[Is secondary myocardial hypertrophy a physiological or pathological adaptive mechanism?].
Physiological hypertrophy is present when the increase in myocardial mass resulting from chronic mechanical loading is associated with normal or enhanced myocardial function and myosin ATPase activity. Morphological alterations occurring during the formation of hypertrophy are fully reversible in physiological hypertrophy. In pathological hypertrophy myocardial function and myosin ATPase activity are depressed and morphological changes do not or only incompletely regress following the elimination of the stimulus of hypertrophy. In the experimental animal myocardial hypertrophy resulting from exercise conditioning or slight to moderate ventricular pressure overload fulfills the criteria of physiological hypertrophy. More severe sudden pressure overload is accompanied by depression of contractile function. These pressure overload models have however, little analogy to the more progressive development of pressure loading in humans. In young dogs and in cats with a gradually increasing pressure load, in vivo ventricular ejection fraction remained within normal limits 37 to 60 weeks after banding of the ventricular outflow vessel. In vitro myocardial function evaluated in the hypertrophied papillary muscle was, however, at least in part depressed, notably when hydroxyproline concentration was augmented. Following debanding in rats with aortic constriction hydroxyproline content did not regress suggesting that fibrosis once established is not reversible. In man myocardial hypertrophy from exercise conditioning is associated with normal ventricular function except in older athletes, who may show a subtle reduction in ventricular shortening. Patients with chronic pressure overload from aortic stenosis or volume overload from aortic insufficiency in whom the angiographic muscle mass is severely increased (greater than or equal to 180 g/m2) elicit a depressed left ventricular contractile function. Preserved left ventricular ejection performance in aortic valve disease is however not associated with normal myocardial structure because interstitial fibrosis evaluated from endomyocardial biopsies or biopsies obtained at surgery was found to be increased. Patients with depressed left ventricular contractility were characterized by having an abnormally high muscle fibre diameter. Normal function after surgery was not accompanied by normalization of myocardial structure: Interstitial fibrosis increased, fibrous content remained the same and cellular hypertrophy regressed incompletely regardless whether angiographic muscle mass had regressed to normal or remained still increased after surgery. In summary, the bulk of available functional and morphological data suggests that the occurrence of true physiological hypertrophy is probably limited to exercise conditioning and eventually to mild chronic mechanical overload. The more severe secondary hypertrophy such as in patients with aortic valve disease who undergo valve replacement, is not a physiological adaptation, but must be considered as a pathological process.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001022:Aortic Valve Insufficiency / Q000473:pathology / Q000601:surgery; D001024:Aortic Valve Stenosis / Q000473:pathology / Q000601:surgery; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology*; D002415:Cats; D004285:Dogs; D006321:Heart / Q000502:physiology*; D006801:Humans; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D010210:Papillary Muscles / Q000503:physiopathology; D005082:Physical Exertion; D051381:Rats; D013318:Stroke Volume
D000251:Adenosine Triphosphatases
Ist die sekundäre Myokardhypertrophie ein physiologischer oder pathologischer Adaptationsmechanismus?