Summary
Background
Left ventricular (LV) longitudinal deformation is a good marker of intrinsic myocardial dysfunction in pressure overload cardiomyopathies.
Aim
To assess the effect of valvuloarterial haemodynamic load on LV longitudinal deformation in patients with aortic valve stenosis (AVS) and preserved LV ejection fraction (LVEF).
Methods
Global LV longitudinal strain (GLS) was measured using speckle tracking imaging in a series of 82 consecutive patients with AVS (mean age 75 ± 10 years; 50% men). The global (valvular + arterial) haemodynamic load imposed on the LV was estimated by the valvuloarterial impedance (Z va ), and was calculated using either arm-cuff systolic peripheral blood pressure or systolic central aortic blood pressure estimated by SphygmoCor ® .
Results
Among this series of 82 patients with preserved LVEF, 79% had reduced LV GLS (< −18%). LV GLS correlated weakly with AVS severity, systemic vascular resistance and systemic arterial compliance. However, there was a good inverse correlation between increase in Z va and impairment of LV GLS ( r = 0.41 p < 0.0001). On multivariable analysis, impaired GLS was associated with increased Z va ( p < 0.0001), increased E/Ea ratio ( p = 0.001) and increased LV end-diastolic volume index ( p = 0.021), while indices of valvular load were not. Utilization of estimated central aortic blood pressure in place of brachial pressure did not improve the performance of Z va to predict GLS.
Conclusion
The magnitude of the global haemodynamic load as reflected by Z va is a powerful determinant of altered LV longitudinal deformation in AVS patients with preserved LVEF. The calculation of Z va may be useful to identify the patients who are potentially at higher risk for the development of myocardial dysfunction. Use of estimated central aortic pressure in the calculation of Z va does not appear to provide any incremental predictive value over that calculated with the simple measurement of brachial pressure.
Résumé
Contexte
La déformation longitudinale du ventricule gauche (VG) est un bon marqueur de dysfonction myocardique intrinsèque dans les cardiomyopathies avec surcharge de pression.
But
Évaluer l’effet de la charge hémodynamique valvulo-artérielle sur la déformation longitudinale du VG de patients porteurs d’une sténose valvulaire aortique et d’une fraction d’éjection préservée.
Méthodes
La déformation globale longitudinale du VG a été mesurée à l’aide de l’imagerie speckle tracking dans une série de 82 patients consécutifs porteurs d’une sténose valvulaire aortique (âge moyen 75 ± 10 ans, 50 % d’hommes). La charge hémodynamique globale (valvulaire + artérielle) imposée au VG a été estimée par l’impédance valvulo-artérielle (Z va ) et a été calculée en utilisant soit la pression périphérique systolique brachiale au brassard, soit la pression systolique centrale aortique estimée par le SphygmoCor ® .
Résultats
Parmi cette série de 82 patients avec une fraction d’éjection préservée, 79 % avaient une déformation globale longitudinale du VG réduite (< −18 %). La déformation globale longitudinale du VG été faiblement corrélée avec la sévérité de la sténose aortique, les résistances vasculaires systémiques et la compliance artérielle systémique. Toutefois, une bonne corrélation était observée entre l’augmentation du Z va et l’altération de la déformation globale longitudinale du VG ( r = 0,41 p < 0,0001). En analyse multivariée, l’altération de la déformation longitudinale du VG était associée avec un Z va ( p < 0,0001), un rapport E/Ea ( p = 0,001) et un volume télédiastolique du VG indexé ( p = 0,021) plus élevés. L’utilisation de l’estimation de la pression aortique centrale en remplacement de la pression brachiale n’améliorait pas la performance du Z va comme déterminant de la déformation longitudinale du VG.
Conclusion
L’importance de la charge hémodynamique globale représentée par le Z va est un déterminant puissant de l’altération de la déformation longitudinale du VG des patients porteurs d’une sténose aortique avec une fraction d’éjection préservée. Le calcul du Z va pourrait être utile pour identifier les patients potentiellement à risque de développement de dysfonction myocardique. L’utilisation de la pression aortique centrale dans le calcul du Z va ne semble pas apporter de valeur prédictive supplémentaire par rapport au calcul incluant la simple mesure de pression brachiale.
Background
Aortic valve replacement is indicated in patients with severe aortic valve stenosis (AVS) when symptoms and/or left ventricular (LV) systolic dysfunction (defined as LV ejection fraction [LVEF] less than 50%) develops. However, LVEF may remain unaltered during the course of the disease despite latent and potentially irreversible alterations in myocardial function. Using M-mode tracings, Dumesnil et al. reported in the 1970s that LV longitudinal systolic shortening is depressed despite normal LVEF in patients with AVS compared with controls . Very recently, Cramariuc et al. demonstrated that a higher degree of LV hypertrophy and concentric remodelling is associated with decreased LV longitudinal deformation assessed by two-dimensional speckle tracking in patients with AVS . In addition, impairment of LV longitudinal shortening or strain correlates with the presence of symptoms in patients with AVS and predicts elicited symptoms during exercise testing in the subset of asymptomatic patients . However, the relatively weak relationship between the LV longitudinal strain and the severity of the valve stenosis suggests that, beyond the narrowed valvular orifice, other factors may impact on LV longitudinal contraction in the setting of AVS . Recently, Briand et al. have demonstrated that systemic arterial compliance (SAC) is frequently reduced in AVS patients . Hence these patients often have a double haemodynamic load: a valvular load caused by the stenosis and an arterial load caused by reduced arterial compliance and/or increased vascular resistance. It is logical to believe that the development of LV dysfunction as well as the occurrence of symptoms and adverse events is related to the global haemodynamic load that results from the additive effects of AVS and hypertension. Briand et al. proposed a new index measurable by Doppler echocardiography – valvuloarterial impedance (Z va ) – to estimate the global haemodynamic load imposed on the left ventricle . This index integrates the mean transvalvular gradient, the brachial systolic blood pressure and the stroke volume index. Recent studies have reported that elevated Z va is an independent predictor of reduced stress-corrected LV midwall fractional shortening and mortality in AVS patients.
Use of central aortic blood pressure instead of peripheral brachial pressure in the calculation of Z va potentially allows a more precise assessment of the global LV haemodynamic load. To this effect, several devices have been developed to estimate non-invasively central aortic pressure. The aim of the present study was to examine the relationship between Z va and LV longitudinal deformation using either arm-cuff systolic blood pressure or estimated aortic systolic blood pressure in a prospective cohort of patients with AVS and preserved LV ejection fraction.
Methods
Clinical data
During a 6-month period, consecutive patients with AVS (peak aortic velocity > 2.5 m/s) and LVEF greater or equal to 50% referred to our echocardiography laboratory were enrolled prospectively into the present study. Exclusion criteria were atrial fibrillation, LV systolic dysfunction (LVEF < 50%), greater than mild aortic or mitral regurgitation and history of myocardial infarction.
Significant coronary artery disease was defined as the presence of a luminal narrowing greater than 50% on coronary angiography. Body mass index was calculated as weight in kilogram divided by height in metre square. Clinical data included age, sex, history of smoking, documented history of hypertension (including antihypertensive medications), hypercholesterolaemia (patients on cholesterol-lowering medication or with a low-density lipoprotein cholesterol concentration greater than 160 mg/dL in the absence of treatment), diabetes mellitus (fasting blood glucose greater than 126 mg/dL on two occasions or patients currently receiving an oral hypoglycaemic medication or insulin). Plasma levels of BNP were measured using the ACS 180 BNP dosage (Bayer ® ).
Vascular function analysis
Patients were studied in the supine position over a 1-hour period following an overnight fast. The radial wave-form was obtained using a high-fidelity micromanometer (Millar Instrument, Houston, Texas) and 20 wave-forms were averaged. A series of radial pressure waves over an 8-second period was together averaged and calibrated for the peak and nadir of the wave, with the best estimate of upper limb systolic and diastolic pressures using a cuff sphygmomanometer and phase I and V, respectively, of Korotkoff sounds. The ascending aorta waveform was obtained by applying a generalized mathematical transfer function to the radial artery waveform using a SphygmoCor ® system device (AtCor Medical System, Australia). This device allowed the determination of the aortic systolic, diastolic, pulse (difference between systolic and diastolic pressure) and mean (diastolic pressure plus one third of pulse pressure) pressures. Measurements were performed by two experienced operators (E.C., M.M.-S.C.) until the operator index, an index of signal quality and reproducibility among the 20 cycles, was greater than 70%.
Pulse wave velocity (PWV) (i.e., the speed at which the pressure waveform travels along the aorta and large arteries during each cardiac cycle) is the gold standard for the assessment of aortic stiffness and is measured using the SphygmoCor ® system. PWV is measured using the foot-to-foot velocity method from femoral and carotid waveforms. The time between the R wave of the electrocardiogram and the foot of each waveform is calculated and the difference between times is the delay (Δt). The distance (D) covered by the waves was calculated as the difference between the sternum femoral distance and carotid sternum distance. PWV is calculated as
D ( m ) / Δ t ( sec ) .
Doppler echocardiographic analysis
Echocardiograms were performed by two experienced echocardiographers (S.M., P.V.E.) using a Vivid 7 ultrasound system (GE Medical Systems, Horten, Norway). Three cardiac cycles were stored for each measurement, for subsequent offline analysis. Measurements were made over at least three cardiac cycles and the average value calculated.
Severity of aortic valve stenosis
Left ventricular outflow tract (LVOT) diameter was measured in mid systole from the parasternal long-axis view after the outflow tract had been magnified. Transvalvular aortic velocity time integral (VTI), mean pressure gradient (MPG) and peak aortic velocity were obtained using non-imaging continuous wave Doppler and the right parasternal view, whenever possible. Aortic valve effective orifice area (EOA) was determined by the continuity equation method using the ratio of the VTI across the valve and in the LVOT obtained using pulsed-wave Doppler and was indexed to body surface area (BSA). The energy loss index (ELI) (i.e., the EOA corrected for pressure recovery) was calculated using the following formula:
E L I = ( E O A ( A a / A a − E O A ) / B S A ) ,
Systemic arterial haemodynamics
Assuming a two-element Windkessel model, systemic arterial compliance (SAC) was calculated as the ratio of stroke volume index (SVi) to pulse pressure (PP) using either aortic PP (SAC Ao ) or brachial PP (SAC b ). The systemic vascular resistance (SVR) was calculated as follows:
( [ 80 × mean blood pressure ] / cardiac output ) ,
Global LV haemodynamic load
As a measure of global LV haemodynamic load, valvuloarterial impedance was calculated as follows:
Z v a = ( M P G + S B P ) / S V i ,
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