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| Hypertrophy of the Heart |
| Etiology •Hypertension of any cause, any type of aortic stenosis or regurgitation, mitral regurgitation, and congenital heart diseases. •Familial dilated and hypertrophic cardiomyopathy (CM). •Idiopathic dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and restrictive CM. •Some secondary CM's due to infectious, vascular, metabolic, toxic, immune,and neoplastic causes. •Alcoholic CM most common secondary form but anatomically same as idiopathic DCM. |
| Pathogenesis •Pressure and/or volume overload stimulate stretched myocytes to enlarge. Mechanism for this mechanogrowth coupling unknown. •Gene expression changes with reappearence of fetal isoforms of contractile proteins requiring less energy and having a slower more sustained contraction than adult forms. •Proto-oncogenes are expressed encoding growth factors, which also result in increased interstitial fibrous tissue., |
| Epidemiology •Known causes of hypertrophy, i.e., hypertensive heart disease , aortic stenosis (AS), and mitral regurgitation (MR) each have unique epidemiologies. •Cardiomyopathies with big hearts, and non-specific histopathology, and by definition of unknown cause, make up a minority among cases of big hearts. |
| General Gross Description •Varies with cause: hypertension - a concentric predominantly left ventricular hypertrophy > 2X normal wt. •AS = hypertension > 3X normal wt. •MR - hypertrophied and dilated heart involving all chambers. •CM : DCM - similar to MR; HCM - similar to hypertension. •Special type of HCM - idiopathic hypertrophic subaortic stenosis (IHSS) with marked interventricular septal thickening obstructing LV outflow. |
| General Microscopic Description •Muscle fibers uniformly thickened in proportion to increased weight. •Nuclei larger, some with pleomorphic shapes. •Hypertrophic cardiomyopathy (HCM): loss of normal structure of formed bundles of parallel fibers cut transversely or lengthwise. Total disorder of fiber grouping with interstial fibrosis. •Restrictive CM - focal or diffuse interstitial fibrosis. |
| Clinical Correlation •Hypertrophy alone without CAD causes coronary insufficiency, i.e. angina pectoris, SCD, etc. •Arrhythmias and CHF. •Prognosis of all forms of idiopathic, familial, and secondary CM's poor with death < 2 years after symptoms begin (ischemic heart disease, congestive heart failure, sudden cardiac death). •Hypertension curable medically . •Valvular lesions and some congenital lesions amenable to surgical management with increased life expectancy. |
| References •Cotran etal. Robbins Pathologic Basis of Disease. 5th ed. Phil: Saunders, 1994, pp. 45-7, 520-3, 540-7, and 558-562 •Harrison's Principles of Internal Medicine, 13th Ed: Isselbach et. al. (eds). NY: McGraw-Hill, 1994, pp. 941-2 and 1088-94 |
| Hypertrophy of the Heart |
| Synopsis by: J. Hasson M.D. (T33010M71000)[145] |
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