2009心脏舒张功能超声诊断标准

D th io . App MD, A. F ista, slo, a, Sp ogra C L A T f p T m c A t T i t p h T T c O U n t v p t e a A T m – T E P C n E TA Pre I F. Limitations 114 VI. Color M-Mode Flow Propagation Velocity 114 c Veloci- From the Method Mayo Clinic Ariz Belgium (T.C.G.); Clinic, Rochester (O.A.S.); Washing University of Erla Barcelona, Spain Reprint requests: Boulevard, Suite * Writing Committ † Writing Commit 0894-7317/$36.00 © 2009 Publishe Echocardiography doi:10.1016/j.ech A. Acquisition, Feasibility, and Measurement 114 B. Hemodynamic Determinants 114 C. Clinical Application 115 D. Limitations 115 VII. Tissue Doppler Annular Early and Late Diastoli ties 115 A. Acquisition and Feasibility 115 B. Measurements 115 C. Hemodynamic Determinants 116 D. Normal Values 116 E. Clinical Application 116 F. Limitations 117 VIII. Deformation Measurements 118 IX. Left Ventricular Untwisting 118 A. Clinical Application 118 ist DeBakey Heart and Vascular Center, Houston, TX (S.F.N.); ona, Phoenix, AZ (C.P.A.); the University of Ghent, Ghent, Eastern Piedmont University, Novara, Italy (P.N.M.); Mayo , MN (J.K.O., P.A.P.); the University of Oslo, Oslo, Norway ton University School of Medicine, St Louis, MO (A.D.W.); the ngen, Erlangen, Germany (F.A.F.); and Hospital Vall d’Hebron, (A.E.). American Society of Echocardiography, 2100 Gateway Centre 310, Morrisville, NC 27560 (E-mail: ase@asecho.org). ee of the European Association of Echocardiography. tee of the American Society of Echocardiography. d by Elsevier Inc. on behalf of the American Society of . o.2008.11.023 GUIDELINES AN Recommendations for Ventricular Diastolic Funct Sherif F. Nagueh, MD, Chair,† Christopher P Paolo N. Marino, MD,* Jae K. Oh, Alan D. Waggoner, MHS,† Frank Patricia A. Pellikka, MD,† and Arturo Evangel Ghent, Belgium; Novara, Italy; Rochester, Minnesota; O Barcelon Keywords: Diastole , Echocardi ontinuing Medical Education Activity for “Recommendations for the Evaluation of eft Ventricular Diastolic Function by Echocardiography” ccreditation Statement: he American Society of Echocardiography is accredited by the Accreditation Council or Continuing Medical Education to provide continuing medical education for hysicians. he American Society of Echocardiography designates this educational activity for a aximum of 1 AMA PRA Category 1 Credits™. Physicians should only claim credit ommensurate with the extent of their participation in the activity. RDMS and CCI recognize ASE’s certificates and have agreed to honor the credit hours oward their registry requirements for sonographers. he American Society of Echocardiography is committed to resolving all conflict of nterest issues, and its mandate is to retain only those speakers with financial interests hat can be reconciled with the goals and educational integrity of the educational rogram. Disclosure of faculty and commercial support sponsor relationships, if any, ave been indicated. arget Audience: his activity is designed for all cardiovascular physicians, cardiac sonographers, ardiovascular anesthesiologists, and cardiology fellows. bjectives: pon completing this activity, participants will be able to: 1. Describe the hemody- amic determinants and clinical application of mitral inflow velocities. 2. Recognize he hemodynamic determinants and clinical application of pulmonary venous flow elocities. 3. Identify the clinical application and limitations of early diastolic flow ropagation velocity. 4. Assess the hemodynamic determinants and clinical applica- ion of mitral annulus tissue Doppler velocities. 5. Use echocardiographic methods to stimate left ventricular filling pressures in patients with normal and depressed EF, nd to grade the severity of diastolic dysfunction. uthor Disclosures: hierry C. Gillebert: Research Grant – Participant in comprehensive research agree- ent between GE Ultrasound, Horten, Norway and Ghent University; Advisory Board Astra-Zeneca, Merck, Sandoz. he following stated no disclosures: Sherif F. Nagueh, Frank A. Flachskampf, Arturo vangelista, Christopher P. Appleton, Thierry C. Gillebert, Paolo N. Marino, Jae K. Oh, atricia A. Pellikka, Otto A. Smiseth, Alan D. Waggoner. onflict of interest: The authors have no conflicts of interest to disclose except as oted above. stimated time to complete this activity: 1 hour STANDARDS e Evaluation of Left n by Echocardiography leton, MD,† Thierry C. Gillebert, MD,* † Otto A. Smiseth, MD, PhD,* lachskampf, MD, Co-Chair,* MD,* Houston, Texas; Phoenix, Arizona; Norway; St. Louis, Missouri; Erlangen, Germany; ain phy, Doppler, Heart failure BLE OF CONTENTS face 108 I. Physiology 108 II. Morphologic and Functional Correlates of Diastolic Dysfunc- tion 109 A. LV Hypertrophy 109 B. LA Volume 109 C. LA Function 110 D. Pulmonary Artery Systolic and Diastolic Pressures 110 III. Mitral Inflow 111 A. Acquisition and Feasibility 111 B. Measurements 111 C. Normal Values 111 D. Inflow Patterns and Hemodynamics 111 E. Clinical Application to Patients With Depressed and Nor- mal EFs 111 F. Limitations 112 V. Valsalva Maneuver 113 A. Performance and Acquisition 113 B. Clinical Application 113 C. Limitations 113 V. Pulmonary Venous Flow 113 A. Acquisition and Feasibility 113 B. Measurements 113 C. Hemodynamic Determinants 114 D. Normal Values 114 E. Clinical Application to Patients With Depressed and Nor- mal EFs 114 107 X X X XI X XV XV PR Th int ing dia fra fail dia tan pu ide na abs pre an are cha tha dia do an tio rec the I. Th cyc allo cha vo tio vo wit pre an Fig hig ve co op tric co pre Th slo co pre su da pa Hg en diff cre pro pre (Co 108 Nagueh et al Journal of the American Society of Echocardiography February 2009 B. Limitations 118 X. Estimation of Left Ventricular Relaxation 119 A. Direct Estimation 119 1. IVRT 119 2. Aortic Regurgitation CW Signal 119 3. MR CW Signal 119 B. Surrogate Measurements 119 1. Mitral Inflow Velocities 119 2. Tissue Doppler Annular Signals 119 3. Color M-Mode Vp 119 I. Estimation of Left Ventricular Stiffness 119 A. Direct Estimation 119 B. Surrogate Measurements 120 1. DT of Mitral E Velocity 120 2. A-Wave Transit Time 120 II. Diastolic Stress Test 120 III. Other Reasons for Heart Failure Symptoms in Patients With Normal Ejection Fractions 121 A. Pericardial Diseases 121 B. Mitral Stenosis 122 C. MR 122 V. Estimation of Left Ventricular Filling Pressures in Special Pop- ulations 122 A. Atrial Fibrillation 122 B. Sinus Tachycardia 123 C. Restrictive Cardiomyopathy 123 D. Hypertrophic Cardiomyopathy 123 E. Pulmonary Hypertension 123 V. Prognosis 126 I. Recommendations for Clinical Laboratories 127 A. Estimation of LV Filling Pressures in Patients With De- pressed EFs 127 B. Estimation of LV Filling Pressures in Patients With Normal EFs 127 C. Grading Diastolic Dysfunction 128 II. Recommendations for Application in Research Studies and Clinical Trials 128 EFACE e assessment of left ventricular (LV) diastolic function should be an egral part of a routine examination, particularly in patients present- with dyspnea or heart failure. About half of patients with new gnoses of heart failure have normal or near normal global ejection ctions (EFs). These patients are diagnosed with “diastolic heart ure” or “heart failure with preserved EF.”1 The assessment of LV stolic function and filling pressures is of paramount clinical impor- ce to distinguish this syndrome from other diseases such as lmonary disease resulting in dyspnea, to assess prognosis, and to ntify underlying cardiac disease and its best treatment. LV filling pressures as measured invasively include mean pulmo- ry wedge pressure or mean left atrial (LA) pressure (both in the ence of mitral stenosis), LV end-diastolic pressure (LVEDP; the ssure at the onset of the QRS complex or after A-wave pressure), d pre-A LV diastolic pressure (Figure 1). Although these pressures different in absolute terms, they are closely related, and they nge in a predictable progression with myocardial disease, such t LVEDP increases prior to the rise in mean LA pressure. Echocardiography has played a central role in the evaluation of LV stolic function over the past two decades. The purposes of this ma ap com cument is to provide a comprehensive review of the techniques d the significance of diastolic parameters, as well as recommenda- ns for nomenclature and reporting of diastolic data in adults. The ommendations are based on a critical review of the literature and consensus of a panel of experts. PHYSIOLOGY e optimal performance of the left ventricle depends on its ability to le between two states: (1) a compliant chamber in diastole that ws the left ventricle to fill from low LA pressure and (2) a stiff mber (rapidly rising pressure) in systole that ejects the stroke lume at arterial pressures. The ventricle has two alternating func- ns: systolic ejection and diastolic filling. Furthermore, the stroke lume must increase in response to demand, such as exercise, hout much increase in LA pressure.2 The theoretically optimal LV ssure curve is rectangular, with an instantaneous rise to peak and instantaneous fall to low diastolic pressures, which allows for the 10 20 TIME (ms) 0040020 PR ES SU RE (m mH g) 10 20 Normal EDP High EDP LV LA rapid filling slow filling atrial contr.IR systole ure 1 The 4 phases of diastole are marked in relation to h-fidelity pressure recordings from the left atrium (LA) and left ntricle (LV) in anesthetized dogs. The first pressure crossover rresponds to the end of isovolumic relaxation and mitral valve ening. In the first phase, left atrial pressure exceeds left ven- ular pressure, accelerating mitral flow. Peak mitral E roughly rresponds to the second crossover. Thereafter, left ventricular ssure exceeds left atrial pressure, decelerating mitral flow. ese two phases correspond to rapid filling. This is followed by w filling, with almost no pressure differences. During atrial ntraction, left atrial pressure again exceeds left ventricular ssure. The solid arrow points to left ventricular minimal pres- re, the dotted arrow to left ventricular pre-A pressure, and the shed arrow to left ventricular end-diastolic pressure. The upper nel was recorded at a normal end-diastolic pressure of 8 mm . The lower panel was recorded after volume loading and an d-diastolic pressure of 24 mm Hg. Note the larger pressure erences in both tracings of the lower panel, reflecting de- ased operating compliance of the LA and LV. Atrial contraction vokes a sharp rise in left ventricular pressure, and left atrial ssure hardly exceeds this elevated left ventricular pressure. urtesy of T. C. Gillebert and A. F. Leite-Moreira.) ximum time for LV filling. This theoretically optimal situation is proached by the cyclic interaction of myofilaments and assumes petent mitral and aortic valves. Diastole starts at aortic valve clo he dia the Hg mi tio dia filli mo dia to pro un my Co of Re chr rel con rel an tha get an res seg ute mo 0.9 inv com dy rel wit be sur stif mo int Ex act an wa rel Th dra wit dy oth the pre LV pre of latt my cur do fun cle sta a d ao (to Ke 1. 2. 3. II. DI A. Alt no rea hy elin ob pa hy com ma 3-d sur usi Ech sho fun usu no dia na filli B. Th ech ob ass tio sto refl vo Journal of the American Society of Echocardiography Nagueh et al 109 Volume 22 Number 2 sure and includes LV pressure fall, rapid filling, diastasis (at slower art rates), and atrial contraction.2 Elevated filling pressures are the main physiologic consequence of stolic dysfunction.2 Filling pressures are considered elevated when mean pulmonary capillary wedge pressure (PCWP) is �12 mm or when the LVEDP is �16 mm Hg.1 Filling pressures change nimally with exercise in healthy subjects. Exercise-induced eleva- n of filling pressures limits exercise capacity and can indicate stolic dysfunction. LV filling pressures are determined mainly by ng and passive properties of the LV wall but may be further dulated by incomplete myocardial relaxation and variations in stolic myocardial tone. At the molecular level, the cyclic interaction of myofilaments leads a muscular contraction and relaxation cycle. Relaxation is the cess whereby the myocardium returns after contraction to its stressed length and force. In normal hearts, and with normal load, ocardial relaxation is nearly complete at minimal LV pressure. ntraction and relaxation belong to the same molecular processes transient activation of the myocyte and are closely intertwined.3 laxation is subjected to control by load, inactivation, and asyn- ony.2 Increased afterload or late systolic load will delay myocardial axation, especially when combined with elevated preload, thereby tributing to elevating filling pressures.4 Myocardial inactivation ates to the processes underlying calcium extrusion from the cytosol d cross-bridge detachment and is affected by a number of proteins t regulate calcium homeostasis,5 cross-bridge cycling,2 and ener- ics.3 Minor regional variation of the timing of regional contraction d relaxation is physiological. However, dyssynchronous relaxation ults in a deleterious interaction between early reextension in some ments and postsystolic shortening of other segments and contrib- s to delayed global LV relaxation and elevated filling pressures.6 The rate of global LV myocardial relaxation is reflected by the noexponential course of LV pressure fall, assuming a good fit (r� 7) to a monoexponential pressure decay. Tau is a widely accepted asive measure of the rate of LV relaxation, which will be 97% plete at a time corresponding to 3.5 � after dP/dtmin. Diastolic sfunction is present when � � 48 ms.1 In addition, the rate of axation may be evaluated in terms of LV dP/dtmin and indirectly h the isovolumetric relaxation time (IVRT), or the time interval tween aortic valve closure and mitral valve opening. LV filling is determined by the interplay between LV filling pres- es and filling properties. These filling properties are described with fness (�P/�V) or inversely with compliance (�V/�P) and com- nly refer to end-diastolic properties. Several factors extrinsic and rinsic to the left ventricle determine these end-diastolic properties. trinsic factors are mainly pericardial restraint and ventricular inter- ion. Intrinsic factors include myocardial stiffness (cardiomyocytes d extracellular matrix), myocardial tone, chamber geometry, and ll thickness.5 Chamber stiffness describes the LV diastolic pressure-volume ationship, with a number of measurements that can be derived. e operating stiffness at any point is equal to the slope of a tangent wn to the curve at that point (�P/�V) and can be approximated h only two distinct pressure-volume measurements. Diastolic sfunction is present when the slope is�0.20 mm Hg/mL.7 On the er hand, it is possible to characterize LV chamber stiffness over duration of diastole by the slope of the exponential fit to the diastolic ssure-volume relation. Such a curve fit can be applied to the diastolic pressure-volume relation of a single beat or to the end-diastolic ssure-volume relation constructed by fitting the lower right corner tim ou multiple pressure-volume loops obtained at various preloads. The er method has the advantage of being less dependent on ongoing ocardial relaxation. The stiffness modulus, kc, is the slope of the ve and can be used to quantify chamber stiffness. Normal values not exceed 0.015 (C. Tschöpe, personal communication). A distinct aspect of diastolic function is related to longitudinal ction and torsion. Torrent-Guasp et al8 described how the ventri- s may to some extent be assimilated to a single myofiber band rting at the right ventricle below the pulmonary valve and forming ouble helix extending to the left ventricle, where it attaches to the rta. This double helicoidal fiber orientation leads to systolic twisting rsion) and diastolic untwisting (torsional recoil). y Points Diastolic function is related to myocardial relaxation and passive LV properties and is modulated by myocardial tone. Myocardial relaxation is determined by load, inactivation, and nonunifor- mity. Myocardial stiffness is determined by the myocardial cell (eg, titin) and by the interstitial matrix (fibrosis). MORPHOLOGIC AND FUNCTIONAL CORRELATES OF ASTOLIC DYSFUNCTION LV Hypertrophy hough diastolic dysfunction is not uncommon in patients with rmal wall thickness, LV hypertrophy is among the important sons for it. In patients with diastolic heart failure, concentric pertrophy (increased mass and relative wall thickness), or remod- g (normal mass but increased relative wall thickness), can be served. In contrast, eccentric LV hypertrophy is usually present in tients with depressed EFs. Because of the high prevalence of pertension, especially in the older population, LV hypertrophy is mon, and hypertensive heart disease is the most common abnor- lity leading to diastolic heart failure. LV mass may be best, although laboriously, measured using imensional echocardiography.9 Nevertheless, it is possible to mea- e it in most patients using 2-dimensional (2D) echocardiography, ng the recently published guidelines of the American Society of ocardiography.10 For clinical purposes, at least LV wall thickness uld be measured in trying to arrive at conclusions on LV diastolic ction and filling pressures. In pathologically hypertrophied myocardium, LV relaxation is ally slowed, which reduces early diastolic filling. In the presence of rmal LA pressure, this shifts a greater proportion of LV filling to late stole after atrial contraction. Therefore, the presence of predomi- nt early filling in these patients favors the presence of increased ng pressures. LA Volume e measurement of LA volume is highly feasible and reliable in most ocardiographic studies, with the most accurate measurements tained using the apical 4-chamber and 2-chamber views.10 This essment is clinically important, because there is a significant rela- n between LA remodeling and echocardiographic indices of dia- lic function.11 However, Doppler velocities and time intervals ect filling pressures at the time of measurement, whereas LA lume often reflects the cumulative effects of filling pressures over e. Importantly, observational studies including 6,657 patients with- t baseline histories of atrial fibrillation and significant valvular heart dis ind isc ma me an fun car sid clin LV C. Th an rel cha fro pa the pu en vo gra be be mi res com AV res dia de con usi LA mi 1.0 M Fig lete pa velo ha rese 110 Nagueh et al Journal of the American Society of Echocardiography February 2009 ease have shown that LA volume index � 34 mL/m2 is an ependent predictor of death, heart failure, atrial fibrillation, and hemic stroke.12 However, one must recognize that dilated left atria y be seen in patients with bradycardia and 4-chamber enlarge- nt, anemia and other high-output states, atrial flutter or fibrillation, d significant mitral valve disease, in the absence of diastolic dys- ction. Likewise, it is often present in elite athletes in the absence of diovascular disease (Figure 2). Therefore, it is important to con- er LA volume measurements in conjunction with a patient’s ical status, other chambers’ volumes, and Doppler parameters of relaxation. LA Function e atriummodulates ventricular filling through its reservoir, conduit, d pump functions.13 During ventricular systole and isovolumic axation, when the atrioventricular (AV) valves are closed, atrial mbers work as distensible reservoirs accommodating blood flow m the venous circulation (reservoir volume is defined as LA ssive emptying volume minus the amount of blood flow reversal in pulmonary veins with atrial contraction). The atrium is also a mping chamber, which contributes to maintaining adequate LV d-diastolic volume by actively emptying at end-diastole (LA stroke lume is defined as LA volume at the onset of the electrocardio- phic P wave minus