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(Circulation. 1997;95:796-799.)
© 1997 American Heart Association, Inc.

Articles

Preload Reduction to Unmask the Characteristic Doppler Features of Constrictive Pericarditis

A New Observation

Jae K. Oh, MD; A. Jamil Tajik, MD; Christopher P. Appleton, MD; Liv K. Hatle, MD; Rick A. Nishimura, MD; James B. Seward, MD

the Division of Cardiovascular Diseases and Internal Medicine (J.K.O., A.J.T., R.A.N., J.B.S.), Mayo Clinic and Mayo Foundation, Rochester, Minn; Division of Cardiovascular Diseases (C.P.A.), Mayo Clinic, Scottsdale, Ariz; and Department of Clinical Physiology (L.K.H.), Linkoping, Sweden.

	Abstract

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Background Respiratory variation of 25% in mitral E velocity is a characteristic Doppler echocardiographic feature in constrictive pericarditis. However, a subset of patients with constriction do not exhibit the typical respiratory change, most likely because of marked increase in the left atrial pressure, and preload reduction may unmask the respiratory variation.

Methods and Results In 12 patients with surgically confirmed constrictive pericarditis who had <25% respiratory variation in mitral E velocity during an initial preoperative examination, the Doppler study was repeated after an attempt to decrease left ventricular filling pressure. At baseline, mean mitral E velocity was similar after inspiration and expiration (0.81±0.24 and 0.84±0.21 m/s, respectively). On repeat Doppler examination, with the patient in a head-up tilt or sitting position, the decrease in mitral E velocity with inspiration (0.61±0.13 m/s) was significant (P<.004), whereas it did not change significantly with expiration. The mean percent respiratory change in E velocity was 5±7% at baseline and 32±28% with preload reduction. Eight (75%) of the 12 patients developed respiratory variation of 25%.

Conclusions When the respiratory variation in Doppler mitral E velocity is blunted or absent during the evaluation of suspected constrictive pericarditis, repeat Doppler recording of mitral flow velocities after maneuvers to decrease preload is recommended to unmask the characteristic respiratory variation in mitral E velocity.

Key Words: blood flow • echocardiography • pericarditis • respiration

	Introduction

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Constrictive pericarditis and restrictive cardiomyopathy have similar clinical presentations; therefore, at times it can be a great challenge to distinguish between the two, even after exhaustive diagnostic testing.^{1 2 3} In constrictive pericarditis, two distinct pathophysiological abnormalities occur: exaggerated ventricular interdependence and dissociation of intrathoracic-intracardiac pressure changes with respiration. These distinctive hemodynamic changes must be demonstrated, either noninvasively or invasively, to establish the diagnosis of constrictive pericarditis. Hatle et al⁴ described the characteristic respiratory variations in Doppler flow velocities in patients with constrictive pericarditis that are not present in those with restrictive cardiomyopathy: 25% expiratory increase in mitral E velocity and expiratory decrease in hepatic vein diastolic flow velocity in conjunction with 25% increase in diastolic flow reversals compared with inspiratory velocities (Fig 1). In our previous study, these typical respiratory changes were present in 88% of patients with constrictive pericarditis. However, a subset of patients with constriction (12%) did not exhibit the characteristic respiratory variation.⁵

View larger version (112K): [in this window] [in a new window]   Figure 1. Typical diagnostic mitral valve (MV) inflow (A) and hepatic vein (HV) Doppler velocity recording (B) in constrictive pericarditis. The mitral inflow pattern is restrictive, with high E and small A velocities and a short deceleration time. In addition, E velocity after expiration (EXP) (1.2 m/s) is 33% higher than after inspiration (INSP) (0.9 m/s). HV forward flow velocity during diastole (D) decreases after onset of EXP, along with a significant diastolic flow reversal (DR).

There are two possible explanations for the absence of typical respiratory changes in Doppler velocities in patients with constriction. Some patients may have a combination of restrictive cardiomyopathy and constrictive pericarditis. Because ventricular filling is limited by a noncompliant restrictive myocardium as well as a constrictive pericardium, full respiratory variation in ventricular filling may not occur. Second, the normal inspiratory intrathoracic pressure decline (5 mm Hg) may not produce significant variation in mitral inflow velocities if the left atrial pressure is markedly increased and mitral valve opening occurs on a steeper than usual portion of the left ventricular pressure curve (Fig 2). In this situation, respiratory variation may be unmasked if the filling pressures are decreased by head-up tilt, sitting, or standing. Traditionally, volume loading is performed in the cardiac catheterization laboratory to induce the hemodynamics of constriction⁶ (ie, dip and plateau and near equalization of intracardiac end-diastolic pressures). These features, however, are also shared by restriction. The present report describes the inducibility of the characteristic respiratory variation in mitral inflow velocities with preload reduction in the subset of patients with constrictive pericarditis who had less than diagnostic (ie, <25%) respiratory change at baseline. Furthermore, diagnostic strategies to enhance echo-Doppler detection of constriction are provided, incorporating the results of this new observation.

View larger version (18K): [in this window] [in a new window]   Figure 2. A possible mechanism of decreased mitral flow velocity variation in some patients with constrictive pericarditis (CP). Left ventricular (LV) pressure decrease and pressure at mitral valve opening (MVO; horizontal arrows) are shown during expiration (exp; solid lines) and inspiration (insp; dashed lines) together with mitral flow velocity and the time from aortic closure (Ac) to the start of mitral flow. Vertical arrows indicate LV isovolumic relaxation time. A, In normal persons, the inspiratory decrease in LV minimal pressure and pressure at MVO is approximately equal, so that there is little change in early diastolic transmitral pressure gradient, mitral flow E velocity, or LV isovolumic relaxation time. B, In contrast, most patients with CP have less inspiratory change in LV minimal pressure than in pressure at MVO, resulting in increased variation in the early diastolic (transmitral) pressure gradient and early mitral flow velocity. C, However, if the constrictive process is severe and filling pressures are markedly increased, the flow velocity variation could be blunted because MVO occurs on a steeper portion of the exponential LV pressure decay where respiratory changes have relatively less effect on the transmitral pressure gradient. In these cases, decreasing left atrial and MVO pressures by head-up tilt or diuresis may result in increased respiratory variation in mitral flow velocities and LV isovolumic relaxation time, as seen in B.

	Methods

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Patients
Since January 1992, 12 patients with surgically confirmed constriction had <25% variation from inspiration to expiration in mitral inflow velocities during an initial preoperative echocardiographic examination, and a Doppler study was repeated after an attempt was made to decrease left ventricular filling pressure by head-up tilting or sitting. The study group included 10 men and 2 women (mean age±SD, 60±7 years; range, 47 to 73 years). All patients presented with evidence of right ventricular failure. The cardiac rhythm was sinus in 10 patients and atrial fibrillation in 2. Before pericardiectomy, all patients had additional evaluation with computed tomography (12 patients) or complete cardiac catheterization (2 patients), which showed findings consistent with constrictive pericarditis.

Echocardiography
Two-dimensional and Doppler echocardiographic examinations were performed in a standard manner with the use of a commercially available cardiac ultrasound unit. A pulsed-wave Doppler study of mitral inflow and hepatic vein flow velocities was performed with simultaneous respiratory recording from a nasal thermistor, as described previously.^{4 5} Doppler velocities were recorded at a paper-strip speed of 50 or 100 mm/s. The first cardiac cycles in which filling and ejection occurred in their entirety during a particular respiratory phase (either inspiration or expiration) were analyzed. Three respiratory cycles were analyzed for the patients with sinus rhythm, and 5 to 10 respiratory cycles for those with atrial fibrillation. The patients were initially placed in the left lateral decubitus or supine position, and a repeat echo-Doppler study was performed with the patient in a sitting or head-up tilt position.

Statistical Analysis
Results are expressed as mean±SD. The degrees of respiratory variation in E velocity were calculated as [(Expiratory E–Inspiratory E)/Inspiratory E]x100%. Values at baseline and after the postural change were compared by use of the paired t test. Differences were considered significant when the probability value was <.05.

	Results

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Doppler Findings
At baseline, mitral flow E velocity was 0.81±0.24 m/s (range, 0.50 to 1.30 m/s) with inspiration and 0.84±0.21 m/s (range, 0.60 to 1.20 m/s) with expiration (Figs 3 and 4A). The mean change in E velocity from inspiration to expiration was 5±7% (range, 0 to 20%). Mitral A velocity in 10 patients with sinus rhythm was 0.39±0.12 m/s (range, 0.25 to 0.60 m/s) with both inspiration and expiration. Deceleration time was shortened (137±29 ms with inspiration and 144±28 ms with expiration).

View larger version (22K): [in this window] [in a new window]   Figure 3. A plot of mitral E velocities with inspiration (Insp) and expiration (Exp) at baseline (A) and after a postural change (B). The mean and SD values are also shown. , Patients with sinus rhythm; , patients with atrial fibrillation.

With the patient in a sitting or head-up tilt position to reduce cardiac preload, there was a significant decrease in E velocity with inspiration (0.61±0.13 m/s; P<.004) compared with baseline E velocity (Figs 3 and 4B). E velocity with expiration (0.78±0.13 m/s) and A velocity with inspiration (0.39±0.11 m/s) and expiration (0.40±0.09 m/s) did not change significantly. The mean percent change in E velocity from inspiration to expiration was 32±28% (range, 0 to 100%), and 8 (75%) of the 12 patients developed respiratory variation of 25%. Deceleration time did not change significantly (127±21 ms with inspiration and 154±22 ms with expiration).

View larger version (151K): [in this window] [in a new window]   Figure 4. A, Baseline pulsed-wave Doppler echocardiographic recording of mitral inflow with patient in left lateral decubitus position. The respirometer recording is displayed at the bottom. Upward and downward deflections indicate the onset of inspiration and expiration, respectively. Mitral E velocity is 0.75 m/s with inspiration (second beat) and increases minimally to 0.85 m/s with expiration (fourth beat). It should be noted that the individual Doppler velocity pattern is restrictive, with short deceleration time (90 ms), small A velocity (0.25 m/s), and increased E/A ratio. B, Doppler echocardiographic study repeated a few minutes after baseline study with patient in upright position. The E velocity decreased during both inspiration (0.50 m/s) and expiration (0.75 m/s), with significant (50%) respiratory variation. The velocity pattern remained restrictive, with a respiratory variation in the deceleration time.

Doppler flow velocities in the hepatic vein were recorded in all patients at baseline. In 1 patient with severe tricuspid regurgitation, flow reversal occurred only during systole. In the 11 other patients, there were marked diastolic flow reversals during expiration.

Two-Dimensional Echocardiography
All patients had normal global left ventricular systolic function, with a mean left ventricular ejection fraction of 58±7%. Ventricular septal motion showing a "respiratory bounce" (septal shift toward the right ventricle during expiration and toward the left ventricle during inspiration) was present in 11 patients. The pericardium was thickened or calcified (or both) in 6 patients. The inferior vena cava was dilated in all the patients, with no inspiratory collapse.

	Discussion

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In patients with symptoms and signs of right ventricular failure, Doppler echocardiography can be diagnostic for constriction if mitral inflow and hepatic vein flow velocities show characteristic respiratory changes.^{4 5} However, our additional clinical experience has demonstrated that a lack of these typical respiratory flow velocity changes should not exclude the diagnosis, because up to 20% of patients may not meet these criteria. As seen in Fig 2, we believe this may occur in many cases because the exponential shape of left ventricular pressure decay dictates that respiratory changes in the early diastolic transmitral pressure gradient are decreased at higher filling pressures.

How, then, is it possible to diagnose constrictive pericarditis when no respiratory variation in flow velocities is shown by Doppler echocardiography? We suggest the following caveats. Most if not all patients with constriction show characteristic two-dimensional echocardiographic abnormalities. These include abnormal ventricular septal motion with prominent respiratory septal "bounce," calcified or thickened pericardium, or dilated inferior vena cava. These abnormal two-dimensional echocardiographic findings should raise the diagnostic possibility of constriction regardless of whether respiratory changes in Doppler flow velocities are present. Also, because patients with constrictive pericarditis have markedly decreased total cardiac compliance and increased filling pressures, both mitral and tricuspid diastolic filling patterns should show restrictive physiology.⁷ If mitral inflow velocity pattern shows an abnormal relaxation pattern (decreased E velocity, increased A velocity, E/A ratio <1, and prolonged deceleration time), this indicates that filling pressures are usually not elevated,⁷ and the diagnosis of constrictive pericarditis should be questioned. In patients with a restrictive diastolic filling pattern and no respiratory variation in mitral inflow velocities, the Doppler echocardiographic study should be repeated with an increased depth of respiration and maneuvers to decrease preload (tilting, sitting, or diuresis) in an effort to determine whether the characteristic Doppler velocity changes with respiration can be demonstrated.

Conclusion
In a subset of patients with constrictive pericarditis, the typical respiratory variation (25%) of mitral E velocity may not be present. This most likely is related to a marked increase in left atrial pressure. Reduction of preload by head-up tilt, upright position, or diuresis may augment or unmask the typical respiratory variation. Therefore, we recommend a repeat Doppler recording of mitral flow velocities simultaneously with a respirometer after maneuvers to decrease preload if there is blunted or absent respiratory variation in Doppler mitral flow velocities during the evaluation of constrictive pericarditis. These patients usually have characteristic two-dimensional echocardiographic features that in conjunction with Doppler echocardiographic findings should be helpful in diagnosing constrictive pericarditis.

	Footnotes

 
Reprint requests to Jae K. Oh, MD, Mayo Clinic, 200 First St SW, Rochester, MN 55905.

Received July 2, 1996; revision received December 16, 1996; accepted December 19, 1996.

	References

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2. Meaney E, Shabetai R, Bhargava V, Shearer M, Weidner C, Mangiardi LM, Smalling R, Peterson K. Cardiac amyloidosis, constrictive pericarditis and restrictive cardiomyopathy. Am J Cardiol. 1976;38:547-556.[Medline] [Order article via Infotrieve]

3. Vaitkus PT, Kussmaul WG. Constrictive pericarditis versus restrictive cardiomyopathy: a reappraisal and update of diagnostic criteria. Am Heart J. 1991;122:1431-1441.[Medline] [Order article via Infotrieve]

4. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation. 1989;79:357-370.[Abstract/Free Full Text]

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