Favorable left ventricular remodeling following large myocardial infarction by exercise training. Effect on ventricular morphology and gene expression.

Continued adverse remodeling of myocardium after infarction may lead to progressive ventricular dilation and heart failure. We tested the hypothesis that exercise training in a healed myocardial infarction-dysfunction rat model can favorably modify the adverse effects of ventricular remodeling including attenuation of abnormal myosin gene expression. Sprague-Dawley rats were subjected to either proximal LAD ligation or sham operation. At 5 wk after the operation, animals were randomly assigned to sedentary conditions or 6 wk of graduated swim training, creating four experimental groups: infarct sedentary (IS), infarct exercise (IE), sham sedentary (SS), and sham exercise (SE). At 11 wk all rats were sacrificed and analyzed. Compared to sedentary infarct controls, exercise training attenuated left ventricular (LV) dilation and allowed more hypertrophy of the non infarct wall. The exercise-trained hearts also showed a reduction in the estimated peak wall tension. Northern blot analysis showed an increase in beta-myosin heavy chain expression in the hearts of the sedentary infarction group soon after infarction when compared to sham controls. However, with exercise training, there was a significant attenuation of the beta-myosin heavy chain expression in the myocardium. Exercise training in a model of left ventricular dysfunction after healed myocardial infarction can improve the adverse remodeling process by attenuating ventricular dilation and reducing wall tension. The abnormal beta-myosin expression was also attenuated in the exercise trained group. This is evidence that abnormal gene expression following severe myocardial infarction dysfunction can be favorably modified by an intervention.

Echocardiographic abnormalities following cardiac radiation.

Five years or more after receiving cardiac radiation, 41 patients with Hodgkin's disease and seminoma in remission were subjected to echocardiography. The abnormalities detected included pericardial thickening in 70%, thickening of the aortic and/or mitral valves in 28%, right ventricular dilatation or hypokinesis in 39%, and left ventricular dysfunction in 39%. In the 23 patients treated by an upper mantle technique with shielding, the incidence of right ventricular abnormalities and valvular thickening was significantly lower than in patients treated with modified techniques. Although no symptoms were attributable to the observed abnormalities, longer follow-up time may reveal important functional implications.

Abnormal thallium kinetics in postoperative coarctation of the aorta: evidence for diffuse hypertension-induced vascular pathology.

After operative correction of congenital coarctation of the aorta, patients continue to have excess cardiovascular mortality, including manifestations of ischemic heart disease. Previous morphologic studies support the concept of direct hypertensive vascular injury in these patients. To determine whether abnormalities of myocardial perfusion were present in an asymptomatic group of patients with coarctation repair, 18 men and 9 women with a mean age of 26 years (range 19 to 41) were studied between 2 and 25 years after operative correction. Stress electrocardiography and quantitative thallium imaging by a circumferential profile technique were used. These patients were compared with a normal group, statistically defined as having a less than 1% prevalence of significant obstructive coronary artery disease. The postoperative coarctation group demonstrated a reduction in global thallium redistribution in each view analyzed. As compared with findings in the control subjects, thallium washout in the anterior view (41.9 versus 48.6%, p = 0.02) and left anterior oblique projection (40.5 versus 48.2%, p = 0.007) was significantly diminished. Although the postoperative coarctation group had a lower thallium redistribution rate in the lateral view (41.4 versus 46.3%, p = 0.09) this difference did not reach statistical significance because of the intrinsic variability of this projection. Plots of the median percent thallium washout revealed independence from circumferential profile angle, indicating global abnormalities in perfusion. No correlation between clinical variables and thallium kinetics could be established, suggesting marked individual variability in the development of this vascular lesion. The observation of abnormal thallium kinetics in patients with coarctation repair may have consequences for long-term follow-up and therapy.

Persistent ventricular adaptations in postoperative coarctation of the aorta.

To evaluate ventricular performance and myocardial contractility after surgical correction of congenital coarctation of the aorta, we studied 25 patients (16 men and 9 women, mean age 26.1 years [range 19 to 34]), an average of 10.6 years (range 2 to 25) after repair. Radionuclide ventriculography at rest and exercise and digitized, quantitative two-dimensional echocardiography were performed. Data from derived, high resolution time-activity curves by radionuclide ventriculography, combined with noninvasive hemodynamic/ventricular volume data, were compared with values in an age- and sex-matched normal population. Despite essentially identical baseline and exercise hemodynamics, postoperative coarctation subjects demonstrated enhanced ventricular contraction, as determined by the peak ejection rate at rest (-3.79 versus -3.20 stroke volume/s, p less than 0.01) and exercise (-3.00 versus -2.90 stroke volume/s, p = NS), and overall ejection fraction at rest (56.4 versus 48.0%, p less than 0.01) and exercise (70.8 versus 59.3%, p less than 0.01). An intrinsic activation-contraction delay was observed, as illustrated by a prolonged time to peak ejection rate at rest (27.7 versus 21.5% of the RR interval, p less than 0.01) and exercise (28.4 versus 21.2% of the RR interval, p less than 0.01), and total systolic time at rest (50.2 versus 43.4% of the RR interval, p less than 0.01) and exercise (56.8 versus 50.4% of the RR interval, p less than 0.01). Although left ventricular meridinal wall stress was statistically indistinguishable (62 versus 74 mm Hg/mm2, p = NS), intrinsic myocardial contractility, as assessed by the peak systolic pressure/volume ratio, was increased in the postoperative coarctation group (1.88 versus 2.87 mm Hg/ml, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary valve replacement in adults late after repair of tetralogy of fallot: are we operating too late?

OBJECTIVES: The purpose of this study is to evaluate right ventricular (RV) volume and function after pulmonary valve replacement (PVR) and to address the issue of optimal surgical timing in these patients. BACKGROUND: Chronic pulmonary regurgitation (PR) following repair of tetralogy of Fallot (TOF) leads to RV dilation and an increased incidence of sudden cardiac death in adult patients. METHODS: We studied 25 consecutive adult patients who underwent PVR for significant PR late after repair of TOF. Radionuclide angiography was performed in all at a mean of 8.2 months (+/- 8 months) before PVR and repeated at a mean of 28.0 months (+/- 22.8 months) after the operation. Right ventricular (RV) end-systolic volume (RVESV), RV end-diastolic volume (RVEDV) and RV ejection fraction (RVEF) were measured. RESULTS: Mean RVEDV, RVESV and RVEF remained unchanged after PVR (227.1 ml versus 214.9 ml, p = 0.74; 157.4 ml versus 155.4 ml, p = 0.94; 35.6% versus 34.7%, p = 0.78, respectively). Of the 10 patients with RVEF > or = 0.40 before PVR, 5 patients (50%) maintained a RVEF > or = 0.40 following PVR, whereas only 2 out of 15 patients (13%) with pre-operative values <0.40 reached an RVEF > or = 0.40 postoperatively (p < 0.001). CONCLUSIONS: Right ventricular recovery following PVR for chronic significant pulmonary regurgitation after repair of TOF may be compromised in the adult population. In order to maintain adequate RV contractility, pulmonary valve implant in these patients should be considered before RV function deteriorates.

Congenitally corrected transposition of the great arteries in the adult: functional status and complications.

OBJECTIVES: We sought to assess the clinical outcome, functional status and complications of adult patients with congenitally corrected transposition of the great arteries. BACKGROUND: Congenitally corrected transposition is a rare form of congenital heart disease, although survival into adult life may be expected. Little information is available on the long-term prognosis of these patients once they have reached adulthood. This study focuses exclusively on patients >18 years old followed up at a single tertiary referral center. METHODS: The charts of all patients with a diagnosis of congenitally corrected transposition of the great arteries from the Toronto Congenital Cardiac Centre for Adults since 1985 were reviewed. Data were available for 52 patients, 26 of whom had undergone radionuclide angiography. Mortality, clinical and functional status, surgical procedures and complications were reviewed. RESULTS: Thirteen patients (25%) died; age at death was 38.5 +/- 12.5 years (mean +/- SD). The current age of survivors is 32.7 years (range 18.2 to 54.3). Of the survivors, 17 had palliative procedures, and 25 had definitive repair, 11 of whom required reoperation. Left ventricle to pulmonary artery conduit replacement was necessary in seven patients. Eighteen patients have permanent pacemakers, nine of whom developed complete heart block perioperatively. Nine patients developed progressive atrioventricular (AV) block unrelated to operation. Supraventricular arrhythmias occurred in 15 patients. Progressive systemic AV valve regurgitation developed in 10 patients and endocarditis in 6. CONCLUSIONS: Congenitally corrected transposition in the adult patient is not a benign condition. Late complications are common and warrant careful, long-term follow-up.

Serial follow-up of adults with repaired tetralogy of Fallot.

OBJECTIVES AND BACKGROUND: Sudden death has long been considered a major contributor to mortality in pediatric patients with corrected tetralogy of Fallot. However, this may not apply to the patient with repaired tetralogy of Fallot who has survived into adulthood. Consequently we followed up a cohort of such adults to establish the clinical outcome and risk factors affecting their survival. METHODS: A baseline group of 151 adult patients with repaired tetralogy of Fallot were followed up for a mean of 3.2 years. The overall mortality rate was low (0.009 death/patient-year). Four patients died during follow-up, but only two deaths can be attributed to tetralogy of Fallot repair, and there were no sudden cardiac deaths. Clinically 94% of patients have remained in New York Heart Association functional class I. A subset of 36 patients were followed up for a mean of 6.7 years. This group had three sets of serial testing at 3-year intervals consisting of right heart catheterization at the initial study only, 24-h Holter ambulatory electrocardiographic (ECG) monitoring, exercise ECG and rest and exercise radionuclide angiography. RESULTS: Exercise capacity assessed by serial exercise stress testing remained stable over the follow-up period, whereas the presence of exercise-induced arrhythmias steadily decreased. Most patients had no significant arrhythmias and had no significant change in severity of arrhythmia with time. Radionuclide angiography showed significant improvement in exercise right ventricular ejection fraction over time but a progressive decrease in left ventricular ejection fraction at both rest and exercise. However, the left ventricular ejection fraction is still within the normal limits for our laboratory. CONCLUSIONS: Adults with repaired tetralogy of Fallot have a very good prognosis and a low risk of sudden death. However, ventricular function may change over time and should be carefully monitored.

Right ventricular form and function after percutaneous atrial septal defect device closure.

OBJECTIVES: We sought to assess the right heart's response to percutaneous device closure of moderate sized atrial septal defects (ASDs) in adults over a one-year follow-up period. BACKGROUND: Percutaneous ASD device closure is a safe and effective means of reducing or eliminating interatrial shunting. The response of the adult's right heart to device closure is incompletely understood. METHODS: Forty consecutive patients had 40 device implantations (32 with the CardioSeal implant and 8 with the Amplatzer device). The patients were assessed with echocardiography, chest radiography and electrocardiography before the procedure and at 1, 6 and 12 months. RESULTS: The mean ASD size was 13+/-4 mm, and the device size ranged from 33 to 40 mm for CardioSeal and 12 to 36 mm for Amplatzer. At one month, heart size (49% vs. 46%), four-chamber right ventricular (RV) size (45 vs. 41 mm), paradoxical septal motion (60% vs. 5%), QRS duration (125 vs. 119 ms), PR interval (181 vs. 155 ms) and echocardiographically determined pulmonary artery systolic pressure decreased significantly and was maintained at 12-month follow-up. At six months, right atrial length decreased from 50 to 47 mm. At one year, 29% of patients had persistent RV enlargement. CONCLUSIONS: Right heart morphology undergoes rapid improvement within one month of defect closure, with associated mechanoelectrical benefit. A small number of patients had persistent RV enlargement or pulmonary hypertension, or both, at one year. Our data support the application of transcatheter methods in achieving excellent hemodynamic and anatomic outcomes.

Cardiopulmonary function in adult patients late after Fontan repair.

OBJECTIVES: The clinical status and exercise assessment of adult patients late after the Fontan operation were reviewed to determine cardiovascular function. BACKGROUND: The Fontan operation is the final operation for many patients with tricuspid atresia or a single ventricle. Follow-up reports describe most patients to be in Canadian Cardiovascular Society functional class I or II. Objective measures of cardiac performance in the pediatric age group have shown significant dysfunction. METHODS: Forty-seven adult patients were seen late after the Fontan operation at the Toronto Congenital Cardiac Centre for Adults. Thirty of these underwent cycle ergometry to determine maximal exercise capacity. Maximal ventilation, maximal oxygen uptake and anaerobic threshold were determined from a ramp exercise protocol. Ejection fraction at rest and during exercise was measured with gated radionuclide angiography. Results were compared with those of eight normal volunteers. Results are given as mean +/- SD. RESULTS: Thirty patients underwent cardiopulmonary exercise testing 6.7 +/- 3.9 years after a first Fontan operation. Clinically 93% were in functional class I or II. The Fontan group patients had a significantly lower maximal work load (548 +/- 171 vs. 1,094 +/- 190 kilopond-meters, p < 0.00001), anaerobic threshold (11.2 +/- 2.9 vs. 23.6 +/- 4.6 ml/kg per min) and maximal oxygen consumption (14.8 +/- 4.5 vs. 42.1 +/- 10.0 ml/kg per min). Systemic ventricular ejection fraction was lower at rest (38 +/- 12% vs. 58 +/- 7%) and during exercise (40 +/- 15% vs. 70 +/- 8%). CONCLUSIONS: Despite a clinical impression of good function, by objective measures adult patients continue to have significant cardiovascular limitation late after the Fontan operation.

Sustained ventricular tachycardia in adult patients late after repair of tetralogy of Fallot.

OBJECTIVES: We sought to determine the features associated with sustained monoform ventricular tachycardia (VT) in adult patients late after repair of tetralogy of Fallot (TOF) and to review their management. BACKGROUND: Patients with repair of TOF are at risk for sudden death. Risk factors for ventricular arrhythmia have been identified from patients with ventricular ectopic beats because of the low prevalence of sustained VT. METHODS: From a retrospective chart review of patients assessed between January 1990 and December 1994, 18 adult patients with VT were identified and compared with 192 with repaired TOF free of sustained arrhythmia. RESULTS: There was no significant difference in age at repair, age at follow-up or operative history. Patients with VT had frequent ventricular ectopic beats (6 of 9 vs. 21 of 101), low cardiac index ([mean +/- SD] 2.4 +/- 0.4 vs. 3.0 +/- 0.8) and more structural abnormalities of the right ventricle (outflow tract aneurysms and pulmonary or tricuspid regurgitation) than control patients. Electrophysiologic map-guided operation was performed in 10 of 14 patients who required reoperation. VT has reoccurred in three of these patients. Four patients did not undergo operation (three received amiodarone; one underwent defibrillator implantation). Two patients with VT also had severe heart failure and died. CONCLUSIONS: Most patients with VT late after repair of TOF have outflow tract aneurysms or pulmonary regurgitation, or both. These patients have a greater frequency of ventricular ectopic beats than arrhythmia-free patients after repair of TOF. A combined approach of correcting significant structural abnormalities (pulmonary valve replacement or right ventricular aneurysmectomy, or both) with intraoperative electrophysiologic-guided ablation may reduce the potential risk of deterioration in ventricular function and enable arrhythmia management to be optimized.

Analysis of adults with and without complex ventricular arrhythmias after repair of tetralogy of Fallot.

Forty-four adult patients with tetralogy of Fallot were studied while clinically well at a mean of 14 years (range 5 to 27) after intracardiac repair to examine the association of postoperative ventricular arrhythmias with historical and postoperative hemodynamic data. Twenty-two patients who demonstrated during 24 hour ambulatory monitoring or maximal graded treadmill exercise testing, or both, ventricular premature beats that were multiform, repetitive or increased in frequency during exercise or recovery after exercise were found to differ from patients without such ventricular premature beats in four respects. The patients with complex or exercise-induced ventricular premature beats had a higher right ventricular systolic blood pressure, a higher incidence of residual left to right intracardiac shunt, lower cardiac index and more frequently abnormal left ventricular ejection fraction measured by rest and exercise-gated radionuclide ventriculography. Adults with complex or exercise-induced ventricular premature beats after intracardiac repair of tetralogy of Fallot are characterized by suboptimal hemodynamic repair and preclinical left ventricular dysfunction.

Clinically unrecognized ventricular dysfunction in young diabetic patients.

Left ventricular function at rest and during supine bicycle exercise was assessed by gated radionuclide angiography in 20 diabetic patients and 18 normal control subjects without clinical evidence of heart disease. The diabetic patients were aged 21 to 44 years and all except one used insulin. No subject developed chest pain or electrocardiographic changes during exercise. Both groups had a similar rest and exercise heart rate and blood pressure, and both achieved similar work loads. The control group had an ejection fraction at rest of 65.4 +/- 6.2% (mean +/- SD) and only 1 of 18 showed a decrease with exercise; peak exercise ejection fraction averaged 77.1 +/- 7.8%. The diabetic group had a mean ejection fraction at rest of 63.7 +/- 6.5%, similar to that of the control group, but 7 of 20 showed a decrease during exercise; the exercise ejection fraction averaged 67.7 +/- 9.7%, significantly lower than that of the control group (p less than 0.01). The diabetic patients varied widely in ejection fraction response to exercise, ranging from an increase of 25% to a decrease of 21%. This response did not correlate with age, sex, duration of diabetes, smoking, retinopathy, exercise heart rate, blood pressure or rate-pressure product, work load attained or ejection fraction at rest. These data suggest that approximately one-third of patients with diabetes have subclinical left ventricular dysfunction without correlation to risk factors for atherosclerosis or other diabetic complications. Whether this is due to unrecognized coronary artery disease or primary myocardial disease remains unknown.

The relationship of cardiac diastolic dysfunction to concurrent hormonal and metabolic status in type I diabetes mellitus.

The presence of diabetic cardiomyopathy and its relationship to concurrent hormonal and metabolic status have not been defined in patients with uncomplicated type I diabetes mellitus. Accordingly, radionuclide left ventricular angiograms and simultaneous metabolic profiles were obtained in 8 type I diabetic patients who had no major diabetic complications and in 11 normal subjects. Occult coronary artery disease was excluded by electrocardiogram exercise testing. Hemodynamics and systolic function did not differ between the groups. However, the peak filling rate (PFR; end-diastolic volumes per s) was less in the diabetic patients at rest [mean, 4.1 +/- 0.2 (+/- SE) vs. 4.8 +/- 0.2; P less than 0.05] and during aerobic (6.8 +/- 0.2 vs. 8.30 +/- 0.3; P less than 0.01) and anaerobic exercise (8.8 +/- 0.3 vs. 9.8 +/- 0.4; P less than 0.05). The time to PFR was prolonged in the diabetic patients at rest (174 +/- 10 vs. 133 +/- 7 ms; P less than 0.01) and during anaerobic exercise (126 +/- 5 vs. 103 +/- 6 ms; P less than 0.01). Plasma glucose and insulin levels were elevated in the diabetic patients at rest and during exercise. Otherwise, the metabolic and hormonal levels did not differ between the groups. In the diabetic patients, no single metabolic or hormonal parameter correlated with PFR or time to PFR. Impairment of diastolic filling also did not correlate with level of glycosylated hemoglobin or duration of diabetes. The alteration in diastolic filling present in type I diabetic patients who have no other diabetic complications may represent the earliest functional effect of diabetic cardiomyopathy.

Prinzmetal's angina with coronary artery spasm. Angiographic, pharmacologic, metabolic and radionuclide perfusion studies.

We studied the effects of coronary artery spasm on perfusion of the microvasculature in a patient with Prinzmetal's angina. Intracoronary injections of 99mTc and 131I-labelled macroaggregated human serum albumin were performed (1) at rest, (2) during spontaneous angina, (3) after the administration of nitroglycerin and (4) during pacing-induced spasm and the resultant scans compared. The resting scan was normal. Pain and spasm were associated with a perfusion defect that was localized to the anterior and inferior walls of the left ventricle. The localization of the perfusion defect corresponded with angiographically demonstrated spasm involving left anterior descending and distal circumflex coronary arteries. A subsequent myocardial infarction was localized by 43K scanning to the same perfusion area. Metabolic and parasympathetic stimulation studies were performed but were inconclusive. The patient's recurrent pains were ultimately controlled with large oral doses of isosorbide dinitrate.

Detection of radiation cardiomyopathy by gated radionuclide angiography.

Twenty-one asymptomatic adults underwent rest and exercise gated radionuclide angiography seven to 20 years after having received mediastinal radiation (2,000 to 7,600 rads) for Hodgkin's disease. None of these patients received cytotoxic chemotherapy. Twelve patients (57 percent) had abnormal left (less than 53 percent at rest and/or greater than 5 percent decrease at peak exercise) and/or right (less than 27 percent at rest and/or greater than 5 percent decrease at peak exercise) ventricular ejection fractions. Previous reports have described myocardial fibrosis occurring late after therapeutic mediastinal radiation; however, the incidence of this occurrence based on clinical follow-up has been low. Rest and exercise radionuclide angiography is a sensitive method for assessing systolic ventricular function and reveals a high prevalence of cardiomyopathy that can be linked to previous radiotherapy.

Repeatability of estimates of left-ventricular volume from blood-pool counts: concise communication.

Radionuclide ventriculography permits nongeometric calculation of ventricular volume. Accurate and reproducible determination of left-ventricular (LV) blood-pool counts is necessary to perform this calculation. Furthermore, to make serial volume determinations one must know the half-time of in vivo blood-pool activity. We compared five methods of LV count determination in nine patients. Interpatient and intrapatient variability of the in vivo half-time of Tc-99m-labeled red blood cells (RBCs) was measured. Left-ventricular count determinations, derived from temporally and spatially smoothed images using a second-derivative algorithm to identify the LV region of interest (ROI), are less variable than those based on manual ROI determinations. The mean in vivo half-time of Tc-99m RBCs is 4.1 hr, and there is significant interpatient (0.9 +/- 0.8 hr) and intrapatient (1.0 +/- 0.9 hr) variability. These findings should be considered in the determination of serial, relative ventricular volume by radionuclide ventriculography.

Cardiac damage produced by direct current countershock applied to the heart.

This study examined the pathophysiology of the myocaridal damage produced by direct current shock over a dose range of 10 to 90 watt-seconds, applied directly to the heart in 26 dosgs. The extent of injury produced was assessed with creatine kinase depletion and light and electron microscopy, and was correlated with in vivo imaging and tissue distributions of the isotopes technetium-99m pyrophosphate and thallium-201. Changes in intramyocardial temperature and regional myocardial blood flow were also measured. Uptake of technetium-99m pyrophosphate occurred exponentially with graded increases in shocks, and this agent was more sensitive than thallium-201 in detecting injury both on imaging and at tissue level. The threshold for significant injury was approximately 30 watt-seconds, and on electron microscopy a characteristic feature was marked dehiscence of the intercalated disks between the damaged myocytes. The use of different-size paddles did not appear to affect the total number of cells damaged. However, with large paddles the injury was more superficial and spread over a wider area. With short time intervals between successive shocks, a greater amount of injury occurred, in part because of a compounding of the thermal component of the damage. Hypothermia can reduce the degree of injury.

Percutaneous catheter closure of the persistently patent ductus arteriosus in the adult.

The USCI patent ductus occluder has been shown to be an effective nonsurgical technique for closure of the persistently patent ductus in a primarily pediatric population. Its clinical impact in the adult has been reported only within small subgroups of larger pediatric studies or for a small population. This study was conducted to determine the feasibility, success rate, and complications of device closure for the persistently patent ductus arteriosus (PDA) in the adult. The population consisted of 55 patients (4 men and 51 women; mean age 38.8 +/- 15.0 years) with follow-up of 2.2 +/- 2.1 years. All patients underwent echocardiography obtained as part of their follow-up assessment. The device was successfully placed in 54 patients, with 75% clinical and echocardiographic closure at the first follow-up assessment 2.4 +/- 2.6 months). One patient with initial clinical and echocardiographic evidence of closure was subsequently found to have an open ductus. Spontaneous closure (2 patients) or second implant (6 patients) resulted in 86% closure at the most recent assessment. Thus, the percutaneous PDA double-umbrella occluder device is a feasible and effective technique for closing persistent PDA in the adult and will result in occlusion of the shunt in most patients without the need for thoracotomy.

Myocardial imaging in a patient with reproducible variant angina.

A unique case is presented of variant angina pectoris with reproducible chest pain and S-T segment elevation in the immediate postexercise period and with normal coronary arteries. Coronary arterial spasm was deomnstrated with arteriography after intravenous administration of ergonivine maleate. Thallium-201 imaging during the pain reproducibility demonstrated malperfusion in the region supplied by the artery with documented spasm.

Catheter occlusion of the persistently patent ductus arteriosus.

Catheter occlusion of a persistently patent ductus arteriosus was attempted in 40 patients (11 men and 29 women, mean age 7.2 +/- 8.3 years, range 244 days to 40 years), using a transvenously placed Rashkind umbrella occluder (USCI). Thirty-one 12-mm and six 17-mm diameter devices were successfully placed in the ductus (internal diameter average 3.9 mm, range 2 to 9 mm). One procedure was abandoned when fluoroscopy failed to visualize the device. There were 2 immediate embolizations subjected to surgical recovery. A residual shunt was present on the immediate postocclusion ventriculogram in 12 of 37 procedures (32%). Twenty-eight patients (75%) have had at least a follow-up at 3 months with Doppler study and 6 (21%) continued to have shunting into the pulmonary artery. Three of 4 patients have undergone successful placement of a second device and 1 patient's shunting spontaneously resolved at 1 year postimplant, leaving only 2 patients (7%) with persistent shunts. There has been 1 episode of probable prosthetic endarteritis and 1 patient has developed mild narrowing of the left pulmonary artery related to device placement. Catheter occlusion of the patent ductus arteriosus using the Rashkind umbrella appears to be a safe and effective method of non-surgical management.