Prehypertension is associated with peripheral arterial disease and low ankle-brachial index.

Patients with prehypertension suffer endothelial dysfunction and are at increased cardiovascular risk. Ankle-brachial index (ABI) constitutes an efficient tool for diagnosing peripheral arterial disease; but also an ABI<0.9 is an independent and positive predictor of endothelial dysfunction and is associated with increased cardiovascular risk and mortality. THE AIM: of this study was testing whether ABI was decreased in prehypertensive patients when compared with normotensive subjects. METHODS: We included 70 prehypertensive patients older than 19 years, in whom the ABI was registered with a 5 megahertz Doppler (Summit Doppler L250, Life Dop., USA). The highest ankle systolic pressure was divided by the highest brachial systolic pressure. We also included 70 normotensive subjects in whom the ABI was registered in the same way. The measurements were performed by the same physician who was blinded about the study. Statistical analysis was performed with odds ratio and student t-test. RESULTS: The ABI values in normotensive subjects were 1.023±0.21, whereas prehypertensive patients significantly had lower ABI (0.90±0.14p=0.00012). We found ABI <0.9 in 30 prehypertensive patients (42.85%) and 13 normotensive patients (18.5%). The odds ratio of ABI <0.90 in prehypertensive patients was 3.288 (IC95 1.5-7.0, p=0.0023). A regression analysis failed to show any independent association between ABI values and any other clinical parameter. CONCLUSIONS: Prehypertensive patients had lower ABI and higher prevalence of peripheral artery disease when compared with normotensive subjects; this fact increases their cardiovascular risk. ABI must be included in global evaluation of prehypertensive subjects.

Diferencias en el grosor de la grasa epicárdica en pacientes con diabetes mellitus tipo 2, prediabetes y sujetos no diabéticos / Differences in the epicardial fat thickness in patients with diabetes mellitus 2, prediabetes and nondiabetic subjects

Resumen OBJETIVO Evaluar si hay diferencias en el grosor de la grasa epicárdica en pacientes con diabetes mellitus 2, prediabetes y sujetos no diabéticos. MATERIAL Y MÉTODO Estudio en el que de enero a agosto de 2017 se evaluaron sujetos divididos en tres grupos: sujetos con diabetes mellitus 2, sujetos con prediabetes y sujetos no diabéticos. En todos se midió el grosor de la grasa epicárdica por ecocardiografía, siguiendo la técnica descrita por Iacobelis, con un equipo Aloka alfa 6, usando un transductor de 3.5 MHz, por dos ecocardiografistas que desconocían los datos clínicos de los pacientes. El método estadístico usado fue ANOVA. RESULTADOS Se incluyeron en el estudio 120 pacientes divididos en los tres grupos (40 pacientes cada grupo); se encontró grosor de la grasa epicárdica de 5.63 mm en el grupo de diabetes mellitus, de 4.43 mm en el grupo de prediabetes y de 4.0 mm en el grupo sin diabetes. No hubo diferencia en el grosor de la grasa epicárdica entre los grupos sin diabetes y prediabéticos (p = 0.09). Sin embargo, sí encontramos diferencia significativa entre el grupo de diabetes mellitus y los grupos prediabetes y sin diabetes (p = 0.00017). CONCLUSIÓN Los pacientes diabéticos tipo 2 tienen mayor grosor de la grasa epicárdica que los prediabéticos y los sujetos no diabéticos, lo que apoya la relación entre grasa visceral y diabetes mellitus tipo 2.

Abstract OBJECTIVE To evaluate the differences in epicardial fat thickness in subjects with type-2 diabetes, prediabetes or non-diabetic. MATERIAL AND METHOD A study was done from January to August 2017 evaluating subjects divided into 3 groups: group with type-2 diabetic patients, group with subjects with prediabetes and group with nondiabetic subjects. In all of them the epicardial fat thickness was measured with an Aloka alfa 6 equipment, by 2 cardiologists who were unaware of the clinical data. Statistical analysis was performed with ANOVA. RESULTS There were included 120 patients divided into three groups of 40 patients each. Epicardial fat thickness was of 5.63 mm in diabetes mellitus group, 4.43 mm in prediabetes group and 4 mm in nondiabetic group. We did not find difference in epicardial fat thickness between nondiabetes and prediabetes groups (p = 0.09). However, we found significantly differences in epicardial fat thickness between diabetes group and groups of prediabetes and nondiabetes (p = 0.00017). CONCLUSION Type-2 diabetic patients have greater nondiabetes than prediabetic and nondiabetic subjects; this fact supports the relationship between visceral fat and the risk of type-2 diabetes.

Serum uric acid levels are associated with homeostasis model assessment in obese nondiabetic patients: HOMA and uric acid.

BACKGROUND: Hyperuricemia leads to insulin resistance, whereas insulin resistance decreases renal excretion of uric acid. The aim of this study was to evaluate whether there is a correlation between serum uric acid levels with homeostatic model assessment (HOMA) 1 in nondiabetic patients. METHODS: We evaluated 88 nondiabetic patients, in whom uric acid levels were measured, in all of them HOMA of ß-cell function (HOMA 1B) and HOMA of insulin resistance (HOMA 1IR) scores were performed. Uric acid and the HOMA 1 values were correlated using the Pearson coefficient. RESULTS: We did not find any correlation between uric acid levels with both HOMA 1B (r = 0.102, p = 0.343), nor with HOMA 1IR (r = 0.158, p = 0.117). When patients were analyzed by sex, we found a significant correlation with HOMA 1IR (0.278, p = 0.01), but not with HOMA 1B (0.138, p = 0.257) in women. We found a correlation with HOMA 1B in men (r = 0.37, p = 0.044), but not with HOMA 1IR: 0.203, p = 0.283. The analysis performed based on body mass index did not show correlation in the patients with normal weight, (HOMA 1B r = 0.08, p = 0.5, HOMA 1IR = 0.034, p = 0.793), nor in the patients who were overweight (HOMA 1B: r = 0.05, p = 0.76, HOMA 1IR r = 0.145, p = 0.43). However, a significant correlation between uricemia with both HOMA 1B (0.559, p < 0.001), and HOMA 1IR (0.326, p < 0.05), was observed in obese patients. CONCLUSION: Our results suggest that serum uric acid levels seem to be associated with insulin resistance in women, and in obese patients, but not in nonobese men. Uric acid also modifies ß-cell function in men and in obese patients.

Circulating Levels of Uric Acid and Risk for Metabolic Syndrome.

Hyperuricemia leads to insulin resistance, whereas insulin resistance decreases renal excretion of uric acid, both mechanisms link elevated serum uric acid with metabolic syndrome. The aim of this study is to evaluate the probability for the development of metabolic syndrome in low-income young adults with hyperuricaemia. METHODS: We evaluated 103 patients less than 40 years of age, from a low-income population, and without history of cardiovascular disease, in all of them the presence of metabolic syndrome was assessed in accordance with the International Diabetes Federation criteria. In all patients, fasting serum uric acid levels were measured; hyperuricaemia was defined as serum uric acid values 6.5 mg/dl in men and 5.1 mg/dl in women. Statistical analysis was performed with odds ratio. RESULTS: 83 of our patients (80.5%) suffered metabolic syndrome, the odds ratio for the presence of metabolic syndrome in patients with hyperuricaemia was 5.1 (p=0.002, I.C 1.8- 14.5). When patients were evaluated by gender a significantly association between hyperuricaemia and metabolic syndrome was found in women (odds ratio 3.6, p=0.048, C.I. 1.0-12.9), and men (odds ratio 10.2, p= 0.015, IC 1.5-13.2). When uric acid was correlated with the components of metabolic syndrome, we only found a positive correlation with waist circumference (r=0.483). CONCLUSION: Our results showed a significant association between hyperuricemia and metabolic syndrome in low-income young adults in Mexico. DR is associated with estimated risk of CVD in type 2 diabetic patients.

Effect of losartan combined with amlodipine or with a thiazide on uric acid levels in hypertensive patients.

Hyperuricemia leads to endothelial dysfunction and insulin resistance, and has been associated with diseases such as hypertension. Antihypertensive drugs modify serum uric acid levels, however, few data are available about their combinations on uricemia. In this study we evaluate the effect of two combinations of losartan, with amlodipine or with hydrochlorothiazide, on serum uric acid levels in hypertensive patients. METHODS: A total of 60 hypertensive patients were randomized in two groups; group LA received losartan/amlodipine (100/5 mg) once a day, whereas LH group received losartan hydrochlorothiazide (100/12.5 mg) once a day for 3 months. In both groups serum uric acid levels were measured at the beginning and end of the study. Patients were evaluated monthly for blood pressure (BP) and adverse events. Statistical analysis was performed with a two-way analysis of variance (ANOVA) for repeated measures. RESULTS: All patients experienced a significant reduction of BP to the same extent (LA 155/94 to 123/79, LH 157/92 to 124/78 mmHg, p > 0.05). In the LA group, serum uric acid decreased from 6.5 ± 1.6 to 4.6 ± 1.3 mg/ml ( p = 0.0001), whereas in the LH group there was a nonsignificant increase from 5.82 ± 1.4 to 5.85 ± 1.5 mg/ml, ( p = 0.936). When both groups were compared, we found a significant reduction ( p < 0.00013) on serum uric acid levels in the LA group. CONCLUSIONS: Both combinations decrease BP values to the same extent, however, LA combination showed a reduction on serum uric acid levels, which may contribute to a reduction in the metabolic risk in hypertensive patients.

Lifestyle changes and surgical treatment for hypertension in the elderly.

Hypertension is a major cardiovascular risk factor that increases morbidity and mortality in the elderly because, numerous factors contribute to development and progression of hypertension in elderly patients, including excessive salt intakes, obesity, physical inactivity and stress. Hypertension treatment usually results in a combination of both, pharmacologic and non-pharmacologic measures. These latter are an essential part of treatment and cannot be replaced by the medication. Non pharmacologic management known as lifestyle modifications has a pivotal role in non-hypertensive and hypertensive individuals. In case of non-hypertensive or pre-hypertensive patients it can prevent hypertension development and in hypertensive people it has the capacity to lower blood pressure levels as well as modify cardiovascular complications. Older people tend more often to treatment resistance so it is increasingly necessary to have other therapeutic resources for patients with difficult control of disease. Minimally invasive techniques are developing that might improve the course of the disease and prevent its complications by a more extended time.In this chapter, we will review components of nonpharmacological treatment of hypertension focusing on the geriatric patient.

Recommendations for the treatment of hypertension in elderly people.

High blood pressure is a major cardiovascular risk factor. The prevalence of hypertension increases with aging. As a consequence of changes in arterial wall that leads to arterial stiffness, the majority of elderly patients suffer isolated systolic hypertension. The evidence strongly supports that hypertension in the elderly is associated with an increase in stroke risk and cardiovascular mortality and morbidity. Several trials have shown the benefits of treating hypertension in elderly patients. Even in the very old patients, the use of antihypertensive agents such as calcium channel blockers, thiazide and thiazide-like diuretics, and inhibitors of the renin-angiotensin system reduce the risk of complications in those patients. However, most patients will need two or more drugs to reach the recommended goals. Hypertension in the elderly has special conditions that must be assessed in the evaluation of the patient (as pseudohypertension and white coat hypertension), and issues that may affect the therapeutic choice and the response to treatment, as comorbidities and polypharmacy.

Diabetic nephropathy and inflammation.

Diabetic nephropathy (DN) is the leading cause of end-stage renal failure worldwide. Besides, diabetic nephropathy is associated with cardiovascular disease, and increases mortality of diabetic patients. Several factors are involved in the pathophysiology of DN, including metabolic and hemodynamic alterations, oxidative stress, and activation of the renin-angiotensin system. In recent years, new pathways involved in the development and progression of diabetic kidney disease have been elucidated; accumulated data have emphasized the critical role of inflammation in the pathogenesis of diabetic nephropathy. Expression of cell adhesion molecules, growth factors, chemokines and pro-inflammatory cytokines are increased in the renal tissues of diabetic patients, and serum and urinary levels of cytokines and cell adhesion molecules, correlated with albuminuria. In this paper we review the role of inflammation in the development of diabetic nephropathy, discussing some of the major inflammatory cytokines involved in the pathogenesis of diabetic nephropathy, including the role of adipokines, and take part in other mediators of inflammation, as adhesion molecules.

Correlation between levels of circulating adipokines and adiponectin/resistin index with carotid intima-media thickness in hypertensive type 2 diabetic patients.

BACKGROUND: Hypoadiponectinemia and hyperresistinemia are associated with cardiovascular disease. The increase in the carotid intima-media thickness (CIMT) assessed by B-mode ultrasound has been directly associated with increased risk of myocardial infarction and stroke. OBJECTIVE: To evaluate the correlation between adipokine levels with CIMT in hypertensive type 2 diabetic patients. METHODS: Serum levels of adiponectin and resistin levels were measured by ELISA in 30 type 2 diabetic patients with never-treated hypertension and in age-matched healthy controls. The CIMT (B-mode color imaging of extracranial carotid arteries using high-resolution ultrasound) was also obtained. The relationship between adipokine levels and the adiponectin/resistin index with the CIMT was assessed by the Pearson correlation coefficient test. RESULTS: Adiponectin was lower (p < 0.05), and resistin higher (p < 0.01) in patients than in controls, CIMT correlated positively with resistin (R = 0.45, p < 0.02) and the adiponectin/resistin index (R = 0.58, p < 0.001), but not with adiponectin levels (r = -0.11, p > 0.1) in patients. Whereas only adiponectin levels correlated - negatively - with CIMT (r = -0.39, p < 0.02) in controls. CONCLUSION: Our results shown that the adiponectin/resistin index seems to be more strongly associated with atherosclerosis than adipokine levels, and may be used as a reliable marker of cardiovascular risk in type 2 diabetic hypertensive patients.

Beneficial effect of combination therapy using an angiotensin-converting enzyme inhibitor plus verapamil on circulating resistin levels in hypertensive patients with type 2 diabetes.

BACKGROUND: Resistin levels are strongly correlated with insulin resistance and vascular inflammation. Type 2 diabetic and hypertensive patients have higher circulating levels of resistin, which is associated with endothelial dysfunction. OBJECTIVE: To compare the effect of trandolapril (T) and its fixed-dose combination with verapamil (FDTV) on resistin levels in hypertensive, type-2 diabetic patients. METHODS: Forty type-2 diabetic patients with never-treated hypertension were randomly assigned to two groups. One group received FDTV 2 mg/180 mg once per day; the other group received T 2 mg once per day. Study drugs were administered for three months in both groups. Resistin levels were measured using ELISA at the beginning of the study and at study end. Patients were evaluated monthly for blood pressure, fasting serum glucose levels and adverse events. Statistical analysis was performed using ANOVA. RESULTS: All patients experienced a significant reduction in blood pressure. Both therapeutic regimens reduced resistin levels; however, FDTV treatment resulted in a greater decrease in resistin levels (mean [± SD] 25.5±13 ng/mL to 17.2±10 ng/mL) when compared with T treatment (22.4±12 ng/mL to 18.5±8 ng/mL) (P<0.05). None of the patients experienced an adverse event. CONCLUSION: Results showed that FDTV resulted in a greater reduction in resistin levels than T treatment alone.

Impact of trandolapril therapy and its combination with a calcium channel blocker on plasma adiponectin levels in patients with type 2 diabetes and hypertension.

INTRODUCTION: Adiponectin is secreted from adipose tissue and exhibits a protective effect against cardiovascular disease; plasma adiponectin concentrations are decreased in type 2 diabetic and in hypertensive patients. OBJECTIVE: The aim of this study was to compare the effect of trandolapril (T) and its fixed-dose combination with verapamil (FDTV) on adiponectin levels in hypertensive type 2 diabetic patients. METHODS: A total of 40 type 2 diabetic patients with never-treated hypertension were randomly assigned to two groups. One group received FDTV 180 mg + T 2 mg, once a day; the other group received T 2 mg once a day, administered for 3 months in both groups. Adiponectin was measured by enzyme-linked immunosorbent assay (ELISA) at the beginning and end of the study. Patients were evaluated monthly for blood pressure, fasting serum glucose and adverse events. Statistical analysis was performed with analysis of variance (ANOVA). RESULTS: All patients experienced a significant reduction of blood pressure. Both therapeutics regimens increased the levels of adiponectin, However, FDTV produces a higher increase in the levels of the hormone (8.15 ± 4.6 to 10.96 ± 5.6 µg/ml) when compared with the T treatment (7.64 ± 3.8 to 8.92 ± 4.4 µg/ml), p < 0.05. None of the patients suffered adverse events. CONCLUSION: Our results show that the addition of FDTV to T produced a greater increase on adiponectin levels than trandolapril alone.

Correlation between circulating adhesion molecules and resistin levels in hypertensive type-2 diabetic patients.

BACKGROUND: Endothelial dysfunction, a common feature among hypertensive and type-2 diabetic patients, has been associated with inflammation and increased concentrations of serum soluble adhesion molecules and resistin, a monocyte-macrophage- and adipocyte-derived cytokine. THE AIM OF THIS STUDY: To determine if there is a correlation between the serum concentrations of ICAM-1, VCAM-1, Eselectin and resistin in hypertensive type-2 diabetic patients. METHODS: Thirty hypertensive type-2 diabetic patients were enrolled in the study. Serum ICAM-1, VCAM-1, E-selectin and resistin concentrations were determined by ELISA and correlated with the Spearman correlation coefficient. RESULTS: The patients' serum resistin concentrations significantly correlated with VCAM-1 (r = 0.31, p= 0.05) concentrations but not with ICAM-1 (r = 0.29, p = >0.05) and E-selectin (r = 0.10, p = 0.24) concentrations. CONCLUSION: VCAM-1 and resistin may participate in the pathophysiology of vascular damage in hypertensive type-2 diabetic patients. Serum resistin concentrations may be a marker of endothelial dysfunction.

Current concepts in combination therapy for the treatment of hypertension: combined calcium channel blockers and RAAS inhibitors.

Recent guidelines for the management of hypertension recommend target blood pressures <140/90 mmHg in hypertensive patients, or <130/80 mmHg in subjects with diabetes, chronic kidney disease, or coronary artery disease. Despite the availability and efficacy of antihypertensive drugs, most hypertensive patients do not reach the recommended treatment targets with monotherapy, making combination therapy necessary to achieve the therapeutic goal. Combination therapy with 2 or more agents is the most effective method for achieving strict blood pressure goals. Fixed-dose combination simplifies treatment, reduces costs, and improves adherence. There are many drug choices for combination therapy, but few data are available about the efficacy and safety of some specific combinations. Combination therapy of calcium antagonists and inhibitors of the renin-angiotensin-aldosterone system (RAAS) are efficacious and safe, and have been considered rational by both the JNC 7 and the 2007 European Society of Hypertension - European Society of Cardiology guidelines for the management of arterial hypertension. The aim of this review is to discuss some relevant issues about the use of combinations with calcium channel blockers and RAAS inhibitors in the treatment of hypertension.

Effectiveness and safety of ezetimibe added to statin therapy in patients with primary dyslipidaemia not achieving the LDL-C treatment goal on statin monotherapy.

BACKGROUND AND OBJECTIVE: Elevated serum low-density lipoprotein cholesterol (LDL-C) is a major cardiovascular risk factor. This study aimed to determine the efficacy and safety of co-administration of the cholesterol absorption inhibitor ezetimibe with an HMG-CoA reductase inhibitor (statin) in the treatment of Mexican patients with dyslipidaemia who had not attained the LDL-C treatment goal with statin monotherapy. MATERIAL AND METHODS: We studied 256 patients with elevated serum LDL-C (as defined by the US National Cholesterol Education Program Adult Treatment Panel III guidelines) despite statin therapy. All patients had lipid profiles performed at baseline and after 6-8 weeks of treatment with statin therapy plus ezetimibe 10 mg/day for 6-8 weeks. RESULTS: Addition of ezetimibe to statin treatment reduced mean serum LDL-C levels significantly (from 160 +/- 42.8 to 100 +/- 36 mg/dL; p<0.001) after 6-8 weeks of treatment, with 61.7% of patients achieving LDL-C values below the goal established according to their coronary risk group. Serum LDL-C goals were achieved at the end of the study in 88.2% of the low-risk coronary group, 75.7% of the moderate-risk group and 47.8% of the high-risk group. Ezetimibe was well tolerated; no hepatic or muscle-related adverse events were observed. CONCLUSION: Addition of ezetimibe to statin treatment was both efficacious and safe when used for further reduction of serum LDL-C in dyslipidaemic patients who had not reached their LDL-C treatment goal while taking statin monotherapy.