Percutaneous transluminal angioplasty in coronary-internal thoracic-subclavian steal syndrome.
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
L C Pelletier
Publications and source records attributed to L C Pelletier.
Cyclosporin A-induced coronary artery vasoconstriction through myogenic and endothelium-dependent mechanisms.
BACKGROUND: The exact mechanism of vascular toxicity of cyclosporin A (CSA) remains unknown. It has been reported that an impairment of endothelium-mediated vascular reactivity may be involved. METHOD AND RESULTS: We studied the response to intracoronary injections of acetylcholine (ACh) (30 ng/kg), adenosine (100 ng/kg), and nitroglycerin (NTG) (1.7 micrograms/kg) before and after intracoronary infusion of CSA (20 mg over 20 minutes) and of L-arginine (10 mg.kg-1.min-1). Experiments were performed on 11 open-chest dogs anesthetized and instrumented for measurements of coronary blood flow (CBF) in the left anterior descending (LAD) and left circumflex (LCx) coronary arteries, left ventricular dP/dt, mean aortic pressure, and coronary sinus pressure. CSA, L-arginine, ACh, adenosine, and NTG were injected into the LAD, and the LCx served as control. The increase in CBF in the LAD with ACh administration averaged 21 +/- 11 mL/min before CSA, 15 +/- 10 mL/min after CSA, and 15 +/- 8 mL/min during L-arginine injection (P = .2). Adenosine caused an increase in CBF in the LAD averaging 20 +/- 10 mL/min before CSA, 10 +/- 8 mL/min after CSA, and 17 +/- 12 mL/min during L-arginine injection (P = .004). NTG caused an increase in CBF in the LAD averaging 21 +/- 10 mL/min before CSA, 13 +/- 11 mL/min after CSA, and 14 +/- 7 after administration of L-arginine (P = .009). CONCLUSIONS: These results suggest that direct intracoronary injection of CSA induces a vasoconstrictive response through endothelium-dependent and myogenic mechanisms. The muscarinic endothelial response was not affected by CSA, whereas the purinergic action of CSA was restored after L-arginine administration.
Acetylcholine↗
Clinical trial of retrograde warm blood reperfusion versus standard cold topical irrigation of transplanted hearts.
BACKGROUND: A prospective, randomized clinical study involving 34 patients undergoing heart transplantation compared myocardial preservation of donor hearts maintained with continuous reperfusion with retrograde warm blood cardioplegia during surgical implantation versus the standard cold topical irrigation. METHODS: Hearts in both groups were arrested with a standard crystalloid solution and maintained in a cold saline solution during transportation. In the retrograde group, cardioplegia was administered through a catheter in the coronary sinus during surgical implantation. An average of 471 +/- 30 mL of hyperkalemic crystalloid solution diluted 1:4 in warm blood from the oxygenator was infused. In the standard group, the heart was kept cold by topical irrigation of cold saline solution and was reperfused only when the ascending aorta was unclamped. RESULTS: Preoperative characteristics of donors and recipients were similar in the two cohorts. Ischemic time average 139 +/- 12 minutes in the retrograde group compared with 130 +/- 11 minutes in the standard group (p = 0.57). Cardiopulmonary bypass time averaged 89 +/- 4 minutes in the retrograde group and 110 +/- 12 minutes in the standard group (p = 0.12). Defibrillation at reperfusion was performed in 4 patients (4/17, 24%) in the retrograde group and 12 patients (12/18, 67%) in the standard group (p = 0.01). There were no deaths in the retrograde group (0/17), whereas in the standard group, 3 patients (3/17) died of early graft failure (p = 0.11). Four early graft failures occurred in the standard group (p = 0.06). Two patients (2/17, 12%) were weaned from bypass with ventricular assist devices in the standard group. The number of subendocardial necrotic cells in the first two weekly endomyocardial biopsy specimens averaged 2.7 +/- 0.8 cells/mm2 in the retrograde group and 5.9 +/- 2.4 cells/mm2 in the standard group (p = 0.12). CONCLUSIONS: Retrograde warm blood reperfusion appears to improve the initial recovery of transplanted hearts. The technique is easy to use and may be a useful approach to graft protection during surgical implantation.
Adult↗
Effect of L-arginine on metabolic recovery of the ischemic myocardium.
BACKGROUND: The release of nitric oxide is decreased after myocardial ischemia and reperfusion. Whereas the precursor L-arginine can stimulate the release of nitric oxide, its effect on metabolic recovery after myocardial ischemia is unknown. METHODS: To study the effect of L-arginine on metabolic recovery after myocardial ischemia, cardioplegia infusion, and reperfusion, 33 dogs were placed on cardiopulmonary bypass and subjected to a sequence of 30 minutes of normothermic global ischemia, 30 minutes of warm blood cardioplegic arrest, and 30 minutes of reperfusion. A pH probe was inserted in the anterior wall of the left ventricle, and tissue pH was measured throughout the experiment. Coronary blood flow in the left anterior descending coronary artery and the circumflex coronary artery was measured. Blood samples from the coronary sinus were taken to measure blood pH and levels of lactate, creatine kinase, and troponin T. RESULTS: In the control group of 9 dogs, tissue pH averaged 6.4 +/- 0.1, 6.5 +/- 0.1, and 6.8 +/- 0.1 after the end of global ischemia, cardioplegia, and reperfusion, respectively. Tissue pH averaged 6.4 +/- 0.1, 6.6 +/- 0.1, and 6.9 +/- 0.1, respectively, in the experimental group of 9 animals with 2 mmol/L of L-arginine added to the cardioplegic solution. Tissue pH averaged 6.2 +/- 0.1, 6.7 +/- 0.1, 7.1 +/- 0.1, respectively, in the third group of 9 animals that received an additional infusion of L-arginine (10 mg.kg-1.min-1) during reperfusion. Tissue pH recovered faster in groups with L-arginine (p = 0.00001). A hyperemic response of coronary blood flow was shown at reperfusion in animals in the control group only. In 6 dogs, L-NAME (N-nitroarginine methyl ester), an inhibitor of nitric oxide synthesis, was injected and resulted in a slower pH recovery on reperfusion compared with that of animals that received L-arginine. CONCLUSIONS: The addition of L-arginine to the cardioplegic solution and the systemic circulation during reperfusion resulted in a significant increase in coronary blood flow during cardioplegia infusion and in a faster recovery of myocardial tissue pH, possibly by increasing coronary blood flow through the release of nitric oxide.
Animals↗
Metabolic recovery after global myocardial ischemia: effects of blood cardioplegic solutions.
OBJECTIVE: To determine the effect of whole blood cardioplegia (WBC) and a mix of crystalloid in blood (CB) hyperkalemic cardioplegic solutions on recovery of the myocardium following global ischemia. DESIGN: Twenty-one dogs were placed on normothermic cardiopulmonary bypass, and a pH probe was inserted in the anterior wall of the left ventricle. Global myocardial ischemia was obtained by clamping the ascending aorta until a decrease in myocardial tissue pH of 0.4 units from baseline value was obtained, at which time cardioplegic solutions were perfused over 30 mins. The aorta was then unclamped and 30 mins of reperfusion was allowed. RESULTS: The aortic cross-clamping time necessary to decrease myocardial tissue pH 0.4 units from baseline averaged 13 +/- 8 mins. Whereas myocardial tissue pH returned to baseline value (6.9 +/- 0.1) after an average of 24 mins with cold (15 degrees C) and warm (35 degrees C) WBC, it took an average of 48 mins to reach control levels when warm CB solutions were used. Moreover, tissue pH decreased temporarily from 6.97 +/- 0.35 to 6.77 +/- 0.37 (P < 0.05) at initiation of normothermic myocardial reperfusion in cold WBC protected animals, and myocardial pH remained normal in the warm WBC group but remained severely acidic in warm CB animals (6.6 +/- 0.3). CONCLUSIONS: Metabolic recovery after global ischemia was faster with WBC cardioplegic protection. Normothermic blood reperfusion in cold WBC protected animals caused a significant but temporary tissue acidosis.
Animals↗
Effect of pentoxifylline on renal toxicity of cyclosporine: results of a clinical trial after heart transplantation.
BACKGROUND: Pentoxifylline was suggested to prevent the renal release of endothelin caused by cyclosporine. METHODS: We studied the renal-sparing effect of pentoxifylline in 44 patients who underwent heart transplantation between 1991 and 1994 and were randomized to a group treated with pentoxifylline (400 mg three times daily) or to a control group. All patients were treated according to the same immunosuppression protocol, including induction with perioperative rabbit anti-thymocyte antibody and maintenance with azathioprine, cyclosporine, and prednisone. Five patients withdrew voluntarily because of lack of compliance, and five patients died during the first month of the study. RESULTS: There was no difference between the two groups in regard to age, sex, initial cardiopathy, the number of acute rejections, and the number of infection episodes. Urinary clearance of creatinine averaged 1.1 +/- 0.1 ml/sec, 1.3 +/- 0.1 ml/sec, and 1.3 +/- 0.1 ml/sec in the control patients (n = 16) and 1.2 +/- 0.1 ml/sec, 1.4 +/- 0.1 ml/sec, and 1.3 ml/sec in patients treated with pentoxifylline (n = 18) at initiation, 12 months, and 24 months of the study (p > 0.05), respectively. At these three times, the serum creatinine levels averaged 106 +/- 4 mmol/L, 119 +/- 4 mmol/L, and 126 +/- 5 mmol/L in the control group and 94 +/- 4 mmol/L, 114 +/- 4 mmol/L, and 127 +/- 5 mmol/L in patients treated with pentoxifylline, respectively (p > 0.05). Trough levels of cyclosporine throughout the study period averaged 212 +/- 8 mmol/L and 206 +/- 8 mmol/L in the control and treated groups, respectively (p > 0.05). Endothelin blood levels averaged 0.4 +/- 0.2 pg/ml for nine control patients and 0.4 +/- 0.1 pg/ml for a group of 10 patients treated with pentoxifylline (p > 0.05). CONCLUSIONS: Pentoxifylline in association with cyclosporine did not result in a significant improvement in renal function during the first 2 years after heart transplantation.
Creatinine↗
[Effect of cyclosporin A on the reactivity of the pulmonary vascular network in dogs].
UNLABELLED: Aside to its immunosuppressive effects, cyclosporine A (CyA) is known as a vasoconstrictor agent. The vasoconstriction appears to be related to an endothelial release of thromboxane A2 (TxA2) and endothelium as well as a decrease endothelial production of nitric oxide. However, no data is available on the effects of CyA on pulmonary artery (PA) network. We designed experiments to study the CyA effects on canine pulmonary artery vasoregulation. Resistance vessels were studied in vivo using a lung (n = 6) steady rate delivery autoperfusion model. The CyA was infused in the left pulmonary artery at incremental doses of 5, 10, and 20 mg; CyA dosage, sampled in the left atrium, were respectively 515 +/- 67, 580 +/- 97, and 1024 +/- 84 nmol/L. No significant increase in tension were registered regardless of the dose infused. Conductance vessels were studied in vitro using third division PA segments (n = 6) suspended for isometric force measurement in organ chambers. PA segments were precontracted (phenylephrine 10(-6) M) and subsequently exposed to incremental dose of CyA and cremophor (CR), the CyA vehicle. CyA specifically induced a dose-dependent contraction. The maximal contraction observed were 159 g +/- 13% with CyA exposure and 106 +/- 3% with the CR (p < 0.05). This contraction was abolished by indomethacin (cyclooxygenase inhibitor), pinane thromboxane A2 (TxA2 antagonist), dexamethasone (phospholipase A2 inhibitor), neomycin (phospholipase C inhibitor), and endothelial mechanical denudation. CONCLUSIONS: In the canine model, in vivo infusion of CyA does not affect pulmonary resistance arteries. However, in vitro, on pulmonary conductance arteries, CyA induces an endothelium-dependent vasoconstriction. This constriction appears to be related to a TxA2 release mediated by a phospholipase A2 phospholipase C pathway.
Animals↗
The Carpentier-Edwards pericardial bioprosthesis: clinical experience with 600 patients.
Carpentier-Edwards pericardial bioprostheses were implanted in 600 patients: 416 aortic valve replacement, 115 mitral valve replacement, 6 isolated tricuspid, and 63 multiple valve replacements. The survival rates were 70% at 10 years after aortic valve replacement, 62% 8 years after mitral valve replacement, and 57% at 8 years with multiple valve replacement. Overall, 69 patients suffered one or more valve-related complications. The 10-year freedom rates from embolism were 91% (aortic valve replacement), 92% (mitral valve replacement), and 89% (multiple valve replacement), and those from endocarditis were 95%, 93%, and 85%, respectively. In 18 of the 35 patients, reoperation was due to primary valve dysfunction. Freedom from primary dysfunction was 87% at 10 years with aortic valve replacement, and at 8 years, it was 79% with mitral valve replacement and 77% with multiple valve replacement. A direct correlation was found between freedom from valve dysfunction and age of the patient at operation, with a 10-year-free rate of 90% among patients older than 59 years. This bioprosthesis has an excellent durability up to 10 years in the aortic position. More data regarding its long-term durability in the mitral position are needed. It is currently our valve substitute of choice when a bioprosthesis is indicated.
Actuarial Analysis↗
Mitroflow pericardial bioprosthesis: clinical performance to ten years.
The Mitroflow pericardial bioprothesis, a second generation pericardial prosthesis, has clinical performance assessment to 10 years. This bioprosthesis was used in 445 operations in 445 patients between 1982 and 1992 inclusive (mean age, 59.1 years; age range, 19 to 94 years). There were 253 aortic valve replacements (AVR), 155 mitral valve replacements (MVR), 31 multiple valve replacements (MR), and 6 tricuspid valve replacements. Concomitant procedures were performed in 40 patients (14.2%). The age group distributions (years) were less than or equal to 35 years, 28 patients; 36 to 50 years, 79; 51 to 64 years, 167; 65 to 69 years, 70; and 70 years or more, 101 patients. The total follow-up was 1,524 patient-years (mean, 5.4 years), 96% complete. The early mortality was 6.3%/patient-year (28 patients) and the late mortality was 4.1%/patient-year (96 patients). Concomitant procedures did not influence either early or late mortality (p = not significant [NS]). The overall patient survival at 10 years was 58% +/- 5% (p = NS by valve position). The overall freedom from structural valve deterioration (SVD) at 8 years was 69% +/- 3% and at 10 years, 45% +/- 7%; and at 8 years AVR 80% +/- 4%, MVR 58% +/- 6%, and MR 38% +/- 11% (p < 0.05, AVR > MVR > MR). The freedom from thromboembolism (TE) was 87% +/- 2%, overall at 10 years, and was not different by valve position (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Antithymocyte globulin and methotrexate therapy of severe or persistent cardiac allograft rejection.
BACKGROUND: The treatment of severe or persistent acute rejection remains difficult despite newer immunosuppressive agents available. METHODS: To evaluate the effectiveness of rabbit antithymocyte globulin and methotrexate as therapy for severe or persistent acute cardiac allograft rejection, we conducted a retrospective analysis of clinical and laboratory data from 150 consecutive heart transplant recipients between 1983 and 1994. RESULTS: Thirteen episodes of severe or refractory acute rejection were treated with rabbit antithymocyte globulin in 10 patients. Rabbit antithymocyte globulin (125 mg/day for 3 consecutive days) was effective in 90% of patients. Therapy was well tolerated, and contributed to one infectious complication, no malignancy, and long-term survival in 8 of 10 patients. Recurrent rejection developed in 60% of patients. Methotrexate (7.5 to 15 mg/wk for 16 weeks) was administered to 8 patients with persistent rejection documented on three consecutive endomyocardial biopsies. Therapy was effective in 6 of the 8 patients, with one infectious complication and no malignancy on follow-up. White blood cell count decreased significantly during therapy (p = 0.008). Seven of the 8 patients in the methotrexate group are long-term survivors. CONCLUSIONS: Rabbit antithymocyte globulin is a valuable alternative in patients with severe or refractory acute rejection. Methotrexate is an important adjunct in patients with persistent rejection unresponsive to conventional immunosuppressive regimens.
Adult↗
[Cyclosporine A decreases coronary blood flow in dogs].
The objective of the present study was to determine the effect of cyclosporine (CSA) on coronary artery reactivity. Six mongrel dogs, weighing 20 to 30 kg were anesthetized with sodium pentobarbital and were artificially ventilated. A median sternotomy was performed to expose the heart. Left anterior and circumflex coronary flows were measured with an electromagnetic flowmeter. Heart rate, mean arterial pressure, coronary sinus pressure and dP/dt were monitored during all experiments. Blood samples were withdrawn from the coronary sinus to measure CSA. Injections of 5 and 10 mg of CSA in the left anterior descending coronary artery were administered to all animals and the measure of the circumflex coronary blood flow was used as control during the experiments. The decrease in left anterior descending coronary artery blood flow averaged 24 +/- 9% (p = 0.002) and 18 +/- 11% (p = 0.009), and the increase in coronary vascular resistance averaged 31 +/- 12% (p = 0.005) and 16 +/- 24% (p = 0.1) after 5 and 10 mg of CSA, respectively. There were no significant changes in circumflex coronary artery blood flow and in dP/dt during the experiments. Cyclosporine blood levels averaged 453 +/- 226 nmol/l and 1087 +/- 199 nmol/l after injections of 5 and 10 mg of CSA, respectively. In conclusion, this study suggests that CSA can cause acute vasoconstriction of the arterial coronary vasculature.
Animals↗
[Effect of the injection of cyclosporine A on the peripheral venous resistance in dogs].
We have studied the effect of cyclosporin on the peripheral venous system. CSA was injected into an isolated hind limb saphenous vein perfused at constant flow in 29 dogs. Reactivity of the vein was tested with infusions of norepinephrine (NE) before and after CSA. In a 1st group of 7 dogs, CSA at doses of 5, 10 and 20 mg was infused over a 10-minute period. In a 2nd group of 8 dogs, 20 mg of CSA was infused over 20 minutes and, injections of 6, 12 and 24 micrograms of NE were administered before and during CSA. In a 3rd (n = 7) and 4th (n = 7) groups of animals, 30 mg of CSA was injected over 60 minutes and injections of 3, 6, 12 micrograms of NE were given before and during CSA. In the last group, an ipsilateral lumbar sympathectomy was performed before CSA injection. The infusion of CSA over periods of 10 and 20 minutes did not cause significant changes in venous perfusion pressure. The infusion of 30 mg of CSA over 60 minutes caused an increase in venous perfusion pressure from 44 +/- 2 mm Hg to 58 +/- 5 mm Hg (p < 0.0001). Surgical sympathectomy prevented the venoconstrictor response to CSA. Injections of 3, 6 and 12 +/- g of NE caused averaged increases of 25 +/- 6, 39 +/- 9 and 53 +/- 10 mm Hg before CSA, and of 45 +/- 7, 69 +/- 12 and 84 +/- 8 mm Hg respectively after CSA injections, a significant increase (p = 0.03). In conclusion, CSA causes a vasoconstriction of the saphenous vein through stimulation of the sympathetic nervous system and potentiates the venoconstrictor effect of NE.
Animals↗
[Assessment of the need for organ transplantation in Quebec].
OBJECTIVES: To evaluate the demand for organs for transplantation and to recommend a reorganization of transplantation services in Quebec. DESIGN: Retrospective study. SETTING: Province of Quebec, 1988 to 1992. PATIENTS: All patients on waiting lists for organ transplantation and patients who received transplants registered in national data banks. MAIN OUTCOME MEASURES: The actual annual demand for organ transplantation and the rate of transplantations performed. RESULTS: The rates of heart transplantation were lower than the actual annual demand, which resulted in many patients dying while awaiting transplantation. The actual annual demand for heart transplantation decreased during the last 5 years from 10.9 per million people in 1987 to 6.7 in 1992. The rates of heart transplantation in Quebec were higher than the Canadian average. The actual demand for lung transplantation was only 2.9 per million people on average in 1992. Demand for liver transplantation increased annually, reaching 8.6 per million in 1992. The rate of transplantation increased likewise but remained insufficient. The demand for kidney transplantation reached 27.2 per million people in 1992, and the transplantation rate was 17.8. CONCLUSIONS: Taking into account the actual demand for and supply of organ transplantation, to insure high-quality service and to control costs associated with organ transplantation, we recommend that the present system in Quebec be reorganized so that transplantations are performed in 12 centres: 7 for kidney transplantation, 2 for hearts, 2 for livers and 1 for lungs.
Databases, Factual↗
Vasoconstrictor effect of cyclosporin on the mesenteric artery in the dog.
To evaluate the effect of cyclosporin (CyA) on the mesenteric arterial bed, studies were performed on the isolated mesenteric artery perfused at a constant flow in 20 dogs. Changes in mesenteric perfusion pressure reflected variations in vascular resistance. Pure powder CyA was dissolved in autologous blood and injected at doses of 5, 10, 20 and 40 mg. Infusions of 5 and 10 mg CyA caused nonsignificant mean increases of 3 +/- 2 mm Hg [95% confidence interval (CI) -2 to +7; P > 0.05] and 3 +/- 3 mm Hg (95% CI -3 to +9; P > 0.05) in mesenteric perfusion pressure, with CyA blood levels in the mesenteric vein averaging 466 +/- 153 and 692 +/- 130 nmol/l, respectively, at the end of the injections. Infusions of 20 and 40 mg CyA caused significant increases in mesenteric perfusion pressure averaging 11 +/- 3 mm Hg (95% CI 3-18; P < 0.05) and 26 +/- 4 mm Hg (95% CI 16-34; P < 0.05), respectively. CyA blood levels at the end of infusion averaged 806 +/- 85 and 1118 +/- 89 nmol/l, respectively, in the mesenteric vein. Blockade of alpha-adrenergic receptors with phentolamine abolished the CyA vasoconstriction of the mesenteric artery, with the increase in perfusion pressure averaging 16 +/- 4 mm Hg before and 3 +/- 3 mm Hg after phentolamine (P < 0.05). Thus, in the dog, CyA causes an acute vasoconstriction of the mesenteric artery through stimulation of alpha-adrenergic receptors.
Animals↗
Effects of cold and warm blood cardioplegia assessed by myocardial pH and release of metabolic markers.
The optimal temperature of blood cardioplegia remains controversial. Interstitial myocardial pH was monitored online with a probe that was inserted in the anterior wall of the left ventricle. Venous pH, lactate production, and creatine kinase and troponin T release were measured in coronary sinus blood obtained in 14 dogs after ischemic arrest periods of 5, 10, 20, and 40 minutes with warm (n = 7; mean myocardial temperature, 35 degrees +/- 2 degrees C) and cold (n = 7; mean myocardial temperature, 12 degrees +/- 1 degree C) blood cardioplegic protection. Blood cardioplegic solution was delivered at a rate of 100 mL/min during the 10 minutes between each ischemic arrest. The interstitial myocardial pH decreased significantly (p < 0.05) from 7.1 +/- 0.3 to 6.53 +/- 0.3 after ischemia in animals perfused with warm blood cardioplegia and from 7.04 +/- 0.3 to 6.64 +/- 0.1 in those receiving cold blood cardioplegic protection; however, the difference between the groups was not significant (p > 0.05). Lactate production and creatine kinase and troponin T release increased significantly after ischemia, but there was no difference in the changes between the warm and cold blood cardioplegia groups. In conclusion, ischemia caused significant changes in all variables measured, and these changes were directly proportional to the duration of ischemia. However, there was no significant difference (p > 0.05) in the myocardial metabolic changes between the warm and cold blood cardioplegia groups in terms of the duration of ischemic arrest studied.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Cholesterol-lowering intervention and coronary artery disease after cardiac transplantation.
Allograft coronary artery disease is a major threat to long-term survival after cardiac transplantation. It has been suggested that hyperlipidemia plays a major role in allograft coronary disease. The objective of the present study was to evaluate the effect of a lipid-lowering intervention with diet and drug therapy after cardiac transplantation. Forty-six patients who underwent transplantation between 1988 and 1991 and who were treated with the American Heart Association phase 1 diet and an HMG coenzyme A reductase inhibitor (lovastatin or simvastatin) when low-density lipoprotein cholesterol levels were higher than 3.4 mmol/L were compared with 35 untreated patients having transplantation between 1983 and 1988. Annual coronary angiograms were obtained in both groups. Cholesterol, triglyceride, and low-density lipoprotein levels were significantly lower in the treated group. Actuarial survival and event-free survival (survival free from allograft coronary artery disease) were similar in both groups. Low-density lipoprotein levels lower than 3 mmol/L at the last follow-up had a positive effect on event-free survival. The cholesterol-lowering intervention was not effective in decreasing the prevalence of allograft coronary artery disease. This study suggests that more aggressive measures to lower low-density lipoprotein levels may be necessary to significantly affect allograft disease. Clinical trials should be developed to address this hypothesis.
Adult↗
Intermittent antegrade warm versus cold blood cardioplegia: a prospective, randomized study.
A prospective, randomized study was performed in 200 patients undergoing coronary artery bypass grafting to compare the myocardial protection obtained with intermittent antegrade warm versus cold blood cardioplegia. Preoperative and surgical characteristics of the two cohorts were similar. Intermittent antegrade infusion of warm blood cardioplegia failed to achieve sustained electromechanical arrest of the heart in 13%. The only difference in clinical outcomes was the more frequent spontaneous return to sinus rhythm after the unclamping of the aorta in the warm group (88% versus 70%, p = 0.002). Mortality (1% each) and myocardial infarction (2% and 4%) rates were similar. Rates of increase in serum activity of the isoenzyme of creatine kinase (CK-MB), CK-MB mass concentration, and cardiac troponin-T level as well as total release of troponin T were significantly lower in the warm group, and fewer patients in this group had a clinically significant increase in serum CK-MB mass (20% versus 39%, p = 0.005) and troponin T (20% versus 56%, p = 0.00001). Thus, intermittent antegrade warm blood cardioplegia is appropriate and clinically safe; the lower release of biochemical markers of myocardial damage suggests improved protection during first-time coronary artery bypass grafting.
Biomarkers↗
[Urinary excretion of acetylated polyamines after heart transplantation in dogs].
Increase in urinary polyamine levels after transplantation was suggested to be an indicator of organ rejection but immunosuppression therapy could also give rise to these polyamines. To test this hypothesis, the urinary excretion of N-acetylputrescine (Nap) and N-acetylspermidine (Nas) was studied in 36 dogs. Two groups (n = 6) underwent cervical heterotopic heart transplantation. Three other groups (n = 6) were given different immunosuppression treatments without having any surgery and one group (n = 6) had a sham cervical operation. Urine samples and percutaneous transmural biopsy of the transplanted heart were collected daily. The acetylated polyamines were measured with high performance liquid chromatography (HPLC). Immunosuppression of the transplanted dogs with cyclosporine, imuran and prednisone during the postoperative period caused a significant increase (p < 0.05) in the excretion of Nas averaging 512 +/- 122, 929 +/- 337, 507 +/- 207, 1008 +/- 665, 674 +/- 273 nmol/mg of creatinine respectively compared to 197 +/- 31, 149 +/- 30, 203 +/- 56, 177 +/- 40, 226 +/- 62 nmol/mg of creatinine. The excreted levels of Nap for the same group were 594 +/- 202, 707 +/- 138, 1007 +/- 270, 1055 +/- 358, 827 +/- 270 nmol/mg of creatinine compared to 71 +/- 24, 169 +/- 36, 150 +/- 23, 136 +/- 29, 197 +/- 32 nmol/mg of creatinine (p < 0.05) in the control group of sham operated animals. A significant excretion of Nas and Nap was also observed between the transplanted dogs under immunosuppression and the immunosuppressed but non-operated animals, as well as with the non-operated animals that were given cyclosporine only.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗