Abstract
Left ventricular hypertrophy is the primary risk factor associated with the appearance of symptomatic heart failure [1]. Why hypertrophic growth of the myocardium would be adaptive in a weight lifter, fostering enhanced cardiac performance during elevations in arterial pressure associated with isometric exercise, and pathologic in the patient with hypertension, is unclear. In seeking to identify the pathogenetic mechanisms responsible for pathologic hypertrophy, basic and applied scientists have hoped to unravel this puzzle. As an outgrowth of this investigation, important insights into the contractile process of cardiac muscle have emerged while potential biochemical abnormalities that would account for impaired ventricular function have been identified [2, 3]. To date, however, no unifying concept has linked abnormalities in the biochemistry of contraction with the clinical appearance of heart failure. Furthermore, it is not clear whether any given abnormality would be a primary or secondary event.
This work was supported in part by NHLBI grant no. R05-HL-31701.
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Silver, M.A., Weber, K.T. (1990). Structural Basis of Left Ventricular Dysfunction: Role of Collagen Network Remodeling and Potential Therapeutic Interventions. In: Brachmann, J., Dietz, R., Kübler, W. (eds) Heart Failure and Arrhythmias. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75326-8_8
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