PakMediNet Discussion Forum : Medicine : about atenolol
12
can some one help me wt the max dose of atenolol (tenormin)u can give to a patient of HTN i knw abt 100 mg od but can u raise dose if his bp is not showing good control
Posted by: ali98029Posts: 9 :: 30-03-2008 ::
I don't think that raising atenolol will help much. There is very little additional benefit you will get by even doubling its dose. Try adding another medication to atenolol such as cholorthalidone or hydrochlorthiazide 25 mg daily (if patients is not already taking thiazides).
Posted by: rqayyumPosts: 199 :: 31-03-2008 ::
Why not ACE inhibitors (having more benefits) rather than thiazide diuretics (having more side effects)?
Posted by: imtiazkPosts: 56 :: 13-04-2008 ::
According to JNC 7
"Thiazide-type diuretics should be used as initial therapy for most patients with hypertension, either alone or in combination with one of the other classes(ACEIs, ARBs, BBs, CCBs)...."
For details read JNC 7 which can be accesssed at http://www.nhlbi.nih.gov/guidelines/hypertension/index.htm
Posted by: rqayyumPosts: 199 :: 14-04-2008 ::
This is an old concept NOT the new one!
Posted by: imtiazkPosts: 56 :: 14-04-2008 ::
JNC 8 is still in preperation and considering the evidence, I don't think that they will change this recommendation.
I would also humbly mention that new concepts don't necessarily save patients' lives. There are several recent examples in medical literature to support this statement.
Posted by: rqayyumPosts: 199 :: 15-04-2008 ::
quote:
There are several recent examples in medical literature to support this statement.
Posted by: imtiazkPosts: 56 :: 15-04-2008 ::
My above statement is for 'new concepts' in general and not for ACE inhibitors. Developing a habit of reading leading medical journals (such as JAMA, NEJM, Lancet, Annals of Internal Medicine) regularly is likely to help in answering questions in your mind.
I will be glad to hear randomized controlled trials enrolling hypertensive patients (not specific subpopulations) which found ACE inhibitors superior to a thiazide diuretics in improving clinical outcomes.
To have a meaningful discussion and support my point, I will direct you to ALLHAT trial, main results were published in JAMA in 2002, issue 288, pages 2981-2997.
Posted by: rqayyumPosts: 199 :: 15-04-2008 ::
This is not the answer of my question rather to conceal it by the method shown.
Posted by: imtiazkPosts: 56 :: 15-04-2008 ::
Be upto date. Your understanding is almost obsolete.
Posted by: imtiazkPosts: 56 :: 19-04-2008 ::
I really don't know what do you mean by suggesting me to be uptodate or that my understanding is obsolete. I referred you to the most recent recommendations (JNC 7) and to the largest comparative trial of antihypertensives (ALLHAT). Would you like to share your 'up to date' knowledge (please provide reference - don't come up with something out of thin air).
The most recent guidelines published on hypertension are by AHA (these are on resistant hypertension) and there too the first class of durg that is discussed (and the only which is discussed at any length) is diuretics. These guidelines are scheduled to be published in June 2008 but are available online at
http://hyper.ahajournals.org/cgi/reprint/HYPERTENSIONAHA.108.189141
Now are these guidelines also obsolete?
Posted by: rqayyumPosts: 199 :: 19-04-2008 ::
Why have you switched on from non-resistant hypertension to the resistant one?
JNC 8 will surely and definitly DO make your concept null and void.
Posted by: imtiazkPosts: 56 :: 21-04-2008 ::
you are not quoting any evidence, just hoping for something to happen to support your point. Why do you think that JNC 8 will reach to a different conclusion. Can you quote any evidence in your support
Posted by: rqayyumPosts: 199 :: 21-04-2008 ::
quote:
Can you quote any evidence in your support.
Posted by: imtiazkPosts: 56 :: 22-04-2008 ::
Thank you, now at least I know you what are the bases of your opinion. Just to remind you, we were talking about the comparison of ACE inhibitors with diuretics, more specifically thiazide diuretics. We are not talking about whether ACE inhibitors are good or not. If any doubt, please see first few posts in this thread again.
Here are the reasons why I think that these articles don’t support what you are saying:
1. First article by Anderson: it is an editorial, not a randomized trial. In addition, this editorial does not even talk about diuretics or thiazides. This article was an editorial commentary to another article published in the same issue of JACC. Here, I will also point out that editorials are opinions of experts and not considered evidence. Clinical evidence are clinical trials, preferably randomized clinical trials. Therefore, if you allow, we can remove this article from the list of your references. For correction of your reference and others who may want to look at this article, this was published in 2003 and not in 2007.
2. Regarding second article by Kaski et al, let me first say that this was not published in 2006 as you have referenced but in 1994. (I am not sure from where you are getting your references that your years keep messing up). This was a crossover randomized trial on TEN patients in which enalapril was compared to PLACEBO (not a thiazide). Outcome in this trial was decrease in exercise–induced ishchemia in patients with syndrome X (patients with angina pectoris, positive exercise stress test, but normal coronaries on angiogram). This study found that total exercise duration and time to 1-mm ST segment depression were prolonged by enalapril as compared to placebo. However, there was no statistical difference in the number of patients who had ischemia when given enalapril as compared to when given placebo. However, this study is also irrelevant to our discussion as it did not compare ACE inhibitors with thiazides. Therefore, we should remove this also from the list of your references.
3. Well your third reference is also incorrect. It is so incorrect that I can’t find the article you want to cite. The article published by Morice et al in NEJM in the Jun 6, 2006 issue was related to drug eluting stents. Here is the correct reference to this article. [Morice MC, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin M, Colombo A, Schuler G, Barragan P, Guagliumi G, Molnàr F, Falotico R; RAVEL Study Group. Randomized Study with the Sirolimus-Coated Bx Velocity Balloon-Expandable Stent in the Treatment of Patients with de Novo Native Coronary Artery Lesions. A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularization. N Engl J Med. 2002;346:1773-80.]. - Can you provide me with correct reference?
4. Again year is incorrect in your 4rth reference (Yusuf et al). Correct year is 2000 and not 2005. You are referring to HOPE trial. This trial was a comparison of rampril with PLACEBO (not thiazide). This trial also does not answer the question which was comparison of thiazide with ACE inhibitors and not ACE Inhibitors versus placebo. Allow me to remove this trial also from your reference list as it does not answer our main question which was comparison of ACE I with thiazides.
5. There again, you got year incorrectly, correct year of publication of this study is 1991 not 2004 as you have written. Again this study does not compare ACE inhibitors with thiazides and is not relevant to the question we are trying to explore.
As you can see from my above comments, none of the studies you have quoted answer the question which initiated this discussion, which was comparison of ACE I with thiazides. Do you have any references to randomized clinical trials that compare ACE I with thiazides, I will be glad to hear. If not, then listen what JNC 7 has to say (link given above).
Posted by: rqayyumPosts: 199 :: 23-04-2008 ::
Provide the EVIDENCE to defend yourself, so far as your detailed reply is concerned!
Note plz, Not the every material is available on net. In a country like USA, if the journals are not available, Give your postal address, I will send you the copies for free.
Posted by: imtiazkPosts: 56 :: 23-04-2008 ::
It is you who need to provide evidence. If you think that JNC 7 is obsolete, or another trial has better and more uptodate evidence than ALLHAT, provide evidence. And if you can't provide evidence, then either agree what JNC 7 has to say or keep quite.
You don't need to tell me that you have access to more journals than me (without knowing limits of my access) while your references are wrong and incorrect. If you enter your references in PubMed (provided you know how to use it) you will find out that your references are incorrect (exactly the same way I have said) and you can put your money to some better use.
Posted by: rqayyumPosts: 199 :: 23-04-2008 ::
Of course, the best use of your money will be to use it for your own education.
Did you check your references on PubMed? or should I ask; do you know how to use PubMed?
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
By the way why are you reluctant to receive the ORIGINAL COPIES of the references for free? What does it mean?
Posted by: imtiazkPosts: 56 :: 24-04-2008 ::
I am not reluctant, I have seen all these articles that you have referenced to except the one whose reference is so incorrect that I can't even find it.
My above detailed posting addresses those articles. Now if you think that I was reading different articles, then say so.
If you are so much dying to send me articles, scan those articles and e-mail me, that will be cheaper. You can use rest of the money for your education (remember, religious duty!).
Still if you want to keep insisting on sending me articles that you yourself have not read (otherwise how can you give wrong references and still insist on those references being correct), you are more than welcome to send to the following address.
Rehan Qayyum, MD
Assistant Professor of Medicine
Johns Hopkins School of Medicine
600 North Wolfe Street, 307-A
Baltimore, MD 21287, USA
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
And for the benefit of those who are following this discussion, I am posting abstracts of articles (when such abstracts are available) here one by one. These are the same abstracts that get published with the article without changing any word.
1: J Am Coll Cardiol. 1994 Mar 1;23(3):652-7.
Effects of angiotensin-converting enzyme inhibition on exercise-induced angina
and ST segment depression in patients with microvascular angina.
Kaski JC, Rosano G, Gavrielides S, Chen L.
Department of Cardiological Sciences, St. George's Hospital Medical School,
London, England, United Kingdom.
OBJECTIVES. This study was conducted to test the hypothesis that
angiotensin-converting enzyme inhibition may lessen myocardial ischemia in
patients with microvascular angina. BACKGROUND. Patients with syndrome X (angina
pectoris, positive findings on exercise testing and normal coronary arteriogram)
have a reduced coronary vasodilator reserve ("microvascular angina" ) and may show
an increased sympathetic drive. Angiotensin-converting enzyme inhibition
attenuates sympathetic coronary vasoconstriction in patients with coronary artery
disease. METHODS. Ten patients (seven women and three men, mean age [+/- SD] 53
+/- 6 years) with syndrome X and a reduced coronary flow reserve underwent a
randomized, single-blind, crossover, placebo-controlled study of the effects of
the angiotensin-converting enzyme inhibitor enalapril on angina and
exercise-induced ST segment depression. Assessment was by symptom-limited
treadmill exercise testing after 2 weeks of treatment with 10 mg/day of enalapril
and after 2 weeks of placebo administration. RESULTS. All patients had positive
findings on exercise testing (> or = 1 mm ST segment depression and angina) while
taking placebo, whereas six patients had a positive test result (four with
angina) during enalapril therapy. Total exercise duration and time to 1 mm of ST
segment depression were prolonged by enalapril over those obtained with placebo
(mean 779 +/- 141 vs. 690 +/- 148 s, p = 0.006 and 690 +/- 204 vs. 485 +/- 241 s,
p = 0.007, respectively). The magnitude of ST segment depression was also less
with enalapril than with placebo (mean 1.1 +/- 0.4 vs. 1.5 +/- 0.2 mm, p =
0.004). Heart rate and blood pressure at peak exercise and at 1 mm of ST
depression were not significantly different during placebo and enalapril
treatment. CONCLUSIONS. Angiotensin-converting enzyme inhibition lessens
exercise-induced ischemia in patients with syndrome X and microvascular angina,
probably by a direct modulation of coronary microvascular tone, which results in
an increased myocardial oxygen supply.
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
Here is your next reference:
1: N Engl J Med. 2002 Jun 6;346(23):1773-80.
A randomized comparison of a sirolimus-eluting stent with a standard stent for
coronary revascularization.
Morice MC, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin M, Colombo A,
Schuler G, Barragan P, Guagliumi G, Molnàr F, Falotico R; RAVEL Study Group.
Randomized Study with the Sirolimus-Coated Bx Velocity Balloon-Expandable Stent
in the Treatment of Patients with de Novo Native Coronary Artery Lesions.
Institut Cardiovasculaire Paris Sud, Massy, France.
BACKGROUND: The need for repeated treatment of restenosis of a treated vessel
remains the main limitation of percutaneous coronary revascularization. Because
sirolimus (rapamycin) inhibits the proliferation of lymphocytes and smooth-muscle
cells, we compared a sirolimus-eluting stent with a standard uncoated stent in
patients with angina pectoris. METHODS: We performed a randomized, double-blind
trial to compare the two types of stents for revascularization of single, primary
lesions in native coronary arteries. The trial included 238 patients at 19
medical centers. The primary end point was in-stent late luminal loss (the
difference between the minimal luminal diameter immediately after the procedure
and the diameter at six months). Secondary end points included the percentage of
in-stent stenosis of the luminal diameter and the rate of restenosis (luminal
narrowing of 50 percent or more). We also analyzed a composite clinical end point
consisting of death, myocardial infarction, and percutaneous or surgical
revascularization at 1, 6, and 12 months. RESULTS: At six months, the degree of
neointimal proliferation, manifested as the mean (+/-SD) late luminal loss, was
significantly lower in the sirolimus-stent group (-0.01+/-0.33 mm) than in the
standard-stent group (0.80+/-0.53 mm, P<0.001). None of the patients in the
sirolimus-stent group, as compared with 26.6 percent of those in the
standard-stent group, had restenosis of 50 percent or more of the luminal
diameter (P<0.001). There were no episodes of stent thrombosis. During a
follow-up period of up to one year, the overall rate of major cardiac events was
5.8 percent in the sirolimus-stent group and 28.8 percent in the standard-stent
group (P<0.001). The difference was due entirely to a higher rate of
revascularization of the target vessel in the standard-stent group. CONCLUSIONS:
As compared with a standard coronary stent, a sirolimus-eluting stent shows
considerable promise for the prevention of neointimal proliferation, restenosis,
and associated clinical events.
--> As you can see, the page numbers, authors and journal, volume number, and issue number are all the same but the title is different.
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
Here is the abstract of the next reference:
1: N Engl J Med. 2000 Jan 20;342(3):145-53.
Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on
cardiovascular events in high-risk patients. The Heart Outcomes Prevention
Evaluation Study Investigators.
Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G.
Canadian Cardiovascular Collaboration Project Office, Hamilton General Hospital,
McMaster University, ON. hope@ccc.mcmaster.ca
BACKGROUND: Angiotensin-converting-enzyme inhibitors improve the outcome among
patients with left ventricular dysfunction, whether or not they have heart
failure. We assessed the role of an angiotensin-converting-enzyme inhibitor,
ramipril, in patients who were at high risk for cardiovascular events but who did
not have left ventricular dysfunction or heart failure. METHODS: A total of 9297
high-risk patients (55 years of age or older) who had evidence of vascular
disease or diabetes plus one other cardiovascular risk factor and who were not
known to have a low ejection fraction or heart failure were randomly assigned to
receive ramipril (10 mg once per day orally) or matching placebo for a mean of
five years. The primary outcome was a composite of myocardial infarction, stroke,
or death from cardiovascular causes. The trial was a two-by-two factorial study
evaluating both ramipril and vitamin E. The effects of vitamin E are reported in
a companion paper. RESULTS: A total of 651 patients who were assigned to receive
ramipril (14.0 percent) reached the primary end point, as compared with 826
patients who were assigned to receive placebo (17.8 percent) (relative risk,
0.78; 95 percent confidence interval, 0.70 to 0.86; P<0.001). Treatment with
ramipril reduced the rates of death from cardiovascular causes (6.1 percent, as
compared with 8.1 percent in the placebo group; relative risk, 0.74; P<0.001),
myocardial infarction (9.9 percent vs. 12.3 percent; relative risk, 0.80;
P<0.001), stroke (3.4 percent vs. 4.9 percent; relative risk, 0.68; P<0.001),
death from any cause (10.4 percent vs. 12.2 percent; relative risk, 0.84;
P=0.005), revascularization procedures (16.3 percent vs. 18.8 percent; relative
risk, 0.85; P<0.001), cardiac arrest (0.8 percent vs. 1.3 percent; relative risk,
0.62; P=0.02), [corrected] heart failure (9.1 percent vs. 11.6 percent; relative
risk, 0.77; P<0.001), and complications related to diabetes (6.4 percent vs. 7.6
percent; relative risk, 0.84; P=0.03). CONCLUSIONS: Ramipril significantly
reduces the rates of death, myocardial infarction, and stroke in a broad range of
high-risk patients who are not known to have a low ejection fraction or heart
failure.
--> Here again, you will find my comments in an earlier post on this page correct.
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
Here is your last reference (your first reference is editorial and as you know (may be you don't know) editorials don't have structured abstracts)
1: N Engl J Med. 1991 Apr 18;324(16):1098-104.
Association of the renin-sodium profile with the risk of myocardial infarction in
patients with hypertension.
Alderman MH, Madhavan S, Ooi WL, Cohen H, Sealey JE, Laragh JH.
Department of Epidemiology and Social Medicine, Albert Einstein College of
Medicine, Bronx, N.Y. 10461-1602.
BACKGROUND. To test the prognostic value of plasma renin activity prospectively,
we determined the pretreatment renin-sodium profile of 1717 subjects with
mild-to-moderate hypertension (mean age, 53 years; 36 percent white; 67 percent
men) in a systematic work-site treatment program. METHODS. Renin profiles,
obtained by plotting plasma renin activity against the urinary excretion of
sodium, were classified as high (12 percent of the subjects), normal (56
percent), and low (32 percent), and there were expected variations according to
age, sex, and race. Modified stepped-care treatment for hypertension, prescribed
without reference to the renin profile, was similar in the three renin groups.
RESULTS. Mean (+/- SD) blood pressure at entry was 151 +/- 19/100 +/- 10 mm Hg in
the subjects with a high renin profile, 151 +/- 19/97 +/- 10 mm Hg in those with
a normal profile, and 151 +/- 20/96 +/- 11 mm Hg in those with a low profile.
During 8.3 years of follow-up, there were 27 myocardial infarctions. As adjusted
for age, sex, and race, the incidence of myocardial infarction per 1000
person-years was 14.7 among the subjects with a high renin profile, 5.6 among
those with a normal profile, and 2.8 among those with a low profile (rate ratio
for high vs. low, 5.3; 95 percent confidence interval, 3.4 to 8.3). The rate of
mortality from all causes was 9.3 in the high-profile group, 5.3 in the
normal-profile group, and 3.9 in the low-profile group. The independent
association of a high renin profile with myocardial infarction (but not with
stroke or noncardiovascular events) was affirmed by Cox analyses (rate ratio for
high vs. normal plus low, 3.2; 95 percent confidence interval, 1.2 to 8.4) after
adjustment for race, sex, age at entry, serum cholesterol level, smoking status,
electrocardiographic evidence of left ventricular hypertrophy, blood glucose
level, body-mass index, history of cardiovascular disease or treatment, blood
pressure, and use of beta-blockers. CONCLUSIONS. In the study population, whose
blood pressure before and during treatment was in a narrow range, and after other
cardiovascular risk factors had been considered, the renin profile before
treatment remained independently associated with the subsequent risk of
myocardial infarction.
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
Now ball is in your court, either accept that your references are incorrect (see my above postings of abstracts of your referenced articles) and provide correct references (this is what an honest person will do) or keep on talking irrelevant or incorrect stuff while trying to mislead others from the current state of evidence.
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
And just to remind you about your references, I have copy-pasted below from your earlier posting:
Anderson HV: Angiotensin-converting enzyme inhibitors: J Am Coll Cardiol 2007 Dec 17; 42(12): 2060-2
Kaski JC, Rosano G, Gavrielides S, Chen L: Effects of angiotensin-converting enzyme inhibitors on various types of hypertension. J Am Coll Cardiol 2006 Mar 1; 23(3): 652-7.
Morice MC, Serruys PW, Sousa JE, et al: A randomized trials of ACE inhibitors and diuretics in the treatment of hypertension: N Engl J Med 2006 Jun 6; 346(23): 1773-80.
Yusuf S, Sleight P, Pogue J, et al: Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med 2005 Jan 20; 342(3): 145-53.
Alderman MH, Madhavan S, Ooi WL, Cohen H, Sealey JE, Laragh JH. Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension. N Engl J Med. Apr 18 2004;324(16):1098-104.
Posted by: rqayyumPosts: 199 :: 24-04-2008 ::
If you are still not satisfied, do go through these references to get your ideas quite null and void.
1. Massaglia G, Mantovani LG, Sturkenboom MCJM, Filippi A, Trifiro G, Cricelli C, Brignoli O, Caputi AP. Patterns of persistence with antihypertensive medications in newly diagnosed hypertensive patients: a retrospective study in primary care. J Hypertens. 2005; 23:2093–2100.
2. Pierdomenico SD, Lapenna D, Bucci A, Di Tommaso R, Di Mascio R, Manente BM, Caldarella MP, Neri M, Cuccurullo F, Mezzetti A. Cardiovasular outcome in treated hypertensive patients with responder, masked, false resistant, and true resistant hypertension. Am J Hypertens. 2005;18:1422–1428.
3. Stergiou GS, Makris T, Papavasiliou M, Efstathiou S, Manolis A. Comparison of antihypertensive effects of an angiotensin-converting enzyme inhibitor and diuretics. J Hypertens. 2005;23:883– 889.
4. Sharma J, Das T, Solangi, S. A prospective study of outcome of monotherapy vs polytherapy in various groups of hypertentions. J. Medol. 2007; Vol,13: 451– 67.
Certainly, YOU are more than one hundred percent WRONG, if you dare to decide (for nothing) without going through original copies of the articles and the references. Isn’t it?
Why should anyone rely on your presented stuff taken from various unauthenticated sites while anyone has the original copies of the articles and the reference? Isn’t it? Latest available relevant books/journals and the other related literature would surely do reject and refute your mediaeval approach.
[Edited by docosama on 03-05-2008 at 08:44 AM GMT]
Posted by: imtiazkPosts: 56 :: 29-04-2008 ::
There you go again; instead of providing correct references you are providing more references. Have you seen full-text articles of your previous references or these references? If you have then why not you post result sections of each of these articles on this site so that everyone can read it.
The first study that you quoted; its first author’s name is not Massaglia as you have written above but rather Mazzaglia. It is a retrospective chart review. This can’t be equated with a randomized controlled trial. (Do you know the difference between the two?) Moreover, it did not look at clinical outcomes such as death, myocardial infarction, and stroke.
Your second study is also not a randomized controlled trial. Moreover, it did not compare diuretics with ACE inhibitors
Your third study did not report on clinical outcomes (such as mortality, myocardial infarction, and stroke). But its results are supportive of my argument. In results it says “The additional effects of amlodipine and chlorthalidone added to valsartan were approximately 6/3.5 mmHg (P < 0.05) greater than that of benazepril.” And it concludes with a statement “The antihypertensive effects of the ARB-diuretic and the ARB-calcium antagonist combinations were superior to that of the ARB-ACE inhibitor combination.” To remind you, this study does not answer question that we were discussing. In this study all patients got valsartan, and then some got diuretic and other ACE inhibitor. Those who got diuretic did better.
What is the name of the journal from which you referenced your fourth article? Can you provide its name?
If you think that PubMed is an ‘unauthenticated site’, then you are making fun of yourself.
Anyway! Note the above challenge, post the result sections of all your references on this site for everyone to view and then judge.
Posted by: rqayyumPosts: 199 :: 29-04-2008 ::
quote:
Have you seen full-text articles of your previous references or these references?
Posted by: imtiazkPosts: 56 :: 29-04-2008 ::