Search

Background: Dialysis patients frequently present with debilitating coronary artery disease but are regarded as challenging patients for coronary artery bypass grafting., Methods: The operative, early postoperative, and late results of 44 dialysis patients undergoing coronary artery bypass grafting from 1984 to 1997 were retrospectively reviewed., Results: Compared with patients in The Society of Thoracic Surgeons database who underwent coronary artery bypass grafting, only cerebrovascular accident and postoperative cardiac arrest occurred more frequently in dialysis patients. However, 73% experienced some type of complication. Operative mortality was 11.4%. Decreased left ventricular ejection fraction and severe distal disease were predictive of increased operative mortality. New York Heart Association angina class fell from 2.8 to 1.5, and New York Heart Association congestive heart failure class fell from 2.6 to 1.8. Overall quality-of-life scores did not improve; however, walking distances remained consistently improved. Actuarial survival at 5 years was 32.0%+/-12.0%. Five-year survival was 0% for smokers and 83.6%+/-7.6% for nonsmokers (p = 0.0142). Causes of late death were myocardial infarction (4), sepsis (1), subdural hematoma (1), stroke (1), and unknown (6)., Conclusions: Coronary artery bypass grafting should be avoided in dialysis patients with severe diffuse disease. A smoking history is associated with poor outcome. Coronary artery bypass grafting in dialysis patients is associated with a higher incidence of complications but can be performed with an acceptable operative mortality and is associated with good symptomatic relief of angina and heart failure.

Background: Radial artery (RA) is being used for coronary artery bypass grafting (CABG) with greater frequency. However, RA is prone to post-CABG vasospasm, which may be neurohormonally mediated. Use of the calcium channel antagonist diltiazem has been advocated as a strategy to reduce post-CABG RA vasospasm. However, whether and to what degree different calcium channel antagonists influence neurohormonally induced RA vasoconstriction remains unknown., Methods: RA segments were collected from patients undergoing elective CABG (n = 13), and isometric tension was examined in the presence of endothelin (10 nM) or norepinephrine (1 microM). In matched RA, endothelin- or norepinephrine-induced contractions were measured in the presence of diltiazem (277 nM), amlodipine (73 nM), or nifedipine (145 nM). These concentrations of calcium channel antagonists were based upon clinical plasma profiles., Results: Endothelin and norepinephrine caused a significant increase in RA-developed tension (0.54+/-0.1 and 0.68+/-0.1 g/mg, respectively; p<0.05). Amlodipine or nifedipine significantly reduced RA vasoconstriction in the presence of endothelin (30+/-6% and 41+/-9%, respectively; p<0.05) or norepinephrine (27+/-8% and 53+/-9%, respectively; p<0.05), whereas diltiazem did not significantly reduce RA vasoconstriction., Conclusions: These results demonstrate that neurohormonal factors released post-CABG can cause RA vasoconstriction, and that calcium channel antagonists are not equally effective in abrogating that response. Both amlodipine and nifedipine, which have a higher degree of vascular selectivity, appear to be the most effective in reducing RA vasoconstriction.

Background: Increased synthesis and release of the potent bioactive peptide endothelin-1 (ET-1) occurs during and after cardiac surgery. However, the cellular and molecular basis for the effects of ET-1 on human left ventricular (LV) myocyte contractility remains unknown., Methods: LV myocyte contractility was examined from myocardial biopsies taken from patients (n = 30) undergoing elective coronary artery bypass. LV myocytes (n = 997, > 30/patient) were isolated using microtrituration and contractility examined by videomicroscopy at baseline and after ET-1 exposure (200 pmol/L). In additional studies, myocytes were pretreated to inhibit either protein kinase C (PKC) (chelerythrine, 1 micromol/L), the sodium/hydrogen (Na/H) exchanger (EIPA, 1 micromol/L), both PKC and the Na/H exchanger, or the ET(A) receptor (BQ-123, 1 micromol/L), followed with ET-1 exposure., Results: Basal myocyte shortening increased 37.8 +/- 6.3% with ET-1 (p < 0.05). Na/H exchanger, PKC, and dual inhibition all eliminated the effects of ET-1. Furthermore, ET(A) inhibition demonstrated that ET-1 effects on myocyte contractility were mediated through the ET(A) receptor subtype., Conclusions: ET-1 directly influences human LV myocyte contractility, which is mediated through the ET(A) receptor and requires intracellular activation of PKC and stimulation of the Na/H exchanger.

Background: All patients undergoing St. Jude Medical valve replacement at the Medical University of South Carolina since January 1979 have been followed prospectively at 12-month intervals., Methods: This report describes long-term experience in 710 adult patients undergoing isolated aortic (AVR) (418) or mitral valve replacements (MVR) (292) with this prosthesis from January 1979 to December 1996., Results: Ages ranged from 19 to 84 years (54.8 +/- 15.1 AVR, 51.8 +/- 12.9 MVR; mean +/- SD). Male gender predominated in the AVR group (70%) and female gender in the MVR group (62%). One hundred and fifty-seven patients (22%) had associated coronary artery bypass grafting (AVR 27%, MVR 15%). Thirty-day operative mortality was 5.3% (22/418) in the AVR group and 5.1% (15/292) in the MVR group. Follow-up is 96.9% complete and ranges from 1 month to 16.9 years (AVR, 2,376 patient-years, mean 5.7 +/- 4.5 years; MVR, 1,868 patient-years, mean 6.4 +/- 4.8 years). In the AVR group, 120 late deaths have occurred and actuarial survival was 78.0 +/- 2.3%, 58.0 +/- 3.2%, and 36.8 +/- 4.8%; at 5, 10, and 15 years, respectively. Forty-six patients have sustained 55 thromboembolic (TE) events (2.3%/patient-year). Fifty-one patients had anticoagulant-related bleeding complications (2.7%/patient-year). The mean improvement in New York Heart Association (NYHA) functional class from preoperative to postoperative was 3.0 +/- 0.8 to 1.7 +/- 0.1 (p < 0.05). In the MVR group, there have been 84 late deaths, and the actuarial survival was 79.3 +/- 2.5%, 60.1 +/- 3.5%, and 49.3 +/- 4.1% at 5, 10, and 15 years, respectively. Fifty-two patients have had 64 TE events (3.5%/patient-year). Twenty-three patients had anticoagulant-related bleeding complications (1.6%/patient-year). The mean improvement in NYHA functional class was from 3.3 +/- 0.6 to 1.8 +/- 0.1. There were no mechanical failures in either group., Conclusions: With a follow-up now extending to 17 years, the St. Jude Medical valve continues to be a reliable mechanical prosthesis with low and stable rates of valve-related complications.

Transient elevations of the potent vasoconstrictive peptide endothelin have been reported to occur with the institution of cardiopulmonary bypass. We measured plasma endothelin levels in a 24-year-old gravid patient undergoing a mitral valve replacement operation. Plasma endothelin levels increased by more than 250% in the first 24 hours postoperatively and remained elevated above baseline values at 36 hours postoperatively.

Background: This study was designed to determine the effects of prolonged hyperkalemic cardioplegic arrest under normothermic or hypothermic conditions with respect to left ventricular myocyte contractile performance and beta-adrenergic responsiveness., Methods: Isolated left ventricular porcine myocytes were randomly assigned to one of three groups: (group 1) normothermic control, (group 2) hypothermic cardioplegic arrest, or (group 3) normothermic cardioplegic arrest. Myocyte contractility was evaluated by high-speed video microscopy at baseline and after beta-adrenergic stimulation with isoproterenol (25 nmol/L)., Results: Myocyte velocity of shortening was decreased after both hypothermic and normothermic cardioplegic arrest (68 +/- 2 and 69 +/- 2 microns/s, respectively) compared with normothermic control values (96 +/- 2 microns/s; p < 0.05). This relative reduction in baseline contractile function was equivalent in both cardioplegia groups (p = 0.5356). With beta-adrenergic stimulation, myocyte velocity of shortening was 186 +/- 4 microns/s in the hypothermic and 176 +/- 3 microns/s in the normothermic cardioplegia groups (p = 0.0563). However, myocyte contractility with beta-adrenergic stimulation was reduced in both cardioplegia groups compared with normothermic controls (205 +/- 4 microns/s; p < 0.05, respectively)., Conclusions: Hyperkalemic cardioplegic arrest under either normothermic or hypothermic conditions resulted in an equivalent reduction in baseline myocyte contractile function with reperfusion/rewarming. Hypothermic cardioplegic arrest may have provided mild protective effects on beta-adrenergic responsiveness. Nevertheless, these results suggest that an important contributory factor for diminished myocyte contractility after simulated cardioplegic arrest was prolonged exposure to a hyperkalemic environment.

Background: Pharmacologic treatment using potassium-channel openers (PCOs) before cardioplegic arrest has been demonstrated to provide beneficial effects on left ventricular performance with subsequent reperfusion and rewarming. However, the PCO treatment interval necessary to provide protective effects during cardioplegic arrest remains to be defined. The present study was designed to determine the optimum period of PCO treatment that would impart beneficial effects on left ventricular myocyte contractility after simulated cardioplegic arrest., Methods: Left ventricular porcine myocytes were assigned randomly to three groups: (1) normothermic control = 37 degrees C for 2 hours; (2) cardioplegia = K+ (24 mEq/L) at 4 degrees C for 2 hours followed by reperfusion and rewarming; and (3) PCO and cardioplegia = 1 to 15 minutes of treatment with the PCO aprikalim (100 micromol/L) at 37 degrees C followed by hypothermic (4 degrees C) cardioplegic arrest and subsequent rewarming. Myocyte contractility was measured after rewarming by videomicroscopy. A minimum of 50 myocytes were examined at each treatment and time point., Results: Myocyte velocity of shortening was reduced after cardioplegic arrest and rewarming compared with normothermic controls (63+/-3 microm/s versus 32+/-2 microm/s, respectively; p < 0.05). With 3 minutes of PCO treatment, myocyte velocity of shortening was improved after cardioplegic arrest to values similar to those of normothermic controls (56+/-3 microm/s). Potassium channel opener treatment for less than 3 minutes did not impart a protective effect, and the protective effect was not improved further with more prolonged periods of PCO treatment., Conclusions: A brief interval of PCO treatment produced beneficial effects on left ventricular myocyte contractile function in a simulated model of cardioplegic arrest and rewarming. These results suggest that a brief period of PCO treatment may provide a strategy for myocardial protection during prolonged cardioplegic arrest in the setting of cardiac operation.

Lung volume reduction surgery is an option for the management of end-stage emphysema. The most frequent surgical complication of lung volume reduction is prolonged air leaks. We describe a patient undergoing a lung volume reduction operation complicated by persistent bilateral air spaces with large air leaks. Treatment with recurrent pneumoperitoneum via a peritoneal dialysis catheter along with chemical sclerosis successfully resolved both problems.

Background: Myocardial precondition, which can be achieved through short intervals of ischemia or hypoxia followed by reperfusion, protects the myocardium with subsequent prolonged periods of ischemia. Accordingly, the present study tested the hypothesis that hypoxic preconditioning before cardioplegic arrest would have direct and beneficial effects on myocyte contractile processes with reperfusion., Methods: Left ventricular porcine myocytes (n = 335) were randomly assigned to one of three treatments: normothermia, maintained in cell media (37 degrees C, 2 hours); cardioplegia, hyperkalemic arrest (24 mEq K+, 4 degrees C, 2 hours) followed by normothermic reperfusion; preconditioning, hypoxia (20 minutes) and reperfusion (20 minutes), and then followed by cardioplegic arrest and rewarming. Myocyte velocity of shortening was measured using computer-assisted videomicroscopy at baseline and with beta-adrenergic receptor stimulation with isoproterenol (25 nmol/L)., Results: In the cardioplegia group, myocyte function was reduced at baseline (22 +/- 1 versus 57 +/- 2 microns/s) and with beta-adrenergic receptor stimulation (81 +/- 5 versus 156 +/- 7 microns/s) compared to normothermic controls (p < 0.05). Preconditioning improved myocyte function at baseline (38 +/- 2 microns/s) and with beta-adrenergic receptor stimulation (130 +/- 6 microns/s) compared to the cardioplegic alone group (p < 0.05)., Conclusions: The important findings from this study are twofold. First, preconditioning can be induced directly at the level of the myocyte, independent of nonmyocyte populations and extracellular influences. Second, myocyte preconditioning provides protective effects on myocyte function and beta-adrenergic responsiveness after cardioplegic arrest and rewarming. These findings suggest that preconditioning may provide a novel approach in protecting myocyte contractile processes during cardioplegic arrest.