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This report documents our early experience with minimally invasive direct-access surgical repair of atrial septal defect (ASD) in adults. We have developed minimally invasive techniques for direct-access ASD repair in adults while maintaining the efficacy of the open operative procedure. Between June 1996 and September 1998, 59 consecutive patients underwent repair of ASD, 34 (58%) of whom underwent minimally invasive direct-access surgical closure of ASD through a right parasternal, submammary, or upper hemisternotomy incision. Twenty-three (68%) were secundum type ASD, 5 (15%) were sinus venosus types, 2 (6%) were primum types, and 4 (122%) were patent foramen ovales. Twenty-six (77%) were women (mean age 39 +/- 15 years, range 18 to 79). The mean pulmonary-to-systemic shunt ratio (Qp/Qs) was 2.3 +/- 0.6 (n = 15). There were no operative or late deaths. Follow-up was 100% complete. Four patients (12%) developed major complications. All were alive and well at the time of follow-up and there was 1 late arrhythmia (atrial fibrillation). In all but 1 patient, New York Heart Association functional class was improved or unchanged (1.47 +/- 0.51 vs 1.06 +/- 0.25, p = 0.0001). These results indicate that minimally invasive direct-access repair of ASD in adults is safe and effective, and is broadly applicable to the entire spectrum of defects. [ABSTRACT FROM AUTHOR]

Although venous thrombosis may occur often after coronary artery bypass grafting, prophylaxis with low-dose heparin is rarely used due to the risk of bleeding. Therefore, we compared the efficacy of 2 mechanical regimens of prophylaxis against deep vein thrombosis (DVT). Consecutive patients undergoing coronary artery bypass without concomitant valve surgery or coronary endarterectomy were randomized to either a more intensive regimen of intermittent pneumatic compression (IPC) plus graduated compression stockings (GCS) versus standard compression stockings alone. Of 611 patients screened, 184 were excluded due to peripheral vascular disease, postoperative intraaortic balloon support, or immediate postoperative anticoagulation. An additional 83 patients refused consent, leaving 172 in each prophylaxis group. The primary study end point was DVT diagnosed by a predischarge leg ultrasound examination performed on postoperative days 4 to 6. Of 344 patients enrolled, 330 (96%) underwent predischarge ultrasonography. DVT was detected in 19% of patients assigned to IPC plus stockings versus 22% assigned to GCS alone (95% confidence interval for the difference, -11% to 6%, p = 0.62). The addition of IPC did not add significant incremental benefit to GCS alone for DVT prophylaxis among patients undergoing coronary artery bypass surgery.

The long-term results of patients undergoing myotomy/myectomy of the ventricular septum for obstructive hypertrophic cardiomyopathy are documented in 31 patients (15 women, 16 men, age range 21 to 80 years [mean 55]) with mean New York Heart Association functional class III to IV congestive heart failure, who underwent radical myotomy/myectomy at the Brigham and Women's Hospital from 1972 to 1991. Preoperative gradients by catheterization or echocardiography ranged from 26 to 240 mm Hg (average 96). There were no operative deaths. Two patients developed early postoperative complete heart block requiring a transvenous pacemaker. Clinical follow-up was 1 to 14 years (mean 6.5). All surviving patients were restudied by echocardiography and clinical examination. The mean postoperative functional class was II. Postoperative gradients ranged from 0 to 30 mm Hg (mean 4.5) (p less than 0.001 compared with preoperative values). There were 5 late deaths (low cardiac output in 2, stroke in 2, and acute respiratory failure in 1); 4 of 5 deaths occurred in patients with concomitant coronary artery disease. Survival at 10 years was 86 +/- 9%. There were no reoperations for subaortic obstruction.

To study the natural history of the hemodynamic performance of bioprosthetic heart valves, Doppler echocardiograms were recorded in a group of clinically stable patients at 2 and 5 years after replacement of native aortic valves with bioprosthetic valves. Eighteen patients completed a 2-year and 26 patients a 5-year follow-up examination. The effective orifice areas of identical models of bioprosthetic valves (Hancock II) were determined in vitro in a left-sided heart pulse duplicator system. In vivo Doppler-derived effective orifice areas were compared with the in vitro measurements for the same valve size. At both the 2- and 5-year follow-up examinations, the Doppler-derived effective orifice area was significantly less than the in vitro area (p less than 0.0001 at each interval). Ten of 16 valves evaluated serially decreased greater than 0.20 cm2 in the Doppler-derived effective orifice area between studies. The mean decrease in effective orifice area in valves evaluated serially was 0.25 +/- 0.29 cm2 (p less than 0.005). The peak transaortic gradient increased from 21 +/- 6 to 27 +/- 8 mm Hg (p less than 0.01). The mean transaortic gradient increased from 12 +/- 4 to 15 +/- 7 mm Hg (p less than 0.05). It is concluded that serial Doppler echocardiographic studies demonstrate a deterioration in the hemodynamic performance of bioprosthetic valves over time in patients with no symptoms or signs of valvular dysfunction and that Doppler echocardiography may be useful for identifying subclinical bioprosthetic valvular dysfunction.

To compare the hemodynamic results of different anuloplasty techniques of primary valve repair for mitral regurgitation, 122 patients were prospectively studied with Doppler echocardiograms 5 to 10 days after operation. Seventy-seven patients had mitral valve prolapse, 27 had coronary artery disease, 13 patients had rheumatic mitral valve lesions and 5 patients had infective endocarditis. Forty-eight patients received the flexible Duran ring, 46 received the more rigid Carpentier ring and 28 patients received no ring. Doppler echocardiography demonstrated a significant decrease in mitral valve area estimated by the pressure half-time method in patients who received either a Carpentier (2.6 +/- 0.8 cm2) or Duran ring (2.8 +/- 0.8 cm2) when compared with patients who received no ring (3.2 +/- 0.7 cm2) (p = 0.01). No significant differences were observed for peak transmitral diastolic velocity, peak transmitral diastolic gradient, or the grade of mitral regurgitation by color flow Doppler mapping between patients with and without rings. The etiology of mitral disease and concomitant surgical procedures accompanying mitral valve repair did not significantly influence mitral valve area, peak velocity or peak gradient. These data suggest that Carpentier and Duran rings decrease the hemodynamic mitral valve area; however, the decrease in valve area is small and not associated with a clinically important increase in transvalvular gradient.

To ascertain relations among site, incidence, and mechanisms of clinically evident failure of porcine bioprosthetic heart valves, the frequency of failure of 1,110 valves in 1,001 adult operative survivors from January 1972 to January 1982 was reviewed and correlated with the pathologic features of 22 consecutive dysfunctional valves. There were 373 mitral, 519 aortic, and 109 double replacements, yielding for study 482 mitral and 628 aortic valves at risk. Infective endocarditis occurred in 1.9% (8 mitral, 7 aortic, and 4 double). Twenty-three valves (13 mitral and 10 aortic) with documented primary dysfunction were explanted, a mean of 55 months (range 9 to 94) after surgery. The primary dysfunction rate for the 333 valves implanted for greater than or equal to 5 years was 6.8% (11 of 161) for mitral and 4.1% (7 of 172) for aortic valves. Valves implanted for less than 5 years had a failure rate of 0.7%. The actuarially determined freedom from primary valve failure was 98 +/- 1% for mitral and 98 +/- 1% for aortic valves at 5 years and 79 +/- 7% for mitral and 91 +/- 4% for aortic valves at 10 years. Recovered valves (12 mitral and 10 aortic) with detailed morphologic analysis were functioning for a mean duration of 52 months (range 12 to 87). Causes of failure included calcification-related tears in 7 (4 mitral and 3 aortic, mean 66 months), tear without calcium deposits in 4 (4 mitral, mean 44 months), cuspal stiffening without tear but with calcium deposits in 2 (1 mitral and 1 aortic, mean 80 months) and thrombosis in 1 (aortic). Late primary dysfunction was most frequently a result of degenerative processes, especially calcification, often with secondary tears, but cuspal tears in the absence of calcium deposits and thrombosis predominated at shorter intervals.

The increase in left ventricular ejection fraction produced by postextrasystolic potentiation or epinephrine infusion has been used to demonstrate inotropic contractile reserve in patients with coronary artery disease and a depressed ejection fraction (less than 0.50). Prior studies have shown that a change in ejection fraction of 0.10 or more after postextrasystolic potentiation or epinephrine infusion is helpful in discriminating those patients with a better short-term (1 year) prognosis whether treated medically or surgically. This study related inotropic contractile reserve to 5 year prognosis in 54 patients receiving postextrasystolic potentiation or epinephrine infusion between 1971 and 1974. Current left ventricular function in surviving patients was assessed with radionuclide ventriculograms whenever possible. Five year survival was significantly better in patients with an initial change in ejection fraction greater than 0.10 in both the surgically treated group (16 of 20 versus 5 of 15, p less than 0.01) and the medically treated group (6 of 8 versus 1 of 11, p less than 0.01). Furthermore, among the surviving patients in the surgical group, current ejection fraction in the radionuclide ventriculogram was significantly greater in patients who demonstrated inotropic contractile reserve in their 1971 to 1974 contrast left ventriculogram. These findings support the concept that coronary revascularization enhances function of ischemic but viable myocardium.

Fluosol DA (20%), a perfluocarbon with high oxygen solubility, was administered by concurrent exchange transfusion (30 ml/kg) to anesthetized open-chested adult greyhounds (n = 9) 1 hour after left anterior descending coronary ligation. Mechanical ventilation using 100% oxygen was used throughout the experiment. A second similar group (n = 9) received 0.9% normal saline solution (30 ml/kg), and a third group (n = 9) received no further intervention. Systemic, right atrial, and left atrial pressures were not altered by the exchange transfusion. Monastryl blue dye was injected through the left atrial line at 6 hours after ligation to define the area of myocardium at risk (AR); the animals were then killed and the heart was excised. The left ventricle was sliced at 5 mm intervals and stained using triphenyltetrazolium chloride, defining areas of necrosis (AN). The ratio of AN/AR and total left ventricular mass were then compared with the use of planimetry. The results were as follows: the AN/AR ratio in the 9 control animals was 90 +/- 2 (mean +/- standard error of the mean); in the 9 animals who received saline solution it was 88 +/- 2; and in the animals who received Fluosol it was 67 +/- 4 (p less than 0.01 compared with control; p less than 0.001 compared with the saline group). Fluocarbon exchange transfusion may reduce infarct size when administered after coronary occlusion.

Among 2,004 patients who underwent their first coronary artery bypass graft operation between January 1970 and December 1980 without concomitant valve replacement or aneurysmectomy, life-table survival was 89% at 5 years and 80% at 8 years after surgery. In a multivariate Cox model analysis, the independent correlates of long-term survival were emergent operation with cardiogenic shock (multivariate mortality rate ratio [RR] = 14.0), use of a postoperative intraaortic balloon pump (RR = 3.9), ejection fraction less than 50% (RR = 2.4), preoperative history of congestive heart failure (RR = 2.2), cardiopulmonary bypass time (RR = 1.4 for each 30-minute increment), uncorrected mitral regurgitation (RR = 1.5 for each increment of angiographic gradation), left main coronary artery narrowing (RR = 1.7) and diabetes (RR = 1.6). After controlling for these factors, age, sex and the percentage of narrowings that were bypassed were not independent correlates of long-term survival.

Doppler echocardiographic studies were performed in 21 consecutive patients (mean age 56 +/- 11 years) to evaluate postoperative results of mitral ring anuloplasty. All patients were symptomatic and all had clinically severe isolated mitral regurgitation (MR). The origin of MR was myxomatous degeneration, coronary artery disease, rheumatic heart disease or congestive cardiomyopathy. In 20 patients ring anuloplasty was performed using the Carpentier ring and 1 patient using the Duran ring. Postoperative Doppler echocardiographic studies were performed to detect and semiquantitate residual MR by flow mapping and to identify left ventricular inflow or outflow obstruction. The severity of MR was assessed by flow mapping in the left atrium and graded from I to IV in increasing severity. Blood flow velocity spectra were recorded from the left ventricular outflow tract during systole and from the left ventricle subjacent to the mitral valve during diastole. Pressure half-time, mitral valve area and mitral valve gradient were derived from digitized mitral diastolic flow velocity spectra. After ring valvuloplasty, 9 patients had no MR and 6 had grade I, 3 grade II, 2 grade III and 1 patient grade IV MR. Peak diastolic mitral valve gradient was 8 +/- 4 mm Hg, mean diastolic gradient was 3 +/- 2 mm Hg and pressure half-time was 83 +/- 17 ms, representing a calculated mean mitral valve area of 2.9 +/- 0.8 cm. Peak velocity in the left ventricular outflow tract was 0.9 +/- 0.2 m/s, indicating no obstruction to outflow. Our study confirms that mitral ring valvuloplasty produces a significant reduction in severity of MR, and this is achieved without obstructing left ventricular inflow or outflow.

Open mitral reconstruction for rheumatic mitral stenosis (MS) was performed in 120 patients, 101 women and 19 men, aged 22 to 75 years (mean 49). Nine patients were functional class II, 106 class III, 5 class IV; 13 only underwent noninvasive studies, including echocardiography, before surgery, while 107 had preoperative cardiac catheterization studies. The latter showed a mean valve area of 1.09 cm2 and a pulmonary artery wedge to left ventricular mean diastolic gradient of 14 mm Hg. Cardiopulmonary bypass was used in all patients for open reconstruction under direct vision. Superior commissurotomy was done in 115 patients, inferior in 114, papillary muscles were incised and chordae lengthened in 39 and calcium was excised from valve leaflets in 23. Suture or ring anuloplasty was not required in any patient. The series was begun January 1972 and terminated in January 1984. Personal follow up was conducted in July 1984. There were no operative deaths in the 120 patients. There were 5 late deaths, all from noncardiac causes. The mean follow-up time was 53 months. The actuarial probability of survival at 10 years was 95 +/- 2%. Thromboemboli occurred in 9 patients; the probability of freedom from thromboemboli at 10 years was 91 +/- 3% and the linearized rate was 1.8%/patient-year of follow-up. Reoperation was required in 9 patients, an absolute incidence of 7.5% and an annual incidence of 1.7%/patient year. At 10 years the probability of freedom from reoperation was 84 +/- 5%.

Patients with congenital cardiac shunts in whom marked functional disability, cyanosis and pulmonary arterial hypertension develop have been considered inoperable or at exceedingly high risk. Three adult patients, 2 with atrial septal defect (ASD) and 1 with patent ductus arteriosus (PDA), presented with New York Heart Association class IV symptoms, bidirectional shunting with cyanosis, polycythemia, severe pulmonary hypertension, and increased pulmonary vascular resistance. Pulmonary arterial pressure did not decrease in response to administration of 100% oxygen in any patient, and 2 had lung biopsy results showing advanced pulmonary vascular obstruction. While a right-to-left shunt caused cyanosis in all patients, the net shunt was left to right (Qp/Qs greater than 1) and the resistance ratio (Rp/Rs) less than 0.5. All 3 patients survived operation, became acyanotic with normal hematocrit, and are in functional class I or II a mean of 36 months postoperatively. At repeat cardiac catheterization, pulmonary arterial pressure and resistance had decreased substantially. This high-risk group of patients with bidirectional shunts, in whom cyanosis due to pulmonary vascular obstruction and polycythemia develop and who appear to be at very high operative risk, should still be considered for surgical correction if the usual criteria for operability exist: net left-to-right Qp/Qs and Rp/Rs less than 0.50.

The degree of progressive inward deflection of the stent posts ("stent creep") during function of Hancock standard orifice porcine aortic valve bioprostheses is unknown. The present investigation determines, using a quantitative geometric analysis of clinically removed bioprostheses, the contribution of stent creep to progressive reduction in the outflow orifice area of these valves. Fifty-four Hancock standard orifice porcine aortic valve bioprostheses obtained at reoperation or at autopsy of 50 patients were studied; 47 of these were removed more than 21 months postoperatively. The projected geometric outflow orifice area of each prosthesis was planimetrically measured. To compare prostheses through the entire range of available sizes, this measured area was divided by that of an unimplanted valve of the same size to calculate a ratio designated the "normalized outflow area ratio" (NOAR). Thus, by definition, for all unimplanted standards, NOAR was 1.00. In 7 prostheses in place for less than 1 month, the NOAR was 1.00 +/- 0.03 (mean +/- standard deviation). In 47 prostheses removed 21 to 126 months postoperative, the NOAR was 0.91 +/- 0.08. The relation between NOAR and duration of function determined by linear regression was NOAR = 0.955 - 4.560 X 10(-4) X Duration (in months). The minimum NOAR found was 0.74; the NOAR was less than 0.80 in 4 prostheses (8% of long-term valves). Thus, stent creep is usually not prominent after long-term function of Hancock standard orifice procine bioprostheses and suggests that clinically important progressive reduction of the geometric outflow orifice is infrequent.

This report describes the diagnosis and surgical treatment of a 48 year old patient with congenital right pulmonary arterial ostial stenosis, no intra- or extracardiac shunts and systemic levels of pressure in the main and left pulmonary artery with pulmonary vascular obstruction in the left lung. Operation consisted of a bypass graft of 10 mm woven Dacron from the main pulmonary artery to the distal right pulmonary artery producing an immediate 50 percent reduction in mean left pulmonary arterial pressure. Late postoperative evaluation revealed equal perfusion of both lungs, maintenance of the reduced pulmonary arterial pressure and improvement from New York Heart Association functional class IV to class I.

Insulin was administered to two patients whose diminished myocardial contractility made it difficult to terminate cardiopulmonary bypass. In both instances, bypass was successfully terminated shortly after the insulin injection. These clinical observations led to experiments under the controlled conditions provided by the isolated, working rat heart preparation. The recovery of contractility after 30 minutes of severe ischemia was assessed in all 11 control and 11 insulin-treated hearts. Myocardial performance, as judged by the product of heart rate and peak systolic blood pressure, was significantly greater in the insulin-treated hearts. These clinical observations and experimental findings suggest the need for more extensive study of the potential value of insulin in treating depressed contractility after prolonged myocardial ischemia.