Showing papers by "European Society of Hypertension published in 2019"

Prevalence and Control of Dyslipidemia in Patients Referred for High Blood Pressure: The Disregarded “Double-Trouble” Lipid Profile in Overweight/Obese

Abstract: We evaluated the prevalence and control of dyslipidemia in a wide sample of patients referred to our ESH “Hypertension Excellence Centre” for high blood pressure (BP). Furthermore, we evaluated the role of adiposity on the serum lipid profile. Observational study on 1219 consecutive outpatients with valid ambulatory BP monitoring (ABPM) referred for high BP. Patients with body mass index (BMI) ≥ 25 kg/m2 were defined as overweight/obese (OW/OB). Dyslipidemia and the control rates of low-density lipoprotein cholesterol (LDLc) were defined according to the 2016 ESC/EAS Guidelines. Mean age: 56.5 ± 13.7 years. Male prevalence: 55.6%. OW/OB patients were 70.2%. The prevalence of dyslipidemia was 91.1%. Lipid-lowering drugs were taken by 23.1% of patients. Patients with controlled LDLc comprised 28.5%, while BP was controlled in 41.6% of patients. Only 12.4% of patients had both 24-h BP and LDLc controlled at the same time. The higher the cardiovascular (CV) risk was, the lower was the rate of LDLc control (p < 0.001). Patients in secondary prevention had worse LDLc control than patients in primary prevention (OR 3.5 for uncontrolled LDLc, p < 0.001). OW/OB showed a more atherogenic lipid profile, characterized by lower high-density lipoprotein cholesterol (HDLc) (p < 0.001), higher non-HDLc (p = 0.006), higher triglycerides (p < 0.001), higher non-HDLc/HDLc (p < 0.001) and higher (non-HDLc + non-LDLc) (p < 0.001). Dyslipidemia is still too often neglected in hypertensives, especially in patients at higher CV risk. OW/OB hypertensives have a “double-trouble” atherogenic lipid pattern likely driven by adiposity. We encourage a comprehensive evaluation of the lipid profile in all hypertensives, especially if they are OW/OB, to correctly assess their CV risk and improve their management. Article processing charges funded by Servier SpA.

PCSK9 is Expressed in Human Visceral Adipose Tissue and Regulated by Insulin and Cardiac Natriuretic Peptides

Abstract: Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to and degrades the low-density lipoprotein receptor (LDLR), contributing to hypercholesterolemia. Adipose tissue plays a role in lipoprotein metabolism, but there are almost no data about PCSK9 and LDLR regulation in human adipocytes. We studied PCSK9 and LDLR regulation by insulin, atrial natriuretic peptide (ANP, a potent lipolytic agonist that antagonizes insulin), and LDL in visceral adipose tissue (VAT) and in human cultured adipocytes. PCSK9 was expressed in VAT and its expression was positively correlated with body mass index (BMI). Both intracellular mature and secreted PCSK9 were abundant in cultured human adipocytes. Insulin induced PCSK9, LDLR, and sterol-regulatory element-binding protein-1c (SREBP-1c) and -2 expression (SREBP-2). ANP reduced insulin-induced PCSK9, especially in the context of a medium simulating hyperglycemia. Human LDL induced both mature and secreted PCSK9 and reduced LDLR. ANP indirectly blocked the LDLR degradation, reducing the positive effect of LDL on PCSK9. In conclusion, PCSK9 is expressed in human adipocytes. When the expression of PCSK9 is induced, LDLR is reduced through the PCSK9-mediated degradation. On the contrary, when the induction of PCSK9 by insulin and LDL is partially blocked by ANP, the LDLR degradation is reduced. This suggests that NPs could be able to control LDLR levels, preventing PCSK9 overexpression.

Relationship of a Body Shape Index and Body Roundness Index with carotid atherosclerosis in arterial hypertension

Abstract: Background and aims A Body Shape Index (ABSI) and Body Roundness Index (BRI) are two new anthropometric adiposity indices that have shown to be associated better than BMI with adipose abdominal tissue, with the onset of diabetes and the risk of premature death. Little is known about the influence of ABSI and BRI on subclinical vascular damage. The study was aimed to assess the relationship between ABSI and BRI with carotid atherosclerosis damage in subjects with arterial hypertension. Methods and results A total of 468 patients with arterial hypertension (30–80 years old) were enrolled; adiposity indices were calculated (BMI, WC, ABSI, BRI) and carotid ultrasonographic examination was performed to detect atherosclerotic damage (IMT or atherosclerotic plaque). BRI, but not ABSI, was higher in subjects with IMT> 0.90 mm in comparison to those with a lower IMT (p Conclusions ABSI may be proposed as a better correlate of carotid atherosclerosis than the traditional measures of adiposity.

Prognostic role of masked and white-coat hypertension: 10-Year mortality in treated elderly hypertensives.

Abstract: White-coat uncontrolled hypertension (WUCH) and masked uncontrolled hypertension (MUCH) are common in the elderly. The prognostic role of these hypertension phenotypes is not completely defined in this subpopulation. Our aim is to evaluate the long-term prognostic role of WUCH and MUCH in treated elderly hypertensives. Observational study conducted on 120 consecutive treated elderly hypertensives. Patients were assessed on a first clinical visit in 2006. Subsequently, such patients or their relatives have been recalled after 10 years to evaluate the survival rates. Main inclusion criteria at baseline: age ≥ 65 years, a previous diagnosis of essential hypertension, a valid 24-h ambulatory blood pressure monitoring (ABPM). All participants received anti-hypertensive drugs during the 10-year period and we considered 10-year mortality for the analysis. General characteristics at baseline: mean age was 71.2 ± 5.3 years; females were 53.3%; 15.1% of patients had sustained controlled hypertension (SCH), 35.8% had WUCH, 10.8% had MUCH and 38.3% had sustained uncontrolled hypertension (SUCH). Thirty-two patients (26.7%) died during the 10-year period. Deceased patients were older, had lower treatment intensity, HDLc levels and eGFR than survivors. After adjusting for these covariates, MUCH (HR 12.30, p < 0.001) and SUCH (HR 4.84, p = 0.007) were associated with higher risk of death, compared to SCH, while no relationship emerged with WUCH (HR 1.58, p = 0.455). In our real-life study on treated elderly hypertensives, MUCH was associated with higher risk of death, compared to SCH and SUCH, while WUCH was not. ABPM is a key tool to improve management and therefore prognosis in this subpopulation.

Association between different lipid parameters and aortic stiffness: clinical and therapeutic implication perspectives.

Abstract: Introduction Recommendations about lipid parameters varied from different guidelines. Aortic stiffness is a marker of vascular aging and may reflect occurrence of cardiovascular diseases. Aortic pulse wave velocity (PWV), a marker of aortic stiffness, can be measured by applanation tonometry. The purpose of our study was to test the associations between lipid parameters and aortic stiffness. Methods A cross-sectional study was conducted from 2012 to 2017, 603 participants were included: 517 patients and 86 'healthy' individuals used to calculate the theoretical PWV. Lipid parameters, including total cholesterol, triglycerides, low-density lipoprotein (LDL), high-density lipoprotein (HDL), non-HDL, total cholesterol/HDL ratio, triglycerides/HDL ratio and LDL/HDL ratio were measured. Theoretical PWV can be calculated according to age, sex, mean blood pressure and heart rate, allowing to form an individual PWV index [(measured PWV - theoretical PWV)/theoretical PWV]. PWV index [(measured PWV - theoretical PWV)/theoretical PWV] greater than 0 defined aortic stiffness. Results In multiple linear regression analyses, total cholesterol (P = 0.03), LDL (P = 0.04), non-HDL (P = 0.03), total cholesterol/HDL (P = 0.01) and LDL/HDL (P = 0.03) were significantly correlated with PWV. In multiple logistic regression analyses, non-HDL [OR = 1.12 (1.04-1.20), P = 0.01, R value: 0.224], total cholesterol/HDL [OR = 1.12 (1.02-1.22), P = 0.03, R value: 0.219] and total cholesterol [OR = 1.11 (1.01-1.23), P = 0.03, R value: 0.209] were significantly associated with aortic stiffness. Conclusion Non-HDL, total cholesterol and total cholesterol/HDL were significantly associated with aortic stiffness than others and especially individually lipid parameters. This result should be considered in future clinical lipid-lowering trials.

Clinic Versus Ambulatory Blood Pressure in Resistant Hypertension: Impact of Antihypertensive Medication Nonadherence: A Post Hoc Analysis the DENERHTN Study.

Abstract: Clinic-ambulatory blood pressure (BP) difference is influenced by patients- and device-related factors and inadequate clinic-BP measurement. We investigated whether nonadherence to antihypertensive...

Renal haemodynamics and coronary atherosclerotic burden are associated in patients with hypertension and mild coronary artery disease.

Abstract: Intrarenal hemodynamic alterations are independent predictors of cardiovascular events in different populations. It has been hypothesized that there is an association between renal hemodynamics and coronary atherosclerotic burden in patients with hypertension. Therefore, the present study examined the associations between renal hemodynamics, coronary atherosclerotic burden and carotid atherosclerotic disease. A total of 130 patients with hypertension aged between 30-80 years who had been referred for an elective coronary angiography were enrolled in the present study. A duplex ultrasound of the intrarenal vasculature was performed to evaluate the resistive index (RI), pulsatility index (PI) and acceleration time (AT). The carotid intima-media thickness was additionally assessed. A coronary angiography was performed to detect the atherosclerotic burden using the Gensini Score (GS). Based on the GS values, subjects were divided into quintiles (I: ≤9; II: 9-17; III: 17-30; IV: 30-44; and V: GS >44) as well as in subjects with mild (GS ≤30) or severe coronary disease (GS >30). A weak significant difference in PI was identified among quintiles (P=0.041), whereas, RI and AT did not differ significantly. PI was associated with GS in the group with low coronary atherosclerotic burden (GS ≤30; P=0.047), whereas, no association was detected in subjects with GS >30. This association remained following adjustment for age and left ventricular ejection fraction (P=0.025). In conclusion, renal vascular alterations were associated with coronary atherosclerotic burden in patients with hypertension with mild coronary disease.

Treatment of Primary Aldosteronism With mTORC1 Inhibitors.

Abstract: CONTEXT Mammalian target of rapamycin complex 1 (mTORC1) activity is often increased in the adrenal cortex of patients with primary aldosteronism (PA), and mTORC1 inhibition decreases aldosterone production in adrenocortical cells, suggesting the mTORC1 pathway as a target for treatment of PA. OBJECTIVE To investigate the effect of mTORC1 inhibition on adrenal steroid hormones and hemodynamic parameters in mice and in patients with PA. DESIGN (i) Plasma aldosterone, corticosterone, and angiotensin II (Ang II) were measured in mice treated for 24 hours with vehicle or rapamycin. (ii) Plasma aldosterone levels after a saline infusion test, plasma renin, and 24-hour urine steroid hormone metabolome and hemodynamic parameters were measured during an open-label study in 12 patients with PA, before and after 2 weeks of treatment with everolimus and after a 2-week washout. MAIN OUTCOME MEASURES (i) Change in plasma aldosterone levels. (ii) Change in other steroid hormones, renin, Ang II, and hemodynamic parameters. RESULTS Treatment of mice with rapamycin significantly decreased plasma aldosterone levels (P = 0.007). Overall, treatment of PA patients with everolimus significantly decreased blood pressure (P < 0.05) and increased renin levels (P = 0.001) but did not decrease aldosterone levels significantly. However, prominent reduction of aldosterone levels upon everolimus treatment was observed in four patients. CONCLUSION In mice, mTORC1 inhibition was associated with reduced plasma aldosterone levels. In patients with PA, mTORC1 inhibition was associated with improved blood pressure and renin suppression. In addition, mTORC1 inhibition appeared to reduce plasma aldosterone in a subset of patients.

Recurrent vertigo is a predictor of stroke in a large cohort of hypertensive patients.

Abstract: Objective Dizziness is associated with hypertension but there are numerous other causes. The aims of the present study were to describe the characteristics and the clinical correlates of dizziness in a large cohort of hypertensive patients, and to test its prognostic value for all-cause, cardiovascular, and stroke mortality. Methods A total of 1716 individuals from the OLD-HTA Lyon's cohort of hypertensive patients recruited in the 1970s were categorized according to the absence or the presence of dizziness. The dizziness group was subdivided into vertigo and other dizziness excluding vertigo. Results Multiple regression analysis demonstrated that presence of dizziness was predicted by age, female sex, coronary artery disease, and the absence of microalbuminuria. During 30 years of follow-up, we observed 956 deaths, 508 of which with a cardiovascular cause, and 114 fatal acute strokes. In the multivariate Cox regression model, the presence of dizziness had no impact on the risk for all-cause mortality [hazard ratio 0.91; 95% CI (0.78-1.06)], cardiovascular mortality [hazard ratio 0.86; 95% CI (0.70-1.05)], or stroke mortality [hazard ratio 1.27; 95% CI (0.85-1.90)]. In an analysis of the different subgroups of dizziness, only vertigo had a prognostic impact. The increased risk was particularly marked on stroke death with a hazard ratio of 2.43 (95% CI 1.33-4.46) vs. patients without dizziness and 2.22 (95% CI 1.21-4.06) vs. patients with dizziness excluding vertigo. Conclusion Hypertensive patients with dizziness did not have a high-risk profile at baseline, but those with vertigo must be carefully followed over years because of the higher stroke mortality.

Self-blood pressure monitoring as a tool to increase hypertension awareness, adherence to antihypertensive therapy, and blood pressure control.

Abstract: For many years, casual blood pressure (BP) taken by a sphygmoma‐ nometer in the clinic or at the physician's office has been used as the standard method for diagnosing hypertension. Even if such mea‐ surement has been the cornerstone on which our understanding of the consequences of hypertension is based, there is a huge and very consistent body of evidence indicating that casual measurements of BP may provide a very unreliable index for the evaluation of hyper‐ tension because of their variability. The two alternative ways of measuring BP that have been most commonly used are measurements made at home by the patient himself (home or self‐BP monitoring—SBPM) and measurements by ambulatory blood pressure recorders.1 Results obtained by these methods have given closer correla‐ tion with a variety of measures of hypertensive end‐organ com‐ plications than casual or office BP.1‐3 Furthermore, the prognostic studies indicate that BP measurements performed in “out‐of‐of‐ fice” settings (using both home and ambulatory monitoring) are superior to office BP in predicting cardiovascular morbidity and mortality.1,4 Moreover, SBPM is a practical, reproducible, easy‐to‐learn, and economical way to reduce some of the pitfalls of relying exclusively on readings taken in the clinic. Most current self‐monitoring elec‐ tronic devices are relatively cheap, simple to operate, will remove observer bias, and allow for multiple measurements in a short time. In addition, it may be possible to reduce or to eliminate the “white‐ coat effect” that influences office BP readings.1 It has been known since the classic study of Ayman and Goldshine in 1940 that home recordings are generally lower than office read‐ ings.5 These authors, working in Boston at Beth Israel Hospital, reasoned that the home environment might be more conducive to obtaining BP readings without the stress associated with an office or clinic visit, recognizing that measurements of pressure at home, outside the clinic, might provide a more accurate assessment of pa‐ tients' usual BP. Clearly, these authors had identified what is now called “white‐coat” or clinic hypertension, although they did not coin these terms. They were the first to propose the concept of “self‐BP measurement”, pioneeringly suggesting that home BP monitoring was useful for (a) instructing the patients about their chronic dis‐ eases, (b) teaching physicians about the natural course of the disease and about factors that affect the disease, (c) learning the prognosis of disease, and (d) increasing the precision of determining the effec‐ tiveness of treatment.5 Nowadays, progress in technology has offered novel approaches to telemonitoring of BP values measured at a patient's home. Blood pressure telemonitoring (BPT) is a telehealth strategy that allows remote data transmission of BP and other information on patients' health status from their dwellings or from a community setting to the doctor's office or the hospital.6,7 For all the above reasons, the use of HBPM is recommended by several national and international guidelines for the management of hypertension, in order to obtain a more representative estimate of the average BP than casual and incidental reading at the clinic or at the office.8‐12 For the most part, the recommendations from the various organizations are similar, as outlined below, although there are some minor differences.

The Unsolved Conundrum of Optimal Blood Pressure Target During Acute Haemorrhagic Stroke: A Comprehensive Analysis.

Abstract: Intracerebral haemorrhage (ICH) is a devastating cerebrovascular disease, which accounts to 15% of all strokes. Among modifiable risk factors for ICH, hypertension is the most frequent. High blood pressure (BP) is detected in more than 75–80% of patients with ICH. Extremely elevated BP has been associated with early hematoma growth, a relatively frequent occurrence and powerful predictor of poor outcome in patients with spontaneous ICH. On the other hand, excessively low BP might cause cerebral hypoperfusion and ultimately lead to poor outcome. This review will analyse the most important trials that have tried to establish how far should BP be lowered during acute ICH. These trials have demonstrated either a small non-significant benefit (INTERACT-2, INTEnsive blood pressure Reduction in Acute Cerebral haemorrhage Trial) or no benefit (ATACH-2, Antihypertensive treatment of acute cerebral haemorrhage II study) when intensive systolic BP reduction was compared with modest or standard BP reduction. The more recent meta-analyses including studies investigating this issue yielded similar conclusions: aggressive BP control in the acute phase of ICH is not beneficial. For these reasons the 2018 European Society of Cardiology/ European Society of Hypertension Guidelines for the management of arterial hypertension, do not recommend treatment to immediately lower BP in patients with acute ICH and systolic BP < 220 mmHg. Careful lowering of SBP to less than 180 mmHg via i.v. Infusion may be considered only in patients with SBP ≥ 220 mmHg.

Isolierte systolische Hypertonie (ISH) – Alt gegen Jung

Abstract: Die isolierte systolische Hypertonie (ISH) ist definiert als erhohter systolischer Blutdruck (BD) mit normalen oder niedrigen diastolischen Werten: > 140/

The nephroprotective effect of sacubitril/valsartan in heart failure: insights from the real-life clinical setting.

Abstract: Sacubitril/valsartan represents the first agent in a new class of drugs developed for heart failure (HF) treatment and termed angiotensin receptor neprilysin (NEP) inhibitors (ARNIs). It is a fixed-dose combination compound containing molecular moieties of valsartan, an angiotensin-type I receptor (AT1)-inhibitor, and the NEP inhibitor sacubitril in a 1:1 molar ratio [1]. Sacubitril is a prodrug that, following oral administration, is rapidly metabolized to the biologically active molecule sacubitrilat. This inhibits the NEP, which is a ubiquitous endopeptidase that is responsible for the breakdown of many vasoactive peptides, including the biologically active natriuretic peptides (NPs), adrenomedullin, substance P, bradykinin, vasoactive intestinal polypeptide, calcitonin gene-related peptide, and enkephalins. Inhibition of NEP increases the levels of these substances, countering the neurohormonal overactivation that contributes to vasoconstriction, sodium retention, and maladaptive remodeling in patients with HF [1]. The NPs are structurally related but genetically different hormones or paracrine factors, that protect the cardiovascular (CV) system from volume overload. The mammalian NP system comprises of mainly 3 NPs: atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). In the kidney, more specifically distal tubular cells, expression of ANP precursor produces a subtype called urodilatin, which helps ANP to regulate renal sodium and water excretion through inhibition of antidiuretic hormone and, Angiotensin II/aldosterone-dependent sodium and water reabsorption [2]. In addition, NPs are known to oppose RAS and have anti-proliferative and anti-hypertrophic effects. As the clinical stage of HF progresses, the responsiveness to NPs, in particular ANP and BNP, decreases. This can be due to downregulation of NPs receptors, increased clearance of BNP by NEP or the NPR-C receptor, or decreased downstream signaling. Blocking NEP with sacubitril/valsartan (S/V) results in greater level of NPs and in increased generation of myocardial cGMP. In this way it is possible to overcome natriuretic resistance, resulting from any one of the previously described mechanisms, thus producing favourable clinical outcomes in patients with HF [2]. Indeed, S/V is the most remarkable pharmacological innovation concerning the treatment of patients with chronic HF and reduced ejection fraction (HFrEF) [3]. In “The Prospective Comparison of ARNI with ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure” (PARADIGM-HF) trial, this drug was studied in 8442 patients with HFrEF, clearly showing superiority above treatment with ACE-inhibitor enalapril [4]. The outcomes of the trial were so overwhelmingly positive that it was stopped early by its data monitoring committee. With a median follow-up of 27 months, the investigators demonstrated a 20% relative risk reduction in the composite of CV death or hospitalization for HF and a 16% relative risk improvement in all-cause mortality, with a number neededto-treat of 35 [4]. Additionally, S/V is also promising in HF with preserved ejection fraction (HFpEF), because it leads to improvement in ventricular diastolic function. The large ongoing “Prospective Comparison of Angiotensin Receptor Neprilysin Inhibitor With Angiotensin Receptor Blocker Global Outcomes in HFpEF” (PARAGON-HF) trial) is testing the hypothesis that S/V would be superior to valsartan in reducing morbidity and mortality in patients with HFpEF [5]. Following the publication of the results of the PARADIGM-HF study, updated guidelines of many cardiologic scientific societies, including the European Society of * Giuseppe Mulè giusemme63@gmail.com