Pressure Wave Transmission along the Human Aorta

O’Rourke, Michael; Blazek, James V.; Morreels, Charles L.; Krovetz, L. Jerome

doi:10.1161/01.res.23.4.567

Cited by 211 publications

(53 citation statements)

References 24 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As the arteries stiffen with age, amplification decreases, and central pressure more closely approximates peripheral pressure. 45 Intraclass correlations for the BP-related variables were as high as one would expect for traits showing a considerable amount of intraindividual variation. Intraclass correlations for peripheral SBP and DBP were very similar to those reported in earlier studies, although heritability estimates in our study were somewhat lower.…”

Section: Snieder Et Al Heritability Of Augmentation Indexdiscussionmentioning

confidence: 85%

Heritability of Central Systolic Pressure Augmentation

et al. 2000

View full text Add to dashboard Cite

Abstract-Less than 50% of the variance in left ventricular mass is explained by conventional factors such as age, blood pressure, and body size. Genetic influences may account for part of the unexplained variance. The central (aortic) pressure augmentation index has been suggested as a noninvasive measure of pulsatile load, which is a likely determinant of left ventricular mass. We quantified the genetic influence on augmentation index and determined the extent to which this influence is dependent on the effects of age, height, heart rate, and blood pressure. We performed a classical twin study composed of 225 monozygotic and 594 dizygotic female white twin pairs aged 18 to 73 years. Augmentation index and mean arterial pressure were based on the central pressure wave derived from the radial waveform as measured by applanation tonometry. Quantitative genetic modeling techniques were used to analyze the data. The heritability of augmentation index was 37%, whereas heritabilities for blood pressure traits varied between 13% and 25%. Most of the variance in augmentation index could be explained by genetic and environmental factors specifically influencing augmentation index. Only a relatively small part of the total variance in augmentation index could be attributed to genes in common with height (3.1%), heart rate (4.6%), and mean arterial pressure (5.6%). Age explained 19% of the total variation in augmentation index. In conclusion, augmentation index has a significant heritable component, which is largely independent of the influence of blood pressure, heart rate, height, and age. Finding genes for the augmentation index could help to unravel pathophysiological mechanisms causing left ventricular hypertrophy and lead to improvements in prevention, diagnosis, and treatment of at-risk populations. 4 It has been suggested that inheritance may account for part of the unexplained variance. [5][6][7] One hemodynamic factor that has been suggested to influence left ventricular mass is pulsatile vascular load, 8 -10 although this has been difficult to measure in large populations. Murgo et al 11 showed that patterns of augmentation index (AI) relate to invasively measured pulsatile vascular load. Recent studies indicate that the AI can be measured accurately noninvasively, providing a reliable method of studying arterial properties in a large population. 12 AI is defined as the ratio of augmented systolic pressure (due to the late systolic peak in the central pressure waveform) to pulse pressure 8 and represents a measure of a combination of factors related to large arterial function. It is increased in association with arterial stiffness, caused by the degeneration of the arterial wall as a result of repetitive cyclic stress, which is a major determinant of increasing systolic pressure with age and in patients with hypertension. 13 Stiffening of the main central arteries also leads to increased velocity of the pulse wave as it travels down the arteries, which causes wave reflections from peripheral sites to return ea...

show abstract

Section: Snieder Et Al Heritability Of Augmentation Indexdiscussionmentioning

confidence: 85%

Heritability of Central Systolic Pressure Augmentation

et al. 2000

View full text Add to dashboard Cite

show abstract

“…[1][2][3][4][5][6] Both the magnitude and timing of the reflected wave(s) are important in assessing their potential physiologic significance. Since a reflected pressure wave adds to the forward wave, a wave returning during systole would increase ventricular afterload.…”

mentioning

confidence: 99%

Arterial wave reflection in heart failure.

Laskey¹,

Kussmaul²

1987

Circulation

121

View full text Add to dashboard Cite

Arterial wave reflection may adversely influence both left ventricular afterload and ejection performance. Therefore, using multisensor catheter manometers, we derived wave reflection indexes from ascending aortic pressure and velocity recordings in 17 subjects with clinical heart failure secondary to idiopathic dilated cardiomyopathy and 11 control subjects free of detectable cardiovascular disease. Patients were studied at rest as well as during submaximal supine bicycle exercise. Eight of the subjects with cardiomyopathy were also studied during infusion of nitroprusside at rest and on exercise. Reflection indexes decreased on exercise in normal subjects but did not consistently do so in the subjects with heart failure. In both groups the reflected wave on exercise returned earlier during the ejection period. Infusion of nitroprusside at rest in subjects with heart failure had dramatic, and significant, effects on the magnitude and timing of arterial wave reflections. THE PRESENCE of arterial wave reflections may be inferred from characteristic alterations in the pressure pulse as it propagates along the aorta. 1-6 Both the magnitude and timing of the reflected wave(s) are important in assessing their potential physiologic significance. Since a reflected pressure wave adds to the forward wave, a wave returning during systole would increase ventricular afterload. Reflected flow waves, however, subtract from the forward flow pulse. Therefore a wave returning during systole diminishes net forward flow and is disadvantageous to ventricular ejection.Changes in systemic vascular resistance have been shown to result in corresponding changes in the reflection properties of the arterial tree. A decrease in peripheral resistance may decrease wave reflections, whereas an increase in peripheral resistance enhances wave reflections.7-9 However, reflections may diminish in the absence of alterations in peripheral resis- acteristic feature of congestive heart failure.1t We reasoned that physiologic or pharmacologic decreases in systemic vascular resistance might result in corresponding, and hopefully beneficial, changes in the reflection characteristics of the arterial tree. Maneuvers that alter the magnitude of reflected waves may also effect a change in their timing. Thus the overall effect(s) of systemic vasodilation may be difficult to predict. To this end, we compared the magnitude and timing of arterial wave reflections in normal subjects, at rest and on exercise, with those in subjects with congestive heart failure. The effects of nitroprusside in the latter subjects were also analyzed to compare physiologic and pharmacologic arteriolar vasodilation in heart failure. MethodsPatients. Seventeen patients (12 men, five women), 24 to 66 years old (mean 44 + 12) with clinical signs and symptoms of congestive heart failure (NYHA class III to IV) were referred to the cardiac catheterization laboratory for endomyocardial biopsy and to rule out the presence of coronary artery disease. Each patient had a dilated, diff...

show abstract

“…Propagation of the PP wave along the arterial tree is influenced by various factors, including the effect of wave frequency on wave velocity, the length of blood vessels, and the rate of damping; high-frequency waves are transmitted faster than low-frequency waves, and this enhances the systolic peak and changes the contour of the pulse wave (more steep) in the distal part of the aorta (6,32,33). When the pulse wave travels further to the periphery, its contour changes because of the damping effect.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, a rise in systolic BP depends on left ventricular performance as well as the stiffness of the central conduit arteries and the degree of systemic resistance (6,32,33). When hardening/stiffness further increases and PWV becomes higher, the difference in contour and magnitude of pulse wave between the proximal and distal aorta becomes small because the wave reflection from the periphery (faster return) enhances the steepness and height of the ascending limb of the pulse wave in the ascending aorta (32). Because in the present study systolic BP was relatively stable in all groups, the widening of PP may primarily be ascribed to the reduction in compliance/hardening of the aortic (arterial) wall.…”

Section: Discussionmentioning

confidence: 99%

Do incremental increases in blood pressure elicit neointimal plaques through endothelial injury?

Ruiz-Feria

Yang

Nishimura

2004

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Fowl (males more than females) show maturation-dependent rises in blood pressure (BP) and formation of neointimal plaques (NPs), resembling balloon catheter injury-induced neointima, in the abdominal aorta (AbA) just above the bifurcation. The plaque comprises neointimal cells containing abundant endoplasmic reticulum and extracellular matrix. Hence, we investigated whether rapid incremental BP increases in male chicks trigger NP formation, possibly via endothelial injury in hemodynamically selective areas. In 6-wk-old chicks (n ϭ 8) treated 4 wk with solvent (Sv; minipump) or arginine supplement (Arg; 0.3% in drinking water), BP increased from 140 Ϯ 5 to 159 Ϯ 4 (Sv) and from 138 Ϯ 4 to 157 Ϯ 3 (Arg) mmHg, whereas propranolol treatment (Prop, 8 mg⅐kg Ϫ1 ⅐day Ϫ1; minipump) prevented the rise. Arg and Prop groups had, respectively, 73% and 77% smaller (P Ͻ 0.05) NP areas and 19% and 25% less (P Ͻ 0.01) AbA medial thickness than Sv controls. In 16-wk-old cockerels, established BP remained high after Sv and Arg treatments. In the Prop group, BP decreased, but neither NP area nor medial thickness was lower than in the Sv group, whereas the Arg group showed greater NP area and medial thickness. Pulse pressure, determined by intravascular transducer, increased as the pulse wave descended the aorta. The results suggest that maturation-dependent rises in BP in chicks may trigger NP formation in the lower segment of the AbA, which was prevented by inhibition of BP increase, or via a possible increase in nitric oxide availability. BP reduction exerts no effect once BP reaches a plateau. Involvement of endothelial injury leading to NP formation and hemodynamic forces selective for the lesion-prone area remain to be determined. arginine supplement; nitric oxide; hypertension; atherosclerosis; fowl model; pulse pressure; endothelial dysfunction; endothelial nitric oxide synthase uncoupling BIRDS, particularly fowl, have higher blood pressure (BP) than most mammals. In both male and female fowl, BP is already ϳ150 mmHg at 2-3 wk after birth, and at plateau levels, mean BP is higher in males (194 Ϯ 4.6 mmHg) than in females (169 Ϯ 3.1 mmHg) (13,29,30). In males, BP tends to increase with maturation and/or age, whereas an age-dependent change is not clear in females (30). Before sexual maturation, vascular neointimal plaques (NPs), comprising deformed endothelial cells, proliferating neointimal cells of synthetic phenotype, increased endoplasmic reticulum, and abundant extracellular matrix, are spontaneously formed without a high-cholesterol or high-fat diet (30). The NP lesions are seen in the abdominal aorta, most frequently just before the aortic bifurcation into the ischiadic arteries (referred to as the lesion-prone area); the size of the NP area increases with maturation and/or age, whereas vascular smooth muscle (SM) exhibits adaptive hypertrophy (30). In humans, aging and hypertension are major factors in the induction of arterial hardening (6, 28), and increased brachial pulse pressure (PP), aortic pulse wave velocity ...

show abstract

Pressure Wave Transmission along the Human Aorta

Cited by 211 publications

References 24 publications

Heritability of Central Systolic Pressure Augmentation

Heritability of Central Systolic Pressure Augmentation

Arterial wave reflection in heart failure.

Do incremental increases in blood pressure elicit neointimal plaques through endothelial injury?

Contact Info

Product

Resources

About