The platelet to lymphocyte ratio (PLR) has recently emerged as a potential inflammatory biomarker. Hence, we assessed the relationship between PLR and the extent/severity of coronary artery disease (CAD) using the Gensini score in association with the inflammatory marker C-reactive protein (CRP) in patients with stable CAD. Angiographic data of 1646 patients were analyzed in this cross-sectional study. Patients were categorized according to Gensini scores as no CAD (control), mild, and severe CAD groups. The PLR in the control group was significantly lower than those of mild and severe CAD groups. In multivariate logistic regression analysis, PLR was found to be an independent predictor of the presence of severe CAD (odds ratio: 1.043 [1.036-1.049], P < .001). Furthermore, there was a significant correlation between PLR and the severity of CAD (r = .370, P < .001) and CRP levels (r = .312, P < .001). In conclusion, PLR was independently and positively associated with the severity of coronary atherosclerosis. These results suggest that PLR is an easily available and cheap inflammatory indicator that can be used in predicting the severity of CAD.

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Red cell distribution width (RDW) is independently associated with morbidity and mortality in cardiovascular diseases. RDW is elevated in hypertensive patients compared with normotensives. Based on the nocturnal course, hypertension classified as dipper and non-dipper. Non-dipper hypertension is associated with higher inflammation and worse prognosis. We aimed to investigate whether RDW and high-sensitive C-reactive protein (hsCRP) are elevated in non-dipper hypertensive patients compared with dippers. The study included total 247 essential hypertensive patients. Twenty-four-hour ambulatory blood pressure monitoring (ABPM) was performed for each patient. Thereafter patients were divided into the two groups on the basis of the results of 24-h ABPM: 127 dipper hypertensives and 120 non-dipper hypertensives. Complete blood count and biochemistry were measured by standard methods and hsCRP was assessed by using BN2 model nephelometer. Non-dippers had significantly higher RDW levels than dippers [14.6 (13.8-17.0) vs 13.0 (12.5-13.4), p < 0.001, respectively]. After adjustment for hemoglobin, low-density lipoprotein-cholesterol, sex, age and hs-CRP, mean RDW values were for dipper and non-dippers 13.4 (12.4-13.2) and 14.5 (13.7-16.8), respectively (p < 0.001). RDW was negatively correlated with the percentage decline of systolic and diastolic BP from day to night (r = - 0.392, p < 0.001 and r = - 0.294, p < 0.001, respectively). Serum hsCRP levels were also significantly higher in the non-dippers (p < 0.001) and it was significantly positively correlated with RDW (r = 0.403, p < 0.001). In receiver-operating characteristic curve analysis, the optimal cut-off value of RDW to predict non-dipping pattern was > 13.8%, with 80% sensitivity and 75% specificity. RDW is significantly increased in patients with non-dipper hypertension compared with the dipper hypertension. Inflammatory activity was closely related to RDW in non-dipper hypertensives. RDW, as easy and quick measurable tool, can predict non-dipping pattern in essential hypertension.

4Triglyceride (TG) to high-density lipoprotein cholesterol (HDL-C) ratio (TG/HDL-C) has been suggested as a simple method to identify unfavorable cardiovascular outcomes in the general population. The effect of the TG/HDL-C ratio on essential hypertensive patients is unclear. About 900 consecutive essential hypertensive patients (mean age 52.9AE12.6 years, 54.2% male) who visited our outpatient hypertension clinic were analyzed. Participants were divided into quartiles based on baseline TG/HDL-C ratio and medical records were obtained periodically for the occurrence of fatal events and composite major adverse cardiovascular events (MACEs) including transient ischemic attack, stroke, aortic dissection, acute coronary syndrome, and death. Participants were followed for a median of 40 months (interquartile range, 35-44 months). Overall, a higher quartile of TG/HDL-C ratio at baseline was significantly linked with higher incidence of fatal and nonfatal cardiovascular events. Using multivariate Cox regression analysis, plasma TG/HDL-C ratio was independently associated with increased risk of fatal events (hazard ratio [HR], 1.25; 95% confidence interval [CI], 1.13-1.37; P≤.001] and MACEs (HR, 1.13; 95% CI, 1.06-1.21; P≤.001). Increased plasma TG/HDL-C ratio was associated with more fatal events and MACEs in essential hypertensive patients.

5Uric acid (UA) is independently associated with the emergence of hypertension. Nocturnal nondipping pattern of hypertension is associated with a greater risk of cardiovascular, renal, and cerebrovascular complications than dippers. The aim of the present study was to evaluate the relationship between the circadian blood pressure rhythm and UA level in patients with newly diagnosed essential hypertension. The study included 112 essential hypertensive patients and 50 healthy controls. The hypertensive patients were divided into two groups according to the results of 24-hour ambulatory blood pressure monitoring, including 60 dippers (35 men, 25 women; mean age, 52.6AE15.8 years) and 52 nondippers (29 men, 23 women; mean age, 55.9AE13.2 years). Nondippers had significantly higher serum UA levels than the dippers and controls (5.8AE0.8, 5.1AE0.9 and 4.2AE0.9 mg ⁄ dL, respectively; P<.001). Serum high-sensitivity C-reactive protein levels were also significantly higher in the nondipper group than the other groups (P<.001) and significantly correlated with serum UA (r=0.358, P<.001). Multivariate logistic regression analysis revealed an independent positive association between serum UA levels and nondipper pattern (odds ratio, 2.28; 95% confidence interval, 1.33-3.94; P=.003). Serum UA is strongly and independently associated with the nondipper circadian pattern in essential hypertension. J Clin Hypertens (Greenwich). 2013; 15:7-13. Ó2012 Wiley Periodicals, Inc.

Early morning blood pressure surge (MBPS) is a risk factor for cardiovascular events (CVEs), but the relationship with uric acid is not well understood. The authors aimed to determine the association between MBPS and increased uric acid and the effect of elevated MBPS and uric acid combination on CVEs. A total of 921 patients underwent 24-hour ambulatory blood pressure monitoring and were followed for a median of 40 months. During this period, 103 (11.2%) CVEs occurred. There was a significant relationship between increasing quartiles of serum uric acid level and increasing values of MBPS (P<.0001). Patients in the highest quartile stratified by elevated MBPS and serum uric acid level had a 3.55 odds of major CVE compared with patients in the lowest quartile. Serum uric acid is associated with MBPS and development of new CVEs. J Clin Hypertens (Greenwich). 2014;16:530-535. ª2014 Wiley Periodicals, Inc.

Developing contrast-induced nephropathy (CIN) after primary percutaneous coronary intervention (pPCI) has a negative impact on survival and morbidity. We assessed the predictive value of serum uric acid (SUA) for the development of CIN in patients with ST-segment elevation myocardial infarction (STEMI) who underwent pPCI. Contrast-induced nephropathy was defined an increase of ≥25% or ≥0.5 mg/dL in creatinine concentrations within 72 hours after pPCI. Patients were divided into 2 groups according to admission median SUA level. Serum uric acid level was <5.4 mg/dL (group 1; n = 222) and ≥5.4 mg/dL (group 2; n = 228). Compared to group 1, development of CIN (12% vs 20%, P < .001) was significantly greater in group 2. Using a cut point of >5.45 mg/dL, the SUA level predicted development of CIN with a sensitivity of 70% and specificity of 67%. In multiple logistic regression analysis, SUA level, diabetes mellitus, left ventricular ejection fraction <50%, contrast volume, estimated glomerular filtration rate, and C-reactive protein level emerged as independent predictors of CIN. In conclusion, elevated SUA is an independent risk factor for the development of CIN after pPCI in patients with STEMI.