A 67-year-old man with hypertension, hyperlipidemia, and a remote history of pulmonary embolism (PE) presented with sudden onset non-pleuritic substernal chest pain while walking around his home. He also noted dyspnea and lightheadedness followed by syncope. Emergency medical services responded and found the patient to have fluid-responsive hypotension (blood pressure of 64/48 improved to 124/57 mmHg with 1L normal saline, initial recorded heart rate of 54 bpm, SpO2 of 99% placed immediately on 2L nasal cannula). He was taken to a nearby hospital.
An electrocardiogram (ECG) on arrival revealed inferior ST-segment depressions. The initial troponin I was elevated (8.9 ng/mL), but laboratory results were otherwise unremarkable. Complete transthoracic echocardiogram (TTE) showed normal right ventricular (RV) size and function and a hyperdynamic left ventricle with an ejection fraction of 70-75%. High-risk non-ST-segment elevation myocardial infarction (MI) was diagnosed, and urgent left heart catheterization revealed an 80% right coronary artery lesion (Thrombolysis in Myocardial Infarction [TIMI] 3 flow, no thrombus) successfully treated with a drug-eluting stent (0% residual lesion, no dissection, TIMI 3 flow). In the hospital, the patient experienced complete resolution of symptoms. Troponin I peaked at 13.6 ng/mL. Upon discharge on hospital day 2, he walked to the nearby Veterans Administration hospital to pick up his prescriptions, and identical symptoms recurred. In the emergency department at that hospital, his vital signs were afebrile, with a heart rate of 67 bpm, blood pressure of 131/62 mmHg, respiratory rate of 20, and SpO2 of 98% on room air. An ECG was done. Troponin I was elevated to 2.7 ng/mL and N-terminal pro-B-type natriuretic peptide was 1004 pg/mL. Renal function was normal. Troponin I down-trended to 2.3 ng/mL 3 hours later.
The correct answer is: C. Computed tomography (CT) pulmonary angiography
- This patient presented with recurrent chest pain after percutaneous coronary intervention (PCI). Differential should include post-PCI complication (coronary dissection, stent thrombosis), de novo coronary thrombosis, pericarditis, or tamponade. Non-cardiac causes of troponin elevation and ECG changes must also be considered.
- One third of patients with acute PE present with chest pain, troponin elevation, and ECG changes.1 Always consider PE in the differential diagnosis of troponin elevation. This patient presented with recurrent symptoms despite successful PCI, a down-trending troponin, and a history of prior PE, all of which point toward PE as a potential etiology of his chest pain and troponin elevation.2
- The optimal imaging modality to diagnose PE is a CT pulmonary angiography (answer C).
- Case closure: CT pulmonary angiography was performed and revealed a saddle PE with reflux of contrast into the inferior vena cava suggestive of RV strain (along with the elevated B-type natriuretic peptide and troponin). In this case, it is likely that this patient's sub-massive PE was initially mistaken for an acute coronary syndrome (ACS) with treatment of an incidental right coronary artery lesion. He subsequently received catheter-directed low-dose thrombolysis to both pulmonary arteries,3 had an uneventful recovery, and was discharged home.
Answer A would be appropriate if there were a concern for an ACS. ECG and resolving troponin were not suggestive of a new ACS or stent thrombosis.
- Acute stent thrombosis is an uncommon (incidence of approximately 1% within the first month) but serious complication of PCI. Features may include presence of ST-segment elevation on ECG, troponin rise, and/or history of dual antiplatelet therapy non-adherence, none of which was present here. It is, however, within the 1-month timeframe of stent placement when this complication is most common. With a 20-45% mortality rate, stent thrombosis should always be considered in post-PCI chest pain.4
- Coronary dissection occurs in <1% of PCI cases5 and can cause chest pain. More serious dissections result in hemopericardium and tamponade, which would present with hypotension with narrowed pulse pressure, jugular venous distension, distant heart sounds (Beck's triad), and pulsus paradoxus. Absence of dissection on angiography immediately following PCI and the patient's hemodynamic stability speak against this diagnosis.
Answer B would identify pericardial effusion that may be concerning for post-PCI coronary dissection or post MI pericarditis (Dressler syndrome). It may also reveal regional wall motion abnormalities that would point toward new coronary ischemia or infarction or evidence of RV strain that could suggest a large PE.
- The patient had no other features of pericarditis such as a friction rub, diffuse ST-segment elevations and PR-segment depressions, fever, or pleuritic chest pain, making this diagnosis less likely. Dressler syndrome also typically presents 2-3 weeks after the MI rather than in such an acute manner.
- Although it is reasonable to obtain an initial bedside TTE to triage further work-up, a complete TTE would delay evaluation for PE, which was the most likely diagnosis.
Answer D would identify aortic dissection, a complication of PCI.
- Aortic dissection would present with tearing chest pain radiating to the back, upper extremity blood pressure discrepancies, and potential hemodynamic instability. In one single-center study, post-PCI aortic dissection occurred in 0.07% of cases.6 This is less likely to be the diagnosis.
- Some facilities offer protocols to assess PE and dissection with CT angiography; however, this often results in suboptimal timing of image acquisition for contrast in either pulmonary arteries or aorta that could delay diagnosis. Because PE is the most likely diagnosis, CT pulmonary angiography is the best imaging technique.
In conclusion, PE can be commonly mistaken for an ACS.
- Kukla P, Długopolski R, Krupa E, et al. How often pulmonary embolism mimics acute coronary syndrome? Kardiol Pol 2011;69:235-40.
- Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2011;123:1788-830.
- Jaber WA, Fong PP, Weisz G, et al. Acute Pulmonary Embolism: With an Emphasis on an Interventional Approach. J Am Coll Cardiol 2016;67:991-1002.
- Reejhsinghani R, Lotfi AS. Prevention of stent thrombosis: challenges and solutions. Vasc Health Risk Manag 2015;11:93-106.
- Dash D. Complications of coronary intervention: abrupt closure, dissection, perforation. Heart Asia 2013;5:61-5.
- Cockburn J, Blows L, Cohen A, et al. Acute ischemic complications of PCI and CABG: who should cover whom for coronary revascularization? J Interv Cardiol 2013;26:372-7.