Faculty Bibliography

BACKGROUND: Although retrograde warm continuous cardioplegia (RWCC) has been recently advocated as a method of myocardial preservation during cardiac surgery, scant data exist on the effects of RWCC on right ventricular function. However, previous data have clearly shown that retrograde cardioplegia is poorly distributed to the right ventricle and interventricular septum. This experiment was performed to analyze functional preservation of the right ventricle after RWCC. METHODS AND RESULTS: Fourteen mongrel dogs were instrumented with sonomicrometers and pressure transducers to determine left and right ventricular (LV, RV) pressure-volume relationships and placed on cardiopulmonary bypass. All dogs underwent 90 minutes of aortic cross-clamping with either (1) RWCC (n = 7) after antegrade warm arrest or (2) retrograde cold multidose cardioplegia (RCMC) (n = 7) with topical hypothermia after antegrade cold arrest. All dogs received identical blood cardioplegia solutions. Ventricular function was measured before arrest and 30 and 60 minutes after unclamping. The end-diastolic-work area relationship was calculated, and the slope is presented as percent of baseline (mean +/- SEM; repeated measures ANOVA). At 30 minutes after unclamping, RWCC provided 68.77 +/- 9.09 for the left ventricle and 41.03 +/- 7.49 (P < .05 for RWCC versus RCMC for RV function at 30 minutes) for the right ventricle, and RCMC provided 62.80 +/- 7.23 for the left ventricle and 79.40 +/- 13.82 for the right ventricle. At 60 minutes after unclamping, RWCC provided 58.24 +/- 12.35 for the left ventricle and 48.05 +/- 9.72 for the right ventricle, and RCMC provided 65.38 +/- 6.76 for the left ventricle and 61.95 +/- 8.70 for the right ventricle. (P = NS for RWCC versus RCMC for LV function at either 30 or 60 minutes). These results demonstrate depressed recovery of RV function after 90 minutes of RWCC (P < .05 at 30 minutes after reperfusion) compared with RCMC. No difference in recovery of LV function was detected. CONCLUSION: RWCC may be harmful to the right ventricle and should be used with caution, particularly in patients with preexisting RV hypertrophy

BACKGROUND: With the widespread application of mitral valve reconstructive techniques, systolic anterior motion (SAM) of the anterior mitral leaflet causing left ventricular outflow tract obstruction has been recognized by several groups. SAM occurred in 9.1% of the first 441 patients operated on for mitral valve reconstruction at our institution. Fortunately, SAM subsided with medical therapy within 1 year for a majority of patients as reported in May 1993. Some surgeons, however, have considered abandoning repair for prosthetic replacement after SAM was detected on intraoperative echocardiogram. METHODS AND RESULTS: Since June 1991, a triangular anterior leaflet resection has been cautiously evaluated in patients with extensive anterior leaflet tissue. This has been performed in 23 of 119 patients. CONCLUSIONS: The frequency of SAM in the 119 study patients has decreased from 9.1% to 3.4%

Some surgeons have suggested that the presence of severe calcification in the mitral valve annulus or leaflets precludes successful repair. Our institution has attempted to repair these calcified valves when good annular and leaflet mobility could be achieved by annular debridement and leaflet resection. From June 1979 through June 1993 558 mitral valve repairs were performed using Carpentier's techniques. When calcified valves were encountered, these techniques were modified to include annular debridement and mechanical leaflet decalcification. Calcification was identified preoperatively in 49 patients (8.8%) by either left ventricular fluoroscopy or echocardiography and was debrided in 64 patients (11.5%). This included 24 annular debridements, 28 leaflet debridements, and 12 annular and leaflet debridements. Patient ages ranged from 13 to 83 years (mean age, 62.3 years), and 25 patients (39.1%, 25/64) had concomitant cardiac procedures. Operative mortality was 6.2% (4/64) overall and 2.6% (1/39) for isolated mitral valve repairs. Calcium debridement was performed in 19.3% (23/119) of patients with a rheumatic cause compared with 9.3% (41/439) of the nonrheumatic patients (p < 0.01). Long-term follow-up revealed the necessity for reoperation in 7.8% (5/64) in patients with calcium debridement as compared with 7.7% (38/494) with no debridement (p = not significant). Cumulative freedom from reoperation at 10 years was 83.3% for all patients, 88.1% for debrided patients, and 82.6% for nondebrided patients (p = not significant). Cox proportional hazards analysis revealed that the presence of rheumatic disease significantly increased the risk of reoperation (odds ratio = 3.28; p < 0.001), whereas calcium debridement had no significant effect. These results demonstrate that when good annulus and leaflet motion can be achieved in calcified mitral valves, calcium debridement allows durable repairs

Neointimal hyperplasia limits the long-term patency of saphenous vein grafts (SVGs), but is notably absent from most internal mammary artery (IMA) grafts. Basic fibroblast growth factor (bFGF) is a local endothelial and vascular smooth muscle mitogen known to be involved in the pathogenesis of neointimal hyperplasia. This study used an animal model to compare the number of available high-affinity (HAR) and low-affinity (LAR) bFGF receptors in SVGs and IMA grafts and to determine whether distention injury causes an increase in receptor availability. The IMA and SVG specimens were harvested from 12 dogs and distended at 25 or 200 mm Hg for 15 minutes, and then the bFGF receptor uptake was measured in them using iodine 125-labeled bFGF. In the IMA conduits distended at low pressure, there were 2.54 +/- 0.10 (mean +/- standard error of the mean) HARs per mm2 of intimal surface area available and 5.19 +/- 0.40 LARs per mm2. High-pressure distention significantly (p < 0.001) increased the number of available HARs to 5.06 +/- 0.27 per mm2 and of LARs to 7.27 +/- 0.042 per mm2. At low pressure, the SVGs had significantly (p < 0.001) more HARs (9.14 +/- 0.84 per mm2) and LARs (18.2 +/- 0.57 per mm2) available than did the IMA conduits, and high pressure significantly (p < 0.001) increased the number of HARs available in SVGs to 24.1 +/- 2.43 per mm2 and the number of LARs to 44.7 +/- 2.34 per mm2.(ABSTRACT TRUNCATED AT 250 WORDS)

BACKGROUND. Basic fibroblast growth factor (bFGF) is a potent local promoter of vascular smooth muscle cell migration and proliferation and may play a major role in the pathogenesis of intimal fibromuscular lesions. Preliminary studies have shown that exogenous bFGF localizes to injured rabbit aorta and suggest that this interaction might be inhibited by anti-bFGF immunoglobulin (Ig) G. This study was designed to evaluate the possible role of polyclonal anti-bFGF IgG in reducing intimal fibromuscular lesion formation in the injured rabbit aorta. METHODS. The abdominal aortic endothelium was subjected to balloon injury in 13 rabbits. Six rabbits received intravenous rabbit anti-bFGF IgG, and seven received irrelevant rabbit IgG (16 micrograms/kg) 30 minutes before injury and daily for 5 days after injury. At 14 days after injury the aorta was fixed and sectioned, and the intimal and medial areas were measured by computerized digital morphometry with the intimal/medial ratio as an index of neointimal lesion formation. RESULTS. In the control group the intimal/medial ratio was 0.538 +/- 0.046 (mean +/- SEM), which was significantly greater than the anti-bFGF-treated group value of 0.148 +/- 0.021 (p < 0.001). CONCLUSIONS. These results show that daily doses of intravenous polyclonal anti-bFGF IgG for 5 days after balloon aortic injury significantly inhibit intimal fibromuscular lesion formation at 14 days. The results suggest that the process of intimal fibromuscular lesion formation may be susceptible to modification by antagonists to bFGF

The goal of this study was to review the short-term and long- term results of aggressive corrective intervention in a consecutive series of patients with atrioventricular canal defects, especially with respect to minimizing progressive valvular insufficiency or pulmonary hypertension. A total of 46 consecutive patients with atrioventricular canal defects had operative repair between 1981 and 1991, using a two-patch technique in all but 4 patients. The median age was 8.5 months, with 29 patients (63%) < 1 year old. Left-to-right shunting was severe in all cases (mean Qp/Qs = 2.9:1), with a mean systolic pulmonary artery pressure of 63.6 mm Hg and a mean pulmonary vascular resistance of 4.03 Wood units. Preoperatively, 35 patients (76.1%) had moderate to severe congestive heart failure. Hospital mortality was 6.5% (3 patients), and the systolic pulmonary artery pressure dropped significantly in all cases, with a postrepair mean of 25.7 mm Hg. The 5 year actuarial survival rate was 70.3%. Late echocardiographic studies graded mitral insufficiency as 0-2+ in 41 patients (95.2%) and 3-4+ in 2 patients (4.6%); 2 patients required reoperation, and 41 (95.2%) were New York heart Association functional class I at follow-up. These data demonstrate excellent lat survival and functional results when complete atrioventricular canal correction is performed in infancy, despite significant preoperative pulmonary hypertension, valvular insufficiency, or symptoms. Prompt operative repair should be done for symptomatic patients and those with valvular incompetence; electrive repair is recommended before 1 year of age for most others