Newsletter

Pharmacologic therapy proved effective in improving morbidity and mortality in hypertensive patients. Since there is no cure from established essential hypertension, it is obvious that once drug therapy is started, it has to be continued for many years and most probably indefinitely. Costs, side effects and accordingly patient’s compliance are important limitations when considering life-long drug treatment. For these reasons initiation of drug therapy is not an easy decision, should not be taken lightly and should be based on strong grounds. From the very beginning it is mandatory to establish the presence of hypertension by repeated and accurate blood pressure (BP) measurements over variable intervals depending upon BP level. Non-pharmacologic treatment should be started in all hypertensive patients whether drug therapy is to be given or not. Four factors determine physician’s decision to initiate drug therapy Level of BP on initial examination, presence of target organ damage, other cardiovascular risk factors and BP response to non-pharmacologic treatment. Patients with moderate and severe hypertension with persistent elevation of SBP>180 mmHg and/or DBP>1 10 mmHg need pharmacologic intervention within one week if BP remains high. Close follow-up and repeated BP measurement over days or weeks, depending on its level, are recommended. In the presence of diabetes mellitus or target organ damage, e.g. left ventricular hypertrophy, heart failure, coronary artery disease, retinopathy, renal failure, transient cerebral ischemic attacks, stroke and peripheral arterial disease, drug treatment should also be initiated within days as soon as high BP is confirmed (> 140/90 mm Hg). Patients with other cardiovascular risk factors such as dyslipidemia, cigarette smoking, male gender, age above 65 years, obesity, impaired glucose tolerance, positive family history of cardiovascular death or events at young age and have mild hypertension (SBP 140-180 mm Hg, DBP 90-110 mm Hg) should continue non-pharmacologic treatment for 3 to 6 months and have their BP checked every 1 to 2 months. Drug therapy should be initiated if BP is persistently above 140/90 mm Hg. Non-pharmacologic treatment includes correction of obesity and weight control, limiting salt and alcohol intake, dietary modification, exercise, stress management and addressing other cardiovascular risk factors. Patients with mild hypertension and without diabetes mellitus, target organ damage or cardiovascular risk factors should continue non-pharmacologic treatment for 6 to 12 months before considering drug therapy. If BP remains elevated at the end of this period, antihypertensive therapy should be initiated.

M. Mohse,: Ibrahim, MD
Prof. & Chairman, Department of Cardiovascular Medicine - Cairo University.
President of The Egyptian Hypertension Society.

THE PRESIDENT’S MESSAGE
HYPERTENSION WHEN TO INITIATE DRUG THERAPY?

M. Mohse,: Ibrahim, MD
Prof. & Chairman, Department of Cardiovascular Medicine - Cairo University.
President of The Egyptian Hypertension Society.

SCIENTIFIC NEWS

• The Kampo medicine Shichimotsukoka-to (SKT) is used to treat hypertension & atherosclerosis in Japan by enhancing serum NO. This suggests that it may become a unique new orally active NO donor.

• An effective choice in patients with hypertension & concomitant dyslipidaemia or type 2 diabetes mellitus is the use of Urapidil. It is a newly introduced formulation with a peripheral postsynaptic &-adrenoceptor antagonistic but with a central agonistic action at serotonin 5-HTIA receptors.

ABPM, beyond being that effective as a diagnostic tool, is advised to be further used as a new determinant of patient’s compliance to treatment.

• For essential hypertension, new antihypertensives are now being tested in clinical practice for the new millennium as Selective I1 imidazoline receptor binding agents, vasopeptidase inhibitors & endothelin antagonists.

CONTENTS

The president message.
Scientific news.
Editorial; Leptin;
Its cardiovasculorenal interlinks.
Abstracts of world literature.
Abstract of local literature.
Challenge yourself.
Patient’s advisory corner:
Diet in hypertension.
Cardiology pearls
EHS news
Calendar

Editorial

LEPTIN:
ITS CARDIOVASCULORENAL INTERLINKS
AMER NOAM
Ass.Prof Physiology, Faculty of Medicine, Alexandria
University

Obesity is rapidly increasing in most industrial societies. In particular upper-body obesity [ android or visceral ] is considered one of the strongest predictors for the development of hypertension along with other cardiovascular morbidity & mortality. No wonder, body adiposity has deserved much concern and its regulation over the long term has been the focus of intense attention.

In this respect, different strategies are invoked to maintain stable adiposity including alterations in food intake, spontaneous activity, metabolism, metabolic efficiency, and thermogenesis. Although all of these responses, or efferent mechanisms, are coordinated by the central nervous system, yet how this can be achieved was not fully clear. Among what has been advocated to illucidate this is the lipostatic theory for the regulation of food intake. This states that an afferent signal produced by, or indirect relation to body adiposity provides the brain with the necessary information to control body fat stores. At a minimum, such proposed afferent signal must be; proportional to body fat, circulates in the blood, acts in the brain and .have predictable effects on behaviour, particularly on food intake and metabolism.

Luckily, after intense molecular research, the promising candidate that satisfied the criteria of a long term regulator of adiposity signal, turned out to be, the ob (obese) gene product leptin (from the Greek leptos meaning “thin”. Thus, ever since the initial report of the ob cDNA in December 1994, the literature concerning leptin is endlessly expanding and its attributes to many diseases is the interest of many researchers.

Now the baseline knowledge states that, obese individuals have high, and lean individuals have low leptin circulating levels; meaning that leptin is found to correlate positively with body adiposity. Subsidiary, ob/ob mouse, which do not produce functional leptin, and the db/db mouse and fa/fa rat, which are insensitive to leptin (now known to have a leptin receptor defect) are profoundly obese and may additionally develop type II diabetes. The treatment of the ob/ob mouse with exogenous leptin normalizes considerably its eating behavior, obesity and metabolism, while this effect is much less marked in the db/db mice and fa!fa rats that are hardly responsive to exogenous leptin.

Beyond this, increasing evidence suggests that leptin influences autonomic, cardiovascular and renal regulations. In this domain, the role of leptin in regulating the sympathetic outflow is evolving whereby leptin-treated animals have higher core temperatures, higher metabolic rates and a simultaneous increase in norepinephrine turnover i.e it is involved in the sympathetic modulation of thermogenic organs. Also, a correlation between basal muscle sympathetic nerve activity (MSNA) [a direct measure of sympathetic nervous outflow] and plasma leptin concentration was of a magnitude similar to that between MSNA and body fat. All such reports emphasize that epinephrine may play a role in mediating the effects of leptin to reduce body weight.

Still tackling the cardiovasculorenal links of leptin, its ICV administration to normal rats, increased their arterial blood pressure by decreasing the arterial flow to skeletal muscles and splanchnic vascular bed. Yet, on the other hand, other experimental studies have cleared, that intravenous leptin administration in anaesthetized rats did not concomitantly induce an overt increase in arterial pressure nor heart rate despite increasing the overall sympathetic nerve activity. This denotes that leptin may have acted simultaneously by other mechanisms to offset the appealing vasoconstrictor effects of increased sympathetic outflow. This was perceived, as to an increase in renal tubular sodium and water excretion, by leptin, that could have ameliorated, on short term, its pressor responses. This highlighted the necessity of a longer term exposure to hyperleptinaemia for full expression of its renal sympathoexcitation, a situation comparable to what actually happens in obese rats subjected to chronic administration of leptin, whereby their arterial pressure and heart rate are found increased.

Clinically, a significant positive correlation between mean arterial blood pressure and leptin was demonstrated in patients with essential hypertension. These data suggest that leptin may serve as a link between obesity and hypertension.

The mechanisms through which leptin cause sympathoactivation are not clear. Given that leptin is transported into cerebrospinal fluid by a specific saturable transport process, the CNS thus becomes the plausible site for the actions of leptin on sympathetic nerve traffic. A receptor-mediated effect is supported by substantially decreased sympathoactivation in Zucker rats, that are known to possess a mutation in the gene for the leptin receptor. Furthermore, specific binding sites for leptin were observed in the adrenal medulla with no specific binding in the adrenal cortex suggesting that leptin may have a direct effect on epinephrine-secreting cells in the adrenal medulla.

In light of the aforementioned and based on the fact that human obesity is associated with circulating hyperleptinaemia, an overview as to the problem of obesity was posed. This conceives obesity in part to be a deficiency in penetration of leptin into the CNS or resistance to its actions. This will be expressed as deficiency in thermogenesis as well as increases in appetite that will recruit obesity. Thus the overall sympathoactivation secondary to resistance to leptin may offer an explanation to the deleterious cardiovascular consequences of obesity and may be clinically relevant to the therapeutic potentialities of leptin administration or its synthetic analogues in preventive cardiology.

BIBLIOGRAPHY:

Harris RBS, Martin RJ. Lipostatic theory of energy balance: Concepts and Signals. Nutr Behav 1984; 1:253-75.
Kuczmarski RJ, Felgal KM, Campbell SM, Jhonson C./ Increasing prevalence of overweight among US adults.
The national health and nutrition examination survey. JAMA 1994: 272: 205-11.
Zhang Y, Proeca R, Maffei M, Barone M, leopold L, Friedman JM. Positional cloning of the mouse obese
gene and its human homologue. Nature 1994; 62:425-32.
Kaiyala KJ, Woods SC, Schwartz MW. New model for the regulation of energy balance and adiposity by
the central nervous system. Am J Clin Nutr 1995; 62(Suppl 5):1123S-34S.
Guagnano MT, Pace-Palitti V, Muri R. The prevalence of hypertension in gynecoid and android obese women.
J Hum Hypertens 1996; 10:6 19-24.
Matson CA, Wiater MF, Weigle DS. Leptin and the regulation of body adiposity. Diabetes Reviews 1996; 4(4):488-508.
Levin N, Nelson C, Gurney A, Vandlen R, DeSauvage F. Decreased food intake does not completely account for adiposity
reduction after ob protien infusion. Proc Nalt Acad Sci USA 1996;93:1726-30.
Collins 5, Kuhn CM, Petro AE, Swick AG, Chruynk BA, Surwit RS. Role of leptin in fat regulation. Nature 1996; 380:677.
Streamson C, Chua SC, Chung WK, Wu-peng XS, Zhang Y, Tartaglia L, Leibel RL. Phenotypes of mouse diabetes and rat
fatty due to mutatins in the OB (leptin) receptor. Science 1996; 271:994-6.
Considine RV, Sinha MK, Heiman ML, Kraiuciunas A, Stephens TW, Nyce MR, Ohannesian JP, Marco CC, Mckee
U, Bauer Tl, Caro JF. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med 1996; 334:292-5.
Haynes WC, Morgan DA, Walsh SA, Mark AL, Sivitz WI. Receptor-mediated regional sympathetic nerve activation by leptin.
J Clin Invest 1997; 1 00(2):270-8.
Agata J, Masuda A, Takada M, Higashiura K, Murakami H, Miyazaki Y, Shimamoto K. High plasma immunoreactive l
eptin level in essential hypertension. Am J Hypertens 1997; 10(10 Pt l):1174.
Golden P, Maccagnan TJ, Pardridge MW. Human blood-brain barrier leptin receptor. Binding and endocytosis in isolated
human brain microvessels. J Clin Invest 1997; 99:14-8.
Tuominen JA, Ebeling, Heiman ML, Stephens T, Koiviston VA. Leptin and thermogenesis in humans. Acta Physiol Scand
1997; 160(l):83-7.
15- Haynes WG, Sivitz WI, Morgan DA, Walsh SA, Mark AL. Sympathetic and cardiorenal actions of leptin. Hypertension
1997; 30(3 Pt 2):619:15-23.
Jackson EK, Li P. Human leptin may function as a diuretic/natriuretic hormone. Hypertension 1998; 31(1 Pt 2):409-14

ABSTRACTS OF WORLD LITERATURE

AGE-RACE SUBGROUP COMPARED WITH RENIN PROFILE AS PREDICTORS OF BLOOD
PRESSURE RESPONSE TO ANTIHYPERTENSIVE THERAPY
Preston RA, Materson BJ, Reda DJ, Williams DW, Hamburger RJ, Cushman WC, Anderson RJ.
Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents, Miami, USA.

Objective: To compare the plasma renin profiling and age-race subgroup methods as predictors of response to single-drug therapy in men with stage 1 and 2 hypertension as defined by the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Design: The Veterans Affairs Cooperative Study on Single-Drug Therapy of Hypertension, a randomized controlled trial. Setting: Fifteen Veterans Affairs hypertension centers. Patients:A total of 1105 ambulatory men with entry diastolic blood pressure (DBP) of 95 to 109 mm Hg, of whom 1031 had valid plasma and urine samples for renin profiling. Interventions. Randomization to 1 of 6 antihypertensive drugs: hydrochlorothiazide, atenolol, Captopril, clonidine, diltiazem (sustained release), or prazosin. Main Outcome Measure-Treatment response as assessed by percentage achieving goal DBP (<90 mm Hg) in response to a single drug that corresponded to patients’ renin profile vs a single drug that corresponded to patients’ age-race subgroup. Results. Clonidine and diltiazem had consistent response rates regardless of renin profile (76%, 67%, and 80% for low, medium, and high renin, respectively, for clonidine and 83%, 82%, and 83%, respectively, for diltiazem for patients with baseline DBP of 95-99 mm Hg). Hydrochlorothiazide and prazosin were best in low and medium-renin profiles; Captopril was best in medium-and high-renin profiles (low-, medium-, and high-renin response rates were 82%, 78%, and 14%, respectively, for hydrochlorothiazide; 88%, 67%, and 40%, respectively, for prazosin; and 51 %, 83%, and 1 00%, respectively, for Captopril for patients with baseline DBP of 95-99 mm Hg). Response rates for patients with baseline DBP of 95 to 99 mm Hg by age-race subgroup ranged from 70% for clonidine to 90% for prazosin for younger black men, from 50% for Captopril to 97% for diltiazem for older black men, from 70% for hydrochlorothiazide to 92% for atenolol for younger white men, and from 84% for hydrochlorothiazide to 95% for diltiazem for older white men. Patients with a correct treatment for their renin profile but incorrect for age-race subgroup had a response rate of 58.7%; patients with an incorrect treatment for their renin profile but correct for age-race subgroup had a response rate of 63.1 % (P= .30). After controlling for DBP and interactions with treatment group, age-race subgroup (P<.001) significantly predicted response to single-drug therapy, whereas renin profile was of borderline significance (P= .05). Conclusions: In these men with stage I and stage 2 hypertension, therapeutic responses were consistent with baseline renin profile, but age-race subgroup was a better predictor of response.

JAMA 1998; 280: 1168-1172.

EFFECTS OF A TRADITIONAL LIFESTYLE ON THE CARDIOVASCULAR RISK PROFILE:
THE AMONDAVA POPULATION OF THE BRAZILIAN AMAZON. COMPARISON WITH
MATCHED AFRICAN, ITALIAN AND POLISH POPULATIONS

Pavan L, Casiglia E, Carvalho Braga LM, Winnicki M, Puato M, Pauletto P, Pessina AC.
Department of Clinical & Experimental Medicine, University of Padova, Italy, Hospital S.
Lucas de Ouro Preto do Oeste, Rondonia, Brazil & Department of Hypertension & Diabetology, University of Gdansk, Poland.

OBJECTIVE: To determine the relationships between lifestyle and cardiovascular risk factors among the Brazilian Amondava, one of the world’s most isolated populations. DESIGN: Cross-sectional, population-based study. Four age- and sex-matched samples from Brazil Africa, Italy and Poland, representing different levels of modernization, were compared. Body weight, height, blood pressure, serum cholesterol and glycaemia were measured, and a standard questionnaire administered. Data concerning dietary habits and physical activity were collected. A personal socioeconomic score was calculated, on the basis of type of economy, level of formal education, type of occupation, type of habitat, availability of piped water and electricity, main source of income, housing conditions, availability of radio, television or personal computer, knowledge of a second language, and organized health facilities.SETTING: Primary epidemiological screening, at an institution. RESULTS: Among the Amondava blood pressure was always < l40/90mmHg, it did not increase with age and was not correlated with any other variable; 46.6% of subjects had systolic blood pressure : < I00mmHg. Blood pressure among the Amondava (109.6 ± 11.1/69.5 ± 6.4mmHg) was on average lower (P < 0.0001) than in all other samples. Among the Amondava, the concentration of total cholesterol was always < 200mg/dl, i.e. similar to that of Africans whose diet included large amounts of vegetable foodstuffs; 90% had glycaemia (< 80mg/dl), and their mean value was the lowest (55.1 ± 14.9mg/dl) of all the groups. CONCLUSIONS: In addition to a possible genetic predisposition not analyzed in this study, a traditional lifestyle (no contact with civilization, diet based on complex carbohydrates and vegetables, high energy expenditure) may protect against the development of hypertension, hypercholesterolaemia, and diabetes.

Hypertension 1999; 17(6): 749-756

ABSTRACTS OF LOCAL LITERATURE
CAROTID ARTERY WALL THICKNESS AND ENDOTHELIAL
DYSFUNCTION IN PATIENTS WITH ESSENTIAL HYPERTENSION

M.EI-Masrv, M. Seteha, M. Salama
Department of Cardiology, Faculty of Medicine, Tanta University. Egypt

The purpose of this study was to evaluate the relationship between the vascular reactivity and carotid intimal-medial thickening (IMT) in essential hypertensive patients. The study population included 20 normotensive subjects and 45 patients with essential hypertension. None were smokers, or had other vascular risk factors. Each subject underwent the following examinations: B-mode ultrasound imaging of the carotid artery, echocardiographic examination, and arterial physiologic testing: the right brachial artery diameter was measured on B-mode ultrasound images with the use of a7.0 MHz linear array transducer (Acusonl28xp) Scans were recorded at rest, during reactive hyperemia (flow mediated dilatation”FMD”= endothelium-dependent dilatation and after sublingual nitroglycerine”NTG” = endothelitim independent dilatation. Carotid wall IMT showed a significant inverse correlation with FMD and age, whereas no correlation was observed with the response to NTG, LV mass index, systolic and diastolic blood pressures, and plasma cholesterol and glucose levels. Moreover, FMD showed no correlation with LV mass index The present data indicate that in patients with essential hypertension, carotid wall thickening is associated with reduced endothelium-dependent in the systemic arteries and suggest that endothelial dysfunction might be involved in the preclinical phase of arterial disease in essential hypertensive patients who are at risk for atherosclerosis and its complications in later life.

Presented in the 26th Annual Meeting of the Egyptian
Society of Cardiology, Cairo, Egypt. February 1999.

STUDY OF HEART RATE VARIABILITY IN HYPERTENSIVE PATIENTS BY USING 24-HOUR AMBULATORY ECG RECORDING

Hanaa M.Fereig, Watia B.Eteiba, Mervat A. Nabih, Osaila H.E1 Khatib.

El-Zahraa Hospital, Faculty of Medicine for Girls, Al-Azhar University & Faculty of Medicine, Am Shams University.

Background It is well known that blood pressure in under the influence of the autonomic nervous system (ANS) . Heart rate variability (HRV) represents a promising non invasive marker of autonomic activity The aim of our study is to evaluate ANS response in hypertensive patients . Methods : The study included 40 subjects, 30 hypertensive patients and 10 normotensive control subjects. We excluded patients with ISCHEMIC heart disease, atrial fibrillation, congestive heart failure, diabetes mellitus, and digitalis medication. All of the 40 subjects were subjected to medical history, cardiac examination, ECG, transthoracic Echocardiography and 24-hr. Holter monitoring. Both time and frequency domain measures of HRV were calculated over 24-hr period. Results: Our results revealed the following: In control versus patients; SDNNi (58.8±12.9) vs (47.1±15.2) rMSSD (46.9±15.3) vs (36.1±22.7) pNN5O (10.4±7.2) vs (6.2±7.2) LF power (890.3±620.6) vs (541.2±493.4) HF power (417.9 ± 251) vs (358.9±501) LF/HF (2.2±0.98) vs
( 2.9±0.75). Conclusions: SDNNi, RMSSD, pNN50 and LF power were significantly decreased in hypertensive subjects. The decrease in HF power and the increase in LF/HF ratio in hypertensive subjects were insignificant.

Presented in the 26th Annual Meeting of the Egyptian
Society of Cardiology, Cairo, Egypt. February 1999.

CHALLENGE YOUR SELF !!!

A 51-year old man had been in his usual state until the day of admission when he complained of acute onset of dyspnea. There had been no previous orthopnea, and he denied angina, palpitation or syncope. He had a 3-year history of hypertension that has been poorly controlled by hydrochlorothiazide. The patient reported episodes of diaphoresis and flushing. Physical examination: Vital signs: pulse 110 and regular, Blood pressure: 240/120, General: moderate respiratory distress. Fundi: arterial narrowing, arteriovenous nicking but no papiloedema Chest: diffuse bilateral rales. Cardiac: Summation gallop, no murmurs. Laboratory findings: CBC: normal. Na: l40mEq/L; K: 4.2m eq/L; Cl: l02meq/L; HCO3:26mEq/L; BUN 30mg/dl; Cr: 1.2 mg/dl. EKG: normal sinus with LVH. Hospital course; After administration of oxygen, nitroglycerine furosemide 40 mg intravenously and sublingually, the patient improved rapidly.

Question,’ What should the evaluation of a patient with severe hypertension include?

Pick up the solution at CARDIOLOGY PEARLS on P. [ 7] of this issue.

PATIENTS’ ADVISORY CORNER
DIET IN HYPERTENSION

• For years, doctors have advised reducing sodium to help lower blood pressure[BP], s’o one should check the levels of sodium listed on food labels. One should avoid canned or prepared foods unless their label clears that no salt is added. Effervescent medication should not be forgotten as a source of high Na intake.

• The quality OF food in the diet also matters. Now, they’ve discovered that a diet rich in fruits, vegetables and low-fat dairy products can lower blood pressure. That is why a new eating guide called the DASH diet, published by Mayo Clinic in April 1998 to help one prevent or guide patients to lower their high BP. The name evolved from the study” Dietary Approaches to Stop Hypertension.” where for 8 weeks, participants followed one of three diets - a diet that matched the average American diet, a diet rich in fruits and vegetables, and a “combination” diet that was reduced in saturated fat and emphasized fruits, vegetables and low-fat dairy products. Sodium consumption in all three was about 3,000 milligrams (mg) a day.

Results revealed that fruits and vegetables and combination diets both lowered BP, but the combination diet was most effective. In that group, the decrease was the greatest for those with high BP(above 140/90) with an average drop of 11.4 points in systolic pressure and 5.5 points in diastolic pressure. That’s about the same effect as some medications. Researchers are n’t sure why the combination diet fared better. However, they believe it’s due to the mixture of nutrients provided, rather than any single ingredient.
The original publication has submitted the following table where the number of servings one should consume daily from each food group is cleared. Serving amounts are based on a diet of 2,000 calories per day.

Food/servings	1 serving equals	Food examples
Grains & grain products 6 to 8 daily	1slice bread 1/2cup dry cereal	Whole wheat breads, English muffins, pita bread, bagels, cereals, oatmeal grits
Fruits & vegetables 4 to 5 fruit servings daily 4 to 5 vegetable servings daily	6 oz. fruit or vegetable juice 1 medium fruit 1/2cup frozen or canned fruit 1 cup raw, leafy or ‘/2 cup cooked vegetables	Apricots, bananas, grapes, orangesgrapefruit, melons, strawberries tomatoes, peas, carrots, potatoes, broccoli, squash, leafy greens
Dairy foods (low-fat or non-fat) 2 to 3 daily 3	8 oz. Milk 1 cup yogurt 1 ½ oz. cheese	Skim or 1% milk, nonfat or low-fat yogurt, nonfat or part-skim cheese
Meats, poultry & fish 2 or fewer daily	3 oz. cooked meat, poultry orfish	Lean meats only; trim visible fatremove skin from poultry; broil, roast or boil
Nuts, seeds & legumes 3 to 4 a week	1/3 Cup nuts 2 tablespoons seeds 1/2 Cup cooked legumes	Almonds, peanuts, mixed nuts sunflower seeds, kidney beans, lentils

The merits of such a diet are many;
If your BP is normal, the DASH diet may help you avoid BP problems. While if it is only slightly elevated, the diet may actually eliminate the need for medication and if sever, it may allow you to reduce your medication. However, don’t stop or alter your medication without first consulting your doctor.

The DASH diet can’t do it alone, but it is important that one takes other steps to control or prevent hypertension, including exercising, losing excess weight, not smoking and limiting alcohol.

Beyond this the DASH diet may improve health in other ways, as fruits and vegetables may reduce the risk for some cancers, the calcium in dairy products can lower risk for osteoporosis and a diet low in saturated fats and cholesterol can reduce cardiovascular disease risk.

Mayo Clinic Health Letter, April 1998.

• Soft drinks containing caffeine should be limited, refraining from alcohol is advisable & smoking should be prohibited.

Focusing on tea in particular, the caffeine within tends to raise the blood pressure acutely temporarily more than expected specially in black tea, while the flavenoids are thought to protect against heart disease and other disorders, specially when present in appropriate concentrations in green tea. However, over long terms neither type of tea were thought to have a significant effect on blood pressure.

In an Australian study, conducted to illustrate the acute effects of administration of regular black tea, Japanese green tea, in comparison to hot water with the same amount of caffeine; the blood pressure after one hour was increased about 6 mm Hg systolic and 3 mm Hg diastolic, by caffeine. However black tea produced a bigger rise [16/8 mm Hg] while green tea produced an intermediate rise [12/6 mm Hg]. When this was repeated in borderline hypertensives that drank 5 cups of tea a day for three weeks, and their 24 hours blood pressure was measured by ambulatory monitoring at the end of each week , then no effect of either tea or caffeine on blood pressure was recorded.

The acute and long term effects of tea deserve to be well delineated in wide scale control trials.

J Hyperten 1999; 17457.

CARDIOLOGY PEARLS

Although many patients with pheochromocytoma have episodic elevations in blood pressure thought typical of the disease, in 50%
of cases the blood pressure is consistently elevated without distinct variations.
Other symptoms, including palpitations, headache, and diaphoreses, are common in phaeochromacytoma but are usually absent in other forms of hypertension.
CT scanning is an excellent diagnostic tool for localizing the tumor once biochemical evidence has established tumors existence.

• The editorial committee of the News Letter of Egyptian Society of Hypertension, is now changing Prof Dr. Mohsen Ibrahim on behalf of the editing board is whole heartily thanking Dr. Mohamed Hamed the former editor for his executive elegant and distinguished collaboration in making this News Letter come to reality and progress throughout the previous years. His words of gratitude implies:

The Egyptian Society of Hypertension members wish to express their thanks to professor Mohamed Hamed M.D, editor of the EHS Newsletter since it was started in 1995. His dedication and interest were manifest in every issue of the paper and helped to make the work and aims of the EHS known to doctors in all health care centers in Egypt and Hypertension Societies abroad. We wish Professor M. Hamed every success in his present endeavor and look forward to his contribution to the newsletter.

M. Mohsen Ibrahim

Now, Prof. Dr. Hassan Khalil, Prof of Cardiology, Alexandria University has been nominated, editor in chief from this June issue and onwards.

• The EHS has held a symposium on the 11th of March in El-Menia at Upper Egypt to enlighten physicians there about hypertension,
its prevalence, its diagnosis and its lines of treatment. Another symposium was held in Cairo on the 13th of May entitled” What’s new
in hypertension?” during which the general assembly of the Society was held and the annual report on scientific activities, publications,
research, finances etc. The assembly settled on dividing active participants into several working committees namely for ; continuous
medical education & symposia, publicity & public education, finances, publication, Internet advertisement & newsletter, scientific
research & drug assessment, communication with international & Pan-Arab Societies, ... etc. These committees will run cyclic
meetings to encompass all such expandable activities of the society.

A book on “Ischaemic Heart Disease.” is due to be completed and issued by the society. Its manuscript has been already
finalized in El Gona on January 1999.
The society has issued a 2nd edition of” Short review on hypertension- Egyptian Hypertension Society Guidelines.” Also
three guideline booklets were issued on ; How to measure blood pressure - Hypertension in pregnancy-Diagnosis of chest pain.
The Internet web site of the society has been logged in.; http://www.ehs-egypt.net.
Our E-mail address is ehs@link.com.eg

LOCAL MEETINGS
The Summer Meeting of the Society	Helnan Palestine Hotel June 24-25^th ,1999		Prof. Dr. Mohamed Sobhy Tel (203)4203288 Fax (203) 420 32 88
1st Annual Meeting of Working Group of Heart Failure	Helnan Palestine Hotel September 9-10, 1999.		Prof Dr. Wagdy Ayad Fax (203) 425 11 57
4th Annual International & Pan-Arab Meeting of Interventional Cardiology	Main Conference Hall Alexandria		Prof Dr. Mohamed Sobhy Tel (203) 420 32 88 Fax (203)
INTERNATIONAL MEETINGS
9th European Meeting on Hypertension	Milan Italy. June 11-15 1999		Contact: AISC via A. Rom,Italy Fax 39-6-8088491
XVII Interamerican Congress Of Cardiology	Buenos Aires ,Argentina Aug 22-25,199911-15 1999		Contact: Argentine Society of Cardiology ,Buenos Aires Fax : [54-1]9616020
XI Congress of European Society of Cardiology [ESC]		Barcelona,Spain.Sep 4-8, 1999	Contact : ECOR,Sophia Antipolis Cedex, France.Fax :+33-492947601
1^st Meeting,Ascian-Pacific Society of Hypertension		Ball,Indonesia,September 16-18,1999	National Cardio Center,Jakarta, Indonesia

President
Vice president
Secretary
Treasurer
Members

M.M. Ibrahim, MD
H.E. Attia, MD
H.H. Rizk, MD
W.EI-Aroussy, MD
A.M. Hassabatlah,MD
M.M. Gomaa, MD
F.A. Maklady, MD S.
EI-Tobgy, MD
O.EI-Khashaab, MD

Editor
Associate editors

Hassan KhaIiI, MD
Ebtihag Hamdi, MD
Omnia Nayel, Ph D
Zeinab Ashour, MD
Fatma Aboul -Enein, MD
Salwa Morkos, MD