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Retinal changes and cardiac remodelling in systemic hypertension

Department of Clinical Medicine and Prevention, University of Milano-Bicocca, Milano, Istituto Auxologico Italiano, Milano, Italy, cesare.cuspidi{at}unimib.it

Francesca Negri

Istituto Auxologico Italiano, Milano, Italy, Department of Clinical Medicine and Prevention, University of Milano-Bicocca, Milano

Valentina Giudici

Istituto Auxologico Italiano, Milano, Italy

Carla Sala

Istituto di Medicina Cardiovascolare, Ospedale Maggiore Policlinico and University of Milano, Italy

The clinical value of left ventricular hypertrophy (LVH), a cardinal manifestation of hypertensive organ damage, in predicting cardiovascular (CV) events, independently of blood pressure (BP) and other accompanying risk factors, has been widely documented and its role in CV stratification indisputability recognized. Although the examination of the fundus oculi provides a unique opportunity to evaluate retinal microvascular abnormalities, which may mirror systemic arteriolar damage due to high BP, no consistent evidence exists, on the prognostic value of mild degrees of retinopathy, encompassing the vast majority of uncomplicated hypertensive subjects. Personal and literature data indicate that: (1) there is a tight association between advanced retinopathy and LVH suggesting the existence of a parallel involvement of retinal tree and cardiac damage in severe untreated or poorly controlled hypertension; (2) in contrast, a firm conclusion about the relationship between early or nonspecific retinal changes (narrowing or arteriovenous crossing) and cardiac damage is not allowed by the majority of the studies; (3) future investigations, based on computer-assisted methods, are further required to document the relation between initial retinal changes with organ damage and more importantly to test their predictive value for clinical outcomes.

Key Words: Left ventricular hypertrophy • retinopathy • hypertension

This version was published on June 1, 2009

Therapeutic Advances in Cardiovascular Disease, Vol. 3, No. 3, 205-214 (2009)
DOI: 10.1177/1753944709103220


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