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Biomedical subjects

V L Gott

Publications and source records attributed to V L Gott.

At least 91 records · Page 5Linked to original sources

Beneficial effects of adding propranolol to multidose potassium cardioplegia.

The use of propranolol with multidose potassium cardioplegia was studied in 32 in situ canine hearts subjected to 90 minutes of global ischemia at 15 degrees C and 60 minutes of reperfusion at 37 degrees C. All hearts received potassium (37 mEq/l) every 30 minutes during ischemia. There were four groups of equal size: group 1 received no propranolol, group 2 received low-dose propranolol and group 3 received high-dose propranolol. Group 4 received high-dose propranolol only with the initial potassium infusion. Myocardial CO2 (PmCO2) was monitored by mass spectrometry as an indicator of metabolic activity. An intraventricular balloon was used to measure isovolumic developed pressure, maximal dP/dt and end-diastolic pressure (EDP) before and after ischemia. During ischemia, peak PmCO2 was significantly higher in group 1 (45.6 +/- 2.8 mm Hg) than in groups 2, 3 and 4 (35.2 +/- 2.8 mm Hg, 33.4 +/- 2.8 mm Hg and 30.4 +/0 2.8 mm Hg, respectively) (p less than 0.05). There were no differences between the four groups in systolic ventricular function assessed by developed pressure and dP/dt. Hearts that received high-dose propranolol had significantly lower EDP after 60 minutes of reperfusion (group 3 13.3 +/- 1.5 mm Hg, group 4 10.4 +/0 1.5 mm Hg) compared with group 1 hearts (25.3 +/- 3.8 mm Hg, p less than 0.05). Hearts in groups 3 and 4 exhibited less ischemic injury as assessed by electron microscopy than hearts in groups 1 and 2. These data show that propranolol added to multidose potassium cardioplegia reduced metabolic activity during ischemia and improved ventricular compliance during reperfusion without depressing systolic function. Because left ventricular compliance and morphologic preservation were similar in groups 3 and 4, it appears that a single high dose of propranolol is sufficient and that subsequent doses do not further enhance the beneficial effects.

Animals↗

Automatic defibrillation in man. The initial surgical experience.

The automatic implantable defibrillator is an electronic device designed to detect and promptly correct malignant ventricular arrhythmias. Nineteen patients, all survivors of multiple cardiac arrests because of ventricular arrhythmias unresponsive to therapy, have undergone implantation of the automatic defibrillator. In seven patients who had had a previous cardiac operation, implantation was performed through a left lateral thoracotomy. A median sternotomy was used in five patients without a previous operation. In six patients cardiac procedures were performed concomitantly with defibrillator implantation. There were no operative deaths. The average follow-up is 6 months, the longest being 14 months. Following implantation, 47 episodes of malignant ventricular arrhythmias were documented. Twenty-six occurred spontaneously (17 of them outside the hospital); all were corrected with a single 25 joule pulse. Seventeen of 21 arrhythmias induced postoperatively were terminated. Although further validation is required, this study demonstrates that the automatic defibrillator is capable of diagnosing and terminating potentially lethal ventricular arrhythmias. Finally, implantation can be safely accomplished in an exceedingly high risk population.

Adolescent↗

Surgical management of patients with the Marfan syndrome and dilatation of the ascending aorta.

Until recently, surgical correction of Marfan defects of the aortic root has been undertaken with some hesitancy because of the high perioperative risk. The Division of Medical Genetics at Johns Hopkins follows about 300 patients with the Marfan syndrome, and during the past 8 years 13 of these were referred to the senior author (V.L.G.) for aortic valve replacement and repair of the ascending aorta. Preoperatively, four of the 13 patients were in New York Heart Association (NYHA) Class IV (3/4 required emergency operation), three patients were in Class III, and six were in Class II. The aortic diameter at the mid-valve level ranged from 5.3 cm to 8.2 cm on M-mode echocardiography. The first two patients received a separate Björk-Shiley prosthesis and a woven Teflon graft and the last 11 patients had a composite valve-graft with direct coronary implantation. There were no hospital deaths. Follow-up ranges from 6 months to 8.1 years and is complete for all 13 patients (mean of 23 months). Two late deaths occurred 2 and 20 months postoperatively from presumed arrhythmia and two late deaths occurred at 4 and 6 months from endocarditis. The actuarial survival rate at 3 years is 61%. Some pathologists claim that the incidence of dissection of the aorta does not increase with increasing aortic dilatation in the Marfan patient. Six of our 13 patients, however, had aortic dissection at the time of surgery (two DeBakey Type I, three Type II, and one Type III). With the low hospital mortality that can now be achieved in the Marfan patient, and with the relatively high incidence of clinically unrecognized dissection, we fell that strong consideration should be given to earlier prophylactic repair in these patients. Operation may be indicated even in the asymptomatic Marfan patient with an aortic root diameter greater than 5.5 cm.

Adult↗

Unstable angina pectoris. Factors influencing operative risk.

Experience was reviewed with 471 consecutive patients who had coronary artery bypass (CAB) operation alone. The hospital mortality rate was 2% in 341 patients operated on for treatment of stable angina pectoris. There were ten deaths (7.7%) in the 130 patients who underwent CAB for treatment of unstable angina. In this series, age greater than 70 years, poor left ventricular function, distal coronary arteries unfavorable for grafting and the presence of main left coronary artery disease were factors associated with increased operative mortality. In 78 patients with unstable angina who had none of these increased risk factors, the mortality rate was 1.3%. Hospital mortality was 33% in patients older than 70 years and 29% in patients with poor left ventricular function and/or distal vessels unfavorable for grafting. In 23 of the 130 patients, the only increased risk factor present was severe stenosis of the main left coronary artery and one of them (4.3%) died. Thus, when elderly patients and patients with poor left ventricular function or poor distal vessels were excluded, the hospital mortality rate associated with CAB in patients with unstable angina was low (2.0%, 2/101 patients) and equal to that for operation in patients with stable angina pectoris.

Adult↗

Comparison of the effects of left ventricular distention during cardioplegic-induced ischemic arrest and ventricular fibrillation.

To evaluate the role of left ventricular distention in the pathophysiology of myocardial injury during cardiac surgery, 40 isolated, perfused feline hearts were subjected to 1 hour of either hypothermic potassium arrest (groups 1, 2 and 3) or 1 hour of hypothermic ventricular fibrilation (groups 4 and 5). During this period, intracavitary left ventricular pressure was maintained at 0 mm Hg in groups 1 and 4, at 30 mm Hg in groups 2 and 5 and 45 mm Hg in group 3. After either reperfusion of defibrillation, myocardial gas tensions, left ventricular function, coronary blood flow, the ration of endocardial to epicardial blood flow, and myocardial water content were measured to evaluate the degree of myocardial injury incurred. In addition, structural changes in the myocardium were assessed using light and electron microscopy. No differences in these parameters were seen in hearts that underwent ischemic arrest, regardless of the presence or absence of significant left ventricular distention. In fibrillating hearts, however, dilatation decreased ventricular performance, impaired subendocaridal blood flow and elevated myocardial CO2 tensions. These results suggest that left ventricular distention per se is not harmful during periods of ischemia. During periods of ventricular fibrillation, howevr, distention produces impaired subendocardial blood flow, resulting increased ischemia and decreased recovery of ventricular performance.

Animals↗

Mass spectrometry and phosphorus-31 nuclear magnetic resonance demonstrate additive myocardial protection by potassium cardioplegia and hypothermia during global ischemia.

Previous studies from this laboratory utilized mass spectrometry to measure myocardial oxygen (PO2) and carbon dioxide (PCO2) tensions in isolated feline hearts subjected to periods of global ischemia and reperfusion. Myocardial carbon dioxide tension was found to increase during ischemia, and its rate of increase was found to correlate inversely with subsequent recovery of myocardial function following reflow. The present study utilized phosphorus-31 nuclear magnetic resonance (NMR) to assess whether the severity of intracellular acidosis or the depletion of high energy phosphate stores would show a similar correlation with recovery of function. Hyperkalemic cardioplegia employed as a myocardial preservation technqiue in combination with hypothermia was compared with hypothermia alone as the control intervention. The experimental results demonstrated that intracellular pH fell to 6.09 +/- 0.13 with hypothermia alone and to 6.31 +/- 0.09 with cardioplegia plus hypothermia. Furthermore, myocardial ATP content fell to 22% +/- 2% of control with hypothermia alone, while falling to 36% +/- 4% of control with the combined therapy. Recovery of myocardial performance was found to correlate inversely with the severity of intracellular acidosis and depletion of ATP during ischemia. In contrast, no relationship was observed between preservation of phosphoryl-creatinine levels either during ischemia or after reflow and recovery of ventricular function. These results suggest that, similar to mass spectrometry, which allows monitoring of myocardial PCO2, 31P NMR permits the on-line monitoring of intracellular pH as well as high energy phosphate compounds, and thereby provides useful metabolic indices of the severity of ischemia. Since tight coupling was found between changes in these parameters and subsequent recovery of contractile performance, further development of 31P NMR for evaluation of techniques designed to minimize the severity of ischemic damage would seem indicated.

Acidosis↗

Routine use of autotransfusion following cardiac surgery: experience in 700 patients.

An autotransfusion technique has been developed for collection and reinfusion of shed mediastinal blood. This system has been routinely applied in the postoperative management of 592 consecutive adult and 108 pediatric cardiac surgical patients. Two hundred seventy-one adult patients (46%) and thirty-six pediatric patients (33%) actually received autologous blood. Autotransfusion volume ranged from 50 to 21,350 ml per patient. In 1976 at our institution, homologous transfusion requirements averaged 8.4 +/- 0.7 units per adult patient. During 1978, with the routine use of postoperative autotransfusion, bank blood transfusions were lowered to 4.2 +/- 0.3 units per patient (p less than 0.001). In contrast to perioperative autotransfusion techniques, collection and reinfusion of shed mediastinal blood is particularly useful for intravascular volume replacement in patients with serious postoperative bleeding.

Adult↗

Beneficial effects of pulsatile perfusion in the hypertrophied ventricle during ventricular fibrillation.

To assess the potential benefit of pulsatile perfusion inthe hypertrophied heart during fibrillation, 10 dogs with left ventricular hypertrophy, produced by previous supravalvular aortic banding, were used to compare linear and pulsatile perfusion in the fibrillating heart during total cardiopulmonary bypass. The mass spectrometer was used to measure subendocardial PCO2 and PO2 (PmCO2 and PmO2), and radioactive microspheres were utilized to measure myocardial blood flow in the same layers. Pulsatile perfusion was established using the recently develop "bubble tubing," which produces a pulse pressure of at least 20 mm Hg and can be used in a standard roller-pump apparatus. Both linear and pulsatile flows were compared at mean aortic root pressures of 80 and 50 mm Hg, and these four combinations of aortic root pressure and type of flow were employed for periods of 30 minutes each. Myocardial ischemia developed during linear coronary perfusion at 50 mm Hg, as evidenced by an elevation of PmCO2. Ischemia was not evident during pulsatile perfusion at the same mean pressure. Reversal ischemia was a result of increased myocardial blood flow and pulsatile perfusion, and this increase was shown to occur maximally in the deeper subendocardial layer. Ischemia was not eviden during linear or pulsatile perfusion at an mean perfusion pressure 80 mm Hg. Thus, if lower perfusion pressures are to be tolerated in patients with left ventricular hypertrophy, pulsatile perfusion with the bubble tubing technique may prevent the development of subendocardial ischemia or infarction.

Animals↗

Comparison of myocardial protection with nifedipine and potassium.

Nifedipine, a slow-channel calcium blocker, is thought to provide useful myocardial protection during prolonged total ischemia and reperfusion. An isolated, isovolumic, feline heart model was used to asses the effectiveness of nifedipine in both cardioplegic (100 microgram/10 ml) and noncardioplegic (10 microgram/10 ml) doses for providing myocardial preservation during 90 minutes of hypothermic ischemic arrest and 45 minutes of normothermic reperfusion. Use of nifedipine was compared to hypothermia (27 degrees C) alone and to hypothermia with potassium cardioplegia. Ventricular function was assessed by recovery of isovolumic left ventricular developed pressure and dP/dt. Myocardial carbon dioxide tension (PCO2) and myocardial oxygen tension (PO2) were measured by mass spectrometry. Potassium cardioplegia and the higher dose of nifedipine resulted in immediate asystole. The rates of rise of PCO were greatest in the group receiving 10 microgram nifedipine and in the control group. The rates of rise in the two cardioplegic groups were significantly lower. Recovery of ventricular function was significantly lower with low-dose nifedipine than with potassium cardioplegia. Higher dose nifedipine resulted in a return of function, which was no different than with potassium cardioplegia. Morphologic protection was better with higher dose nifedipine and potassium cardioplegia than with either low-dose cardioplegia or hypothermia alone. These results demonstrate that nifedipine in a cardioplegic dose results in preservation of myocardial structure and function that is similar to that obtained with potassium cardioplegia. In lower noncardioplegic dose, nifedipine does not appear to offer additional protection compared to hypothermia alone. Whether persistent depression of ventricular contractility will limit nifedipine's clinical usefulness as a myocardial protection agent will require further study.

Animals↗