Constrictive pericarditis

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Definition: A chronic inflammatory condition in which the visceral and parietal layers of pericardium are adherent, thickened, fibrous or calcific. This rigid pericardium limits the diastolic ventricular filling and impairs ventricular function.

Contents

Etiology

The most common causes of pericardial constriction are repeated episodes of pericarditis of various etiologies, previous cardiac surgery procedures, radiation therapy, tuberculosis.[1][2] Other causes such as neoplastic disease, autoimmune diseases, uraemia are less frequent.

Pathophysiology

Because of the surrounding rigid pericardium the main pathophysiological feature of constrictive pericarditis is an impaired diastolic filling of the heart. In early diastole there is an abnormally rapid filling which suddenly stops when the fibrous pericardium reaches its maximum distensibility. On pressure tracings this filling pattern is recognised as dip-plateau or square-root sign. The haemodynamics in constrictive pericarditis is characterised by disassociation between intrathoracic and intracardiac pressures and an exaggerated ventricular interdependence. The thickened fibrous pericardium hampers full transmission of the intrathoracic pressure changes that occur with respiration to the cardiac chambers. Inspiratory decrease in intrathoracic pressure and pulmonary venous pressure is not transmited to the left heart and so, with inspiration, there is a decrease in the pressure gradient between pulmonary veins and the left atrium which normally induces left heart filling and in the transmitral flow. The rigid pericardium increases the ventricular interdependence. Therefore, reciprocal respiratory changes occur in the left and right ventricle filling, the decrease in left ventricle filling with inspiration inducing an increased right ventricle filling. Consequently, the ventricular septum shifts to the left, and the tricuspid inflow E velocity and hepatic vein diastolic forward flow velocity increase. With expiration opposite changes occur in diastolic ventricular filling. [1][3][4] Two-dimensional and Doppler echocardiography findings demonstrate these heamodynamic characteristics of constrictive pericarditis.

Figure 1. Transthoracic echocardiography, two-dimensional examination in parasternal long axis view in constrictive pericarditis: increased echogenicity in the region of the pericardium. Note the decreased angle between posterior walls of the left atrium and ventricle (less than 150°) (red arrow).
Figure 2. Transthoracic echocardiography, M-mode in parasternal short axis view at papillary muscles level in constrictive pericarditis: septal bounce with abnormal septum movement in early diastole (arrow).

Two-dimensional and M-mode echocardiographic features of constrictive pericarditis

Diagnosis of constrictive pericarditis is sustained by direct signs such as thickening of the pericardium (normal pericardial thickness = 1-2 mm) or calcifications (increased echogenicity) and by indirect signs of constriction. The two-dimensional an M-mode echocardiographic findings[1][3][5][6] in constrictive pericarditis are:

  • Left and right atrial enlargement due to chronic increased atrial pressure [Video 1]
  • Normal size and systolic function of ventricles [Video 1]
  • Abnormal left atrial-left ventricular junction with an angle between posterior walls of the left atrium and ventricle less than 150° [Figure 1]
  • Multiple parallel echo-densities posterior to left ventricular epicardium on M-mode recordings
  • No increase in left ventricle internal diameter after early rapid filling phase
  • Abnormal interventricular septum motion (septal bounce) which is better seen with M-mode: abrupt posterior septum motion in early diastole, then flat motion in mid-diastole and abrupt anterior motion following atrial contraction. This motion reflects dip-plateau phenomenon and the ventricular interdependence. During early diastole there is rapid blood inflow into the ventricles; because right ventricular filling begins slightly before left ventricular filling, the change in pressure induces the paradoxical leftward motion of the interventricular septum. The septal bounce is accentuated during inspiration when venous return to the right ventricle increases and reverses with expiration [Figure 2, Video 1]
  • Inferior vena cava and hepatic veins dilation with restricted respiratory variation
  • Pericardial thickness of ≥ 3mm on trans-esophageal echocardiography has a high sensitivity and specificity for detecting thickened pericardium.

Doppler echocardiography findings in constrictive pericarditis

Pulse wave Doppler recordings reflect the haemodynamic changes in constrictive pericarditis resulting from the lack of intrathoracic pressure transmission to the cardiac chambers and the exaggerated ventricular interdependence, namely typical pattern of left and right atrial filling, respiratory variations in left and right ventricular filling and in the isovolumic relaxation time (IVRT). Characteristic features of pulse wave Doppler flow pattern at each level of recording are as follows: [1][2][3][5][6]

Figure 3. Transthoracic echocardiography, apical four-chamber view, pulse wave Doppler recording of mitral inflow: inspiratory decrease in E-wave velocity (arrow) in constrictive pericarditis.
Figure 4. Transthoracic echocardiography, apical four-chamber view, pulse wave Doppler recording of tricuspid inflow: inspiratory increase in E-wave velocity by 35% (arrow) in constrictive pericarditis.
Figure 5. Transthoracic echocardiography, subcostal view, pulse wave Doppler recording of hepatic vein inflow: slight increase in S- and D-wave velocities and increased flow reversals (arrows) with inspiration in constrictive pericarditis.>
  • Mitral inflow (left ventricular filling): increased early diastolic filling velocity (high E wave) with an E/A ratio > 2 and short E-wave deceleration time (EDT) <160 ms due to rapid early diastolic ventricular filling which abruptly ceases after the elevation of left ventricular pressure. There is little ventricular filling in late diastole due to the constrictive effect of rigid pericardium, with a small A-wave following atrial contraction. With inspiration, there is an increase in the intrathoracic pressure which is not fully transmitted to the left atrium due to the rigid pericardium. Thus, the pressure gradient between the pulmonary veins and the left atrium is reduced and the E-wave velocity decreases by >25% and IVRT increases by >20% with inspiration; opposite changes are seen with expiration [Figure 3].
  • Tricuspid inflow (right ventricular filling): increased early diastolic filling velocity (E wave) with E >A due to initial high atrial-to-ventricular pressure gradient resulting in a rapid early diastolic filling. Because of ventricular interdependence, the decrease in left ventricular filling with inspiration induces an increased right ventricular filling, thus E-wave velocity increases by >35% with inspiration; opposite changes are seen with expiration [Figure 4].
  • Pulmonary vein flow: both systolic (S wave) and diastolic (D wave) flows are present with S/D ratio =1. With inspiration, there is a decrease in both S and D velocities due to the effect of changes in intrathoracic pressure; opposite changes are seen with expiration.
  • Hepatic vein flow: diastolic forward flow velocity is equal or higher than systolic forward flow velocity in the hepatic vein because in constrictive pericarditis maximum cardiac volume is reached in early diastole and pericardial constriction has its minimum effect in end-systole. With inspiration, there is a slight increase in S and D velocities as decreased filling allows increased right ventricular filling; with expiration, left ventricular filling increases limiting right ventricular filling and hepatic vein diastolic forward flow (D wave) decreases, with pronounced flow reversals [Figure 5].
  • Superior vena cava flow: diastolic dominant pattern, minimal respiratory variation as right atrial pressure is constantly elevated.
  • Aortic and pulmonary flow: aortic flow velocity decreases (-14 ± 5%) and pulmonary flow velocity increases (16 ± 4%) with inspiration, as a consequence of exaggerated ventricular interdependence [Figure 6].


Possible pitfalls in pulse wave Doppler recordings of atrial and ventricular filling:[3][6]

  • Similar respiratory variation in mitral inflow velocity may occur in several clinical settings such as acute dilatation of the heart, pulmonary embolism, right ventricular infarct, conditions in which a dilated right ventricle helps in the differential diagnosis
  • Increased respiratory variation in mitral and tricuspid inflow velocities are seen in chronic obstructive lung disease without pericardial constriction due to respiratory changes in intrathoracic pressure. In this setting, E/A ratio is lower, EDT is more prolonged and there is a more pronounced respiratory variation in superior vena cava flow with increase in forward flow and systolic dominant flow with inspiration
  • Persistence of respiratory variation in mitral and tricuspid inflow velocities after pericardiectomy
  • Absence of respiratory variation in mitral inflow velocity in cases of markedly elevated left atrial pressure
  • Reduced respiratory variation in mitral inflow velocity in atrial fibrillation, with more pronounced respiratory change in D-wave velocity in this setting.


Color M-mode echocardiography in constrictive pericarditis enables measurement of mitral flow propagation velocity (Vp) which is normal or even increased (frequently >100 cm/s)[2] due to a normal myocardial relaxation [Figure 7].


Tissue Doppler imaging may contribute to constrictive pericarditis diagnosis. Mitral annular e’ velocity is normal or increased (≥8 cm/s) in cases without associated myocardial involvement. This is due to the exaggerated longitudinal motion of the heart which compensates for the limited radial motion because of the rigid pericardium. The longitudinal motion increases more as the constriction worsens with higher filling pressures. Thus, in constrictive pericarditis, E/e’ ratio is inversely proportional to the pulmonary capillary wedge pressure, and this phenomenon was termed annulus paradoxus.[3] Also, due to the calcific pericardium mitral annular e’ velocity at septal site is higher than at lateral site (opposite to normal higher lateral e’ velocity), phenomenon termed annulus reversus.[7]

Figure 6. Transthoracic echocardiography, apical five-chamber view, pulse wave Doppler recording of aortic flow: inspiratory decrease in aortic flow velocity (arrow) in constrictive pericarditis.
Figure 7. Transthoracic echocardiography, apical four-chamber view, color M-mode flow propagation velocity: normal value in constrictive pericarditis (82 cm/s).

References

  1. 1.0 1.1 1.2 1.3 Otto C.M. Pericardial Disease. In: Otto CM. Textbook of Clinical Echocardiograhy, 4th edition. Saunders Elsevier 2009:242-258.
  2. 2.0 2.1 2.2 Maisch B, Seferović PM, Ristić AD, et al. Guidelines on the Diagnosis and Management of Pericardial Diseases. Eur Heart J 2004;25:587-610.
  3. 3.0 3.1 3.2 3.3 3.4 Oh JK, Seward JB, Tajik AJ. The Echo Manual, 3rd edition. Lippincott, Williams and Wilkins 2006: 290-310.
  4. Klein AL, Craig RA. Diseases of the pericardium, restrictive cardiomyopathy and diastolic dysfunction. In: Topol EJ. Textbook of Cardiovascular Medicine, 3rd edition. Lippincott, Williams and Wilkins 2007:421-460.
  5. 5.0 5.1 Feigenbaum H, Armstrong WF, Ryan T. Feigenbaum's Echocardiography. 6th edition. Lippincott, Williams and Wilkins;2005:556-583.
  6. 6.0 6.1 6.2 Ginghină C, Beladan CC, Iancu M, et al. Respiratory maneuvers in echocardiography: a review of clinical applications. Cardiovascular Ultrasound 2009;7:42.
  7. Reuss CS, Wilansky SM, Lester SL, et al. Using mitral ‘annulus reversus’ to diagnose constrictive pericarditis. Eur J Echocardiogr 2009;10:372-5.
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