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MicroRNAs (miRs) regulate gene expression at the post-transcriptional level and are found to be present in monocytes. This study aimed to investigate miR-221-5p, miR-21-5p, and miR-155-5p, their expression in monocytes, and their role in coronary arterial disease (CAD). The study population comprised 110 subjects, and RT-qPCR was used to examine the miR-221-5p, miR-21-5p, and miR-155-5p expressions in monocytes. Results: the miR-21-5p (p = 0.001) and miR-221-5p (p < 0.001) expression levels were significantly higher in the CAD group, and the miR-155-5p (p = 0.021) expression levels were significantly lower in the CAD group; only miR-21-5p and miR-221-5p upregulation was found to be associated with an increased CAD risk. The results show significant increases in miR-21-5p in the unmedicated CAD group with the metformin patients vs. the healthy control group (p = 0.001) and vs. the medicated CAD group with metformin (p = 0.022). The same was true for miR-221-5p in the CAD patients unmedicated with metformin vs. the healthy control group (p < 0.001). Our results from Mexican CAD patients show that the overexpression in monocytes of miR-21-5p and miR-221-5p increases the risk of the development of CAD. In addition, in the CAD group, the metformin downregulated the expression of miR-21-5p and miR-221-5p. Also, the expression of endothelial nitric oxide synthase (NOS3) decreased significantly in our patients with CAD, regardless of whether they were medicated. Therefore, our findings allow for the proposal of new therapeutic strategies for the diagnosis and prognosis of CAD and the evaluation of treatment efficacy.

Coronary artery disease (CAD) is the leading cause of death around the world, and its rate of presentation is increasing at young ages. Despite the evidence that secondary prevention in CAD reduces the risk of recurrent major adverse cardiovascular events (MACE), no studies have analyzed the composite control of blood pressure, lipids, and glucose control in premature CAD.This was a real-world prospective cohort study of patients with premature CAD. The composite control in blood pressure140/80 mmHg, LDL-C70 mg/dL, non-HDL-C100 mg/dL, and Hemoglobin A1c8% was considered as metabolic control. The primary endpoint was the occurrence of non-fatal and fatal MACE. The data included 1042 patients with premature CAD. The mean age of the patients was 54.1 ± 8.1 years, 18.5% were women, and had a median follow-up of 59.1 ± 11.8 months. Of them, 7% had non-fatal MACE, and 4% had a fatal MACE. Overall, 21.3% achieved metabolic control, and 3.0% did not achieve any target. Cox regression analysis showed that percutaneous coronary intervention (Hazzard ratio = 1.883 [95% CI, 1.131-3.136]), C-reactive protein (1.046 [1.020-1.073]), blood pressure140/90 mmHg (2.686 [1.506-4.791]), fibrates (2.032 [1.160-3.562]), calcium channel blockers (2.082 [1.158-3.744]) had greater risk to present a recurrent non-fatal MACE; whereas familial history of premature CAD (2.419 [1.240-4.721]), heart failure (2.139 [1.032-4.433]), LDL-C70 mg/dL (4.594 [1.401-15.069]), and diuretics (3.328 [1.677-6.605]) were associated with cardiovascular mortality.The composite goal achievement in lipids, blood pressure and glucose, reduced the risk for recurrent MACE in 80%.

ATP-binding cassette membrane transporters (ABC), functions as an outflow facilitator of phospholipids and cellular cholesterol, playing an important role in the development of atherosclerosis and arterial hypertension. ABC’s transporters could post-transcriptionally regulated by miRs. Evaluate the association in the transporters ABCA1 and ABCG1 with the expression of miR-33a and miR-144 and the carotid intima media thickness (cIMT) in patients with essential arterial hypertension. The miR-33a-5p, miR-144-3p and mRNA ABCA1 and ABCG1 expression in monocytes from Mexican hypertensive patients were examined by RT-PCR. The miR-33a and miR-144 expression in monocytes and mRNA ABCA1 and ABCG1 from Mexican hypertensive patients were examined by RT-PCR. This study involved 84 subjects (42 normotensive subjects and 42 patients with essential hypertension). Our study revealed that miR-33a expression (p = 0.001) and miR-144 (p = 0.985) were up-regulated, meanwhile, ABCA1 and ABCG1 transporters were down-regulated (p = 0.007 and p = 0.550 respectively) in hypertensive patients compared with the control group. The trend remains for miR33a/ABCA1 in presence of cIMT. Moreover, an inverse correlation was found with the expression levels of ABCA1 and ABCG1 as well as in HDL-C with miR-33a and miR-144. Our results showed an increase in the expression of miR-33a and miR-144 and an inverse correlation in their target ABCA1 and ABCG1; it may be associated with essential arterial hypertension in patients with cIMT and as consequence for atheromatous plaque.

Background: In subjects without a history of coronary heart disease (CHD), type 2 diabetes mellitus (T2DM) is associated with carotid artery plaques (CAP), which is a better marker than high carotid intima-media thickness (hCIMT) for predicting first or recurrent cardiovascular events. Objective: The objective of this study is to analyze the association of T2DM with CAP and hCIMT in premature CHD patients. Methods: Premature CHD was considered before the age of 55 years in men and before 65 in women. T2DM was defined according to the American Diabetes Association criteria. CAP was defined as a focal structure encroaching the arterial lumen by at least 50% of the surrounding IMT value or with a thickness > 1.5 mm. Results: Among 1196 patients (CHD duration 1.5 years [interquartile range: 0.4-5.6]), 37.2% had T2DM, and 97.8% were on antihypertensive, 94.4% on lipid-lowering, and 97.3% on anti-aggregate treatment. hCIMT prevalence was similar in patients with or without T2DM, whereas CAP prevalence was higher among T2DM patients (17.7% vs. 30.9%; p < 0.001). T2DM showed association with CAP, independently of CHD evolution and glycemic control (odds ratio: 1.57; 95% confidence interval: 1.09-2.26). Conclusions: T2DM has an independent association with CAP. Early detection of recurrent cardiovascular events, with CAP identification, could be useful to prevent complications in patients with CHD. (REV INVEST CLIN. 2018;70:301-9)

miR-33a has been described as a key regulator in the initiation and progression of atherosclerosis. However, its role in arterial hypertension (HTA) has not been elucidated. Therefore, the aim of this study was to determine the association between the expression of miR-33a (5p and 3p) and the carotid intima-media thickness (cIMT) in samples of monocytes and serum from hypertensive patients. The miR-33a-5p and miR-33a-3p expression in monocytes and serum from Mexican hypertensive patients were examined by RT-PCR. This study involved 84 subjects (42 normotensive subjects and 42 patients with essential hypertension). Our study revealed that miR-33a-5p expression was significantly upregulated in the monocytes of hypertensive patients compared with the control group (p = 0.001), while miR-33a-3p was significantly downregulated (p = 0.013). miR-33a-5p upregulation [OR: 5.53, 95% CI: 2.01–15.20; p = 0.001], as well as miR-33a-3p downregulation [OR: 3.32, 95% CI: 1.45–7.60; p = 0.004] in monocytes, was associated with an increased risk of developing hypertension. In addition, miR-33a-5p upregulation in hypertensive patients was associated with an increased risk of presenting cIMT [OR: 5.99, 95% CI: 1.10–32.85; p = 0.039]. Moreover, we found no significant differences in the expression of both strands of miR-33a in serum of our patients. Our results showed an upregulation of miR-33a-5p and downregulation of miR-33a-3p in monocytes, these data are associated with cIMT, which could be a risk factor for the development of hypertension. In addition, upregulation of miR-33a-5p in monocytes from Mexican hypertensive patients could be involved in the development of atherosclerosis.

Microalbuminuria is an early marker of atherosclerosis. Ethnic differences for both conditions have been reported. We studied microalbuminuria prevalence and its association with coronary artery calcification as an early atherosclerosis marker in a Mexican-Mestizo population free of diabetes and hypertension (healthy), as well as in hypertensive and diabetic subjects.In 1,472 adults (53.3 ± 9.4 years old, 50.3% women), anthropometric measurements, fasting blood glucose, and lipid profile were determined. A spot urine sample was used to quantify the albumin-to-creatinine ratio and to define microalbuminuria (20-200 mg/g in men, and 30-300 mg/g in women). A coronary artery calcification score was obtained by electron-beam computed tomography and subclinical atherosclerosis was defined as a score0.Overall microalbuminuria prevalence was 9.3% (5.4% in healthy, 11.6% in obese, 12% in hypertensive, and 25% in diabetic subjects). Compared to "healthy" subjects without microalbuminuria, those with microalbuminuria had a ∼3-fold higher prevalence of coronary artery calcification0, while normal-high albumin-to-creatinine ratio (OR: 1.8; p0.05) and microalbuminuria (OR: 2.6; p0.001) was independently associated with coronary artery calcification0 only among diabetic subjects.Microalbuminuria and high-normal albumin-to-creatinine ratio were independently associated with subclinical atherosclerosis, suggesting that they may confer a higher risk of future cardiovascular events.

Non-alcoholic fatty liver (FL) has a high prevalence and is associated with clinical conditions such as dyslipidemia, arterial hypertension, diabetes, and coronary artery disease.To investigate the association of physical activity (PA) and nutritional factors on the presence of FL, and to analyze the association of the energy intake/energy expenditure (EI/EE) index with FL.We studied 786 nondiabetic subjects without a history of hepatic or cardiovascular disease, and alcohol consumption20 g/d. Diet and PA were assessed using standardized questionnaires, and visceral abdominal fat (VAF) and liver fat by tomography. The energy intake/energy expenditure (EI/EE) index effect on the presence on FL was analyzed.No macronutrient was associated with FL. After adjusting for age, gender, VAF, and total kilocalories, PA significantly reduced the risk of FL (OR: 0.86; 95% CI: 0.74-0.99; p = 0.03). In logistic regression analysis adjusted for confounding factors, the EI/EE index was associated with the presence of FL (OR: 1.69; 95% CI: 1.02-2.82; p = 0.04).These results suggest that independent of macronutrient composition, a high hypercaloric diet with physical inactivity favours the development of fatty liver.