Question

Why can an enlarged heart be both a blessing and a curse?

Answer 1

Enlarged heart _due to cardiac hypertrophy.It can be both beneficial and disadvantageous.Thus can be called double edge sword.

Valvular [Pressure overlody Disease Hypertension (pressure I Infarction Myocardial Regional Twith volume dynyünetion Overload overload) ↑ Cardiac Work 1 a wall stress Cell stretch Hypertrophy and/or dilation Characterized by • ↑ Heart size & mars I protein synthesis Induction immediate early genes induction fetal genie programme Abnormal proteins. • fibrosis Inadequate vasculateure Cardiac dysfunction Characterized by Heart failure (ayatolie / digcartolic) Arnhythmias newro humo and stimulation

Sustained increase in mechanical work due to pressure or volume overload(e.g.systemic hypertension or aortic stenosis) or trophic signals(e.g,those mediated through activation of beta adrenergic receptors)cause myocytes to increase in size and weight.

Hypertrophy requires increased protein synthesis,thus enabling the assembly of additional sarcomeres and mitochondrias. These have enlarged nuclei,attributed to increased DNA ploidy resulting from DNA replicatiin in the absence of cell division.Finally ,heart weight,tather than wall thicknesd,is the best measure of hypertrophy in dilated hearts.

cardiac hypertrophy can be substantial in clinical heart disease.Jeart weights of 2 or 3 times normal are common in patients with systemic hypertension,ischemic heart disease,aortic stenosis,mitral regurgitation,or dilated cardiomyopathy,and heart weights can be 3-4 fold greater thsn normal in those with aortic regurgitation or hypertrophic cardiomyopathy.

Important changes at tisdue level occour with cardiac hypertrophy.Important point tobe considered is,myocyte hyprtrophy isnot accompanied by a proportional increase in capillary numbers.As a result the supply of oxygen and nutrients to the hypertrophied heart,perticularly one undergoing pressure overload hypertrophy,is more tenous than the normal heart.At the same time,oxygen consumption by the hypertrophied heart is elevated due to increased work load that drives the process.Hypertrophy is also accompanied by deposition of fibrous tissue(interdtitial fibrosis).With prolonged hemodynamic overload ,there may be a shift to gene expression pattern resembling that seen during fetal cardiac development(including selective expression of embryonic forms of beta-myosin heavy chain,natri uretic peptides and collagen.

At functional level,cardiac hypertrophy is asdociated with heightened metabolic demands due to increased mass,heart rate,and contractility_allof which increase cardiac oxygen consumption.As a redult of these changes ,the hypertrophied heart is vulnerable to ischemia related decompensation,which can evolve to cardiac failure and eventually lead to death.Thus the molecular and cellular changes in hypertrophied heart that initially mediate enhanced function may themselves contribute to the development of heart failure.