No abstract

Metabolic adaptation of the ischemic human heart includes release of lactate, augmented uptake of glucose and glutamate, together with increased release of citrate and alanine. In the present study exchanges of these metabolites were examined in relation to left ventricular function (LVF) in pig hearts during reperfusion after hypothermic cardioplegic-induced global ischemia and storage. Three groups of pig hearts were studied. Group I consisted of 11 hearts subjected to 9 minutes of warm ischemia prior to cold chemical cardioplegia with Bretschneider's cardioplegic solution (CCC), and hypothermic storage (HS), for a total of 180 minutes. Groups II and III, 8 hearts in each, were subjected to 90 and 180 minutes of CCC and HS, without precardioplegic warm ischemia. All hearts were reperfused in an isolated blood-perfused Langendorff model. Myocardial oxygen uptake and LVF were two-fold depressed in Group I compared to Groups II and III during the first 25 minutes of reperfusion. An increased uptake of glucose (p < 0.05) and augmented release of lactate (p < 0.01) and citrate (p < 0.001) were found during the reperfusion period in the hearts subjected to precardioplegic warm ischemia, indicating an increased total ischemic burden compared to Groups II and III. No significant changes in LVF or myocardial metabolism were noted between Groups II and III during reperfusion. In all three heart groups a substantial release or loss of glutamate was found at start of reperfusion, although in the preischemic state prior to cardioplegia pig hearts were found to extract glutamate from the circulation to an extent similar to that of the human heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Six-hundred-and-three patients who underwent 720 vascular prosthetic graft operations caudal to the diaphragm were studied retrospectively. Wound complications appeared in 99 patients. Prophylactic antibiotics were not used. Serous secretion was found after 27 arterial graft procedures (3.8%), superficial wound infection after 41 (5.7%), and prosthetic graft infection after 31 (4.3%). Of the 31 patients with prosthetic graft infection, 10 recovered (32%). Four of these patients recovered after removal of the Staphylococcus aureus-infected prosthesis. Three received a replacement prosthesis with systemic antibiotic treatment and closed antibiotic irrigation, and one patient's prosthesis was replaced with an autologous vein graft with antibiotic treatment. Twelve patients (39%) underwent amputation and 9 died. The frequency of graft occlusion was greater when the prosthesis was infected with Staphylococcus aureus than with other microorganisms. The aggressive approach used in the 4 above-mentioned cases could be a treatment modality in prosthetic graft infection with Staphylococcus aureus, especially because of the high incidence of graft occlusion associated with these microorganisms.

From 1976 through 1986, 188 patients (female/male ratio: 2/1, age 20-77 years, mean 58 years) with isolated mitral valve disease underwent valve replacement using the Carpentier-Edwards porcine bioprothesis (CEPB). Nine hospital deaths (4.8%) were excluded from further analysis. Follow-up was 0.2-11.3 years (mean 5.2 years); preoperatively, 74% had atrial flutter/fibrillation, and 75% were in NYHA-classes III-IV. All patients were put on life-long coumadin treatment. Preoperative predictability of long-term survival and prosthesis-related complications was examined using Cox regression analysis. Five preoperative variables were found to have independent predictive value as regards long-term survival: myxomatous degeneration of the valve (p = 0.002), chronic regurgitation (p = 0.003), age (p = 0.004), NYHA-class III-IV (p = 0.05), and atrial flutter/fibrillation (p = 0.05). A prognostic index calculated form the final Cox model identified six risk groups (I-VI) having cumulative 10-year survivals +/- SE of: I (n = 9) 100%, II (n = 10) 90 +/- 9%, III (n = 30) 73 +/- 10%, IV (n = 70) 51 +/- 9%, V (n = 43) 17 +/- 10%, and VI (n = 17, 7-year survival) 16 +/- 13% (p less than 0.0001). The incidence of late valve-related complications (%/patient-years) were: hemorrhage, 1.2; thromboembolism, 0.5; Endocarditis, 1.0; paravalvular leak, 0.2; and primary tissue failure, 1.5. Previous closed comissurotomy adversely influenced the occurrence of hemorrhage, while calcified mitral annulus were predictive of endocarditis. Younger age (less than or equal to 45 years) had a strong predictive influence of primary tissue failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased glutamate utilization is a part of the metabolic adaptation to oxygen deprivation by the heart. The effect of low-dose L-glutamate (2 mmol/L) during continuous reperfusion after aortic unclamping on postcardioplegic recovery was studied in pig hearts similar in size, anatomy, and function to the human adult heart. After cold crystalloid cardioplegic arrest (CCC) with Bretschneider solution no 3, hearts were excised from pigs weighing 70-80 kgs (heart weight, average +/- SEM: 308 +/- 4 grams), and reperfused in an isolated blood-perfused heart model for 120 minutes. Three groups of hearts were compared. One group of hearts was subjected to 30 minutes of CCC only (30 min group; n = 9), another group of hearts to 90 minutes of CCC and storage (Control group: n = 16), and a third group to 90 minutes of CCC and storage, but with L-glutamate added to the blood reperfusate (2 mmol/L) (Glutamate group: n = 18). In the Control group 14 of 16 hearts (88%) needed electrical defibrillation after start of reperfusion, significantly more (p < 0.05) than the 8 of 18 (44%) in the Glutamate group; the difference between the 30-min (2 of 9 [22%]) and the Glutamate group was not significant (p = 0.48). Developed left-ventricular pressure (DLVP) and positive dP/dtmax (+dP/dtmax) was significantly higher in the Glutamate group than in the Control group during early reperfusion (DLVP: p < 0.05: +dP/dtmax: p < 0.01) and the entire reperfusion (DLVP and +dP/dtmax: p < 0.05), while reperfusion responses in the Glutamate and 30-min groups were not significantly different. Furthermore, myocardial oxygen uptake was significantly higher in the Glutamate group than in the Control group (p < 0.001), but not higher than that in the 30-min group. Decreased lactate release was found in the Glutamate group compared to the Control group during early reperfusion (p < 0.01), and the entire reperfusion (p < 0.001). No differences were found between the Control and Glutamate groups in alanine exchange. Thus, L-glutamate has a beneficial effect in pig hearts on both functional and metabolic recovery after cold crystalloid cardioplegia and storage when present in a concentration even as low as 2 mmol/L during continuous reperfusion after aortic unclamping. A possible mechanism is a glutamate-induced stimulation of the malate-aspartate shuttle leading to increased intramyocardial lactate utilization.