- Email: [email protected]
Comparison of left ventricular systolic and diastolic function in patients with idiopathic dilated cardiomyopathy and mild heart failure versus those with severe heart failure
Comparison of Left Ventricular Systolic and Diastolic Function in Patients With Idiopathic Dilated Cardiomyopathy and Mild Heart Failure Versus Those With Severe Heart Failure Barbara M. Richartz,
MD,
Gerald S. Werner, MD, Markus Ferrari, Hans R. Figulla, MD
MD,
and
The pathogenesis of acute pulmonary edema in idiopathic dilated cardiomyopathy (IDC) is not completely understood. Because pulse-wave tissue Doppler imaging (TDI) allows a direct comparison between systolic as well as diastolic wall motion velocities, we tested the hypothesis that acute pulmonary edema is caused by both systolic and diastolic failure. We prospectively studied 65 patients. Forty patients had IDC (group 1), 15 of whom had recent-onset pulmonary congestion (group 1a, New York Heart Association [NYHA] functional classes III and IV) and 25 of whom were in clinically stable condition without signs of pulmonary congestion (group 1b, NYHA I and II). All of these patients were restudied after 3, 7, and 45 days. Groups 1a and 1b were compared with 25 subjects without evidence of heart disease (group 2). Peak systolic wall motion velocity (Vs), peak wall motion velocity of the early (Ve), and late (Va) filling waves were measured by TDI; mitral
inflow pattern was determined by pulse-wave Doppler and left ventricular (LV) ejection fraction (EF) by 2-dimensional echocardiography. In those patients without pulmonary edema (controls and group 1b, n ⴝ 50), we found a positive correlation between LVEF and Vs (r ⴝ 0.72, p <0.001) and between LVEF and Ve (r ⴝ 0.79, p <0.001). Early diastolic wall motion velocity always exceeded peak systolic wall motion velocity (Ve/Vs ratio >1). In patients with IDC with recent-onset pulmonary congestion (group 1a), Ve was significantly lower compared with group 1b (3.5 ⴞ 0.2 vs 4.9 ⴞ 0.4 cm/s, p <0.01, Ve/Vs ratio <1). Clinical improvement was paralled by a gradual increase in Ve (3.5 ⴞ 0.2 to 6.8 ⴞ 0.3 cm/s, p <0.01) but not in Vs or LVEF. Thus, in patients with IDC acute pulmonary edema is exclusively caused by diastolic rather than systolic failure. 䊚2002 by Excerpta Medica, Inc. (Am J Cardiol 2002;90:390 –394)
issue Doppler imaging (TDI) is a new ultrasound technique that allows direct quantification of myoT cardial diastolic and systolic wall motion velocities
to our hospital for invasive diagnostic procedures. Forty of the 65 patients had IDC (group 1) identified by an enlargement of the left ventricle, systolic dysfunction, angiographic exclusion of coronary artery disease, and valvular heart disease. The remaining 25 patients, who did not have clinical, echocardiographic, and angiographic evidence of heart disease (group 2), served as control group; they had normal systolic function, no coronary artery disease, and no segmental wall motion abnormalities and none had mitral regurgitation or an enlargement of the left atrium. All patients of the IDC group were restudied after 3, 7, and 45 days. Fifteen patients had signs of acute pulmonary edema (dyspnea, pulmonary edema on chest x-ray, New York Heart Association [NYHA] functional classes III and IV, group 1a), that initiated intensified medication with increased doses of diuretics and IV nitrates. Clinical improvement was defined as weight loss ⱖ3 kg, absence of rales, and no pulmonary congestion on chest x-ray. The remaining 25 patients were in clinically stable condition without signs of pulmonary edema (NYHA I and II, group 1b). Echocardiographic studies: Studies were performed with patients in the left lateral decubitus position using a Toshiba Power Vision 8000 (Toshiba Corp., Tokyo, Japan) with a multifrequency transducer with TDI
throughout the full cardiac cycle.1,2 In this technique, high velocities and small Doppler signals generated by blood flow are eliminated, and low velocities and large Doppler signals generated by the myocardial wall are selectively displayed as a color or spectral wave Doppler image.3 In the present study, we tested the hypothesis that acute pulmonary edema is caused by diastolic and systolic failure and that TDI may distinguish between acute congestion and chronic stable heart failure in idiopathic dilated cardiomyopathy (IDC).
METHODS
Patient population: We prospectively studied 65 consecutive patients who were in sinus rhythm and referred
From the Department of Internal Medicine III, Division of Cardiology, Friedrich-Schiller-University Jena, Jena, Germany. Manuscript received February 28, 2002; revised manuscript received and accepted April 18, 2002. Address for reprints: Barbara M. Richartz, MD, Friedrich-SchillerUniversity Jena, Department of Internal Medicine III, Division of Cardiology, Erlanger Allee 101, 07740 Jena, Germany. E-mail: barbara. [email protected].
390
©2002 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 90 August 15, 2002
0002-9149/02/$–see front matter PII S0002-9149(02)02495-5
pulse-wave Doppler mitral flow velocities were recorded from the apical 4-chamber view by placing the sample volume between the tip of the leaflets in the center of the stream to obtain peak rapid filling velocity (E), peak atrial filling velocity (A), the E/A ratio, and the E-wave deceleration time. Systolic and diastolic mitral annular velocities determined by tissue Doppler imaging: In the TDI technol-
ogy, a modified wall filter was used to display lowamplitude myocardial velocity. Gains were minimized to allow for a clear tissue signal with minimal background noise. Images were taken from the apical 4-chamber view with a 5-mm sample volume placed at the septal and lateral side of the mitral annulus. To minimize errors in the quantification of myocardial velocities related to cardiac translation and rotation, the transducer was angled such that the systolic movement occurred within a 30° arc (maximum of 15° on FIGURE 1. Typical tissue Doppler velocity spectrum with a posieach side).2 A typical tissue Doppler velocity spective wave during systole (s), and 2 main negative waves during diastole (e and a). trum shows a positive wave during systole when the mitral ring moves toward the cardiac apex (peak systolic wall motion velocity, Vs), and 2 main negative TABLE 1 Patient Characteristics waves during diastole, when the miIDC IDC Control Group tral annulus moves toward the base NYHA III–IV NYHA I–II Group 2 away from the apex, 1 that reflects (n ⫽ 15) (n ⫽ 25) (n ⫽ 25) early filling (peak wall motion velocAge (yrs) 52 ⫾ 4 49 ⫾ 5 54 ⫾ 6 ity of the early diastole, Ve) and 1 Women/men 4/11 6/19 10/15 that relates to atrial contraction (peak Heart rate (beats/min) 87 ⫾ 9 81 ⫾ 6 75 ⫾ 8 wall motion velocity of the late diasMean arterial blood pressure (mm Hg) 88 ⫾ 5 91 ⫾ 6 103 ⫾ 8 tole, Va) (Figure 1). The peak sysLVEF (%) 24 ⫾ 8 26 ⫾ 7 61 ⫾ 6 tolic and diastolic velocities were measured online at a sweep speed of 50 mm/s. The average value of 3 consecutive measurements was calculated. Because velocities in systole and diastole were opposite in value, absolute velocity data are used for comparison. Cardiac catheterization: After providing written informed consent, all patients underwent cardiac catheterization for ⱖ1 of the following indications: impaired LV function, exertional dyspnea, angina, and pathologic stress test. Data analysis: All data are expressed as mean ⫾ SD. To validate TDI, LV ejection fraction (EF) was compared with Vs, Ve, and Va by use of simple regression analysis. Analysis of variance was performed by F test. Intragroup comparisons FIGURE 2. The relation between peak systolic wall motion velocity (Vs) and LVEF. were performed by Student’s paired t test. Intergroup comparisons were performed by an unpaired Student’s technology in standard views and techniques accord- t test. A difference was considered significant at p ing to the recommendations of the American Society ⬍0.05. of Echocardiography.4,5 Mitral flow velocities determined by pulse-wave Doppler: Left ventricular (LV) diastolic function was
assessed from the transmitral flow velocities. The
RESULTS Table 1 lists the patient characteristics of the IDC
CARDIOMYOPATHY/PULMONARY EDEMA IN DILATED CARDIOMYOPATHY
391
Mitral annular systolic and diastolic velocities versus left ventricular ejection fraction: TDI spectral veloc-
ities were obtained from all patients to correlate peak systolic, peak early diastolic, and peak late diastolic wall motion velocities in both patients with chronic stable heart failure and controls (n ⫽ 50). A linear correlation was present between Vs and LVEF (r ⫽ 0.72, p ⬍0.001; Figure 2). Similarly, there was a linear correlation between Ve and LVEF (r ⫽ 0.79, p ⬍0.001; Figure 3). No correlation was found between Va and LVEF (r ⫽ 0.31, p ⫽ 0.40). Mitral annular early diastolic and systolic velocities: Furthermore, we
FIGURE 3. The relation between peak early diastolic wall motion velocity (Ve) and LVEF.
FIGURE 4. Comparison of peak systolic wall motion veloctiy (Vs, white column) and peak early diastolic wall motion velocity (Ve, black column).
compared peak early diastolic wall motion velocities with peak systolic wall motion velocities from both group 1b (IDC group without signs of congestive heart failure, n ⫽ 25) and the control group (n ⫽ 25). In this set of patients, peak early diastolic wall motion velocity was higher than peak systolic wall motion velocity (6.4 ⫾ 2.5 vs 5.5 ⫾ 1.8 cm/s, p ⬍0.01) with a Ve/Vs ratio ⬎1. Irrespective of the LVEF, Ve/Vs was ⬎1 as long as symptoms of heart failure were missing. In general, the better the global (systolic and diastolic) myocardial function, the greater the Ve/Vs ratio (Figure 4). Mitral annular early diastolic and systolic velocities in acute pulmonary edema: In the IDC group we com-
pared 15 patients with acute pulmonary congestion (group 1a, NYHA classes III and IV) and 25 patients TABLE 2 Doppler Echocardiographic Baseline Data with stable heart failure (group 1b, IDC IDC Control Group NYHA classes I and II). Table 2 NYHA III–IV NYHA I–II Group 2 lists the baseline data of the 2 (n ⫽ 15) (n ⫽ 25) (n ⫽ 25) groups. At baseline, Ve was signifE-wave velocity (m/s) 0.7 ⫾ 0.3 0.5 ⫾ 0.2* 0.7 ⫾ 0.2 icantly lower in patients in NYHA A-wave velocity (m/s) 0.6 ⫾ 0.2 0.7 ⫾ 0.3 0.9 ⫾ 0.4 class III and IV (group 1a) comE/A ratio 1.2 ⫾ 0.3 0.7 ⫾ 0.2* 0.9 ⫾ 0.3 pared with patients in NYHA class E-wave deceleration time (ms) 167 ⫾ 51 246 ⫾ 65* 216 ⫾ 43 I and II (group 1b), whereas Vs did Peak systolic wall motion velocity (cm/s) 4.1 ⫾ 0.2 4.4 ⫾ 0.2 7.1 ⫾ 1.3† Early diastolic wall motion velocity (cm/s) 3.5 ⫾ 0.2 6.0 ⫾ 0.4* 10.6 ⫾ 1.2† not differ significantly between the Late diastolic wall motion velocity (cm/s) 5.0 ⫾ 0.7 8.7 ⫾ 0.8* 11.5 ⫾ 2.1† groups. Thus, patients with acute Ve/Vs ratio 0.85 ⫾ 0.2 1.36 ⫾ 0.2* 1.48 ⫾ 0.2 pulmonary edema showed a Ve/Vs *p ⬍0.05 compared with NYHA classes III and IV (group 1a). ratio ⬍1. In contrast, in patients in † p ⬍0.05 compared with NYHA classes III and IV (group 1a) and NYHA classes I and II (group 1b). NYHA classes I and II, the Ve/Vs ratio was ⬎1 (Table 2). With respect to peak early diastolic wall motion velocity, 2 distinct patterns (groups 1a and 1b) and control groups. Demographics were identified: at baseline, Ve was significantly and baseline hemodynamic data were similar among lower in patients in NYHA classes III and IV than in patients in NYHA classes I and II and the Ve/Vs ratio the groups. 392 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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transient deterioration of systolic function. TDI provides direct assessment of wall motion abnormalities both in systole and diastole,1,2 in which Vs reflects systolic and Ve diastolic function. Thus, the Ve/Vs ratio has the potential to distinguish between acute pulmonary congestion and clinically stable heart failure. In the latter group, early diastolic wall motion velocity was always higher than peak systolic wall motion velocity (Ve/Vs ratio ⬎1) and remained unchanged over 6 weeks. In contrast, in patients with heart failure who had acute pulmonary congestion, Ve was significantly lower with a Ve/Vs ratio ⬍1 and clinical improvement was paralleled exclusively by an increase of Ve, whereas Vs and LVEF failed to improve with symptomatic recovery. Currently, Doppler echocardiography is the most accurate method to noninvasively assess diastolic function.6 The transmitral Doppler flow pattern7–10 has been introduced to focus on diastolic dysfunction. Impaired LV relaxation is seen in the early stages of diastolic dysfunction and is detected by a decrease in early transmitral LV filling (E wave) and an increase in the atrial filling component (A wave).11 During acute pulmonary edema, decreased LV chamber compliance FIGURE 5. Changes of peak early wall motion velocity (Ve, solid line), peak systolic and elevated left atrial pressures wall motion velocity (Vs, dashed line), and the Ve/Vs ratio (columns) by time (1: basecause a large inflow velocity E line, 2: 3 days, 3: 7 days, 4: 45 days). (A) Patients with IDC of group 1a (NYHA wave and an impaired filling during classes III and IV) with acute pulmonary edema. (B) Patients with IDC of group 1b atrial contraction.12 Moreover, LV (NYHA classes I and II) without evidence of acute pulmonary edema. stiffness is markly increased, causing a progressive shortening of the mitral deceleration time,11 as seen was ⬍1. Clinical improvement was paralleled by a in our patients. The deceleration time is useful in gradual increase of Ve but not of LVEF (24 ⫾ 8% vs estimating pulmonary capillary wedge pressure, such 26 ⫾ 6%, ns) or Vs. With improving symptoms, the as deceleration time ⬍120 ms indicates pulmonary Ve/Vs ratio was ⬎1 within 3 days. In contrast, in the capillary wedge pressure ⬎20 mm Hg.13 Although patients of group 1b, Ve was significantly higher than noninvasive estimation of pulmonary wedge pressure Vs with a Ve/Vs ratio ⬎ 1. Ve, Vs, and the Ve/Vs appears to be an attractive concept, it has not been ratio were unchanged with longitudinal follow-up closely correlated with pulmonary congestion in pa(Figure 5). tients with heart failure.14 Therefore, a less load deTransmitral flow velocities: The mean ratio of the pendent noninvasive parameter would facilitate the peak transmitral flow velocity of the E and A waves was detection of acute pulmonary edema. As recently lower after treatment, because E-wave velocity de- shown, TDI has the potential to evaluate diastolic creased. In addition, deceleration time was prolonged function independently of loading conditions.15–17 In after treatment. This implies a trend toward of a restric- addition, pulsed TDI allows direct assessment of both tive filling pattern in acute pulmonary edema, and a the relation between systolic and diastolic wall motion relaxation abnormality in the recompensated state. velocities, and interdependent changes in systolic and diastolic abnormalities. Diastolic failure is a filling disturbance and results in “backward failure” with DISCUSSION We showed that acute pulmonary edema in IDC is decreased Ve and preserved Vs. This can be—at least exclusively caused by diastolic failure and not by a partially— explained by the fact that tissue Doppler CARDIOMYOPATHY/PULMONARY EDEMA IN DILATED CARDIOMYOPATHY
393
velocity reflects functional wall motion changes (endocardial excursion and myocardial thickening), whereas mitral Doppler inflow velocity portrays blood flow dynamics, dependent on pressure gradient between left atrium and left ventricle, LV relaxation, and viscoelastic properties.9,18 Another explanation might be that in patients with acute pulmonary congestion, ventricular compliance is almost lost and therefore prevents early diastolic filling (no shift of the mitral annulus toward the base) and causes a significant decrease in Ve,16,19 but not of Vs, leading to a Ve/Vs ratio ⬍1. 1. Donovan C, Amstrong W, Bach D. Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects. Am Heart J 1995; 130:100 –104. 2. Miyatake K, Yamagishi M, Tanaka N, Uematsu M, Yamazaki N, Mine Y. New method for evaluating left ventricular wall motion by color-coded tissue Doppler imaging: in vitro and in vivo studies. J Am Coll Cardiol 1995;25:717–724. 3. Sutherland G, Stewart M, Groundstroem K, Moran C, Fliming A, Guell-Peris F. Color Doppler myocardial imaging: a new technique for the assessment of myocardial function. J Am Soc Echocardiogr 1994;7:441–458. 4. Henry WL, DeMaria A, Gramiak R, King DL, Kisslo JA, Popp RL, Sahn DJ, Schiller NB, Tajik A, Teichholz LE, Weyman AE. Report of the American Society of Echocardiography nomenclature and standards in two-dimensional echocardiography. Circulation 1980;62:212–215. 5. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silvermann NH, Tajik AJ. Recommendation for quantification of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358 –367. 6. Nishimura RA, Abel MD, Hatle LK, Tajik AJ. Assessment of diastolic function of the heart: background and current applications of Doppler echocardiography. Mayo Clin Proc 1989;64:181–204. 7. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined
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hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988; 12:426 –440. 8. Werner GS, Schaefer C, Dirks R, Figulla HR, Kreuzer H. Doppler echocardiographic assessment of left ventricular filling in dilated cardiomyopathy during a one-year follow-up: relation to the clinical course of the disease. Am Heart J 1993;126:1408 –1416. 9. Ishida Y, Meisner JS, Tsujioka K, Gallo JI, Yoran C, Frater RWM. Left ventricular filling dynamics: influence of left ventricular relaxation and left atrial pressure. Circulation 1986;74:187–196. 10. Rossvoll O, Hatle LK. Pulmonary venous flow velovities recorded by transthoracic Doppler ultrasound: relation to left ventricular diastolic pressures. J Am Coll Cardiol 1993;21:1687–1696. 11. Ohno M, Cheng CP, Little WC. Mechanismus of altered filling patterns of left ventricular filling during the development of congestive heart failure. Circulation 1984;89:2241–2250. 12. Pinamonti B, Zecchin M, Di Lenarda A, Gregori D, Sinagra G, Camerini F. Persistance of restrictive left ventricular filling pattern in dilated cardiomyopathy: an ominous prognostic sign. J Am Cardiol 1997;29:604 –612. 13. Nishimura RA, Tajik AJ. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinican’s Rosetta Stone. J Am Coll Cardiol 1997;30:8 –18. 14. Chacco CS, Woska D, Martinez H. Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care. Am J Med 1991:90. 15. Rodriguez L, Garcia M, Arez M, Griffin BP, Nakatani S, Thomas JD. Assessment of mitral annular dynamics during diastole by Doppler tissue imaging: comparison with mitral Doppler inflow in subjects without heart disease and in patients with left ventricular hypertrophy. Am Heart J 1996;131:982–987. 16. Nagueh SF, Middelton KJ, Kopelen HA, Zoghbi WA, Quinones MA. Doppler tissue imaging: a noninvasive technique for evaluation of the left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 1997;30:1527– 1533. 17. Oki T, Tabata T, Yamada H, Wakatsuki T, Mishiro Y, Abe M, Onose Y, Iuchi A, Ito S. Left ventricular diastolic properties of hypertensive patients measured by pulsed tissue Doppler imaging. J Am Soc Echocardiogr 1998;11:1106 –1112. 18. Myreng Y, Smiseth OA. Assessment of left ventricular diastolic function by Doppler echocardiography: comparison of isovolumic relaxation time and transmitral flow velocities with time constant of isovolumic relaxation. Circulation 1990;81:260 –266. 19. Nicolic S, Yellin EL, Tamura K, Vetter H, Tamura T, Meisner JS, Frater RW. Passive properties of cannin left ventricle: diastolic stiffness and restoring forces. Circ Res 1988;62:1210 –1222.
AUGUST 15, 2002
MD,
Gerald S. Werner, MD, Markus Ferrari, Hans R. Figulla, MD
MD,
and
The pathogenesis of acute pulmonary edema in idiopathic dilated cardiomyopathy (IDC) is not completely understood. Because pulse-wave tissue Doppler imaging (TDI) allows a direct comparison between systolic as well as diastolic wall motion velocities, we tested the hypothesis that acute pulmonary edema is caused by both systolic and diastolic failure. We prospectively studied 65 patients. Forty patients had IDC (group 1), 15 of whom had recent-onset pulmonary congestion (group 1a, New York Heart Association [NYHA] functional classes III and IV) and 25 of whom were in clinically stable condition without signs of pulmonary congestion (group 1b, NYHA I and II). All of these patients were restudied after 3, 7, and 45 days. Groups 1a and 1b were compared with 25 subjects without evidence of heart disease (group 2). Peak systolic wall motion velocity (Vs), peak wall motion velocity of the early (Ve), and late (Va) filling waves were measured by TDI; mitral
inflow pattern was determined by pulse-wave Doppler and left ventricular (LV) ejection fraction (EF) by 2-dimensional echocardiography. In those patients without pulmonary edema (controls and group 1b, n ⴝ 50), we found a positive correlation between LVEF and Vs (r ⴝ 0.72, p <0.001) and between LVEF and Ve (r ⴝ 0.79, p <0.001). Early diastolic wall motion velocity always exceeded peak systolic wall motion velocity (Ve/Vs ratio >1). In patients with IDC with recent-onset pulmonary congestion (group 1a), Ve was significantly lower compared with group 1b (3.5 ⴞ 0.2 vs 4.9 ⴞ 0.4 cm/s, p <0.01, Ve/Vs ratio <1). Clinical improvement was paralled by a gradual increase in Ve (3.5 ⴞ 0.2 to 6.8 ⴞ 0.3 cm/s, p <0.01) but not in Vs or LVEF. Thus, in patients with IDC acute pulmonary edema is exclusively caused by diastolic rather than systolic failure. 䊚2002 by Excerpta Medica, Inc. (Am J Cardiol 2002;90:390 –394)
issue Doppler imaging (TDI) is a new ultrasound technique that allows direct quantification of myoT cardial diastolic and systolic wall motion velocities
to our hospital for invasive diagnostic procedures. Forty of the 65 patients had IDC (group 1) identified by an enlargement of the left ventricle, systolic dysfunction, angiographic exclusion of coronary artery disease, and valvular heart disease. The remaining 25 patients, who did not have clinical, echocardiographic, and angiographic evidence of heart disease (group 2), served as control group; they had normal systolic function, no coronary artery disease, and no segmental wall motion abnormalities and none had mitral regurgitation or an enlargement of the left atrium. All patients of the IDC group were restudied after 3, 7, and 45 days. Fifteen patients had signs of acute pulmonary edema (dyspnea, pulmonary edema on chest x-ray, New York Heart Association [NYHA] functional classes III and IV, group 1a), that initiated intensified medication with increased doses of diuretics and IV nitrates. Clinical improvement was defined as weight loss ⱖ3 kg, absence of rales, and no pulmonary congestion on chest x-ray. The remaining 25 patients were in clinically stable condition without signs of pulmonary edema (NYHA I and II, group 1b). Echocardiographic studies: Studies were performed with patients in the left lateral decubitus position using a Toshiba Power Vision 8000 (Toshiba Corp., Tokyo, Japan) with a multifrequency transducer with TDI
throughout the full cardiac cycle.1,2 In this technique, high velocities and small Doppler signals generated by blood flow are eliminated, and low velocities and large Doppler signals generated by the myocardial wall are selectively displayed as a color or spectral wave Doppler image.3 In the present study, we tested the hypothesis that acute pulmonary edema is caused by diastolic and systolic failure and that TDI may distinguish between acute congestion and chronic stable heart failure in idiopathic dilated cardiomyopathy (IDC).
METHODS
Patient population: We prospectively studied 65 consecutive patients who were in sinus rhythm and referred
From the Department of Internal Medicine III, Division of Cardiology, Friedrich-Schiller-University Jena, Jena, Germany. Manuscript received February 28, 2002; revised manuscript received and accepted April 18, 2002. Address for reprints: Barbara M. Richartz, MD, Friedrich-SchillerUniversity Jena, Department of Internal Medicine III, Division of Cardiology, Erlanger Allee 101, 07740 Jena, Germany. E-mail: barbara. [email protected].
390
©2002 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 90 August 15, 2002
0002-9149/02/$–see front matter PII S0002-9149(02)02495-5
pulse-wave Doppler mitral flow velocities were recorded from the apical 4-chamber view by placing the sample volume between the tip of the leaflets in the center of the stream to obtain peak rapid filling velocity (E), peak atrial filling velocity (A), the E/A ratio, and the E-wave deceleration time. Systolic and diastolic mitral annular velocities determined by tissue Doppler imaging: In the TDI technol-
ogy, a modified wall filter was used to display lowamplitude myocardial velocity. Gains were minimized to allow for a clear tissue signal with minimal background noise. Images were taken from the apical 4-chamber view with a 5-mm sample volume placed at the septal and lateral side of the mitral annulus. To minimize errors in the quantification of myocardial velocities related to cardiac translation and rotation, the transducer was angled such that the systolic movement occurred within a 30° arc (maximum of 15° on FIGURE 1. Typical tissue Doppler velocity spectrum with a posieach side).2 A typical tissue Doppler velocity spective wave during systole (s), and 2 main negative waves during diastole (e and a). trum shows a positive wave during systole when the mitral ring moves toward the cardiac apex (peak systolic wall motion velocity, Vs), and 2 main negative TABLE 1 Patient Characteristics waves during diastole, when the miIDC IDC Control Group tral annulus moves toward the base NYHA III–IV NYHA I–II Group 2 away from the apex, 1 that reflects (n ⫽ 15) (n ⫽ 25) (n ⫽ 25) early filling (peak wall motion velocAge (yrs) 52 ⫾ 4 49 ⫾ 5 54 ⫾ 6 ity of the early diastole, Ve) and 1 Women/men 4/11 6/19 10/15 that relates to atrial contraction (peak Heart rate (beats/min) 87 ⫾ 9 81 ⫾ 6 75 ⫾ 8 wall motion velocity of the late diasMean arterial blood pressure (mm Hg) 88 ⫾ 5 91 ⫾ 6 103 ⫾ 8 tole, Va) (Figure 1). The peak sysLVEF (%) 24 ⫾ 8 26 ⫾ 7 61 ⫾ 6 tolic and diastolic velocities were measured online at a sweep speed of 50 mm/s. The average value of 3 consecutive measurements was calculated. Because velocities in systole and diastole were opposite in value, absolute velocity data are used for comparison. Cardiac catheterization: After providing written informed consent, all patients underwent cardiac catheterization for ⱖ1 of the following indications: impaired LV function, exertional dyspnea, angina, and pathologic stress test. Data analysis: All data are expressed as mean ⫾ SD. To validate TDI, LV ejection fraction (EF) was compared with Vs, Ve, and Va by use of simple regression analysis. Analysis of variance was performed by F test. Intragroup comparisons FIGURE 2. The relation between peak systolic wall motion velocity (Vs) and LVEF. were performed by Student’s paired t test. Intergroup comparisons were performed by an unpaired Student’s technology in standard views and techniques accord- t test. A difference was considered significant at p ing to the recommendations of the American Society ⬍0.05. of Echocardiography.4,5 Mitral flow velocities determined by pulse-wave Doppler: Left ventricular (LV) diastolic function was
assessed from the transmitral flow velocities. The
RESULTS Table 1 lists the patient characteristics of the IDC
CARDIOMYOPATHY/PULMONARY EDEMA IN DILATED CARDIOMYOPATHY
391
Mitral annular systolic and diastolic velocities versus left ventricular ejection fraction: TDI spectral veloc-
ities were obtained from all patients to correlate peak systolic, peak early diastolic, and peak late diastolic wall motion velocities in both patients with chronic stable heart failure and controls (n ⫽ 50). A linear correlation was present between Vs and LVEF (r ⫽ 0.72, p ⬍0.001; Figure 2). Similarly, there was a linear correlation between Ve and LVEF (r ⫽ 0.79, p ⬍0.001; Figure 3). No correlation was found between Va and LVEF (r ⫽ 0.31, p ⫽ 0.40). Mitral annular early diastolic and systolic velocities: Furthermore, we
FIGURE 3. The relation between peak early diastolic wall motion velocity (Ve) and LVEF.
FIGURE 4. Comparison of peak systolic wall motion veloctiy (Vs, white column) and peak early diastolic wall motion velocity (Ve, black column).
compared peak early diastolic wall motion velocities with peak systolic wall motion velocities from both group 1b (IDC group without signs of congestive heart failure, n ⫽ 25) and the control group (n ⫽ 25). In this set of patients, peak early diastolic wall motion velocity was higher than peak systolic wall motion velocity (6.4 ⫾ 2.5 vs 5.5 ⫾ 1.8 cm/s, p ⬍0.01) with a Ve/Vs ratio ⬎1. Irrespective of the LVEF, Ve/Vs was ⬎1 as long as symptoms of heart failure were missing. In general, the better the global (systolic and diastolic) myocardial function, the greater the Ve/Vs ratio (Figure 4). Mitral annular early diastolic and systolic velocities in acute pulmonary edema: In the IDC group we com-
pared 15 patients with acute pulmonary congestion (group 1a, NYHA classes III and IV) and 25 patients TABLE 2 Doppler Echocardiographic Baseline Data with stable heart failure (group 1b, IDC IDC Control Group NYHA classes I and II). Table 2 NYHA III–IV NYHA I–II Group 2 lists the baseline data of the 2 (n ⫽ 15) (n ⫽ 25) (n ⫽ 25) groups. At baseline, Ve was signifE-wave velocity (m/s) 0.7 ⫾ 0.3 0.5 ⫾ 0.2* 0.7 ⫾ 0.2 icantly lower in patients in NYHA A-wave velocity (m/s) 0.6 ⫾ 0.2 0.7 ⫾ 0.3 0.9 ⫾ 0.4 class III and IV (group 1a) comE/A ratio 1.2 ⫾ 0.3 0.7 ⫾ 0.2* 0.9 ⫾ 0.3 pared with patients in NYHA class E-wave deceleration time (ms) 167 ⫾ 51 246 ⫾ 65* 216 ⫾ 43 I and II (group 1b), whereas Vs did Peak systolic wall motion velocity (cm/s) 4.1 ⫾ 0.2 4.4 ⫾ 0.2 7.1 ⫾ 1.3† Early diastolic wall motion velocity (cm/s) 3.5 ⫾ 0.2 6.0 ⫾ 0.4* 10.6 ⫾ 1.2† not differ significantly between the Late diastolic wall motion velocity (cm/s) 5.0 ⫾ 0.7 8.7 ⫾ 0.8* 11.5 ⫾ 2.1† groups. Thus, patients with acute Ve/Vs ratio 0.85 ⫾ 0.2 1.36 ⫾ 0.2* 1.48 ⫾ 0.2 pulmonary edema showed a Ve/Vs *p ⬍0.05 compared with NYHA classes III and IV (group 1a). ratio ⬍1. In contrast, in patients in † p ⬍0.05 compared with NYHA classes III and IV (group 1a) and NYHA classes I and II (group 1b). NYHA classes I and II, the Ve/Vs ratio was ⬎1 (Table 2). With respect to peak early diastolic wall motion velocity, 2 distinct patterns (groups 1a and 1b) and control groups. Demographics were identified: at baseline, Ve was significantly and baseline hemodynamic data were similar among lower in patients in NYHA classes III and IV than in patients in NYHA classes I and II and the Ve/Vs ratio the groups. 392 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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transient deterioration of systolic function. TDI provides direct assessment of wall motion abnormalities both in systole and diastole,1,2 in which Vs reflects systolic and Ve diastolic function. Thus, the Ve/Vs ratio has the potential to distinguish between acute pulmonary congestion and clinically stable heart failure. In the latter group, early diastolic wall motion velocity was always higher than peak systolic wall motion velocity (Ve/Vs ratio ⬎1) and remained unchanged over 6 weeks. In contrast, in patients with heart failure who had acute pulmonary congestion, Ve was significantly lower with a Ve/Vs ratio ⬍1 and clinical improvement was paralleled exclusively by an increase of Ve, whereas Vs and LVEF failed to improve with symptomatic recovery. Currently, Doppler echocardiography is the most accurate method to noninvasively assess diastolic function.6 The transmitral Doppler flow pattern7–10 has been introduced to focus on diastolic dysfunction. Impaired LV relaxation is seen in the early stages of diastolic dysfunction and is detected by a decrease in early transmitral LV filling (E wave) and an increase in the atrial filling component (A wave).11 During acute pulmonary edema, decreased LV chamber compliance FIGURE 5. Changes of peak early wall motion velocity (Ve, solid line), peak systolic and elevated left atrial pressures wall motion velocity (Vs, dashed line), and the Ve/Vs ratio (columns) by time (1: basecause a large inflow velocity E line, 2: 3 days, 3: 7 days, 4: 45 days). (A) Patients with IDC of group 1a (NYHA wave and an impaired filling during classes III and IV) with acute pulmonary edema. (B) Patients with IDC of group 1b atrial contraction.12 Moreover, LV (NYHA classes I and II) without evidence of acute pulmonary edema. stiffness is markly increased, causing a progressive shortening of the mitral deceleration time,11 as seen was ⬍1. Clinical improvement was paralleled by a in our patients. The deceleration time is useful in gradual increase of Ve but not of LVEF (24 ⫾ 8% vs estimating pulmonary capillary wedge pressure, such 26 ⫾ 6%, ns) or Vs. With improving symptoms, the as deceleration time ⬍120 ms indicates pulmonary Ve/Vs ratio was ⬎1 within 3 days. In contrast, in the capillary wedge pressure ⬎20 mm Hg.13 Although patients of group 1b, Ve was significantly higher than noninvasive estimation of pulmonary wedge pressure Vs with a Ve/Vs ratio ⬎ 1. Ve, Vs, and the Ve/Vs appears to be an attractive concept, it has not been ratio were unchanged with longitudinal follow-up closely correlated with pulmonary congestion in pa(Figure 5). tients with heart failure.14 Therefore, a less load deTransmitral flow velocities: The mean ratio of the pendent noninvasive parameter would facilitate the peak transmitral flow velocity of the E and A waves was detection of acute pulmonary edema. As recently lower after treatment, because E-wave velocity de- shown, TDI has the potential to evaluate diastolic creased. In addition, deceleration time was prolonged function independently of loading conditions.15–17 In after treatment. This implies a trend toward of a restric- addition, pulsed TDI allows direct assessment of both tive filling pattern in acute pulmonary edema, and a the relation between systolic and diastolic wall motion relaxation abnormality in the recompensated state. velocities, and interdependent changes in systolic and diastolic abnormalities. Diastolic failure is a filling disturbance and results in “backward failure” with DISCUSSION We showed that acute pulmonary edema in IDC is decreased Ve and preserved Vs. This can be—at least exclusively caused by diastolic failure and not by a partially— explained by the fact that tissue Doppler CARDIOMYOPATHY/PULMONARY EDEMA IN DILATED CARDIOMYOPATHY
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velocity reflects functional wall motion changes (endocardial excursion and myocardial thickening), whereas mitral Doppler inflow velocity portrays blood flow dynamics, dependent on pressure gradient between left atrium and left ventricle, LV relaxation, and viscoelastic properties.9,18 Another explanation might be that in patients with acute pulmonary congestion, ventricular compliance is almost lost and therefore prevents early diastolic filling (no shift of the mitral annulus toward the base) and causes a significant decrease in Ve,16,19 but not of Vs, leading to a Ve/Vs ratio ⬍1. 1. Donovan C, Amstrong W, Bach D. Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects. Am Heart J 1995; 130:100 –104. 2. Miyatake K, Yamagishi M, Tanaka N, Uematsu M, Yamazaki N, Mine Y. New method for evaluating left ventricular wall motion by color-coded tissue Doppler imaging: in vitro and in vivo studies. J Am Coll Cardiol 1995;25:717–724. 3. Sutherland G, Stewart M, Groundstroem K, Moran C, Fliming A, Guell-Peris F. Color Doppler myocardial imaging: a new technique for the assessment of myocardial function. J Am Soc Echocardiogr 1994;7:441–458. 4. Henry WL, DeMaria A, Gramiak R, King DL, Kisslo JA, Popp RL, Sahn DJ, Schiller NB, Tajik A, Teichholz LE, Weyman AE. Report of the American Society of Echocardiography nomenclature and standards in two-dimensional echocardiography. Circulation 1980;62:212–215. 5. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silvermann NH, Tajik AJ. Recommendation for quantification of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358 –367. 6. Nishimura RA, Abel MD, Hatle LK, Tajik AJ. Assessment of diastolic function of the heart: background and current applications of Doppler echocardiography. Mayo Clin Proc 1989;64:181–204. 7. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined
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