Perioperative myocardial damage and the incidence of type 2 myocardial infarction in patients with intermediate and high cardiovascular risk.

OBJECTIVE: Perioperative myocardial infarction is a major cause of morbidity and mortality in patients undergoing surgical operations. We aimed to determine the incidence of perioperative myocardial infarction in patients with intermediate- or high-risk Framingham scores. METHODS: One hundred and one patients (62 males, 39 females) over 40 years of age (mean age 72±11 years) median 73 (65-81), min- max (46-96), with Framingham risk scores of 10% or higher, and scheduled for surgical interventions in the orthopedics and urology departments of our hospital were included in the study. Patient demographics, comorbidities, blood pressures, and biochemical data were recorded. Troponin values and electrocardiographic findings were obtained during the immediate preoperative period and on postoperative day 2 and then compared. Perioperative myocardial injury and infarction were diagnosed using the third universal definition of myocardial infarction. RESULTS: In 44 (43%) patients, postoperative troponin values were compared with the preoperative values. In 26 (25%) patients, the changes were consistent with myocardial ischemia or damage. Alterations in troponin values with significant electrocardiogram (ECG) changes were found in 6 patients (6%). CONCLUSION: The risk of postoperative myocardial damage was high in our patients with intermediate or high-risk Framingham scores. This im-plies that close follow-up of these patients with abnormal ECG and troponin values during the pre- and postoperative period is required.

Lowering Uric Acid With Allopurinol Improves Insulin Resistance and Systemic Inflammation in Asymptomatic Hyperuricemia.

BACKGROUND: Hyperuricemia is an independent predictor of impaired fasting glucose and type 2 diabetes, but whether it has a causal role in insulin resistance remains controversial. Here we tested the hypothesis that lowering uric acid in hyperuricemic nondiabetic subjects might improve insulin resistance. METHODS: Subjects with asymptomatic hyperuricemia (n = 73) were prospectively placed on allopurinol (n = 40) or control (n = 33) for 3 months. An additional control group consisted of 48 normouricemic subjects. Serum uric acid, fasting glucose, fasting insulin, HOMA-IR (homeostatic model assessment of insulin resistance), and high-sensitivity C-reactive protein were measured at baseline and at 3 months. RESULTS: Allopurinol-treated subjects showed a reduction in serum uric acid in association with improvement in fasting blood glucose, fasting insulin, and HOMA-IR index, as well as a reduction in serum high-sensitivity C-reactive protein. The number of subjects with impaired fasting glucose significantly decreased in the allopurinol group at 3 months compared with baseline (n = 8 [20%] vs n = 30 [75%], 3 months vs baseline, P < 0.001). In the hyperuricemic control group, only glucose decreased significantly and, in the normouricemic control, no end point changed. CONCLUSIONS: Allopurinol lowers uric acid and improves insulin resistance and systemic inflammation in asymptomatic hyperuricemia. Larger clinical trials are recommended to determine if lowering uric acid can help prevent type 2 diabetes.

Effects of allopurinol on endothelial dysfunction: a meta-analysis.

OBJECTIVE: Several studies have assessed the effect of allopurinol on endothelial function, but these studies were relatively small in size and used different methods of evaluating endothelial function. We conducted a meta-analysis to investigate the effect of allopurinol on both endothelial-dependent and -independent vasodilatation. METHODS: Electronic databases, Medline, PubMed, EMBASE, SCOPUS, EBSCO and the Cochrane Library Central Register of Clinical Trials were searched from January 1985 to July 2013 on clinical trials (randomized and non-randomized) which assessed the effect of allopurinol on endothelial function. We conducted a sensitivity analysis to assess the contribution of each study to the pooled treatment effect by excluding each study one at a time and recalculating the pooled treatment effect for the remaining studies. Treatment effect was significant if p < 0.05. We assessed for heterogeneity in treatment estimates using the Cochran Q test and the χ(2) statistic (with substantial heterogeneity defined as values >50%). RESULTS: The final analysis consisted of 11 studies (2 observational and 9 randomized). For the endothelial-dependent vasodilatation there were 6 studies, including 257 patients, that evaluated flow-mediated dilatation and 5 studies with 87 patients that reported data on forearm blood flow response to acetylcholine or flow-dependent vasodilatation. Overall, there was a significant increase in the endothelium-dependent vasodilatation with allopurinol treatment (MD 2.69%, 95% CI 2.49, 2.89%, p < 0.001; heterogeneity χ(2) = 319.1, I(2) = 96%, p < 0.001). There was only 1 study (100 patients) assessing nitrate-mediated dilatation and 4 studies (73 patients) evaluating forearm blood flow response to sodium nitroprusside as measures of endothelial-independent vasodilatation. The overall analysis (MD -0.08, 95% CI -0.50, 0.34, p = 0.70; heterogeneity χ(2) = 9.0, I(2) = 44%, p = 0.11) showed no effect of allopurinol treatment on endothelium-independent vasodilatation. CONCLUSIONS: We found that treatment of hyperuricemia with allopurinol is associated with an improvement in the endothelial-dependent, but not with the endothelial-independent vasodilatation.