BackgroundAutonomic dysregulation represents a hallmark of coronary artery disease (CAD). Therefore, we investigated the effects of exercise‐based cardiac rehabilitation (CR) on autonomic function and neuro‐cardiovascular stress reactivity in CAD patients.Methods and ResultsTwenty‐two CAD patients (4 women; 62±8 years) were studied before and following 6 months of aerobic‐ and resistance‐training–based CR. Twenty‐two similarly aged, healthy individuals (CTRL; 7 women; 62±11 years) served as controls. We measured blood pressure, muscle sympathetic nerve activity, heart rate, heart rate variability (linear and nonlinear), and cardiovagal (sequence method) and sympathetic (linear relationship between burst incidence and diastolic blood pressure) baroreflex sensitivity during supine rest. Furthermore, neuro‐cardiovascular reactivity during short‐duration static handgrip (20s) at 40% maximal effort was evaluated. Six months of CR lowered resting blood pressure (P<0.05), as well as muscle sympathetic nerve activity burst frequency (48±8 to 39±11 bursts/min; P<0.001) and burst incidence (81±7 to 66±17 bursts/100 heartbeats; P<0.001), to levels that matched CTRL and improved sympathetic baroreflex sensitivity in CAD patients (P<0.01). Heart rate variability (all P>0.05) and cardiovagal baroreflex sensitivity (P=0.11) were unchanged following CR, yet values were not different pre‐CR from CTRL (all P>0.05). Furthermore, before CR, CAD patients displayed greater blood pressure and muscle sympathetic nerve activity reactivity to static handgrip versus CTRL (all P<0.05); yet, responses were reduced following CR (all P<0.05) to levels observed in CTRL.ConclusionsSix months of exercise‐based CR was associated with marked improvement in baseline autonomic function and neuro‐cardiovascular stress reactivity in CAD patients, which may play a role in the reduced cardiac risk and improved survival observed in patients following exercise training.
In this study we evaluate the impact of ischemic heart disease (IHD) and cardiac rehabilitation (CR) on cerebrovascular control and peripheral vascular health. Patients with IHD are at greater risk for stroke, a risk determined in part by cerebrovasoreactivity tests (i.e., dilation or constriction to a known stimulus). Exercise provides cerebrovascular health benefits in the aging population; yet, effects of IHD and CR (exercise) on cerebrovascular health indicators and cerebral blood flow control are not understood. We explored cerebrovascular control (i.e., vasoreactivity and autoregulation), peripheral vascular health, brain volume, and white matter hyperintensities (WMH) in a group of healthy adults (CTL), and patients with IHD after cardiac event (pre‐CR) and following 6 months CR (post‐CR) comprised of 2–3 sessions/week of 30 minutes moderate intensity aerobic exercise and 30 minutes of resistance training. In 23 participants (CTL: 11, IHD: 12; age range: 40–75 years), we measured changes in cross‐sectional area (ΔCSA) divided by changes in end‐tidal CO2 (ΔPetCO2: CTL: 2.3±1.2, pre‐CR: 4.1±3.2, post‐CR: 5.2±2.2 mmHg)] during hypercapnic (5% CO2, 95% oxygen; ADInstruments) conditions using a 3 Tesla (Siemens) scanner and T1‐weighted pulse sequence (0.7 mm isotropic). Vasoreactivity was calculated for the basilar (BA), left (L) and right (R) internal carotid (ICA), anterior (ACA), middle (MCA), and posterior cerebral arteries (PCA) using OsiriX software. Autoregulation of the MCA was assessed by measuring relative changes in MCA flow velocity with respect to changes in mean arterial pressure during a sit‐to‐stand task, quantified by rate of regulation (ROR). Peripheral vascular health metrics included brachial artery flow‐mediated dilation (FMD; %) and common carotid artery (CCA) intima media thickness (mm) using duplex ultrasound. Compared to CTL, those with IHD had lower CSA reactivity (mm/mmHg; mean±SD; p<0.05) in the BA (CTL: 0.74±0.73, pre‐CR: 0.29±0.29, post‐CR: 0.14±0.24), LICA (CTL: 1.1±0.86, pre‐CR: 0.93±1.03, post‐CR: 0.42±0.51), RICA (CTL: 0.93±0.71, pre‐CR: 0.48±0.35, post‐CR: 0.27±0.34), LMCA (CTL: 0.67±0.53, pre‐CR: 0.37±0.48, post‐CR: 0.14±0.12), and RMCA (CTL: 0.93±0.95, pre‐CR: 0.33±0.37, post‐CR: 0.29±0.33), which were not improved with CR. Compared to CTL, those with IHD had greater CCA IMT (CTL: 0.43±0.05, pre‐CR: 0.58±0.09, post‐CR: 0.59±0.07) which was not improved with CR, as well as lower ROR (CTL: 0.18±0.02, pre‐CR: 0.14±0.03, post‐CR: 0.16±0.03) and lower FMD (CTL: 9.1±4.3, pre‐CR: 4.7±2.3, post‐CR: 6.1±1.3; p<0.05) which were improved with CR. Finally, brain volume and white matter lesions were similar across groups. Therefore, compared to healthy individuals, the IHD patients exhibited impaired cerebrovascular control and peripheral endothelial function. Peripheral vascular health, and cerebrovascular autoregulation, were improved with 6 months of CR in these IHD patients.Support or Funding InformationCanadian Institute of Health Research (201503MOP‐342412‐MOV‐CEEA).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Aging patients with ischemic heart disease (IHD) have impaired cerebrovascular vasodilation in response to hypercapnia, but whether this is due to endothelial dysfunction or impairment in the vascular smooth muscle remains unknown. Further, despite being a standard drug given to patients with cardiovascular disease, the role of an exogenous nitric oxide donor (sodium nitroglycerin – NTG, which acts independently of the endothelium) in the cerebrovasculature in these patients is not known. This study tested the hypothesis that age and IHD impair nitric oxide‐mediated dilation (sodium nitric oxide, 0.4 mg spray) of the nine larger cerebral arteries in the Circle of Willis (3 Tesla MRI), as well as mean flow velocity [transcranial Doppler ultrasound; right middle cerebral artery (MCA)] and calculated MCA cerebral blood flow. These measures were made in groups of IHD (n=10, 49–77 years), older controls (CTL; n=5, 51–78 years) and young healthy (YH; n=10, 20–26 years) individuals. Compared to baseline, right MCA velocity [V (cm/s)] decreased similarly in all three groups [ΔIHD: −5.8 ± 5.0 cm/s; ΔCTL: −5.8 ± 3.2 cm/s; ΔYH: −6.3 ± 4.4: all p<0.05 versus baseline; mean ± S.D.]. However, a main effect of drug indicated that NTG induced artery dilation in all six basal and the three extracranial arteries [average range of cross sectional area values for all vessels provided here: BL: 3.3 – 16.5 mm2; NTG: 3.9 – 17.9 mm2, p<0.05, mean], and this dilation was similar across all 3 groups [e.g. right MCA CSA – ΔIHD: 1.3 ± 1.4 mm2; ΔCTL: 0.7 ± 1.2 mm2; ΔYH: 1.3 ± 0.9 mm2, p>0.05 versus baseline; mean ± S.D.]. As a result, NTG exerted no change in MCA blood flow versus baseline. These results demonstrate that age and IHD have little impact on vascular smooth muscle responses to exogenous nitric oxide.Support or Funding InformationSupported by Canadian Institute for Health Research (201503MOP‐342412‐MOV‐CEEA)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Markers of arterial wall stiffness are used commonly as indicators of cardiovascular risk. Stiff conduit vasculature transmits pulse waves with increased velocities, which may lead to end‐organ microvascular damage. However, the association of peripheral vascular stiffness to the brain's vulnerability for vascular impairment has not been established. In the brain, this microvascular damage could include breakdown of the blood‐brain barrier causing leakage of fluid through the cerebrovascular endothelial layer. Fluid‐attenuated inversion recovery (FLAIR) imaging allows the visualization of fluid‐abnormalities in subcortical tissue, which can be quantified as white matter lesions (WML). These WML have been linked to cognitive impairment, and labelled as risk factors for stroke, dementia, and cardiovascular mortality. This research tested the hypothesis that peripheral arterial stiffness predicts levels of WML volume. We examined normotensive controls (CTRL; n = 12; 6 males; age: 42–69 years) as well as normotensive ischemic heart disease patients (IHD; n = 17; 14 males; age: 40–75 years). Common carotid artery diameters were measured during systole and diastole (B‐mode ultrasound images with ECG‐gating), and time‐aligned corresponding blood pressure values were used for measures of arterial strain (strain), arterial stiffness index (β), carotid distensibility, carotid compliance, and arterial elastic modulus. All measures were taken in the supine posture. Magnetic resonance FLAIR imaging at T2 was used to assess periventricular WML volume (WMLv) using SPM software. The IHD and CTRL cohorts had similar WMLv (4.4 ± 3.2 vs. 3.2 ± 3.5 mL; p = 0.33). Also, all participants were normotensive. Therefore, the data were pooled (n = 29) to examine the association between WMLv and peripheral arterial stiffness. Following multiple linear regressions while adjusting for age and BMI, WMLv was correlated with arterial stiffness index (r2 = 0.39, p = 0.001), strain (r2 = 0.37, p = 0.002), carotid distensibility (r2 = 0.36, p = 0.004), carotid compliance (r2 = 0.26, p = 0.009), and absolute change in carotid diameter across one cardiac cycle (r2 = 0.24, p = 0.01). Regardless of the age, BMI, and participant cohort, structural periventricular WMLv correlated with markers of arterial stiffness. These findings support the emerging hypothesis that systemic arterial stiffness affects damage in the microvasculature of the brain. Further, the resulting subcortical structural damage is apparent in older populations regardless of ageing and vascular pathology.Support or Funding InformationSupported by the Canadian Institute of Health Research (201503MOP‐342412‐MOV‐CEEA).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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