SCIENTIFIC NEWS

• The pulsatile component of BP as reflected by pulse pressure is now in focus, being proved to dictate the mechanotransductional haemodynamic response of vessels and heart to pressure constrains. New investigational aspects to correlate its assessment to the progression of disease are being sought.
• Apoptosis plays a major role in vascular homeostasis, and its inhibition during hypertensive vascular remodeling is now recognized. Markers of apoptosis are now probed in hypertensives and are also used to assess the efficiency of antihypertensives to induce reverse remodeling.
• Intensive combination therapies of two or more antihypertensives and a lipid-lowering agent are thought essential in the treatment of patients with diabetes and hypertension in light of recent data from the UKPDS and HOT trials.

CONTENTS

• The president message.
• Scientific news.
• Editorial; Endothelial function and myocardial infarction
• Abstracts of world literature.
• Abstracts of local literature.
• Challenge yourself.
• Practical considerations: Hypertensive women
• Environmental hazards: Cigarette smoking
• Bed-side tips Cardiology pearls
• National & international recognition
• EHS news
• Calendar

EDITORIAL

ENDOTHELIAL FUNCTION AND
MYOCARDIAL INFARCTION
SamirAbd-Ulkader, MD
Prof. of Cardiol, Cardiology Unit, Faculty of Medicine,
University of Assuit.

Until relatively recently, the endothelium was regarded simply as an inert nonthrombogenic diffusional barrier separating the blood from the vascular smooth muscle cell. It influences not only vascular tone but also vascular remodelling, through production of growth-promoting and inhibiting substances, and haemostasis and thrombosis through the antiplatelet, anticoagulant and fibrinolytic effects.

Abnormalities in the function of the endothelium has been coined to play a crucial role in the etiopathogenesis of hypertension & are likely to play an important role too in the pathogenesis of coronary artery disease. This occurs, whether the latter associates, as a functional derangement to the existing hypertension or exists, as a comorbid structural atherosclerotic derangement, in adjuvance to the already existing dysfunction reported in hypertensives. Indeed, coronary blood flow and coronary flow reserve have been found encroached upon in hypertension per se, more if prehypertrophic or overt LVH superadds and still even more if atherosclerotic changes intervene. The denominator of all that is being endothelial dysfunction with the decrease in NO dilating potentials that can trigger coronary spasm or with the loss of its protecting potentials that can cascade the development of atherosclerosis.

Focusing on atherosclerotic vessels, it is known that oxidised LDL increases adhesion molecules expression and produces monocyte chemotactic proteins that facilitates monocyte adhesion and migration through the vessel wafl, It also stimulates the release of epidermal growth factor and platelet derived growth factor, which contribute to SMC migration and proliferation in the Intima. All of these processes potentially serve to further predispose the vessel wall to plaque rupture and thrombosis.

Impaired vasodilation was found in the coronary arteries of patients with advanced atherosclerosis. Reduced coronary vasodilator function in infarcted and normal myocardium was demonstrated following myocardial infarction. The dysfunction has been found to extend beyond the acute setting so that patients with chronic stable angina due to single vessel disease have been shown to have reduced maximal myocardial blood flow, not only in territories perfused by the stenosed artery but also in regions supplied by "'normal" coronaries.

Endothelial dysfunction significantly predates the acute myocardial event. This lends further support to the idea that the process of atherogenesis that ultimately leads to myocardial infarction is intimately related to the presence and severity of endothelial dysfunction.

How might endothelia dysfunction contribute to myocardial ischaemia?

Obstructive coronary stenoses are usually thought to contribute to angina by providing a fixed limitation to coronary flow during periods of increased myocardial oxygen demand. Impaired endotbeliurn-dependent dilatation at the site of coronary plaques may result in paradoxical vasoconstriction during exercise or mental stress. Microvascular endothelial dysfunction may p lay a significant role in the pathogenesis of myocardial ischaemia and infarction. After an acute infarction, the coronary vasodilator response in the infarcted myocardiurn remains severely impaired, despite successful recanalisation of the infarct-artery by thrombolysis. This impairment has been attributed to endothelial dysfunction of the resistance vessels in the infarcted tissue. Impairment of endothelium-dependent dilatation persists for much longer than the acute insult (thrombosis), even in the myocardium remote from the site of infarction.

In conclusion, with such a background of understanding, it seems prudent to weigh that, in our therapeutic approaches to control hypertension, whether with or without LVH, or coronary atherosclerotic changes. This is to safeguard against the progression of hypertensive heart disease, through Ischaemic syndromes or overt myocardial infarction, ending up with all its morbidity & mortality consequences.

References:

Quyyum A.A., Cannon R. 0. Ill Panzo JA., Diodati and Epstein S.E; Endothelial dysfunction in patients with chest pain and normal coronary arteries. Circulation 1992;86. 1864-1871.
Forstermann U., Pollock JS. And Nakane M NO system, Trends syntheses in the cardiovasetdar
Cardiovasc. Med 1993; 3:104-1 1 0.
Dorckier f, Hanet C,, Stoleru L., et al. Effects of endot helium on pat hophysiology of coronary perfusion. J Cardiovascular Research Pharmacol; 199423:212-2/9.
Hasdai D., Koniowski R. and Battler A. Endothelium and myocardial ischemia. Cardiovasc Drugs Ther 1994; 8: 589-599. Pernow J and Wang Q. D. Endotheliun in myocardial ischemia and reperfusion. Cardiovascular Research 1997; 33. 518-526

ABSTRACTS OF WORLD LITERATURE
AN ECONOMIC EVALUATION OF THE JNC HYPERTENSION GUIDELINES
USING DATA FROM A RANDOMIZED CONTROLLED TRIAL.
JOINT NATIONAL COMMITTEE.

Ramsey SD; Neil N; Sullivan SD; Perfetto E
Department of Medicine, University of Washington, Seattle, USA.

BACKGROUND: We wanted to determine the clinical cost of managing hypertension when following the Joint National Committee on Hypertension (JNC) guidelines, including drug therapy, the cost of monitoring for and treating side effects, compliance, and the cost of switching after therapeutic failures.
METHODS: The base-case analysis considers antihypertensive agents from four therapeutic classes that were recently evaluated in a large randomized trial: enalapril, Amlodipine, acebutolol, and chlorthalidone. Clinical evaluation, therapy, and monitoring for hypertension are modeled with an incidence-based Markov model. Clinical inputs include agent efficacy, side effects, and compliance with dosing schedules. JNC-recommended clinical and laboratory monitoring schedules are followed for each agent. Drug and medical care costs are valued in 1995 US dollars.
RESULTS: Although patients whose hypertension was initially treated with Amlodipine achieved control more readily than patients who were given the other agents, the initial costs to achieve and maintain hypertension control were lowest for chlorthalidone ($641), followed by acebutolol ($920), Amlodipine ($946), and enalapril ($948). Maintenance costs were lowest for chlorthalidone. For all agents except chlorthalidone, drug costs were the largest component of overall costs, followed by the costs of office visits, laboratory monitoring, and switching between classes for therapeutic failures. CONCLUSION: By following JNC guidelines, a slightly higher percentage of patients will achieve hypertension control with a newer class calcium channel blocker (Amlodipine) but at a substantially higher cost than with a generic diuretic (chlorthalidone).

J Am Board Fam Pract, 1999 Mar, 12:2, 105-14.

EVALUATION OF NONINVASIVE BLOOD PRESSURE RECORDING
BY PHOTOPLETHYSMOGRAPHY
IN CLINICAL STUDIES USING ANGIOTENSIN CHALLENGES.
Buclin T; Buchwalder Csajka C; Brunner HR; Biollaz J
Division of Clinical Pharmacology, CHUV, Lausanne, Switzerland.

AIMS: Continuous noninvasive blood pressure measurement by PHOTOPLETHYSMOGRAPHY has been regularly used in the experimental paradigm of Angiotensin challenges, applied to the phase I clinical testing of Angiotensin-converting enzyme inhibitors and Angiotensin receptor antagonists. This work aims to evaluate the performance of this measurement method, in terms of reliability, reproducibility and dependence on technical settings.
METHODS: Data have been gathered from 13 clinical studies on antihypertensive drugs, using the Finapres device for measuring the response to exogenous Angiotensin challenges. The agreement between simultaneous recordings at different fingers and the influence of the reading method are assessed. A literature review addresses the question of the concordance between results obtained noninvasively and through arterial cannulation.
RESULTS: The relative precision of blood pressure monitoring by PHOTOPLETHYSMOGRAPHY allows reproducible determination of Angiotensin-induced blood pressure peaks (agreement limits for systolic and diastolic peaks:12 and 6 mmHg respectively). The reading method influences the results to a similar extent. As compared with blood pressure measured intra-arterially, the difference is usually within limits of clinical acceptability.
CONCLUSION: In the context of phase 1 studies using the Angiotensin challenges methodology, the reliability and reproducibility of noninvasive blood pressure measurement appear satisfactory, despite the technical limitations of this method. The impact of selected changes in the settings and reading methods is limited.

Br J Clin Pharinacol, 1999 Oct, 48:4, 586-93.

ABSTRACTS OF LOCAL LITERATURE

EVALUATION OF CORONARY FLOW RESERVE IN HYPERTENSIVE PATIENTS
BY DIPYRIDAMOLE TRANSESOPHAGEAL DOPPLER ECHOCARDIOGRAPHY

M Hamouda, H. Kassem, M. Salama, N. Shaban, E. Sadek
Cardiac Department, Tanta University Hospital, Tanta, Egypt.

OBJECTIVE: To evaluate the coronary flow reserve (CFR) in hypertensive patients with and without left ventricular hypertrophy (LVH). METHODS: The CFR was assessed by Transesophageal Doppler Echocardio-graphy in 15 normal subjects (group 1), 21 hypertensive patients without LVH (group ID, and 27 hypertensive patients with LVH (Group Ill). All hypertensive patient were complaining of typical anginal pain with normal coronary angiography. The sample volume was placed at the bifurcation of the left main and left anterior descending coronary arteries. Coronary blood flow velocities were evaluated at rest, 2 minutes after dipyridamole infusion, and 2 minutes after IV aminophylline. The ratio of dipyridamole to rest peak diastolic and systolic velocities (D/R PDV and D/R PSV) were considered as indices of CFR. RESULTS: The D/R PDV was significantly lower in group Ill than group 1 and 11(1.63 ± 0.24,1.73 ± 0.41, and 2. 1 ± 0. 15, respectively; P< 0. 005), and it was significantly lower in group 11 than I (PO. 05). the DIR PSV was also significantly lower in group Ill than group I and II (1. 65 ± 0. 28, 2. 8 + 0. 32, and 2. 09 ± 0. 21, respectively; P<O.05),and it was Significantly lower in group II than I (P<O.05).CONCLUSION:The CFR is significantly impaired in hypertensive patients, especially those with LVH as compared with healthy subjects. So, the impaired CFR is one of the important mechanisms for the occurrence of typical anginal Pam in hypertensive LVH..

Presented at the 4th World Congress of Echocardiography &
Vascular Ultrasound Cairo-Egypt January 2000

ABNORMAL LEFT VENTRICULAR DIASTOLIC FUNCTION IN FIELD SURVEYS. INCIDENCE & CLINICAL PROFILE: DATA FROM THE EGYPTIAN NATIONAL HYPERTENSION PROJECT
Amal Khalifa MD, Sherief M. Helmy, MD. Mohsen Ibrahim, MD.

Cardiology Department, Cairo University, Egypt.

BACKGROUND: No reports of studies assessing prevalence of echocardiographically determined ventricular diastolic dysfunction in population-based surveys are available. OBJECTIVE: to study prevalence of abnormal left ventricular (LV) diastolic function in a nation-wide hypertensive prevalence survey (National Hypertension Project, NHP) conducted in Egypt (1990 - 1992). METHODS: In a cohort of 2313 participants of NHP 1981 males, 1332 females aged 25-95, 1559 hypertensive (HT) and 754 normotensive (NT) subjects], we retrospectively analyzed data from abnormal LV diastolic function (Doppler E/A< 1). These were subjected to clinical, biochemical and echo-Doppler examinations. RESULTS: 252 (10.9%) excluded (56.3%) [ages 25-95 with 74%> 45 years, 242 NT (32%) and 919 HT (58.9%)]. Other cardiovascular risk factors were higher in patients with diastolic dysfunction comparing them to those with normal function; Obesity % [36.8* vs 31], DM% [18* vs 6.3], Hypercholestrolemia % [18.2* Vs 8.8] Hypertriglyceridemia% [19.8* Vs 12.0] respectively. Clinical heart failure (HF) [two or more major cardiac symptoms, dyspnea. Pedal oedema, pulmonary congestion, raised JVP and or S3 gallop], was present in 121 (10.4%) patients with diastolic dysfunction. Their gender% (F) [64.3 vs 77.6], age(yrs) [55.85 ± 14.9 vs 57.3 ± 11.0], systolic pressure (SBP) ( mmHg) [120±11.5 vs 158 + 24.1*] and diastolic pressure (DBP) ( mmHg) [75.1 ±8.8 vs 87.7 +17*] in NT vs HT, respectively.[ * P<0.001] Impaired systolic function (% FS < 25) was present in 43 (3.70 o) patients with diastolic dysfunction. CONCLUSION : Diastolic LV dysfunction is common in Egyptian population (32% NT & 59% HT). It is more prevalent in older population (74% above age of 45). Other cardiovascular risk factors were significantly higher in patients with abnormal diastolic function. Clinical heart failure was present in 10.4% of patients with diastolic dysfunction with higher incidence among females. Incidence of low %FS was low (3.7%).

Presented in 4th Annual Meeting of the Egyptian Hypertension
Society, Cairo, Egypt,. January 2000.

ROLE OF AMBULATORY BLOOD PRESSURE MONITORING IN PREDICTING
OF LEFT VENTRICULAR HYPERTROPHY IN HYPERTENSIVE PATIENTS
(COMPARATIVE STUDY WITH CASUAL BLOOD PRESSURE)
Abdel Moniem A, Ammar S, Abdel Salam M*, Zohair E*, Youssef A
Cardiology Dept. Benha Faculty of Medicine, Zagazig University & National Heart institute*, Egypt

AIM: The aim of this study was to evaluate blood pressure changes (through 24-h) by non invasive ambulatory blood pressure monitoring (ABPM) is a predictor of left ventricular hypertrophy (LVH) in patients with essential hypertension. PATIENTS & METHODS: Eighty patients were studied in this study. 60 hypertensive patients as a test group and 20 normotensive subjects as a control group. All subjects were subjected to 24 hours ABPM, electrocardiogram and echocardiography. According to echocardio graphic parameters, hypertensive patients were classified into two groups, hypertensives with LVII and hypertensives without LVH.
RESULTS:ABPM is more closely related to left ventricular mass (LVM) (P<0.05) than causal blood pressure. A co r relation of SBP over DBP to the degree of hypertrophy was observed. A significant increase in LVM in hypertensives with marked fluctuations in BP throughout 24 hours versus those without such fluctuations and in hypertensive non-dippers versus hypertensive dippers (P<0.05) were also recorded.
CONCLUSION: these results underline the importance of ambulatory blood pressure monitoring (ABPM) in evaluating the effects of hypertension in relation to left ventricular hypertrophy .

Presented in the 27th Annual Congress of the Egyptian
Society of Cardiology, February 21st - 25th, 2000. Cairo, Egypt

SODIUM NITROPRUSSIDE INHIBITS THE INTRACELLULAR CALCIUM STORAGE AND RELEASE IN RABBIT AORTA
Hassan Heialy Abo Rahma
Department of Pharmacology, Assiut Faculty of Medicine, Assiut, Egypt

Department of Pharmacology, Assiut Faculty of Medicine, Assiut, Egypt Sodium nitroprusside (SNP) is a potent vasodilator used clinically as an antihypertensive agent for several years. Its mechanism of action is still not totally understood. Previous reported results showed that SNP activates guanylate cyclase, increases cGMP level which in turn reduces the intracellular Ca2+. It was hypothesised that the SNP-induced reduction of the intracellular Ca2+ may be due to opening of the K+ channels and the resultant hyperpolarization with the subsequent inhibition of the voltage operated Ca2+ channels (VOCs). Other possibilities include direot inhibition of the VOCs or activation of the plasma membrane or Sarcoplasmic
Ca2+ pump. The aim of the present study was to clarify these reported suggestions by studying the possible involvement of the K+ channels by performing concentration response curves of SNP on KCI precontracted aorta. The efect of SNP on the process of Ca2+ release from intracellular stores by studying its effects on phenylephrine-induced contractions in Ca2+ free solution, was also studied. The effect of SNP on the process of filling of the intracellular stores after their emptying by repeated application of phenylephrine in Ca2+ free solution and before the filling period in which the aorta was incubated in normal salt solution containing Ca2+ was evaluated. The possible involvement of the endothelium in the SNP-induced vasorelaxation was also investigated. The results of the present study show that the relaxant effect of SNP is not endothelium-dependent, SNP completely abolished contractions induced by low K+ (20 mM) and partially abolished contractions induced by high K2 concentrations (50 mM). SNP produced a significant (p<0.01) dose dependent inhibition of the process of filling of the intracellular stores of Ca2+ - and the process of Ca2+ release from these stores.

Presented at the Joint International Conference of Egyptian Society of
Pharmacology & Experimental Therapeutics, the Union of African Societies of
Pharmacology & the Arab Union of Pharmacology. Cairo, Egypt, December 1999.

 

CHALLENGE YOUR SELF !!!

A 65-years-old woman with known hypertension developed atrial fibrillation several months earlier, which converted to regular sinus rhythm with quindine after ventricular rate control with digoxin and a blocking agent. She subsequently developed fever and diarrhea that disappeared after stopping the Quinidine. Regular sinus rhythm could not be maintained with the use of B-blockers, disopyramide, or procainamde. The ventricular response to persistent atrial fibrillation was controlled with digoxin and a
B-blocker.
Physical Examination: Vital signs; pulse; 65-70 (irregular); BP; 130/85. Neck: no venous distension. Chest: clear to auscultation and percussion. Cardiac: no murmurs or extrasounds.
Laboratory investigation; CBC, urinalysis, and thyroid profile : normal. EKG: Atrial fibrillation with satisfactory ventricular response at rest and with moderate exercise. Echocardiogram: normal chamber sizes, valves appeared normal; ejection fraction greater than 50%

Question: Should this patient be on long-term oral anticoagulations?
Pick up the solution at CARDIOLOGY PEARLS on p. [7] of this issue.
Cardiology Pearls. Hanley & Be/fits, Inc. 1994.

PRACTICAL CONSIDERATIONS:
HYPERTENSIVE WOMEN

When your patient happens to be a woman;
ON ORAL CONTRACEPTIVES:

Explain that oral contraceptives contribute to a small but detectable rise in SBP & DBP and that the incidence of hypertension is two to three times higher in those who are on the pills specially in obese and elderly women. So if hypertension developed while she is on the pills it is advisable to stop, as BP will normalize within a few months.

If high BP persists, and other contraceptive methods are not suitable, antihypertensives should be instituted beside the pill and the patients should have their BP monitored on a semiannual basis..

Explain that cigarette smoking and oral contraceptives have synergistic effect on BP and it is prudent to stop smoking.

When your patient happens to be a woman in;
NEED OF HORMONE REPLACEMENT THERAPY

Explain that hypertension is not a contraindication to postmenopausal estrogen replacement therapy; as the BP is insignificantly affected by this therapeutic modality whether the woman is hypertensive or not.

Clarify that this therapeutic approach has a beneficial effect on overall cardiovascular risk profiles and osteoporosis.

However, since very few women may experience a rise in BP attributable to the estrogen component, it is recommended to have the BP monitored more frequently after therapy is instituted.

The 6th report of the JNC on Prevention, Detection, Evaluation and Treatment of High Blood Pressure.
NIH Publication 1997.

ENVIRONMENTAL HAZARDS: CIGARETTE SMOKING; ITS PRO-OXIDANT PROFILE

Cigarette smoke-induced lipid peroxidation is one of the morbid outcomes of smoking. In this respect, it was demonstrated that cigarette smoke exposure directly stimulates proliferation and enhances the free radical-producing activity of polymorphonuclear Leukocytes and other macrophages. Moreover, it also inhibits plasma paraoxanase, the enzyme which protects LDL against oxidation by modifying the enzyme's free thiol. Taken together, the monocyte / macrophage recruitment and the provocation of LDL-oxidation by smoking is apt to cascade lipid peroxidation,. This, aside what has been suggested in relation to the ability of cigarette smoke to mobilize iron from ferritin, which initself presents a specific prooxidant mechanism, will all in all add to sculpture the vascular changes in smokers.

A further indirect mechanism, through which cigarette smoke exposure can induce lipid peroxidation, could be via depletion of plasma and tissue antioxidants due to their destruction by cigarette smoke-free radicals Ii namely; peroxy radicals (ROO.), superoxide anion, nitrogen dioxide.. . etc.]. This has been confirmed, by retrieving a reduction in plasma levels of Vitamin E, uric acid and ascorbic acid and recording an associated decrease in total-SH content in the respiratory system in smokers when compared with non-smokers. Aside, depletion of tissue GSH stores by the interaction of cigarette smoke oxidants with GSH leads to its consumption. Furthermore, the inhibition of glutathione reductase, the enzyme responsible for conversion of oxidized- to reduced glutathione- via inhibition of glucose-6- phosphate [G6P] dehydrogenase with subsequent decrease in formation of NADPH the substrate needed for reduction of oxidized glutathione ] is another added factor of contribution. This was confirmed, upon comparing erythrocyte G6P-dehydrogenase activity, and finding it significantly lower in smokers than in nonsmokers, probably due to decreased selenium status.

However, other different clinical studies cleared, that erythrocyte SOD and catalase activities were not significantly altered in smokers versus non smokers [aged 18-45 year], though being decreased in smokers[aged 46- 80 years]. This finding highlights the inability of the antioxidant system in the elderly to adapt with imposed prooxidant conditions conferred by cigarette smoke.

The consequence of all this, is the development of endothelial damage that ignites the atherosclerotic cascade, the formation of advanced glycation end-products that destroys collagen and precipitates premature arteriolar stiffness and arteriosclerosis and the mitogenic signals of oxidative BI-products that causes vascular smooth muscle cells hypertrophy characteristic of hypertensive remodeling. Needless to emphasis on the ability of prooxidants in cigarette smoke to encroach on NO vasodilating potentialities, that hastens the perpetuation of hypertension or the precipitation of coronary vasospastic anginal attacks that superimpose on the already progressing obliterative lesions.

Atherosclerosis 1994;109(Suppl) : 52-3.
Am J Respir Grit Care Med 1995; 151: 43 1-5.
Atherosclerosis 1995; 112: 9 1-9. J Lipid Res 1995; 36: 322-3 1.
AmHJ l996;131:39784.
Atherosclerosis 1997;129: 169-76.
Biochem Mol Biol Int 1997; 42: 1-10.
Biophys Res Commun 1997; 636: 289-93

BED-SIDE TIPS:

Sincere Practitioner please remember that; successful approach to manage hypertension is to encourage lifestyle modification first [i.e. exercise and weight loss, diet high in fruits vegetables, whole grain, and low in diary-fat products and sodium]. Emphasis to patients, that medications work better when a healthy lifestyle is followed. If this does not fulfil the reduction required, then pick up an appropriate agent of choice to start and up-titrate, to its full dose, if needed. If still blood pressure is not optimally controlled, then it is wise to continue with the preferable medication and add an appropriate second agent [diuretic is synergistic to most therapeutics] taking in consideration that its dose-response may be steeper, when in combination. Do not attempt to reduce pressure abruptly as this causes adverse effects [lightheadedness, headache, drowsiness, fatigue,]. Titration should be slow as most medications need 4 weeks to achieve maximal benefits. Increasing the dose or adding another therapy should be better conducted on 6 weeks interval. Close follow-up from the physician's behalf and adherence to therapy from patient's perspectives are the tools of success

5th American Collage of Cardiology Meeting Report, 1999.

CARDIOLOGY PEARLS
Diagnosis: The patient has hypertension & chronic atrial fibrillation and should receive long-term anticoagulant.

1. Overall, approximately 30% of patients with atrial fibrillation will have a cerebral embolism during their lifetime.
2. Chronic atrial fibrillation regardless of the cause can shorten life.
3. Patients with lone atrial fibrillation under age 60 have a low risk of stroke.
4. Unless there is contraindication, all patients with chronic atrial fibrillation should receive low dose warfarin [target prothrombin ratio, 1:2 to 1:5 ]. Patients with lone atrial fibrillation under the age of 60 should be given aspirin.

NATIONAL & INTERNATIONAL RECOGNITION:

• Prof. Dr. Hassan H. KHALIL, professor of cardiology, in Cardiology Unit, Faculty of Medicine, Alexandria University and the editor of this News Letter has been awarded the Alexandria University Merit Award, 1999. This is not the first time as he has been awarded the Outstanding Contribution Award and Medal of Alexandria University 1984 and the State Award & Medal for Medical Research 1964. It is worth mentioning that he established the 1st Coronary & Critical Care Unit in Egypt at the Main University Hospital in Alexandria 1972.
  Earlier, Professor Hassan KI-JALIL served as a full time research scientist National Aerospace Medical Research Institute, Pensacola, Florida, USA [1964-1968] Since then Dr. KHALIL was allowed four U.S. Patents in cardiovascular devices Nos.: 3,359,974 ; 4,217,910 ;4,240,441 & 5,056,526. At present he is conducting an ongoing research on the coronary circulation.
  

EHS News & Calendar

EHS NEWS:

• The President of the Society is invited to chair one of the ninety minutes major sessions (called a Parallel session), at the 18th Scientific Meeting of the International Society of Hypertension (ISH 2000), between Monday, August 21 and Thursday, August 24,2000 in Chicago, Illinois - USA.
• The Egyptian Hypertension Society has held its IV Annual Meeting on; January 26th-28th 2000., In Marriott Hotel Cairo. The basic scope of the meeting was " Hypertension in the Third Millennium." Prof. Dr. Mokhtar Gomma has delineated the general theme of the meeting i.e. to invite some foreign guest speakers from; Canada, Hungary, Italy, UAE, UK & USA, most of the participants were Egyptians, holding distinguished posts in reputable centers abroad. Those in particular, were most cognizant of the preponderance of medical problems in Egypt and take the opportunity of their presence to share and submit their experience with colleagues in their home country. Beside such guests, the majority of speakers were Egyptians, whether cardiologists or relevant academic scientists, belonging to the intermediate generations, who have attained the knowledge, talent and vision to deliver original presentations, on national and international Events . The scientific program included molecular biology, genetics, epidemiology, pathophysiology, target end-organ affection, diagnosis of comorbid diseases, risk assessment and stratification. It also discussed, ways of prevention and updated approach to hypertension control whether by' life-style modification or pharmacological therapies. The ZODIAC, the first calendar in the world, was discovered on the ceiling of an ancient Pharaonic Temple at Dandara in upper Egypt. Prof. M. GQMAA chose it as the logo of the conference to emphasize the significance of time, discipline and achievements in our daily life. This valuable relic is exhibited at the Louvre in Paris.

LOCAL MEETINGS
1st International Meeting on Critical Care Medicine	Marriot Hotel , Cairo, Egypt. April 8-11, 2000.	Prof. Dr. SherifMok.htar Tel:   (202) 3926650, Telefax : (202) 3602800 / 3958000
Advanced Course in Cardiology	Meridian Hotel, Cairo Egypt April 19-21 7000	Prof Dr. Mohsen Ibrahim Tel:   (202)362-4803 -Fax: (202) 3639895 E-mail:ehs@1ink.com.eg
The Summer Meeting of the Egyptian Society of Cardiology	Palastine Hotel, Alexandria, Egypt June 1st –2nd 2000.	Prof Dr. Said E1-Sakka Tel (203) 5978849 - Fax (203) 4868887
INTERNATIONAL MEETINGS
49th Annual Scientific Sessions, American Collage of Cardiology	Anaheim, CA, USA. March 12th-15th  , 2000	American Collage of Cardiology, Bethesda, USA. Fax: +1-301 8979745
Future of Arrhythmology	Maastricht, The Netherlands.  April 15th –18th ,2000	Cardiol Dept. Academic Hospital, Maastricht Tel: +31(0)433875095-Fax : +31(0) 433877081
4th Asian Vascular Society International Congress.	Qeuezon City, Philippines May 24th-27th, 2000	Tel: (632) 9252401- Fax: : (632) 928-1414
10th European Meeting of Hypertension	Goteborg, Sweden. May 29th- June 3rd  2000	Organizng Secretariat:: AISC, Via, A. Ristori 38-00197 Rome, Italy
7 World Congress on Heart Failure; Mechanism & Management.	Vancouver, B.C., Canada. July, 9th –12th, 2000	Prof. Asher Kimchi, U.S.A. Tel: +13 106577887 (77) Fax: + 13102758922

 

EHS EXECUTIVE BOARD:		EDITORIAL COMMITTEE:
President Vice president Secretary Treasurer Members	M.M. Ibrahim,MD H.E. Attia, MD H.H. Rizk, MD W.EI-Aroussy, MD A.M. Hassaballah, MD M.M. Gomaa, MD F.A. Maklady, MD S.El-Tobgy, MD O.EI-Khashaab, MD	Editor Associate editors	Ebtihag Hamdi, MD Omnia Nayel, Ph D Zeinab Ashour, MD Fatma Aboul -Enein, MD Salwa Morkos, MD