Arterial Stiffness: Implications and Interventions

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Arterial Stiffness: A Review in Type 2 Diabetes

Deconditioning After SCI, not only the skeletal muscles used for limb movement are affected, but also the smooth muscles lining the arteries experience rapid deconditioning and stiffness. The correlation of injury levels to high level cervical or low level thoracic is also an important issue, because individuals with higher lesion levels experience more severe CV abnormalities, such as sudden bouts of hypertension.

These improvements can vary depending on the intensity of exercise employed and the severity of arterial stiffness of the individual. Some research does contradict the effectiveness of only upper body exercise due to the lack of other muscle groups being activated. This suggests that a more integrated knowledge and research is required to assess the role of specific lower or upper body exercise in relieving arterial stiffness. Dietary interventions show a reduction in arterial stiffness.

These include the incorporation of omega-3 polyunsaturated fats especially EPA and DHA , plant-derived isoflavones found in legumes and beans, and fermented milk products. Long-term caffeine avoidance is advised because of the immediate effects of caffeine constricting the arteries. Even though sodium increases blood pressure, decreasing its consumption is not viable.

This is due to the very important role sodium plays in maintaining a healthy blood volume in the body. Additionally, a low-cholesterol and low-saturated-fat diet for 8 weeks yielded a decreased aPWV. Several pharmacological drugs have been tested to reduce arterial stiffness.

Antihypertensive drugs have shown the most promise by far to reduce vascular stiffness in the non-SCI population. These drugs reduce effectiveness of the systemic mechanisms that increase blood pressure and volume. Reiffel et al. Is arterial stiffness a contributing factor to atrial fibrillation in patients with hypertension? A preliminary investigation. Am J Hypertens ; Click here to see the Library ] did not report any association between arterial stiffness and AF in a small group of hypertensive and normotensive subjects.

On the other hand, several recent therapeutic trials have shown that treatments reducing arterial stiffness [ 23 Mahmud A, Feely J. Arterial stiffness is related to systemic inflammation in essential hypertension.

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J Am Coll Cardiol ; Finally, we used brachial PP and not central PP. Peripheral PP, most often measured at the site of the brachial artery, does not fully reflect central PP, measured at the carotid site. Indeed, in peripheral arteries, reflection sites are closer than in central arteries, and reflected waves travel faster on peripheral arteries than on central arteries, which are less stiff in young subjects. However, these discrepancies are probably attenuated in our study patients, who had an average age of 53 years. This question is largely a matter of speculation and requires caution because of the limitations highlighted above.

There is, however, a rapidly growing number of papers in the literature on the participation of genes, particularly those involved in matrix proteins, in the thickening process [ 27 Durier S, Fassot C, Laurent S, et al. Physiological genomics of human arteries: quantitative relationship between gene expression and arterial stiffness. For example, Medley et al.

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Matrix metalloproteinase-9 genotype influences large artery stiffness through effects on aortic gene and protein expression. Arterioscler Thromb Vasc Biol ; Click here to see the Library ] showed that matrix metalloproteinases are potential candidates to explain arterial wall remodeling, especially MMP3 and MMP9 genes. Interestingly, Nakano et al. Matrix metalloproteinase-9 contributes to human atrial remodeling during atrial fibrillation. Click here to see the Library ] found a similar role for one of these genes MMP9 as a candidate for atrial remodeling during AF.

Other genes involved in cell-matrix connections, like integrins, provide additional examples, being activated during vascular and atrial remodeling [ 3 Laurent S, Boutouyrie P, Lacolley P. In light of these findings, one might speculate that, for some reason and maybe simply because of age, similar genes are up-regulated both in the atria and vessel wall, contributing to a concomitant remodeling of both, possibly on top of mechanical effects.

Inflammation may also be involved since it has been shown that arterial stiffness was related to an increased level of C-reactive protein as well as of other markers like IL-6 and TNF [ 23 Mahmud A, Feely J. C-reactive protein and paroxysmal atrial fibrillation: evidence of the implication of an inflammatory process in paroxysmal atrial fibrillation. Acta Cardiol ; Stiffening at the vascular level may trigger an inflammatory process, a condition associated with a greater occurrence of AF [ 32 Dernellis J, Panaretou M. In conclusion, these results provide a new possible pathophysiological link between arterial stiffness and stroke, and consequently may open the way for a new approach to AF prevention.

This concept has recently been illustrated by the LIFE trial, which showed that the drug regimen producing the most important decrease in left atrial size had the greatest effect at preventing AF [ 33 Gerdts E, Wachtell K, Omvik P, et al. Left atrial size and risk of major cardiovascular events during antihypertensive treatment: losartan intervention for endpoint reduction in hypertension trial. Previous Article Mechanical circulatory assistance in myocardial infarction with refractory cardiogenic shock: clinical experience in 10 patients at a teaching hospital in Rouen D.

Brunet, H. Eltchaninoff, M. Kerkeni, C. Tron, B. Baala, P. Litzler, J. Bessou, A. Journal page Archives Sommaire. Gueret, K. Khalife, Y. Jobic, E. Fillipi, K. Isaaz, S. Tassan-Mangina, C.

Arterial Stiffness Implications and Interventions SpringerBriefs in Physiology

Baixas, P. Motreff, C. Meune, on behalf of the study investigators. Article Article Outline. Access to the text HTML. Access to the PDF text If you experience reading problems with Firefox, please follow this procedure. Recommend this article. Save as favorites. Body mass index, waist circumference, hip circumference and waist-to-hip ratio were measured and calculated as per established guidelines. All data analysis was done in a blinded manner. Sixty-five subjects responded to the advertisement in local publications and were screened.

Thirteen subjects did not meet inclusion and exclusion criteria including four subjects excluded on the basis of a positive stress test. In all, 52 subjects 30 males and 22 females were randomized to the AT and NA groups. Randomization resulted in 25 subjects in the AT group 13 males and 12 females and 27 in the NA group 17 males and 10 females.

As shown in Table 1 , at the time of entry into the study, there was no significant difference between AT and NA subjects with respect to demographic data, resting HR, resting blood pressure, fasting blood sugar, glycosylated hemoglobin or lipid profile. There was no difference between the two groups with respect to the prescription of various types of medications.

Only one patient in the NA group changed their medication during the intervention discontinued their statin agent. The difference in response was primarily due to a decrease in both radial and femoral PWV in the AT group after 3 months of training that was not maintained at the 6-month mark for either radial or femoral PWV Figure 1. By comparison, the NA group demonstrated a 0. None of these reductions in PWV observed in the AT group were maintained throughout the course of the intervention Figure 1.

Aerobic training temporarily reversed multifactorial geriatric age, T2DM, hypertension and hypercholesterolemia arterial stiffness, as shown by significant decreases in both radial and femoral PWV. Although these improvements after 3 months of aerobic training were quite large in magnitude, they became attenuated over the course of the training intervention.

In fact there was no statistical difference between the two groups at the 6-month mark, suggesting that the underlying mechanisms behind arterial stiffening in a high cardiometabolic risk population have some constituents that are both progressive and irreversible.

The attenuation of the aerobic training effect on arterial stiffness occurred despite a maintenance of improved aerobic fitness as measured by VO 2max throughout the course of the intervention. The present study is novel in that the subjects were at high cardiometabolic risk geriatric age, T2DM, hypertension and hypercholesterolemia , and that the intervention was longer in duration than most previous studies 6 months. Most previous studies have examined short-term interventions, middle-aged subjects and populations with a single risk factor.

The benefits of aerobic exercise on arterial stiffness have been demonstrated previously through cross-sectional data on middle-aged normal subjects, 2 prospective interventions in young athletes 1 and prospective interventions in middle-aged healthy persons. Long-term aerobic training has been shown to improve arterial stiffness in normal older adults 3 and short-term aerobic training has successfully reduced arterial stiffness in middle-aged subjects with T2DM.

A cross-sectional study of hypertensive adults has previously demonstrated that there is no relationship between aerobic fitness and arterial stiffness. Overall, this suggests that in older adult population with multiple cardiovascular risk factors, there is a component of arterial stiffness that is unresponsive to aerobic training interventions.

Of these structural changes, it has been theorized that non-enzymatic glycation would be the most responsive to aerobic exercise, through pulsatile stretching and breaking of collagen crosslinks. The fact that we were unable to demonstrate any training-induced improvements in fasting blood glucose, blood pressure and lipid levels might be one explanation for the training-resistant nature of arterial stiffness in our high-risk subjects over the longer term.


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In persons with diabetes, previous research has strongly established the relationship between vascular stiffness and cardiovascular mortality. Although aerobic exercise has numerous well-established benefits in older adults 35 our findings suggest that in the longer term, arterial stiffness in a high-risk population is resistant to aerobic training.

This suggests that with respect to vascular compliance, the timely prescription of aerobic training to prevent hypertension, diabetes and high cholesterol might impact vascular health more than starting aerobic training once patients are already at high cardiometabolic risk. Since our exercise intervention was only 6 months in duration, it is possible that an even longer intervention might have successfully reduced arterial stiffness. There were trends for a reduction in weight, SBP and fasting blood glucose that might have eventually resulted in a decline in arterial stiffness if the intervention had been continued for longer than 6 months.

Further research is needed to determine the pathophysiological mechanism for the short-term reduction in radial and femoral PWV with aerobic exercise in our population. Our study was unable to detect any significant training effect on weight, body mass index, waist circumference or fasting blood glucose but this is consistent with the other aerobic training literature in older adults with cardiovascular risk factors.

It is also possible that the active control group NA group had some degree of aerobic training since it is impossible to completely separate strength from aerobic training, although there was no significant difference in the response of VO 2max to training between the aerobic and non-aerobic groups. It is also possible that a mild strength training effect in the NA group might have skewed the results, but this is unlikely given that the intervention only involved an exercise ball and very light weights that were not progressed.

Although all subjects had to be non-smokers for at least 5 years, we do not have data on lifetime smoking habits.

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There might have been some selection bias toward healthier subjects, since all of our subjects were recruited from newspaper advertisements. The present study demonstrated that aerobic exercise has no long-term impact on arterial stiffness in older adults with multiple cardiometabolic risk factors.

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Short-term aerobic exercise improves arterial stiffness in type 2 diabetes. Diabetes Res Clin Pract ; 65 2 : 85— Aging habitual exercise, and dynamic arterial compliance. Circulation ; 11 : — Effect of acute and long-term aerobic exercise on arterial stiffness in the elderly. Hypertens Res ; 30 10 : — Aizawa K, Petrella RJ. Acute and chronic impact of dynamic exercise on arterial stiffness in older hypertensives. Open Cardiovasc Med J ; 2 : 3—8.

Effect of exercise on blood pressure in older persons: a randomized controlled trial. Arch Intern Med ; 7 : — Physical activity and older adults: expert consensus for a new research agenda. Gerontologist ; 51 6 : — Effects of continuous vs interval exercise training on blood pressure and arterial stiffness in treated hypertension. Hypertens Res ; 33 6 : — American Diabetes Association. Diabetes Care ; 35 Suppl 1 : S1—S2. Hypertension ; 43 1 : 1—3. Clinical Practice Recommendations Diabetes Care ; 28 Suppl 1 : S1— Christmas C, Andersen RA.


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  6. Exercise and older patients: guidelines for the clinician. J Am Geriatr Soc ; 48 3 : — Medicine ACoS. Lippincott Williams and Wilkins: Philadelphia, The Hawthorne Effect: a randomised, controlled trial. Clinical applications of arterial stiffness: therapeutics and pharmacology.



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