Impact of tachycardia and sympathetic stimulation by cold pressor test on cardiac diastology and arterial function in elderly females

Abstract

Abnormal vascular-ventricular coupling has been suggested to contribute to heart failure with preserved ejection fraction in elderly females. Failure to increase stroke volume (SV) during exercise occurs in parallel with dynamic changes in arterial physiology leading to increased afterload. Such adverse vascular reactivity during stress may reflect either sympathoexcitation or be due to tachycardia. We hypothesized that afterload elevation induces SV failure by transiently attenuating left ventricular relaxation, a phenomenon described in animal research. The respective roles of tachycardia and sympathoexcitation were investigated in n = 28 elderly females (70 ± 4 yr) carrying permanent pacemakers. At rest, during atrial tachycardia pacing (ATP; 100 min(-1)) and during cold pressor test (hand immersed in ice water), we performed Doppler echocardiography (maximal untwist rate analyzed by speckle tracking imaging of rotational mechanics) and arterial tonometry (arterial stiffness estimated as augmentation index). Estimation of arterial compliance was based on an exponential relationship between arterial pressure and volume. We found that ATP produced central hypovolemia and a reduction in SV which was larger in patients with stiffer arteries (higher augmentation index). There was an associated adverse response of arterial compliance and vascular resistance during ATP and cold pressor test, causing an overall increase in afterload, but nonetheless enhanced maximal rate of untwist and no evidence of afterload-dependent failure of relaxation. In conclusion, tachycardia and cold provocation in elderly females produces greater vascular reactivity and SV failure in the presence of arterial stiffening, but SV failure does not arise secondary to afterload-dependent attenuation of relaxation.

Association between baseline blood pressure variability and left heart function following short‐term extreme cold exposure

“…In subsequent studies, the focus was primarily on changes in LV function during cold pressor testing. Notably, the E/A ratio was significantly decreased but as untwisting velocity increased, diastolic relaxation may not actually be impaired 25,26 . While several studies found only minor changes in EDV, ESV, and EF without achieving statistical significance, cardiac output (CO) and cardiac work index were both significantly increased compared to baseline levels after cold pressor testing.…”

“…Notably, the E/A ratio was significantly decreased but as untwisting velocity increased, diastolic relaxation may not actually be impaired. 25,26 While several studies found only minor changes in EDV, ESV, and EF without achieving statistical significance, cardiac output (CO) and cardiac work index were both significantly increased compared to baseline levels after cold pressor testing. This increase can be interpreted as a compensatory adaptation to maintain oxygen supply for cardiac muscle cells.…”

Effect of increasing heart rate on finger photoplethysmography fitness index (PPGF) in subjects with implanted cardiac pacemakers

“…Studies on the effects of increased HR on TPR are limited in the literature. Previous studies have observed that pacing reduced TPR [20, 26], while several studies observed no change [18, 27]. Generally, TPR will decrease if pacing has adequately increased the MAP/DBP ratio or CO, as this stimulates the activation of the arterial baroreceptors with subsequent deactivation of sympathetic activity [28].…”

Vocal complaint in physical education teachers and its association with the cardiovascular system

“…In this context, a previous study reported intensification in speaking rate which was indicated by a decrease in the length of phonation in males and females subjects during the cold pressor test [ 22 ]. Considering that the cold pressor test is an autonomic test that increases the sympathetic nervous system activity [ 23 ], the authors [ 22 ] suggested that increased sympathetic activity induces phonation length. These data do not support the negative association between parasympathetic indices of HRV and the domain 2 of the vocal handicap index.…”