Charalampos I. Liakos

2013 ESH/ESC Guidelines for the Management of Arterial Hypertension: What Has Changed in Daily Clinical Practice?

This is a review article aiming to make focus on the changes made in the European Society of Hypertension (ESH)/European Society of Cardiology (ESC) guidelines for the management of arterial hypertension with some criticism for each element discussed in the text. Given that in the real world clinical practice physicians would hardly spend the time needed for studying the 77 pages manuscript of the recently released 2013 ESH/ESC hypertension guidelines, the present review summarizes all the significant updates (along with their clinical implications) compared to the 2007 ESH/ESC hypertension guidelines and the 2009 reappraisal document.

Apelin and Visfatin Plasma Levels in Healthy Individuals With High Normal Blood Pressure

BACKGROUND High normal blood pressure (BP; 130-139/85-89 mm Hg) is related with increased cardiovascular (CV) risk compared to normal BP (120-129/80-84 mm Hg) or/and optimal BP (<120/80 mm Hg). Low apelin plasma levels have been associated with arterial hypertension and atherosclerosis, while high visfatin plasma levels may promote vascular inflammation and atherosclerotic plaque destabilization and have been evaluated as a marker for identifying stages of essential hypertension. We sought to compare the apelin and visfatin plasma levels between subjects with high normal BP and subjects with normal or optimal BP matched for age, gender, smoking, and body mass index (BMI). METHODS Twenty-five subjects with high normal BP (office BP 136±3/88±2 mm Hg, age 57±4 years, 76% males, 32% smokers, BMI 24.0±1.7 kg/m2) and 35 subjects with normal or optimal BP (office BP 118±2/78±2 mm Hg, age 55±7 years, 63% males, 29% smokers, BMI 23.2±1.4 kg/m2) were studied. The apelin and visfatin plasma levels were determined with the enzyme-linked immunosorbent assay. RESULTS Compared to normal or optimal BP subjects, apelin levels were significantly lower (205±108 vs. 325±152 pg/ml, P < 0.001) and visfatin levels significantly higher (11.0±2.0 vs. 7.2±0.9 ng/ml, P = 0.002) in high normal BP subjects. No significant differences were found between the 2 groups (P = NS) regarding the basic clinical characteristics, the glycemic/lipid profile, and the renal function parameters. CONCLUSIONS The emerging, from the present study, data raise the hypothesis that lower apelin and higher visfatin plasma levels in high normal BP subjects compared to normal or optimal BP individuals could partially explain the higher CV risk of the high normal BP group.

The Interplay of Exercise Heart Rate and Blood Pressure as a Predictor of Coronary Artery Disease and Arterial Hypertension

J Clin Hypertens (Greenwich). 2012;00:00–00. ©2012 Wiley Periodicals, Inc.

Correlation of 24-Hour Blood Pressure and Heart Rate Variability to Renal Function Parameters in Hypertensive Patients. The Effect of Smoking

Intrarenal hemodynamics depend on blood pressure (BP), heart rate (HR), and smoking. Although BP levels have been associated with kidney function, the effect of HR levels, BP, and HR variability on renal function are less well clarified. This cross‐sectional study sought to determine the association of 24‐hour BP and HR variability with kidney function in hypertensive patients, stratified by smoking. The study comprised 9600 nondiabetic, never‐treated hypertensive individuals without evident renal impairment examined from 1985 to 2014 (aged 53.3±13.4 years, 55.3% males). The 24‐hour systolic BP (SBP) and HR variability were estimated via their coefficient of variation (CV=standard deviation×100/mean value) derived from ambulatory recording. The CVSBP‐to‐CVHR ratio (CVR) was used as a marker of the interplay between 24‐hour SBP and HR variability. Renal function was estimated via 24‐hour urine creatinine clearance (CrCl), estimated glomerular filtration rate (eGFR), albumin‐to‐creatinine ratio (ACR), and 24‐hour urine α1‐microglobulin. After adjustment for age, sex, and smoking, CVSBP was found to be weakly correlated to eGFR (r=−0.017, P=.1) and somewhat more strongly to CrCl, ACR, and α1‐microglobulin (r=−0.032, 0.072, and 0.065; P=.002, <.001 and <.001, respectively). CVHR was much better related to renal function, with stronger adjusted correlations to CrCl, eGFR, ACR, and α1‐microglobulin (r=0.185, 0.134, −0.306, −0.247; all P<.001, respectively). CVR also showed equally good adjusted correlations (r=−0.175, −0.125, 0.336, 0.262; all P<.001, respectively). Most adjusted correlations for CVHR and CVR were even better in smokers (r=0.213, 0.158, −0.332, −0.272 and −0.183, −0.118, 0.351, 0.275, respectively; all P<.001). CVHR and CVR emerge as better related to kidney function than CVSBP, especially in smokers. The correlation of CVHR and CVSBP to renal function is inverse to each other. ACR and α1‐microglobulin are better related to variability indices than CrCl and eGFR. However, causal relations cannot be proved.

Twenty‐Four–Hour Urine α1‐Microglobulin as a Marker of Hypertension‐Induced Renal Impairment and Its Response on Different Blood Pressure–Lowering Drugs

The purpose of this study was to assess the role of urine α1‐microglobulin as a marker of hypertension‐induced renal damage compared with estimated glomerular filtration rate, (eGFR), urine albumin, and urine albumin‐to‐creatinine ratio (ACR). Its response on different blood pressure (BP)–lowering drugs was also studied. Sixty never‐treated hypertensive patients (65.0% men, 46.9 years, BP 141.4/94.0 mm Hg) were randomized to an irbesartan (an angiotensin receptor blocker [ARB]) or a diltiazem (a nondihydropyridine calcium channel blocker [CCB])‐based regimen. Patients with diabetes or established cardiovascular, renal, or liver disease were excluded. Blood samples and 24‐hour urine were analyzed at baseline and 6 months after pharmaceutical BP normalization. Serum creatinine was measured and eGFR was calculated. Urine albumin, creatinine, and α1‐microglobulin were measured and ACR was calculated. Minor changes (P=not significant [NS]) in eGFR were noted during follow‐up in both groups (from 111.0 mL/min/1.73 m2 to 108.4 mL/min/1.73 m2 in the ARB group and from 111.3 mL/min/1.73 m2 to 114.0 mL/min/1.73 m2 in the CCB group). Twenty‐four–hour urine indices were all significantly improved (P<.01) in the ARB group (albumin from 19.4 mg/L to 8.2 mg/L, ACR from 21.5 mg/g to 10.0 mg/g, α1‐microglobulin from 5.06 mg/L to 3.64 mg/L) but not (P=NS) in the CCB group (albumin from 15.6 mg/L to 13.9 mg/L, ACR from 17.6 mg/g to 17.1 mg/g, α1‐microglobulin from 4.94 mg/L to 4.79 mg/L). These differences between groups remained significant (P<.05) after adjusting for office heart rate and BP. α1‐Microglobulin was significantly correlated (P<.05) with albumin and ACR both at baseline (r=0.283 and 0.299, respectively) and at the end of follow‐up (r=0.432 and 0.465, respectively) but not (P=NS) with eGFR. It was also significantly related (P<.05) to cardiovascular risk scores (Framingham and HeartScore) both at baseline (r=0.264 and 0.436, respectively) and at the end of follow‐up (r=0.308 and 0.472, respectively). Urine α1‐microglobulin emerges as a potentially usable marker of hypertension‐induced renal impairment. Its excretion rate and its response to treatment appears similar to that of albumin. Irbesartan but not diltiazem seems to be associated with reduced excretion of α1‐microglobulin in urine.

Arterial hypertension and aortic valve stenosis: Shedding light on a common “liaison”

Arterial hypertension and aortic valve stenosis are common disorders and frequently present as concomitant diseases, especially in elderly patients. The impact of hypertension on heart haemodynamics is substantial, thus affecting the clinical presentation of any coexisting valvulopathy, especially of aortic stenosis. However, the interaction between these 2 entities is not thoroughly discussed in the European or/and American guidelines on the management of hypertension or/and valvular heart disease. The present review summarizes all available evidence on the potential interplay between hypertension and aortic valve stenosis, aiming to help physicians understand the pathophysiology and select the best diagnostic and therapeutic strategies (medical or/and interventional) for better management of these high-risk patients, taking into account the impact on outcome as well as the risk-benefit-ratio.

Epidemiology of Erectile Dysfunction in Hypertension

Erectile dysfunction is a microvascular-endothelial disease that affects the quality of life. Hypertension is a major cardiovascular risk factor, while antihypertensive therapy is associated with dramatic reduction in cardiovascular events. Large community-based studies indicate that hypertension increases substantially the risk for erectile dysfunction. Erectile dysfunction is approximately twice as prevalent in hypertensive patients compared to normotensive individuals. Of major clinical importance, erectile dysfunction is usually more severe in hypertensive compared to normotensive subjects and tends to be more prevalent in treated than in untreated hypertensive patients, suggesting that antihypertensive therapy may, at least in part, contribute to erectile dysfunction. Age, duration, and severity of hypertension, comorbidities, and the type of antihypertensive therapy are the major determinants of erectile dysfunction in hypertensive patients. This review aims to summarize epidemiological data regarding the prevalence of erectile dysfunction in hypertensive patients compared to normotensive individuals, the determinants of erectile dysfunction in hypertensive patients, and critically evaluate available data.

Genetic Variant in the CYP19A1 Gene Associated with Coronary Artery Disease.

The CYP19A1 gene encodes the enzyme aromatase, which is responsible for the biosynthesis of estrogens. The rs10046 polymorphism of CYP19A1 gene has been investigated in two studies on the occurrence of hypertension, but there are no studies on its correlation with coronary artery disease (CAD). We investigated 189 subjects who were hospitalized at “KAT” General Hospital of Athens and underwent coronary angiography. Of these, 123 were found with CAD with an average age of 60 years and constituted the patients group and 66 subjects with an average age of 58 years without damage in the coronary vessels and constituted the control group (healthy). The frequencies of genotypes CC, CT, and TT of rs10046 polymorphism are significantly different between the group of CAD patients and the control group (0.34, 0.48, and 0.18 versus 0.20, 0.48, and 0.32, resp., P = 0.034) as the frequency of C allele (0.58 versus 0.44, resp., OR = 1.771 and P = 0.010). We found similar results for men, but not for women (small sample). The results of this study show that the rs10046 (C/T) polymorphism of CYP19A1 gene exhibits correlation with CAD and that patients with C allele have an increased probability of manifesting the disease.

Impaired glucose homeostasis in non-diabetic Greek hypertensives with diabetes family history. Effect of the obesity status.

Arterial hypertension (AH) and diabetes mellitus (DM) are established cardiovascular risk factors. Impaired glucose homeostasis (IGH; impaired fasting glucose or/and impaired glucose tolerance) or pre-diabetes, obesity, and DM family history identify individuals at risk for type 2 DM in whom preventive interventions are necessary. The aim of this study was to determine the glycemic profile in non-diabetic Greek adult hypertensive men and women according to DM family history and the obesity status. Diabetes family history, obesity markers (waist-to-hip ratio, WHR; body mass index, BMI), glycemic parameters (fasting and 2-hour post-load plasma glucose, if necessary; glycated hemoglobin, HbA1c; fasting insulin), insulin resistance indices (homeostasis model assessment, HOMA; quantitative insulin sensitivity check index, QUICKI; Bennett; McAuley), and IGH prevalence were determined in a large cohort of 11,540 Greek hypertensives referred to our institutions. Positive DM family history was associated with elevated fasting glucose (98.6 ± 13.1 vs 96.5 ± 12.3 mg/dL), HbA1c (5.58% ± 0.49% vs 5.50% ± 0.46%), fasting insulin (9.74 ± 4.20 vs 9.21 ± 3.63 μU/mL) and HOMA (2.43 ± 1.19 vs 2.24 ± 1.01) values, lower QUICKI (0.342 ± 0.025 vs 0.345 ± 0.023), Bennett (0.285 ± 0.081 vs 0.292 ± 0.078) and McAuley (6.73 ± 3.43 vs 6.95 ± 3.44) values, and higher IGH prevalence (45.3% vs 38.7%); P < .01 for all comparisons. The difference in the prevalence of IGH according to DM family history was significant (P < .01) in both genders and every WHR and BMI subgroup (except for women with BMI <20 kg/m(2)). Non-diabetic hypertensives with positive DM family history present with higher IGH prevalence and worse glycemic indices levels compared with those with negative family history, especially in the higher WHR/BMI subgroups.