The predictive value of the epicardial adipose thickness in the rate of expansion of the aortic root.

BACKGROUND: Epicardial adipose tissue (ECAT) is metabolically active and is involved in the development of atherosclerosis. The thickness of ECAT has been positively correlated with the dimensions of the ascending aorta. We aimed to examine whether ECAT thickness predicted the expansion of the aortic dimensions. METHODS: The imaging results of patients who had undergone transthoracic echocardiographic (TTE) examinations more than twice during the period 2005-2015 were surveyed. We included adult patients who had undergone TTE examinations at least 1 year apart. The ECAT was measured in the parasternal long-axis view from the index TTE study. End-diastolic dimensions in three consecutive beats were averaged for all measurements. The annulus, root, and sinotubular junction (STJ) were also measured. The amount of increase (if any) in aortic dimensions per year was calculated and the correlation of this increase with the initial thickness of the ECAT was analyzed. RESULTS: In total, 429 examinations were performed with 197 patients (17 females), from which 394 examinations were analyzed. The ECAT thickness was 8.6 ± 3.6 mm. In the initial examinations, the annulus, STJ, and root measured 23 ± 4, 28 ± 4, and 34 ± 4 mm, respectively. In univariate analysis, for every 1 mm of ECAT thickness, the STJ expanded 0.056 (95% CI: 0.001-0.112 mm/year; p = 0.030) and the aortic root expanded 0.088 mm/year (p < 0.001). In multivariate analysis, ECAT thickness remained an independent predictor of the aortic root expansion. For every 1­mm increase in ECAT thickness, the aortic root expanded by 0.036 mm (95% CI: 0.010-0.062) per year (p = 0.007). CONCLUSION: The thickness of the ECAT is a predictor of more rapid increases in the dimensions of the aortic root. Further studies of patients with established aortic aneurysm are warranted.

Intraoperative administration of vasopressin during coronary artery bypass surgery is associated with acute postoperative kidney injury.

BACKGROUND: Severe vasodilatation is commonly seen upon weaning from cardiopulmonary bypass (CPB). We examined the effects of vasopressin (arginine vasopressin [AVP]) on acute kidney injury (AKI) in postoperative period. METHODS: The records of 483 patients undergoing coronary bypass surgery on CPB from 2004 to 2008 were retrospectively reviewed. Demographic, anthropometric, comorbid condition, and perioperative clinical/laboratory data were collected along with postoperative complications. Patients were grouped based on the perioperative use of AVP, and AKI was used as the primary end point. Univariate and multivariate logistic regression analyses were used, followed by propensity score matching for AKI. Null hypothesis was rejected at P < .05. RESULTS: Postoperative AKI occurred in 14.5% of patients. Arginine vasopressin was administered to 280 patients during the perioperative period. The prevalence of AKI in AVP was 20%, whereas it was 6.1% in controls (P < .0001). Arginine vasopressin was an independent factor that predicted the occurrence of AKI (odds ratio, 3.60; 95% confidence interval, 1.22-10.62; P = .02). However, after propensity score matching, the association between AKI and AVP was lost (P = .073). CONCLUSION: Acute kidney injury is a common complication after cardiac surgery, and vasopressin use increases its incidence; however, this effect may rely on several clinical factors, and its true effect should be examined by large randomized trials.

Adjuvant therapy with intrathecal clonidine improves postoperative pain in patients undergoing coronary artery bypass graft.

BACKGROUND: Alpha2 adrenergic agonists have long been employed as analgesics and to sedate patients undergoing surgical procedures. In addition, their therapeutic response synergizes that elicited by opioids. Although this response is well known, the role of alpha2 agonists, such as clonidine, during various painful surgical procedures remains to be elucidated. The goal of our study was to evaluate the effects of the intrathecal administration of clonidine on postoperative pain control and time to extubation in patients undergoing coronary artery bypass grafting. METHODS: Eighty-five patients undergoing coronary artery bypass grafting randomly received either an intrathecal injection of preservative free morphine 0.5 mg (MOR) or a combination of morphine 0.5 mg and clonidine 100 microg (CMC) before induction of anesthesia. Anesthesia was induced and maintained using a balanced anesthesia technique. Patients were transferred to the intensive care unit while intubated and weaned from mechanical ventilation following an established weaning protocol. Postoperative pain, opioid use within the first 24 hours, and time to extubation were used as primary outcome variables. Data were analyzed by a 2-tailed t test for continuous variables and Fisher exact test for nonparametric variables. RESULTS: There were no demographic differences between the CMC and MOR groups. Postoperative pain, as assessed by a visual analog scale, was milder in the CMC group when compared with that of the MOR group (2.2+/-0.36 vs. 3.4+/-0.33, P<0.05). Similarly, patients in the CMC group required lower doses of morphine within 24 hours compared with the MOR group (2.02+/-0.36 vs. 6.47+/-0.49 mg, P<0.0001). Time to extubation was significantly shorter in patients receiving CMC than in those who received MOR (592+/-52 vs. 887+/-75 min, P<0.05). There was no mortality in either group. There was a trend for increased vasopressin use in the CMC group compared with the MOR group, although this was not statistically significant (P=0.07). CONCLUSIONS: Addition of clonidine to neuraxial opioids improves the quality of analgesia postoperatively and expedites the process of weaning from mechanical ventilation. There were no serious adverse events in the cohort of the patients studied. However, the safety profile of this medication remains to be examined with a larger group of patients.

Anesthetic myocardial protection with sevoflurane.

OBJECTIVE: To examine the role of sevoflurane in myocardial protection in patients undergoing coronary artery bypass graft (CABG) surgery. DESIGN: Prospective, randomized, controlled, double-blinded study. SETTING: Veterans Administration Medical Center (VAMC), Buffalo, New York. SUBJECTS: Twenty-one patients undergoing CABG were included in the study. Eleven patients were randomized to receive sevoflurane, and 10 patients served as controls. INTERVENTION: Total intravenous anesthesia was provided for both study and control groups by infusion of propofol, fentanyl, and midazolam. Sevoflurane 2% was added to the cardioplegia solution in the experimental group. MEASUREMENTS AND MAIN RESULTS: Neutrophil beta-integrins (CD11b/CD18), tumor necrosis factor alpha (TNF-alpha), and interleukin (IL)-6 were measured as indicators of the inflammatory response to myocardial ischemia-reperfusion injury. Blood samples were obtained from the aorta and coronary sinus before (T1) and immediately after cardiopulmonary bypass (CPB) (T2) and, in addition, from a peripheral artery 6 hours (T3) after CPB. Myocardial function was determined in all patients at each time point. Left ventricular stroke work index (LVSWI) was calculated as an estimation of left ventricular function. Left ventricular regional wall motion abnormality (RWMA) was assessed by transesophageal echocardiography at T1 and T2 time points. TNF-alpha was detectable only in the control group in arterial samples at T3. IL-6 levels (pg/mL) were found to be lower in the sevoflurane group compared with controls at T2 arterial circulation (38.2 +/- 21.1 v 60.6 +/- 19.1, p < 0.05) as well as in the coronary circulation (38.4 +/- 19.9 v 118.2 +/- 23.5, p < 0.01) at T2. CD11b/CD18 increased 79% after CPB in the control group while only increasing 36% in the sevoflurane group (p < 0.05). The post-CPB LVSWI was back to its baseline values in the sevoflurane group, whereas it was still significantly depressed in the control group. Eight of 10 patients in the control group showed a transient new-onset RWMA in either the septal or anteroseptal regions. Only 2 of 11 patients in the sevoflurane group showed transient RWMA of the LV. CONCLUSIONS: Sevoflurane decreases the inflammatory response after CPB, as measured by the release of IL-6, CD11b/CD18, and TNF-alpha. Myocardial function after CPB, as assessed by RWMA and LVSWI, was also improved with sevoflurane. The role of sevoflurane in myocardial protection and the inflammatory response to myocardial reperfusion should be considered.