Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Expanding the horizons in secondary prevention of stroke and transient ischaemic attacks
- Sumantra Ray, Alexander SF Doney and Ronald S MacWalter (11 February 2004)
-
PROGRESS is about reducing blood pressure not promoting drugs.
- Martin G Duerden (12 February 2004)
-
Secondary prevention after stroke and TIA
- Richard M Darling (18 February 2004)
-
STROKE DISTINCTIONS ARBITRARY
- DR. MANJUNATH P DESAI (19 February 2004)
|
|
|||
|
Sumantra Ray, Clinical Research Fellow & Honorary Clinical Teacher Stroke Studies Centre, Ninewells Hospital & Medical School, University of Dundee DD1 9SY, Alexander SF Doney and Ronald S MacWalter
Send response to journal:
|
Dear Editor, An acute stroke or transient ischaemic attack (TIA) are real emergencies and a wealth of data is now emerging regarding secondary prevention. Dr KW Muir has presented recently accrued evidence, demonstrating that reduction of blood pressure and cholesterol levels, regardless of baseline values, have an unequivocal benefit in secondary prevention of strokes and TIAs. There are also other pertinent areas in secondary prevention that merit attention. It is important to realise that there is no real boundary between acute treatment and secondary prevention therapy. Secondary prevention should start as early as possible and this is best done in an acute stroke unit. Such units dedicated to stroke care, enhance the multidisciplinary approach and minimise lag time, leading to a better recovery after an acute stroke.(1) There is increasing evidence that high blood glucose is detrimental after an acute stroke. A blood glucose level of 10 mmol/l and higher suggests that an insulin regime may be needed. Although the exact underlying mechanisms still remain unclear, there is an evidence base which clearly demonstrates clinical worsening in stroke patients with hyperglycaemia. There is also evidence to show that the risk of a second stroke greatly increases with poor long term control.(2),(3),(4),(5) Non-fasting total homocysteine is another independent risk factor for stroke in men and women aged 60 years or older. Screening for elevated homocysteine levels and folate therapy may thus play an important part in secondary prevention of stroke, as levels above 14 µmol/L are associated with an 80% increased risk of total stroke.(6), (7) However, reducing homocysteine levels have not shown a convincing effect till date and further data is required in this area. Although there are significant resource implications associated with the possible over diagnosis of TIAs in the community as suggested by Dr KW Muir, it must also be pointed out that the estimated risk of a stroke after a TIA or minor stroke is 8-12 % at 7 days and 11-15 % at 1 month. (8) Thus for stroke prevention to be effective, public education is needed to seek urgent medical attention and better organisation of stroke services is also required so that all patients with a suspected TIA or minor stroke are seen immediately and receive appropriate secondary prevention at the earliest opportunity.(8) However, Further research is essential to clearly define which interventions or combinations thereof, offer maximum benefit in the secondary prevention of stroke and TIA. Yours Sincerely, Dr S Ray; Clinical Research Fellow, Dr ASF Doney; SpR and Dr RS MacWalter; Consultant Physician Stroke Studies Centre, The Institute of Cardiovascular Research, Division of Medicine & Therapeutics Ninewells Hospital & Medical School, University of Dundee, Scotland DD1 9SY References: 1) MacWalter RS, Shirley CP: Managing Strokes and TIAs in Practice. Royal Society of Medicine 2003. 2) Bruno A, Biller J, Adams HP Jr et al: Acute blood glucose level and outcome from ischaemic stroke. Trial of ORG 10172 in acute stroke treatment (TOAST) investigators. Neurology 1999; 52:280-284. 3) Bruno A, Levine SR, Frankel MR et al: Admission glucose level and clinical outcomes in the NINDS rtPA stroke trial. Neurology 2002; 59: 669- 674. 4) Weir CJ, Murray GD, Dyker AG, Lees KR. Is hyperglycaemia an independent predictor of poor outcome after an acute stroke? Results of a long term follow up study. BMJ 1997; 314 1303-1306. 5) Pulsinelli WA, Levy DE, Sigsbee B, Scherer P, Plum F: Increased damage after ischemic stroke in patients with hyperglycemia with or without established diabetes mellitus. Am J Med 1983;74:540-544. 6) AG Bostom et al. Nonfasting plasma total homocysteine levels and stroke incidence in elderly persons: The Framingham Study. Annals of Internal Medicine 1999 131: 352-355. 7) Clarke R et al. Homocysteine Studies collaboration. Homocysteine and risk of coronary heart disease and stroke. Homocysteine Metabolism, 3rd International Conference 1-5 July 2001. Abstract 109. 8) AJ Coull, JK Lovett, PM Rothwell: Population based study of early risk of stroke after transient ischaemic attack or minor stroke - implications for public education and organisation of services. BMJ, Feb 2004; 328: 326 - 0. Competing interests: None declared |
|||
|
|
|||
|
Martin G Duerden, General Practitioner Meddygfa Gyffin, Conwy, LL32 8LT
Send response to journal:
|
Editor – The editorial by Muir on secondary prevention for stroke and transient ischaemic attack (TIA)[1] seems biased in favour of implementing the results of the Perindopril Protection against Recurrent Stroke Study (PROGRESS) by promoting the combination of perindopril and indapamide as preferred agents. Is this justified? There are a wealth of blood pressure studies exploring which drugs work best, a comparison not made in PROGRESS. Putting all of these together suggests that blood pressure lowering is the most important effect rather than drug choice[2]. Occasionally an individual drug has caused some concerns – doxazosin, for example[3]. Of late the role of thiazides as a class has come to the fore as drugs of first choice because they appear safe and well-tolerated, and in particular reduce stroke risk[4]. Muir states that several factors favour the PROGRESS regimen. Firstly, the combination was well tolerated. This is all very well but what evidence is provided concerning the tolerability of other agents? Without making some comparison this seems a sweeping conclusion. Secondly, Muir says that dose titration of perindopril is rapid and simpler than other ACE inhibitors. As far as I am aware there is no evidence to support this assertion as relevant to hypertension. It may be an advantage of perindopril used in heart failure, but even that point is debatable. Thirdly, the claim is made that perindopril may reduce blood pressure without impairing global cerebral blood flow, even in patients with moderate to severe carotid stenosis. Where is the evidence on how this compares with other drugs? The final claim (unreferenced) is that indapamide differs pharmacologically from other thiazides, with less propensity for adverse metabolic effects and some vasodilating actions. I would also like to see robust evidence supporting this statement. An equally valid alternative interpretation of PROGRESS, pointed out in a subsequent letter[5], is that perindopril was an inactive component, and all benefit could be attributed to the thiazide, indapamide. This fits with other studies supporting use of thiazide, such as ALLHAT[6]. Possibly because of inadequacy in the PROGRESS trial design, which allowed physician choice of using perindopril alone, or combined with indapamide, according to their assessment of risk, this remains a major problem with the interpretation of this study. PROGRESS should be used to promote blood-pressure lowering after a stroke or TIA, not to promote particular drugs or regimens. [1] Muir K W. Secondary prevention for stroke and transient ischaemic attacks. BMJ 2004;328:297-298. [2] Blood Pressure Lowering Treatment Trialists’ Collaboration. Effects of different blood-pressure-lowering regimens on major cardiovascular events: results of prospectively-designed overviews of randomised trials. Lancet 2003; 362: 1527–35. [3] The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major Cardiovascular Events in Hypertensive Patients Randomized to Doxazosin vs Chlorthalidone: The Antihypertensive and Lipid- Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 2000; 283: 1967 - 1975. [4] Chobanian AV, Bakris GL, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. JAMA 2003; 289: 2560 - 2571. [5] Cates C. Letter: The lowering of blood pressure after stroke. Lancet 2001;358:1993. [6] Appel LJ. The verdict from ALLHAT - thiazide diuretics are the preferred initial therapy for hypertension. JAMA 2002;288:3039-42. Competing interests: None declared |
|||
|
|
|||
|
Richard M Darling, GP Riverbank Medical Centre, Weston super Mare, BS22 7YZ
Send response to journal:
|
That lowering blood pressure and lipid levels, irrespective of their initial levels, after stroke and TIA helps to prevent further episodes should surprise no-one. TIA and stroke are strongly associated with atherosclerosis. Atherosclerosis is strongly associated with blood pressure and an adverse lipid profile ( for which total serum cholesterol is a very poor marker), as well as other factors such as genetic make-up, smoking history and the presence of insulin resistance. Other factors being equal, reducing blood pressure and improving lipid profiles will slow the progression of atherosclerosis and thus reduce the likelihood of further events. One day we will realise that this applies to all atherosclerotic diseases ie CHD, PVD and cerebrovascular disease in addition to stroke and TIA. Competing interests: None declared |
|||
|
|
|||
|
DR. MANJUNATH P DESAI, CLINICAL OBSERVER LEICESTER ROYAL INFIRMARY LE1 5WW
Send response to journal:
|
Dear Editor, I read the article by a learned Neurologist and found it very informative.My compliments to the author. I have some basic questions regarding diferrent clinical syndromes of strokes.Strokes are clasified as TIAs,RINDs or a full blown Thrombosis . Here I am talking about only ischaemic strokes and not intracranial haemorrhages. I believe the syndrome of TIA as it is presently defined is absolutely arbitrary and not very usefulin terms of understanding the further risks to the patient.Although all the neurological deficits that revert back within 24 hours are called TIAs , I feel it might have diferrennt repurcussions to diferrnt patients. We actually need a sudy which proves beyond dought that all the stroke syndromes which revert back within 24 hours have similar pathophysiology. And I think it is very unlikely. I have seen in my personal experience that most of the elderly people with conventional risk factors like Hypertension , Diabetes mellitus , hypercholesterolemia and obesity present with Vertebro basilar TIAs rather than TIAs in the carotid artery systems. I think we also need to understand why certain individuals recover from fullblown strokes very well with minimal residual deficits and where as others dont. A controlled study in this regard would be a good and useful project. Thank you and best wishes. Dr. Manjunath Desai. Competing interests: None declared |
|||