**5. Constrictive pericarditis**

Constrictive pericarditis is a condition that occurs when a thickened or calcified pericardium loses elasticity resulting in the reduction of diastolic filling. It is a syndrome that is the end result of chronic pericarditis and pericardial effusion gradually progressing to fibrosis [2, 15, 29, 60]. Such impairment overtime causes the reduction of pericardial space, which in turn uncouples intrathoracic and intracardiac pressures generating increased interventricular interdependence visible on echocardiogram [2, 35, 61, 62].

#### **5.1 Etiology**

Constrictive pericarditis can occur as a result of inflammation and effusion from any pericardial disease [2, 31, 63]. A combination of studies has found that 42 to 61% of cases were idiopathic or viral, 11 to 37% postcardiac surgery, 2 to 31% postradiation, 3 to 7% due to connective tissue disorders, 3 to 15% bacterial or tuberculous, and 1 to 10% related to malignancy, trauma, drug toxicity, sarcoidosis, or uremic pericarditis [64–69]. Tuberculosis remains a major global cause of constrictive pericarditis especially in endemic nations [2, 70].

#### **5.2 Clinical presentation**

Patients with constrictive pericarditis usually present with symptoms of right heart failure in the absence of ventricular function impairment. Symptoms are consistent with volume overload, such as edema, pleural effusion, dyspnea, ascites,

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*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

of constrictive pericarditis when the SAI is >1.1 [74].

related cardiac pathology.

**6. Cardiac tamponade**

**5.4 Treatment**

pericarditis [65].

**5.3 Diagnostics**

or low output states such as exertional dyspnea and fatigue [2]. As high as 93% of patients present with elevated jugular venous pressure (JVP) [65], while only approximately 20% of patients present with pulsus paradoxus or Kussmaul's sign [64, 65, 71]. A pericardial knock has been noted in 47% of patients with constrictive

Although the diagnosis of constrictive pericarditis can be made by echocardiography [72], an ECG and chest X-ray should also be obtained as part of the initial evaluation. There are no specific ECG changes consistently indicative of constrictive pericarditis; however, an ECG may be helpful in ruling out other cardiac pathology. The chest X-ray may show the evidence of pericardial calcification in which the presence of right heart failure would be strongly suggestive of constrictive pericarditis; however, the absence of such a finding would not rule out the disease [2]. All patients with suspected pericardial disease should be evaluated with echocardiography [2, 73]. Septal bounce and pericardial thickening on M-mode and 2-dimensional echocardiography would be suggestive of a constrictive pattern. On Doppler echocardiography, increased interventricular interdependence is associated with pericardial fibrosis, and the ratio of the right ventricular (RV) area to the left ventricular (LV) area, known as systolic area index (SAI), is virtually diagnostic

CT imaging can show pericardial thickening and calcification but is not necessary to diagnose constrictive pericarditis. However, the identification of important vascular structures on CT can prove useful if planning for pericardiectomy [75]. Positron emission tomography (PET)/CT can also be helpful in predicting response to corticosteroid therapy [76]. CMRI may show characteristic changes of constrictive pericarditis, such as pericardial thickening, dilation of the inferior vena cava, or ventricular interdependence, but is usually necessary unless investigating other

Treatment of constrictive pericarditis is dependent on the course of the disease

Cardiac tamponade is characterized by the accumulation of pericardial fluid causing significant impairment in cardiac function due to the pressure effect of external pericardial content causing compression of all cardiac chambers. Increase in intrapericardial pressure reduces the myocardial transmural pressure with a reduced ventricular wall diastolic compliance and a decrease in cardiac output and blood pressure. In cardiac tamponade, unlike constrictive pericarditis, most of the inspiratory decline in the intrathoracic pressure is transmitted through

at the time of evaluation. For early subacute disease in patients who are hemodynamically stable, medical therapy similar to that used for acute pericarditis is recommended. Patients who present with the evidence of late chronic disease (cachexia, pericardial calcifications, and hepatic dysfunction) or those who have failed conservative management with anti-inflammatory therapy can be treated with pericardiectomy [63]. The majority of patients achieve symptomatic relief with early surgical removal of the inflamed pericardium [69] with one study reporting up to 69% of patients being symptom-free at 4 year follow-up [65].

or low output states such as exertional dyspnea and fatigue [2]. As high as 93% of patients present with elevated jugular venous pressure (JVP) [65], while only approximately 20% of patients present with pulsus paradoxus or Kussmaul's sign [64, 65, 71]. A pericardial knock has been noted in 47% of patients with constrictive pericarditis [65].
