Rereplacement of the mitral valve with represervation of the subvalvular apparatus.
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Biomedical subjects
Publications and source records attributed to G N Olinger.
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Saphenous veins are placed frequently in storage solutions before use as coronary bypass grafts. Controversy remains regarding which solution is optimal for the preservation of endothelium and vascular smooth muscle viability. Thus, this study measured the effect of four different storage solutions on saphenous vein smooth muscle and endothelial cell function. Saphenous vein segments from five baboons were stored for 3 h in one of four storage solutions consisting of physiological salt solution (PSS), University of Wisconsin solution (UWS), normal saline solution (NSS), or autologous whole blood (WB). Following storage, veins were suspended for isometric tension recording in tissue baths filled with PSS. Veins stored in PSS, UWS, and NSS showed similar contractile amplitude and agonist sensitivity to norepinephrine (10(-8) -10(-4) M) and KCl (20-100 mM). However, veins stored in WB contracted 31% less to KCl on average than those stored in the other three solutions (p < 0.05). The direct vascular muscle vasodilator, papaverine (10(-7) -10(-4) M), and the endothelium-dependent dilator, A23187 (10(-5) M), relaxed all vein preparations equally well. These results suggest that after storage in PSS, UWS, and NSS, contractile and relaxant vascular responses are similar in isolated saphenous veins. However, although veins stored in WB show comparable relaxation responses, they demonstrate an impaired vascular contraction immediately after storage. We conclude that storage of veins in blood may immediately modify vascular smooth muscle function.
Temporary atrial pacing leads have uncontested utility for diagnosis and treatment of postoperative supraventricular arrhythmias. Sensing and capture thresholds may be inconsistent, however. We evaluated intraoperative atrial sensing amplitude and capture thresholds in 25 patients after coronary bypass using six bipolar and four unipolar lead combinations based on four lead positions: A, atrial appendage; B, 1 cm above the presumed sinoatrial node at the atrial-superior-vena caval junction; C, interatrial groove at the right superior pulmonary vein; and D, caudal inferolateral free wall. Unipolar lead B and bipolar lead B-D had the best voltage pacing threshold and system resistance (p less than 0.05). The lowest current was also observed with unipolar lead B and bipolar lead B-D, but the difference was not significant (p greater than 0.05). P-wave amplitude was not significantly different for any lead combination. Location C, in unipolar or bipolar combinations, frequently paced the phrenic nerve. These data provide new guidelines for establishment of postoperative temporary atrial pacing leads.
This study was designed to measure the effect of ambient temperature (25 degrees C) on papaverine-induced relaxations in canine saphenous veins. Segments of vein were suspended in water-jacketed tissue baths at 37 degrees C, and isometric tension was recorded. After equilibration, veins were preconstricted by a median effective dose of norepinephrine 2 x 10(-6) mol/L at either 25 degrees C or 37 degrees C. Consequent dose-dependent relaxations showed that papaverine (10(-7) to 10(-3) mol/L was three times more potent as a dilator at 37 degrees C than at 25 degrees C, with half-maximal relaxations occurring at 2.2 x 10(-5) mol/L and 6.4 x 10(-5) mol/L, respectively. A 10(-4) mol/L dose of papaverine completely relaxed veins at 37 degrees C, whereas veins at 25 degrees C never fully relaxed even at ten times the standard concentration. In addition, the time for half-maximal relaxation with a 10(-4) mol/L dose of papaverine averaged 40 minutes at 25 degrees C compared with 22 minutes at 37 degrees C; this is indicative of a reduced relaxation rate at the lower temperature. These data show that papaverine is a slower and less potent dilator of canine saphenous veins at 25 degrees C than at 37 degrees C. This may have implications for the use of papaverine in the operating room, where it is usually applied at ambient temperature to reduce vasospasm of the saphenous vein during coronary artery bypass procedures.
Clinical application of hypothermic pharmacologic cardioplegia in pediatric cardiac surgery is less than satisfactory, despite its well known benefits in adults. Protection of the ischemic immature rabbit heart with hypothermia alone is better than with hypothermic St. Thomas' II cardioplegic solution. Control of cellular calcium is a critical component of cardioplegic protection. We determined whether the existing calcium content of St. Thomas' II solution (1.2 mmol/L) is responsible for suboptimal protection of the ischemic immature rabbit heart. Modified hypothermic St. Thomas' II solutions (calcium content, 0 to 2.4 mmol/L) were compared with hypothermic Krebs bicarbonate buffer in protecting ischemic immature (7- to 10-day-old) hearts. Hearts (n = 6 per group) underwent aerobic "working" perfusion with Krebs buffer, and cardiac function was measured. The hearts were then arrested with a 3-minute infusion of either cold (14 degrees C) Krebs buffer (1.8 mmol calcium/L) as hypothermia alone or cold St. Thomas' II solution before 6 hours of hypothermic (14 degrees C) global ischemia. Hearts were reperfused, and postischemic enzyme leakage and recovery of function were measured. A bell-shaped dose-response profile for calcium was observed for recovery of aortic flow but not for creatine kinase leakage, with improved protection at lower calcium concentrations. Optimal myocardial protection occurred at a calcium content of 0.3 mmol/L, which was better than with hypothermia alone and standard St. Thomas' II solution. We conclude that the existing calcium content of St. Thomas' II solution is responsible, in part, for its damaging effect on the ischemic immature rabbit heart.
Relatively few methods have been described for the creation of valvular insufficiency in an animal model. Those presented involve limitations such as permanent destruction of the valves or lack of control over the degree of regurgitation produced. We describe a method of acute reversible tricuspid insufficiency that can be easily created and controlled in anesthetized dogs. The model employs a wire spiral that is advanced through the atrioventricular canal from the right atrium. The spiral causes regurgitation by preventing complete apposition of the valve leaflets while permitting retrograde flow to occur through the spiral lumen. The degree of regurgitation can be controlled by the use of spirals of different sizes. Creation of tricuspid insufficiency is demonstrated by the onset of right atrial pressure V waves, a "ballooning" of the right atrium during ventricular systole, palpation of an atrial thrill, or by color Doppler echocardiography. In 14 dogs, right atrial pressure increased from a control value of 9 +/- 3 (mean +/- SD) mmHg to 10 +/- 3 and 12 +/- 3 mmHg, respectively, with spirals of 1.5 and 2.2 cm in diameter (both P less than 0.05). With the 2.2-cm spiral, aortic blood pressure decreased from a control value of 104 +/- 20 to 83 +/- 17 mmHg (P less than 0.05), and cardiac output decreased from 73 +/- 26 to 59 +/- 19 ml.min-1.kg-1 (P less than 0.05). This model is reversible, allows repeated trials of various grades of regurgitation, does not require ventriculotomy, and is relatively nonarrhythmogenic.
The objectives of this study were to determine whether veins subjected to barotrauma in situ undergo lipid uptake and morphologic changes to the same extent as veins grafted into the arterial circulation. Saphenous veins in seven stump-tailed macaque monkeys were exposed bilaterally and were circumferentially dissected free from surrounding tissue only at isolated sites. Segments of the veins were distended for 1 minute at hydrostatic pressures of 125 or 350 mm Hg. An undistended segment served as control. A cephalic vein graft was interposed in the femoral artery for comparison with in situ veins. The animals were fed a diet that sustains plasma cholesterol levels of approximately 225 mg/dl. Saphenous veins and the cephalic vein grafts were explanted at 3 months for biochemical and histologic analyses. Cholesterol content in undistended saphenous veins was similar to that in veins distended at 125 or 350 mm Hg--105 +/- 15, 122 +/- 14, and 109 +/- 30 micrograms/100 mg wet tissue weight, respectively. Cholesterol content in cephalic vein grafts, 473 +/- 122 micrograms/100 mg, was greater (p less than 0.001) than in saphenous veins at all distention pressures studied. There was no difference among the distention pressures in the intimal fraction of saphenous vein wall, with the pooled value being 20% +/- 12%. This contrasted with the value of 59% +/- 11% in cephalic vein grafts (p less than 0.01). Endothelial coverage of the luminal surface in saphenous veins was similar among the levels of barotrauma, with the pooled value being 83% +/- 15%. Less of the lumen was covered with endothelium in cephalic vein grafts, 46% +/- 18% (p less than 0.01). Slightly more medial fibrosis was observed in cephalic vein grafts as compared with saphenous veins (p less than 0.05). These data demonstrate that barotrauma alone does not cause veins that remain in the venous system to undergo the lipid uptake or morphologic changes that occur in veins grafted into the arterial circulation in nonhuman primates.
Computed tomography is used with increasing frequency to evaluate blunt chest trauma. Since traumatic aortic rupture (TAR) is a rapidly lethal condition, unnecessary CT scanning may not be justified. To determine the accuracy of chest CT scanning for TAR, we reviewed 17 patients who underwent both chest CT scanning and aortography. Five patients had TAR by aortography. CT scanning yielded three true positives and two false negatives. In 12 patients with a negative aortogram, CT scanning recorded four false positives and eight true negatives. The specificity was 23% and the sensitivity was 83% compared with aortography. The overall accuracy for CT scanning was 53%. From these data we conclude that in the presence of an unstable patient or where there is a strong clinical suspicion of TAR the patient should proceed directly to aortography.
The known benefits of hypothermic pharmacological cardioplegia in protecting the ischemic adult heart may not extend to children. Protection of the ischemic immature rabbit heart with hypothermic Krebs-Henseleit bicarbonate buffer is better than with hypothermic St. Thomas' II cardioplegic solution. We investigated whether the availability of oxygen in the preischemic perfusate is responsible for the increased tolerance to ischemia of immature (7- to 10-day-old) hearts perfused with Krebs buffer in comparison with St. Thomas' II solution immediately before ischemia. After obtaining preischemic control data in the "working" mode, we perfused hearts (n = 8 per group) for 3 minutes with hypothermic (14 degrees C) Krebs buffer or hypothermic St. Thomas' II solution saturated with 0%, 25%, or 95% oxygen. This was followed by 2 hours of global ischemia at 14 degrees C. Hearts were reperfused for 15 minutes in the Langendorff mode and 35 minutes in the working mode, and recovery of function was measured. For preischemic oxygen concentrations of 0%, 25%, and 95%, recovery of aortic flow in hearts protected by hypothermia alone during ischemia was 74% +/- 9%, 82% +/- 4%, and 99% +/- 2% of preischemic values, respectively. In hearts protected by hypothermia plus cardioplegia, the values were 69% +/- 6%, 72% +/- 3%, and 86% +/- 5%, respectively. Thus, at equal oxygen concentrations, recovery of postischemic function was better in hearts protected by hypothermia alone compared with hypothermia plus cardioplegia. We conclude that factors other than oxygen availability are responsible for the damaging effect of St. Thomas' II solution on the ischemic immature rabbit heart.
Elevated pulmonary vascular resistance (PVR), differential cardiac dynamics, and increased lung water following cardiopulmonary bypass (CPB) have been proposed as limitations to the accuracy of the pulmonary artery occlusion pressure (PAOP) in estimating left ventricular preload. A prospective study of 22 patients undergoing elective myocardial revascularization is described wherein PAOP was compared with directly measured left atrial pressure (LAP). The reliability of PAOP to estimate LAP in the hour immediately following CPB and at 1, 4, 8, and 12 hours post-CPB was examined with repeated measures analysis of variance. Relationships between the PAOP-LAP difference and PVR, core temperature, arterial CO2 tension, and right and left ventricular stroke work indices (RVSWI, LVSWI) were tested by linear regression analysis. There was greater variability in measurements at 15, 30, and 45 minutes immediately after CPB, demonstrated by a pooled correlation coefficient of 0.73 versus 0.90 in the postoperative period. The degree of discrepancy between PAOP and LAP lessened with time. There was no determinable relationship of the PAOP-LAP gradient to PVR, level of PCO2, temperature, RVSWI, or LVSWI. Potential sources of discrepancy include airway pressure effects, position of the measuring catheters, positive end-expiratory pressure, infusion of protamine sulfate, extremes of pulmonary artery pressures, and effects of an open pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)
The objective of this study was to determine the early influence of platelet inhibition on the histologic, morphometric, and biochemical evolution of vein bypass grafts in a nonhuman primate model. Cephalic vein grafts were interposed bilaterally in the femoral arteries of 15 stump-tailed macaque monkeys fed a diet that sustains plasma cholesterol levels of approximately 225 mg/dl. All animals received in combination aspirin, 80 mg/day, and dipyridamole, 50 mg/day. Grafts were excised from five animals for analysis on each of postoperative days 3, 7, 14, 30, 60, and 90. In animals subjected to platelet inhibition, cholesterol content in the graft was 170 +/- 52 micrograms/100 mg at 90 days, 205% of the level in ungrafted vein (p less than 0.01). This change was small in comparison with the increase to 686% of ungrafted vein observed in our study of control animals. In stepwise regression analysis, cholesterol content of grafts was best predicted by prevalence of foam cells (r2 = 0.82), and the proportion of intima as a fraction of total wall area was best predicted by the presence of macrophages (r2 = 0.69). Platelet inhibition did not decrease the extent of intimal hyperplasia. The prevalence of adherent platelets (r = -0.72) and the amount of fibrin (r = -0.78) correlated inversely with the amount of endothelium present during the first 14 days. The strength of these correlations declined with time, despite persistent lack of endothelium in some areas. Medial fibrosis occurred to the same extent as in control grafts, as did the early appearance of platelet factor VIII and fibronectin and the lack of vasa vasorum at 3 days followed by reappearance at 7 days. These data demonstrate that platelet inhibition dramatically reduces lipid uptake by grafts in the first 90 days but has less influence over histologic or morphometric changes.
The objective of this study was to define the histologic and morphometric evolution that accompanies the increase in cholesterol content of vein bypass grafts in a nonhuman primate model. Cephalic vein grafts were interposed bilaterally in the femoral arteries of 15 stump-tailed macaque monkeys (Macaca arctoides), which were fed a diet that sustains plasma cholesterol levels of approximately 225 mg/dl. Grafts were excised from five animals for analysis on each of postoperative days 3, 7, 14, 30, 60, and 90. Cholesterol content increased from 69 +/- 24 micrograms/100 mg (mean +/- standard deviation) in ungrafted vein to 473 +/- 122 micrograms/100 mg in grafts 90 days after implantation (p less than 0.05). By stepwise regression analysis, cholesterol content was best predicted by abundance of foam cells (r2 = 0.82). Intima comprised 13% +/- 5% of the total cross-sectional area of the wall in ungrafted vein and 59% +/- 11% at day 90 (p less than 0.001). With cholesterol content excluded from the stepwise regression, intimal area was best predicted by the presence of foam cells (r2 = 0.39). There was consistently an increase in the prevalence of polymorphonuclear leukocytes on the luminal surface and in both the intima and media during the first 14 days after grafting. Vasa vasorum, which were always present in ungrafted vein, were sparse at 3 days but reappeared by day 7. Medial fibrosis occurred in grafts, and in the 30- to 90-day interval it was directly correlated with the number of adventitial vasa vasorum present (r = 0.64, p less than 0.05). Immunohistochemistry revealed prominent staining for both platelet factor VIII and fibronectin during the first month, with a gradual decline in staining intensity thereafter. The evolution of changes in vein bypass grafts documented in this report are in general agreement with graft changes observed in humans and support the validity of our model in evaluating the histologic correlates of increased graft cholesterol content.
Hypothermia combined with pharmacologic cardioplegia protects the globally ischemic adult heart, but this benefit may not extend to children, resulting in poor postischemic recovery of function and increased mortality. The relative susceptibilities to ischemia modified by hypothermia alone and by hypothermia plus cardioplegia were assessed in isolated perfused neonatal (3- to 4-day-old) rabbit and pig hearts. Hearts were perfused aerobically with Krebs buffer solution in the working mode for 30 minutes and aortic flow was recorded. This was followed by 3 minutes of hypothermic (14 degrees C) coronary perfusion with either Krebs or St. Thomas' Hospital cardioplegic solution No. 2 followed by hypothermic (14 degrees C) global ischemia (rabbits 2, 4, and 6 hours; pigs 2 and 4 hours). Hearts were reperfused for 15 minutes in the Langendorff mode and 30 minutes in the working mode, and recovery of postischemic aortic flow was measured. Hypothermia alone provided excellent protection of the ischemic neonatal rabbit heart, with recovery of aortic flow after 2 and 4 hours of ischemia at 91% +/- 4% and 87% +/- 5% (mean +/- standard deviation) of its preischemic value. Recovery after 6 hours of ischemia was depressed to 58% +/- 9% of its preischemic value. Ischemic neonatal pig hearts protected with hypothermia alone recovered 94% +/- 3% of preischemic aortic flow after 2 hours; none was able to generate flow after 4 hours. St. Thomas' Hospital solution No. 2 decreased postischemic aortic flow after 4 hours of ischemia in rabbit hearts from 87% +/- 5% to 70% +/- 7% (p less than 0.05, hypothermia alone versus hypothermia plus cardioplegia) but improved postischemic recovery of aortic flow in pig hearts after 4 hours of ischemia from 0 to 73% +/- 13% (p less than 0.0001, hypothermia alone versus hypothermia plus cardioplegia). This effect was dose related in both species. We conclude that the neonatal pig heart is more susceptible to ischemia modified by hypothermia alone than the neonatal rabbit and that St. Thomas' Hospital solution No. 2 improves postischemic recovery of function in the neonatal pig but decreases it in the neonatal rabbit. This species-dependent protection of the neonatal heart may be related to differences in the extent of myocardial maturity at the time of study.
The objectives of this study were to elucidate the long-term influence on vein bypass grafts of platelet inhibition and its late discontinuation. Cephalic vein grafts were interposed bilaterally in the femoral arteries of stump-tailed macaque monkeys fed a diet that sustains plasma cholesterol levels of approximately 225 mg/dl. Fifteen animals were divided into three groups of five animals each. Group I received no medications and served as a control group. Group II received for the full duration of the study a combination of aspirin, 80 mg/day, and dipyridamole, 50 mg/day. Group III received the same regimen of platelet inhibition as in group II during the first 9 months, but were not treated during the subsequent 9-month interval. Grafts were excised for analysis from groups I and II at both 9 and 18 months and from group III at 18 months. Cholesterol content in group I grafts was 470 +/- 89 micrograms/100 mg at 9 months and 388 +/- 127 micrograms/100 mg at 18 months. In group II grafts, cholesterol content was 208 +/- 72 micrograms/100 mg at 9 months (p less than 0.001 compared with group I) and 266 +/- 84 micrograms/100 mg at 18 months. In group III grafts, cholesterol content was 249 +/- 71 micrograms/100 mg at 18 months. Differences in cholesterol content among the three groups of grafts at 18 months were not found to be statistically significant. Stepwise regression analysis at 18 months showed that cholesterol content was best predicted by medial fibrosis (r2 = 0.66) followed by abundance of foam cells (increase in r2 = 0.26) in group I, by fibrin in group II (r2 = 0.63), and by prevalence of macrophages in group III (r2 = 0.74). In all groups, platelets, fibrin, and polymorphonuclear leukocytes were less abundant than they had been at 3 months. Cross-sectional area occupied by the intima was not influenced by platelet inhibition.
This study was designed to evaluate separately the influence of restoration of distal pulse pressure and the influence of factors related to operation upon hemodynamic and hormonal alterations accompanying repair of canine aortic coarctation. Eight normal adult dogs underwent a sham operation and served as controls. In 10 dogs the thoracic aorta was transfected and reanastomosed. In 10 dogs aortic coarctation was created within 1 week of birth by banding the aorta just proximal to the ductus ligament, thereby fixing lumenal diameter at 1 to 2 mm. Studies were performed in the latter animals 18 months after operation. These dogs were subdivided into two groups: one (n = 6) underwent surgical repair of the coarctation; in the other (n = 4), the coarctation was repaired and an occluder was placed on the aorta to maintain distal aortic pulse pressure at its diminished preoperative level. Normal distal pulse pressure was restored in these animals by releasing the occluder 1 week after recovery from the repair of coarctation. Each dog was studied in the conscious state before the definitive procedure and again 24 hr later. Plasma renin activity increased significantly after operation in the sham and in the transection groups. Renin activity and proximal blood pressure were significantly elevated and distal pulse pressure was diminished preoperatively in both the repair and the occluder groups. After their respective definitive procedures, the elevation in renin activity and in proximal pressure persisted in the repair group but decreased in the occluder group.(ABSTRACT TRUNCATED AT 250 WORDS)
The automatic implantable cardioverter-defibrillator is tested intraoperatively with defibrillation trials to ensure effectiveness. It is unknown if the energy requirement for internal defibrillation remains stable and that once demonstrated effective, if the device will continue to be effective in terminating lethal ventricular arrhythmias. In this study, the defibrillation energy requirement was compared in 56 patients at the time of lead implantation to that obtained at the time of generator replacement. Mean time to generator replacement was 17. +/- 6.6 months. The defibrillation threshold was stable over that time (11.9 +/- 6.7 joules compared to 12.7 +/- 8.4 joules, NS). There was no relation between transmyocardial impedance and defibrillation threshold. In addition, no effect on defibrillation threshold was demonstrated by the use of various cardiac medications, concomitant surgery or the occurrence of clinical shocks during follow-up.
Paradoxical hypotension during rapid infusion of plasma protein fraction (PPF) has been attributed to vasodilation by bradykinin in PPF. This study employed a canine, controlled right heart bypass preparation to assess changes in systemic vascular resistance and venous capacitance during infusion of PPF and other possibly vasoactive mediators. Plasma protein fraction caused consistent vasodilation, whereas purified human albumin did not. This vasodilation could be ascribed entirely to acetate, present in PPF as a buffer. Bradykinin in PPF had no effect during venous infusion. Acetate is used widely as a buffer in intravenous and dialysate solutions. Its vasoactive properties must be recognized when such solutions are administered to patients with limited capacity to compensate for sudden vasodilation.
Major noncardiac surgery is a serious hazard to patients with advanced coronary disease. Perioperative infarction is common, and preliminary coronary bypass is often unwarranted. We suggest that the use of the intra-aortic balloon pump (IABP) for perioperative support of such patients makes perioperative infarction unlikely and permits otherwise hazardous operations. Three patients with advanced coronary disease (unstable angina in two) had major thoracotomies for lung masses without cardiac complications. This management plan has wider implications for other noncardiac surgical problems in such patients, particularly for mandatory operations wuch as relieving intestinal obstructions.