Dataset Information

Arterial load and ventricular-arterial coupling: physiologic relations with body size and effect of obesity.

ABSTRACT: Accurate quantification of arterial function is crucial to distinguishing disease states from normal variants. However, there are little data regarding methods to scale arterial load to body size in humans. We studied 2365 adults aged 35 to 55 years free of overt cardiovascular disease. We assessed arterial hemodynamics and ventricular-vascular coupling with carotid tonometry and Doppler echocardiography. To define normal (physiological) relationships between hemodynamic indices and body size, we used nonlinear regression to analyze a selected reference subsample (n=612) with normal weight (body mass index 18 to 25 kg/m(2)), waist circumference, and metabolic parameters. Most arterial hemodynamic indices demonstrated important relationships with body size, which were frequently allometric (nonlinear). Allometric indexation using appropriate powers (but not ratiometric indexation) effectively eliminated the relationships between indices of arterial load and body size in normal subjects. In the entire sample (n=2365), the adverse effects of obesity on arterial load and end-systolic ventricular stiffening were clearly demonstrated only after appropriate indexation to account for the expected normal relationship to body size. After adjustment for age and sex, a progressive increase in indexed systemic vascular resistance, effective arterial and ventricular end-systolic elastance, and a decrease in total arterial compliance were seen from normal weight to obesity (P<0.0001). Arterial load relates to body size in an allometric fashion, calling for scaling with the use of appropriate powers. Obesity exerts adverse effects on arterial load and ventricular stiffening that go beyond the normal relationship with body size. Allometric normalization should allow more accurate quantification of arterial load in future studies.

SUBMITTER: Chirinos JA

PROVIDER: S-EPMC2780003 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Arterial load and ventricular-arterial coupling: physiologic relations with body size and effect of obesity.

Chirinos Julio A JA Rietzschel Ernst R ER De Buyzere Marc L ML De Bacquer Dirk D Gillebert Thierry C TC Gupta Amit K AK Segers Patrick P

Hypertension (Dallas, Tex. : 1979) 20090706 3

Accurate quantification of arterial function is crucial to distinguishing disease states from normal variants. However, there are little data regarding methods to scale arterial load to body size in humans. We studied 2365 adults aged 35 to 55 years free of overt cardiovascular disease. We assessed arterial hemodynamics and ventricular-vascular coupling with carotid tonometry and Doppler echocardiography. To define normal (physiological) relationships between hemodynamic indices and body size, w ...[more]

PMID: 19581507

Similar Datasets

Project description:Age is the dominant risk factor for cardiovascular diseases. Understanding the coupling between the left ventricle (LV) and arterial system, termed arterial-ventricular coupling (E(A)/E(LV)), provides important mechanistic insights into the complex cardiovascular system and its changes with aging in the absence and presence of disease. E(A)/E(LV) can be indexed by the ratio of effective arterial elastance (E(A); a measure of the net arterial load exerted on the LV) to left ventricular end-systolic elastance (E(LV); a load-independent measure of left ventricular chamber performance). Age-associated alterations in arterial structure and function, including diameter, wall thickness, wall stiffness, and endothelial dysfunction, contribute to a gradual increase in resting E(A) with age. Remarkably there is a corresponding increase in resting E(LV) with age, due to alterations to LV remodeling (loss in myocyte number, increased collagen) and function. These age-adaptations at rest likely occur, at least, in response to the age-associated increase in E(A) and ensure that E(A)/E(LV) is closely maintained within a narrow range, allowing for optimal energetic efficiency at the expense of mechanical efficacy. This optimal coupling at rest is also maintained when aging is accompanied by the presence of hypertension, and obesity, despite further increases in E(A) and E(LV) in these conditions. In contrast, in heart failure patients with either reduced or preserved ejection fraction, E(A)/E(LV) at rest is impaired. During dynamic exercise, E(A)/E(LV) decreases, due to an acute mismatch between the arterial and ventricular systems as E(LV) increases disproportionate compared to E(A) (≈200 vs. 40%), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. However, with advancing age the reduction in E(A)/E(LV) during acute maximal exercise is blunted, due to a blunted increase E(LV). This impaired E(A)/E(LV) is further amplified in the presence of disease, and may explain, in part, the reduced cardiovascular functional capacity with age and disease. Thus, although increased stiffness of the arteries itself has important physiological and clinical relevance, such changes also have major implications on the heart, and vice versa, and the manner in the way they interact has important ramifications on cardiovascular function both at rest and during exercise. Examination of the alterations in arterial-ventricular coupling with aging and disease can yield mechanistic insights into the pathophysiology of these conditions and increase the effectiveness of current therapeutic interventions.

Dataset Information

Arterial load and ventricular-arterial coupling: physiologic relations with body size and effect of obesity.

Publications

Arterial load and ventricular-arterial coupling: physiologic relations with body size and effect of obesity.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets