Longitudinal outcomes after endovascular repair of abdominal aortic aneurysms.

OBJECTIVE: Endovascular abdominal aneurysm repair (EVAR) is increasingly used, but there is insufficient evaluation of long-term outcomes. METHOD: Retrospective cohort study using the linked Washington State hospital discharge database. RESULT: 3,350 patients underwent elective repair of AAA (1181 EVAR) between 2000 and 2005. EVAR patients were older and had higher comorbidity scores. The 30-day readmission rate after EVAR was 11.6%. The 30-day readmissions included cardiac complications (18.5%) and device complications (10.4%). 46% of the 30-day readmissions after EVAR underwent procedures: abdominal/ iliac angiography (7.4%), angioplasty (8.9%), and device revision (8.2%). Mean time to late interventions was 611 days. CONCLUSION: Readmission, reintervention, and complication rates after EVAR occur more commonly than previously described. Cardiac complications were the most common readmission. Almost half of the 30-day readmissions required a secondary intervention. Long-term complications after EVAR occurred before two years. Population-based assessment may be more reflective of "real world" complication rates after EVAR.

NO metabolites accumulate in erythrocytes in proportion to carbon dioxide and bicarbonate concentration.

It is not known whether the ratio between the concentrations of NO metabolites (NOx) in plasma (pNOx) and in erythrocytes (eNOx) is constant or correlates with chemical parameters of the blood. We measured pH, PO(2), and PCO(2) and calculated bicarbonate concentration in 19 blood samples from the aorta, coronary sinus, and leg veins of 7 dogs. Erythrocytes were then separated by centrifugation and lysed with distilled water, and the lysate was ultrafiltered with a molecular cutoff of 50 kDa to remove the hemoglobin. NOx were measured in plasma and in the ultrafiltrate. NOx concentration was higher in erythrocytes, with eNOx/pNOx ranging from 4.38 to 14.60. Linear and significant correlations were found between the natural logarithm of eNOx/pNOx and PCO(2) (r = 0.70, P < 0.001) or bicarbonate concentration (r = 0.72, P < 0.001). These results demonstrate, for the first time, that plasma NOx cannot be considered as a constant fraction of the total NOx in blood but varies dramatically in proportion to the CO(2)/bicarbonate concentration. To prevent an underestimation of venous-arterial difference of NOx across organs, NOx should be measured in whole blood.

Reduced nitric oxide production and altered myocardial metabolism during the decompensation of pacing-induced heart failure in the conscious dog.

The aim of the present study was to determine whether cardiac nitric oxide (NO) production changes during the progression of pacing-induced heart failure and whether this occurs in association with alterations in myocardial metabolism. Dogs (n=8) were instrumented and the heart paced until left ventricular end-diastolic pressure reached 25 mm Hg and clinical signs of severe failure were evident. Every week, hemodynamic measurements were recorded and blood samples were withdrawn from the aorta and the coronary sinus for measurement of NO metabolites, O2 content, free fatty acids (FFAs), and lactate and glucose concentrations. Cardiac production of NO metabolites or consumption of O2 or utilization of substrates was calculated as coronary sinus-arterial difference times coronary flow. In end-stage failure, occurring at 29+/-1.6 days, left ventricular end-diastolic pressure was 25+/-1 mm Hg, left ventricular systolic pressure was 92+/-3 mm Hg, mean arterial pressure was 75+/-2.5 mm Hg, and dP/dtmax was 1219+/-73 mm Hg/s (all P<0.05). These changes in hemodynamics were associated with a fall of cardiac NO metabolite production from 0.37+/-0.16 to -0.28+/-0.13 nmol/beat (P<0.05). O2 consumption and lactate uptake did not change significantly from control, while FFA uptake decreased from 0.16+/-0.03 to 0.05+/-0.01 microEq/beat and glucose uptake increased from -2.3+/-7.0 to 41+/-10 microgram/beat (P<0.05). The cardiac respiratory quotient also increased significantly by 28%. In 14 normal dogs the same measurements were performed at control and 1 hour after we injected 30 mg/kg of nitro-L-arginine, a competitive inhibitor of NO synthase .O2 consumption increased from 0.05+/-0.002 mL/beat at control to 0.071+/-0.003 mL/beat after nitro-L-arginine, while FFA uptake decreased from 0.1+/-0.01 to 0.06+/-0.01 microEq/beat, lactate uptake increased from 0.15+/-0.04 to 0.31+/-0.03 micromol/beat, glucose uptake increased from 8.2+/-5.0 to 35.4+/-9.5 microgram/beat, and RQ increased by 23% (all P<0.05). Our results indicate that basal cardiac production of NO falls below normal levels during cardiac decompensation and that there are shifts in substrate utilization. This switch in myocardial substrate utilization also occurs after acute pharmacological blockade of NO production in normal dogs.