Compensatory hypertrophy comes at a cost. The oxygen requirements of hypertrophic myocardium are amplified owing to increased myocardial cell mass. Because the myocardial capillary bed does not expand in step with the increased myocardial oxygen demands, the myocardium becomes vulnerable to ischemic injury. Hypertrophy also typically is associated with altered patterns of gene expression reminiscent of fetal myocytes, such as changes in the dominant form of myosin heavy chain produced. Altered gene expression may contribute to changes in myocyte function that lead to increases in heart rate and force of contraction, both of which improve cardiac output, but which also lead to higher cardiac oxygen consumption. In the face of ischemia and chronic increases in workload, other pathologic changes eventually supervene, including myocyte apoptosis, cytoskeletal alterations, and increased extracellular matrix (ECM) deposition.
Pathologic compensatory cardiac hypertrophy is correlated with increased mortality; indeed, cardiac hypertrophy is an independent risk factor for sudden cardiac death. By contrast, the volume-loaded hypertrophy induced by regular aerobic exercise (physiologic hypertrophy) typically is accompanied by an increase in capillary density, with decreased resting heart rate and blood http://ebooksmedicine.net
Fig. 11.1 Leftventricularhypertrophy.(A)Pressurehypertrophyduetoleftventricularoutflowobstruction.Theleftventricleisonthelower right inthisapicalfour-chamberviewoftheheart.(B)Leftventricularhypertrophywithandwithoutdilation,viewedintransverseheartsections.Comparedwithanormalheart(center), thepressure-hypertrophiedhearts(left and in A) haveincreasedmassandathickleftventricularwall,whilethehypertrophied,dilatedheart(right) hasincreasedmassandanormalwallthickness.(C)Normalmyocardium.(D)Hypertrophiedmyocardium(panelsC andD arephotomicrographsatthesamemagnification).Notetheincreasesinbothcellsizeandnuclearsizeinthehypertrophiedmyocytes.(A and B, Reproduced with permission from Edwards WD: Cardiac anatomy and examination of cardiac specimens. In Emmanouilides GC, et al, editors: MossandAdamsheartdiseaseininfants,children,andadolescents:includingthefetusandyoungadults,ed 5,Philadelphia,1995,Williams & Wilkins,p 86.) pressure. These physiologic adaptations reduce overall
MORPHOLOGYcardiovascular morbidity and mortality. In comparison, static exercise (e.g., weight lifting) is associated with pressure hypertrophy and may not have the same beneficial effects.
Heart failure can affect predominantly the left or the right side of the heart or may involve both sides. The most common causes of left-sided cardiac failure are ischemic heart disease (IHD), systemic hypertension, mitral or aortic valve disease, and primary diseases of the myocardium (e.g., amyloidosis). The morphologic and clinical effects of left-sided CHF stem from diminished systemic perfusion and elevated back-pressures within the pulmonary circulation.