Systolic Reserve Maintains Left Ventricular-Vascular Coupling When Challenged by Adverse Breathing Mechanics and Hypertension in Healthy Adults

Augmented negative intrathoracic pressures (nITP) and dynamic hyperinflation (DH) are adverse breathing mechanics (ABM) associated with chronic obstructive pulmonary disease that attenuate left ventricular (LV) preload and augment afterload. In COPD, hypertension (elevated systemic arterial load) commonly adds additional afterload to the LV. Combined ABM and hypertension may profoundly challenge ventricular-vascular coupling and attenuate stroke volume (SV), particularly if LV systolic reserve is limited. However, even in the healthy heart, the combined impact of ABM and systemic arterial loading on LV function and ventricular-vascular coupling has not been fully elucidated. Healthy volunteers (10M/9F, 24±3 years) were challenged with Mild (-10cmH2O nITP and 25% DH) and Severe (-20cmH2O nITP and 100% DH) ABM, without and with post-exercise ischemia (PEI) at each severity. LV SV, chamber geometry, and end-systolic elastance (Ees), arterial elastance (Ea), and ventricular-vascular coupling (Ees:Ea) were quantified using echocardiography. Compared to resting Control (58±13mL), SV decreased during Mild ABM (51±13mL), Mild ABM+PEI (51±11mL), Severe ABM (50±12mL), and Severe ABM+PEI (47±11mL) (P<0.001); similar trends were observed for LV end-diastolic volume. The end-diastolic radius of septal curvature increased, indicating direct ventricular interaction, during Severe ABM and Severe ABM+PEI (P<0.001). Compared to Control (1.99±0.41mmHg/mL), Ea increased progressively with Mild ABM (2.21±0.47mmHg/mL) and Severe ABM (2.50±0.56mmHg/mL); at each severity Ea was greater with superimposed PEI (P<0.001). However, well-matched Ees increases occurred, and Ees:Ea was unchanged throughout. ABM pose a challenge to ventricular-vascular coupling that is accentuated by superimposed PEI; however, in healthy younger adults, the LV has substantial systolic reserveto maintain coupling.

Reversed Septal Curvature Is Associated with Elevated Troponin Level in Hypertrophic Cardiomyopathy

The aim of study was to compare patients with hypertrophic cardiomyopathy divided according to septal configuration assessed in a 4-chamber apical window. The study group consisted of 56 consecutive patients. Reversed septal curvature (RSC) and non-RSC were diagnosed in 17 (30.4%) and 39 (69.6%) patients, respectively. Both RSC and non-RSC groups were compared in terms of the level of high-sensitivity troponin I (hs-TnI), NT-proBNP (absolute value), NT-proBNP/ULN (value normalized for sex and age), and echocardiographic parameters, including left ventricular outflow tract gradient (LVOTG). A higher level of hs-TnI was observed in RSC patients as compared to the non-RSC group (102 (29.2-214.7) vs. 8.7 (5.3-18) (ng/l), p = 0.001 ). A trend toward increased NT-proBNP value was reported in RSC patients (1279 (367.3-1186) vs. 551.7 (273-969) (pg/ml), p = 0.056 ). However, no difference in the NT-proBNP/ULN level between both groups was observed. Provocable LVOTG was higher in RSC as compared to non-RSC patients (51 (9.5-105) vs. 13.6 (7.5-31) (mmHg), p = 0.04 ). Furthermore, more patients with RSC had prognostically unfavourable increased septal thickness to left LV diameter at the end diastole ratio. Patients with RSC were associated with an increased level of hs-TnI, and the only trend observed in this group was for the higher NT-proBNP levels. RSC seems to be an alerting factor for the risk of ischemic events. Not resting but only provocable LVOTG was higher in RSC as compared to non-RSC patients.

P735 Septal curvature - a novel, semi-automated parameter to aid in recognition of basal septal hypertrophy in arterial hypertension

Funding Acknowledgements Horizon 2020 European Commission Project MSCA-ITN-2016 (764738), Grant from Fundacio La Marató de TV3 (040310). Background and aim Localized basal septal hypertrophy (BSH) is a known marker of increased afterload and localized deformation impairment, and can be seen in one-fifth of patients with arterial hypertension. Although there is variability in the classification, BSH is mainly defined from ratios between several wall thickness measurements. We hypothesize that the curvature of the septum is reflective of localized hypertrophy and will be significantly increased in patients with BSH. Speckle tracking endocardial delineations of the left ventricle (LV) can be used to quantify curvature, with the potential to create a novel, semi-automatized parameter for recognition of patients with an increased impact of afterload on cardiac structure and function. Methods An echocardiogram was performed on a total of 149 patients with a diagnosis of long-standing hypertension, treated with at least one antihypertensive drug and on 19 healthy age and sex-matched controls. The interventricular septum thickness was measured at basal and mid-level in the parasternal long axis (PLAX) and 4-chamber (4C) views. BSH was identified from a two-part criterion: both a positive visual assessment of an abrupt change in septal thickness seen in the 4C or PLAX views and a basal to mid-septal ratio ≥ 1.4. A dedicated software for speckle tracking was used to trace the endocardial border of the LV in 4C and 3C view. In post-analysis, we quantified the maximal curvature of the antero- and inferoseptal segments from the exported myocardial contour. Curvature, measured in m-1, was defined as the reciprocal value of the radius of the circle fitted into the curve defined by three subsequent neighboring points in the myocardial contour. Curvature was considered negative if the curve was convex with respect to the LV long-axis. Results Using septal wall thickness measurements, 19% (n = 28) of hypertensive patients were classified as having BSH, whereas all healthy controls had normal geometry. Basal antero- and inferoseptal wall thickness was significantly increased in the BSH group, which was coupled with regional deformation impairment (basal inferoseptum, controls vs. non-BSH vs. BSH: 16.1 ± 2.33 vs. 15.14 ± 2.8 vs. 13.02 ± 2.98 %, p &lt; 0.001). The curvature of the basal inferoseptum was significantly higher in the BSH group (controls vs. non-BSH vs BSH: -23.4 (-27.2, -10.9) vs. -28.3 (-40.2, -19.3) vs. -50.5 (-66.8, -33.9) m-1, p &lt; 0.001) (Figure 1), with the same trend seen in the basal anteroseptum. The inferoseptal curvature showed a moderately strong correlation with the inferoseptal basal-to-mid wall thickness ratio (R = 0.527, p &lt;0.001). Conclusion Increased septal curvature is an easily quantifiable, single-value, semi-automated parameter reflective of localized thickening that could easily be incorporated into the output of the LV speckle tracking workflow, possibly aiding in the recognition of hypertensive patients in need of a closer clinical follow-up. Abstract P735 Figure 1

Severe right ventricular dilatation after repair of Tetralogy of Fallot is associated with increased left ventricular preload and stroke volume

Aims Pulmonary regurgitation (PR) and right ventricular (RV) dilatation are common in repaired tetralogy of Fallot (rTOF). Left ventricular (LV) dysfunction is an important risk factor in rTOF. The effect of PR/RV dilatation on LV performance and RV-LV interactions in rTOF are incompletely understood. We examined LV responses and exercise capacity in rTOF, both before and after pulmonary valve replacement (PVR). Methods and results Cardiac magnetic resonance imaging scans in 126 rTOF patients (age 17.3 ± 7.6 years) were analysed, comparing subjects with indexed RV end-diastolic volume (RVEDVi) <170 mL/m2 (mild/moderate dilatation, n = 95) and RVEDVi ≥170 mL/m2 (severe dilatation, n = 31). Indexed PR volume (PRVi), RV end-systolic (RVESVi), RV end-diastolic (RVEDVi), RV stroke volume (RVSVi), net pulmonary forward flow (NPFFi), LV end-diastolic (LVEDVi), LV end-systolic (LVESVi), LV stroke volume (LVSVi), RV and LV ejection fraction (EF), and diastolic septal curvature were obtained. Peak aerobic capacity (VO2 max) was measured. In a subset (n = 30), measures were obtained pre-and-post surgical PVR. Compared to those with mild/moderate RV dilatation, patients with severe RV dilation had greater PRVi (38 ± 12 vs. 24 ± 9 mL/m2, P < 0.0001), NPFFi (53 ± 9 vs. 44 ± 11 mL/m2, P < 0.0001), LVEDVi (87 ± 14 vs. 73 ± 13 mL/m2, P < 0.0001), LVESVi (39 ± 12 vs. 30 ± 8 mL/m2, P < 0.0001), and LVSVi (48 ± 7 vs. 43 ± 8 mL/m2, P = 0.002) but lower RV ejection fraction (46 ± 8 vs. 53 ± 7%, P < 0.0001). Septal curvature and VO2 max were similar in both groups. After PVR, there was no change in LVEDVi, LVSVi, septal curvature, or VO2 max. Conclusions Chronic PR with severe RV dilatation is associated with increased NPFFi, LVEDVi, and LVSVi. This may potentially explain preserved exercise capacity in rTOF with severe PR and RV dilatation.