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(Stroke. 2003;34:2385.)
© 2003 American Heart Association, Inc.
Original Contributions |
Instituto de Neurociencias Buenos Aires (INEBA), and Cátedra de Neurología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Left ventricular hypertrophy (LVH) has been increasingly recognized in the last decade as a risk factor for cardiovascular disease and stroke. However, at least in this guest editors experience, LVH is seldom or never mentioned, in everyday practice, among the risk factors considered relevant in a patient with cerebrovascular disease, whether because it is forgotten, neglected, or even despised. Why is this so?
LVH is usually considered a consequence of arterial hypertension: the left ventricle increases its mass and wall thickness to oppose a rise in the pressure load. Patients with LVH whose blood pressure is normal are thought to be "probably hypertensive," albeit with "nonsustained hypertension." In this line of reasoning, the relevant risk factor is hypertension and not the "secondary" consequence of LVH. In other instances, LVH is dismissed as a phenomenon linked to "aging," akin to the "sclerosis" of the aortic valve or the "stiffness" of the arterial vessels often found in ultrasound studies of the elderly. Embolism is considered the necessary mechanism to ascribe a stroke to cardiac disease, and LVH is not regarded as a cardiac source of embolism. In myocardial diseases, it is dilated and not hypertrophic cardiomyopathy that is deemed liable to cause stroke.
However, after adjusting for hypertension and other recognized factors, LVH remains an independent risk factor for stroke. Different patterns of LVH have now been described, and a coherent picture seems to be slowly emerging. In the current issue of Stroke, Di Tullio and coworkers present further evidence relating
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