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The 2018 resistant hypertension scientific statement offers new treatment recommendations. To determine the implications of these changes, we sought to ascertain the prevalence of apparent treatment resistant hypertension (aTRH) and the therapies used to treat it in an US national ambulatory cardiovascular registry before these recent developments. Using the PINNACLE Registry from 2013 to 2014, we identified all patients receiving treatment for hypertension and then determined the proportion with aTRH as those who met the following criteria over ≥2 consecutive visits: (1) 3 blood pressure medication classes including a diuretic and blood pressure >140/90, OR (2) ≥4 blood pressure medications. Among those with aTRH, we examined past use of therapies now recommended in guidelines including: (1) first-line therapy with an angiotensin-converting enzyme inhibitor or angiotensin-II receptor blocker, calcium channel blocker and a thiazide diuretic, (2) use of chlorthalidone, and (3) use of a mineralocorticoid receptor antagonist (MRA) for those requiring a 4th medication. Of 84,624 patients on treatment for hypertension, 11,147 (13.1%) met criteria for prevalent aTRH. Among these patients: (1) Of those on 3 antihypertensive agents (n = 1,255), 315 (25%) were on the first-line regimen now recommended in guidelines, (2) 520 (6.7%) of the 7,930 patients on thiazides were using chlorthalidone, and (3) 3061 (27%) were using a MRA; another 4,523 (40.6%) were eligible for its addition. In conclusion, our findings of low historic use of therapies now recommended in guidelines suggest opportunities to improve care among patients with aTRH., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Objective: Use of amlodipine for treatment of arterial hypertension and stable coronary artery disease (CAD) is sometimes limited by occurrence of peripheral edema and headache. We aimed to explore the true magnitude of this phenomenon by determining the rate and placebo-adjusted rate of these side effects., Methods: We performed a meta-analysis by including all randomized, placebo-controlled trials reporting edema and headache with amlodipine in patients with arterial hypertension and CAD. Placebo-adjusted rate (%) was determined as follows: (SE amlodipine % - SE placebo %)/SE amlodipine %., Results: Data from 7226 patients of 22 trials were analyzed. Rate of edema was higher on amlodipine vs. placebo (16.6 vs. 6.2%, risk ratio: 2.9, 95% CI: 2.50-3.36, P < 0.0001). The placebo-adjusted rate was 63%, indicating that 37% of edema cases were unrelated to amlodipine. Treatment with low/medium doses (2.5-5 mg) resulted in lower rates of edema (risk ratio: 2.01, 95% CI: 1.41-2.88, P = 0.0001) vs. high dose (10 mg) (risk ratio: 3.08, 95% CI 2.62-3.60, P < 0.0001, Pforinteraction = 0.03). Incidence of headache was reduced using amlodipine vs. placebo (7.9 vs. 10.9%, risk ratio: 0.77, 95% CI: 0.65-0.90, P = 0.002) and was driven by use of low/medium doses (risk ratio: 0.52, 95% CI: 0.40-0.69, P < 0.00001 vs. risk ratio: 0.92, 95%-CI: 0.74-1.15, P = 0.45, for high doses, Pforinteraction = 0.002)., Conclusion: Although risks of peripheral edema are three-fold higher on amlodipine, up to one-third of edema cases on amlodipine might not be induced by amlodipine. Headache is reduced on amlodipine treatment, mainly driven by use of this drug at low/medium doses.

Beta-blockers are commonly used medications, and they have been traditionally considered "cardioprotective." Their clinical use appears to be more widespread than the available evidence base supporting their role in cardioprotection. Beta-blockers counteract neurohumoral activation in heart failure with reduced ejection fraction and offer both symptomatic improvement and reduction in adverse events. On the other hand, the use of beta-blockers in uncomplicated hypertension results in suboptimal outcomes compared to the established first-line antihypertensive agents. Providers at all levels should be familiar with common misconceptions regarding beta-blocker use in routine clinical practice., (Copyright © 2019 Elsevier Inc. All rights reserved.)

: A physiologically lower heart rate, such as that seen in athletes, has been associated with better survival in epidemiological studies. In patients with coronary artery disease, heart rate is considered an independent risk factor for adverse outcomes. Higher heart rate increases cardiac work load and oxygen demand and reduces coronary perfusion by decreasing the amount of time spent in diastole, which in patients with obstructive coronary artery disease can trigger angina and myocardial infarction. Whether pharmacological reduction in heart rate by using a beta-blocker or ivabradine improves prognosis has been debated. In this review, we explore the effect of pharmacological heart rate lowering with a beta-blocker or ivabradine on cardiovascular outcomes in patients with cardiovascular disease and address the question as to whether pharmacological heart rate reduction is ready for prime time in the management of patients with coronary artery disease. Although physiologically lower heart rates are associated with improved survival, the effect of pharmacological heart rate reduction with beta-blockers (in patients without heart failure or postmyocardial infarction) or ivabradine on improvement in survival is weak at best.

Until recently, intraindividual visit-to-visit variability of cardiovascular risk factors has been dismissed as random fluctuation. This simplistic concept was challenged by demonstrating that visit-to-visit blood pressure variability, independent of average blood pressure, was a powerful risk factor for stroke. Subsequently, variability of other cardiovascular risk factors such as cholesterol, glycemia, and body weight was documented to increase risk independent of their absolute values. Variability of these risk factors has been demonstrated to be a powerful predictor for all-cause and cardiovascular mortality, stroke, coronary artery disease, heart failure, end-stage renal disease, and dementia. With the notable exception of heart rate, cardiovascular risk factors must now be defined by 2 components: the magnitude and duration of sustained risk factor elevation and, equally important, the variability of the same risk factor over time., (Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Introduction: Angiogenic and inflammatory factors have been shown to play an important role in the pathogenesis of preeclampsia. However, there is little information on their interaction. The aims of this study were to investigate the longitudinal pattern of inflammatory markers, such as interleukin-6 (IL-6) and C-reactive protein (CRP) using a novel ultra-high sensitive assay method (uhsCRP), and to explore their relationship with angiogenic factors such as placental growth factor (PLGF), soluble fms-like tyrosine kinase-1 (sFlt-1), and vascular endothelial growth factor (VEGF) in normal pregnancies and pregnancies complicated by preeclampsia., Materials and Methods: Serum levels of uhsCRP, IL-6, PLGF, VEGF and s-Flt-1 were longitudinally determined in 16 women with normal, singleton healthy pregnancies at 7-13, 17-22, 27-31 and 37-41 weeks of gestation by ELISA. uhsCRP was measured using a ultra-high sensitivity ELISA test. Serum of women with preeclampsia (n = 15) was available only once, usually in the third trimester of pregnancy. Women with premature rupture of membranes (PROM) or infection such as chorioamnionitis were excluded. Spearman rank correlation, logistic regression, ROC analysis, ANOVA and Mann-Whitney U-test were used for statistical purposes., Results: In normal pregnancies, serum uhsCRP showed a gestational age-dependent increase (r = 0.40; P < 0.001). In women suffering from preeclampsia, uhsCRP levels were higher than in gestational age-matched controls (18010 ± 4763 versus 3026 ± 587 ng/ml; P < 0.001). Similarly, serum IL-6 levels increased throughout pregnancy and correlated with uhsCRP in normal pregnancies and in preeclampsia (n = 64, r = 0.37; P < 0.01 and n = 15, r = 1.00, P < 0.0001). uhsCRP levels were positively correlated with sFlt-1 levels (n = 64, r = 0.34; P < 0.01)., Conclusion: The increases in uhsCRP (and IL-6) serum levels with advancing gestation indicate a shift towards an inflammatory state during normal pregnancy. The excessive rise in uhsCRP and sFlt-1 in preeclampsia indicate that both may be involved in its pathogenesis. uhsCRP may be useful as an early marker for preeclampsia and studies defining the pattern of its rise throughout pregnancies at risk are urgently needed.

Background: Polycythemia is characterized by increased blood viscosity and a chronic inflammatory state possibly giving rise to excessive thromboembolic events and hypertensive cardiovascular disease. We aimed to study the relationship between polycythemia and cardiac risk factors using a large national registry., Methods: Patients more than 18 years with a diagnosis of polycythemia were identified from the National Inpatient Sample 2009-2010 database using International Classification of Diseases; Ninth Edition (ICD-9) code 238.4. Demographics, cardiac risk factors, and cardiovascular events were identified., Results: Polycythemia was present in 0.1% (n = 37 922) of hospital-discharged patients. Patients with polycythemia had a significantly increased prevalence of all cardiac risk factors and events, except for diabetes mellitus and chronic kidney disease. Hypertension was more prevalent in polycythemia compared to controls (61 vs. 46%; P < 0.0001). After adjusting for age, sex, race, diabetes mellitus, hyperlipidemia, tobacco use, obesity, coronary artery disease, heart failure, and chronic kidney disease, polycythemia was still a determinant of hypertension [1.37 (1.28-1.45); P < 0.001]., Conclusion: Polycythemia had high prevalence of all cardiac risk factors and was independently associated with increased prevalence of hypertension even after adjusting. Our findings from the National Inpatient Sample provide an epidemiological correlate of Gaisböck's original observation of the association of polycythemia and hypertension more than a century ago.

Background: Assisted reproductive technologies (ART) have been shown to induce premature vascular aging in apparently healthy children. In mice, ART-induced premature vascular aging evolves into arterial hypertension. Given the young age of the human ART group, long-term sequelae of ART-induced alterations of the cardiovascular phenotype are unknown., Objectives: This study hypothesized that vascular alterations persist in adolescents and young adults conceived by ART and that arterial hypertension possibly represents the first detectable clinically relevant endpoint in this group., Methods: Five years after the initial assessment, the study investigators reassessed vascular function and performed 24-h ambulatory blood pressure (BP) monitoring (ABPM) in 54 young, apparently healthy participants conceived through ART and 43 age- and sex-matched controls., Results: Premature vascular aging persisted in ART-conceived subjects, as evidenced by a roughly 25% impairment of flow-mediated dilation of the brachial artery (p < 0.001) and increased pulse-wave velocity and carotid intima-media thickness. Most importantly, ABPM values (systolic BP, 119.8 ± 9.1 mm Hg vs. 115.7 ± 7.0 mm Hg, p = 0.03; diastolic BP, 71.4 ± 6.1 mm Hg vs. 69.1 ± 4.2 mm Hg, p = 0.02 ART vs. control) and BP variability were markedly higher in ART-conceived subjects than in control subjects. Eight of the 52 ART participants, but only 1 of the 43 control participants (p = 0.041 ART vs. controls) fulfilled ABPM criteria of arterial hypertension (>130/80 mm Hg and/or >95th percentile)., Conclusions: ART-induced premature vascular aging persists in apparently healthy adolescents and young adults without any other detectable classical cardiovascular risk factors and progresses to arterial hypertension. (Vascular Dysfunction in Offspring of Assisted Reproduction Technologies; NCT00837642.)., (Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Purpose of Review: Evidence that artificial intelligence (AI) is useful for predicting risk factors for hypertension and its management is emerging. However, we are far from harnessing the innovative AI tools to predict these risk factors for hypertension and applying them to personalized management. This review summarizes recent advances in the computer science and medical field, illustrating the innovative AI approach for potential prediction of early stages of hypertension. Additionally, we review ongoing research and future implications of AI in hypertension management and clinical trials, with an eye towards personalized medicine., Recent Findings: Although recent studies demonstrate that AI in hypertension research is feasible and possibly useful, AI-informed care has yet to transform blood pressure (BP) control. This is due, in part, to lack of data on AI's consistency, accuracy, and reliability in the BP sphere. However, many factors contribute to poorly controlled BP, including biological, environmental, and lifestyle issues. AI allows insight into extrapolating data analytics to inform prescribers and patients about specific factors that may impact their BP control. To date, AI has been mainly used to investigate risk factors for hypertension, but has not yet been utilized for hypertension management due to the limitations of study design and of physician's engagement in computer science literature. The future of AI with more robust architecture using multi-omics approaches and wearable technology will likely be an important tool allowing to incorporate biological, lifestyle, and environmental factors into decision-making of appropriate drug use for BP control.

Most guidelines for the management of patients with cardiovascular disease recommend angiotensin-converting enzyme (ACE) inhibitors as first-choice therapy, whereas angiotensin receptor blockers (ARBs) are merely considered an alternative for ACE inhibitor-intolerant patients. The aim of this review was to compare outcomes and adverse events between ACE inhibitors and ARBs in patients. In patients with hypertension and hypertension with compelling indications, we found no difference in efficacy between ARBs and ACE inhibitors with regard to the surrogate endpoint of blood pressure and outcomes of all-cause mortality, cardiovascular mortality, myocardial infarction, heart failure, stroke, and end-stage renal disease. However, ACE inhibitors remain associated with cough and a very low risk of angioedema and fatalities. Overall withdrawal rates because of adverse events are lower with ARBs than with ACE inhibitors. Given the equal outcome efficacy but fewer adverse events with ARBs, risk-to-benefit analysis in aggregate indicates that at present there is little, if any, reason to use ACE inhibitors for the treatment of hypertension or its compelling indications., (Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Arterial hypertension is a prevalent disease with great harming potential. After the age of 55 years the remaining lifetime risk of hypertension amounts to 90%. Despite the constant advances some important issues such as the cut-off blood pressure for the initiation of antihypertensive therapy or the therapeutic goal are debated. In this review, we present - based on the available literature - the current concepts concerning the pathophysiology, epi-demiology and antihypertensive therapy in patients aged 65 years or older. The pathophysiology of hypertension in older patients in principle rests on stiffening of large conduit arteries, which leads to greater systolic and lower diastolic blood pressure. This in most older patients results in isolated systolic hypertension. Additionally most of these patients have low-renin hypertension. Data from large-scale clinical trials indicate that therapy of such individuals with thiazide-like diuretics and long-acting dihydropiridine calcium channel blockers as first-line medications reduces risk of complications. Based on results of recently published trials, meta-analyses, and prospective observations, the optimal on-treatment blood pressure values for most older hypertensive patients should be set within the 130-139 mmHg range. At present, lower values of standard office blood pressure in this group of patients have not been shown to be associ-ated with additional benefits, and may be associated with a greater risk of adverse events. In conclusion, we recommend that for most patients aged 65 years or more, standard office systolic blood pressure should be cautiously reduced to within 140 and 130 mmHg, preferably with a thiazide-like diuretic, long acting dihydropiridine calcium channel blocker or their combination.