The Egyptian Hypertension Society is
planning to prepare a new book containing its recommendations
and guidelines for management of heart failure. The
success of our two previous guideline books titled"
Management of Hypertension" and "Management
of Coronary Artery Disease" has stimulated the
board of directors of the Egyptian Hypertension Society
to approve, in its meeting on March 24th 1999, the establishment
of a heart failure guidelines working group to prepare
a new book titled "Heart Failure". The book
will be addressing the practitioner, the internist and
the cardiologist. It will contain the essential and
modern information that will guide our Egyptian physicians
in their everyday practice. Heart failure is possibly
the most important cause of hospital admission to cardiology
and general medical departments. Furthermore, developments
in drug therapy in the past decade have changed favorably
the course and outcome of this serious disorder in many
patients. For a number of reasons heart failure has
become an increasingly important problem in our clinical
practice. First, there is a rising incidence of heart
failure in the population, and it is expected that this
trend will continue to increase in the coming years.
The incidence of heart failure rises with aging. There
is a worldwide increase in average life expectancy with
an increase in the number of the elderly in many countries.
Furthermore, the introduction in the recent years of
effective therapies for hypertension, coronary artery
disease and valvular heart disease has prolonged survival
in many cardiac patients and delayed the development
of heart failure.
Second, in the last two decades, a number
of new therapeutic interventions were introduced for
the management of heart failure. Many of these interventions
not only improved patients' symptoms and quality of
life but also prolonged survival of patients with heart
failure and decreased rates of hospitalization and cardiovascular
events. Angiotensin converting enzyme inhibitors (ACEI),
beta adrenergic blockers, Angiotensin receptor blockers
and spironolactone have now an established role in the
routine management of heart failure patients. In addition,
to these established drugs, new pharmacologic agents
are under extensive investigation, which include neutral
endopeptidase inhibitors (NEPI) (Candoxatrilat), combined
NEPI and ACEI (Omipatrilat), endothelin receptors antagonists
(Bosentan), natriuretic peptide (Nesiritide), tumor
necrosis factor receptor antagonists (Etanercept), new
classes of inotropic agents with a novel mode of action
independent of the cyclic adenosine monophosphate (cAMP)
pathway such as calcium sensitizers. These agents proved
effective in improving the hemodynamics and effort tolerance
in short term studies. The plethora of pharmacological
agents combined with non-pharmacological interventions
such as cardiac pacing, LV assist devices, surgery,
gene and immunotherapy make the management of heart
failure patients something more than simple digitalis,
diuretics and bed rest.
Finally, the recognition that asymptomatic
left ventricular dysfunction is a common condition,
being the precursor of clinical heart failure in about
one third of patients and the observation that ACEI
therapy can delay the progression into overt heart failure,
have two implications. First, that echocardiography
should assume a central role as a screening tool for
asymptomatic impaired LV function. Second, there are
new insights into the possibility of prevention of heart
failure through early intervention, particularly with
the use of drugs (ACEI and beta blockers) in asymptomatic
patients.
M.
Mohsen Ibrahim M.D.
Prof & Chairman, Department of Cardiovascular Medicine-Cairo
University
President of The Egyptian Hypertension Society
THE
PRESIDENT'S MESSAGE
INCREASING IMPORTANCE OF HEART FAILURE
The Egyptian Hypertension Society is
planning to prepare a new book containing its recommendations
and guidelines for management of heart failure. The
success of our two previous guideline books titled"
Management of Hypertension" and "Management
of Coronary Artery Disease" has stimulated the
board of directors of the Egyptian Hypertension Society
to approve, in its meeting on March 24th 1999, the establishment
of a heart failure guidelines working group to prepare
a new book titled "Heart Failure". The book
will be addressing the practitioner, the internist and
the cardiologist. It will contain the essential and
modern information that will guide our Egyptian physicians
in their everyday practice. Heart failure is possibly
the most important cause of hospital admission to cardiology
and general medical departments. Furthermore, developments
in drug therapy in the past decade have changed favorably
the course and outcome of this serious disorder in many
patients. For a number of reasons heart failure has
become an increasingly important problem in our clinical
practice. First, there is a rising incidence of heart
failure in the population, and it is expected that this
trend will continue to increase in the coming years.
The incidence of heart failure rises with aging. There
is a worldwide increase in average life expectancy with
an increase in the number of the elderly in many countries.
Furthermore, the introduction in the recent years of
effective therapies for hypertension, coronary artery
disease and valvular heart disease has prolonged survival
in many cardiac patients and delayed the development
of heart failure.
Second, in the last two decades, a number
of new therapeutic interventions were introduced for
the management of heart failure. Many of these interventions
not only improved patients' symptoms and quality of
life but also prolonged survival of patients with heart
failure and decreased rates of hospitalization and cardiovascular
events. Angiotensin converting enzyme inhibitors (ACEI),
beta adrenergic blockers, Angiotensin receptor blockers
and spironolactone have now an established role in the
routine management of heart failure patients. In addition,
to these established drugs, new pharmacologic agents
are under extensive investigation, which include neutral
endopeptidase inhibitors (NEPI) (Candoxatrilat), combined
NEPI and ACEI (Omipatrilat), endothelin receptors antagonists
(Bosentan), natriuretic peptide (Nesiritide), tumor
necrosis factor receptor antagonists (Etanercept), new
classes of inotropic agents with a novel mode of action
independent of the cyclic adenosine monophosphate (cAMP)
pathway such as calcium sensitizers. These agents proved
effective in improving the hemodynamics and effort tolerance
in short term studies. The plethora of pharmacological
agents combined with non-pharmacological interventions
such as cardiac pacing, LV assist devices, surgery,
gene and immunotherapy make the management of heart
failure patients something more than simple digitalis,
diuretics and bed rest.
Finally, the recognition that asymptomatic
left ventricular dysfunction is a common condition,
being the precursor of clinical heart failure in about
one third of patients and the observation that ACEI
therapy can delay the progression into overt heart failure,
have two implications. First, that echocardiography
should assume a central role as a screening tool for
asymptomatic impaired LV function. Second, there are
new insights into the possibility of prevention of heart
failure through early intervention, particularly with
the use of drugs (ACEI and beta blockers) in asymptomatic
patients.
M.
Mohsen Ibrahim M.D.
Prof & Chairman, Department of Cardiovascular Medicine-Cairo
University
President of The Egyptian Hypertension Society
SCIENTIFIC NEWS
Unraveling some of the etiopathogenic
aspects in hypertension cleared that a difference in
endothelium activity was detected between black and
white population and was suggested to play a major role
in the clinical differences observed among them and
the therapeutic outcome specially in relevance to the
different antihypertensives available..
Novel therapies to treat cardiovascular
diseases as hypertension are aimed at striking the critical
steps in vascular disease progression. This includes
reversing endothelial cell dysfunction, correcting dysregulated
cell growth and Apoptosis ,modulating vascular phenotype,
modifying mechano-transduction and reversing vascular
remodeling.
CONTENTS
- The president message.
- Scientific news.
- Editorial;
- Insulin resistance & hypertension
- 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
INSULIN RESISTANCE AND
ESSENTIAL HYPERTENSION
Mona Aboul-Seoud, MD
Endocrine Unit, Internal Medicine, Department,
Faculty of Medicine, University of Alexandria.
The past decades have witnessed a major
surge of interest in the cardiovascular actions of insulin.
On one hand, this interest has stemmed from epidemiological
studies demonstrating an association between obesity,
insulin resistance, and hypertension, which has been
named the "insulin hypothesis of hypertension.'
On the other hand, this interest has been stimulated
by experimental evidence suggesting that the vascular
actions of insulin contributes to its essential role
in promoting glucose uptake in skeletal muscles.
In such a domain, two tenets have emerged
about how insulin may exert its cardiovascular actions.
Thus, it is firmly established that acute insulin administration
stimulates sympathetic nerve activity in both animals
and humans. Also, increasing evidence clear that insulin
stimulates muscle blood flow, an effect that appears
to be mediated, at least, in part, by an endotheliumdependent
mechanism.
In this respect, insulin is thought
to stimulate endothelial NO production or may act directly
to enhance hyperpolarization of vascular smooth muscle
cell membranes via stimulation of their Na+-H+ exchanger
and Na+-K+ ATPase, leading to the consequent closure
of their voltage-gated Ca2+ channels. While glucose
uptake, may determine peripheral blood flow via stimulation
of ATP-dependent ion pumps with consequent vasorelaxation.
Beyond this, a "third factor"
may collectively contribute to both insulin resistance
and endothelial dysfunction in cardiovascular disease.
Candidates to this include; skeletal muscle fibre type
and capillary density, distribution of adiposity and
endogenous corticosteroid production.
The aformentioned can highlight how
hyperinsulinemia that commonly associates hypertension
in the metabolic syndrome-X, can perpetuate the functional
and structural alteration in vessels characteristic
to essential hypertension. This hyperinsulinemia is
attributed to the presence of decreased insulin sensitivity,
or insulin resistance, with consequent compensatory
insulin secretion.
When the hypothesis of decreased insulin
clearance present in hypertensive subjects and its contribution
to hyperinsulinemia [independent of the degree of insulin
resistance] was tested; it was found that essential
hypertension is independently associated with decreased
insulin metabolic clearance rate in addition to insulin
resistance. Thus, a low insulin metabolic clearance
rate may be a contributory factor to the hyperinsulinernia
observed in essential hypertension.
The pathophysiological mechanisms linking
hyperinsulinemia to hypertension are varied. Insulin
might increase blood pressure through sympathetic nervous
system stimulation and enhancement of renal sodium absorption.
Evidence exists linking both of these mechanisms to
hypertension. Also, insulin is independently associated
with myocardial infarction and microalbuminuria, two
long-term complications of high blood pressure. While
experimentally induced decreases in insulin resistance
and hyperinsulinemia have been associated with decreased
blood pressure. Moreover, normotensive offspring of
hypertensive parents are also, as a group, insulin resistant
and hyperinsulinemic.
The relationship between hyperinsulinemia,
insulin resistance and hypertension is more marked in
the obese, yet is present in lean hypertensive as well.
However this relationship is not present in secondary
forms of hypertension and may persist despite adequate
antihypertensive therapy.
When the impact of therapeutic agents
on insulin resistance were raised, their appeared that
treatment of essential hypertension with beta-blockers
and diuretics has been associated with increased risk
of developing diabetes mellitus in three prospective
cohort studies. While prospective, randomized studies
with antihypertensive drugs have demonstrated differences
between different classes of drugs regarding effects
on insulin sensitivity. Accordingly, treatment with
beta-blockers or diuretics is associated with impairment
in insulin sensitivity, whereas most modern calcium
channel blockers and Angiotensin converting enzyme (ACE)
inhibitors are neutral. However, still to hold, there
are exceptions within the different classes. For instance,
Captopril seems to differ from other ACE inhibitors
and results in improvement of insulin sensitivity yet
the most pronounced improvements have been obtained
with alpha1 blockers.
Despite of the raised therapeutic control,
new concepts in therapy of insulin resistance are endlessly
added, realizing how much this syndrome is rapidly expanding
in industrialized countries, with its dramatic consequences
on public health.
For instance, insulin sensitivity can
be improved by non-pharmacological means as, the essential
reduction of excessive body weight, the promotion of
regular physical activity and the modification of dietary
habits, as well as, the possibility of cessation of
smoking and correction of subclinical magnesium deficiency.
While the currently available pharmacological means
should mainly include the biguanide compound metformin
and possibly anti-obesity agents, such as dexfenfluramine,
fluoxetine and benfluorex. New compounds aiming at improving
the action of insulin, that are called 'insulin sensitizers"
as the thiazolidinedione derivatives like troglitazone
and pioglitazone are better added. By this therapeutic
modality, hopefully the cardiovascular prognosis of
numerous individuals having some or all components of
the insulin resistance syndrome is improved.
In conclusion, evidence suggests that
hyperinsulinemia and insulin resistance exert a pro-hypertensive
effect that contributes to the pathogenesis of hypertension
and hypertensive complications in some patients with
essential hypertension. The associated complex interaction
between endothelial dysfunction, abnormal skeletal muscle
blood flow and reduced insulin-mediated glucose uptake
observed, links between insulin resistance, blood pressure,
impaired glucose tolerance and the risk of cardiovascular
disease. An understanding of the primary mechanisms
resulting in these phenotypes may reveal new targets
to therapeutically strike when tempting to achieve appropriate
control. While in those at high risk for diabetes mellitus,
it may be justified to select drugs that improve insulin
sensitivity when treating hypertension in insulin resistant
individuals
BIBLIOGRAPHY:
- Landsberg L. Insulin sensitivity
in the pathogenesis of hypertension and hypertensive
complications. Clin Exp Hypertens 1996; 18 (3-4):
33 7-46.
- Natali A, Quinones Galvan A, Arzilli
F, Taddei 5, Pecori N, Frascerra 5, Salvetti A, Ferrannini
E. Renovascular hypertension and insulin sensitivity.
Eur J Gun Invest 1996; 26 (7): 556-63.
- Lithell HO. Hyperinsulinemia, insulin
resistance, and the treatment of hypertension. Am
J Hypertens 1996;9(1l): 1505-1545.
- Scherer U, Sartori C. Insulin as
a vascular and sympathoexcitatory hormone: implications
for blood pressure regulation, insulin sensitivity,
and cardiovascular morbidity. Circulation 1997; 96
(11): 4 104-13.
- Lender D, Arauz-Pachero C, Adams-Huet
B, Raskin P. Essential hypertension is associated
with decreased insulin clearance and insulin resistance.
Hypertension 1997; 29 (lPt 1): 111-4.
- Scheen Al. Perspective in the treatment
of insulin resistance. Hum Reprod 1997; 12 (Suppl
1): 63-7 1.
- Cleland Si, Petrie JR, Ueda 5, Elliott
HL, Connell JM. Insulin as a vascular hormone: implications
for the pathophysiology of cardiovascular disease.
Clin Exp Pharmacol Physiol 1998; 25 (3-4): 175-84.
ABSTRACTS OF
WORLD LITERATURE
ECHOCARDIOGRAPHIC DEFINITION OF LEFT VENTRICULAR HYPERTROPHY
IN THE HYPERTENSIVE: WHICH METHOD OF INDEXATION OF LEFT
VENTRICULAR MASS?
P Gosse, V Jullien, P Jarnier,
P Lemetayer & J Clementy
Hôpital Saint André, I rue Jean Burguet,
33075 Bordeaux cedex, France
Objectives: It has been suggested that
hypertensives at high risk of cardiovascular complications
can be identified on the basis of their left ventricular
mass as determined echographically. However, there is
as yet a lack of consensus on the mode of indexation
(body surface area, height, height2.7) of left ventricular
mass (LVM), and on the cut-off values for definition
of left ventricular hypertrophy (LVH). The main objective
of this study is to test the influence of the different
modes of indexation for LVM on the prevalence of LVH
in a population of never treated hypertensive patients
on the basis of cut-off for LVM based upon its relationship
with ambulatory blood pressure (BP)measurement.
Methods: A population of 363 untreated
hypertensives was investigated using a standardised
procedure. The men and women were analyzed separately.
We studied the relationship between mean daytime ambulatory
systolic BP and LVM and calculated the LVM cut-off for
a BP of 135 mm Hg using three different methods of indexation.
On the basis of these criteria, the population was divided
into those with and those without LVH.
Results: Th prevalence of LVH was found
to be higher when LVM was indexed to height 2.7 (50.40o)
or height (50.1%). Prevalence was lowest when LVM was
indexed to body surface area (48.20o), which tended
to minimize the hypertrophy in obese individuals. Only
indexation by height2.7 fully compensates for relationships
between height and ventricular mass in this population.
Conclusions: Indexing LVM to height
2.7 thus appeared to give a more sensitive estimate
of LVH by eliminating the influence of growth. Cut-off
of 47 g/m 2.7 in women and 5 g/m2.7 in men corresponded
to a cardiovascular risk indicated by a daytime systolic
BP 135 mm Hg.
I Hypertension 1999;13 (8): 559- 563.
TRIALS OF ANTIHYPERTENSIVE THERAPIES
IN CHILDREN.
Wells TG
Divisions of Pediatric, Nephrology and Pediatric Clinical
Pharmacology and Toxicology, University of Arkansas
for Medical Sciences and the Arkansas Children's Hospital,
Little Rock, Arkansas, USA.
Clinical trials assessing the safety,
effectiveness and pharmacokinetics of new antihypertensive
medications have been numerous as new classes of medications
have been developed and brought to market over the past
two decades. However, very few clinical trials have
been initiated and completed in children with hypertension.
Excluding diuretics, only one antihypertensive medication
marketed within the past 20 years has any pediatric
pharmacokinetic or dosing information published in the
drug label and none have a pediatric indication. There
are many reasons that these studies have not been done.
Summation of the data collected in large epidemiologic
studies that establish normal blood pressure and define
hypertension using casual measurements have been a relatively
recent event in pediatrics. Although ambulatory blood
pressure measurement has been studied for the past decade
there is still uncertainty with respect to the standardization
of devices, measurement technique and normal values
in a multi-racial pediatric population. As a result,
no large scale, industry-sponsored clinical trials involving
antihypertensive therapy have employed this measurement
technique in children. In recognition of this problem,
US Congress passed the Food and Drug Administration
Modernization Act in 1997. Among the many provisions
of this law, the US Food and Drug Administration (FDA)
is required to publish a list of approved drugs for
which additional information may prove beneficial for
children. This law and subsequent action by the FDA
also provides a mechanism by which manufacturers may
gain six months of additional market exclusivity if
adequate and well-controlled pediatric trials are completed
and submitted to the FDA in response to a formal written
request for these studies. Because such studies have
not been previously undertaken and the new rules provide
a significant financial incentive, written requests
have been issued for pediatric studies involving more
than a dozen antihypertensive agents. The FDA published
a sample written request for oral antihypertensives
in children and several potential study designs were
presented.
Blood Press Monit l999;4(3):189-192
ABSTRACTS OF
LOCAL LITERATURE
PRO INFLAMMATORY CYTOKINES IN ISCHEMIC HEART DISEASE:
EFFECT OF CONVERTING ENZEME INHIBITORS.
Saraa Abd EI-Sha.fee, Ahmed
Abd El-Aziz,, Abd EI-Hameed Ibrahim, Abeer Mohamed,
Sobhy Said, Sherif Mokhtar.
Critical Care Medicine, Cairo
University & Clinical Pharmacology, Helwan University.
Pro-inflammatory CYTOKINES are mediators
released from leucocytes and vascular endothelium in
response to various inflammatory and noxious stimuli,
but have recently been reported also in myocardial ischemia
and different grades of heart failure (HF). The exact
pathogenic role and mechanism of production in HF and
Ischaemic heart disease have not been clearly explained.
Moreover the role of converting enzyme inhibition has
not been elucidated in this work, we assessed the level
of Cytokines and studied the effect of Angiotensin converting
enzyme (ACE) inhibition on such mediators using Captopril
(75 mglday) and Benazepril 5-10 mg /day in 2 groups
of pts with ischeamic heart disease (IHD). Group 1:
comprized 16 pts with chronic myocardial ischemia (12
males, mean age 49± 15) all complicated by heart
failure (class 11 NYHA). Group 11: comprized 20 pts
(17 males, mean age 52 - 10) with acute myocardial infarction
complicated by left ventricular dysfunction (Killp's
classification 11). Following admission all patients
had clinical and laboratory evaluation including serum
estimation of Cytokines I L6 and 1 L8 measured by chemiluminescence
immunometric assay technique. Converting enzyme inhibition
was started in the absence of contraindication using
Captopril and Benazepril for one week with repeated
measurement of serum Cytokines. Compared to the group
of pts with chronic IHD, those with acute myocardial
infarction had significantly higher levels of interleukin
6 (180 vs 10 pg/rn) and interleukin 8 (400 vs 20 pg/rn),
respectively prior to treatment with ACE inhibitors.
Following ACE therapy there was significant reduction
in interleukin 1L6 (from 180 to 20 pg/ml) and 1L8 (from
400 to 90 pg/mI) in groupll. We concluded that pro-inflammatory
Cytokines are elevated in acute MI apparently as a response
to the acute Ischaemic insult rather than being related
to heart failure. More important, converting enzyme
inhibitors were shown for the first time to significantly
reduce the pro-inflammatory Cytokines in acute myocardial
infarction a further addition to their cardiac protective
action. Presented at the 3rd Scientific meeting of the
Egyptian Hypertension Society, Port Said, Egypt. December
1998.
BETA ADRENOCEPTOR MEDIATED VASORELAXATION
OF RABBIT AORTA IS ENDOTHELIUM-DEPENDENT: ROLE OF PROSTAGLANDINS
AND SODIUM PUMP
Hassan Heialy Abo Rahma
Department of Pharmacology, Assiut Faculty of Medicine,
Assiut, Egypt
B-adrenoceptor mediated vasorelaxation
is thought to be through activation of adenylate cyclase
within the smooth muscles. Such a mechanism is not dependent
on the presence of the intact endothelium. There are
now several findings suggesting that the B-adrenoceptor
induced vasodilatation is endothelium dependent. However,
others have shown that isoprenaline-induced relaxations
in rat aorta are not endothelium dependent. Moreover,
there is accumulated evidence showing that hyperpolarization
through opening of K-ATP channels partly mediates vasodilatation
induced by B-adrenoceptors. Recently, it was reported
also that nitric oxide mediated Na+ pump as well as
cyclooxygenase activation are also involved. The present
study was designed to evaluate the role of endothelium
in 3-adrenoceptor mediated vasorelaxation in isolated
rabbit aortic rings by using the selective 32 agonist,
terbutaline and to investigate the possible involvement
of other mediators e.g. prostaglandins and other cellular
components e.g. Na+-K+ ATPase (sodium pump) in the
B-adrenoceptor mediated vasorelaxation.
The results of the present work indicate that the removal
of the endothelium reduces significantly the relaxant
effect of terbutalin Propranolol treatment reduced significantly
(p< 0.05) the terbutaline induced vasorelaxation
& shifted its cumulative dose-response curve to
the right. Terbutaline concentration response curves
were obtained after treatment of the aortic rings with
the prostaglandin synthesis inhibitors, dexamethasone
and aspirin. The results showed that the terbutaline
induced vasorelaxation was significantly augmented (p<0.0l)
in presence of dexamethasone. This means that not only
the prostaglandins are involved but also other substances
e.g. adenosine, leukotrienes, etc. may be involved and
the net result depends on the proportion of the vasodilator
and the vasoconstrictor agents that may be affected
by the cyclooxygenase and the phospholipase A2 inhibitors.
Pretreatment of the aortic rings with the sodium pump
inhibitor, digoxin, produced a significant reduction
(p<O.01) of the terbutaline induced vasorelaxation:
pretreatment with dexamethasone, aspirin and digoxin
didn’t affect significantly the endothelium independent
sodium nitroprusside induced vasodilatation. In conclusion,
B-adrenoceptor vasorelaxation is mediated partly by
NO release from the endothelium. The results of the
present work suggests also the involvement of other
mediators e.g. prostaglandins and the sarcolemmal sodium
pump in the B-adrenoceptor mediated vasorelaxation of
the rabbit aorta
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 73-years old man with known hypertension
for many years was admitted for evaluation of progressive
exertional dyspnea that developed over several days
and for the sudden onset of severe dyspnea. He denied
recent chest pain but did note that 1 year earlier he
had experienced several episodes of nonspecific chest
pain. He underwent coronary arteriography at that time,
which demonstrated normal coronary arteries. He had
no history of diabetes and did not smoke.
Physical Examination: Vital signs; pulse;
1 00;BP 220/120. General: severe dyspnea. Neck: no venous
.distension. Chest: crackles throughout all lung fields.
Cardiac: no S3 or murmur. Laboratory investigation;
Cardiac enzymes: normal. Chest radiography: pulmonary
edema with normal heart size. EKG: normal. Echocardiogram
and Doppler study: normal chamber sizes with some left
ventricular hypertrophy and an ejection fraction of
600 o; mitral flow revealed a reduction of the F to
A ratio.
Question: What is the cause
of this patient's acute pulmonary oedema?
Pick up the solution at CARDIOLOGY PEARLS
on p. [7 ] of this issue. PRACTICAL CONSIDERATIONS:
HYPERTENSIVE WOMEN
When your patient happens to be a woman
please;
àConcentrate on the ways to make
this patient day by day live healthier and feel better
and emphasize that it's a task every woman can do.
à Explain the dimension of the
problem first and clear that three of every four women
with high blood pressure know they have it, yet fewer
than one in three are controlling it.
àEncourage overweight patients
to a gradual loss of weight either by a lower calorie
intake or increased physical activity and preferably
both... Advice from a registered dietitian, or a qualified
nutritionist to plan for a sensible, balanced eating
pattern to lose weight slowly should be encouraged.
àExplain the importance of physical
activity for the heart and blood vessels and for maintaining
optimal weight to look and feel better. Luckily, this
can be achieved without having to run marathons. Just
a 30 minutes of moderate activity would be a brisk walking,
gardening, cycling, swimming... .Breaking this into
periods of at least 10 minutes, helps one to get started.
If the issue that your patient is pressed for time,
just make it clear that physical activity doesn't need
that much time for a reward and a sense of accomplishment.
àExplain that women, should have
no more than 2,400 milligrams of sodium a day (about
1 teaspoon) and clear, that this amount includes all
of the salt and sodium consumed in processed foods,
added during cooking, and used at the table. The importance
of this hold of salt, is equal, whether there is high
blood pressure, high-normal blood pressure, or to prevent
high blood pressure.
àWhen you prescribe an antihypertensive,
be sure that your patient understands the instructions
and secure that if something is not clearly understood,
she should call back and ask. Explain that, as with
all drugs, side effects like; sleepiness, being tired,
rash or cough etc, could happen. So it is important
that she should pay attention to how she feels and notify
any change that issues.
--
Guidelines to which antihypertensives allowed during
pregnancy, lactation, with contraception or better avoided
in special health problems will be highlighted in the
forthcoming editions.
High Blood Pressure Information for
the General Public
: NHLBJ Home Page A collaboration of the Alliance for
Aging Research,
National Heart, Lung, and Blood Institute, National
Institutes of Health & Sponsored by Hoechst Marion
Roussel, Inc.
ENVIRONMENTAL HAZARDS:
CIGARETTE SMOKING: A GLOBAL LOOK
Many epidemiological and experimental
studies has recognized and established the links between
cigarette smoking and its cardiovascular hazardous impacts
on morbidity & mortality.
Speaking of its relevance to hypertension
per se, it was reported that smoking a cigarette raises
the blood pressure by 5-10 mm Hg for about 30 minutes
and lowers coronary reserve for 20 minutes. This aggravates
and lasts longer if this is combined with drinking a
cup of coffee.
Despite of this, numerous epidemiological
studies have found that people with hypertension are
not more likely to be smokers than those with normal
blood pressure, and conversely that smokers are not
more likely to be hypertensive than non-smokers. One
possible explanation for this, might be, that smokers
tend to weigh less than non-smokers, and that the effects
of obesity and smoking on blood pressure cancel each
other out. But even when smokers and nonsmokers of the
same body weight are compared, their blood pressures
are the same. This is probably because the rise of daytime
pressure, after one smokes a pack a day, will raise
your average pressure by about 5 mm Hg, a value that
might not be detected during an office visit to the
physician.
However, the important thing about smoking,
is not what it does solely to your blood pressure, [the
mechanisms through which remains to be clarified] but
is centered more to how it greatly increases the vascular
and cardiac risks, the extent of end organ damage and
the likelihood of co-morbid conditions. These issues
then, will even weigh more.
Moreover, breathing sidestream smoke
[passive smoking] is also partially associated with
the same detrimental effects as active smoking. To imagine
how figures could be striking, the U.S. Environmental
Protection Agency estimated that in USA 30,000 to 60,000
cardiac deaths are associated with passive smoke exposure.
The question that will pose itself at this juncture
is: Will these risks go down, if one quit smoking? The
answer will be a big ' YES". This statement is
based on the findings of several studies clearing that
if you smoke, your risk of heart disease is about three
times higher than if you don't. If you quit, it will
go down to twice the normal risk in two years, and after
that, it will be the same as if you had never smoked.
Realizing all this, calls on the need
to really under stand why and how cigarette smoking
does all this.
So let us know first, what are some of the noxious chemicals
in tobacco smoke???
It was reported that tar, phenol, benzopyrene, nirtosamine
and polycyclic aromatic hydrocarbons are all carcinogenic
and some are pro-oxidants thus perpetuating lipid peroxidation,
endothelial disruption and impairing NO vasodilatory
potentials, which are all relevant to hypertension and
comorbid atherosclerotic changes. While formaldehyde
and oxides of nitrogen are severe bronchial irritants
and toxic to epithelial, endothelial,.. .etc structures.
In addition, carbon monoxide impairs oxygen transport
and utilization and shares in a pattern of Ischaemic
myocardial insults that may also be linked to microvascular
ischaemias in hypertensive heart disease. Lastly nicotine
the known ganglion stimulant and depressant, beyond
being carcinogenic, it sets the sympathetic drive of
blood pressure regulation, at a higher regulatory setpoint.
The impact of some of such hazardous
products and there relevance to vascular and cardiac
functional and structural integrity will be more detailed
in the forthcoming editions.
Br Med J 1994; 309: 901
JAMA 1995; 273: 1047.
N Engl J Med 1996; 334: 1189.
J Hum Hypertens 1996 Feb;10 Suppl 2:S13-6
Basic Pathology. W.B . Saunders Company
Publicationsl997; 8: 221.
PATIENT'S TIPS:
Help your patients stop smoking by initiating
therapy with the antihypertensive mecamylamine HCI [Inversine]
10 days before their quit day starting by 2.5 mg twice
daily for five days & going up to 5 mg twice a day.
Mecamylamine reduces nicotine craving because it blocks
ganglionic receptors. So tell the patient to stop smoking
completely & start wearing the nicotine patch. By
this you can strike a double benefit ; cessation of
smoking & improving the therapeutic outcome of any
antihypertensive intended to be used.
Modem Medicine 1998; 15 : 32.
CARDIOLOGY PEARLS
- Diagnosis: Pulmonary oedema secondary
to hypertension with diastolic dysfunction.
- One-third of patients with signs
of congestive heart failure have diastolic dysfunction
and normal systolic function.
- Diastolic dysfunction should be suspected
in a patient with signs and symptoms of congestive
heart failure who has normal-sized heart and normal
ejection fraction.
- The differentiation of systolic versus
diastolic dysfunction is important, as therapy is
different for these two causes of heart failure. Inotropic
agents and arterial vasodilators used for unloading
therapy may be harmful in diastolic dysfunction
NATIONAL & INTERNATIONAL
RECOGNITION:
- Prof Dr. Mohsen Ibrahirn, Head of
Dept. Cardiology, Faculty of Medicine, Cairo University
and the President of the Society, has been chosen
a member of the Editorial Board for the Journal of
Hypertension, for a term of three years. This journal
happens to be the official Journal of the International
Society of Hypertension (SH) and the European Society
of Hypertension (ESH).
- Prof. Dr. Ebtihag A Hamdi, Prof in
Cardiology Unit, Faculty of Medicine, Alexandria University
and a senior member of the editing board of this News
Letter has been elected as a member of the High Blood
Pressure Council, the Scientific Council of the American
Heart Association, starting from 1st June 1999 with
a membership ID 000106559901
EHS News &
Calendar
EHS NEWS:
- The EHS has held its annual social
event of getting together in Ramadan at Cairo Sheraton
Hotel on Friday the 24th of this month. The members
enjoyed the splendid iftar and the whole heartily
gathering in this holy month . Prof Dr. Mokhtar Gomma
clarified the final arrangements and theme of organization
he has adopted in the forthcoming annual congress
of the society next January. Also, Prof Dr. Soliman
Gareeb highlighted the preliminary data pooled from
the scientific committee of the Egyptian Hypertension
Project that is conducted to test the efficacy and
tolerability of anti-hypertensives among Egyptian
hypertensive population. A short statement was addressed
by Prof Dr. Omnia Nayel on the current status of the
news letter of the society an the topics that has
been added to the issues. Lastly Prof Dr. Mohsen Ibrahim
delivered a small lecture to delineate the criteria
that should be fulfilled when probing the utility
of an antihypertensive agent He also handed out a
questionnaire form termed " Physician Hypertension
Survey" to investigate Egyptian physician's knowledge
and attitudes regarding hypertension.
CALENDAR:
$th Meeting of the Egyptian
Society of Atherosclerosis
|
Mena-House Oberoi,Cairo
Egypt.
January 21-23, 2000. |
Prof Dr. Osama Abdel Aziz
Tel: (202) 3926650,
Telefax: (202) 3602800 / 3958000 |
The fourth Scientific Meeting of
the EHS |
Marriot Hotel, Cairo Egypt
January 28-29th 2000
|
Prof Dr. Mokhtar Gomma
Tel: (202) 3026871 -Fax (202) 3026871
E-mail : mogomaa@idscl.gov.eg |
7th Annual Meeting of Egyptian
Society of Cardiothoracic Surgery |
Sheraton El Gizzera Hotel
Cairo,Egypt,
February,9-11,2000 |
Prof Dr.Shabaan Abul-Ela
Tel : (2050) 374111.Fax (2050) 360138
E-mail : SHAABANABUELA@netscape.net |
The 27th Annual Congress of the
Egyptian Society of Cardiology |
Marrior Hotel ,Cairo Egypt
February 21st -25th ,2000. |
Prof Dr.Adel Imam
Tel (202) 3489383-Fax (202) 3489383
E-mail : emam@internetegypt.com |
4th World Congress of Echo-
cardiography & vascular Ultrasound. |
Mena-House Oberoi,Cairo.
Egypt.
January 19-2 1, 2000. |
Prof Dr. Osama Abdel Aziz
Tel : (202) 3926650,
Telefax: (202) 3602800 / 3958000
|
3rd Conference of the Pan -Arab
Hypertension Society |
Abu Dhabi, 5-9 February,
2000
Intercontinental Hotel |
Conference Secretarial Office:
Tel:+ 97 1(2) 347478-Fax 349225
E-Mail: yassinl@emirates.net.ae |
9th International Congress on
Cardiovascular Pharmacotherapy |
Salvador, Bahia, Brazil.
March 2000 |
Congress Secretariat; JZ Promocoes,
E Assessproa De.
Tel.: +55215391 299, Fax: + 55215379134 |
| 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. I-Iassaballah, 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 |
