Compensatory Hyperfunction of the Heart and Cardiac Insufficiency

Меерсон, Ф. З.

doi:10.1161/01.res.10.3.250

Cited by 141 publications

(59 citation statements)

References 11 publications

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“…Cardiac hypertrophy is a universal response of the heart to injury or overload, which according to the Law of Laplace acts to normalize increased wall stress (1). Initially described as a beneficial and necessary response to maintain cardiac output under conditions of overload (1), hypertrophy has more recently been recognized as a risk factor for increased mortality (2).…”

Section: Introductionmentioning

confidence: 99%

“…Initially described as a beneficial and necessary response to maintain cardiac output under conditions of overload (1), hypertrophy has more recently been recognized as a risk factor for increased mortality (2). A large number of studies now collectively demonstrate that modulation of the hypertrophic growth of the heart is feasible without provoking hemodynamic compromise (3), despite increased wall stress (4).…”

Section: Introductionmentioning

confidence: 99%

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Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction

Perrino¹

2006

Journal of Clinical Investigation

226

162

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For over a century, there has been intense debate as to the reason why some cardiac stresses are pathological and others are physiological. One long-standing theory is that physiological overloads such as exercise are intermittent, while pathological overloads such as hypertension are chronic. In this study, we hypothesized that the nature of the stress on the heart, rather than its duration, is the key determinant of the maladaptive phenotype. To test this, we applied intermittent pressure overload on the hearts of mice and tested the roles of duration and nature of the stress on the development of cardiac failure. Despite a mild hypertrophic response, preserved systolic function, and a favorable fetal gene expression profile, hearts exposed to intermittent pressure overload displayed pathological features. Importantly, intermittent pressure overload caused diastolic dysfunction, altered b-adrenergic receptor (bAR) function, and vascular rarefaction before the development of cardiac hypertrophy, which were largely normalized by preventing the recruitment of PI3K by bAR kinase 1 to ligand-activated receptors. Thus stress-induced activation of pathogenic signaling pathways, not the duration of stress or the hypertrophic growth per se, is the molecular trigger of cardiac dysfunction.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction

Perrino¹

2006

Journal of Clinical Investigation

226

162

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“…It has not been fully elucidated whether or not myocardial hypertrophy adversely effects myocardial function during PCM. It has been reported (Meerson 1962 ;Gudbjarnason et al 1964) that pressure overload to the myocardium enhances uptake of amino acids and increases production of myocardial proteins resulting in myocardial hypertrophy and a gradual adaptation to pressure overload. However, oxygen and energy demands increase with left ventricular pressure overload and therefore, myocardial dysfunction may appear at an earlier stage of starvation.…”

Section: Discussionmentioning

confidence: 99%

Biochemical and hemodynamic changes in the hypertrophied dog heart subjected to chronic protein-calorie malnutrition.

Tabayashi

Iguchi

Arai

et al. 1987

Tohoku J. Exp. Med.

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Biochemical and hemodynamic changes were assessed in 13 dogs subjected to sub-coronary valvular aortic stenosis and chronic protein-calorie malnutrition (PCM). Red blood cell, hemoglobin, serum albumin, free fatty acids, blood glucose, cholinesterase and blood amino acid levels were measured. The dynamic geometry of the left ventricle (LV) was assessed with chronically implanted sonomicrometric piezoelectric crystals. Cardiac function was evaluated by mean velocity of circumferential fiber shortening (mean VcF) and the relationship between LV end-systolic pressure (LVESP) or LV wall stress (LVWst) and LV end-systolic diameter (LVESD). The following results were obtained : 1) A decrease in body weight and increases in free fatty acids and 3-Methylhistidine were observed following long-term PCM. 2) Mean VcF was not depressed in dogs subjected to PCM. 3) The relationship between LVESP or LVWst and LVESD shipted downward and to the right after PCM, indicating reduced myocardial contractility. These findings suggest that the left ventricle in hypertrophied dog hearts subjected to PCM retains normal pump function, despite a low state in the myocardium.protein-calorie malnutrition ; sub-coronary aortic stenosis ; free acid ; 3-Methylhistidine ; myocardial contractility

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“…Согласно классической парадигме естественного течения гипертонического сердца, предложенной кори-феем отечественной и американской патофизиологии Феликсом Залмановичем Меерзоном [16] и подтверж-денной экспериментальными данными других иссле-довательских групп [17,18], бессимптомная концен-трическая ГЛЖ рано или поздно приводит к снижению сократимости ЛЖ. О возможности развития СД ЛЖ у больных с гипертоническим сердцем косвенно свиде-тельствует тот факт, что у многих больных с ГЛЖ и нор-мальной ФВ с помощью показателей деформации мио-карда можно выявить начальные нарушения сократимо-сти ЛЖ [19,20].…”

Section: развитие систолической дисфункции лж у больных с гипертоничеunclassified

Structure and function features and adverse prognostic factors of compensated hypertensive heart disease

Овчинников¹,

Ozhereljeva²,

Масенко³

et al. 2017

RHJ

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Compensatory Hyperfunction of the Heart and Cardiac Insufficiency

Cited by 141 publications

References 11 publications

Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction

Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction

Biochemical and hemodynamic changes in the hypertrophied dog heart subjected to chronic protein-calorie malnutrition.

Structure and function features and adverse prognostic factors of compensated hypertensive heart disease

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