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Pericardial Constriction

“Constrictive pericarditis is a rare but severely disabling consequence of the chronic inflammation of the pericardium, leading to an impaired filling of the ventricles with reduced function.”
Pericardial Diseases Guidelines, Eur Heart J 2004;25:587.

Clinical picture
– Asthenia and shortness of breath
– Signs of venous congestion (giugular distension, peripheral edema, ascites)
– Reduction of cardiac output

The pericardial thickening / adhesions can be:
– Diffuse (global)
– At the atrio-ventricular junction (symmetrical or prevalently right / left)
– Along the left or right ventricular free wall
– With or without associated atrophy of the underlying myocardium (to a varying extent).

Figure 78. Hemodynamics of pericardial constriction
Figure 78.

– Increased right and left ventricular diastolic pressures with equalization (within 5 mmHg) (Fig. 79)
– “Dip and plateau” pattern of right and left diastolic pressures (Fig. 78 and 79, red arrow= “dip”, black arrow= “plateau” ).
– “W“ pattern of the right atrial pressure curve with prevalent “y” nadir (Fig. 78 and 79, red arrow= “y” nadir)
– Inspiratory increase in right atrial pressure (Kussmaul sign)
– Reduction of cardiac output, which may be preserved by tachycardia

Figure 79. Left ventricular and right ventricular pressure tracings, constrictive pericarditis
Figure 79. LV and RV pressure tracings, constrictive pericarditis
Figure 80. Right atrial pressure tracing, constrictive pericarditis
Figure 80. RA pressure tracing, constrictive pericarditis

Seminal paper by prof. L. Hatle: Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357.

Figure 81. Left and right heart hemodynamics in pericardial constriction
Figure 81.

Figure 81. The right ventricular pressure increases during inspiration while systolic and diastolic LV pressures are decreasing (Fig. 81, left panel). The respiratory variations of the pulmonary wedge pressure (PCW) are greater than those of LV diastolic pressure (Fig. 81, right panel), leading to a reduction in the difference between wedge pressure and LV pressure during inspiration – which decreases the mitral peak E wave – and an increase of the pressure difference during expiration which causes an increase in the mitral peak E wave. Maximum peak E wave velocity is regularly observed at the first expiratory beat.

Figures 81-82. A case of outcomes of partial pericardiectomy with pericardial thickening and adhesions of the LV postero-lateral wall. There are no signs of pericardial constriction.

Figure 81.2D parasternal long axis, left ventricle
Figure 82. 2D paratsernal short axis, left ventricle

Figure 83-85. Pericardial constrictive syndrome after aortic valve replacement (Carpentier bioprosthesis) and CABG.
Note abnormal septal motion with abrupt leftwards shift during inspiration (Fig. 83) and pericardial adhesions of the LV lateral wall (Figs. 84 and 85).

Figure 83. 2D apical 4-chamber
Figure 84.2D apical 4-chamber
Figure 85. 2D subcostal 4-chamber