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(Circulation Research. 2007;100:e45.)
© 2007 American Heart Association, Inc.

Letter to the Editor

Adaptive and Maladaptive Cardiac Hypertrophy: What Is the Effective Role of Heat Shock Transcription Factor 1?

Piercarlo Ballo, Arianna Bocelli, Sergio Mondillo

Cardiology Operative Unit, S. Andrea Hospital, La Spezia;, Meyer Hospital, University of Florence;, Department of Cardiovascular Diseases, University of Siena, Italy

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

To the Editor:

In the recent interesting article by Sakamoto et al,¹ the authors found that rats undergoing exercise training showed lower degree of left ventricular (LV) hypertrophy, higher expression and activity of heat shock transcription factor 1 (HSF1), and preserved LV systolic function in comparison with rats exposed to sustained pressure overload by surgical constriction of the transverse aorta (TAC). They also observed that transgenic mice expressing constitutively active HSF1 showed less evident hypertrophic response and better systolic function than their wild-type littermates 5 weeks after TAC. Conversely, HSF1-deficient mice showed similar degree of LV hypertrophy but worse systolic function in comparison with their wild-type littermates after 4 weeks of exercise or 1 week after TAC. These data support the intriguing hypothesis that HSF1 upregulation in cardiac myocytes may play a key role in preventing LV systolic impairment in the exercise-induced hypertrophy model, and in determining the adaptive or maladaptive nature of the hypertrophic response.

An important issue in the interpretation of these findings derives from the method used for the assessment of LV systolic performance. The use of unadjusted echocardiographic indices measured at the level of endocardium, such as the M-mode-derived fractional shortening used by the authors, overestimates the real performance of circumferentially oriented LV fibers, that are mostly distributed within the midwall layers.^2,3 Determination of fractional shortening at the midwall is a more reliable method to explore effective LV systolic function, particularly in the presence of LV hypertrophy or altered LV geometry, and its feasibility in mice . . . [Full Text of this Article]