Cardiac hypertrophy pathological

In patients with cardiac hypertrophy from chronically pressure-loaded human left ventricles due to aortic valve stenosis, a general reduction in gap junction surface area per unit cell volume by about 40% (0.0031 versus 0.0051 pm2/ pm3) has been observed [Peters et al., 1993]. The gap junctions in the pathological tissue were larger than normal. The estimated gap junction content per cell was reduced [Peters et al., 1993]. A reduction by 30% in the gap junction surface per cell was observed [Peters, 1996]. However, the number of intercalated disks per myocyte and the mean density of packing of connexons at freeze-fracture in these hearts remained unchanged as compared to control hearts. 

Cellular and Morphological Adaptations of Pathological and Physiological Cardiac Hypertrophy... 

Delaughter, M.C., Taffet, G.E., Fiorotto, M.L., Entman, M.L., and Schwartz, R.L. 1999. Local insulin-like growth factor expression induces physiologic, then pathologic, cardiac hypertrophy in transgenic mice. FASEB J. 13 1923-1929. 

Iemitsu, M., Miyauchi, T., Maeda, S., Sakai, S., Kobayashi, T., Fujii, N., Miyazaki, H., Matsuda, M., and Yamaguchi, I. 2001. Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat. Am. J. Physiol. 281 R2029-R2036. 

McMullen, J., Shioi, T., Zhang, L., Tamavaski, O., Sherwood, M.C., Kang, P.M., and Izumo, S. 2003. Phosphoinositide 3-kinase (pi 10a) plays a critical role for the induction of physiological, but not pathological cardiac hypertrophy. Proc. Natl. Acad. Sci. USA 100 12355-12360. 

Hypertrophy is an increase in the size of the cells due to synthesis of more sub-cellular components. An increase in the size of the organ results. Take, for example, cardiac hypertrophy in response to increased workload. The increased load is often a result of some pathological condition such as heart valve incompetence or stenosis of an outflow path. Hypertrophy of the muscles of a body builder is another good example, in which the increased workload is due to continued weight training. 

Pathological cardiac hypertrophy develops in response to stresses, and can be concentric, eccentric, or both. An excess pressure load placed on the heart, for example, resulting from uncorrected hypertension or valvular disease, results in concentric hypertrophy. This hypertrophy is initially believed to be adaptive, normalizing systolic wall stress, though it is not clear that hypertrophy is necessary to maintain systolic function in the face of moderately elevated pressure loads. Eccentric hypertrophy results most often from volume loads such as those in valvular insufficiency. Einally, the hypertrophy that occurs in the remote noninfarcted myocardium, as part of the remodeling process following a myocardial infarction, may be both concentric and eccentric. 

---