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(Circulation. 2002;105:1025.)
© 2002 American Heart Association, Inc.

Editorial

Peroxisome Proliferator-Activated Receptor as a Genetic Determinant of Cardiac Hypertrophic Growth

Culprit or Innocent Bystander?

Daniel P. Kelly, MD

From the Center for Cardiovascular Research, Departments of Medicine, Molecular Biology and Pharmacology, and Pediatrics, Washington University School of Medicine, St Louis, Mo.

Correspondence to Daniel P. Kelly, MD, Center for Cardiovascular Research, Washington University School of Medicine, 660 S Euclid Ave, Campus Box 8086, St Louis, MO 63110. E-mail dkelly@imgate.wustl.edu

Key Words: Editorials • hypertrophy • metabolism • genetics • hormones

Left ventricular hypertrophy (LVH) occurs in response to a long-term increase in hemodynamic load related to a variety of physiological and pathophysiological conditions. The cardiac hypertrophic response is considered to be purely adaptive during postnatal growth stages and in response to exercise training. In contrast, pathological forms of LVH, such as that caused by hypertension, often enter a phase of pathological remodeling that leads to contractile dysfunction and ultimately to heart failure. These observations suggest that certain components of the pathological cardiac hypertrophic response are maladaptive, contributing to a pathological remodeling response. Previous studies have demonstrated that left ventricular (LV) mass is a risk factor for future cardiac events in patients with pathological forms of LVH.^1,2 Of interest is the fact that clinical studies also have revealed significant variability in LV mass, independent of blood pressure, among individuals with LVH, suggesting that the hypertrophic response is influenced by genetic and environmental factors.^3,4

See Circulation. 2002;105:950–955.

Peroxisome Proliferator-Activated Receptor Gene as a Candidate Determinant of the Ventricular Hypertrophic Growth Response

Despite evidence for genetic determinants of the LVH phenotype in humans, little is known about the specific genes involved. The results of previous studies have suggested a role for the angiotensin-converting enzyme (ACE) insertion/deletion genotype as a predictor of the cardiac hypertrophic response.^5,6 Hypertrophic cardiomyopathy is caused by mutations in genes encoding a variety of sarcomeric proteins, providing another potential genetic link.⁷ However, convincing evidence for genetic modifiers of the ventricular hypertrophic response due to common diseases such as hypertension generally is lacking.

In the February 26, 2002, issue of Circulation, the report . . . [Full Text of this Article]

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