Much has been published in the past 20 years on the use of measurements of arterial stiffness in animal and human research studies. This summary statement was commissioned by the American Heart Association to address issues concerning the nomenclature, methodologies, utility, limitations, and gaps in knowledge in this rapidly evolving field. The following represents an executive version of the larger online-only Data Supplement and is intended to give the reader a sense of why arterial stiffness is important, how it is measured, the situations in which it has been useful, its limitations, and questions that remain to be addressed in this field. Throughout the document, pulse-wave velocity (PWV; measured in meters per second) and variations such as carotid-femoral PWV (cfPWV; measured in meters per second) are used. PWV without modification is used in the general sense of arterial stiffness. The addition of lowercase modifiers such as “cf” is used when speaking of specific segments of the arterial circulation.

The ability to measure arterial stiffness has been present for many years, but the measurement was invasive in the early times. The improvement in technologies to enable repeated, minimal-risk, reproducible measures of this aspect of circulatory physiology led to its incorporation into longitudinal cohort studies spanning a variety of clinical populations, including those at extreme cardiovascular risk (patients on dialysis), those with comorbidities such as diabetes mellitus (DM) and hypertension, healthy elders, and general populations.

In the ≈3 decades of clinical use of PWV measures in humans, we have learned much about the importance of this parameter. PWV has proven to have independent predictive utility when evaluated in conjunction with standard risk factors for death and cardiovascular disease (CVD). However, the field of arterial stiffness investigation, which has exploded over the past 20 years, has proliferated without logistical guidance for clinical and …

Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness: A Scientific Statement From the American Heart Association

Prevention of atherosclerosis from childhood

PURPOSE OF REVIEW: 

To detail recent developments linking modifiable youth risk factors with preclinical markers of cardiovascular disease such as carotid artery intima-media thickness, pulse-wave velocity (PVW) and large artery stiffness, brachial artery flow-mediated dilatation, left ventricular geometry, and coronary artery calcification in adulthood.

RECENT FINDINGS: 

Population-based data from prospective cohort studies beginning in youth with follow-up into adulthood have shown that the modifiable youth risk factors of elevated blood lipids, blood pressure, and adiposity, smoking (active and passive), metabolic disorders, physical inactivity, low cardiorespiratory fitness, and diet associate with preclinical markers of cardiovascular disease in adulthood. The data suggest that, in some instances, those who amend their trajectory by not maintaining these risk factors into adulthood experience reductions in preclinical markers to levels associated with never having had the risk factor.

SUMMARY: 

Though avoidance of risk factors in youth is ideal, there is still a window for intervention where long-lasting cardiovascular effects might be avoided. Health-enhancing changes in the rates of active and passive smoking, adiposity, increased physical activity, accentuated fitness, modified diet, and socioeconomic position in the transition from youth to adulthood might be important in modifying an individual's trajectory from high risk in youth to low risk in adulthood.

When to prevent cardiovascular disease? As early as possible: lessons from prospective cohorts beginning in childhood

A limited number of observational studies were commenced in the 1970s and 1980s that have aimed to examine the child and adolescent origin of cardiovascular disease. These studies have provided, and continue to provide, critical evidence that have enhanced our understanding of the disease process, the early-life factors involved, and have informed public health and clinical guideline statements. Using data on preclinical markers of vascular health in adulthood, these studies have recently described the important role for youth lifestyle for later vascular health, provided information on the critical age in youth when risk factor associations with adult vascular health emerge, and have reported on the potential vascular benefits of resolving youth at-risk status in the transition from youth to adulthood. It is these works that we cover in detail in this review. Despite all the achievements from these studies, it is tantalizing that their most important contributions are still to come. That is, once sufficient clinical end points accrue so that analyses linking early life health to hard outcomes can be performed. These studies are a commodity and an invaluable resource that, with minimal re-investment, will provide increasing returns on cardiovascular health into the future.

What the Long Term Cohort Studies that Began in Childhood Have Taught Us about the Origins of Coronary Heart Disease

Background. It is unknown how much precociously the cigarette smoking (CS) may compromise the integrity of the cardiovascular (CV) system. Myocardial function can be routinely assessed by conventional echocardiography, but abnormalities are only detected when somewhat a remodelling has already occurred. These limitations could be overcome by strain imaging. Methods. We evaluated whether young smokers with normal left ventricular (LV) geometry, wall motion and ejection fraction may present abnormalities in myocardial deformation, both at rest and during physical effort. We selected 50 young smokers with no additional CV risk factors, and 60 non-smokers to undergo a standardized exercise-test. Consistently, we evaluated the CV adaptation to exercise by both conventional echocardiography and speckle-tracking analysis (2D-STE). Results. We found no difference between smokers and controls regarding baseline characteristics; as expected, smokers presented with lower HDL-cholesterol (p < 0.005), and higher fibrinogen, C-reactive protein (CRP), and interleukin-6 (p < 0.001). Conventional echocardiography parameters were not different between groups, while we detected a different behaviour of global longitudinal strain (GLS), global circumferential strain (GCS) and twist by 2D-STE during exercise-test. Indeed, GLS, GCS and twist behaved differently during exercise test in smokers with respect to controls. We found an association between CS, inflammation and LV mechanics changes uncovered by physical effort, and regression analysis confirmed that the intensity of the exposure to cigarette smoking, together with the inflammatory status (CRP, fibrinogen and Il-6) plasma levels, drive this impairment. Conclusions. We confirm strain imaging (2D-STE) as a very useful tool to identify early changes in cardiac mechanics, as adaptation to exercise; our findings may reflect a very precocious functional abnormality in active smokers, likely long before structural damage occurs.

/pdf/abnormal-left-ventricular-global-strain-during-exercise-test-47zm9lfkhl.pdf

Abnormal left ventricular global strain during exercise-test in young healthy smokers.

Objectives: To investigate the associations between smoking in adolescence and adulthood, and changes in smoking behaviour between these age periods, with arterial stiffness in young adults; and whether any such associations could be explained by concomitant smoking-related levels of inflammation and endothelial dysfunction. Methods: We studied 424 individuals (216 women) in whom smoking status was assessed in adolescence (age 15 years) and again in young adulthood (mean age of 22.6 ± 1.6 years), along with aorto-iliac, aorto-radial, and aorto-dorsalis pedis pulse wave velocity (PWV), and markers of inflammation (i.e. C-reactive protein and fibrinogen) and endothelial dysfunction (i.e. von Willebrand factor and tissue-plasminogen activator antigen) in young adulthood only. Results: Smoking in adolescence was associated with higher aorto-iliac PWV, as well as with inflammation and endothelial dysfunction levels (expressed as two scores), independently of other adolescent and adult lifestyles. Compared with never smokers, continuing smokers, but not starters nor quitters, showed higher aorto-iliac PWV, independent of changes in other lifestyle variables: +0.157 m/s (95% confidence interval 0.026-0.288). This difference was attenuated to 0.124 m/s (-0.009 to 0.257) after adjustment for changes in traditional biological risk factors, but was not materially affected when adjusted for the inflammation and endothelial dysfunction scores, despite the continuing smoking-related higher levels of inflammation and endothelial dysfunction. Smoking was not associated with aorto-radial and aorto-dorsalis pedis PWV. Conclusion: Starting to smoke in adolescence and continuing to do so up to young adulthood is adversely associated with aortic stiffness. The continuing smoking-related aortic stiffness was not explained by concomitant higher inflammation and endothelial dysfunction. Prevention of smoking should target the young to prevent arterial stiffness in young adults.

/pdf/continuing-smoking-between-adolescence-and-young-adulthood-3yl0e99eth.pdf

Continuing smoking between adolescence and young adulthood is associated with higher arterial stiffness in young adults: the Northern Ireland Young Hearts Project

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Continuing smoking between adolescence and young adulthood is associated with higher arterial stiffness in young adults: the Northern Ireland Young Hearts Project