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Diverse Effects of Aging on the Cardiac Response in Pathological Left Ventricular Remodeling and Dysfunction
Author(s) -
Boer Martine,
Deel Elza D.,
Kleijnen Marion,
Hoeijmakers Jan H.J.,
Duncker Dirk J.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1194.2
Subject(s) - cardiology , medicine , pressure overload , heart failure , diastole , left ventricular hypertrophy , ventricular remodeling , muscle hypertrophy , concentric hypertrophy , cardiac function curve , myocardial infarction , pathological , blood pressure , cardiac hypertrophy
The aging heart undergoes structural and functional changes that are reminiscent of the failing heart, and which thus may increase cardiac vulnerability to develop heart failure. To test this hypothesis, we subjected mice to pressure overload by transverse aortic constriction (TAC) or myocardial infarction (MI) at 3, 12 and 24 months of age. Eight weeks after TAC or MI, left ventricular (LV) geometry and function were measured. Aging mildly affected cardiac geometry and function in sham operated animals. TAC produced marked LV hypertrophy, cardiac dysfunction, pulmonary congestion and right ventricular (RV) hypertrophy in all age groups. MI produced LV dilation, cardiac dysfunction and LV and RV hypertrophy in all age groups. Interestingly, the hypertrophic responses to TAC and MI were diminished with aging, but whereas the blunted hypertrophic response in TAC was associated with aggravated LV dysfunction, LV function tended to improve in MI. Thus, aging aggravated the TAC‐induced decrease in LV dP/dt P40 and LV dP/dt min and the increase in lung fluid and RV weight in the 24 vs. 3 months old mice. In contrast, MI‐induced diastolic dysfunction was slightly blunted with aging as demonstrated by decreases in tau and LV end diastolic pressure in the 24 vs. 3 months old mice. These observations indicate that the effects of aging on the cardiac response to hemodynamic overload depend critically on the underlying pathology. Supported by a NHF Grant 2007B024