Arterial and Cardiac Remodeling Associated With Extra Weight Gain in an Isolated Abdominal Obesity Cohort

Introduction: This study aims to assess the changes in cardiovascular remodeling attributable to bodyweight gain in a middle-aged abdominal obesity cohort. A remodeling worsening might explain the increase in cardiovascular risk associated with a dynamic of weight gain.Methods: Seventy-five middle-aged subjects (56 ± 5 years, 38 women) with abdominal obesity and no known cardiovascular disease underwent MRI-based examinations at baseline and at a 6.1 ± 1.2-year follow-up to monitor cardiovascular remodeling and hemodynamic variables, most notably the effective arterial elastance (Ea). Ea is a proxy of the arterial load that must be overcome during left ventricular (LV) ejection, with increased EA resulting in concentric LV remodeling.Results: Sixteen obese subjects had significant weight gain (>7%) during follow-up (WG+), whereas the 59 other individuals did not (WG–). WG+ and WG– exhibited significant differences in the baseline to follow-up evolutions of several hemodynamic parameters, notably diastolic and mean blood pressures (for mean blood pressure, WG+: +9.3 ± 10.9 mmHg vs. WG–: +1.7 ± 11.8 mmHg, p = 0.022), heart rate (WG+: +0.6 ± 9.4 min−1 vs. −8.9 ± 11.5 min−1, p = 0.003), LV concentric remodeling index (WG: +0.08 ± 0.16 g.mL−1 vs. WG−: −0.02 ± 0.13 g.mL−1, p = 0.018) and Ea (WG+: +0.20 ± 0.28 mL mmHg−1 vs. WG−: +0.01 ± 0.30 mL mmHg−1, p = 0.021). The evolution of the LV concentric remodeling index and Ea were also strongly correlated in the overall obese population (p < 0.001, R2 = 0.31).Conclusions: A weight gain dynamic is accompanied by increases in arterial load and load-related concentric LV remodeling in an isolated abdominal obesity cohort. This remodeling could have a significant impact on cardiovascular risk.

Arterial Load and Norepinephrine Are Associated With the Response of the Cardiovascular System to Fluid Expansion

BackgroundFluid responsiveness has been extensively studied by using the preload prism. The arterial load might be a factor modulating the fluid responsiveness. The norepinephrine (NE) administration increases the arterial load and modifies the vascular properties. The objective of the present study was to determine the relationship between fluid responsiveness, preload, arterial load, and NE use. We hypothesized that as a preload/arterial load, NE use may affect fluid responsiveness.MethodsThe retrospective multicentered analysis of the pooled data from 446 patients monitored using the transpulmonary thermodilution before and after fluid expansion (FE) was performed. FE was standardized between intensive care units (ICUs). The comparison of patients with and without NE at the time of fluid infusion was performed. Stroke volume (SV) responsiveness was defined as an increase of more than 15% of SV following the FE. Pressure responsiveness was defined as an increase of more than 15% of mean arterial pressure (MAP) following the FE. Arterial elastance was used as a surrogate for the arterial load.ResultsA total of 244 patients were treated with NE and 202 were not treated with NE. By using the univariate analysis, arterial elastance was correlated to SV variations with FE. However, the SV variations were not associated with NE administration (26 [15; 46]% vs. 23 [10; 37]%, p = 0.12). By using the multivariate analysis, high arterial load and NE administration were associated with fluid responsiveness. The association between arterial elastance and fluid responsiveness was less important in patients treated with NE. Arterial compliance increased in the absence of NE, but it did not change in patients treated with NE (6 [−8; 19]% vs. 0 [−13; 15]%, p = 0.03). The changes in total peripheral and arterial elastance were less important in patients treated with NE (−8 [−17; 1]% vs. −11 [−20; 0]%, p < 0.05 and −10 [−19; 0]% vs. −16 [−24; 0]%, p = 0.01).ConclusionThe arterial load and NE administration were associated with fluid responsiveness. A high arterial load was associated with fluid responsiveness. In patients treated with NE, this association was lower, and the changes of arterial load following FE seemed to be driven mainly by its resistive component.

The isobaric pulmonary arterial compliance in pulmonary hypertension

Pulmonary hypertension (PH) is associated with stiffening of pulmonary arteries which increases right ventricular pulsatile loading. High pulmonary artery wedge pressure (PAWP) in postcapillary PH (Pc-PH) further decreases PA compliance (PAC) at a given pulmonary vascular resistance (PVR) compared to precapillary PH, thus responsible for a higher total arterial load. In all other vascular beds, arterial compliance is considered as mainly determined by the distending pressure, due to non-linear stress-strain behaviour of arteries. We tested the applicability, advantages and drawbacks of two comparison methods of PAC depending on the level of mean PA pressure mPAP (isobaric PAC) or PVR.Right heart catheterisation data including PAC (stroke volume/pulse pressure) were obtained in 112Pc-PH (of whom 61 had combined postcapillary and precapillary PH) and 719 idiopathic pulmonary arterial hypertension (iPAH).PAC could be compared over the same mPAP range (25–66 mmHg) in 792/831 patients (95.3%) and over the same PVR range (3–10.7 WU) in only 520/831 patients (62.6%). The main assumption underlying comparisons at a given PVR was not verified as the PVR×PAC product (RC-time) was not constant but on the contrary more variable than mPAP. In the 788/831 (94.8%) patients studied over the same PAC range (0.62–6.5 mL·mmHg−1), PVR and thus total arterial load tended to be higher in iPAH.Our study favours comparing PAC at fixed mPAP level (isobaric PAC) rather than at fixed PVR. A reappraisal of the effects of PAWP on the pulsatile and total arterial load put on the right heart is needed, and this point deserves further studies.

Aortic Stiffness, Central Blood Pressure, and Pulsatile Arterial Load Predict Future Thoracic Aortic Aneurysm Expansion

Thoracic aortic aneurysm is a disease associated with high morbidity and mortality. Clinically useful strategies for medical management of thoracic aortic aneurysm are critically needed. To address this need, we sought to determine the role of aortic stiffness and pulsatile arterial load on future aneurysm expansion. One hundred five consecutive, unoperated subjects with thoracic aortic aneurysm were recruited and prospectively followed. By combining arterial tonometry with echocardiography, we estimated measures of aortic stiffness, central blood pressure, steady, and pulsatile arterial load at baseline. Aneurysm size was measured at baseline and follow-up with imaging; growth was calculated in mm/y. Stepwise multivariable linear regression assessed associations of arterial stiffness and load measures with aneurysm growth after adjusting for potential confounders. Mean±SD age, baseline aneurysm size, and follow-up time were 62.6±11.4 years, 46.24±3.84 mm, and 2.92±1.01 years, respectively. Aneurysm growth rate was 0.43±0.37 mm/y. After correcting for multiple comparisons, higher central systolic (β±SE: 0.026±0.009, P =0.007), and pulse pressures (β±SE: 0.032±0.009, P =0.0002), carotid-femoral pulse wave velocity (β±SE: 0.032±0.011, P =0.005), amplitudes of the forward (β±SE: 0.044±0.012, P =0.0003) and reflected (β±SE: 0.060±0.020, P =0.003) pressure waves, and lower total arterial compliance (β±SE: −0.086±0.032, P =0.009) were independently associated with future aneurysm growth. Measures of aortic stiffness and pulsatile hemodynamics are independently associated with future thoracic aortic aneurysm growth and provide novel insights into disease activity. Our findings highlight the role of central hemodynamic assessment to tailor novel risk assessment and therapeutic strategies to patients with thoracic aortic aneurysm.

Potential benefits of ambulatory blood pressure monitoring in coarctation of aorta

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

Impact of arterio–ventricular interaction on first-phase ejection fraction in aortic stenosis

Aims First-phase ejection fraction (EF1), the EF at the time to peak aortic jet velocity, has been proposed as a novel marker of peak systolic function in aortic stenosis (AS). This study aimed to explore the association of myocardial contractility and arterial load with EF1 in AS patients. Methods and results Data from a prospective, cross-sectional study of 114 patients with mild, moderate, and severe AS with preserved left ventricular EF (>50%) were analysed. EF1 was measured as the volume change from end-diastole to the time that corresponded to peak aortic jet velocity. Myocardial contractility was assessed by strain rate measured by speckle tracking echocardiography. Arterial stiffness was assessed by central pulse pressure/stroke volume index ratio (PP/SVi). The total study population included 48% women, median age was 73 years, and mean peak aortic jet velocity was 3.47 m/s. In univariable linear regression analyses, lower EF1 was associated with higher age, higher peak aortic jet velocity, lower global EF, lower global longitudinal strain, lower strain rate, and higher PP/SVi. There was no significant association between EF1 and heart rate or sex. In multivariable linear regression analysis, EF1 was associated with lower strain rate and higher PP/SVi, independent of AS severity. Replacing PP/SVi by valvular impedance did not change the results. Conclusion In patients with AS, reduced myocardial contractility and increased arterial load were associated with lower EF1 independent of the severity of valve stenosis.