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Arterial elastance and wave reflection augmentation of systolic blood pressure: deleterious effects and implications
1Department of Medicine, University of Florida College of Medicine, Gainesville, FL 32610, USA.
Insights
Systolic blood pressure is a better predictor of cardiovascular events than diastolic pressure. Increased arterial stiffness elevates systolic pressure, impacting heart function and potentially leading to atherosclerosis.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Biomedical Engineering
Background:
- Systolic blood pressure (SBP) and pulse pressure (PP) are stronger predictors of cardiovascular events and mortality than diastolic pressure (DBP).
- Increased arterial elastance (stiffness) in central elastic arteries, due to arterial wall degeneration and hyperplasia, is a primary cause of elevated SBP and PP with aging and in cardiovascular disease.
- Elevated elastance leads to earlier wave reflection, augmenting central aortic pressure and increasing left ventricular afterload, myocardial oxygen demand, and potentially causing myocardial ischemia.
Purpose of the Study:
- To elucidate the mechanisms by which arterial stiffness influences cardiovascular hemodynamics and outcomes.
- To explain the physiological basis for SBP and PP being superior predictors of cardiovascular disease compared to DBP.
- To evaluate the impact of vasodilator drugs on arterial wave reflection and central hemodynamics.
Main Methods:
- Analysis of arterial hemodynamics, focusing on wave reflection, pulse wave velocity, and arterial elastance.
- Examination of the relationship between arterial wall properties and cardiovascular risk factors.
- Assessment of the effects of vasodilator medications on central and peripheral arterial pressures and wave characteristics.
Main Results:
- Increased arterial elastance is linked to higher SBP, lower DBP, augmented wave reflection, and increased left ventricular afterload.
- Elevated SBP increases arterial wall stress, promoting atherosclerosis.
- Vasodilator drugs reduce wave reflection and augmentation by decreasing elastance in peripheral muscular arteries, leading to decreased SBP and arterial stress, effects underestimated by brachial artery measurements.
Conclusions:
- Arterial stiffness is a critical determinant of cardiovascular risk, primarily through its effects on systolic pressure and wave reflection.
- Understanding the complex interplay between arterial properties and hemodynamics is crucial for effective cardiovascular disease management.
- Pharmacological interventions targeting arterial stiffness and wave reflection may offer significant benefits in reducing cardiovascular events, particularly when central hemodynamics are considered.
Abstract:
Systolic and pulse blood pressures are stronger predictors of stroke, coronary heart disease, myocardial infarction, heart failure, end-stage renal disease, and cardiovascular mortality than diastolic pressure. Furthermore, diastolic pressure is inversely related to coronary heart disease and cardiovascular mortality. Increased elastance (or stiffness, inverse of compliance) of the central elastic arteries is the primary cause of increased systolic and pulse pressure with advancing age and in patients with cardiovascular disease, including hypertension, and is due to degeneration and hyperplasia of the arterial wall; diastolic pressure decreases as arterial elastance increases. As elastance increases, transmission velocity of both forward and backward (or reflected) traveling waves increases, which causes the reflected wave to arrive earlier in the central aorta and augments pressure in late systole. These changes in arterial wall properties cause an increase in left ventricular afterload and myocardial oxygen consumption and a decrease in myocardial perfusion pressure, which may induce an imbalance in the supply-demand ratio, especially in hypertrophied hearts with coronary artery disease. Also, an increase in systolic pressure increases arterial wall circumferential stress, which promotes fatigue and development of atherosclerosis. Vasodilator drugs have little direct active effect on large elastic arteries but can markedly reduce wave reflection amplitude and augmentation index by decreasing elastance of the muscular arteries and reducing pulse wave velocity of the reflected wave from the periphery to the heart. This decrease in intensity (or amplitude) and increase in travel time (or delay) of the reflected wave causes a generalized decrease in systolic pressure and arterial wall stress and an increase in ascending aortic flow during the deceleration phase. The decrease in systolic pressure brought about by this mechanism is grossly underestimated when systolic pressure is measured in the brachial artery.