Ventricular-vascular Coupling Research Articles

Elimination of Transcoarctation Pressure Gradients Has No Impact on Left Ventricular Function or Aortic Shear Stress After Intervention in Patients With Mild Coarctation

This study sought to investigate the impact of transcatheter intervention on left ventricular function and aortic hemodynamics in patients with mild coarctation of the aorta (COA). The optimal method and timing of transcatheter intervention for COA remains unclear, especially whenthe severity of COA is mild (peak-to-peak transcoarctation pressure gradient<20 mmHg). Debate rages regarding the risk/benefit ratio of intervention versus long-term effects of persistent minimal gradient in this heterogeneous population with differing blood pressures, ventricular function, and peripheral perfusion. We developed a unique computational fluid dynamics and lumped parameter modeling framework based on patient-specific hemodynamic input parameters and validated it against patient-specific clinical outcomes (before and after intervention). We used clinically measured hemodynamic metrics and imaging of the aorta and the left ventricle in 34 patients with mild COA to make these correlations. Despite dramatic reduction in the transcoarctation pressure gradient (catheter and Doppler echocardiography pressure gradients reduced by 75% and 47.3%, respectively), there was only modest effect on aortic flow and no significant impact on aortic shear stress (the maximum time-averaged wall shear stress in descending aorta was reduced 5.1%). In no patient did transcatheter intervention improve left ventricular function (e.g., stroke work and normalized stroke work were reduced by only 4.48% and 3.9%, respectively). Transcatheter intervention that successfully relieves mild COA pressure gradients does not translate to decreased myocardial strain. The effects of the intervention were determined to the greatest degree by ventricular-vascular coupling hemodynamics and provide a novel valuable mechanism to evaluate patients with COA that may influence clinicalpractice.

Reduced haemodynamic coupling and exercise are associated with vascular stiffening in pulmonary arterial hypertension

ObjectiveInadequate right ventricular (RV) and pulmonary arterial (PA) functional responses to exercise are important yet poorly understood features of pulmonary arterial hypertension (PAH). This study combined invasive catheterisation with echocardiography...

Right ventricular end-diastolic stiffness heralds right ventricular failure in monocrotaline-induced pulmonary hypertension.

Recent studies suggest right ventricular (RV) stiffness is important in pulmonary hypertension (PH) prognosis. Smaller stroke volume (SV) variation after a certain RV end-diastolic pressure (EDP) respiratory variation as assessed by spectral transfer function (STF) may identify RV stiffness. Our aim was to evaluate RV stiffness in monocrotaline (MCT)-induced PH progression and to validate STF gain between EDP and SV as marker of stiffness. Seven-week-old male Wistar rats randomly injected with 60 mg/kg MCT or vehicle were divided into three groups (n = 12 each) according to cardiac index (CI): controls (Ctrl), preserved CI (MCT pCI), and reduced CI (MCT rCI). All underwent RV pressure-volume (PV) evaluation 24-34 days after MCT, under halogenate anesthesia and constant positive-pressure ventilation. End-diastolic stiffness (βi), end-systolic elastance (Eesi), arterial elastance for indexed volumes (Eai), and preload recruitable stroke work (PRSW) were obtained and beat-to-beat fluctuations during ventilation assessed by STF. Eai was the strongest determinant of CI, alongside βi but not PRSW. MCT rCI showed impaired ventricular-vascular coupling (VVC) and higher βi, along with low end-diastolic pressure (EDP) and stroke volume index (SVi) STF gain, denoting impaired preload reserve. On multivariate analysis βi and not Eesi correlated with EDP-SVi STF gain (P < 0.001). Receiver-operating characteristics (ROC) curve analysis of EDP-SVi STF gain showed an area under curve of 0.84 for βi prediction (P = 0.002). Afterload, impaired VVC and RV stiffness are major players in RV failure. RV stiffness can be assessed by STF gain analysis of respiratory fluctuations between EDP and SVi, which may constitute a prognostic tool in PH.

Magnetic resonance and applanation tonometry for noninvasive determination of left ventricular load and ventricular vascular coupling in the time and frequency domain.

Cardiac magnetic resonance (CMR) is potentially more useful than Doppler ultrasound for quantifying ascending aortic flow velocity in the presence of complex flow patterns. Our aim was to characterize flow velocity wave patterns in the ascending aorta with age and their use with central (carotid) pressure waves to estimate ascending aortic impedance as left ventricular (LV) load and interpret vascular/ventricular interaction. Ascending aortic flow velocity was measured noninvasively, using velocity-encoded CMR, in 50 healthy individuals (21-70 years) by averaging flow velocities across the aortic cross-section. Pressure waves were measured noninvasively by carotid tonometry as a surrogate of aortic pressure. Impedance was determined in modulus and phase from corresponding harmonics of pressure and flow velocity waves. With increasing age, ascending aortic peak flow velocity decreased from 67 ± 18 cm/s in younger persons (≤50 years) to 48 ± 13 cm/s in older persons (>50 years) (P < 0.0001), largely attributable to increase in aortic diameter 2.5 ± 0.3 cm for third decade to 3.3 ± 0.2 cm for seventh decade (P < 0.001). With ageing, carotid pressure augmentation index increased (r = 0.52, P < 0.001), as expected from increased aortic stiffness, whereas ascending aortic flow pressure augmentation index decreased during the mid-to-late systolic period (r = 0.26, P < 0.001), attributable to progressive impairment in LV contractility. Ascending aortic impedance spectra showed ageing changes seen in previous invasive studies and as predicted from modelling. CMR provides noninvasive measures of LV pulsatile load in time and frequency domain, with expected differences between young and older persons. This conforms with and extends the new American Heart Association recommendations for LV afterload and vascular/ventricular interaction.

Right Ventricular Functional Reserve in Pulmonary Arterial Hypertension.

Right ventricular (RV) functional reserve affects functional capacity and prognosis in patients with pulmonary arterial hypertension (PAH). PAH associated with systemic sclerosis (SSc-PAH) has a substantially worse prognosis than idiopathic PAH (IPAH), even though many measures of resting RV function and pulmonary vascular load are similar. We therefore tested the hypothesis that RV functional reserve is depressed in SSc-PAH patients. RV pressure-volume relations were prospectively measured in IPAH (n=9) and SSc-PAH (n=15) patients at rest and during incremental atrial pacing or supine bicycle ergometry. Systolic and lusitropic function increased at faster heart rates in IPAH patients, but were markedly blunted in SSc-PAH. The recirculation fraction, which indexes intracellular calcium recycling, was also depressed in SSc-PAH (0.32±0.05 versus 0.50±0.05; P=0.039). At matched exercise (25 W), SSc-PAH patients did not augment contractility (end-systolic elastance) whereas IPAH did (P<0.001). RV afterload assessed by effective arterial elastance rose similarly in both groups; thus, ventricular-vascular coupling declined in SSc-PAH. Both end-systolic and end-diastolic RV volumes increased in SSc-PAH patients to offset contractile deficits, whereas chamber dilation was absent in IPAH (+37±10% versus +1±8%, P=0.004, and +19±4% versus -1±6%, P<0.001, respectively). Exercise-associated RV dilation also strongly correlated with resting ventricular-vascular coupling in a larger cohort. RV contractile reserve is depressed in SSc-PAH versus IPAH subjects, associated with reduced calcium recycling. During exercise, this results in ventricular-pulmonary vascular uncoupling and acute RV dilation. RV dilation during exercise can predict adverse ventricular-vascular coupling in PAH patients.

Effects of chronic carotid baroreceptor activation on arterial stiffness in severe heart failure.

Heart failure with reduced ejection fraction (HFrEF) is characterized by activation of the sympathetic nervous system and increased arterial stiffness, leading to an impaired ventricular-vascular coupling. Baroreflex activation therapy (BAT) has been shown to reduce muscle sympathetic nerve activity (MSNA) and improve clinical status of patients with HFrEF. The purpose of this investigation was to determine the effects of BAT on arterial stiffness in HFrEF. MSNA, clinical variables, and parameters of central blood pressure (BP) and arterial stiffness were collected in 18 NYHA Class III HFrEF patients, nine receiving BAT and nine continuing with optimal medical management alone. Patients were followed for 3months, with measurements at that time compared to baseline evaluation. Baseline characteristics of the groups were well matched. At 3months, BAT did not improve central BP and arterial stiffness despite a significant amelioration of MSNA, NYHA class, Minnesota living with heart failure questionnaire score, number of heart failure medications and six-minute walking distance. The control group exhibited no significant changes in all the measured variables. Despite significant reductions in MSNA and clinical improvement, BAT does not appear to chronically modify arterial stiffness within this HFrEF cohort. Additional study is required to determine if this result applies to the HFrEF population as a whole.

Effect of acute nitrate ingestion on central hemodynamic load in hypoxia

Acute hypoxia results in local vasodilation that may temporarily unload the left ventricle (LV) through nitric oxide (NO)-mediated mechanisms. Whether increasing NO levels augments LV unloading and improves ventricular-vascular coupling in hypoxia remains unknown. PurposeInvestigate the effect of acute nitrate ingestion on central hemodynamic load in hypoxia. Methods20 Healthy men (23 ± 3 yrs, BMI 24.6 ± 2.8 kg m−2) consumed 70 mL of either a) 0.45 g nitrate (NIT) or b) an inert placebo (PLA) prior to 105 min of normobaric hypoxia (11.6 ± 0.1%) in this randomized, double-blind, crossover-design study. Wave reflection index (RIX; ratio of forward to reflected wave pressure), augmentation index (AIX75) and pulse wave velocity were calculated as measures of wave reflection magnitude and aortic stiffness, respectively, from the aortic blood pressure (BP) waveform. LV wasted pressure effort (WPE) was calculated as an index of LV work due to wave reflections. Subendocardial viability ratio (SEVR) was assessed a measure of myocardial O2 supply/demand ratio. ResultsAortic diastolic BP decreased in hypoxia compared to normoxia (p < 0.05). Aortic RIX, AIX75, and LV WPE significantly decreased in hypoxia compared to normoxia (p < 0.05). Aortic systolic BP, SEVR, and PWV were unaffected by hypoxia (p > 0.05). Compared to placebo, nitrate ingestion did not significantly alter central hemodynamics in hypoxia (p > 0.05). ConclusionsAcute hypoxic exposure unloads the LV (WPE, AIX75, and RIX) without disturbing myocardial O2 supply-demand ratio (SEVR). Reductions in LV work with hypoxia are likely due to reductions in pressure from wave reflections as hypoxia had negligible effects on aortic stiffness. Nitrate ingestion did not affect the central hemodynamic response to acute systemic hypoxia.

Assessment of N-terminal prohormone B-type natriuretic peptide as a measure of vascular and ventricular function in pediatric pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a progressive disease that puts excessive mechanical loads on the ventricle due to a gradual increase in pulmonary vascular impedance. We hypothesize that the increase in right ventricular (RV) afterload is reflected in the concentration of circulating biochemical markers of ventricular strain and stress (B-type natriuretic peptide [BNP] and N-terminal prohormone BNP [NT-proBNP]). We retrospectively analyzed right heart catheterization (RHC) and serum biochemical analysis data ([Formula: see text]) for a pediatric PAH cohort with no sign of left ventricular dysfunction. Using RHC data, we computed an estimate of pulmonary vascular resistance (PVR), compliance, and ventricular-vascular coupling. We also compared how the early onset of interventricular decoupling (characterized as septal flattening) impacts serum NT-proBNP concentrations. Our data revealed correlated NT-proBNP expression with both the resistive and reactive components of RV afterload, an estimate of ventricular-vascular coupling, and a significant increase in biomarker expression in patients with a flattened interventricular septum. Furthermore, the strong correlation between PVR and NT-proBNP appears to break down under flat septum morphology. Over 80% of resistive RV afterload variance is reflected in serum NT-proBNP concentration in pediatric patients with PAH with no sign of left ventricular dysfunction. Reactive afterload appears to contribute to myocardial NT-proBNP release at advanced stages of PAH. Therefore, in mild-to-moderate PAH, resistive afterload is likely the greatest contributor to RV wall stress. These findings could also be used to estimate invasive RHC measurements from serum biochemical analysis, but more work is needed to improve correlations and overcome the issue of interventricular decoupling.

Gender Differences in Ventricular-vascular Coupling Following Exercise.

To study the differences of cardiovascular system between men and women in response to exercise stress. Forty healthy youth were tested according to Bruce protocol of exercise stress. They were detected by ultrasonography during the rest, peak exercise, and recovery stages, respectively. The left ventricular diastolic elastance (Ed), effective arterial elastance (Ea), left ventricular end-systolic elatance (Ees), ventricular-vascular coupling index (VVI), and total stiffness index (TSI) were measured and calculated according to the formulas. The results of all stages were compared according to genders. All stages, the Ed, TSI, and VVI of women were higher than those of men, but the Ees was lower than that of men (all P<0.05); there was no significant difference in Ea between men and women. The Ed, Ees, Ea, and TSI were closely related with left ventricular oxygen consumption and heart function, and women showed more closely. Before and after exercise, the changes were different in Ed, Ees, Ea, TSI, and VVI (all P<0.05), and VVI changed least. Before and after exercise, the ventricular stiffness matched well with arterial stiffness and maintained within a narrow range. For women, the tolerance of exercise was lower than that of men.

Echo-Doppler-derived indexes of ventricular stiffness and ventriculo-arterial interaction as predictors of new-onset atrial fibrillation in patients with heart failure.

BackgroundAtrial fibrillation (AF) is common in patients with heart failure (HF) and worsens their prognosis. Vulnerability to changes in loading is an important factor in the development of AF and is strongly influenced by ventricular stiffness and ventriculo-arterial interaction. The aim of this study was to investigate predictors of AF development in patients with HF.MethodsWe studied 349 patients with stable HF. The following parameters of ventricular stiffness and ventriculo-arterial interaction were derived from echo-Doppler measurements: left ventricular (LV) diastolic elastance (Ed), effective arterial elastance (Ea), LV end-systolic elastance (Ees) and ventricular–vascular coupling index (VVI).ResultsAF occurred in 57 (16.3 %) patients over a median follow up of 30.3 months. Echo-Doppler–derived parameters of ventricular stiffness and ventriculo-arterial interaction were closely associated with HF severity. Ed was independently associated with AF after adjustment for age, hypertension, diabetes mellitus, and left atrial volume index (hazard ratio [HR] 5.49, p = 0.018). Ea and VVI were also associated with new-onset AF (HR 1.66, p = 0.027, and HR 1.06, p = 0.001, respectively).ConclusionsEcho-Doppler indexes of ventricular stiffness are closely associated with HF severity. LV diastolic elastance (Ed) is the strongest predictor of new-onset AF in HF patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12947-016-0050-y) contains supplementary material, which is available to authorized users.

Abstract 13470: RV Ejection Efficiency Measured in the Phasic Pulmonary Flow; a CMR Approach in PAH

Introduction: Measurements of RV function, such as RVEF and RV-measured ventricular-vascular coupling (VVC), maybe important in predicting survival in PAH, but are dependent on load and mathematical assumptions. However, independent measures, such as flow efficiency (FEI) within the main PA may be better predictors. FEI is dependent on the natural ratio between MPA area to pulsatile blood wavelength (λ), where λ is proportional to the product of λ velocity and the pulse time, but is difficult to measure directly. Hypothesis: We hypothesize pulmonary FEI will correlate with the VVC and RVEF. Methods: CMR was performed on 18 pts with PAH to assess RV function. Eight pts additionally underwent RV CMR during physiologic stressors: 1) inhaled NO 2) dobutamine (20μ/kg/min) and 3) volume challenge (500ml NaCl). MPA flow was measured via phase velocity mapping (PVM). The RVEF, VVC ratio and ejection time (ET) were calculated from CMR. The MPA area was measured from the PVM images along with avg velocity (Vel avg . Pulmonary FEI = (average Vel avg x ET) / MPA area. Results: A total of 38 unique measures of RVEF (52±12%), VVC (0.89±.3) and MPA flow conditions were measured: Vel avg (49±15cm/s), MPA area (51±11mm 2 ) and ET (295±61ms). The FEI correlated with RVEF and VVC via log term: RVEF = 11.5 log nat (FEI) + 37.2; and VVC = 0.34 log nat (FEI) + 1.17.Bland-Altman analysis of the measured RVEF vs. the FEI modeled RVEF (Fig 1) has an offset bias of 0, a four SD range of ±14.4; r=0. 0.8, while the measured VVC vs. modeled has a bias of 0 and a 4 SD range of ± 0.45; r = 0.74. Conclusions: The linear combination of average pulmonary blood velocity, ejection time and MPA area combine to form a pulmonary FEI that strongly correlates with RVEF and VVC. Importantly, it is devoid of the afterload/preload assumptions of RVEF and the multitude of assumptions of V 0 and RVEDP in VVC. As such, this index may provide additional clinical value since it reflects the directly measured intrinsic efficiency of integrated RV-PA conditions.

Abstract 14123: Circulating miRNAs as Biomarkers of Afterload, Acute Vascular Reactivity, and Ventricular-Vascular Coupling in Pediatric Idiopathic Pulmonary Arterial Hypertension: Initial Clinical Studies

Introduction: Although it is known that structural remodeling of the pulmonary arteries (PA) leads to increases in right ventricular (RV) afterload in pediatric idiopathic pulmonary arterial hypertension (iPAH), evaluating such changes early in the process continues to be challenging. Since biological markers such as microRNAs may manifest earlier than functional markers, and since such markers may be detected using simple blood draws, identifying correlations between microRNAs and RV or pulmonary vascular functional parameters would be particularly useful in tracking this disease. Methods: Blood was collected for 14 pediatric patients with iPAH while undergoing right heart catheterization (RHC). Taqman Low Density Arrays (TLDA) was used to quantify miRNA expression in each patient. RHC data was used to compute pulmonary vascular impedance, ventricular-vascular coupling (VVC), and other hemodynamic markers. VVC was computed from the pressure tracing using the single beat pressure method (Vanderpool RR, et al. Heart 2015;101:37–43). Results: miR-21, which frequently appears in the PAH literature, was well correlated with pulmonary vascular resistance index (PVRi) (r = 0.81, P &lt; 0.001, see Fig. 1a). Fig. 1b shows that the ratio of miR-150/571 is an excellent predictor of VVC (r = 0.91, P &lt; 0.05). Random Forest statistical machine learning identified miR-683 as a classifier of acute vascular reactivity, confirmed with receiver operating curves (AUC = 0.88, see Fig. 1c) Conclusion: Over a dozen circulating miRNAs were identified as potential biomarkers for pediatric iPAH from the aforementioned arrays, with several having strong correlations to afterload and acute vascular reactivity. The ratio of miR-150 (recognized as biomarker of PAH) and miR-571 (recognized as biomarker of heart failure) appears particularly promising as a predictor of ventricular-vascular decoupling.

Abstract 15835: Cold Air Inhalation Induces Differential Effects on Coronary Microvascular Resistance and Flow Depending on Presence of Significant Coronary Artery Disease

Introduction: Cold temperatures increase the incidence of myocardial infarction. Precise mechanisms remain unclear. Sudden severe myocardial oxygen supply/demand mismatch may be responsible. We measured coronary flow and myocardial work during cold air inhalation (CAI), invasively and with cardiac magnetic resonance imaging (CMR), aiming to elucidate the dominant mechanisms. Methods: All data were acquired at rest and peak stress during CAI: 5minutes -15oC via a face-mask. Simultaneous intracoronary pressure and flow velocity data were acquired in a target artery from 20 patients (10 with normal coronary arteries, 10 with a significant stenosis (CAD). Coronary flow average peak velocity (APV), microvascular resistance (MVR) and buckberg index (BI: a surrogate for subendocardial ischemia) were calculated. Wave intensity analysis also differentiated waves that accelerate and decelerate coronary flow. Separately CMR perfusion was performed in 7 patients with a significant stenosis to quantify myocardial perfusion reserve (MPR) and transmural perfusion gradients (TPG). Results: At rest MVR is lower in CAD patients, maintaining APV (1a,b). During CAI, although myocardial work increased similarly in normal and CAD patients (rate pressure product mean difference 2312 and 2651mmHg.min-1 respectively), there was a differential response in coronary flow, with a significant increase and a downward trend in APV respectively (1a). Relative hypoperfusion of stenosed segments was also noted on MPR (2a). This inability of CAD patients to augment APV is explained by a significant increase in MVR (1b) collaborating with a reduction in accelerating flow waves (1c). These cause a relative subendocardial perfusion deficit, demonstrated by a significant decrease in BI (1d) and increase in TPG (2b). Conclusions: CAI increases myocardial work but CAD patients are unable to augment flow due to microvascular vasoconstriction and adverse ventricular-vascular coupling.

17β-Estradiol Attenuates Conduit Pulmonary Artery Mechanical Property Changes With Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH), a rapidly fatal vascular disease, strikes women more often than men. Paradoxically, female PAH patients have better prognosis and survival rates than males. The female sex hormone 17β-estradiol has been linked to the better outcome of PAH in females; however, the mechanisms by which 17β-estradiol alters PAH progression and outcomes remain unclear. Because proximal pulmonary arterial (PA) stiffness, one hallmark of PAH, is a powerful predictor of mortality and morbidity, we hypothesized that 17β-estradiol attenuates PAH-induced changes in mechanical properties in conduit proximal PAs, which imparts hemodynamic and energetic benefits to right ventricular function. To test this hypothesis, female mice were ovariectomized and treated with 17β-estradiol or placebo. PAH was induced in mice using SU5416 and chronic hypoxia. Extra-lobar left PAs were isolated and mechanically tested ex vivo to study both static and frequency-dependent mechanical behaviors in the presence or absence of smooth muscle cell activation. Our static mechanical test showed significant stiffening of large PAs with PAH (P<0.05). 17β-Estradiol restored PA compliance to control levels. The dynamic mechanical test demonstrated that 17β-estradiol protected the arterial wall from the PAH-induced frequency-dependent decline in dynamic stiffness and loss of viscosity with PAH (P<0.05). As demonstrated by the in vivo measurement of PA hemodynamics via right ventricular catheterization, modulation by 17β-estradiol of mechanical proximal PAs reduced pulsatile loading, which contributed to improved ventricular-vascular coupling. This study provides a mechanical mechanism for delayed disease progression and better outcome in female PAH patients and underscores the therapeutic potential of 17β-estradiol in PAH.

Relationship between muscle sympathetic nerve activity and aortic wave reflection characteristics in aerobic- and resistance-trained subjects.

Increased arterial stiffness is associated with an impairment of ventricular-vascular coupling efficiency and increased risk of cardiovascular mortality. Recently, it has been suggested that an increase in arterial stiffness is associated with resistance exercise training. Therefore, the aims of this study were to compare augmentation index (AIx) and left ventricular wasted pressure energy (LVEW) as markers of arterial stiffness and ventricular-vascular coupling efficiency in young aerobic-trained (AT) and resistance (RT)-trained subjects. We also investigated the relationship of muscle sympathetic nerve activity (MSNA) and flow-mediated dilation (FMD) to AIx in both sets of subjects to determine if endothelial function or sympathetic outflow could explain any differences in arterial stiffness. To achieve our aims, we measured MSNA in 15 male subjects (8 RT, 7 AT) using microneurography. We also used applanation tonometry of the radial pressure waveform to noninvasively synthesize aortic pressure waveforms. FMD was calculated as percent dilation of the radial artery from baseline following a 5 min occlusion. RT subjects had an increased AIx (12 ± 3 vs. -7 ± 2; P < 0.01), LVEW (429 ± 111 vs. -360 ± 77; P < 0.01) and MSNA burst incidence (34 ± 4 vs. 26 ± 4; P < 0.01) when compared with AT subjects. There was no difference in FMD between groups. MSNA burst incidence was also significantly related to AIx in subjects (R (2) = 0.61; P < 0.01) with a distinct demarcation between RT and AT subjects. These results confirm previous reports of a positive association between MSNA and AIx in young male resistance-trained subjects. Furthermore, RT is associated with increased arterial stiffness and elevated sympathetic outflow.

Influence of vascular function and pulsatile hemodynamics on cardiac function.

Interactions between cardiac and vascular structure and function normally are optimized to ensure delivery of cardiac output with modest pulsatile hemodynamic overhead. Aortic stiffening with age or disease impairs optimal ventricular-vascular coupling, increases pulsatile load, and contributes to left ventricular (LV) hypertrophy, reduced systolic function, and impaired diastolic relaxation. Aortic pulse pressure and timing of peak systolic pressure are well-known measures of hemodynamic ventricular-vascular interaction. Recent work has elucidated the importance of direct, mechanical coupling between the aorta and the heart. LV systolic contraction results in displacement of aortic and mitral annuli, thereby producing longitudinal stretch in the ascending aorta and left atrium, respectively. Force associated with longitudinal stretch increases systolic load on the LV. However, the resulting energy stored in the elastic elements of the proximal aorta during systole facilitates early diastolic LV recoil and rapid filling. This review discusses current views on hemodynamics and mechanics of ventricular-vascular coupling.

Aortic biomechanics in hypertrophic cardiomyopathy

Background: Ventricular-vascular coupling is an important phenomenon in many cardiovascular diseases. The association between aortic mechanical dysfunction and left ventricular (LV) dysfunction is well characterized in many disease entities, but no data are available on how these changes are related in hypertrophic cardiomyopathy (HCM). Aim of the work: This study examined whether HCM alone is associated with an impaired aortic mechanical function in patients without cardiovascular risk factors and the relation of these changes, if any, to LV deformation and cardiac phenotype. Methods: 141 patients with HCM were recruited and compared to 66 age- and sex-matched healthy subjects as control group. Pulse pressure, aortic strain, stiffness and distensibility were calculated from the aortic diameters measured by M-mode echocardiography and blood pressure obtained by sphygmomanometer. Aortic wall systolic and diastolic velocities were measured using pulsed wave Doppler tissue imaging (DTI). Cardiac assessment included geometric parameters and myocardial deformation (strain and strain rate) and mechanical dyssynchrony. Results: The pulsatile change in the aortic diameter, distensibility and aortic wall systolic velocity (AWS') were significantly decreased and aortic stiffness index was increased in HCM compared to control (P < .001) In HCM AWS' was inversely correlated to age(r = − .32, P < .0001), MWT (r = − .22, P < .008), LVMI (r = − .20, P < .02), E/Ea (r = − .16, P < .03) LVOT gradient (r = − 19, P < .02) and severity of mitral regurg (r = − .18, P < .03) but not to the concealed LV deformation abnormalities or mechanical dyssynchrony. On multivariate analysis, the key determinant of aortic stiffness was LV mass index and LVOT obstruction while the role LV dysfunction in aortic stiffness is not evident in this population. Conclusion: HCM is associated with abnormal aortic mechanical properties. The severity of cardiac phenotype, not LV deformation, is interrelated to aortic stiffness in patients with HCM. The increased aortic stiffness seems to be promising module that can be added as clinical risk parameter in HCM.

Non-invasive determination by cardiovascular magnetic resonance of right ventricular-vascular coupling in children and adolescents with pulmonary hypertension.

BackgroundPediatric pulmonary hypertension (PH) remains a disease with high morbidity and mortality in children. Understanding ventricular-vascular coupling, a measure of how well matched the ventricular and vascular function are, may elucidate pathway leading to right heart failure. Ventricular vascular coupling ratio (VVCR), comprised of effective elastance (Ea, index of arterial load) and right ventricular maximal end-systolic elastance (Ees, index of contractility), is conventionally determined by catheterization. Here, we apply a non-invasive approach to determining VVCR in pediatric subjects with PH.MethodsThis retrospective study included PH subjects who had a cardiovascular magnetic resonance (CMR) study within 14 days of cardiac catheterization. PH was defined as mean pulmonary artery pressure (mPAP) ≥ 25 mmHg on prior or current catheterization. A non-invasive measure of VVCR was derived from CMR-only (VVCRm) and compared to VVCR estimated by catheterization-derived single beat estimation (VVCRs). Indexed pulmonary vascular resistance (PVRi) and pulmonary vascular reactivity were determined during the catheterization procedure. Pearson correlation coefficients were calculated between PVRi and VVCRm. Receiver operating characteristic (ROC) curve analysis determined the diagnostic value of VVCRm in predicting vascular reactivity.ResultsSeventeen subjects (3 months-23 years; mean 11.3 ± 7.4 years) were identified between January 2009-August 2013 for inclusion with equal gender distributions. Mean mPAP was 35 mmHg ± 15 and PVRi was 8.5 Woods unit x m2 ± 7.8. VVCRm (range 0.43–2.82) increased with increasing severity as defined by PVRi (p < 0.001), and was highly correlated with PVRi (r = 0.92, 95 % CI 0.79–0.97, p < 0.0001). Regression of VVCRm and PVRi demonstrated differing lines when separated by reactivity. VVCRm was significantly correlated with VVCRs (r = 0.79, CI 0.48–0.99, p <0.0001). ROC curve analysis showed high accuracy of VVCRm in determining vascular reactivity (VVCR = 0.85 had a sensitivity of 100 % and a specificity of 80 %) with an area under the curve of 0.89 (p = 0.008).ConclusionMeasurement of VVCRm in pediatrics is feasible. Pulmonary vascular non-reactivity may be contribute to ventricular-vascular decoupling in severe PH. Therapeutic intervention to maintain a low vascular afterload in reactive patients may preserve right ventricular functional reserve and delay the onset of RV-PA decoupling. Use of VVCRm may have significant prognostic implication.

Ventricular-vascular coupling in Marfan syndrome and familial aortic aneurysm

Ventricular-vascular coupling in Marfan syndrome and familial aortic aneurysm

Ventricular-vascular coupling in hypertension: methodological considerations and clinical implications.

The present review is addressed to analyse the complex interplay between left ventricle and arterial tree in hypertension. The different methodological approaches to the analysis of ventricular vascular coupling in the time and frequency domain are discussed. Moreover, the role of hypertension-related changes of arterial structure and function (stiffness and wave reflection) on arterial load and how ventricular-vascular coupling modulates the process of left ventricular adaptation to hypertension are analysed.The different interplay between vascular bed and left ventricle emerges as the pathophysiological basis for the development of the multiple patterns of ventricular structural adaptation in hypertension and provides a pathway for the interpretation of systolic and diastolic functional abnormalities observed in hypertensive patients. Targeting the therapeutic approach to improve ventricular-vascular coupling may have relevant impact on reversing left ventricular hypertrophy and improving systolic and diastolic dysfunction.