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Objective: We sought to investigate the changes of velocity profiles in the left anterior descending coronary artery after coronary artery bypass grafting using transthoracic Doppler echocardiography., Methods: Forty-five patients who received a bypass graft to the left anterior descending coronary artery were studied. Before coronary artery bypass grafting, Doppler velocity profiles of the distal left anterior descending coronary artery were recorded with transthoracic Doppler echocardiography. Peak systolic velocity, mean systolic velocity, peak diastolic velocity, mean diastolic velocity, total velocity time integral, systolic velocity time integral, and diastolic velocity time integral were measured. Three weeks after coronary artery bypass grafting, left anterior descending coronary artery antegrade flow in the distal portion of the anastomosis was obtained by using the same method. Coronary angiography was performed before and 3 weeks after coronary artery bypass grafting., Results: The overall success rate of measuring the left anterior descending coronary artery flow was 60.0% preoperatively and 80.0% postoperatively. In 25 patients, in whom all parameters were obtained both before and after coronary artery bypass grafting, the following increased significantly after coronary artery bypass grafting: peak systolic velocity (14.86 +/- 7.50 vs 25.07 +/- 17.02 cm/s, P =.0045), mean systolic velocity (9.86 +/- 5.42 vs 18.03 +/- 12.94 cm/s, P =.0026), peak diastolic velocity (24.26 +/- 12.54 vs 48.28 +/- 31.66 cm/s, P =.0021), mean diastolic velocity (14.94 +/- 6.65 vs 30.36 +/- 20.71 cm/s, P =.0022), diastolic velocity time integral (7.22 +/- 2.88 vs 15.55 +/- 10.39 cm, P =.0009), total velocity time integral (10.50 +/- 4.48 vs 19.27 +/- 12.63 cm, P =.0034), and diastolic-to-systolic velocity time integral ratio (3.09 +/- 1.53 vs 4.97 +/- 2.75, P =.0044). Angiography showed graft patency and no significant change in left anterior descending coronary artery stenosis in all patients., Conclusions: Transthoracic Doppler echocardiography showed a significant increase in some parameters in left anterior descending coronary artery flow after coronary artery bypass grafting. Measurement of left anterior descending coronary artery flow by means of transthoracic Doppler echocardiography might be a noninvasive method to evaluate the effect of bypass grafting on the left anterior descending coronary artery.

Prior experiments on hypothermic ischemia/reperfusion have shown that (1) leukocytes have an important role in the injury resulting from hypothermic ischemia/reperfusion and (2) endothelial dysfunction with reduced release of nitric oxide occurs after hypothermic ischemia/reperfusion. L-Arginine is a nitric oxide precursor, and the effects of nitric oxide released from endothelial cells include vasorelaxation and inhibition of leukocyte adhesion to endothelium. The potential roles of an interaction between endothelial dysfunction and leukocyte-mediated injury were examined in neonatal hearts. Thirty-two isolated, blood-perfused neonatal lamb hearts were subjected to 2 hours of 10 degrees C cardioplegic ischemia. Group L-arginine received a 3 mmol/L dose of L-arginine during the first 20 minutes of reperfusion. In group leukocyte depletion, leukocytes were depleted (Sepacell filter) from the perfusate before reperfusion. In group L-arginine+leukocyte depletion, leukocytes were depleted and a 3 mmol/L dose of L-arginine was infused during early reperfusion. The control group had no intervention during reperfusion. At 30 minutes of reperfusion, left ventricular maximum developed pressure, positive maximum and negative maximum first derivative of left ventricular pressure (dP/dt), developed pressure at V10 (volume that produces a left ventricular endiastolic pressure of 10 mm Hg at baseline measurement), and dP/dt at V10 were measured. Coronary blood flow was continuously monitored and oxygen consumption was also measured to evaluate the metabolic recovery. In each heart, we also tested coronary vascular resistance response to the endothelium-dependent vasodilator acetylcholine 10(-7) mol/L and the endothelium-independent vasodilator trinitroglycerin 3 x 10(-5) mol/L to assess endothelial function. Results are given as mean percent recovery of baseline values +/- standard deviation. Group L-arginine+leukocyte depletion showed significantly greater recovery of left ventricular function than the other three groups, and groups L-arginine and leukocyte depletion also showed better recovery than the control group (positive maximum dP/dt: control group = 68.3% +/- 8.8%, group L-arginine = 88.8% +/- 3.8%, group L-arginine+leukocyte+leukocyte depletion = 100.6% +/- 8.7%, group leukocyte depletion = 79.3% +/- 8.1%; p < 0.05). Groups L-arginine and L-arginine+leukocyte depletion had higher postischemic coronary blood flow than other groups (control group = 133.0% +/- 31.6%, group L-arginine = 203.2% +/- 32.1%, group L-arginine+leukocyte depletion = 222.0% +/- 30.4%, group leukocyte depletion = 156.3% +/- 29.0%; p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

The pH-stat strategy compared with the alpha-stat strategy provides more rapid recovery of brain high-energy phosphate stores and intracellular pH after 1 hour of hypothermic circulatory arrest in pigs. Possible mechanisms for this difference are (1) improved oxygen delivery and homogeneity of brain cooling before deep hypothermic circulatory arrest and (2) greater cerebral blood flow and reduced reperfusion injury owing to extracellular acidosis during the rewarming phase. To identify which of these mechanisms is predominant, we studied 49 4-week-old piglets undergoing 1 hour of deep hypothermic circulatory arrest. Four groups were defined according to cooling/rewarming strategy: alpha/alpha, alpha/pH, pH/alpha, and pH/pH. In 24 animals cerebral high-energy phosphate levels and intracellular pH were measured by magnetic resonance spectroscopy (alpha/alpha group 7, alpha/pH group 5, pH/alpha group 7, pH/pH group 5). In 25 animals cerebral blood flow was measured by labeled microspheres, cerebral metabolic rate by oxygen and glucose extraction, and the redox state of cytochrome aa3 and hemoglobin oxygenation by near infrared spectroscopy (alpha/alpha group 7, alpha/pH group 5, pH/alpha group 7, pH/pH group 6). Cerebral blood flow was greater with pH-stat than alpha-stat during cooling (56.3% +/- 3.7% versus 32.9% +/- 2.1% of normothermic baseline values, p < 0.001). Cytochrome aa3 values became more reduced during cooling with alpha-stat than with pH-stat (p = 0.049). Recovery of adenosine triphosphate levels in the initial 45 minutes of reperfusion was more rapid in group pH/pH compared with that in the other groups (p = 0.029). Recovery of cerebral intracellular pH in the initial 30 minutes was faster in group pH/pH compared with that in group alpha/alpha (p = 0.026). Intracellular pH became more acidic during early reperfusion only in group alpha/alpha, whereas it showed continuous recovery in the other groups. This study suggests that there are mechanisms in effect during both the cooling and rewarming phases before and after deep hypothermic circulatory arrest that could contribute to an improved cerebral outcome with pH-stat relative to more alkaline strategies.

Unlabelled: Previous studies have suggested that a simple crystalloid "cerebroplegic" solution may prolong the safe duration of hypothermic circulatory arrest. We tested the hypothesis that pharmacologic modification of the cerebroplegic solution would further enhance cerebral protection. Forty-six 4-week-old miniature piglets underwent core cooling to 15 degrees C nasopharyngeal temperature and 2 hours of hypothermic circulatory arrest. Twelve animals had a 50 ml/kg dose of saline infused into the carotid artery system at the onset of hypothermic circulatory arrest and repeat doses of 10 ml/kg every 30 minutes during arrest. Eleven animals received the same initial and repeat doses of University of Wisconsin organ preservation solution and 10 received University of Wisconsin solution with 7.5 mg/L of MK-801, an excitatory neurotransmitter antagonist. In 13 control animals blood was partially drained from the piglet before 2 hours of circulatory arrest at 15 degrees C and no cerebroplegic solution was infused. All solutions were delivered at 4 degrees C. Brain temperature (n = 24) at the onset of hypothermic circulatory arrest was 15.0 degrees +/- 0.1 degrees C (mean +/- standard error). Brain temperature after cerebroplegic infusion dropped to 13.0 degrees +/- 0.3 degrees C and stayed lower than brain temperature in the control group throughout the hypothermic circulatory arrest period. Recovery of cerebral adenosine triphosphate and intracellular pH determined by phosphorus 31 magnetic resonance spectroscopy (n = 22) was significantly improved by saline infusion and was further improved with University of Wisconsin solution and University of Wisconsin solution plus MK-801 (p < 0.001). Recovery of cerebral blood flow measured by microspheres (n = 24) also was augmented by University of Wisconsin solution (p < 0.001) but not in the presence of MK-801. The vascular resistance response to acetylcholine and nitroglycerin suggested that MK-801 has a direct vasoconstrictive effect. Recovery of cerebral oxygen consumption (n = 24) was increased by University of Wisconsin solution and University of Wisconsin solution with MK-801 (p = 0.002). Brain water content (n = 46) was significantly lower in all cerebroplegia-treated groups than in controls (p < 0.001)., Conclusion: Cerebroplegia improves short-term recovery after 2 hours of circulatory arrest in hypothermic piglets. Pharmacologic modification with University of Wisconsin solution further improves the recovery of cerebral blood flow and metabolism. MK-801 does not augment the protective effects of University of Wisconsin solution and reduces the recovery of cerebral blood flow by a direct vascular action. Modified cerebroplegia may provide a novel approach to improved cerebral protection when prolonged hypothermic circulatory arrest is necessary.

Hypothermia is believed to improve the tolerance to both ischemia and cardiopulmonary bypass and is commonly used during heart operations, particularly in the neonate. However, hypothermia also causes calcium to accumulate in the myocyte experimentally, and an increase in intracellular calcium during ischemia may worsen the effect of ischemia and impair the postischemic recovery of function. This effect of hypothermia on intracellular calcium has generally not been considered in experiments that attempt to optimize the composition of cardioplegic solutions. We have evaluated the impact of hypothermia before cardioplegic ischemia on the efficacy of two common cardioplegic solutions, one with calcium (St. Thomas' Hospital cardioplegia) and the other without calcium (glucose-potassium cardioplegia), in 37 isolated blood-perfused neonatal lamb hearts. Left ventricular maximal developed pressure, positive maximum of the first derivative of left ventricular pressure, left ventricular stiffness constant at 10 mmHg end-diastolic pressure, coronary blood flow, and myocardial oxygen consumption were measured before and 30 minutes after 2 hours of cold ischemia. After baseline measurements were made, two groups of hearts (ST-C and GK-C) had perfusion-cooling for 10 minutes to 17 degrees C myocardial temperature, and two other groups (ST-NC and GK-NC) had the same period of normothermic perfusion. Then the hearts were arrested with 4 degrees C St. Thomas' cardioplegic in groups ST-C and ST-NC and with glucose-potassium cardioplegia in groups GK-C and GK-NC. In the groups without preischemic cooling, both St. Thomas' (group ST-NC) and glucose-potassium (group GK-NC) cardioplegia resulted in a similar recovery of function compared with baseline levels (group ST-NC: developed pressure = 91.3% +/- 9.2%, dP/dt = 88.1% +/- 8.9%, left ventricular stiffness constant = 96.1% +/- 3.3%; group GK-NC: developed pressure = 89.3% +/- 6.9%, dP/dt = 82.6% +/- 8.8%, left ventricular stiffness constant = 99.4% +/- 2.0%; data are mean plus or minus the standard deviation). However, with preischemic cooling, St. Thomas' cardioplegia (group ST-C) resulted in a significantly reduced recovery of both systolic and diastolic function (developed pressure = 81.6% +/- 6.2%, dP/dt = 75.1% +/- 8.4%, left ventricular stiffness constant = 103.7% +/- 2.7%) compared with that for both glucose-potassium cardioplegia (group GK-C: developed pressure = 92.4% +/- 8.7%, dP/dt = 83.7% +/- 6.0%, left ventricular stiffness constant = 100.5% +/- 2.1%) and St. Thomas' cardioplegia without preischemic cooling (group ST-NC) (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Hypothermia has been reported to increase intracellular ionized calcium, which may aggravate injury resulting from ischemia and reperfusion. The effects of plasma ionized calcium concentration ([Ca2+]) during hypothermic perfusion on recovery after 2 hours of cold cardioplegic ischemia were evaluated in 32 isolated, blood-perfused neonatal lamb hearts. Three groups of hearts (B, C, and D) were perfusion-cooled for 10 minutes to a myocardial temperature of 17 degrees C and then arrested with St. Thomas' Hospital cardioplegic solution. Group A had 10 minutes of normothermic perfusion before cardioplegia. Group B had cooling with normal [Ca2+]. Group C had citrate added as cooling was started to lower [Ca2+] (0.26 mmol/L), and it was not normalized until 15 minutes into reperfusion. Group D received citrate plus Ca2+ to give normal [Ca2+] during cooling. Groups B and D showed a significantly reduced recovery (p < 0.05) in left ventricular systolic function (developed pressure and the rate of pressure rise) and diastolic function (stiffness constant) than groups A and C. During preischemic cooling, oxygen consumption per beat and coronary vascular resistance increased significantly in groups B and D, but both oxygen consumption and coronary vascular resistance were significantly lower in group C than in groups B and D so long as [Ca2+] was low. The data show that preischemic hypothermia results in reduced postischemic recovery of function compared with simultaneous induction of cardioplegia and hypothermia. Low [Ca2+] during preischemic hypothermia and early reperfusion offsets this deleterious effect of hypothermia.

To elucidate the effects of mitral valve surgery on right ventricular function in 11 patients with mitral stenosis, pre- and postoperative right ventricular function were quantified using gated equilibrium blood pool radionuclide ventriculography at rest and during exercise. The preoperative right ventricular ejection fraction was 39 +/- 4% at rest and 36 +/- 9% during exercise, which during exercise was lower than control values (51 +/- 5%) (p < 0.01). When the preoperative right ventricular ejection fraction was lower during exercise than at rest, postoperative right ventricular ejection fraction during exercise was lower than normal values (42 +/- 3% versus 51 +/- 5%) (p < 0.01). When the preoperative right ventricular ejection fraction did not decrease during exercise, the postoperative right ventricular ejection fraction was within normal limits during exercise (54 +/- 5%). In addition, postoperative right ventricular ejection fraction during exercise increased to normal values in patients whose preoperative right ventricular ejection fraction during exercise had been 40% or higher. Preoperative peak ejection rate was -1.81 +/- 0.19 EDV/sec at rest and -1.72 +/- 0.39 EDV/sec during exercise, which during exercise was lower than control values (-2.44 +/- 0.53 EDV/sec) (p < 0.01). Postoperatively, peak ejection rate during exercise (-2.50 +/- 0.37 EDV/sec) increased (p < 0.05) to normal levels. Preoperative peak filling rate was 1.61 +/- 0.47 EDV/sec at rest and 1.88 +/- 0.54 EDV/sec during exercise, which during exercise was lower than control values (2.58 +/- 0.62 EDV/sec) (p < 0.01). Postoperatively, peak filling rate during exercise (2.82 +/- 0.62 EDV/sec) increased (p < 0.05) to normal values in all patients. Preoperative changes in both right ventricular ejection fraction and peak ejection rate from rest to exercise inversely correlated with the preoperative pulmonary vascular resistance at rest (right ventricular ejection fraction, r = -0.79, p < 0.005; and peak ejection rate, r = -0.67, p < 0.05). In conclusion, right ventricular systolic function improved in about half of the patients with mitral stenosis, and diastolic function improved in all patients during exercise following surgery. When the preoperative pulmonary vascular resistance was elevated, the right ventricular systolic dysfunction persisted.

A stable prostacyclin analog (OP-41483) was evaluated for myocardial protective effect against global ischemia with the use of cardioplegia. Isolated canine hearts (n = 25) were exposed to 60 minutes of warm (37 degrees C) global ischemia after the arrest by crystalloid cardioplegia. Prostaglandin analog was given in three different ways: preadministration (700 ng/kg body weight per minute) before ischemia for 30 minutes (group I, n = 5), given as a component of cardioplegic solution (600 ng/ml, group II, n, = 6), and post-administration (25 ng/kg body weight per minute) during reperfusion for 30 minutes (group III, n = 7). During reperfusion, coronary sinus blood flow, 6-keto-prostaglandin F1 alpha in coronary sinus blood, and myocardial oxygen consumption were measured during reperfusion. As a result, groups II and III showed significantly better global left ventricular function (developed pressure, maximum dP/dt, and diastolic compliance) than the control group (without prostaglandin analog, n = 7) and group I. Myocardial oxygen consumption at reperfusion (1 minute) was significantly larger in group II than in the control group. 6-keto-prostaglandin F1 alpha flux was significantly larger in group II than in the other three groups during reperfusion. The results indicated that prostaglandin analog has a beneficial effect on myocardial protection under global ischemia with cardioplegia, particularly when used as a component of cardioplegic solution and also during reperfusion. The mechanism may relate to the cytoprotective effect (including protection of endothelium with enhanced endogenous prostacyclin production at reperfusion and also to the modulation of reperfusion per se.