TY - JOUR
T1 - Altered coronary vascular control during cold stress in healthy older adults
AU - Gao, Zhaohui
AU - Wilson, Thad E.
AU - Drew, Rachel C.
AU - Ettinger, Joshua
AU - Monahan, Kevin D.
PY - 2012/1
Y1 - 2012/1
N2 - Cardiovascular-related mortality increases in the cold winter months, particularly in older adults. Previously, we reported that determinants of myocardial O2 demand, such as the rate-pressure product, increase more in older adults compared with young adults during cold stress. The aim of the present study was to determine if aging influences the coronary homodynamic response to cold stress in humans. Transthoracic Doppler echocardiography was used to non invasively measure peak coronary blood velocity in the left anterior descending artery before and during acute (20 min) whole body cold stress in 10 young adults (25 ± 1 yr) and 11 older healthy adults (65 ± 2 yr). Coronary vascular resistance (diastolic blood pressure/peak coronary blood velocity), coronary perfusion time fraction (coronary perfusion time/ R-R interval), and left ventricular wall stress were calculated. We found that cooling (via a water-perfused suit) increased left ventricular wall stress, a primary determinant of myocardial O2 consumption, in both young and older adults, although the magnitude of this increase was nearly twofold greater in older adults (change of 9.1 ± 3.5% vs. 17.6 ± 3.2%, P < 0.05, change from baseline in young and older adults and young vs. older adults). Despite the increased myocardial O2 demand during cooling, coronary vasodilation (decreased coronary vascular resistance) occurred only in young adults (3.22 ± 0.23 to 2.85 ± 0.18 mmHg·cm-1·s-1, P < 0.05) and not older adults (3.97 ± 0.24 to 3.79 ± 0.27 mmHg·cm-1·s-1, P > 0.05). Consistent with a blunted coronary vascular response, absolute coronary perfusion time tended to decrease (P = 0.13) and coronary perfusion time fraction decreased (P < 0.05) during cooling in older adults but not young adults. Collectively, these data suggest that older adults demonstrate an altered coronary homodynamic response to acute cold stress.
AB - Cardiovascular-related mortality increases in the cold winter months, particularly in older adults. Previously, we reported that determinants of myocardial O2 demand, such as the rate-pressure product, increase more in older adults compared with young adults during cold stress. The aim of the present study was to determine if aging influences the coronary homodynamic response to cold stress in humans. Transthoracic Doppler echocardiography was used to non invasively measure peak coronary blood velocity in the left anterior descending artery before and during acute (20 min) whole body cold stress in 10 young adults (25 ± 1 yr) and 11 older healthy adults (65 ± 2 yr). Coronary vascular resistance (diastolic blood pressure/peak coronary blood velocity), coronary perfusion time fraction (coronary perfusion time/ R-R interval), and left ventricular wall stress were calculated. We found that cooling (via a water-perfused suit) increased left ventricular wall stress, a primary determinant of myocardial O2 consumption, in both young and older adults, although the magnitude of this increase was nearly twofold greater in older adults (change of 9.1 ± 3.5% vs. 17.6 ± 3.2%, P < 0.05, change from baseline in young and older adults and young vs. older adults). Despite the increased myocardial O2 demand during cooling, coronary vasodilation (decreased coronary vascular resistance) occurred only in young adults (3.22 ± 0.23 to 2.85 ± 0.18 mmHg·cm-1·s-1, P < 0.05) and not older adults (3.97 ± 0.24 to 3.79 ± 0.27 mmHg·cm-1·s-1, P > 0.05). Consistent with a blunted coronary vascular response, absolute coronary perfusion time tended to decrease (P = 0.13) and coronary perfusion time fraction decreased (P < 0.05) during cooling in older adults but not young adults. Collectively, these data suggest that older adults demonstrate an altered coronary homodynamic response to acute cold stress.
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U2 - 10.1152/ajpheart.00297.2011
DO - 10.1152/ajpheart.00297.2011
M3 - Article
C2 - 22003058
AN - SCOPUS:84255182348
SN - 0363-6135
VL - 302
SP - H312-H318
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 1
ER -