Acute Pericarditis Emory Family Medicine Susan Schayes M.D. Assistant Professor-CT Family Medicine, Emory University School of Medicine IAFP 2002

The Pericardium A fibroelastic sac composed of visceral and parietal layers Both these layers are separated by a pericardial cavity. The cavity normally contains 15 to 50 ml of straw-colored fluid. Visceral layer is in contact with the epicardium (ST elevation)

The Clinical problem Can be an isolated entity or part of a systemic disease 0.1% of all hospitalized patients 5% of ER visits for chest pain without an MI

Etiology-Acute Pericarditis Infectious Viral : Coxsackie, Echo, EBV, Influenza, HIV Bacterial: TB, staph, hemophilus, pneumococcal, salmonella Fungal/other: histo/blasto/coccidio, rickettsial Rheumatologic SLE, Sarcoid, RA, Dermatomyositis, Ankylosing Spondylitis, Scleroderma, PAN Neoplastic Primary: angiosarcoma, mesothelioma Metastatic: breast, lung, lymphoma, melanoma, leukemia Immunologic Celiac sprue, Inflammatory Bowel Disease Drug Hydralazine, Procainamide Other MI, Dressler’s, Post Pericardiotomy, Chest Trauma, Aortic dissection Uremic, Post Radiation IDIOPATHIC

Other Pearls Viral and Autoimmune causes constitute > 50% of cases of acute pericarditis Pericardial disease is the most frequent cardiovascular manifestation of AIDS The typical diffuse ST elevation is not seen in uremic pericarditis,in which there is fibrin deposition in the parietal layer but no epicardial inflammation.

Clinical Presentation Chest pain Pericardial friction rub Diffuse ST segment elevation on EKG Pericardial effusion Presence of at least two of the above features is necessary to make the diagnosis

Chest Pain Retrosternal in location Sudden in onset Pleuritic and sharp in nature Exacerbated by inspiration Worsens when supine and improves upon sitting upright or leaning forward. Can often radiate to the neck, arms, or left shoulder. Radiation to one or both trapezius muscle ridges, suggests a probable pericarditis (phrenic nerve traverses the pericardium)

Pericardial Friction Rub Present in 85% of cases of pericarditis Highly specific with a variable sensitivity A high-pitched scratchy or squeaky sound best heard with the diaphragm at the LSB with the patient leaning forward. Corresponds temporally to the movement of heart within the pericardial sac. Has 3 components, which correspond to atrial systole, ventricular systole, and early diastole. Pericardial friction rub is audible throughout the respiratory cycle, whereas the pleural rub disappears when respirations are on hold.

EKG in Pericarditis Widespread upward concave ST-segment elevation and PR-segment depression If the ratio of ST-segment elevation to T-wave amplitude in V6 > 0.24, acute pericarditis is almost always present. The EKG changes have 4 phases during the course of illness

EKG Stages Stage I Stage II Stage III Stage IV first few days  2 weeks ST elevation, PR depression up to 50% of pt with symptoms / rub do NOT have or evolve into stage I Stage II last days  weeks Normalization of ST and PR segments ST returns to baseline, flat T waves Stage III after 2-3 weeks, lasts several weeks Widespread T wave inversion Stage IV lasts up to several months gradual resolution of T wave changes

Acute pericarditis – Stage I

Pericarditis-Stage II 60 y/o man with acute pericarditis on presentation and after 1 month of resolution of symptoms

Pericarditis-Stage III T wave inversions

Differential Diagnoses Clinical Myocardial Infarction Myocarditis Pulmonary embolism Pneumothorax Pneumopericardium Musculoskeletal EKG (ST elev) AMI Early Repolarization Myocarditis Hyperkalemia Ventricular Aneurysm Normal Variant

Pericarditis vs Early Repolarization Acute Pericarditis Early Repolarization Sex Either Usually Male Age Any Usually < 40 PR segment dev Common Uncommon T waves nl, blunt tall, peaked J-ST / T ampl > 25% <25% Tallest precordial R Usually V5 Usually V4

Early Repolarization J point and ST segment elevation is most prominent in V4 to V6. The ST segment maintains its normal configuration and is slightly concave

Pericarditis vs AMI Pericarditis MI ST segment Diffuse,concave elevation in all leads except aVR+ V6 w/o reciprocal changes Height Not > 5mm Localized, convex, with reciprocal changes in infarct Height may be > 5 mm PR depression Frequent Almost never Q waves Not usual, unless with infarct Common with q wave infarct T waves Inverted after J returns to baseline T inversions and ST ↑ are not seen simultaneously on the same EKG Inverted while ST still elevated T inversions and ST ↑ can be seen simultaneously on the same EKG Arrhythmias Rare Conduction disturbances frequent

Acute Anterior MI

Laboratory testing Laboratory abnormalities CBC – very high WBC (purulent pericarditis) ↑ESR Chem-7 (uremic etiology) ↑CRP HIV in selected cases ANA Rheumatoid factor Blood cultures if febrile Viral cultures and antibody testing not indicated

Cardiac Isoenzymes - ? helpful MB fraction of CK and Troponin I are modestly elevated The rise in TnI is related to the extent of myocardial inflammation. Features associated with a rise in Tn I are younger age,male gender,presence of effusion and a recent infection Enzyme rise is transient,resolving within the first week, persistent ↑ suggest myopericarditis Not reliable to differentiate MI vs pericarditis Two studies that included 187 patients with idiopathic pericarditis ,TnI was detectable in 32-49% and in 8-22% it was >1.5 mcg/ml Another 2 year ER based study- Out of 14 pts with 2/3 findings (typical CP, rub, and ECG changes) 71% had elevated Tn I with negative CAD workup

Other Studies Tuberculin skin testing Echocardiogram Chest X-ray Normal unless there is an effusion Presence of effusion supports the diagnosis, but absence does not exclude it. The ACC/AHA/ASE all recommend to obtain an echo in any suspected pericardial disease Chest X-ray Recommended in all cases Typically normal Enlarged cardiac silhouette in effusion (with clear lung fields)

Need for hospitalization Many physicians tend to admit them, but this may not be necessary. Uncomplicated acute pericarditis can undergo initial evaluation in a same day hospital facility or clinic, with an outpatient follow-up Features of high risk include: Subacute symptoms (eg, developing over several days or weeks) High fever (>38ºC [100.4ºF]) and leukocytosis Evidence suggesting cardiac tamponade A large pericardial effusion Immunosuppressed state A history of oral anticoagulant therapy Acute trauma Failure to respond within seven days to NSAID therapy, a generous allocation of time Elevated cardiac troponin, suggestive of myopericarditis

Complications Pericardial Effusion/ Tamponade Constrictive Pericarditis can be “transient” – 10% may have transient within 1st month, resolves by 3 months Recurrent Pericarditis (15-32%) Recurrent sx after the initiating event is no longer active Most likely an autoimmune etiology Rx : NSAIDS/ Colchicine +/- steroids

Treatment Goals of acute therapy: Relieve Pain Treat the inflammation Prevent Cardiac tamponade Most viral infections are self-limited Treat the underlying disease process Drain purulent effusions Symptomatic therapy None of the treatments unfortunately, have not been proven to prevent the complications.

NSAIDs May require weeks to months of treatment with high doses of NSAIDs The choice is usually empiric, based on the physician’s familiarity with the agent and/or its availability. Rapidly titrate the dose within 1–2 days to achieve maximum symptomatic relief Evaluate for a response within 1–2 wks,Sx usually subside in a week. If adequate clinical response,continue NSAIDs for 1 wk after complete resolution of Sx and then taper in 2–3 days.

Preferred in patients with CAD Ibuprofen NSAIDs Aspirin 2-6 gm daily650mg Q3-4 hrs Preferred in patients with CAD Ibuprofen 1600-3200 mg daily400-800 mg q 6-8 hrs above average response rate and has a very good side effect profile Indomethacin 75-225 mg daily Try to avoid, unless absolutely needed as it can ↓ coronary blood flow. Nonsteroidal Anti-inflammatory Drugs in the Treatment of Pericarditis: Clinical Review SCHIFFERDECKER, BRANISLAV MD; SPODICK, DAVID H. MD, DSc Cardiology Review ; Volume 11(4), July/August 2003, pp 211-217

Colchicine A prospective, randomized, open-label design was used. 120 patients with a first episode of acute pericarditis were randomly assigned to conventional treatment with aspirin (group I) or conventional treatment plus colchicine 1.0 to 2.0 mg for the first day and then 0.5 to 1.0 mg/d for 3 months (group II). Colchicine significantly reduced the recurrence rate (10.7% vs 32.3%; P=0.004;) and presence of symptoms at 72 hours (11.7% vs 36.7%; P=0.003). Based upon this, addition of it to the Rx regimen for an initial episode of acute pericarditis is an option for physicians. Colchicine in Addition to Conventional Therapy for Acute Pericarditis Results of the COlchicine for acute PEricarditis (COPE) Trial Circulation. 2005;112:2012-2016 10.1161/CIRCULATIONAHA.105.542738eeeeew

Steroids In patients refractory to NSAIDs and colchicine Steroid therapy with initial episode is more likely associated with recurrent episodes. Evidence available argues against the routine administration of corticosteroids during a first episode of acute pericarditis Specific conditions that will benefit: Acute pericarditis due to connective tissue diseases Auto-immune pericarditis Uremic pericarditis

Myocardial Infarction-Associated Pericarditis Early post MI pericarditis is a consequence of transmural infarction. Aspirin is the drug of choice in this setting. (650 mg Q4h) Late MI associated pericarditis (Dressler syndrome), occurs days to months after infarction, Autoimmune in etiology. NSAIDs are the treatment of choice. Colchicine seems to be the most effective if NSAIDs fail Corticosteroids seem to provide symptomatic benefit but do not prevent recurrence. Pericardiectomy is only rarely curative

Summary Etiology of Acute Pericarditis Clinical Presentation and EKG findings Differential Diagnosis Evaluation Treatment