Late Systolic Pressure Augmentation Research Articles

Prospective risk factors for increased central augmentation index in men and women.

Arterial wave reflections are important determinants of central pressure pulsatility and left ventricular afterload. The augmentation index (AIx) is the most widely used surrogate of arterial wave reflections. Despite multiple cross-sectional studies assessing the correlates of AIx, little prospective data exist regarding changes in AIx over time. We aimed to assess the predictors of changes in AIx over time in adults from the general population. We performed radial arterial tonometry assessments a median of 3.18 ± 0.4 years apart on 143 nondiabetic adult participants in the population-based PREVENCION study. Central AIx was obtained using the generalized transfer function of the Sphygmocor device. Predictors of the change in AIx over time were investigated. Among men (n = 67), the change in AIx was predicted by abdominal obesity (standardized β for waist circumference = 0.34; P = 0.002), impaired fasting glucose (standardized β = 0.24; P = 0.009), and the change in heart rate (standardized β = -0.78; P < 0.001). Among women (n = 76), the change in AIx was predicted by non-high-density lipoprotein cholesterol (standardized β = 0.33; P = 0.001), C-reactive protein levels (standardized β = 0.24; P = 0.02), change in mean arterial pressure (standardized β = 0.33; P = 0.001), and change in heart rate (standardized β = -0.52; P < 0.001). Metabolic and inflammatory factors predicted changes in AIx over time, with important sex differences. Metabolic factors, such as abdominal obesity and impaired fasting glucose, predicted changes in AIx in men, whereas C-reactive protein and non-high-density lipoprotein cholesterol levels predicted changes in women. Our findings highlight the impact of sex on arterial properties and may guide the design of interventions to favorably impact changes in late systolic pressure augmentation.

Left Ventricular Responses to Acute Changes in Late Systolic Pressure Augmentation in Older Adults

Changes in the cardiovascular system with age may predispose older persons to development of heart failure with preserved ejection fraction. Vascular stiffening, aortic pressure augmentation, and ventricular-vascular coupling have been implicated. We explored the potential for acute reductions in late systolic pressure augmentation to impact left ventricular relaxation in older persons without heart failure. Sixteen older persons free of known cardiovascular disease with the exception of hypertension had noninvasive tonometry and cardiac ultrasound to evaluate central augmentation index (AI) and diastolic function at baseline and after randomized, blinded administration of intravenous B-type natriuretic peptide (BNP) and hydralazine in a crossover design. AI was significantly reduced after BNP (11.4±8.9 to -0.2±14.7%; P = 0.02) and nonsignificantly reduced after hydralazine (14.7±8.4% to 11.5±8.8%; P = 0.39). With decreased AI during BNP, a trend toward worsened myocardial relaxation by tissue Doppler imaging occurred (E' velocity pre- and post-BNP: 10.0±2.5 and 8.8±2.0cm/s, respectively; P = 0.06). There was a significant fall in stroke volume with BNP (68.5±18.3 to 60.9±18.1ml; P = 0.02), suggesting that changes in preload overwhelmed effects of afterload reduction on ventricular performance. With hydralazine, neither relaxation nor stroke volume changed. Acute changes in late systolic aortic pressure augmentation do not necessarily lead to improved systolic or diastolic function in older people. Preload may be a more important determinant of cardiac performance than afterload in older people with compensated ventricular function. The potential for changes in preload to impair rather than enhance left ventricular systolic and diastolic function in older people warrants further study. This study is registered at clinicaltrials.gov as NCT00204984.

Right Ventricular Pressure Waveform and Wave Reflection Analysis in Patients With Pulmonary Arterial Hypertension

Cardiac index is an important determinant of outcome in patients with idiopathic pulmonary artery hypertension (IPAH). An implantable hemodynamic monitor (IHM) [Chronicle; Medtronic; Minneapolis, MN; a system limited to investigational use only] that records right ventricular (RV) pressure waveforms continuously may increase our understanding of IPAH and improve therapeutic selections and outcomes. The aim of this study was to investigate whether the RV pressure waveform utilizing an IHM can be used to estimate the magnitude of pressure wave reflection and cardiac index in patients with IPAH in acute settings. In eight patients with pulmonary arterial hypertension, RV pressure waveforms were recorded utilizing the IHM, and breath-by-breath cardiac index was recorded during acute IV epoprostenol infusion at 3, 6 and 9 ng/kg/min. Late systolic pressure augmentation and cardiac index were estimated using the RV pressure waveforms and correlated with direct measurement of cardiac index. At baseline, the cardiac index was 2.1 +/- 0.2 L/min/m(2), total pulmonary resistance index was 38 +/- 2 Wood U/m(2), and RV systolic pressure was 92 +/- 4 mm Hg. Wave reflection accounted for 29 +/- 1 mm Hg of the RV systolic pressure. During epoprostenol infusion, total pulmonary resistance index and wave reflection decreased (- 15 +/- 4 Wood U/m(2), p < 0.001, and - 5 +/- 2 mm Hg, p < 0.05, respectively). The breath-by-breath cardiac index correlated with the RV pressure waveform cardiac index estimates (r(2) = 0.95). RV pressure waveform analysis provides continuous hemodynamic assessments including cardiac index in acute settings. Once confirmed in long-term settings, this information may prove useful in optimizing a treatment regimen in patients with IPAH.

Triangulating the Peaks of Arterial Pressure

Increased arterial stiffness and excessive pressure pulsatility have emerged as important risk factors for a number of common disorders of aging, including cardiovascular disease, stroke, cognitive impairment, and renal disease. The triple-threat combination of robust associations between arterial stiffness and the foregoing disorders, a marked increase in arterial stiffness with advancing age and the graying of our society, has led to intensive efforts to identify mechanisms that contribute to arterial stiffening and widening pulse pressure to define interventions to prevent or reverse stiffness and potentially reduce the substantial burden of related disease. Wave reflections complicate the task of evaluating arterial hemodynamics and play an unclear role in the foregoing diseases. When the heart ejects, ventricular outflow interacts with characteristic impedance of the proximal aorta to produce the forward pressure wave, which travels down the normally compliant aorta at a finite pulse wave velocity (PWV). When the forward wave encounters impedance mismatch, such as a branch point or a change in diameter or wall properties, a partial reflection occurs. Innumerable reflections arising from locations distributed throughout the arterial tree summate into a remarkably discrete reflected pressure wave with amplitude ≈40% of the incident wave. The summated reflected wave returns to the central aorta in midsystole, creating an inflection point and secondary late systolic pressure rise that often augments central aortic systolic and pulse pressure.1 Variable timing of this retrograde-traveling reflected wave creates regional inequalities in systolic and pulse pressure and, therefore, complicates interpretation of single point pressure measurements, such as standard brachial blood pressure, which may differ from central aortic pressure. Augmentation index (AI), which expresses late systolic pressure augmentation as a percentage of pulse pressure, is frequently used to assess wave reflection (Figure). AI, which depends on both timing and amplitude of the reflected wave, has also been widely …

Enhanced Radial Late Systolic Pressure Augmentation in Hypertensive Patients With Left Ventricular Hypertrophy

Wave reflection augments central blood pressure (BP) in late systole, thus increasing cardiac afterload. We examined the relationship between late systolic pressure augmentation in the peripheral radial artery pulse wave and the existence of left ventricular hypertrophy (LVH) in hypertension. Brachial BP, radial augmentation index (AI(r)), and carotid-femoral pulse wave velocity (PWV(cf)) were determined in 77 untreated hypertensive patients aged 56 +/- 10 years. Cardiac structure and function were assessed by ultrasound, and LVH was defined based on the LV mass index (LVMI). Using multivariate analysis, patient characteristics were compared between those with (+) and without (-) LVH. The LVMI was correlated independently and positively with AI(r) (beta = 0.33, P = .004) and the brachial mean arterial pressure (MAP; beta = 0.25, P = .03). The ratio of early to atrial peak velocities (E/A ratio) of the diastolic transmitral flow tended to be correlated negatively with the AI(r). The LVH (+) group had a significantly higher AI(r) than the LVH (-) group [LVH (+), 97% v LVH (-), 89%, P = .003]; this difference remained significant even after adjustment for age, gender, MAP, and heart rate. The adjusted relative risk of LVH was 1.99 for each 10% AI(r) increase (P = .005). In contrast, LVMI was not correlated with the PWV(cf), and the PWV(cf) was not different between the LVH (+) and LVH (-) groups. Moreover, there was no significant correlation between PWV(cf) and AI(r). These results suggest that the peripheral AI(r) measurement is clinically useful in predicting LVH. Enhanced wave reflection may be related to the development of LVH in hypertensive patients.

The relationship between late systolic pressure augmentation and left ventricular mass in a healthy population

The relationship between late systolic pressure augmentation and left ventricular mass in a healthy population

Late systolic pressure augmentation: role of left ventricular outflow patterns.

Late systolic augmentation of the ascending aortic pressure waveform is believed to be caused by particular impedance patterns but also could be caused by particular left ventricular outflow patterns. Using a linear mathematical model of the entire human arterial tree, we derived realistic impedance patterns by altering 1) Young's modulus of the arterial wall of the individual branches, 2) peripheral reflection coefficients, and 3) distal compliances at the terminations. These calculated impedance patterns were then coupled to realistic left ventricular outflow patterns determined by unique 1) end-diastolic and end-systolic pressure-volume relationships, 2) preload-recruitable stroke work relationships, and 3) shortening paths simulated by altered aortic flow contours. As determined by the ratio of the individual parameter coefficient of determination (r(2)) to the overall model r(2), late systolic pressure augmentation was more strongly determined by left ventricular outflow patterns than by arterial impedance parameters (r(2) ratio: 53% vs. 33%). Thus left ventricular outflow patterns are at least as important as impedance parameters in determining late systolic pressure augmentation in this model.

Assessment of vasoactive agents and vascular aging by the second derivative of photoplethysmogram waveform.

To evaluate the clinical application of the second derivative of the fingertip photoplethysmogram waveform, we performed drug administration studies (study 1) and epidemiological studies (study 2). In study 1, ascending aortic pressure was recorded simultaneously with the fingertip photoplethysmogram and its second derivative in 39 patients with a mean+/-SD age of 54+/-11 years. The augmentation index was defined as the ratio of the height of the late systolic peak to that of the early systolic peak in the pulse. The second derivative consists of an a, b, c, and d wave in systole and an e wave in diastole. Ascending aortic pressure increased after injection of 2.5 microg angiotensin from 126/74 to 160/91 mm Hg and decreased after 0.3 mg sublingual nitroglycerin to 111/73 mm Hg. The d/a, the ratio of the height of the d wave to that of the a wave, decreased after angiotensin from -0.40+/-0.13 to -0.62+/-0.19 and increased after nitroglycerin to -0.25+/-0.12 (P<0.001 and P<0.001, respectively). The negative d/a increased with increases in plethysmographic and ascending aortic augmentation indices (r=0.79, P<0.001, and r=0.80, P<0.001, respectively). The negative d/a reflects the late systolic pressure augmentation in the ascending aorta and may be useful for noninvasive evaluation of the effects of vasoactive agents. In study 2, the second derivative of the plethysmogram waveform was measured in a total of 600 subjects (50 men and 50 women in each decade from the 3rd to the 8th) in our health assessment center. The b/a ratio increased with age, and c/a, d/a, and e/a ratios decreased with age. Thus, the second derivative aging index was defined as b-c-d-e/a. The second derivative wave aging index (y) increased with age (x) (r=0.80, P<0.001, y=0.023x-1.515). The second derivative aging index was higher in 126 subjects with any history of diabetes mellitus, hypertension, hypercholesterolemia, and ischemic heart disease than in age-matched subjects without such a history (-0.06+/-0.36 versus -0.22+/-0.41, P<0.01). Women had a higher aging index than men (P<0.01). The b-c-d-e/a ratio may be useful for evaluation of vascular aging and for screening of arteriosclerotic disease.

The influence of changes in loading patterns on left ventricular relaxation in humans.

This clinical investigation was designed to determine the effect of changes in loading patterns on left ventricular (LV) relaxation when heart rate was maintained constant. Not only were changes noted in total load or time in which load is changed, but also the contour of the ascending aortic systolic pressure wave. Twenty patients were studied. LV and ascending aortic pressure were measured by a multisensor catheter under baseline conditions (C) and after an intravenous injection of 2.5 microg angiotensin (A) and sublingual administration of 0.3 mg nitroglycerin (N). A bipolar pacing catheter was placed in the right atrium to maintain a constant heart rate throughout the protocol. The augmentation index (AI), which characterizes the contour of the ascending aortic systolic pressure wave, was defined as the ratio of the height of the late systolic shoulder/peak to that of the early systolic shoulder/peak in the pulse. The rate of isovolumic LV pressure decline was calculated as a time constant (Tau). Ascending aortic systolic pressures (mmHg) were 127+/-29 (C), 158+/-20 (A) and 109+/-15 (N). AI were 1.61+/-1.14 (C), 2.08+/-1.11 (A) and 1.27+/-1.14 (N). Tau values (msec) were 49+/-4 (C), 54+/-4 (A) and 45+/-5 (N). Tau was prolonged proportionally with increasing AI (p<0.001, r=0.64). It was concluded that late systolic pressure augmentation in the ascending aorta is one important factor that influences the rate of isovolumic left ventricular pressure decline in humans.