Impact of metabolic syndrome on development of contrast-induced nephropathy after elective percutaneous coronary intervention among nondiabetic patients.

BACKGROUND: Identifying patients who are vulnerable to development of contrast-induced nephropathy (CIN) is essential because of its association with prolonged hospitalization, increased cost, and increased in-hospital and long-term mortality rates. HYPOTHESIS: Individual components of metabolic syndrome (MetS) are well-established risk factors for kidney injury. Nondiabetic patients diagnosed with MetS might be at an increased risk of developing CIN after elective percutaneous coronary intervention (PCI). METHODS: A total of 599 nondiabetic patients were enrolled, of whom 313 met the MetS criteria and 286 were included in the control group. Patients were evaluated for development of CIN after elective PCI. RESULTS: Contrast-induced nephropathy occurred in 9.3% (29 of 313) of the MetS group and 4.9% (14 of 286) of the control group (P = 0.04). The multivariable regression model revealed that baseline glomerular filtration rate < 30 mL/min, multivessel intervention, and MetS increased and use of statin decreased the probability of CIN independent from confounding factors (odds ratio [OR]: 7.84, 95% confidence interval [CI]: 3.46-24.36, P < 0.01 for baseline glomerular filtration rate < 30 mL/min; OR: 0.82, 95% CI: 0.42-0.96, P = 0.02 for statin use; OR: 2.64, 95% CI: 1.46-6.56, P < 0.01 for multivessel intervention; and OR: 1.66, 95% CI: 1.12-2.61, P = 0.03 for MetS). CONCLUSIONS: Metabolic syndrome is a risk factor for CIN in patients with stable coronary artery disease who undergo elective PCI. We suggest that clinicians recognize the patients with MetS before elective coronary interventions.

Overcoming aspirin resistance with loading clopidogrel earlier in elective percutaneous coronary intervention.

We aimed to analyze the clinical effect of clopidogrel loading time on adverse cardiovascular events among patients with aspirin resistance. Recurrent adverse events may still occur despite dual antiplatelet therapy after coronary stenting. Aspirin resistance is one of the possible reasons of this trouble. Optimal antiplatelet strategy for coronary stenting is unknown among patients with aspirin resistance. A total of 980 patients scheduled for elective coronary stenting were enrolled and allocated into two groups according to the loading time of clopidogrel more or less than 6 hours before coronary intervention (early- or late-loaded groups, respectively). Aspirin resistance was determined according to the urinary levels of 11-dehydrothromboxane B2. Overall 240 patients who were allocated to early- and late-loaded groups were identified as aspirin resistant according to the urinary levels of 11-dehydrothromboxane B2. After a follow-up period of 12 months major adverse cardiac events were observed among 16 patients (13.9%) in the early-loaded group and 30 patients (25.8%) in the late-loaded group (p = 0.02). Early loading of clopidogrel was an independent predictor of lower rate of cardiac events (hazard ratio = 0.46 [0.32-0.76, 95% confidence interval], p = 0.001). The rates of bleeding events and periprocedural myocardial infarction were similar in early- and late-loaded groups. The current study demonstrated that loading of clopidogrel earlier than 6 hours before elective coronary stenting among aspirin-resistant patients was associated with increased benefits for ischemic events with similar bleeding rates.

Effect of angiotensin converting enzyme inhibitors on periprocedural myocardial infarction in patients with metabolic syndrome.

BACKGROUND: Metabolic syndrome (MetS) has been reported as a risk factor for cardiovascular events. The aim of the present study is to investigate the association between chronic angiotensin-converting enzyme inhibitors (ACE-I) therapy and the rate of periprocedural myocardial infarction (PMI) after elective coronary stenting among patients with MetS. METHODS: The inclusion criteria were MetS and plan for elective percutaneous coronary intervention. To assess the effect of ACE-I treatment on the incidence of PMI, measurements of cardiac biomarkers (CK-MB mass and troponin I) were performed at baseline and 24 h after the procedure. RESULTS: A total of 459 patients fulfilling the inclusion criteria were recruited to chronic ACE-I treatment and ACE-I naive groups in a 2/1 ratio. Baseline troponin I and CK-MB levels were similar in both treatment groups, whereas they were significantly lower in ACE-I group 24 h after the procedure. Univariate analysis identified body mass index (BMI), LDL cholesterol, nitrate and ACE-I use as significant factors for the development of PMI. Multivariate regression model revealed that body mass index increased and use of nitrate and ACE-I decreased the probability of PMI independent from confounding factors (OR 1.14, 95% CI 1.05-1.23, p = 0.002 for BMI; OR 0.26, 95% CI 0.14-0.48, p = 0.01 for nitrate use, OR 0.51, 95% CI 0.27-0.93, p = 0.03 for ACE-I use). CONCLUSIONS: This prospective observational cohort trial demonstrated that chronic ACE-I therapy was an independent predictor for reduced PMI among patients with MetS who underwent elective coronary intervention.