Cardiology & Internal Medicine & Family Medicine
Péricardite | Clinique Omicron Québec
Pericarditis is an inflammation of the pericardium - the double-layered fibro-serous sac that surrounds the heart and the origins of the great vessels - the acute form of which typically manifests as acute pleuritic chest pain, pericardial rub on auscultation and characteristic electrocardiographic changes. It accounts for around 5 % of non-ischemic chest pain assessed in emergency departments, and preferentially affects young men aged between 20 and 50, with a male predominance of 5:1. The etiology is viral (or presumed viral) in 70 to 90 % of cases in developed countries - an upper respiratory or gastrointestinal infection preceding the episode of pericarditis by 1 to 3 weeks in 50 to 80 % of cases - which has led to the majority of acute pericarditis being classified as idiopathic or viral-idiopathic in origin, with a generally excellent prognosis when the disease remains uncomplicated. Other etiologies include bacterial (tuberculosis in endemic countries, staphylococci), autoimmune (systemic lupus erythematosus, rheumatoid arthritis, scleroderma), neoplastic (pericardial carcinosis), iatrogenic (thoracic radiotherapy, drugs), metabolic (uremia in end-stage chronic renal failure) and post-infarction (Dressler syndrome). The most dreaded complication is cardiac tamponade - accumulation of pericardial effusion sufficiently rapid and abundant to compress the heart chambers, reduce diastolic filling and cause obstructive shock - a hemodynamic emergency requiring emergency pericardiocentesis (pericardial evacuation puncture). Progression to chronic constrictive pericarditis - fibrosis and calcification of the pericardium limiting cardiac filling - is a rare (less than 1 % of viral pericarditis) but potentially serious complication requiring surgical pericardectomy.
Etiologies
| Etiology | Causal agents and frequency | Distinctive features |
|---|---|---|
| Viral or idiopathic - most frequent (70-90 %) | Enterovirus (Coxsackievirus B1-B5 ++) + Echovirus + adenovirus + influenza + parvovirus B19 + EBV + CMV + HIV + SARS-CoV-2 + in the vast majority of cases in current practice in Canada: no specific viral agent is identified because exhaustive virological investigation is costly and rarely available → pericarditis qualified as idiopathic | Viral syndrome often present (rhinopharyngitis + flu-like illness 1-3 weeks before) + usually good prognosis + response to NSAIDs and colchicine + moderate fever (38-38.5°C) + high CRP |
| Bacterial (5-10 % in developed countries) | Tuberculosis (Mycobacterium tuberculosis) - major cause in developing countries + staphylococcus + pneumococcus + meningococcus + streptococcus + gram-negative germs (in the immunocompromised) + high fever + altered general condition + abundant effusion | Purulent pericarditis (purulent exudate) = medical emergency + puncture for diagnostic and therapeutic purposes + surgical drainage often required + systemic antibiotic therapy + tuberculosis: 6-month anti-tuberculosis treatment + corticosteroids to prevent constriction. |
| Autoimmune | SLE (systemic lupus erythematosus) - pericardial involvement in 20-30 % of lupus + rheumatoid arthritis + systemic scleroderma + Sjögren's syndrome + dermatomyositis + SAPL + vasculitides + adult Still's syndrome (fever + arthritis + salmon rash + pericarditis) | Context of known or undiscovered autoimmune disease + systematic autoimmune workup if recurrent or young patient + AAN + anti-dsDNA + FR + CRP very high in Still disease |
| Neoplastic | Pericardial metastases (breast + lung ++ + lymphoma + melanoma) + primary pericardial mesothelioma (rare) + leukemia + pericardial carcinosis is the most frequent cause of abundant pericardial effusion in adults over 60 years of age | Effusion often abundant and rapidly recurring after puncture + cytological analysis of fluid (tumor cells) + surgical pericardial window if frequent recurrence |
| Post-infarction and post-surgery | Early pericarditis (D1-J4 post-IDM): direct inflammation of myocardial necrosis + Dressler syndrome (D2-8 weeks post-IDM): late autoimmune reaction + postpericardiotomy (cardiac surgery) + post-radiofrequency ablation | Obvious cardiovascular context + early post-IDM pericarditis: contraindication to NSAIDs and ibuprofen (reduced myocardial healing) → aspirin preferred + Dressler syndrome: NSAIDs + colchicine |
| Iatrogenic and metabolic | Thoracic radiotherapy (acute or chronic pericarditis months to years later) + drugs (hydralazine + procainamide + isoniazid + methotrexate + checkpoint inhibitors - anti-PD1/PD-L1) + uraemia (end-stage renal disease - uraemic pericarditis) | Uremic pericarditis: painless + occurs if urea > 60 mmol/L + responds to intensified dialysis + NSAIDs are contraindicated in advanced CKD → aspirin + colchicine cautious |
Clinical presentation and diagnosis
- Pleuritic chest pain: acute retrosternal or precordial pain + side-stitch-like + aggravated by deep inspiration + coughing + and supine position + relieved by sitting bent forward (anteflexia or rifle-hound position) + frequently radiates to the left trapezius (characteristic of phrenic nerve irritation) + may mimic pain of coronary origin
- Pericardial friction: leathery rubbing or squeaking sound on cardiac auscultation + heard best in a seated position leaning forward with the diaphragmatic tip of the stethoscope firmly applied + often intermittent + may have 2 or 3 components (systolic + early diastolic + presystolic) + pathognomonic of pericarditis but present in only 33-50 % of cases
- ECG - characteristic changes in 4 stages : stage I (acute phase): diffuse ST elevation + concave upward + affecting several leads (generally all except aVR and V1, which show ST elevation) + PR segment depression (PR elevation in aVR) - very specific sign of pericarditis + stage II (J3-J7): ST normalization + flattening of T waves + stage III: T wave negativation + stage IV: complete normalization
- Biology : elevated CRP (marker of inflammatory activity + guides duration of treatment) + CBC (moderate leukocytosis + eosinophilia if parasitic or drug-induced) + troponin (may be elevated if associated myopericarditis - paradoxically a good prognostic sign in viral pericarditis) + creatinine + liver work-up + NAA if autoimmune cause suspected
- Transthoracic echocardiography (TTE) : indicated in all cases of acute pericarditis + looks for pericardial effusion + assesses its size (slight) > < 10 mm + moderate 20 mm) + look for signs of compression (tamponade) + assess systolic function (associated myocarditis) + an absent effusion does not rule out pericarditis
- Poor prognostic factors («high concern» signs) : fever > 38°C + subacute course (> 7 days) + abundant effusion + tamponade + non-response to NSAIDs after 7 days + immunosuppression + anticoagulant therapy + chest trauma + suspected non-viral bacterial cause → hospitalization recommended for further investigation.
ℹ️
The ECG distinction between acute pericarditis and ACS (acute coronary syndrome) with ST elevation is essential, as their treatments are opposed. In pericarditis: DIFFUS ST elevation (several territories not corresponding to a single coronary artery) + upward concave (saddle-shaped) + PR segment depression + no mirror image. In ACS-STEMI: LOCALIZED ST elevation (territory of a single artery: V1-V4 for IVA, II-III-aVF for CD) + upwardly convex (domed) + mirror images + rapid progression to Q wave and T inversion.
Treatment
- NSAIDs (non-steroidal anti-inflammatory drugs) - first-line treatment : ibuprofen 600 mg × 3/day × 1 to 2 weeks (anti-inflammatory dose) + or aspirin 500-1,000 mg × 3-4/day × 1 to 2 weeks + gradual reduction over 2 to 4 weeks (reduction of 200-400 mg/week for ibuprofen) depending on clinical response and CRP normalization + aspirin is preferred to ibuprofen in the post-IDM context (no reduction in myocardial healing) + systematic gastroprotection (PPI) if treatment is prolonged
- Colchicine - compulsory background treatment : colchicine 0.5 mg × 2/day (if weight > 70 kg) or 0.5 mg × 1/day (if weight ≤ 70 kg) × 3 months as first-episode treatment + reduction in recurrences of 50 % in the COPE (Imazio 2005) and ICAP (Imazio 2013 - NEJM) trials + anti-inflammatory mechanism: inhibition of microtubule assembly and neutrophil activation + side effects: diarrhea (20 % - reduce dose if diarrhea rather than stop) + rare myalgias + contraindications: pregnancy + severe renal impairment (GFR < 30 mL/min) + drug interactions (cyclosporine + clarithromycin)
- Restriction of physical activity: strict restriction of physical activity until symptoms disappear + normalization of CRP and ECG + in competitive athletes: restriction for at least 3 months (including after complete clinical recovery) + risk of arrhythmia and myocarditis aggravated by intense exercise
- Corticosteroids - second or third line only : prednisone 0.2-0.5 mg/kg/day × 2 weeks then gradual decrease + indicated if: contraindication to NSAIDs + failure of NSAIDs + specific causes (lupus + scleroderma + Still's syndrome) + uremic pericarditis + to be avoided in first-line treatment as it is associated with a higher risk of relapse and chronic pericarditis (COPE trial) + slow decrease mandatory to avoid relapse
- Anakinra (anti-IL-1) - refractory recurrent pericarditis : anakinra 100 mg/day SC × 6 months (Kineret®) → anti-interleukin-1 biologiq + indicated in recurrent pericarditis with auto-inflammatory syndrome refractory to NSAIDs + colchicine + corticosteroids (at least 2 lines of treatment) + AIRTRIP trial (Brucato 2016 - NEJM) + rilonacept (Arcalyst®) also FDA-approved for recurrent pericarditis (2021)
- Abundant pericardial effusion and tamponade - emergency : urgent pericardiocentesis (echocardiography-guided evacuation puncture) if hemodynamic signs of tamponade (hypotension + jugular turgor + muffled heart sounds - Beck's triad) + or if circular effusion > 20 mm with echocardiographic signs of compression (collapse of right cavities) + prolonged pericardial drainage by catheter if recurrent effusion
Absolute emergency - dial 911
Call 911 or go immediately to the emergency room if acute chest pain is accompanied by progressive shortness of breath + chest pressure + low blood pressure + or syncope - these signs may suggest cardiac tamponade (compression of the heart by pericardial effusion) or acute coronary syndrome, two cardiac emergencies requiring immediate intervention. Never delay calling 911 in the face of acute chest pain, waiting to see if symptoms improve.
For evaluation of pleuritic chest pain, ECG and echocardiography, initiation of treatment with NSAIDs and colchicine, and cardiological referral, Clinique Omicron offers medical consultations at its points of service in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
Consult at Clinique Omicron
Clinique Omicron's specialized physicians and nurse practitioners (NPs) assess patients presenting with pleuritic chest pain, perform an ECG to identify diffuse elevation and PR-segment depression of pericarditis, prescribe a biological work-up (CRP + troponin + CBC) and echocardiography, initiate treatment with NSAIDs and colchicine for mild to moderate forms, and refer to cardiology for forms with abundant effusion, recurrences or signs of poor prognosis. Consultations are available at several points of service in Quebec, as well as via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The contents of this page are provided for information purposes only and do not replace the advice of a physician or cardiologist. Any acute chest pain should be urgently evaluated medically to exclude acute coronary syndrome before attributing the picture to pericarditis.
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