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Cardiac Hypertrophy and Altered Cellular Electrical Activity of the Myocardium

Possible Electrophysiologic Basis for Myocardial Contractility Changes
  • Robert E. Ten Eick
  • Arthur L. Bassett
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 34)

Abstract

The myocardial cell hypertrophies in response to a sustained increase in workload. Increased workload can result from factors including: pressure overload due to ventricular or systemic hypertension; volume overload because of an AV fistula, other defects in the heart pump, or hypervolemia; sustained increase in heart rate. It can be subsequent to regional damage brought about by acute or chronic ischemia and infarction, by nutritional and hormonal disturbances, and by dynamic [1] and isometric exercise [2]. There are numerous physiologic changes concomitant with and perhaps associated with hypertrophy of the myocardial cell. These include mechanical, biochemical, structural and ultrastructural, and most recently described, electrophysiologic alterations. The notion has developed that hypertrophy is compensatory, allowing the heart to meet the increased workload, and that cardiac failure ensues if hypertrophy is insufficient [3, 4]. The literature on hypertrophy and failure is extensive. This review will be limited to an examination of changes occurring in a common (and the most studied) form of hypertrophy, i.e., that provoked by pressure overload. We described the electrophysiologic changes associated with this form of hypertrophy and consider pertinent mechanical, structural, and biochemical data which are concomitant and may be related to the electrical changes. We will refer to other models or to naturally occurring disease-induced hypertrophy when they reflect areas of special significance or pertinence. The interested reader is directed to several recent reviews of biochemical changes in the myocardium during hypertrophy, including those of Rabinowitz and Zak [5], Wikman-Coffelt et al. [4], and Zak and Rabinowitz [6].

Keywords

Cardiac Hypertrophy Papillary Muscle Action Potential Duration Pressure Overload Intercalate Disc 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer Science+Business Media Dordrecht 1984

Authors and Affiliations

  • Robert E. Ten Eick
  • Arthur L. Bassett

There are no affiliations available

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