Preoperative skeletal muscle density is associated with postoperative mortality in patients with cardiovascular disease.

OBJECTIVES: Although skeletal muscle density (SMD) is useful for predicting mortality, the cut-off in an acute clinical setting is unclear, especially in patients with cardiovascular disease (CVD). This study was performed to determine the preoperative SMD cut-off using the psoas muscle and to investigate the effect on postoperative outcomes, including sarcopaenia, in CVD patients. METHODS: Preoperative psoas SMD was measured by abdominal computed tomography in CVD patients. Postoperative sarcopaenia was defined according to the criteria of the Asia Working Group for Sarcopaenia. The Youden index was used to test the predictive accuracy of survival models. The prognostic capability was evaluated using multivariable survival and receiver operating characteristic curve analyses. RESULTS: Continuous data were available for 1068 patients (mean age 65.5 years; 63.6% male). A total of 105 (9.8%) deaths occurred during the 1.99-year median follow-up period (interquartile range 0.71-4.15). The psoas SMD cut-off estimated by the Youden index was 45 Hounsfield units with high sensitivity and moderate specificity for all-cause mortality and was consistent in various stratified analyses. After adjusting for the existing prognostic model, EuroSCORE II, preoperative and postoperative physical status, psoas SMD cut-off was predicted for mortality (hazard ratio 2.42, 95% confidence interval 1.32-4.45). The psoas SMD cut-off was also significantly associated with postoperative sarcopaenia and provided additional prognostic information to EuroSCORE II on receiver operating characteristic curve analysis (area under the curve 0.627 vs 0.678, P = 0.011). CONCLUSIONS: Reduced psoas SMD was associated with postoperative mortality and added information prognostic for mortality to the existing prognostic model in CVD patients.

Protective effect of urinary trypsin inhibitor on myocardial mitochondria during hemorrhagic shock and reperfusion.

OBJECTIVE: To examine the mitochondrial function in the myocardium after hemorrhagic shock and reperfusion and to evaluate the protective effect of urinary trypsin inhibitor (UTI) on mitochondria. DESIGN: Animal experiment. SETTING: University research laboratory. SUBJECTS: Wistar rats receiving 50,000 units/kg/hr of UTI (n = 27; UTI group) and control rats (n = 26; control group). INTERVENTIONS: Rats were subjected to low-perfusion ischemia with the left ventricular systolic pressure maintained at 50 mm Hg for 60 mins by bleeding, followed by a 60-min reperfusion by transfusion of shed blood. UTI was infused continuously from 10 mins before bleeding. Cardiac function was measured before bleeding, after bleeding, and after transfusion; at each determination point, the myocardial contents of adenosine triphosphate (ATP), creatine phosphate (P-Cr), pyruvate (Pyr), and lactate (Lac) were measured enzymatically. The cytosolic phosphorylation potential (PP) as well as the redox potential of the oxidized form of nicotinamide adenine dinucleotide/reduced form of nicotinamide adenine dinucleotide couple in mitochondria (Eh(NAD+/NADH)) and change of Gibbs free energy in ATP hydrolysis (deltaG(ATP hydrolysis) energy) were calculated. MEASUREMENTS AND MAIN RESULTS: Cardiac function decreased during hemorrhagic shock but improved significantly in the UTI group after transfusion compared with the control group. Lac and the Lac/Pyr ratio were significantly lower in the UTI group than in the control group after transfusion. ATP and P-Cr were significantly higher in the UTI group than in the control group after transfusion. PP (x10(3) M-1), Eh(NAD+/NADH) (x - 1 mV), and deltaG(ATP hydrolysis) (x - 1 kcal/mol) were 1.9 +/- 0.4, 266 +/- 4, and 9.7 +/- 0.2, respectively, in the control group and 4.0 +/- 0.9, 274 +/- 5 and 13.0 +/- 0.2, respectively, in the UTI group after transfusion (p <.001, p <.001, and p <.001, respectively). CONCLUSIONS: In reperfusion after hemorrhagic shock, oxidative phosphorylation in myocardial mitochondria is impaired and energy production remains reduced, even after reperfusion. UTI contributed to the recovery of cardiac function after reperfusion, probably by reducing the severity of mitochondrial dysfunction during a state of shock and by maintaining energy production.