Acute Pericarditis Hours After Uncomplicated Diagnostic Cardiac Catheterization

DISCUSSION

This case describes acute pericarditis with a new small pericardial effusion occurring approximately 4 hours after diagnostic coronary angiography without PCI or a documented procedural complication. The timing, absence of an acute culprit coronary lesion, down-trending troponin pattern, pleuritic and positional chest pain, and new pericardial effusion favored acute pericarditis rather than acute coronary syndrome. The case is clinically important because diagnostic catheterization is generally safe, and isolated postdiagnostic catheterization pericarditis is much less represented in the literature than pericarditis after PCI, coronary perforation, chronic total occlusion intervention, or other complex intracardiac procedures.^1,4,5,8,9

The literature more commonly describes pericardial inflammation or effusion after therapeutic or complicated procedures. Imazio and Hoit reported that post–cardiac injury syndrome after percutaneous cardiac interventions is uncommon, with estimated rates of <1% to 5% depending on the trigger, and report the rate of post-PCI pericarditis as <0.5%.² Rodevič et al reported acute pericarditis 6 hours after unsuccessful chronic total occlusion PCI without documented contrast extravasation,⁴ Yang et al described pericarditis 36 hours after PCI complicated by guidewire perforation and contrast extravasation,⁵ Gungor et al described pericarditis 48 hours after a prolonged and technically difficult PCI without coronary perforation or dissection,⁸ and Faraj et al reported post–cardiac injury syndrome 4 hours after PCI with suspected guidewire-related distal coronary perforation.⁹ These reports support that early postprocedural pericarditis can occur after PCI, but they differ from the present case because they involved attempted or completed coronary intervention, complex lesion manipulation, or documented procedural injury.

Procedure-related pericardial effusion and tamponade are discussed in a related but distinct literature base. Lekhakul et al described hemopericardium after invasive cardiology procedures and management with pericardiocentesis,¹⁰ while Holmes et al emphasized that iatrogenic pericardial effusion and tamponade have been documented after both diagnostic and therapeutic percutaneous cardiac procedures, are often related to cardiac perforation, and require prompt clinical and echocardiographic assessment.¹¹ Li et al described tamponade after chronic total occlusion revascularization despite no visible contrast leakage on final angiography, illustrating that clinically important pericardial complications may occasionally be occult at the end of the procedure.¹² Delayed constrictive pericarditis has also been reported after PCI or coronary perforation, but these cases represent later and more severe outcomes than the presentation in our patient.^13,14

Several mechanisms may explain early postcatheterization pericarditis. First, immune-mediated inflammation after myocardial or pericardial injury is the classic framework for post–cardiac injury syndrome.^2,3 Second, direct pericardial irritation from localized procedural trauma or occult procedure-related pericardial bleeding or effusion is biologically plausible, especially because iatrogenic effusion and tamponade are well described after invasive cardiac procedures.^10,11 Third, wire manipulation during PCI may cause angiographically occult vascular injury, ranging from micro-extravasation through the vessel wall to sealed perforations or subadventitial hematoma, that is sufficient to produce pericardial irritation or even tamponade despite no contrast extravasation on final angiography.⁴ This mechanism has been proposed in cases of early post-PCI pericarditis in which guidewires may have exited the vessel architecture during chronic total occlusion revascularization attempts, causing micro-extravasation not visible during the procedure yet provoking inflammatory cytokine release and pericardial fluid accumulation.⁴ The possibility of angiographically occult vascular injury is further supported by a report of frank pericardial tamponade after chronic total occlusion revascularization in which no contrast leakage was identified angiographically, yet at thoracotomy, a hematoma was found on the coronary artery surface without a definite rupture site.¹² A contrast-related inflammatory mechanism is theoretically possible, but direct evidence for contrast-induced isolated acute pericarditis after diagnostic angiography is limited in the available literature. Further, the absence of allergic-type symptoms, hemodynamic instability during contrast exposure, or other systemic features in our patient makes this mechanism less compelling than localized procedural trauma or early inflammatory pericardial response.

Post–cardiac injury syndrome can be difficult to diagnose because its clinical presentation may mimic myocardial infarction.² In our patient, the early postcatheterization chest pain and mild troponin elevation appropriately triggered concern for acute coronary syndrome, and heparin was started while the evaluation was ongoing. However, serial electrocardiograms did not show ischemic evolution or the typical diffuse ST-segment elevation or PR-segment depression described in acute pericarditis. The diagnosis was supported by characteristic pleuritic, positional chest pain and a new pericardial effusion on transthoracic echocardiography, satisfying 2 guideline-supported diagnostic criteria for acute pericarditis.³ This diagnostic sequence highlights the value of early echocardiography in patients with postcatheterization chest pain when the clinical pattern is not fully explained by acute coronary occlusion.

Aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) with colchicine as adjunctive therapy are recommended as first-line treatment for acute pericarditis.³ In the Investigation of Colchicine for Acute Pericarditis randomized trial, colchicine added to conventional anti-inflammatory therapy reduced persistent symptoms at 72 hours and significantly lowered the rate of incessant or recurrent pericarditis.¹⁵ Low-dose corticosteroids are not recommended as first-line therapy and should be reserved for select patients in whom aspirin or NSAIDs are contraindicated, not tolerated, or ineffective and when an infectious cause has been excluded.³ Our patient's prompt symptomatic improvement after initiation of ibuprofen and colchicine was consistent with guideline-supported treatment for acute pericarditis.³

Early recognition of postprocedural pericarditis and pericardial effusion is clinically important because severe outcomes may include cardiac tamponade, hemodynamic collapse, and the need for urgent pericardiocentesis, with constrictive pericarditis reported less commonly as a delayed complication of pericardial inflammation.^10,11,13,14 In this case, prompt recognition allowed discontinuation of empiric heparin after acute coronary syndrome became less likely and initiation of anti-inflammatory therapy. The patient remained hemodynamically stable, had no echocardiographic tamponade, and improved without invasive pericardial intervention.