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Highlights from the 21st Annual Scientific Meeting of the Egyptian Hypertension Society

PART OF Manage Hypertension Online FEATURE
Highlights from the 21st Annual Scientific Meeting of the Egyptian Hypertension Society
  • Cardiometabolic
  • Hypertension


Resource type



renal artery stenosis



This scientific meeting was held at: Grand Nile Tower Hotel, Cairo, Egypt, 4-5 April 2018

As in previous Egyptian Hypertension Society (EHS) meetings, much of the scientific program was devoted to continuous medical education and recent advances in hypertension research. Professor Marcelo Orias, Vice President of the World Hypertension League, was guest speaker and delivered two key lectures.

This year’s meeting included a report on the first year of the specialized hypertension clinics inaugurated last year, as well as sessions covering hypertension in those with:

  • Metabolic syndrome
  • Concomitant stress
  • Gestational hypertension
  • Chronic kidney disease

Sessions also discussed the role of herbal treatment, the problem of white coat hypertension, whether β-blockers are still the first-line of drug therapy and target blood pressure levels following the new guidelines from the USA.

      Are phenotypes in young hypertensive patients important? asked Professor Marcelo Orias (National University of Córdoba, Argentina). In his lecture, Professor Orias discussed hypertension in young patients, the pathophysiology and genetics of hypertension, pulse pressure phenotypes and predominantly diastolic hypertension.

            Cardiac events in young patients with diastolic hypertension are related to the degree of blood pressure elevation,1 a finding confirmed by recent studies.2,3 All types of hypertension (isolated systolic hypertension [ISH], isolated diastolic hypertension [IDH] and systolic-diastolic hypertension [SDH]) increase with age of the patient, but hypertension in the young is mainly IDH, and is predominantly (70-85% of cases) secondary hypertension. Blood pressure determinants are either genetic or environmental and the genetic determinants are either monogenic human hypertension associated with either hypokalemia, for example Liddle’s disease or with hyperkalemia, such as Gordon’s syndrome. An increase in blood pressure in late adolescence in both males and females is associated with increased morbidity and mortality – indeed, among younger individuals, those with ISH are at higher risk of death from cardiovascular disease or coronary heart disease compared with those with optimal-normal blood pressure over long-term follow-up.4 ISH in young individuals carries a relatively low risk of developing hypertension needing treatment when central blood pressure is low.5 Predominantly diastolic hypertension is more common in young patients, and is characterized by increased systemic vascular resistance associated with reduced cardiac output, cardiac index and stroke volume coupled with a relative increase in heart rate.5

Professor Orias concluded that hypertension is a complex syndrome with genetic and environmental influence, for which we need better phenotyping to increase genetic and pathophysiological knowledge, and that peripheral blood pressure measurement is not enough to comprehend the hemodynamic mechanisms.

Professor Omar El Khashab (Department of Renal Medicine, Cairo University, Egypt) presented on the control of blood pressure in regular hemodialysis patients. Regular hemodialysis patients are those with pre-dialysis blood pressure or 4-hour post-dialysis blood pressure of >140/90, and who show a night-time ‘dipping’ pattern and blood pressure variability.

There are several possible causes of hypertension in those with end-stage renal disease, including volume overload, increased vasopressor activity, reduced vasodilator capacity, hyperparathyroidism or erythropoietin treatment. The end-stage renal disease cardiovascular risk profile includes hypertension, cardiovascular autonomic dysfunction, increased arterial stiffness, anemia and sleep apnea, which leads to left ventricular hypertrophy, coronary artery disease, myocardial infarction and congestive heart failure. Consequently, hypertension in hemodialysis can cause left ventricular hypertrophy, coronary artery disease, arrhythmias and increased mortality.6

Factors impacting sudden cardiac death in hemodialysis patients include cardiomegaly, aortic stiffness, hypertension and volume overload,7 and there is a correlation between systolic blood pressure and cerebral hematoma size in end-stage renal disease. Nocturnal blood pressure and 24-hour pulse pressure are potent indicators of mortality in hemodialysis patients.8

            Strategies to manage hypertension in dialysis patients include reducing weight to dry weight, reducing sodium intake and dialysing sodium, modifying the dialysis strategy and lastly, using drugs. Modifying dialysis strategy includes using a longer treatment time and a slower ultrafiltration rate,9 selecting between nocturnal hemodialysis and daily hemodialysis and the effects of intensive hemodialysis. The type of dialysis can affect the degree of anemia and inflammation.10 Drug therapy aims for a target blood pressure reading of <140/90, with the optimum level being <120/80.  The preferred methodology is to control extracellular volume, and all classes of antihypertensives are effective:

  • Beta-blockers: Beneficial because hemodialysis patients have increased sympathetic activity; are dialyzable, but atenolol needs dose adjustment. Combined beta- and alpha-blockers are preferred.
  • Combined beta-alpha-blockers: Carvedilol has proved to be an inhibitor of progenitor endothelial cells and reduces intradialytic hypertension, without needing dose adjustment. Carvedilol leads to improvement of the ejection fraction relative to placebo11 and significant improvement in survival.12
  • Calcium channel blockers (CCB) are safe, effective and do not require dose adjustment.
  • Renin-angiotensin-aldosterone system (RAAS) inhibitors are the group of hypertensive medications most effective in reducing left ventricular hypertrophy.13 Follow up of serum potassium is needed, and there is no role for aldosterone antagonists.
  • ACEI need dose adjustment.
  • Diuretics: Rarely used, and only if patients are not oliguric.

Hypertension is an important contributor to mortality and morbidity in hemodialysis patients, for whom prolonged treatment and achieving a true dry weight are important factors in controlling blood pressure. Although all groups of hypertension drugs may be used, RAAS inhibitors and beta-blockers are particularly useful.

In his second lecture, Professor Marcelo Orias (National University of Córdoba, Argentina) examined the value of albuminuria as a surrogate biomarker, stating that a valid biomarker should predict a hard end-point risk and, if modified, the hard end-point should improve.

            In dialysis patients, age-adjusted cardiovascular mortality is 10-100 fold higher than in the general population and there is a relationship between the degree of albuminuria and the cardiovascular disease risk.14 Albuminuria can also predict renal events,15 with the deterioration of renal function directly related to the degree of microalbuminuria (MAU). Renal dysfunction can be improved by proper management in diabetic hypertensive patients.16

            As a predictor of cardiovascular and renal events, albuminuria is not ideal for many patients. Antihypertensive therapy producing an effective stable lowering of blood pressure can improve albuminuria and reduce the decline in the glomerular filtration rate – with the decrease in renal events dependent on the average quartile of blood pressure.17

            Combined angiotensin inhibition doesn’t improve morbidity and mortality in diabetic nephropathy,17 although albuminuria can improve, there is no effect on the glomerular filtration rate. Also, the combination can cause acute kidney injury in some patients and can increase the incidence of hyperkalemia.18 In the LIFE study19 the decrease in cardiovascular events correlated with the reduction of albuminuria and was associated with significant reductions in both systolic and diastolic pressure. However, all studies which have shown a beneficial effect of aggressively lowering albuminuria have done so in post-hoc analysis.

All diabetes guidelines suggest ordering an albuminuria test every year, although no prospective studies have demonstrated that microalbuminuria is lowered once blood pressure and low density lipoprotein goals are reached. Hence, cardiovascular and renal hard end-points shouldn’t be reduced and in low-to-intermediate risk patients, management is mainly dependent on controlling blood pressure. The FDA have advised against using microalbuminuria as a surrogate marker20 and in the PREVEND IT trial, combination fosinopril and pravastatin improved event-free survival in subjects with microalbuminuria.21 These data all suggest that microalbuminuria is a weak predictor.

The subject of ‘renal artery stenosis (RAS) “when to suspect” - How underlying pathology affects your management’ was tackled by Professor Mohamed Abd El Ghany (Department of Cardiology, Cairo University, Egypt). Significant RAS is generally considered when ≥60% blood flow reduction is apparent. Renovascular disease includes asymptomatic incidental RAS, renovascular hypertension, accelerated cardiovascular disease (congestive heart failure, stoke) and ischemic nephropathy. RAS can be unilateral (unilateral atherosclerotic RAS, unilateral fibromuscular dysplasia) or it can be bilateral (bilateral RAS, aortic coarctation).

            The main causes of RAS are either atherosclerotic, which causes >90% of renovascular hypertension and occurs in 6.8% of the general population, or non-atherosclerotic, which affects <1% of the general population. Renovascular hypertension should be suspected with recent onset hypertension, refractory or malignant hypertension or when hypertension is associated with abdominal or flank bruit.22 RAS presents clinically as onset of hypertension in those <30 years, onset of severe hypertension in those >55 years, or rapid worsening of previously controlled hypertension, resistant hypertension, hypertension associated with abdominal bruit or flash pulmonary edema.

            Management of RAS generally involves life-style modification, control of risk factors and pharmacological therapy. The CORAL study23 compared medical therapy with interventional therapy for the management of RAS, but found no difference in event-free survival between the groups. There was also no difference between the two groups in analysis of secondary end-points including myocardial infarction, stroke and heart failure. Indeed, no randomized clinical trial to date has demonstrated a clinical advantage of lifestyle intervention over medical therapy. Guidelines from ACC/AHA, ESC and SCAI all recommend medical therapy as first-line treatment for RAS. The ACC/AHA recommend beta-blockers for treatment of hypertension associated with RAS. The ESC considers the use of antiplatelet agents as part of best medical practice, and the use of statins, which are associated with improved survival, slow lesion progression and reduced restenosis risk after renal stenting.

            The CORAL trial also reported no benefit in revascularization from endovascular therapy compared with medical therapy. Revascularization of RAS should only be considered in symptomatic patients with signs of organ ischemia, or those in whom renal balloon angioplasty has failed. Percutaneous transluminal angioplasty alone (without stenting) can improve blood pressure control and even normalize blood pressure, especially in patients with recent onset hypertension or resistant hypertension. Guidelines from ACC/AHA recommend surgical revascularization for the following indications (evidence level Class I):

  • Fibromuscular dysplasia, especially in those with complex disease
  • Atherosclerotic RAS and primary branching of the renal artery
  • Atherosclerotic RAS in combination with para-renal aortic reconstruction

ESC gives Class II recommendation for the consideration of surgical revascularization in patients undergoing repair of the aorta or with complex anatomy of renal arteries or after failure of endovascular treatment.


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  2. Grebla R, et al. J Hypertens 2010;28:15-23.
  3. SPRINT Research Group, Wright JT Jr, et al. N Engl J Med. 2015 Nov 26;373(22):2103-16.
  4. Yano Y, et al. J Am Coll Cardiol 2015;65:327-35.
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  16. Perkins BA, et al. N Engl J Med 2003;348:2285-93.
  17. Pohl MA, et al. J Am Soc Nephrol 2005 Oct;16(10):3027-37.
  18. Fried LF, et al. N Engl J Med 2013;369:1892-1903.
  19. Ibsen H, et al. Hypertension 2005;45(2):198-202
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  23. Cooper CJ, et al.  N Engl J Med 2014;370(1):13-22.

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