Cardiovascular-related mortality peaks during cold winter months, particularly in older adults. Acute physiological responses, such as increases in blood pressure, in response to cold exposure may contribute to these associations. To determine whether the blood pressure-raising effect (pressor response) of non-internal body temperature-reducing cold stress is greater with age, we measured physiological responses to 20 min of superficial skin cooling, via water-perfused suit, in 12 younger [25 +/- 1 (SE) yr old] and 12 older (65 +/- 2 yr old) adults. We found that superficial skin cooling elicited an increase in blood pressure from resting levels (pressor response; P < 0.05) in younger and older adults. However, the magnitude of this pressor response (systolic and mean blood pressure) was more than twofold higher in older adults (P < 0.05 vs. younger adults). The magnitude of the pressor response was similar at peripheral (brachial) and central (estimated in the aorta) measurement sites. Regression analysis revealed that aortic pulse wave velocity, a measure of central arterial stiffness obtained before cooling, was the best predictor of the increased pressor response to superficial skin cooling in older adults, explaining approximately 63% of its variability. These results indicate that there is a greater pressor response to non-internal body temperature-reducing cold stress with age in humans that may be mediated by increased levels of central arterial stiffness.

determine whether skin surface cooling increases left ventricular preload and contractility to a greater extent in older compared with young adults we studied 11 young (28 Ϯ 2 yr; means Ϯ SE) and 11 older (64 Ϯ 3 yr) adults during normothermia (35°C water perfused through a tube-lined suit) and cooling (15°C water perfused for 20 min) using standard and tissue Doppler echocardiography. Cooling significantly decreased skin surface temperature in young (⌬2.8 Ϯ 0.3°C) and older (⌬3.0 Ϯ 0.3°C) adults and increased rate-pressure product, an index of myocardial oxygen demand, in older (6,932 Ϯ 445 to 7,622 Ϯ 499 mmHg · beats/ min for normothermia and cooling, respectively), but not young (7,085 Ϯ 438 to 7,297 Ϯ 438 mmHg · beats/min) adults. Increases in blood pressure (systolic and mean blood pressure) during cooling were greater (P Ͻ 0.05) in older than in young adults. Cooling increased preload in older (left ventricular end-diastolic volume from 106 Ϯ 7 to 126 Ϯ 9 ml and left ventricular internal diameter in diastole from 4.69 Ϯ 0.12 to 4.95 Ϯ 0.14 cm; both P Ͻ 0.01), but not young adults (left ventricular end-diastolic volume from 107 Ϯ 7 to 111 Ϯ 7 ml and left ventricular internal diameter in diastole from 4.70 Ϯ 0.10 to 4.78 Ϯ 0.10 cm). Indices of left ventricular contractility (ejection fraction, myocardial acceleration during isovolumic contraction, and peak systolic mitral annulus velocity) were unchanged during cooling in both young and older adults. Collectively, these data indicate that cooling increases left ventricular preload, without affecting left ventricular contractility in older but not young adults. Greater increases in preload and afterload during cooling in older adults contribute to greater increases in indices of myocardial oxygen demand and may help explain the increased risk of cardiovascular events in cold weather.tissue Doppler imaging; echocardiography; age CARDIOVASCULAR-RELATED MORTALITY increases in the cold winter months, particularly in older adults (10,12,23,24,28,40). Associations between increased cardiovascular-related mortality and cold temperatures may be mediated, in part, by acute physiological responses to cold, which include peripheral and visceral vasoconstriction, elevated plasma norepinephrine, and diuresis (33, 38). Recently, we reported an augmented increase in arterial blood pressure during acute cold exposure (nonpainful and noninternal temperature lowering) in older adults (15). This augmented pressor response to cold stress in older adults was strongly associated with increased levels of central arterial stiffness before cooling and an increase in rate-pressure product during cooling (15). This effect appears to be confined to older adults as neither rate-pressure product nor cardiac minute work increase during similar cold exposure in young adults (36,38).Myocardial oxygen demand is affected by a number of factors (17) that may be altered by acute (i.e., cold stress) and chronic processes (i.e., aging). For instance, cold stress that does not induce shivering or d...

116 patients from 4 clinics participated in a double blind study to assess the efficacy of (BAY l 5240), a nifedipine-acebutolol fixed combination (10 mg + 100 mg), as compared to nifedipine 20 mg in essential hypertension. During the 10 week study, the mean recumbent blood pressure decreased 1 to 3 h after treatment from 175.5/105.2 to 148.3/88.0 mmHg in the BAY l 5240 group and from 174.3/102.9 to 150.3/86.5 mmHg in the nifedipine group. The results also showed a comparable decrease in the mean systolic (SBP) and diastolic (DBP) blood pressures before treatment (24 h after last tablet) and after physical exertion before and after either drug given for 4 weeks. Doubling of the dose for 4 additional weeks produced a moderate and similar additional decrease in blood pressure. The results show the possibility of treating essential hypertension with a low dose of a beta-adrenergic blocking agent in combination with 10 mg nifedipine. Both regimens were well tolerated. One patient in the BAY l 5240 group and 2 in the nifedipine group, all treated by the same investigator, were withdrawn from the study because of headache during the nifedipine pre-period.

Skin‐surface cooling acutely increases arterial blood pressure, left‐ventricular (LV) afterload, and myocardial oxygen demand. To determine whether skin surface cooling increases LV preload and contractility more in older than in young adults, we measured indices of LV preload and myocardial contractility using standard and tissue‐Doppler imaging (TDI) echocardiography in 6 young (23 ?1 yrs; mean ?SE) and 6 older (65 ?3 yrs) adults during normothermia (35° C water perfused through a tube‐lined suit) and skin‐surface cooling (15‐18° C water perfused for 20 min). Cooling increased LV end‐diastolic volume (EDV, from 98±1 to 108±1 ml, P<0.001) and LV internal diameter in diastole (IDd, from 4.61±0.03 to 4.77±0.03 cm, P<0.01) in older, but not young adults (EDV=101±1 and 99±1 ml, IDd=4.67±0.03 and 4.62±0.03 cm, for normothermia and cooling, respectively). In contrast LV ejection fraction and TDI myocardial functional indices (myocardial acceleration during contraction and peak velocities during systole and diastole) were unchanged by cooling in both young and older adults. These data indicate that skin surface cooling acutely increases LV preload, without influencing LV contractility in older, but not young adults. Increases in LV preload and afterload likely contribute to greater increases in myocardial oxygen demand during cold exposures in older than in young adults.Support: NIH AG24420 and M01 RR10732

Cardiovascular‐related mortality increases in the cold winter months, particularly in older adults. To determine whether coronary artery blood flow responses to skin surface cooling differ with age, we studied 9 young (25±1 yrs) and 10 older healthy adults (65±2 yrs). We hypothesized that left anterior descending coronary artery blood velocity (CBV) responses, measured using Doppler transthoracic echocardiography, to skin surface cooling (15–18° C water perfused suit for 20 min) would be impaired with age. We found that cooling increased left ventricular wall stress, a determinant of myocardial oxygen consumption, in young (185.6±6.5 to 202.9 ±10.4 mmHg, P < 0.05) and older adults (189.1±8.8 vs. 222.7±14.7 mmHg, P < 0.01) although the magnitude of this response was twofold greater in older adults (Δ9.13±3.48% vs. Δ17.62±3.24%, young and older, respectively; P=0.09). Despite increased left ventricular wall stress during cooling in young and older adults CBV increased only in the young (20.86±1.32 to 25.56±1.24 cm/s, p<0.01) and not older group (17.60±1.09 to 19.93 ±0.97 cm/s, p=0.11). These data suggest that an impaired coronary vasodilator response to cold stress may contribute to age‐dependent increases in cardiovascular‐related mortality during the winter months in healthy adults.Support: NIH HL92309, AG24420 and M01 RR10732

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To test the hypothesis that mild skin surface cooling acutely increases central arterial stiffness and alters timing and amplitude of central wave reflections we measured aortic pulse wave velocity (PWV), central augmentation index, and transit time of the reflected wave before and during 20 min of cooling (water perfused suit) in 12 adults (25 ?1 years old, mean ?SE). Cooling decreased skin temperature (Δ‐3.6 ±0.4° C; P<0.05) without effecting sublingual temperature. Arterial blood pressure increased during cooling (Δ10±1 and Δ8±1 mmHg for systolic and diastolic blood pressure, respectively; P<0.05). Arterial stiffness, measured as aortic PWV, was unchanged (6.1±0.2 vs. 6.6±0.3 m/s for baseline and cooling, respectively; P>0.40) by cooling. In contrast timing and amplitude of central wave reflections were modified by cooling as assessed by measures of augmentation index (6±2% vs. 14±4%; P<0.05) and transit time of the reflected wave (169±7 vs. 152±5 ms; P<0.05). None of these measures changed during a separate control trial. Collectively, these data indicate that mild skin surface cooling does not acutely increase central arterial stiffness (aortic PWV) although it does modify the timing and amplitude of central wave reflections. These latter responses likely result from cold induced splanchnic, renal, and cutaneous vasoconstriction.Support: NIH AG24420, HL77670, M01 RR10732

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