Acute pericarditis is usually brief and benign in course in most instances with symptom resolution within 1-2 weeks after nonsteroidal anti-inflammatory treatment.

Viral infection is the most common cause with other etiologies,  including bacterial or other infections, autoimmune disease, renal failure, iatrogenic or post traumatic causes, and various drugs.

Classically associated with sharp pleurisy chest pain that changes with position and varies with respiration, but may manifest as dull chest discomfort and may mimic myocardial ischemia.

Diagnostic criteria include two of the following: pericardial chest pain, pericardial rub, new widespread EKG changes, and pericardial effusion.

Hospitalization usually not necessary unless associated with poor prognostic factors including associated myocarditis, malignancy, pericardial effusion in excess of 2 cm, trauma, with anticoagulation and with purulent pericarditis.

Associated with pleuritic chest pain that worsens in the supine position.

Deep inspiration can exacerbate pleuritis, whereas leaning forward reduces stress on the pericardium.

Triphasic pericardial friction rub results from the inflamed layers of the pericardium and is highly specific for pericarditis.

Fibrinous pericarditis may be associated with a pericardial friction rub which waxes and wanes and sounds like scraping or grating.

Presence of a an audible pericardial friction rub found in a minority of patients at presentation.

Pericardial friction rub, if heard, tends to be variable and transient.

Pericardial friction rub has poor sensitivity for diagnosis of pericarditis.

Widespread ST elevation across the precordial leads and limb leads with upward concave ST segments and PR segment depression is characteristic of pericarditis.

The ratio of ST segment elevation in millimeters to T-wave amplitude in millimeters in excess of 0.24 in lead V6 supports diagnosis of pericarditis, and helps distinguish pericarditis from other repolarization abnormalities.

Serial electrocardiographic changes begin with PR depression, PR elevation in lead aVR, followed by diffuse ST-segment elevation.

Classical electrocardiographic changes early in the course of acute pericarditis are ST segment elevation in all leads except aVR, and V1, in which there is reciprocal ST segment depression.

PR-segment depression typically accompanies ST-segment elevation in the early stage of disease, and as the disease progresses, the ST and PR segments normalize and are followed by T-wave inversion and then normalization of the T waves.

ST-segment elevation seen in 65-70% of cases.

ST-segment elevations difficult to distinguish from ST-segment elevation myocardial infarction (STEMI).

ST elevation in acute pericarditis is diffuse and nonfocal as seen with myocardial infarction.

Cardiac biomarkers are sometimes elevated secondary to the inflammatory process that involves the epicardium and subsequent myocardial necrosis.

Incidence of elevated cardiac troponin I in viral or idiopathic acute disease reported to be present in 32.2% of cases, and 23% of patients have elevated troponin levels above the myocardial threshold range upon presentation (Imazio).

Troponin elevation with acute pericarditis suggest myocardial involvement and possibly myopericarditis.

Temporal relationship f troponin elevation mirrors that of acute myocardial infarction.

Elevated levels of cardiac biomarkers not of prognostic significance but does complicate diagnosis.

Hospitalization required for most patients with initial presentation to determine etiology and to observe for the development of cardiac tamponade of the pericardium.

Constrictive pericarditis is a result of inflammation, scarring, and fibrosis of the pericardium.

Constrictive pericarditis results in an inelastic pericardial sac that impairs the diastolic filling of the heart.

Constrictive pericarditis is a rare late complication of cardiac surgery and can manifest as congestive heart failure.

Causes of constrictive pericarditis include prior surgery, radiation treatment, tuberculosis, malignancies, trauma, and inflammatory diseases such as lupus or sarcoidosis, but the majority of cases are idiopathic.

Symptoms of constritive pericarditis or primarily related to systemic venous congestion and low cardiac output.

Elevated jugular venous pressure is seen in all patients with constrictive pericarditis, but only 25% of patients have peripheral edema, especially early in the disease, and less thanHe is 6% present with abdominal symptoms (Ling LH et al).

Pericardial thickening can noted on CT or MRI of the chest in up to 28% of patients with proven constrictive pericarditis (Talreja DR et l).

Typically in constrictive pericarditis echocardiograms indicate normal systolic function, a full inferior vena cava, restrictive mitral inflow with respiratory variation, reversal of inexpiratory hepatic-vein flow, septal motion suggesting enhanced ventricular interaction, and elevated early diastolic mitral annular velocity (Oh JK et al, Troughton RW et al).

With constrictive pericarditis the myocardium being encased in a constrictive pericardial sac prevents lack of cardiac stretch and therefore BNP levels are normal or only slightly elevated.

With constrictive pericarditis cardiac catheterization indicates elevated and equalized diastolic pressures with rapid ventricular filling early and blunted by stiffened pericardial sac late, with a characteristic steep y descent of right atrial pressures and the dip and plateau of ventricular pressure (Hansen AT et al, Meaney E et al).

Constrictive pericarditis is generally treated with a surgical peri-cardiectomy with removal of adherent pericardium.

In areas of the world where there is a high burden of HIV infection, tuberculosis pericarditis accounts for 50% and greater than 90%, respectively, of large pericardial infusions in HIV-negative and HIV-positive patients (Mayosi BM).

Recurrent pericarditis is characterized by chronic and debilitating pericardial inflammation, with effects on physical function, well-being, and productivity.
Proximately 15-30% of patients with pericarditis will have a recurrence despite treatment with colchicine.
Interleukin-1 has been implicated in recurrent pericarditis
Recombinant Interleukin-1-receptor antagonist anakinra with colchicine resistant idiopathic recurrent pericarditis has demonstrated some advocacy.
Low-dose colchicine is a first-line treatment for either acute recurrent pericarditis (Imazio M et al).
Rilonacept an interleukin-1 Alpha and interleukin-1 beta cytokine trap  in patients  with recurrent pericarditis lead to rapid resolution of episodes and a significant lower risk of recurrence and than placebo.

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