Pericarditis is an inflammation of the pericardium (heart sac) usually caused by a virus infection. The echocardiogram may show pericardial effusion of any size, pericardial thickening or a normal pericardium. A cardiac tamponade is a feared complication of pericarditis. This occurs when the pressure in the pericardium exceeds the pressure in the cardiac chambers, resulting in impaired cardiac filling and depends on the volume and rate of fluid accumulation.
Echocardiographic findings of pericarditis
|M-mode||Rapid early diastolic and flat mid-diastolic movement of LV and aortic root.|
|Early diastolic notch in movement pattern of interventricular septum.|
|End-diastolic notch, followed by forward movement of septum.|
|2D images||Thickened Pericardium (often difficult to detect, much more reliable MRI).|
|Septal motion to LV at inspiration (AP4CH).|
|Septal motion to RV at expiration (AP4CH).|
|Early opening of pulmonary valve.|
|Gedilateerde vena cava inferior met nauwelijks respiratoire variatie.|
With inspiration an increase of RV volume (shift in septal motion towards the LV in diastole and towards the RV in systole) and a decrease during expiration is seen. This is called interdependence. Due to inspiration the intrathoracic pressure becomes more negative and enhanced RV filling limits the LV diastolic filling. This corresponds with the physical finding of pulsus paradoxus.
Echocardiographic findings in inflow obstruction
|Doppler||Increased respiratory variation in peak velocity of mitral valve (> 25%) and tricuspid valve (> 40%)|
|2-D images||Dilated inferior vena cava without respiratory variation in diameter|
|Late diastolic to early systolic collapse of right and left atrium|
|Early diastolic collaps of right ventricle|
The RV early diastolic filling velocity is augmented with inspiration, while the LV diastolic filling velocity is diminished. The E/A ratio of the mitral and tricuspid-inflow pattern will be >1. The deceleration time of the mitral E-wave will also be shortened (>180 msec.) In the pulmonary vein flow, the S-wave will be smaller than the D-wave.?This is different in a constrictive pericarditis. A respiratory variation in MV inflow (at at the beginning of inspiration increase of the E-wave >25%) and TV inflow (at the beginning of inspiration increase of the E-wave >40%) is seen. Also a respiratory variation in the pulmonary vein is seen, in which the flow at the beginning of expiration, the diastolic forward flow increases >10%. This respiratory variation can also be observed at atrial fibrillation and in patients with severe obstructive lung disease. In these cases the flow from the vena cava towards the RV will increase However in a constrictive pericarditis, the flow will not increase. After a pericardectomy an abnormal filling pattern is often observed. It is believed that this is due to incomplete pericardectomy. On the other hand the myocardium sometimes is involved in the disease process. The early diastolic velocity of the septal mitral valve annulus (é) is often reduced postoperatively, which indicates a relaxation disorder of the myocardium. This could be explained by increased myocardial fibrosis found at autopsies. Development of constrictive pericarditis after pericardectomy is associated with a worse prognosis.
In constrictive pericarditis the pericardium is thickened, and fibrotic. This limits the heart to function normally. It is characterized by impaired diastolic cardiac filling due to the abnormal pericardium, which acts as a rigid box. There is a rapid early diastolic filling with a abrupt cessation of ventricular filling and increase of diastolic pressure. It is important to realize that the abnormalities seen in a constrictive pericarditis are not specific for this syndrome. They can also be found in other diseases and it’s the combination of abnormalities that could give a strong indication of a constrictive pericarditis.
Test Performance Characteristics for the Diagnosis of Surgically Confirmed Constrictive Pericarditis
|Variable||Sensitivity, %||Specificity, %||Positive Predictive Value, %||Negative Predictive Value, %|
|No. 1 ventricular septal shift||93||69||92||74|
|No. 2 change in mitral E velocity||84||73||92||55|
|No. 3 medial e' velocity 0 .9 cm/s||83||81||94||57|
|No. 4 medial e'/lateral e'||75||85||95||50|
|No. 5 HV ratio in expiration||76||88||96||49|
|Combinations among Nos. 1, 3, and 5*|
|No. 1 (with or without Nos. 3 and 5)||93||69||92||74|
|Nos. 1 and 3 (with or without No. 5)||80||92||97||56|
|No. 1 with No. 3 or 5||87||91||97||65|
|No. 1 with both Nos. 3 and 5||64||97||99||42|
|HV indicates hepatic vein; and ROC, receiver operating characteristic.
*Combinations limited to factors significant from final selected multivariable model. Cut points for continuous variables were selected from ROC
Constrictive pericarditis vs. Restrictive cardiomyopathy
Both are characterized with a good systolic LV function with diastolic dysfunction. But there are differences that can be distinguished by echocardiography. In a restrictive cardiomyopathy there is a primary dysfunction of the myocardium. In amyloidosis a mottled aspect of the myocardium, thickened valves, thickened atrial septal and a reduced systolic function can often be observed. Valve abnormalities and dilated atria are often seen in In a restrictive cardiomyopathy in contrast to constrictive pericarditis. The mitral inflow patterns in a restrictive cardiomyopathy show a more pronounced restrictive filling pattern, a E/A ratio >2 with deceleration time < 140msec. A significant pulmonary hypertension (>50mmHg) sometimes occur in a a restrictive cardiomyopathy. In a constriction there is rarely found a pulmonary pressure above 50mmHg.
Pericarditis constriction vs restriction
|Septal motion||Respiratory shift||Normal|
|Mitral E/A ratio||>1.5||>1.5|
|Mitral DecT (ms)||<160||<160|
|Mitral inflow respiratory variation||Usually present||Absent|
|Hepatic vein doppler||Expiratory diastolic flow reversal||Inspiratory diastolic flow reversal|
|Mitral septal É (cm/s)||>7||<7|
|Mitral lateral É||< septal É||> septal É|
|Ventricular septal strain||Normal||Reduced|
Am J Cardiol. 2001 Jan 1;87(1):86-94. Circ Cardiovasc Imaging. 2014;7:526-534 J Am Coll Cardiol. 2016 May 3;67(17):2061-76