Secondary prevention for stroke and transient ischaemic attacks
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《英国医生杂志》
EDITOR—Although I agree with Ray et al that increased public recognition of stroke is necessary, it is salutary that 50% of UK stroke patients already reach hospital within six hours: thereafter, institutional barriers delay investigation and treatment.1 Although logical, acute institution of secondary preventive treatments has not been tested specifically in trials, but if beneficial, the present outpatient referral-based assessment of transient ischaemic attack must be re-evaluated, including anachronistic discrimination based on symptom duration.
Duerden may be correct that blood pressure lowering, rather than specific agents, and indapamide rather than perindopril were responsible for benefit in PROGRESS: both issues were discussed. Chemically, indapamide is a sulfonamide, not a thiazide, and differs with respect to metabolic profile, and possibly regression of left ventricular hypertrophy.2 3 Perindopril seems not to reduce global cerebral blood flow in stroke patients with carotid stenosis,4 and data are lacking for other agents. Whether these differences matter in terms of vascular risk reduction is unclear.
Unfortunately, there are few data to permit comparison of drug regimes in secondary prevention, and PROGRESS and PATS included 76% of all randomised subjects (11 770/15 527).5 Extrapolation from primary prevention trials may be biologically inappropriate (stroke patients are generally older and may have impaired cerebral autoregulation or occlusive extracranial vascular disease) and uninformative since conventionally "normotensive" populations have not been studied. The possible importance of specific mechanisms is indicated by heterogeneity of outcome related to drug class.5 Further trials in secondary prevention are needed to clarify these issues.
Keith W Muir, senior lecturer in neurology
University of Glasgow, Division of Clinical Neurosciences, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF k.muir@clinmed.gla.ac.uk
Competing interests: KM has received honorariums for speaking at educational meetings sponsored by Servier and has received a grant from Servier (value ￡7000) towards a community study of the prevalence of stroke.
References
Harraf F, Sharma AK, Brown MM, Lees KR, Vass RI, Kalra L. A multicentre observational study of presentation and early assessment of acute stroke. BMJ 2002;325: 17.
Perry HM, Jr. Some wrong-way chemical changes during antihypertensive treatment: comparison of indapamide and related agents. Am Heart J 1983;106: 251-7.
Senior R, Imbs JL, Bory M, Amabile G, Denis B, Zannad F, et al. Indapamide reduces hypertensive left ventricular hypertrophy: an international multicenter study. J Cardiovasc Pharmacol 1993;22(suppl 6): S106-10.
Walters MR, Bolster A, Dyker AG, Lees KR. Effect of perindopril on cerebral and renal perfusion in stroke patients with carotid disease. Stroke 2001;32: 473-8.
Rashid P, Leonardi-Bee J, Bath P. Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review. Stroke 2003;34: 2741-8.
Duerden may be correct that blood pressure lowering, rather than specific agents, and indapamide rather than perindopril were responsible for benefit in PROGRESS: both issues were discussed. Chemically, indapamide is a sulfonamide, not a thiazide, and differs with respect to metabolic profile, and possibly regression of left ventricular hypertrophy.2 3 Perindopril seems not to reduce global cerebral blood flow in stroke patients with carotid stenosis,4 and data are lacking for other agents. Whether these differences matter in terms of vascular risk reduction is unclear.
Unfortunately, there are few data to permit comparison of drug regimes in secondary prevention, and PROGRESS and PATS included 76% of all randomised subjects (11 770/15 527).5 Extrapolation from primary prevention trials may be biologically inappropriate (stroke patients are generally older and may have impaired cerebral autoregulation or occlusive extracranial vascular disease) and uninformative since conventionally "normotensive" populations have not been studied. The possible importance of specific mechanisms is indicated by heterogeneity of outcome related to drug class.5 Further trials in secondary prevention are needed to clarify these issues.
Keith W Muir, senior lecturer in neurology
University of Glasgow, Division of Clinical Neurosciences, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF k.muir@clinmed.gla.ac.uk
Competing interests: KM has received honorariums for speaking at educational meetings sponsored by Servier and has received a grant from Servier (value ￡7000) towards a community study of the prevalence of stroke.
References
Harraf F, Sharma AK, Brown MM, Lees KR, Vass RI, Kalra L. A multicentre observational study of presentation and early assessment of acute stroke. BMJ 2002;325: 17.
Perry HM, Jr. Some wrong-way chemical changes during antihypertensive treatment: comparison of indapamide and related agents. Am Heart J 1983;106: 251-7.
Senior R, Imbs JL, Bory M, Amabile G, Denis B, Zannad F, et al. Indapamide reduces hypertensive left ventricular hypertrophy: an international multicenter study. J Cardiovasc Pharmacol 1993;22(suppl 6): S106-10.
Walters MR, Bolster A, Dyker AG, Lees KR. Effect of perindopril on cerebral and renal perfusion in stroke patients with carotid disease. Stroke 2001;32: 473-8.
Rashid P, Leonardi-Bee J, Bath P. Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review. Stroke 2003;34: 2741-8.