Clinical Applications of Arterial Stiffness, Task Force III: Recommendations for User Procedures

Deterioration in endothelial function and arterial stiffness are early events in the development of cardiovascular diseases In adults, noninvasive measures of atherosclerosis have become established as valid and reliable tools for refining cardiovascular risk to target individuals who need early intervention With limited pediatric data, the use of these techniques in children and adolescents largely has been reserved for research purposes Therefore, this scientific statement was written to (1) review the current literature on the noninvasive assessment of atherosclerosis in children and adolescents, (2) make recommendations for the standardization of these tools for research, and (3) stimulate further research with a goal of developing valid and reliable techniques with normative data for noninvasive clinical evaluation of atherosclerosis in pediatric patients Precise and reliable noninvasive tests for atherosclerosis in youth will improve our ability to estimate future risk for heart attack and stroke Currently, large longitudinal studies of cardiovascular risk factors in youth, such as the Bogalusa and Muscatine studies, lack sufficient adult subjects experiencing hard outcomes, such as heart attack and stroke, to produce meaningful risk scores like those developed from Framingham data

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Noninvasive Assessment of Subclinical Atherosclerosis in Children and Adolescents: Recommendations for Standard Assessment for Clinical Research: A Scientific Statement From the American Heart Association

BACKGROUND We wished to assess the respective roles of the antihypertensive and blood pressure (BP)-independent effects of antihypertensive drugs on arterial hemodynamics and left ventricular hypertrophy (LVH) in end-stage renal disease (ESRD) patients. METHODS AND RESULTS In a double-blind study, 24 ESRD patients with LVH were randomized to 12 months9 administration of either the angiotensin-converting enzyme (ACE) inhibitor perindopril (n = 14) or the calcium channel blocker nitrendipine (n = 10). Repeated measurements of the following parameters were performed: BP (mercury sphygmomanometry), left ventricular mass (LVM, echocardiography), cardiac output (aortic cross-section and velocity integral), total peripheral resistance (cardiac output and mean BP), aortic and large-artery compliance (pulse wave velocity, Doppler flowmeter), and arterial wave reflections (augmentation index, applanation tonometry). Radioimmunoassay was used to determine plasma renin activity, aldosterone, and plasma catecholamine levels. Two-way (time-treatment) ANOVA for repeated measures was used for statistical analysis. Perindopril and nitrendipine induced significant and similar decreases in BP, total peripheral resistance (P CONCLUSIONS In ESRD patients with LVH, ACE inhibition decreases LVM independently of its antihypertensive effect and of associated alterations in arterial hemodynamics. The decrease in LVM was due primarily to a decrease in LV volume, which may have resulted in these patients from chronic volume overload.

Cardiac hypertrophy, aortic compliance, peripheral resistance, and wave reflection in end-stage renal disease. Comparative effects of ACE inhibition and calcium channel blockade.

The effects of inactivity and exercise training on established and novel cardiovascular risk factors are relatively modest and do not account for the impact of inactivity and exercise on vascular risk. We examine evidence that inactivity and exercise have direct effects on both vasculature function and structure in humans. Physical deconditioning is associated with enhanced vasoconstrictor tone and has profound and rapid effects on arterial remodelling in both large and smaller arteries. Evidence for an effect of deconditioning on vasodilator function is less consistent. Studies of the impact of exercise training suggest that both functional and structural remodelling adaptations occur and that the magnitude and time-course of these changes depends upon training duration and intensity and the vessel beds involved. Inactivity and exercise have direct “vascular deconditioning and conditioning” effects which likely modify cardiovascular risk.

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Impact of inactivity and exercise on the vasculature in humans

Most (if not all) tumors emerge and progress under a strong evolutionary pressure imposed by trophic, metabolic, immunological, and therapeutic factors The relative impact of these factors on tumor evolution changes over space and time, ultimately favoring the establishment of a neoplastic microenvironment that exhibits considerable genetic, phenotypic, and behavioral heterogeneity in all its components Here, we discuss the main sources of intratumoral heterogeneity and its impact on the natural history of the disease, including sensitivity to treatment, as we delineate potential strategies to target such a detrimental feature of aggressive malignancies The many levels of heterogeneity within tumors dictate their response to therapy and should be considered in future therapeutic regimes

Intratumoral heterogeneity in cancer progression and response to immunotherapy.

Serotonin-mediated cardiovascular responses to electrical stimulation of the raphe nuclei in the rat.

Effects of captopril, clonidine, hydralazine, metoprolol, and prazosin on the circadian variability of blood pressure (BP) and heart rate (HR) as well as on BP and HR rises at awakening were studied in spontaneously hypertensive rats (SHR). An on-line computerized system was used for continuous intraarterial (i.a.) recording of BP and HR. Drugs were infused intravenously (i.v.) with osmotic minipumps. Circadian BP patterns were more pronounced and variable in SHR than in Wistar-Kyoto normotensive control rats. HR patterns were similar in both groups. Antihypertensive treatment resulted in differential effects on the expression of the circadian BP and HR patterns in SHR. Reductions in BP variability and reductions in the awakening increase in BP were not correlated with the BP-lowering efficacy of agents. Treatment with clonidine reduced both circadian variability of BP and HR and the awakening increase. Prazosin reduced circadian BP variability and its awakening increase, whereas metoprolol reduced circadian HR variability only. Hydralazine and captopril did not cause any major effects on the circadian variability of BP and HR. These data indicate that circadian rhythms of BP and HR are under sympathetic control in SHR and are not influenced by nonsympatholytic vasodilators.

Modification of circadian blood pressure and heart rate variability by five different antihypertensive agents in spontaneously hypertensive rats.

Intrahypothalamic serotonin and cardiovascular control in rats.

https://www.kidney-international.org/article/S0085-2538(15)57587-X/pdf

Harry A.J. Struyker-Boudier

Papers

Serotonin-mediated cardiovascular responses to electrical stimulation of the raphe nuclei in the rat.

Modification of circadian blood pressure and heart rate variability by five different antihypertensive agents in spontaneously hypertensive rats.

Intrahypothalamic serotonin and cardiovascular control in rats.

Compliance and reactivity of the peripheral venous system in chronic intermittent hemodialysis

Diurnal pattern of vessel-wall properties of large arteries in healthy men.