Biomedical subjects
Publications and source records attributed to L Golding.
The Cleveland Clinic continuous flow blood pump is the central element of our innovative ventricular assist system (IVAS). Recent progress has been made in the design/fabrication of a pulsatile mock loop, journal bearing materials testing, and evaluation of a system control algorithm. These results have allowed an acceleration of our program.
The neutrophil respiratory burst was examined by the technique of luminol-dependent chemiluminescence (LDCL) triggered by submaximal concentrations of N-formyl-methionyl-leucyl-phenylalanine (fMLP) in diluted whole blood. We sought to identify the chemical species responsible for LDCL in whole blood, to examine the role of leukotriene B4 (LTB4) and other arachidonic acid metabolites as mediators of the fMLP signaling pathway, and to investigate the effect of peroxynitrite on this response. Both sodium azide and taurine significantly inhibited LDCL (93% inhibition with 100 microM azide, 52% inhibition with 10 mM taurine). More modest inhibition was seen with superoxide dismutase (SOD), catalase, the nitric oxide synthase inhibitor monomethyl-L-arginine (L-NMMA), and with inhibitors of the cyclooxygenase (indomethacin), lipoxygenase (AA-861; no effect), and cytochrome P-450 (SKF 525-A) pathways of arachidonic acid metabolism. The nitric oxide donor SIN-1 (1-100 microM) and peroxynitrite (10-300 microM) also augmented fMLP-induced LDCL. The augmentation seen with peroxynitrite and SIN-1 was attenuated by SOD. Despite the increase in LDCL, peroxynitrite caused a dose-related inhibition of fMLP-stimulated LTB4 release. In summary, our results indicate that (1) LDCL elicited by fMLP in diluted whole blood appears primarily mediated by hypochlorous acid derived from myeloperoxidase; (2) pretreatment with the nitric oxide donor SIN-1 or with peroxynitrite augments LDCL; and (3) LTB4 release does not contribute to fMLP-stimulated LDCL or in the modulation of LDCL by SIN-1 or peroxynitrite.
The response of the body and the blood pump was evaluated in animals with a pulsatile artificial heart (total artificial heart [TAH]) and those with a nonpulsatile artificial heart (nonpulsatile biventricular bypass [NPBVB]) subjected to the same exercise load. The animals used in this study were 5 calves implanted with a pusher-plate type TAH (45-206 days) and 5 calves implanted with a nonpulsatile centrifugal pump (34-99 days). The pre-exercise pump flow rate was 92.1 +/- 8.1 ml/kg/min for the TAH group and 94.8 +/- 9.1 ml/kg/min for the NPBVB group, with no significant difference between the two groups. The workload was administered at a rate of 1.5 mph for 15 min. The artificial heart driving conditions were kept constant throughout the test period. Sequential changes in hemodynamic response and metabolism were determined before, during, and for 30 min after exercise. Both TAH and NPBVB calves showed excellent tolerance of the workload (1.5 mph exercise); in NPBVB calves, oxygen demand was compensated for by an increase in the arteriovenous oxygen difference during exercise; and norepinephrine showed a greater response in the NPBVB group. Based on the results presented, the nonpulsatile pump seems to lend itself to a mechanically driven artificial heart of the complete implantation type because of its small size, high efficiency, and the lack of need for a compliance chamber.
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Internal defibrillation leads were placed at time of coronary revascularization in 79 patients. In 34, an implantable cardioverter defibrillator (ICD) was placed simultaneously (group I). A two-stage strategy (selective implantation of the ICD in patients with postoperative spontaneous or inducible ventricular tachycardia [VT]) was followed in 45 patients (group II). Group I patients had failed more antiarrhythmic drug trials (2.9 +/- 1.6 vs 1.5 +/- 1.6; P = 0.02), including amiodarone (62% vs 20%; P less than 0.001). There were four operative deaths in each group. Postoperatively, VT was present in 27 group II patients (60%), 25 of whom received an ICD (two refused device implantation). Patients with postoperative VT had a lower left ventricular ejection fraction than those without VT (33 +/- 9 vs 47 +/- 16; P = 0.01). Actuarial survival at 1, 2, and 3 years was 88 +/- 6, 88 +/- 7, and 88 +/- 10 in group I; and 83 +/- 6, 76 +/- 7, and 76 +/- 11 in group II (NS). No patient without an ICD (based on the postoperative electrophysiological study [EPS]) died suddenly. Five patients (6%) had ICD system infection. Sudden death was largely prevented by either strategy, but relatively high rates of operative mortality and ICD system infection were observed. Prospective studies should identify patients more likely to benefit from one or another strategy.
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We analyzed the long-term outcome of 198 patients after unsuccessful percutaneous transluminal coronary angioplasty. Forty-nine percent underwent emergency coronary artery bypass grafting surgery, 17% had elective bypass surgery, and 34% were treated medically. The in-hospital mortality rate was 4%, and myocardial infarction occurred in 36% of patients. Follow-up was completed in 100% of patients with a mean follow-up period of 35 +/- 22 months. Actuarial cardiac survival at 4 years was 97% in the emergency bypass surgery group, 100% in the elective bypass surgery group, and 86% in the medically treated group. Actuarial event-free survival (freedom from myocardial infarction, bypass surgery, coronary angioplasty, and cardiac death) at 4-year follow-up was 81% in 198 patients, 90% in the emergency bypass surgery group, 85% in the elective bypass surgery group, and 65% in the medically treated group. Results of multivariate analysis showed that emergency or elective bypass surgery after failed coronary angioplasty, normal or mildly impaired left ventricular function, and male sex were predictors of better outcome at 4 years.
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