Constrictive pericarditis: definition, causes, diagnosis & echocardiography
Constrictive pericarditis: the end stage of pericardial inflammation Constrictive pericarditis is the result of chronic inflammation of the pericardium. In principle, all causes…
Constrictive pericarditis: the end stage of pericardial inflammation
Constrictive pericarditis is the result of chronic inflammation of the pericardium. In principle, all causes of pericarditis can result in constrictive pericarditis. In high-income countries, idiopathic pericarditis, radiation to the pericardium and surgical interventions are the most common causes of constrictive pericarditis. Of these three, idiopathic pericarditis is the most common cause of constrictive pericarditis. It usually takes several years to develop the constriction, but in some cases, it may appear a few months after the inflammation has occurred.
In constrictive pericarditis, the pericardium becomes fibrotic (rigid) and thickened (about 80% have thickening). The parietal and visceral leaves of the pericardium are most often fused. The process most often affects the entire pericardium. Constrictive pericarditis is most often chronic, but in some cases, the condition may be transient. Pericardiotomy can be curative, which is why it is important to detect the disease early in the course.
Hemodynamic effects of constrictive pericarditis
Diastolic heart failure and right heart failure
The rigid pericardium prevents all four heart chambers from dilating adequately during diastole. This leads to increased and equivalent diastolic pressure in all rooms. Because pressure is high in the atria, filling of the ventricles occurs fast at the beginning of diastole, but it becomes incomplete because the ventricles cannot expand normally. This leads to diastolic heart failure. The systolic function is usually unaffected, but the shock volume and ejection fraction (EF) may be reduced because the end-diastolic volume of the ventricle (EDV) is reduced. Constrictive pericarditis also leads to right-sided heart failure, which is explained by the fact that high pressure in the right atrium leads to a decrease in atrial filling.
Respiratory variations in E-wave velocity
Under normal circumstances, intrathoracic pressure decreases during inhalation, which lowers pressure in the pulmonary veins and left atrium; this facilitates blood flow from the pulmonary veins to the left atrium. In constrictive pericarditis, the pericardium is so rigid that it is not affected by pressure changes in the thorax. This leads to the fact that the pressure in the left atrium does not decrease when inhaled and, as a result, the blood flow from the pulmonary vein to the left atrium is hampered. This reduces the filling of the left atrium and, accordingly, the left ventricle. The reduced flow over the mitral valve results in reduced E-wave velocity during inhalation. Since the left ventricle is not filled normally, there is more room for the right ventricle, the filling of which increases and the septum bulges into the left ventricle. During exhalation, the conditions are the reverse; the flow increases above the mitral valve and instead decreases the pressure difference between the right atrium and the inferior vena cava, which causes the blood to flow in the retrograde direction (from the atrium to the inferior vena cava).
In constrictive pericarditis, the E wave velocity varies during inspiration and expiration. The E wave velocity is lower during inspiration.
Differential diagnosis: restrictive cardiomyopathy
It is important to be able to differentiate constrictive pericarditis from restrictive cardiomyopathy, as a result of which the myocardium is rigid and imperative, which also leads to an increase in diastolic pressure in the ventricles and atria. At present, echocardiography is the first choice in investigating suspected constrictive pericarditis. The ECG can show low voltage and nonspecific ST-T changes. Conventional thoracic X-ray sometimes reveals calcification of the pericardium. With MRI or CT, the thickness of the pericardium can be measured and in most cases, a thickening is noted. Table 1 presents the similarities and differences between restrictive cardiomyopathy and constrictive pericarditis.
Table 1. Differentiation between constrictive pericarditis and restrictive cardiomyopathy.
| Parameter | Constrictive pericarditis | Restrictive cardiomyopathy |
| Thickened pericardium and moderate pericardial effusion | Occurs | Rarely |
| Dilated vena cava inferior | Yes, with respiratory variation | Yes |
| Premature opening of pulmonary valve | Yes, due to increased right ventricular pressure | No |
| Septal bounce | Yes. Septum moves into the left ventricle during inspiration | No |
| E-wave velocity | Increased | Increased |
| Respiratory variation in E wave velocity | >25% | None |
| E/A ratio | Increased | Increased |
| Deceleration time | <160 msec | <160 msec |
| Retrograde flow in vena cava inferior during expiration | Yes | No |
| Increased pulmonary vein flow during expiration | Yes | No |
| é velocity | Normal or increased | Decreased |
| E/é ratio | Normal or decreased (max 8). High filling pressure with normal E/é ratio is patognomonous for constrictive pericarditis. | Increased (usually 15 or more) |
| Lateral é < medial é | Yes. The lateral part of the mitral annulus is attached to the pericardium, giving it slower speed in constrictive pericarditis. | No |
| Longitudinal strain (é mitral annulus). | Normal or increased | Reduced |
Symptoms of constrictive pericarditis
Symptoms of constrictive pericarditis are related to diastolic heart failure, low cardiac output, high atrial pressure, and right ventricular heart failure. This means that the patient suffers fatigue, dyspnoea, leg edema, hepatic edema, ascites, cervical vein stasis, etc.