NEW DIMENSIONS IN THE TREATMENT OF HYPERTENSION
Dr.Omar Abboud. QATAR

Session Start: Thu Feb 17 17:04:00 2000

[17:04] (MJesus) hello Abboud! welcome!
[17:04] (JBover) WELCOME Dr Abboud!!!!!
[17:04] (Enrique) se de su mercado :)
[17:05] (JBover) THANK YOU VERY MUCH FOR COMING!!!!!
[17:05] (Abboud) hello Maria
[17:05] (MJesus) hou are you ?
[17:05] (JBover) We really thank you for coming.....
[17:05] (Enrique) Hello Dr. Abboud
[17:06] (MJesus) Abboud, thank!! here is nphrologist from Spain, USA, Venezuela....
[17:06] (JBover) we know that your agenda is very busy but we thank your great effort and support
[17:06] (Abboud) I am fine
[17:06] (Abboud) Hello everybody
[17:06] (Ramon) :-)
[17:06] (MADiaz) Wellcome, abboud
[17:06] (Abboud) I am thankful to you for your invitation to me to join in this great effort
[17:07] (JBover) Unfortunately this is a very early hour in Europe
[17:07] (JBover) and many nephrologists would love to be here but they are probably still working
[17:07] (Abboud) I do understand that it is an early hour and that many people are still working
[17:08] (Enrique) same here in the U.S., it is 10 a.m.!!!
[17:08] (Abboud) unfortunatley the time of my flight would not allow a later time
[17:09] (JBover) shall we start then????
[17:09] (Abboud) O K
[17:10] (JBover) We usually post online your contribution first
[17:10] (Abboud) In my article I concentrated on
[17:10] (JBover) we do it automatically ..thus, YOU DONT NEED TO TYPE IT AGAIN!!!!!!
[17:11] (JBover) however you could give us an introduction or summary first
[17:11] (JBover) :-)))
[17:11] (Abboud) I concentrated on highlighting the current
[17:11] (Abboud) trends in treating hypertension
[17:12] (Abboud) as far as the target BP that should be
[17:12] (Abboud) aimed at is concerned, which is now
[17:13] (Speaker) Until the early 1990's the World Health Organization's definition for the upper limit of a
[17:13] (Speaker) normal blood pressure was 160/95. Other hypertension professional bodies had similar
[17:13] (Speaker) views and it was widely accepted that treatment for lower levels of blood pressure was not
[17:13] (Speaker) beneficial (1).
[17:13] (Speaker) The quest for newer drugs for the treatment of hypertension continues. The ability to produce
[17:13] (Speaker) such new therapies stems from increasing knowledge of the different mechanisms that
[17:13] (Speaker) contribute to the production of hypertension.
[17:14] (Speaker) This article will review the change in trends concerning the definition and guidelines for
[17:14] (Speaker) treatment of hypertension and highlight some of the newer therapies, which were recently
[17:14] (Speaker) introduced or are in the process of validation in clinical trials.
[17:14] (Speaker) Evidence Review and Newer Concepts
[17:14] (Abboud) much lower than had been accepted previoulsly
[17:14] (Abboud) I reviewed some evidence i.e. the main trials
[17:14] (Abboud) that have led us to reaching the current status
[17:14] (Speaker) The level to which the blood pressure should be lowered in patients with hypertension had
[17:14] (Speaker) been a matter of controversy. The two major issues of debate were the level at which
[17:14] (Speaker) maximal protection against cerebro- and cardiovascular events and renal damage could be
[17:14] (Speaker) achieved and whether harm could be produced by rather low levels of blood pressure i.e.:
[17:14] (Speaker) J-effect(2). More recently data from different trials pointed towards linear relationship
[17:15] (Speaker) between increased protection and more aggressive blood pressure control to levels much
[17:15] (Speaker) lower than what had been accepted previously. Meta-analysis of data from 17 trials which
[17:15] (Speaker) examined the protective effect of anti-hypertensive therapy was published by MacMahon and
[17:15] (Speaker) Rodgers(3) . Those trials included 47,653 patients with a mean age of 57 years and follow-up
[17:15] (Speaker) period of 4.9 years. The blood pressure was lowered by 10-12 mm Hg (systolic) and 5-6 mm
[17:15] (Speaker) Hg (diastolic) in the treated group compared to the control group. Although the blood
[17:15] (Speaker) pressure reduction was only very modest, there was a significant reduction of 38% in the
[17:16] (Speaker) incidence of cerebrovascular accidents and 16% decrease in coronary heart disease
[17:16] (Speaker) events.
[17:16] (Speaker) In the Systolic Hypertension in the Elderly Programme (SHEP) benefit and safety were
[17:16] (Speaker) shown to occur with progressive reduction of both systolic and diastolic blood pressures but
[17:16] (Speaker) cardiac events were not stratified with the diastolic blood pressure levels and therefore, a
[17:16] (Speaker) J-effect could not be ruled out.
[17:16] (Speaker) The Modification of Diet in Renal Disease (MDRD) study compared the rate of decline in
[17:17] (Speaker) glomerular filtration rate (GFR) in 840 patients with various chronic renal diseases who were
[17:17] (Speaker) randomized either to usual or low blood pressure goals (mean blood pressure 107 or 92 mm
[17:17] (Speaker) Hg). The rate of decline in GFR and the proteinuria were reduced in the low blood pressure
[17:19] (Speaker) The Hypertension Optimal Treatment (HOT) trial was designed to assess the optimum target
[17:20] (Speaker) diastolic blood pressure and whether a J-effect exists. It was a large prospective multi-centre
[17:20] (Speaker) study that recruited 19,193 hypertensive patients, from 26 countries, aged 50-80 years
[17:20] (Speaker) (mean 61.5 years). The baseline diastolic blood pressure was between 100 and 115 mm
[17:20] (Speaker) Hg. They were assigned to three diastolic blood pressure target levels: 90 mm Hg, 85
[17:20] (Speaker) mm Hg or 80 mm Hg. The calcium antagonist felodipine was used in all patients in
[17:20] (Speaker) step-wise dose increments with addition of other hypotensive agents as necessary to
[17:20] (Speaker) achieve the target blood pressures in each group(4). The study gave some indication of the
[17:20] (Speaker) minimum blood pressure i.e. the values around which the maximum benefit of treatment can
[17:20] (Speaker) be expected, these being systolic 130 to 140 mm Hg and diastolic values between 80 and
[17:20] (Speaker) 85 mm Hg. Efforts to lower blood pressure further, to 120 mm Hg systolic and 70 mm Hg
[17:20] (Speaker) diastolic, did not confer further benefit, but did nor cause any significant additional risk i.e.
[17:20] (Speaker) there was no evidence of a J-effect for cardiovascular events, myocardial infarction, all
[17:21] (Speaker) stroke and cardiovascular mortality. The lowest achieved BP was 120 mm Hg systolic and
[17:21] (Speaker) 70 mm Hg diastolic.
[17:21] (Speaker) A seven-country research group has recently published the results of a trial that investigated
[17:21] (Speaker) the relation between blood pressure and long-term mortality from coronary heart disease in
[17:21] (Speaker) which 12,031 men were followed-up for 25 years(5). The relative risk from coronary heart
[17:21] (Speaker) disease was found to rise progressively with increasing levels of systolic and diastolic blood
[17:21] (Speaker) pressures. Sustained decrease of 10 mm Hg in systolic and 5 mm Hg in diastolic blood
[17:21] (Speaker) pressures were each associated with a 28% drop in the risk of death from coronary heart
[17:21] (Speaker) disease. Interesting findings in the results of this trial are the absence of abrupt increase in
[17:21] (Speaker) the mortality risk above the blood pressure levels typically used as criteria for hypertension
[17:21] (Speaker) and the absence of a clearly defined lower level of blood pressure below which the risk did
[17:22] (Speaker) not continue to decline. Any difference in blood pressure between persons is associated with
[17:22] (Speaker) approximately constant difference in relative risk from coronary heart disease irrespective of
[17:22] (Speaker) whether they have hypertension or not.
[17:22] (Speaker) Such cumulative data have led the professional organizations concerned with hypertension
[17:22] (Speaker) to establish new definitions for hypertension and guidelines for treatment. The Joint National
[17:22] (Speaker) Committee for the Prevention, Detection, Evaluation and Treatment of High Blood Pressure
[17:22] (Speaker) 6th report (JNC-6) expressed those new developments and similar guidelines were
[17:22] (Speaker) published by the International Society of Hypertension and the World Health Organization
[17:22] (Speaker) (ISH-WHO). The JNC-6(6) uses the following classification:
[17:22] (Speaker) * Optimal blood pressure = systolic 120 and diastolic 80 mm Hg
[17:23] (Speaker) * Normal blood pressure = systolic 120-129 and diastolic 80-84 mm Hg
[17:23] (Speaker) * High-normal blood pressure = systolic 130-139 or diastolic 85-89 mm Hg
[17:23] (Speaker) * Hypertension:
[17:23] (Speaker) ? Stage 1 = systolic 140-159 or diastolic 90-99 mm Hg
[17:23] (Speaker) ? Stage 2 = systolic 160-179 or diastolic 100-109 mm Hg
[17:23] (Speaker) ? Stage 3 = systolic ? 180 or diastolic ? 110 mm Hg
[17:24] (Speaker) The systolic and diastolic pressures are of equal importance; if there is a disparity in
[17:24] (Speaker) category, the higher value determines the blood pressure class or the severity of
[17:24] (Speaker) hypertension. When considering treatment this classification takes in consideration other
[17:24] (Speaker) major risk factors (smoking, dyslipidaemia, diabetes mellitus, age above 60 years and
[17:24] (Speaker) family history of cardiovascular disease) and target organ damage. Even in the high normal
[17:24] (Speaker) group drug therapy is recommended if heart failure, diabetes mellitus or renal insufficiency
[17:24] (Speaker) co-exist.
[17:24] (Speaker) Microalbuminuria has emerged as an important risk marker in hypertension indicative of
[17:24] (Speaker) end-organ damage. It is a predictor for the development of premature coronary vascular
[17:24] (Speaker) disease in diabetics, development of clinical proteinuria and progression of renal damage. It
[17:25] (Speaker) is best measured on a timed urine collection but early morning or random urine specimens
[17:25] (Speaker) can be used. Accuracy can be increased by calculating the albumin creatinine excretion
[17:25] (Speaker) ration.
[17:25] (Speaker) Newer Drug Therapies
[17:25] (Speaker) A.Angiotensin II Receptor Antagonists
[17:25] (Speaker) Angiotensin II (A II ) is produced in plasma by the sequential processing of circulating
[17:25] (Speaker) angiotensinogen by renin and Angiotensin I Converting Enzyme (ACE). Renin, produced by
[17:25] (Speaker) the kidney, is a major factor in regulating the production of A II in the circulation. Recently it
[17:25] (Speaker) has been recognized that local A II production also occurs in several tissues such as the
[17:25] (Speaker) brain, adrenal glands, the heart and blood vessels. In these tissues A II levels are regulated
[17:26] (Speaker) by uptake of A II from the circulation as well as by local formation and degradation of A II via
[17:26] (Speaker) a tissue renin angiotensin system (RAS). In the tissues Chymase and other enzymes convert
[17:26] (Speaker) angiotensin I (A I ) to A II in a process independent of blood ACE. In animal experiments
[17:26] (Speaker) ACE inhibition reduced basal A II formation by only 25%. A II receptor antagonists selectively
[17:26] (Speaker) compete with the binding of A II to its type I (AT1 ) receptor. AT1 receptor is present in all
[17:26] (Speaker) tissues and is responsible for most of the known actions of A II . The first four A II receptor
[17:26] (Speaker) antagonists are:
[17:26] (Speaker) Losartan which produces a short surmountable AT1 receptor blockade but its metabolite,
[17:26] (Speaker) EXP 3174, has a long duration of action and produces an insurmountableAT1 blockade. It is
[17:26] (Speaker) 20 times more potent than the parent drug(7).
[17:27] (Speaker) Valsartan is also a potent AT1 antagonist. The parent compound is the active drug. It has a
[17:27] (Speaker) half-life of 6-9 hours and is excreted in bile (70%) and by the kidneys (30%)(8).
[17:27] (Speaker) Irbesartan and Candesertan are long acting and produce insurmountable A II blockade.
[17:27] (Speaker) Irbesartan has a half-life of 11-15 hours, and is mainly cleared by the liver (78%) and by the
[17:27] (Speaker) kidneys (22%)(9). Candesertan is a pro-drug and unlike other A II receptor antagonists, is
[17:27] (Speaker) cleared mainly by the kidneys (60%)(10). Those latter two drugs differ from Losartan and
[17:27] (Speaker) Valsartan in that they have a clear dose-response relationship, which was not established
[17:27] (Speaker) with Losartan or Valsartan.
[17:27] (Speaker) When A II receptor antagonists were compared with other hypotensive drugs, they were
[17:27] (Speaker) found to have an efficacy equivalent to that of ACE inhibitors, calcium antagonists and
[17:28] (Speaker) B-blockers(,7,8,9,10). When the RAS is blocked, blood pressure becomes salt sensitive; thus
[17:28] (Speaker) diuretics enhance the BP lowering effect of A II antagonists. This has been demonstrated in
[17:28] (Speaker) several clinical studies(11). A II receptor antagonists as a class have excellent tolerability
[17:28] (Speaker) profile with an incidence of side effects similar to that of placebo. Unlike the ACE inhibitors,
[17:28] (Speaker) they do not induce cough. The only interclass difference is the ability of Losartan to increase
[17:28] (Speaker) urinary uric acid excretion and lower plasma uric acid.
[17:28] (Speaker) Combining ACE inhibitors and A II receptor antagonists:
[17:28] (Speaker) Long term use of ACE inhibitors produces marked elevation of A I in the circulation because
[17:28] (Speaker) its conversion to A II is blocked . This excessively available A I is taken by the tissue
[17:28] (Speaker) enzymes and is converted to A II locally giving A II actions which by-pass the circulation ACE
[17:29] (Speaker) block. Therefore the use of A II receptor antagonists to block the effect of this local A II on the
[17:29] (Speaker) AT1 receptor can be complementary to the use of ACE inhibitors enhancing the hypotensive
[17:29] (Speaker) effect. In spite of this potential beneficial combination, the combined use of ACE inhibitors
[17:29] (Speaker) and A II receptor antagonists in the treatment of hypertension has not been thoroughly
[17:29] (Speaker) studied in well designed controlled trials. A preliminary study conducted on normotensive
[17:29] (Speaker) volunteers has suggested that combined administration of an ACE inhibitor and A II receptor
[17:29] (Speaker) antagonist induces an additional blood pressure reduction(11). On the other hand other
[17:29] (Speaker) therapeutic benefits of the combination of ACE inhibitors and A II receptor antagonists have
[17:29] (Speaker) been probed: in a pilot study on anterior myocardial infarction, the authors concluded that the
[17:29] (Speaker) addition of Losartan to Captopril improved the beneficial effects of ACE inhibition in patients
[17:29] (Speaker) with anterior myocardial infarction(12). The effect of the combination was also studied on
[17:29] (Speaker) proteinuria: the use of the combination produced more reduction in proteinuria than that
[17:30] (Speaker) which was effected by ACE inhibition or A II receptor antagonism alone. The main drawback
[17:30] (Speaker) of this study is the small number of patients(13).
[17:30] (Speaker) (B)Endothelin antagonists.
[17:30] (Speaker) The Endothelins encompass a family of three 21-amino acid isopeptides ET 1,2,3. The most
[17:30] (Speaker) important, Endothelin-1 (ET-1), is produced by endothelial, mesangial, glomerular epithelial
[17:30] (Speaker) and medullary collecting duct cells. The final step in the formation of ET-1 is the cleavage of
[17:30] (Speaker) Proendothelin (big ET) by an Endothelin-converting enzyme (ECE) (Fig1). ET-1 is the most
[17:30] (Speaker) potent endogenous vasoconstrictor yet identified: it is hundred times more potent than
[17:30] (Speaker) norepinephrine when compared on equimolar basis. It acts on two main receptors: ETa and
[17:30] (Speaker) ETb. Stimulation of the former receptor is responsible for the vasoconstrictive effect of ET-1,
[17:31] (Speaker) while ETb has a vasodilator effect conducted through stimulating the production of nitric
[17:31] (Speaker) oxide and prostaglandins. ET-1 is implicated in the pathogenesis of hypertension and its
[17:31] (Speaker) level was elevated in some of the studies on patients with essential hypertension(14). It was
[17:31] (Speaker) also found to contribute to increased vascular tone (15).
[17:31] (Speaker) Drugs against ET-1 have been developed with their actions mainly exerted at two sites: ET
[17:31] (Speaker) receptor and ECE.
[17:31] (Speaker) (i) ET receptor antagonist: the first member of this class is Bosentan, an orally
[17:31] (Speaker) administered blocker of both ETa and ETb receptors. Initial trials have shown it to be
[17:31] (Speaker) effective in lowering blood pressure(16). In a dose of 100 to 500 mg per day it was found to
[17:31] (Speaker) produce a blood pressure lowering effect equivalent to Enalapril 20mg per day. Doses of up
[17:31] (Speaker) to 2000 mg were well tolerated but contributed no additional therapeutic benefit. An
[17:32] (Speaker) additional advantage of Bosentan is the absence of reflex increase in heart rate,
[17:32] (Speaker) norepinephrine blood level, plasma renin activity or angiotensin II . This could have important
[17:32] (Speaker) useful implications in cardiovascular disease particularly in patients with heart failure(16,17).
[17:32] (Speaker) The main adverse effects were headache, flushing and lower limb oedema. No serious side
[17:32] (Speaker) effects were reported. New ET receptor antagonists are being developed, some of which
[17:32] (Speaker) like BQ-123 are specific to the ETa receptor which is likely to make them more potent
[17:32] (Speaker) hypotensive agents (Fig 2). ET antagonists are likely to create a new class of hypotensive
[17:32] (Speaker) drugs, which will widen the range of our armamentarium for the treatment of hypertension.
[17:32] (Speaker) (ii) ECE inhibitors: Phosphoramidon is the first ECE inhibitor but has other non-specific
[17:32] (Speaker) actions. More selective agents are being developed by a number of pharmaceutical firms.
[17:33] (Speaker) Genetics and Hypertension
[17:33] (Speaker) With the development in molecular biology, the field of genetics is progressing rapidly. Some
[17:33] (Speaker) developments are helping in the understanding of the pathophysiology and management of
[17:33] (Speaker) hypertension. Examples of such developments are:
[17:33] (Speaker) A.ACE Gene and I/D Polymorphism With DNA cloning it was possible to identify the
[17:33] (Speaker) structure of the ACE gene with 26 exons and spans 21 Kb on chromosome 17 (18). I/D
[17:33] (Speaker) polymorphism consists of the presence (Insertion -I-) or absence (Deletion - D -) of 287
[17:33] (Speaker) base pair fragments in intron 16 resulting in 3 genotypes: Insertion homozygotes (II),
[17:33] (Speaker) Insertion/Deletion heterozygotes (ID) and Deletion homozygotes (DD).
[17:33] (Speaker) II individuals have relatively low plasma concentrations of ACE compared to DD
[17:34] (Speaker) individuals who have high levels, while the heterozygotes ID have intermediate plasma
[17:34] (Speaker) ACE levels.
[17:34] (Speaker) The DD genotype has been linked to essential hypertension, left ventricular hypertrophy
[17:34] (Speaker) and development of nephropathy in insulin and non-insulin-dependent diabetes
[17:34] (Speaker) mellitus. It may also be a potential genetic marker in hypertensives at risk of renal
[17:34] (Speaker) complications (19) .
[17:34] (Speaker) Unlike the DD geneotype, which has good antiproteinuric response to ACE inhibitors,
[17:34] (Speaker) the II genotype response is limited. This could be explained by the fact that the II has
[17:34] (Speaker) naturally low plasma ACE levels allowing no significant drop with the use of ACE
[17:34] (Speaker) inhibitors.
[17:35] (Speaker)
[17:35] (Speaker) B.AT II Type 1 Receptor (AT1) Polymorphism
[17:35] (Speaker) Recently AT II type 1 receptor (AT1) polymorphism has been described in which there
[17:35] (Speaker) is either an adenine (A) or cytosine (C) base at position 1166 in the 3' untranslated
[17:35] (Speaker) region of the gene(20) according to which persons can be typed as AA or AC/CC.
[17:35] (Speaker) Recent studies have suggested a predictive value of those types to the effect of AT II
[17:35] (Speaker) receptor antagonists. Losartan was found to increase the GFR and lower the mean
[17:35] (Speaker) arterial pressure in the AC/AA group but did not influence these parameters in the AA
[17:35] (Speaker) group(21).
[17:35] (Speaker) Conclusion
[17:36] (Speaker) Trends have changed concerning the definition of hypertension, the levels of blood pressure
[17:36] (Speaker) at which treatment should be started and the target levels of treatment. Associated risk
[17:36] (Speaker) factors are given more weight in the management of patients with hypertension emphasizing
[17:36] (Speaker) the importance of multifactorial aetiology in the production of cerebro- and cardiovascular
[17:36] (Speaker) disease. The effort to introduce newer classes of drugs for the treatment of hypertension
[17:36] (Speaker) continues giving physicians more options as far as efficacy and avoidance of adverse
[17:36] (Speaker) effects are concerned.
[17:36] (Speaker) With the developments in molecular biology the field of genetics is rapidly progressing which
[17:36] (Speaker) may help in understanding the pathophysiology and in the management of hypertension
[17:37] (Speaker) 4 that is all!!
[17:37] (MJesus) 4 thank ypu very much, Dr. Abboud!!
[17:37] (JBover) geee.......JUST GREAT!!!!!
[17:37] (Enrique) very good presentation, congratulations Dr. Abboud!
[17:37] (gerardo) Thank dr aabboud
[17:38] (JBover) you couldnt say more in such a short presentation!
[17:38] (JBover) may I ask a question???
[17:38] (Abboud) Thanks to you
[17:38] (MJesus) I'm have a difficult question.....
[17:38] (Abboud) sure
[17:39] (Abboud) I will try to answer
[17:39] (JBover) other important effects related to ACE inhibitors and AII blockers are related to their action on TGF-B production.....
[17:39] (JBover) are you aware of any comparative data between them in this regard???
[17:39] (MJesus) Dr.Abboud.... como hace para poder llegar a todo.. ahora aqui dando una confernecia y dentro de pocas horas volando a Marruecos?
[17:40] (Abboud) no I am not aware of any comparative studies
[17:40] * JBover will translate later MJesus question
[17:40] (JBover) :-)
[17:41] (JBover) Mjesus asked how do you manage to be EVERYWHERE...now here with us and in Morocco in a few hours!!!!!!
[17:41] (JBover) THAT IS A DIFFICULT ONE!!!!!
[17:41] (Abboud) this secret cannot be released
[17:42] (perico) may I have a question?
[17:42] (gerardo) What is you opinion about the use the ARAll in diabetic nephropaty.
[17:42] (Abboud) I think they are as effective as...
[17:43] (Abboud) ACE inhibitors
[17:43] (gerardo) thanks
[17:43] (Abboud) One addition could be..
[17:43] (Abboud) that they could be used in hypotensive patients..
[17:43] (Abboud) because they may reduce the proteinuria..
[17:44] (Abboud) without much further drop..
[17:44] (Abboud) in the BP...
[17:45] (perico) do you think that the association of ACE and ARA II is dangerous?, for instance with potassium level in diabetics or in patients with some grade of renal failure
[17:45] (Abboud) yes I think in such patients..
[17:46] (Abboud) the combination could be dangerous..
[17:46] (Abboud) many times something...
[17:46] (Abboud) that appear logical may not turnout to be so...
[17:46] (Abboud) when are actually tried.
[17:47] (Abboud) There is very little literature..
[17:47] (Abboud) on the combination..
[17:47] (Abboud) and none on patients with renal impairment
[17:47] (Abboud) I suppose this could be tried with great care
[17:48] (MJesus) abboud ?
[17:49] (Abboud) yes
[17:49] (MJesus) ok... I supose you are off side by lag
[17:50] (Abboud) I suppose if there are no further comments or questions
[17:50] (gerardo) the antagonist ET have they some efect about LVH?
[17:50] (Abboud) This has not been studied yet...
[17:51] (Abboud) the main studies are on hypertension
[17:51] (Abboud) and I suppose that it needs time..
[17:51] (Abboud) to see the effect on LVH
[17:52] (MJesus) please.... when your question/answer finished, writte *
[17:53] (MJesus) gerardo, more question?
[17:53] (gerardo) thanks
[17:53] (JBover) is there any advantage between ACE inhibitors or AII blockers for the treatment of cardiac failure?
[17:54] (JBover) which is a bit different than prevention of LVH***
[17:54] (Abboud) No the effect is the same..
[17:54] (JBover>I amost forgot the ****
[17:54] (Abboud) thus the main advantage will be...
[17:55] (Abboud) in those patients who cannot tolerate..
[17:55] (Abboud) the ACEI because of cough or other side effects...
[17:56] (Abboud) but the combination could have an addtive ...
[17:56] (Abboud) advantageous effect. Finished
[17:56] (JBover) I still do not understand why AII blockers are better tolerated in hypotensive patients...maybe I missed the point or I misunderstood***
[17:57] (Abboud) A study on Losartan..
[17:57] (Abboud) showed that it can produce lowering...
[17:58] (Abboud) in protienuria with a smaller dose when compared to Enalapril
[17:58] (Abboud) at this dose the effect on..
[17:58] (Abboud) protienuria is the same as enalapril..
[17:58] (Abboud) but the effect on the BP is less. Finished
[17:59] (JBover) shall we talk a bit about hypertensive CRISIS??? not emergencies what drugs can we use?? any new approaches but avoiding nifedipine????***
[18:00] (Abboud) Yes I suppose nifedipine , the short acting, is abandoned by most..
[18:00] (Abboud) because of the preciptous drop in BP and the short action.
[18:01] (Abboud) I suppose still drugs like Na nitroprusside hold fort because of its titratable effect and short action when stopped
[18:01] (JBover) what do you use in CRISIS???***
[18:03] (Abboud) I use nitroprusside and if there is contrindication I use hydaralaizine and occasionally labetolol
[18:03] (Abboud) What is your view on that?
[18:04] (JBover) welll....that's a major drug! maybe more for EMERGENCIES ...do you treat in the emergency room Hypertensive patients with remarkable blood pressure (i.e. 200/130) if they only have headache? whta do you use in the ER???
[18:05] (JBover) I like labetalol a lot for some emergencies before nitroprussiate....fenoldopam is also used in my hospital....anesthesiologists like Uropidil
[18:05] (JBover) Nitroprusiate has that cumbersome effect of accumulation of metabolites
[18:07] (Abboud) I agree about nitroprusside and is thus useful for short term and if there is no renal impairment
[18:07] (MJesus) do you use polymorphisms to take any clinical decission??***
[18:07] (Abboud) Maria , no we don't use the polymorphism..
[18:07] (Abboud) yet for taking decisions..
[18:08] (Abboud) it is not readily..
[18:08] (Abboud) available but I suppose it may..
[18:08] (Abboud) not be long before it could be of benefit
[18:09] (Abboud) ..I suppose here there could be an economic.
[18:09] (JBover) Dr Abboud...are you tired????? you gotta know that we would be talking with you FOR AGES!!!!!!!!
[18:09] (Abboud) factor and it will continue for some time..
[18:09] (Abboud) to be cheaper to try the drug clinically first,. Finished
[18:10] (JBover) you should stop us whenever you feel like or it is getting late for you!!!!!!
[18:10] (Abboud) Yes I would be grateful..
[18:10] (gerardo) Dr abboud thanks
[18:10] (Abboud) if you could execuse me..
[18:10] (JBover) Dr Abboud THANK YOU VERY MUCH FOR YOUR PATIENCE!!!!!!!!
[18:10] (Abboud) now because I have to catch..
[18:10] (Abboud) my flight to Morocco
[18:11] (MJesus) thank you very much!!
[18:11] (Abboud) i did enjoy this and thank you
[18:11] (JBover) THANK YOU VERY MUCH for helping us with this new venue!!!!!!!
[18:11] (JBover) watch out with water!!!!!!!!
[18:11] (Abboud) I will tell the colleagues in Morocco
[18:11] (Abboud) about this congress
[18:12] (Abboud) Best regards
[18:12] * JBover stands up and keeps on clapping
[18:12] (Abboud) Thanks
[18:12] (JBover) have a good flight!!!!!!!!!!!!!
[18:12] (MJesus) yes.. we need more diffusion in Marocco and in all around th eworld