Current Hypertension Reviews - Volume 10, Issue 3, 2014

There is increasing evidence that not only the elevation of systolic and diastolic blood pressure (BP) but also the increase in BP variability (or fluctuation) are associated with hypertensive organ damages and the morbidity and mortality of cerebrovascular and cardiovascular events. However, the molecular mechanism whereby the increase in BP variability aggravates hypertensive organ damages remains unknown. Thus, we created a rat chronic model of a combination of hypertension and large BP variability by performing bilateral sino-aortic denervation in spontaneously hypertensive rat. A series of our studies using this model revealed that large BP variability induces chronic myocardial inflammation by activating local angiotensin II and mineralocorticoid receptor systems and thereby aggravates cardiac hypertrophy and myocardial fibrosis, leading to systolic dysfunction, in hypertensive hearts. In addition, large BP variability induces the aggravation of arteriolosclerotic changes and ischemic cortical fibrosis in hypertensive kidney via local angiotensin II system.

Background: With 29% of the world’s adult population projected to have hypertension by the year 2025, prevention and management of hypertension have become a public health priority. Hypertension also referred to as high blood pressure, in which the arteries have persistent high blood pressure. This results in a condition where the heart has to work harder than normal to flow blood through the vessels. A few years ago, there was no sufficient information about the epidemiology of hypertension, treatment protocols and its consequences in Egypt. Lately, there has been a major change in health system in Egypt, including research development. Objectives: To evaluate the existing data on prevalence, levels of awareness, treatment and control of hypertension in Egypt with a view of suggestive actions that could enhance control of hypertension and improve quality of life of the patients. Methods: Six databases (Pub Med, Cochrane, MEDLINE, Sciencedirect, MedEase, Embase) were searched in November 2013, applying the following criteria: published from January 1995 to November 2013 written in English and carried out on human subjects. Results: 21 studies were included in the systematic review of the prevalence, awareness, and control of hypertension in Egypt. The sample size ranged from 27 subjects to 12008 subjects, and the age range from 6-95 years. Every study had both male and female representatives. In most of the studies, the women were more than the men. Conclusion: There are declines in the levels of awareness of hypertension and even lower levels of control. Research is required to reveal reasons behind these near to the ground levels of control and treatment, and especially awareness, in order to put in the picture policy for the improvement of quality of life of hypertensive patients in Egypt.

Prevalence of Heart Failure with Preserved Ejection (HFPEF) has been rising steadily in the recent past. Studies have shown that at least half of patients presenting with symptoms and signs of heart failure (HF) have preserved left ventricular ejection fraction, i.e. HFPEF, and that this portion of the HF population consists predominantly of women, older age group, and people with hypertension and other cardiovascular risk factors. The morbidity and mortality associated with HFPEF are much higher than the normal population. Chronic hypertension is the most common cause in addition to age, with suggestion of up to 60% of patients with HFPEF being hypertensive. Addressing the specific aetiology and aggressive risk factor modification remain the mainstay in the treatment of HFPEF. Current guidelines recommend the management should involve treatment of hypertension, control of heart rate, venous pressure reduction, and prevention of myocardial ischemia. This review aims to discuss the role of hypertension in the pathophysiology, risk stratification and prognosis of HFPEF, as well as the current available data on various antihypertensive options in this population.

Published guidelines for the management of hypertension (HTN) do not discuss HTN in patients with aortic stenosis (AS). Some clinicians have considered severe AS to be a relative contraindication to the use of antihypertensive agents. We sought to determine the incidence of syncope in AS patients who were treated with antihypertensive agents. We identified 89 patients with asymptomatic severe AS and normal ejection fraction. The prevalence of HTN, its treatment, and the occurrence of syncope was abstracted from medical records. HTN was documented in 63 of the 89 patients with severe AS; 62 were being treated (mean 2.2 drugs). The incidence of syncope (mean follow-up: 44 months) was similar in patients with treated HTN compared to those without HTN (8 vs 11%, p=NS). Of the 62 with treated HTN, those with syncope were older than those without syncope (88+/- 6 vs 78 +/- 9 years, p=0.02). When those with treated HTN and syncope were compared to an age and sex matched cohort without syncope there were no significant differences in severity of AS, ejection fraction, or arterial pressure. Patients with treated HTN and syncope had a lower stroke volume index than those without syncope (32 +/- 4 vs 40 +/- 6 mL/m2, p=0.01). In conclusion, the risk of syncope in patients with severe AS and treated HTN is low and similar to that seen in AS patients without HTN. Syncope is related to age, female sex, and a low stroke volume index.

The treatment of hypertension in patients with chronic kidney disease is still controversial, particularly in regards to the intensity of blood pressure lowering. The 2014 guidelines for the management of hypertension in adults released by the Eighth Joint National Committee (JNC 8) have sparked criticism from nephrologists, and various societies have issued differing guidelines. In this article we present a few case vignettes and provide a brief review of the various guidelines, particularly in regards to patients with chronic kidney disease. We review some of the landmark trials that have influenced guidelines and the practice of nephrology, as well as the limitations of the evidence on which the current guidelines are based. We discuss treatment for the patients presented in the case vignettes in light of the guidelines and the evidence. Finally, it will be clear that there is no single BP goal or single drug that is appropriate for all patients, and that our knowledge base for optimal treatment of hypertension in chronic kidney disease is still limited.

Renalase was described in 2005 as a new flavoprotein expressed mainly in the kidney that functions as a flavin adenine dinucleotide (FAD)- and nicotinamide adenine dinucleotide (NADH)-dependent amine oxidase. In contrast to other monoamine oxidases, renalase can be secreted into both plasma and urine where it has been suggested to metabolise catecholamines and contribute to blood pressure control. Renalase was first reported to be undetectable in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD), suggesting a causal link between the reduced plasma renalase levels, increased plasma catecholamine, and heightened cardiovascular risk that are well documented in this population. Plasma renalase deficiency has been consistently reported in studies using animal models of CKD. However, in studies with 3/4 nephrectomised (3/4nx) rats, the reduced circulating renalase levels were accompanied by increased plasma renalase activity that appeared to be related to decreased inhibition of circulating enzyme. By contrast, a series of recent studies in human subjects provides evidence suggesting that plasma renalase levels are negatively correlated with renal function. Though, similar to that found in the rat remnant kidney, the increased plasma renalase activity in patients with ESRD was associated with decreased inhibition of the circulating enzyme.

Hypertension is common in chronic kidney disease patients especially in those undergoing hemodialysis (HD). Usually, blood pressure falls after the HD session but in some patients a paradoxical increase has been observed during or immediately after HD. This phenomenon is referred as intradialytic hypertension. HD patients with intradialytic hypertension or increased blood pressure during HD present higher cardiovascular (CV) morbidity and mortality rates. The underlying mechanism of intradialytic hypertension is multifactorial. Activation both of renin-angiotensinaldosterone system (RAAS) and sympathetic nervous system, volume and sodium overload with concomitant increase in cardiac output, and endothelial dysfunction have been implicated in the pathogenesis of intradialytic hypertension. Given the lack of clinical trials regarding the pathophysiology and management of intradialytic hypertension, current treatment strategies are based mainly on experts’ opinion. The purpose of this review is to describe the pathophysiology of intradialytic hypertension and discuss current strategies in order to improve intradialytic blood pressure management and concomitant HD patients’ outcomes.