Effective Arterial Elastance Index Research Articles

TAPSE/SPAP ratio stratifies mortality risk in mild-to-moderate idiopathic pulmonary fibrosis.

<sec id="st1"><title>BACKGROUND</title>Due to paucity of literature data, we aimed at evaluating the prognostic role of the ratio of tricuspid annular plane systolic excursion (TAPSE) to systolic pulmonary artery pressure (SPAP) in idiopathic pulmonary fibrosis (IPF) patients without severe pulmonary hypertension and at assessing its correlation with effective arterial elastance index (EaI).</sec><sec id="st2"><title>METHODS</title>Multi-instrumental data obtained in 60 IPF patients (73.2 ± 6.8 years) and 60 matched controls were retrospectively analysed. Primary endpoint was all-cause mortality, while secondary endpoint was the composite of all-cause mortality and re-hospitalisations for all-causes over medium-term follow-up.</sec><sec id="st3"><title>RESULTS</title>At baseline, TAPSE/SPAP was significantly lower in patients with IPF than in controls (0.36 ± 0.25 vs. 0.77 ± 0.18 mm/mmHg; P < 0.001). TAPSE/SPAP was inversely correlated with EaI (r = -0.96) in IPF patients. During follow-up (3.5 ± 1.5 years), 21 patients died and 25 were re-hospitalised due to cardiopulmonary causes. TAPSE/SPAP was independently associated with both primary (HR 0.79, 95%CI 0.65-0.97) and secondary (HR 0.94, 95%CI 0.92-0.97) endpoints. A TAPSE/SPAP ratio of <0.20 and <0.44 mm/mmHg showed the greatest sensitivity and specificity for predicting primary (AUC 0.98) and secondary (AUC 0.99) endpoints, respectively.</sec><sec id="st4"><title>CONCLUSIONS</title>TAPSE/SPAP is a strong predictor of adverse outcomes in mild-to-moderate IPF. The strong correlation between TAPSE/SPAP and EaI might be an expression of a systemic fibrotic process which involves the heart, lungs and circulation.</sec>.

Noninvasive Assessment of Sex Differences in Arterial Load in Healthy Adults

BackgroundWomen have higher risk of heart failure than their male counterparts. Although the mechanical inefficiency of myocardium against an excessive afterload is an important reason of heart failure, little attention has been paid to the sex differences in arterial load and its clinical relevance.ResultsThe effective arterial elastance index (EaI), total arterial compliance index (TACI), and systemic vascular resistance index (SVRI) were determined using transthoracic echocardiography combined with cuff-measured brachial blood pressure in 460 healthy adults (230 men). The sex differences in these arterial load indexes were analyzed. No statistical difference was found in the age, heart rate, and stroke volume index (all P < 0.05). After adjustment for the cuff-measured blood pressure; the estimated marginal means (95% CIs) of the EaI was higher in women than in men [0.972 (0.952–0.991) vs 0.743 (0.724–0.763) mmHg m2/mL, P < 0.001], the TACI was lower in women than in men [0.924 (0.905–0.944) vs 1.055 (1.036–1.075) mL/mm Hg m2, P < 0.001], and no statistical difference was found in the SVRI between sexes (P > 0.05).ConclusionsFor any given cuff-measured blood pressure, greater integrated and pulsatile arterial load are imposed on left ventricle in women than in men, which is a piece of evidence that women have higher risk of heart failure than their counterparts.

Incremental prognostic value of arterial elastance in mild-to-moderate idiopathic pulmonary fibrosis.

Previous reports suggested that poor pulmonary function was associated with increased arterial elastance (Ea) in patients with chronic obstructive pulmonary disease and systemic sclerosis. The mechanisms connecting pulmonary function and Ea have not yet been accurately studied in patients with idiopathic pulmonary fibrosis (IPF). The present study was designed to assess Ea in IPF patients without chronic severe pulmonary hypertension and to determine its prognostic role over a medium-term follow-up. This retrospective study included 60 consecutive patients with mild-to-moderate IPF (73.8 ± 6.6years, 75% males) and 60 controls matched by age, sex and cardiovascular risk factors. All patients underwent physical examination, spirometry, blood tests, modified Haller index (MHI, chest transverse diameter over the distance between sternum and spine) assessment, conventional transthoracic echocardiography implemented with speckle tracking analysis of left atrial positive global strain (LA-GSA+ ) and finally carotid Doppler ultrasonography, at basal evaluation. The effective arterial elastance index (EaI) was calculated as the ratio of end-systolic pressure to stroke volume index. During follow-up period, we evaluated the composite endpoint of (1) pulmonary or cardiovascular hospitalizations; (2) all-cause mortality. At baseline, EaI was significantly higher in IPF patients than controls (4.1 ± 1.3 vs 3.5 ± 1.0mmHg/ml/m2, p = 0.01). EaI was strongly correlated to the following variables: C-reactive protein (CRP) (r = 0.86), forced vital capacity (FVC) (r = - 0.91), E/e' ratio (r = 0.91), LA-GSA+ (r = - 0.92), common carotid artery-cross sectional area (CCA-CSA) (r = 0.89) and MHI (r = 0.86), in IPF patients. Mean follow-up time was 2.4 ± 1.3years. During follow-up, 12 patients died and 17 were hospitalized due to major adverse clinical events. At univariate Cox analysis, CRP (HR 1.51, 95% CI 1.25-1.82), FVC (HR 0.88, 95% CI 0.85-0.91), LA-GSA+ (HR 0.85, 95% CI 0.77-0.94), CCA-CSA (HR 1.12, 95% CI 1.03-1.22) and EaI (HR 2.43, 95% CI 1.75-3.37) were significantly associated with outcome. At multivariate Cox analysis, only EaI (HR 1.60, 95% CI 1.03-2.50) retained statistical significance. An EaI ≥ 4mmHg/ml/m2 showed 100% sensitivity and 99.4% specificity for predicting outcome (AUC = 0.98). In patients with mild-to-moderate IPF, an EaI ≥ 4mmHg/ml/m2 is a negative prognostic factor over a medium-term follow-up.

Exercise Intolerance in Heart Failure With Preserved Ejection Fraction: Arterial Stiffness and Abnormal Left Ventricular Hemodynamic Responses During Exercise

BackgroundArterial stiffness is thought to contribute to the pathophysiology of heart failure with preserved ejection fraction (HFpEF). We sought to examine arterial stiffness in HFpEF and hypertension and investigate associations of arterial and left ventricular hemodynamic responses to exercise. Methods and ResultsA total of 385 symptomatic individuals with an EF of ≥50% underwent upright cardiopulmonary exercise testing with invasive hemodynamic assessment of arterial stiffness and load (aortic augmentation pressure, augmentation index, systemic vascular resistance index, total arterial compliance index, effective arterial elastance index, and pulse pressure amplification) at rest and during incremental exercise. An abnormal hemodynamic response to exercise was defined as a steep increase in pulmonary capillary wedge pressure relative to cardiac output (∆PCWP/∆CO > 2 mm Hg/L/min). We compared rest and exercise measures between HFpEF and hypertension in multivariable analyses. Among 188 participants with HFpEF (mean age 61 ± 13 years, 56% women), resting arterial stiffness parameters were worse compared with 94 hypertensive participants (mean age 55 ± 15 years, 52% women); these differences were accentuated during exercise in HFpEF (all P ≤ .0001). Among all participants, exercise measures of arterial stiffness correlated with worse ∆PCWP/∆CO. Specifically, a 1 standard deviation higher exercise augmentation pressure was associated with 2.15-fold greater odds of abnormal LV hemodynamic response (95% confidence interval 1.52–3.05; P < .001). Further, exercise measures of systemic vascular resistance index, elastance index, and pulse pressure amplification correlated with a lower peak oxygen consumption. ConclusionsExercise accentuates the increased arterial stiffness found in HFpEF, which in turn correlates with left ventricular hemodynamic responses. Unfavorable ventricular–vascular interactions during exercise in HFpEF may contribute to exertional intolerance and inform future therapeutic interventions.

Potential benefits of ambulatory blood pressure monitoring in coarctation of aorta

Abstract Background Ambulatory blood pressure monitoring (ABPM) is more sensitive than resting BP assessment in detecting hypertension in patients with coarctation of aorta (COA). However, it is not known whether ABPM provides a better measure of left ventricular (LV) pressure load and LV remodeling as compared to resting BP. LV pressure overload is the lynchpin in the pathogenesis of cardiovascular mortality in COA patients, because it leads to LV remodeling, LV dysfunction and heart failure, which sets-the-stage for cardiovascular death. Therefore identifying a sensitive clinical metric that reflects LV pressure load and LV remodeling, is an important step towards optimizing antihypertensive therapy to prevent LV dysfunction and mortality. We hypothesized that ambulatory systolic BP (SBP) has better correlation with arterial load and LV remodeling indices as compared to resting SBP. Methods Our study cohort comprised of adults with isolated COA without significant residual coarctation (Doppler peak velocity ≤2.5 m/sec), aortic or mitral valve disease. All patients underwent BP measurement at rest, followed by ABPM. Arterial load (LV pressure load) was assessed using Doppler-derived effective arterial elastance index (EAI). LV remodeling was assessed using: LV mass index (LVMI), and E/e'. We divided the cohorts into 4 categories (normotensive, masked, white-coat, and overt hypertension). Results Of the 106 patients (male 69 [65%); age 39±11 years), 98 (93%) had prior COA intervention at 6±5 years. Resting SBP was 132±17, daytime ambulatory SBP was 142±16, and nighttime ambulatory SBP was 128±12 mmHg. The mean arterial load and LV remodeling indices were: EAI 3.4±0.8 mmHg/ml·m2, LVMI 106±21 g/m2, and E/e'11±4. Compared to resting SBP, ambulatory SBP had better correlation with EAI, LVMI, and E/e'. EAI, LVMI and E/e' were significantly different between hypertension categories (Figure 1). Conclusions In this study, we demonstrated that ambulatory SBP had better correlations with arterial load and LV remodeling indices as compared to resting SBP. This suggests that ambulatory SBP was a more robust metric of LV pressure overload and remodeling, and can improve detection of vascular stiffness, LV hypertrophy and elevated LV filling pressure as compared to resting SBP. The results of the current study have important clinical implications with regards to initiation and titration of antihypertensive therapy. If ABPM is used as the gold standard for diagnosis of hypertension, the masked hypertension group (who would have been misclassified as normotensive based on resting SBP alone) will qualify for antihypertensive therapy. Additionally, since ambulatory SBP had better correlation with LV remodeling indices, perhaps titration of antihypertensive therapy using ABPM will potentially reduce the risk of LV hypertrophy and dysfunction due to hypertension. Figure 1 Funding Acknowledgement Type of funding source: None

Doppler-Derived Arterial Load Indices Better Reflect Left Ventricular Afterload Than Systolic Blood Pressure in Coarctation of Aorta.

Patients with vascular stiffening may display increased arterial afterload that is out of proportion to systolic blood pressure (SBP). Since vascular and endothelial dysfunction develop in patients with coarctation of aorta (COA), we hypothesized that for any SBP, patients with mild COA (COA peak velocity <2 m/s) will have a higher arterial afterload and increased left ventricular mass index (LVMI) compared with controls, and that Doppler-derived arterial load indices would be a better predictor of LVMI compared with SBP alone. We studied 204 COA patients (age 35±12 y) and 204 matched controls. Doppler-derived arterial afterload was assessed using effective arterial elastance index and total arterial compliance index. Despite similar SBP, the mild COA group displayed higher arterial afterload as evidenced by a higher elastance index (3.3±0.9 versus 2.9±0.7 mm Hg/mL·m2; P<0.001) and lower total arterial compliance index (0.8±0.3 versus 1.2±0.5 mL/mm Hg·m2; P<0.001). This was associated with higher LVMI in COA (109±35 versus 93±32, g/m2; P<0.001). Compared with SBP (β=0.24 [95% CI, 0.02-0.45]), elastance index (β=20.2 [95% CI, 15.8-44.1]) and total arterial compliance index (β=-32.5 [95% CI, -43.8 to -123.6]) were better predictors of LVMI. Elastance index (but not SBP) was predictive of longitudinal increases in LVMI (r=0.43, P<0.001). COA patients had higher arterial afterload compared with controls with similar SBP. In comparison to SBP, Doppler-derived arterial load indices correlate more strongly with LV hypertrophy. These data suggest that SBP may underestimate LV afterload in this population. This has important clinical implications since titration of antihypertensive therapy is currently based on SBP.

Mild Coarctation of Aorta is an Independent Risk Factor for Exercise-Induced Hypertension.

Exercise-induced hypertension is a predictor of cardiovascular events in patients with coarctation of aorta (COA). However, it is unclear whether mild COA diagnosis is an independent risk factor of exercise-induced hypertension. We hypothesized that for every unit increase in exercise, patients with COA (without hemodynamically significant coarctation) will have a higher rise in systolic blood pressure (SBP) compared with matched controls. One hundred forty-nine patients with COA (aortic coarctation peak velocity <2 m/s) who underwent exercise testing were matched 1:1 to controls using propensity score method based on age, sex, body mass index, hypertension diagnosis, and SBP at rest. We compared exercise-induced change in SBP between patients with COA and controls and also assessed the correlation between Doppler-derived aortic vascular function indices (effective arterial elastance index and total arterial compliance index) and exercise-induced changes in SBP. Compared with controls, patients with COA had a greater change in SBP per unit metabolic equivalent (β=2.86; 95% CI, 1.96-4.77 versus 1.07, 95% CI, -0.15 to 1.75; P=0.018) and per unit oxygen pulse (β=4.57; 95% CI, 2.97-7.12 versus 1.45, 95% CI, -0.79 to 2.09, P<0.001). There was a correlation between SBPpeak-SBPrest and elastance index (r=0.38, P=0.032) and between SBPpeak-SBPrest and total arterial compliance index (r=-0.51, P=0.001), suggesting an association between vascular dysfunction and exercise-induced BP changes. Patients with COA, without significant obstruction, had higher exercise-induced changes in SBP after adjustment for other risk factors for hypertension. Considering the already known prognostic importance of exercise-induced hypertension, the current study highlights the potential role of exercise testing for risk stratification of patients with mild COA.

Vascular-ventricular coupling during exercise is not affected by exaggerated blood pressures in endurance-trained athletes.

This study sought to examine whether cardiovascular performance during exercise, assessed using the vascular-ventricular coupling index (VVC), was affected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. Subjects were middle-aged endurance-trained men and women. Blood pressure measurements and left ventricular echocardiography were performed in a semiupright position at rest and during steady-state cycling at workloads that elicited 100-110 beats/min (stage 1) and 130-140 beats/min (stage 2). These data were used to calculate effective arterial elastance index (EaI), left ventricular end-systolic elastance index (ELVI), and their ratio (VVC). Additional measurements of left ventricular volumes and function (i.e., stroke volume, cardiac output, and longitudinal strain) and indirect assessments of peripheral vascular function (i.e., total arterial compliance and peripheral vascular resistance) were examined. Fourteen subjects with EBP (EBP+, 50% men) and 14 sex-matched subjects without EBP (EBP-) participated, with results presented as EBP+ versus EBP-. EaI and ELVI increased from rest to exercise while VVC decreased, but only ELVI was different between groups at stage 1 [7.6 (1.8) vs. 6.4 (1.0) mmHg·ml-1·m-2, P = 0.045] and stage 2 [10.3 (1.6) vs. 8.0 (1.7) mmHg·ml-1·m-2, P < 0.001]. Additional comparisons revealed no group difference in the contribution of the Frank-Starling mechanism or left ventricular and peripheral vascular function during exercise. The cardiovascular adjustment to exercise in athletes with EBP is achieved through a matched increase in both EaI and ELVI, and the absence of between-group differences in left ventricular or peripheral vascular function suggests that other factors may contribute to the EBP response.NEW & NOTEWORTHY Cardiovascular performance during submaximal exercise, assessed using vascular-ventricular coupling, is unaffected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. The underlying mechanisms of EBP in athletes remain unknown as changes in left ventricular and peripheral vascular function during exercise were similar in athletes with and without EBP.

Small proximal aortic diameter is associated with higher central pulse pressure and poor outcome in patients with congestive heart failure

A small proximal aortic diameter (AoD) is thought to be associated with a higher characteristic impedance of the proximal aorta. However, there has been no evidence of a relationship between directly evaluated AoD and directly measured central aortic pressure or the outcome of patients with cardiovascular diseases. (a) In 135 patients without heart failure (HF), who underwent coronary catheterization, we retrospectively examined the relationship between the AoD and the central aortic pressure or aortic elastance. The AoD adjusted with covariates was inversely correlated with the central pulse pressure (cPP; coefficient=-0.75; P=0.04; model R(2)=0.575) and the effective arterial elastance index (coefficient=-0.12; P=0.001; model R(2)=0.366). (b) In 197 patients who were hospitalized due to HF, we examined the relationship between the AoD (evaluated using echocardiography) and the outcome using a Cox proportional hazard model. Fifty-three patients died from various causes during the follow-up period (2.2±1.1 years). Multivariable analysis revealed that the AoD remained an independent risk factor for all-cause death (hazard ratio for 1 s.d. increase of the AoD: 0.68, 95% confidence interval: 0.50-0.92, P=0.013) and cardiovascular death (hazard ratio for 1 s.d. increase of the AoD: 0.63, 95% confidence interval: 0.43-0.93, P=0.019). A small AoD was associated with a higher cPP and aortic stiffening in the patients without HF, as well as with a poor outcome for HF patients. Although it is easy to evaluate the AoD, it may offer important information regarding the pulsatile load and may be useful for risk stratification of HF patients.

Augmentation Index Immediately after Maximal Exercise in Patients with Type 2 Diabetes Mellitus

Patients with type 2 diabetes mellitus (T2DM) have exaggerated brachial and central (ascending aortic) blood pressure (BP) during exercise, which is associated with adverse outcomes. Central systolic loading, represented by the augmentation index (AIx), may contribute to exaggerated exercise central BP. This study sought to compare the central AIx response to peak exercise in T2DM and control patients and to identify mechanisms of altered exercise central AIx. Central BP and AIx were quantified by radial tonometry at rest and immediately after peak treadmill exercise in 106 patients with T2DM and 106 nondiabetic controls, pair-matched by age, gender, peak exercise brachial BP, and postexercise HR corresponding to tonometry acquisition. Cardiac volumes (by echocardiography) were assessed in a subgroup (22 T2DM and 22 controls) to derive rest and postexercise arterial-ventricular coupling parameters, including cardiac index (stroke volume index × HR), peripheral vascular resistance index (cardiac index / mean BP), and effective arterial elastance index (end-systolic pressure / stroke volume index). Reserve parameters (exercise--rest) were also defined. Patients with T2DM had lower postexercise central AIx (-1% ± 13% vs 3% ± 14%, P = 0.038) and greater central AIx reserve (-24% ± 13% vs -20% ± 11%, P = 0.002) compared with controls, despite raised postexercise peripheral vascular resistance index (P = 0.013) and effective arterial elastance index (P = 0.011); these parameters independently predicted higher central AIx at rest (P < 0.01) but not after exercise. Moreover, T2DM was independently associated with lower postexercise central AIx (β = -0.21, P = 0.006). Cardiac index reserve, which was blunted in T2DM (P = 0.004), represented the only independent correlate of central AIx reserve (r = 0.39, P = 0.01). Patients with T2DM have significantly (and paradoxically) lower postexercise central AIx and greater central AIx reserve, which may be explained by an impaired cardiac functional reserve.

Elevated augmentation index derived from peripheral arterial tonometry is associated with abnormal ventricular–vascular coupling

Although typically derived from the contour of arterial pressure waveform, augmentation index (AIx) may also be derived from the digital pulse volume waveform using finger plethysmography (peripheral arterial tonometry, PAT). Little is known regarding the physiologic correlates of AIx derived from PAT. In this study, we investigated the relation of PAT-AIx with measures of ventricular-vascular coupling. Pulse volume waves were measured via PAT and used to derive AIx. Using 2-dimensional echocardiography, effective arterial elastance index (EaI) was estimated as end-systolic pressure/stroke volume index. Left ventricular (LV) end-systolic elastance index (E(LV)I) was calculated as end-systolic pressure/end-systolic volume index. Ventricular-vascular coupling ratio was defined as EaI/E(LV)I. Given the bi-directional nature of ventricular-vascular uncoupling as measured by echocardiography, patients were separated into three groups: low EaI/E(LV)I (<0.6, n = 21), optimal EaI/E(LV)I (mean 0.6-1.2, n = 16) and high EaI/E(LV)I (>1.2, n = 10). Adjusting for potential confounders (age, mean arterial pressure, height and heart rate), patients with optimal EaI/E(LV)I had lower AIx (1 +/- 4%, P<0.05) compared to those with low EaI/E(LV)I (13 +/- 4%) and high EaI/E(LV)I (19 +/- 5%). Abnormal ventricular-vascular coupling, arising from either increased effective arterial elastance or increased ventricular elastance, is associated with increased AIx as measured by PAT. Additional research is needed to examine other vascular correlates of PAT-AIx.

A non-invasive cardiovascular index for the quantification of arterial load.

Our aim is to quantify steady and pulsatile components of arterial load in a concise and sensitive way by means of a new non-invasive cardiovascular index (NICI). NICI is based on non-invasively measured pressure (sphygmomanometer), stroke volume index and cardiac index (Doppler echocardiography and ECG) and yields a numerical value (in mm Hg). It expresses the difference between the actual arterial load and reference loading conditions as determined in a control group (29 M/35 F, age 34 +/- 13 yr.) of healthy subjects, with blood pressure 116/61 mm Hg (systolic/diastolic), stroke volume index (SVI) 34 +/- 18 ml.m-2 and cardiac index (CI) 2.1 +/- 0.5 l.min-1.m-2. NICI was calculated in the control group and in 23 borderline hypertensive subjects (10 M/13 F, age 65 +/- 12 yr.) with blood pressure 156/79 mm Hg, SVI 36 +/- 10 ml.m-2 and CI 2.4 +/- 0.6 l.min-1.m-2. NICI was higher in borderline hypertensives (33 +/- 51 vs. 0 +/- 34 mm Hg; P < 0.001) and was strongly correlated with total peripheral resistance index (r = 0.89; P < 0.001) and with the ratio of SVI and pulse pressure (r = -0.89; P < 0.001), expressing the combined effect of both known determinants of cardiac load. NICI was also correlated with effective arterial elastance index (r = 0.89; P < 0.001). NICI quantifies, within a logical biomechanical framework, the arterial load as seen by the ejecting ventricle. It combines steady and pulsatile components of arterial load and has a single control value of zero mm Hg.