Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2003;34:e208
Published online before print October 16, 2003, doi: 10.1161/01.STR.0000099063.62084.3C
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
34/11/e208    most recent
01.STR.0000099063.62084.3Cv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Stöllberger, C.
Right arrow Articles by Finsterer, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stöllberger, C.
Right arrow Articles by Finsterer, J.

(Stroke. 2003;34:e208.)
© 2003 American Heart Association, Inc.


Letters to the Editor

Angiotensin-Converting Enzyme Inhibitors and Stroke Prevention: What About the Influence of Atrial Fibrillation and Antithrombotic Therapy?

Claudia Stöllberger, MD Jörg Slany, MD

Second Medical Department, Krankenanstalt Rudolfstiftung, Wien, Austria

Michael Brainin, MD

Neurosciences Centre, Donau-Universität,, Department of Neurology, Donauklinikum, Maria Gugging, Austria

Josef Finsterer, MD

Neurologic Department, Krankenanstalt Rudolfstiftung, Wien, Austria


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor

The Heart Outcomes Prevention Evaluation (HOPE) trial and Losartan Intervention For Endpoint Reduction in Hypertension Study (LIFE) have shown that ramipril and losartan lower the risk of ischemic vascular events, including strokes.1–3 This effect, which is independent of lowering blood pressure, is explained by pharmacological mechanisms, which are further consequences of inhibition of the renin-angiotensin system in the plasma and vascular wall. These potential mechanisms comprise reduction in proliferation of vascular smooth muscle cells, enhancement of endogenous fibrinolysis, stabilization of plaques, decrease in angiotensin II–mediated atherosclerosis, plaque rupture, and vascular occlusion.4 Atherosclerosis, however, is not the only cause of stroke. Stroke may also be due to embolism, vasculitis, or coagulation abnormalities. Stroke may be due to cardiogenic embolism, most frequently in atrial fibrillation. Atrial fibrillation is an independent risk factor for stroke, and {approx}16% of ischemic strokes are associated with atrial fibrillation.5

Although the participants in the HOPE study had a 12-lead ECG at baseline, at 2 years, and at study end and some ECG findings have been reported, the prevalence of atrial fibrillation has not been mentioned.1,2,6 It can be expected that the prevalence of atrial fibrillation in the patients of the HOPE study is high, because the same risk factors, which were inclusion criteria for the HOPE study, have been identified by epidemiological studies to also be risk factors for the development of atrial fibrillation: increased age, hypertension, coronary heart disease, elevated serum cholesterol levels, and smoking.7 Uninformed about the prevalence of atrial fibrillation and . . . [Full Text of this Article]