Background Elevated preoperative hemoglobin A1c (HbA1c) is a predictor of poor outcomes following coronary artery bypass grafting (CABG), but the role of increased postoperative glucose variability (GV) is unknown. We hypothesized that short-term postoperative GV is associated with an increased risk of postoperative atrial fibrillation following isolated CABG. Methods Multicenter retrospective study of 2073 patients who underwent isolated CABG from January 2012 to March 2018. Postoperative GV in the first 24 hours was measured by standard deviation, coefficient of variation, and mean amplitude of glycemic excursions. Multivariate logistic regression assessed the independent association of GV with postoperative atrial fibrillation. Results A total of 2073 patients met the study criteria, and 446 patients (21.5%) developed postoperative atrial fibrillation. Using multivariate logistic regression to adjust for covariates, postoperative atrial fibrillation was associated with increased 24-hour GV (odds ratio [OR] = 1.16, 95% confidence interval [CI], 1.05-1.27, P < 0.01) and increased 24-hour mean glucose (OR = 1.14, 95% CI, 1.08-1.21, P < 0.01). Thus, for every 10% increase in 24-hour GV or 10 mg/dL increase in mean glucose, there was a 16% or 14% increased risk of postoperative atrial fibrillation respectively. Conclusions Increased 24-hour GV and mean glucose are predictors of atrial fibrillation after CABG. Preoperative HbA1c is not a risk factor for postoperative atrial fibrillation after adjusting for postoperative mean glucose and GV. Further investigation is needed to determine the relationship between adherence to strict glucose control and adverse events following CABG.
Reduction of the leukocyte population during postischemic coronary reperfusion results in decreased neutrophil-mediated tissue injury. However, the importance of leukocyte adhesion to coronary endothelium for postischemic ventricular dysfunction after global hypothermic myocardial ischemia is unknown. Neutrophil integrins (CD11b/CD18) upregulate in response to cardiopulmonary bypass and ischemic stress, and their role in generating postoperative ventricular dysfunction was examined in this study.An in vivo, in situ model of neonatal cardiac surgery was established in which neutrophil adherence was manipulated by administering NPC 15669 (an inhibitor of neutrophil CD11b/CD18 surface receptor upregulation). Seventeen 3- to 5-day-old piglets (8 controls and 9 NPC 15669-treated animals) were instrumented with a coronary sinus catheter, sonomicrometry crystals across the short axis of the left ventricle (LV), and a micromanometer positioned in the LV. Hearts were subjected to 90 minutes of hypothermic ischemia after a single dose of cold crystalloid cardioplegia. Myocardial granulocyte accumulation during ischemia and reperfusion was reduced in NPC animals compared with controls (myeloperoxidase activity, 43.4 +/- 2.6 and 75.8 +/- 6.3 mumol/10 mg tissue, respectively; P < or = .005). This was associated with a reduction in coronary vascular resistance in NPC animals compared with controls (P < or = .02) and decreased release of myocardial creatine phosphokinase throughout reperfusion (P < or = .05). NPC animals demonstrated an improved preservation of the end-systolic pressure-volume relation after discontinuation of cardiopulmonary bypass (71 +/- 6% and 96 +/- 6% at 60 minutes, respectively; P < or = .05). There was no difference in ventricular compliance between groups.These data demonstrate that inhibition of neutrophil CD11b/CD18 surface adherence receptor upregulation reduces granulocyte accumulation in myocardium after hypothermic global ischemia, reduces myocyte damage, and improves ventricular systolic function.
Reports of clinical improvement in human studies of dynamic cardiomyoplasty lack support by consistent objective hemodynamic evidence. Animal studies have also yielded conflicting results, likely due to nonuniform models, particularly the use of unconditioned wraps, and to limitations in commonly used study modalities caused by exaggerated heart motion during wrap stimulation. Our purpose was to assess the primary functional properties of the heart wrapped by conditioned muscle using pressure-volume relation analysis based on conductance catheter volume data. Compared with the unstimulated state, 1:1 stimulation caused an increase in contractility and decreases in end-diastolic volume and stroke work. Assisted beats during 1:2 stimulation showed an increase in contractility and a decrease in end-diastolic volume. Unassisted beats (1:2) showed decreases in end-diastolic volume and stroke work. There was no augmentation of cardiac output or ejection fraction with stimulation (1:1 or 1:2). We conclude that in the nonfailing heart, increased contractility does not augment cardiac output, ejection fraction, and stroke work because of a simultaneous decrease in end-diastolic volume. These changes in contractility and end-diastolic volume may prove therapeutic for dilated cardiomyopathy.
