for relief of coarctation of the aorta. All had intractable congestive heart failure, despite aggressive medical therapy. Each infant had other cardiac anomalies, including patent ductus arteriosus (83 percent) and ventricular septal defect (74 percent). All patients underwent closure of the ductus arteriosus and patch angioplasty of the aorta to produce a luminal diameter of at least 16 mm. In addition, 9 of the 17 patients (53 percent) with a large shunt ventricular septal defect underwent pulmonary arterial banding. There was one hospital death 42 days after operation secondary to bowel perforation and sepsis. Hospitalization beyond 21 days postoperatively was always due to other unrepaired cardiac lesions. The three late deaths at 3, 9 and 18 months after operation were associated with additional major anomalies. Fourteen patients have had postoperative catheterization. No gradient was found across the site of coarctation repair, but one patient had a gradient between the left carotid and left subclavian arteries. Surgical repair of critical coarctation of the aorta in infants can safely be offered despite the presence of other cardiac anomalies.

Ruptured ductus arteriosus. Aneurysm in an infant. Report of a survivor.

The diagnosis of a large ductus arteriosus aneurysm was made in a 3 1/2-month-old infant by cardiac catheterization following massive hemoptysis. Prompt surgical correction accounted for the patient's survival. Differential diagnosis of an intrathoracic mass should include a ductus arteriosus aneurysm even in the newborn period.

Epicardial corkscrew lead fracture: an underreported cause of pacing failure?

Three children with a pacemaker sustained similar lead fractures within a two-year period. Each fracture occurred in the corkscrew portion of a Medtronic Model 6917 epicardial lead. All patients were boys. The leads had been in place for 12, 45, and 43 months prior to fracture. None of the patients had sustained major trauma. Fracture of the corkscrew lead has been considered an uncommon complication. However, three lead fractures in the corkscrew area in a population of 60 children followed at this institution indicate that this may be a more common cause of pacemaker-system malfunction than previous data suggest. A plea is made for reporting all pacing failure to the manufacturer.

Late complications following surgical repair of total anomalous pulmonary venous return below the diaphragm.

Between May, 1975, and June, 1977, we surgically repaired an infracardiac total anomalous pulmonary venous return in 4 infants under deep hypothermic cardiac arrest. All patients had pulmonary hypertension and a patent ductus arteriosus. All survived operation and required positive end-expiratory pressure with mechanical ventilation. Late complications included patent ductus arteriosus not visualized at initial catheterization, breakdown of an oversewn atrial septal defect repair, and pulmonary venous obstruction despite an anastomosis diamter of 1.5 to 2.5 cm. At reoperation, there was scarring and contraction at the junction of the pulmonary veins and left atrium. One infant with these complications died post-operatively. In another patient, there was kinking of the left lower pulmonary vein at its juncture with the left atrium. In view of these complications we currently recommend the following: ligation of the ductus arteriosus regardless of catheterization findings; a right-sided approach to avoid pulmonary vein kinking; prosthetic patch closure of the atrial septal defect to avoid excessive tension on suture lines and to maintain maximum left atrial size; stellate anastomosis to provide the largest possible drainage channel; awareness that an unusually high positive end-expiratory pressure may be required postoperatively; and early recatheterization.

Left atrial appendage aneurysm: correlation of noninvasive with clinical and surgical findings: report of a case.

Congenital left atrial appendage aneurysm is rarely diagnosed on the basis of an abnormal cardiac silhouette. Patients with a left atrial appendage aneurysm often present with symptoms of systemic emboli or supraventricular arrhythmias. A patient with left atrial appendage aneurysm was diagnosed by correlation of two noninvasive techniques echocardiography and radionuclide scintiscanning. Angiography was confirmatory and aneurysmectomy was successfully performed.