Pericarditis

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.

Nonischemic chest pain that is typically sharp, pleuritic and worse, when supine (90%).

EKG changes characterized by new widespread ST segment elevations and PR segment depressions, a new or worsening pericardial effusion, or  pericardial friction rub are additional diagnostic findings.

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.

A pericardial friction rub is high-pitched, maybe transient, and is typically triphasic.

The pericardial friction rub is best heard with the patient leaning forward.

Pericardial friction rub has poor sensitivity for diagnosis of pericarditis.

Chest pain is usually sharp, pleuritic and changes with position.

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.

Approximately 4% of patients with acute pericarditis present with atrial fibrillation/flutter.

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.

In patients with acute pericarditis, the patients should be assessed for the presence of tuberculosis, associated malignancies, a systemic, and autoimmune disease.

Laboratory evaluation, in patients with acute or viral pericarditis reveals a high percentage of patients (78%) have an elevated CRP.

Patients should have measurement of cardiac troponins, which can give some indication of prognosis.

Patient should be evaluated for their risk of tuberculosis, antinuclear antibody test should be evaluated when there is a suggestion of a systemic autoimmune disease.

Pericardiocentesis may be performed with acute pericarditis to evaluate for bacterial, tuberculous, or malignant causes of pericardial effusion.

Pericardial fluid can be assessed with a cell count, Gram stain and cultures and cytology.

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, chronic kidney failure, non-tuberculosis bacterial infection, such as Staph or Streptococcus, or underlying systemic autoimmune disease. but the majority of cases are idiopathic.

The most common causes of pericarditis are idiopathic or viral, followed by pericarditis after cardiac procedures or operations.

Acute pericarditis is most often idiopathic or presumed to be a viral infection and recurrs  in 15 to 30% of cases.

Postcardiac injury syndrome follows myocardial infection is 45% cases, cardiac procedures in about 10%,  after ablation for atrial fibrillation, or cardiac procedures or operations, 20 to 30%, and is characterized by pericarditis or pleuritic, chest pain, fever, pericardial, or plural rubs, pericardial effusion or pleural effusion with elevated C reactive protein level.

In areas with TB it is endemic,  TB is the most common cause of pericarditis.

Among patients with a malignant pericardial effusion the most common causes are lung, breast, and hematologic malignancies.

Peritonitis may occur up to 20% of patients with systemic lupus.

Up to 30 to 50% of patients with rheumatoid arthritis may have an asymptomatic pericardial effusion.

Patients with the acute idiopathic pericarditis rarely develop constrictive pericarditis at less than .5% or pericardial tamponade at less than 3%.

Life-threatening complications of pericarditis, such as constrictive pericarditis or pericardial tamponade are more associated with bacterial, or tuberculosis infections.

Pericardial tamponade is characterized by a precipitous increase in pericardial pressure with diastolic chamber collapse, severe impairment in diastolic filling and reduction in stroke volume.

Signs of tamponade include compensatory, tachycardia, elevated, jugular venous pressure, hypertension, and pulsus paradoxus.

About 20% of patients with incessant pericarditis develop constrictive pericarditis.

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).

All patients with acute pericarditis should have echocardiography to assess for a thickened and hyperechoic pericardium, evaluation for a pericardial effusion, and to define the hemodynamic consequences of pericardial abnormality.

A chest x-ray is routinely evaluated for underlying causes of acute pericarditis such as TB or malignancy.

An increased cardiac cardiothoracic ratio occurs only with pericardial effusion succeeding 300 mL.

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.

Approximately 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  acute recurrent pericarditis (Imazio M et al).

Recurrent pericarditis is defined as by return of pericarditis symptoms after clinical remission of at least 4-6 weeks.

Recurrent pericarditis with an inflammatory phenotype usually is related to an abnormal imimmune response, with inappropriate activation of the NLRP3 inflammation.

The NLRP3 inflammation is multiprotein complex that forms in response to infectious pathogens or tissue damage.

The NLRP3 inflammation complex activates caspase-1 dependent release of pro-inflammatory cytokines that can cause an autoinflammatory cycle leading to recurrent pericarditis, whereas inhibiting the NLRP3 inflammation or downstream attenuates this response.

After a first recurrence of pericarditis, subsequent episodes may occur up to 50% of patients and is associated with impairment of quality of life, related to pain, impaired physical and mental health, sleep disturbance and decreased work.

Patients with autoimmune associated pericarditis have significantly higher risk of recurrent episodes of pericarditis than those with idiopathic pericarditis: approximately 50% increase risk of recurrent pericarditis.

Patients with elevated inflammatory markers have a higher risk of recurrence.

After a first episode of idiopathic or viral pericarditis recurrence may occur 15 to 30% of patients.

The majority of recurrences occur within 3 to 6 months and recurrence beyond 12 months is unusual.

 TREATMENT:

Firstly, avoidance of vigorous exercise for up to three months is of recommended for acute period -itis because recurrences may be related to exercise.

NSAIDs are typically used to provide pain relief using high doses and tapering once chest pain has resolved and levels and inflammatory markers have normalized.

Gastrointestinal protection with an  PPI is recommended for patients, taking high dose and sides.

Studies of found the colchicine added to standard NSAIDs is efficacious.

A three month course of colchicine  is recommended for acute idiopathic pericarditis to prevent recurrence.

Colchicine following cardiac surgery reduces the development of pericarditis significantly.

The use of colchicine with acute or recurrent pericarditis is recommended.

Corticosteroids are frequently used to treat acute/recurrent pericarditis without clinical trial evidence.

Steroids, especially at high doses is associated with an increased risk of recurrent pericarditis.

Corticosteroids should only be prescribed at low to moderate doses in patients who do not improve with NASAIDs/colchicine or have adverse outcomes from these drugs.

Additional indications for cortico steroids include systemic autoimmune disease, or post cardiac surgery for symptoms not responsive to colchicine and for patients contraindicated to high dose NSAIDS.

Interleukin 1 blockers are approved for treatment and prevention of recurrent pericarditis.

These agent have efficacy in

patients who have an auto inflammatory phenotype, characterized by elevated CRP.

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.