Background/Aims. Carotid intima media thickness (CIMT) tracks atherosclerotic vascular disease. Hypertension and diabetes chiefly contribute to atherosclerosis with 75% of symptomatic cardiovascular disease cases having dysglycaemia even in normal cases. Hypothesising that postprandial hyperglycaemia contributes to cardiovascular morbidity, we sought to determine if any relationship existed between glycaemic profile in nondiabetic hypertensives and atherosclerosis. Methods. In a study of CIMT in nondiabetic, statin-naïve hypertensives, we evaluated fasting blood glucose (FBG) and 2-hour postprandial sugar (2hPPBG) in the patients and compared them with the CIMT. CIMT was measured on both sides, 1 cm proximal to the carotid bulb using a 7.5 mHz transducer of ALOKA SSD-3500 ultrasound machine. Results. The subjects with complete data were 86 (63 F). The mean (SD) of CIMT was 0.89 (0.15) mm, FBG 4.8 (0.097) mmol/L, and 2hPPBG 6.5 (1.81) mmol/L. There was no significant correlation between FBG and 2hPPBG with CIMT. Blood pressure had no bearing on this. When blood glucose data were divided into quartiles and post hoc multiple comparison was done, there was significant difference in CIMT for the different ranges. This was not so for 2hPPBG. Conclusion. Though expected from other studies, we did not show any significant correlation between FBG and 2hPPBG status and CIMT. This may be our pattern as the degree of excursion of 2hPPBG was low. There may be a threshold level above which PPBG starts to impact CIMT.
Background. Angiotensin 1-7 (Ang1-7) plays an important role in renal circulation. Hemorrhagic shock (HS) may cause kidney circulation disturbance, and this study was designed to investigate the renal blood flow (RBF) response to Ang1-7 after HS. Methods. 27 male Wistar rats were subjected to blood withdrawal to reduce mean arterial pressure (MAP) to 45 mmHg for 45 min. The animals were treated with saline (group 1), Ang1-7 (300 ng·kg(-1) min(-1)), Ang1-7 in hypertonic sodium chloride 7.5% (group 3), and hypertonic solution alone (group 4). Results. MAP was increased in a time-related fashion (P time < 0.0001) in all groups; however, there was a tendency for the increase in MAP in response to hypertonic solution (P = 0.09). Ang1-7, hypertonic solution, or combination of both increased RBF in groups 2-4, and these were significantly different from saline group (P = 0.05); that is, Ang1-7 leads to a significant increase in RBF to 1.35 ± 0.25 mL/min compared with 0.55 ± 0.12 mL/min in saline group (P < 0.05). Conclusion. Although Ang1-7 administration unlike hypertonic solution could not elevate MAP after HS, it potentially could increase RBF similar to hypertonic solution. This suggested that Ang1-7 recovers RBF after HS when therapeutic opportunities of hypertonic solution are limited.
Background. Paraoxonase-1 (PON1) is the crucial antioxidant marker of high-density lipoproteins. The present study is aimed at assessing the effect of simvastatin treatment on PON1 activity and its relationship to Q192R and M55L polymorphisms in subjects with stable coronary artery disease (CAD). Methods. The patient group was composed of 53 individuals with stable CAD, and the control group included 53 sex-matched police officers without CAD. CAD patients were treated with simvastatin 40mg/day for 12 months. Respectively, flow mediated dilatation (FMD), serum hs-CRP and TNF-α levels, urinary 8-iso-PGF2α concentrations, and PON1 activity were evaluated in definitive intervals. Results. There was no effect of simvastatin treatment on urinary 8-iso-PGF2α . Simvastatin treatment significantly increased FMD value, decreased CRP and TNF-α concentration. After adjusting for PON1 genotypes, significantly higher PON1 activity was noted in the 192R allele carriers, in both groups. Regardless of genotype, PON1 activity remained stable after simvastatin treatment. Conclusions. The present study confirms a positive effect of simvastatin therapy on endothelial function and inflammatory markers in secondary prevention. Simvastatin treatment shows no effects on PON1 activity and 8-isoprostanes level. The effect of simvastatin therapy on PON1 activity is not modulated by Q192R and M55L polymorphisms.
Background. In Sri Lanka the ABPI has not been used as a screening tool to detect peripheral arterial disease (PAD) in epidemiological studies. This study was conducted to determine the best cutoff value of ABPI to detect PAD in Sri Lankan population. Methods. The ABPI measured by arterial Doppler to detect PAD was validated against colour duplex scan as the criterion using 165 individuals referred to vascular laboratory, National Hospital Sri Lanka. In all selected individuals ABPI was measured and lower limb colour duplex scan was performed. Narrowing of luminal diameter of lower limb arteries 50% or more was considered as haemodynamically significant and having PAD. The discriminative performance of the ABPI was assessed using Receiver Operator Characteristic (ROC) curve and calculating the area under the curve (AUC). The sensitivity and specificity of different threshold levels of ABPI and the best cutoff value of ABPI to detect PAD were determined. Results. ABPI 0.89 was determined as the best cutoff value to identify individuals with PAD. At this level of ABPI high sensitivity (87%), specificity (99.1%), positive predictive value (98.9%), and negative predictive value (88.4%) were observed. Conclusion. ABPI ≤ 0.89 could be used as the best cut off value to detect PAD.
Objective. The pentraxin family, including high-sensitivity C-reactive protein (hs-CRP), serum amyloid P (SAP), and pentraxin 3 (PTX3), has been identified as playing a key role in inflammatory reactions such as in atherosclerosis and cardiovascular disease. In this study, we examined the relationship between peripheral arterial disease (PAD) and serum levels of pentraxins. Methods. This study was undertaken via a retrospective review of PAD patients with surgical intervention for lesions of the common femoral artery. We evaluated the preoperative patient conditions, hemodynamic status, such as ankle brachial index (ABI), and clinical ischemic conditions according to Rutherford classification. Preoperatively, we collected blood samples for determining the serum levels of hs-CRP, SAP, and PTX3. Results. Twelve PAD patients with common femoral arterial lesions were treated and examined. The hemodynamic severity of PAD was not negatively correlated with hs-CRP, SAP, or PTX3. The clinical severity evaluated by Rutherford classification was significantly positively correlated with the serum level of PTX3 (p = 0.019). Conclusion. We demonstrated that PTX3 might be a better marker of PAD than hs-CRP and SAP. Furthermore, PTX3 might be a prognostic marker to evaluate the severity of PAD.