P866Noninvasive and comprehensive evaluation of the impact of left ventricular pressure overload on both systolic and diastolic function using speckle tracking echocardiography

Purpose: Thyroid hormones (TH) play a central role for cardiac function. TH influence heart rate and cardiac contractility, and altered thyroid function is associated with increased cardiovascular morbidity and mortality. The precise role of TH in onset and progression of heart failure still requires clarification.Methods: Chronic left ventricular pressure overload was induced in mouse hearts by transverse aortic constriction (TAC). One week after TAC, alteration of TH status was induced and the impact on cardiac disease progression was studied longitudinally over 4 weeks in mice with hypo- or hyperthyroidism and was compared to euthyroid TAC controls. Serial assessment was performed for heart function (2D M-mode echocardiography), heart morphology (weight, fibrosis, and cardiomyocyte cross-sectional area), and molecular changes in heart tissues (TH target gene expression, apoptosis, and mTOR activation) at 2 and 4 weeks.Results: In diseased heart, subsequent TH restriction stopped progression of maladaptive cardiac hypertrophy and improved cardiac function. In contrast and compared to euthyroid TAC controls, increased TH availability after TAC propelled maladaptive cardiac growth and development of heart failure. This was accompanied by a rise in cardiomyocyte apoptosis and mTOR pathway activation.Conclusion: This study shows, for the first time, a protective effect of TH deprivation against progression of pathological cardiac hypertrophy and development of congestive heart failure in mice with left ventricular pressure overload. Whether this also applies to the human situation needs to be determined in clinical studies and would infer a critical re-thinking of management of TH status in patients with hypertensive heart disease.

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P3548Noninvasive estimation of left ventricular diastolic function in patients with hypertension and normal ejection fraction using 3-dimensional speckle tracking echocardiography

European Heart Journal ◽

10.1093/eurheartj/ehz745.0411 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

S Minatoguchi ◽

R Tanaka ◽

T Yoshizane ◽

T Deguchi ◽

H Sato ◽

...

Keyword(s):

Diastolic Function ◽

Speckle Tracking ◽

Speckle Tracking Echocardiography ◽

Diastolic Pressure ◽

Left Ventricular Diastolic Function ◽

Left Ventricular ◽

Peak Strain ◽

Myocardial Stiffness ◽

The Impact ◽

Lv Diastolic Function

Abstract Background Left ventricular (LV) relaxation (eTau) and pulmonary capillary wedge pressure (ePCWP) were reported to be estimated by speckle tracking echocardiography (STE). LV camber stiffness (e-c stiffness) may be estimated with the use of 2 diastolic pressure-volume coordinates. The minimum diastolic pressure (mP) is reported to have a strong correlation with Tau. Purpose We sought to examine the impact of hypertension on LV diastolic function and LA properties and to elucidate the feature of hypertensive heart failure with preserved EF (HFpEF). Methods The e', E/e', Tau, PCWP, LVEDP, LV stiffness, LAV, LA emptying function (LAEF) and LA strain were examined in 53 controls (age 66±11), 136 hypertensive patients (HTN) with normal EF (69±11) and 39 HFpEF (77±14). ePCWP and estimated EDP (eEDP) was calculated as previously reported. Tau was calculated as isovolumic relaxation time/(ln 0.9 x systolic blood pressure − ln PCWP). Myocardial stiffness (e-m stiffness) was estimated as LVED stress/LV strain. LV c-stiffness was calculated as LV pressure change (from mP to EDP) obtained by catheterization divided by LV volume change. Estimated LV c-stiffness (e-c-stiffness) was noninvasively obtained using e-mP and e-EDP. The eTau, eEDP and e-mP by STE were validated by catheterization (n=126). Results The mP had a good correlation with Tau (r=0.70, p<0.01). The eTau, eEDP and e-mP by STE had a good correlation with those by catheterization (r=0.75, 0.63 and 0.70, p<0.01). Multivariate analysis revealed that ePCWP and LA strain were independent predictors of HFpEF. LV diastoric function Variables Control HTN HFpEF LVEF, % 68±6 68±8 63±9*+ LV longitudinal strain x (s–1) 19.1±3.0 16.8±4.3* 14.5±5.1*+ E/e' 9.2±2.6 11.6±4.5* 15.9±7.9*+ eTau, ms 35±12 48±17* 59±17*+ ePCWP, mmHg 7.3±2.7 8.3±4.3 15.0±4.4*+ eLVEDP, mmHg 9.4±2.2 10.4±3.5 15.9±3.7*+ LV e-myocardial stiffness, kdynes/cm 0.56±0.25 0.69±0.56 1.27±0.71*+ LV e-chamber stiffness, mmHg/ml 0.19±0.06 0.20±0.08 0.36±0.19*+ Maximum LAVI, ml/m2 42±15 50±21* 68±17*+ Total LAEF, % 55±7 51±11 36±12*+ LA peak strain 41±15 40±17 19±8*+ *p<0.05 vs Control, +p<0.05 vs HTN. Conclusion We demonstrated that LV diastolic function in HTN may be accurately and noninvasively evaluated by STE.

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