Published online before print September 18, 2003, doi: 10.1161/01.STR.0000094582.60549.25
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(Stroke. 2003;34:2385.)
© 2003 American Heart Association, Inc.
Original Contributions |
Editorial Comment—Left Ventricular Hypertrophy: An Unseemly Risk Factor for Stroke?
Instituto de Neurociencias Buenos Aires (INEBA), and Cátedra de Neurología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina
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 editor’s 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 LVH to stroke, and new evidence relating LV geometric patterns to stroke risk and stroke subtypes in a tri-ethnic population. The authors did not find statistically significant differences between the groups they studied. LVH appeared thus to be independently associated with stroke, across age, sex, and ethnicity.
Although 38.5% of the cases in their series were cryptogenic, concentric remodeling and concentric hypertrophy were associated more with lacunar than with other stroke subtypes, and eccentric hypertrophy with an excess of cardioembolic strokes (26.5%). Concentric remodeling, in which the LV mass index remains normal and only changes in relative wall thickness (RWT) occur, was associated with 26.2% of lacunar strokes. Overall, concentric remodeling carried only a slight increase in stroke risk, but RWT was independently associated with stroke after adjusting for LV mass. Lacunar strokes were more prevalent in the concentric hypertrophy group (32.7%), which carried the highest stroke risk. The increased risk was independent of the presence of hypertension. In a previous article, RWT was found to be a predictor for asymptomatic lacunar lesions.1 Therefore, concentric remodeling emerges as a marker for stroke risk, small-vessel disease, and lacunar stroke, and as a predictor of concentric hypertrophy and stroke recurrence. Recently, concentric hypertrophy has also been shown to be related to asymptomatic cerebrovascular disease.2
Concentric remodeling occurs in elderly nonhypertensive subjects. It has been linked to aging and shown to parallel age-related arterial stiffening and elevation of systolic blood pressure.3 These factors may be associated with lacunar strokes. Concentric remodeling is associated with carotid intima-media thickening in hypertensive patients.4 Patients with concentric hypertrophy also show an increase in arterial wall thickness, even in general population studies.5,6 Concentric remodeling has even mysteriously been linked to insulin resistance in elderly men, suggesting as yet unknown disease mechanisms connecting the myocardium to metabolic disturbances.7
It is not yet entirely clear whether LVH represents "a marker, a limited adaptative process or a pathological process,"8 amenable to different therapeutic strategies. But it seems clear that it responds to treatment. The same group reporting the present data has found that physical activity decreases stroke risk in patients with increased left ventricular mass.9 Antihypertensive treatment reduces LV mass and RWT,10 and concentric remodeling often goes untreated.11 And if eccentric hypertrophy is confirmed as a risk factor for cardioembolism in future studies, a rationale for antithrombotic treatment would reasonably follow.
Perhaps we may now understand better why also normotensive patients showed a reduction in stroke risk in recent trials with antihypertensive agents12: they may have decreased LVH. It looks as if physicians should now do well to think again before dismissing LVH as irrelevant for cerebrovascular disease.
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- Kohara K, Zhao B, Jiang Y, Takata Y, Fukuoka T, Igase M, Miki T, Hiwada K. Relation of left ventricular hypertrophy and geometry to asymptomatic cerebrovascular damage in essential hypertension. Am J Cardiol. 1999; 83: 367–370.[CrossRef][Medline] [Order article via Infotrieve]
- Selvetella G, Notte A, Maffei A, Calistri V, Scamardella V, Frati G, Trimarco B, Colonnese C, Lembo G. Left ventricular hypertrophy is associated with asymptomatic cerebral damage in hypertensive patients. Stroke. 2003; 34: 1766–1770.
[Abstract/Free Full Text] - Ganau A, Saba PS, Roman MJ, de Simone G, Realdi G, Devereux RB. Ageing induces left ventricular concentric remodelling in normotensive subjects. J Hypertens. 1995; 13: 1818–1822.[Medline] [Order article via Infotrieve]
- Cuspidi C, Lonati L, Sampieri L, Pelizzoli S, Pontiggia G, Leonetti G, Zanchetti A. Left ventricular concentric remodelling and carotid structural changes in essential hypertension. J Hypertens. 1996; 14: 1441–1446.[CrossRef][Medline] [Order article via Infotrieve]
- Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults. J Am Coll Cardiol. 1996; 28: 751–756.[Abstract]
- Muiesan ML, Salvetti M, Zulli R, Pasini GF, Bettoni G, Monteduro C, Rizzoni D, Castellano M, Agabiti-Rosei E. Structural association between the carotid artery and the left ventricle in a general population in Northern Italy: the Vobarno study. J Hypertens. 1998; 16: 1805–1812.[CrossRef][Medline] [Order article via Infotrieve]
- Sundstrom J, Lind L, Nystrom N, Zethelius B, Andren B, Hales CN, Lithell HO. Left ventricular concentric remodeling rather than left ventricular hypertrophy is related to the insulin resistance syndrome in elderly men. Circulation. 2000; 101: 2595–2600.
[Abstract/Free Full Text] - Gosse P, Dallocchio M. Left ventricular hypertrophy: epidemiological prognosis and associated critical factors. Eur Heart J. 1993; 14 (suppl D): 16–21.
- Rodríguez CJ, Sacco RL, Sciacca RR, Boden-Albala B, Homma S, Di Tullio MR. Physical activity attenuates the effect of increased left ventricular mass on the risk of ischemic stroke: the Northern Manhattan Stroke Study. J Am Coll Cardiol. 2002; 39: 1482–1488.
[Abstract/Free Full Text] - Wachtell K, Dahlof B, Rokkedal J, Papademetriou V, Nieminen MS, Smith G, Gerdts E, Boman K, Bella JN, Devereux RB. Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Am Heart J. 2002; 144: 1057–1064.[CrossRef][Medline] [Order article via Infotrieve]
- Abergel E, Chatellier G, Battaglia C, Menard J. Can echocardiography identify mildly hypertensive patients at high risk, left untreated based on current guidelines? J Hypertens. 1999; 17: 817–824.[CrossRef][Medline] [Order article via Infotrieve]
- PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood pressure-lowering regimen among 6105 patients with previous stroke or transient ischemic attack. Lancet. 2001; 358: 1033–1041.[CrossRef][Medline] [Order article via Infotrieve]
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