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Relation of hemodynamic volume load to arterial and cardiac size
E C Jones1, R B Devereux, M J O'Grady
1Department of Medicine, New York Hospital-Cornell Medical Center, New York 10021, USA.
Insights
Doppler stroke volume (SV) correlates with left ventricular (LV) and carotid artery enlargement, independent of blood pressure. However, SV does not explain the link between cardiac and arterial size.
Area of Science:
- Cardiovascular physiology
- Echocardiography
- Vascular biology
Background:
- Hemodynamic volume load influences left ventricular (LV) hypertrophy beyond blood pressure (BP) effects.
- Understanding the relationship between cardiac structure and arterial dimensions is crucial for cardiovascular health.
Purpose of the Study:
- To assess the association between Doppler stroke volume (SV) and cardiac (LV) and carotid artery size.
- To determine if volume load explains the parallelism between cardiac and arterial dimensions.
Main Methods:
- Doppler echocardiography was used to measure SV in 342 adults.
- Measurements included LV mass, LV internal dimension (LVID), wall thickness, carotid lumen diameter, intimal-medial thickness (IMT), and cross-sectional area (CSA).
- Multivariate analyses controlled for BP, age, and other relevant factors.
Main Results:
- SV positively correlated with LV mass, LVID, wall thickness, carotid diameter, CSA, and IMT.
- SV independently predicted LV mass and chamber size, and carotid artery dimensions, even after controlling for BP and age.
- LV and carotid dimensions were interrelated independently of SV.
Conclusions:
- Doppler-measured SV is linked to LV and carotid artery enlargement and eccentric hypertrophy, independent of arterial pressure, contractility, age, and body size.
- SV and other assessed variables do not fully account for the observed parallelism between cardiac and arterial structure.
Objectives:
This study sought to assess the relation of Doppler stroke volume (SV) to cardiac and carotid artery size and to determine whether volume load accounts for the parallelism between the two.
Background:
It has been suggested that altered hemodynamic volume load can modify the degree and pattern of left ventricular (LV) hypertrophy from that predicted from blood pressure (BP) alone.
Methods:
We related Doppler echocardiographic SV in 342 normotensive or unmedicated asymptomatic hypertensive adults to echocardiographic LV mass, LV internal dimension (LVID), wall thickness, carotid ultrasound arterial lumen diameter, intimal-medial thickness (IMT) and cross-sectional area (CSA).
Results:
SV was positively related to LV mass (r = 0.42), LVID (r = 0.45), ventricular wall thickness (r = 0.20 to 0.29) and carotid diameter (r = 0.23, all p < 0.0001); CSA (r = 0.17, p < 0.002); and IMT (r = 0.12, p = 0.03). In multivariate analyses controlling for awake ambulatory BP and the circumferential end-systolic stress/end-systolic volume index ratio, SV remained an independent predictor of LV mass and chamber size (both p < 0.0001) but not LV wall thickness. SV also predicted carotid diameter (p < 0.0002), CSA (p = 0.001) and, to a lesser degree, IMT (p = 0.02) after controlling for mean awake BP and age. In additional analyses, LV and carotid dimensions were significantly interrelated independent of SV.
Conclusions:
SV measured by invasively validated Doppler echocardiography is associated with LV and carotid artery enlargement and eccentric hypertrophy, independent of arterial pressure, LV contractility, age and body size; however, SV and other variables do not account for the previously documented parallelism between cardiac and arterial structure.