Pulmonary Embolism Initially Misdiagnosed as Perimyocarditis in a Young Patıent

Abstract

Pulmonary embolism is a common cardiovascular emergency. In case of delayed diagnosis and treatment morbidity and mortality is high. In this report, we presented a case of pulmonary embolism without apparent risk factors, which was initially misdiagnosed as peri/myocarditis.

INTRODUCTION

Acute chest pain is one of the most common presenting complaints to the emergency departments. The causes range from relatively benign to life-threatening conditions and include acute coronary syndromes (ACS), pulmonary embolism (PE), and pericarditis.[1] Although the diagnosis can be made on the basis of thorough medical history, physical examination, electrocardiography (ECG), and simple laboratory variables in most patients, the diagnosis remains a challenge, particularly in patients without clear symptoms or specific ECG changes. On the other hand, misdiagnoses in patients with chest pain can lead to serious consequences for the patients and can be a substantial liability for the physician.[2] In this report, we presented a case of PE without apparent risk factors, which was initially misdiagnosed as peri/myocarditis.

CASE REPORT

A 23--year-old male with no previous cardiac history presented with stabbing pain on the left side of his chest that was increasing with deep inspiration. He did not report any additional symptoms, including dyspnea or syncope. However, he had an upper respiratory tract infection (URTI) 2 weeks ago. Physical examination was unremarkable except for a scar of a previous workplace accident happened 3 years ago. Concave ST-segment elevation was present in the inferior and lateral leads, with ST-segment depression in aVR in the initial ECG [Figure 1]. Laboratory findings were within normal ranges apart from high troponin levels and increased white blood cells (14,000/mm³). Bedside echocardiography did not show any findings suggestive of PE, such as right heart dilatation or septal flattening. Considering the patients presentation, recent history of an URTI and ST-elevation pattern, patient was admitted with a diagnosis of pericarditis. Increased troponin levels were suggestive of associated myocarditis. Cardiac magnetic resonance imaging was scheduled to confirm myocardial involvement. A non-steroidal anti-inflammatory drug (NSAID) was administered along with colchicine. However, troponin levels continued to increase (at admission: 0.346 ng/L, peak: 1.82 ng/L, cutoff: 0.014 ng/L), despite stable clinical status. At this point, a coronary angiogram was considered to exclude coronary artery disease (CAD), including coronary anomalies. However, taking patient's age into account and low probability of CAD, we proceeded with a coronary computed tomography angiography (CCTA) which showed massive thrombus in the right main pulmonary artery without any obstruction in the coronary arteries [Figures 2 and 3a]. NSAID and colchicine was stopped and low-molecular weight heparin was started. A screening for deep vein thrombosis, including subclavian veins was normal. Genetic analysis revealed a homogeneous MTHFR gene mutation. Other blood tests including lupus anticoagulants and homocysteine were normal. The patient was discharged on dabigatran 150 mg b.i.d. Patient was asymptomatic and the pulmonary computed tomography angiography was normal at the 3-month follow-up [Figure 3c].

Figure 1.

Concave ST-segment elevation was present in the inferior and lateral leads, with ST-segment depression in aVR in the initial ECG

Figure 2.

CT angiography shows unobstructed coronary arteries; (a) right coronary artery; (b) left circumflex coronary artery; (c) left anterior descending coronary artery

Figure 3.

(a) CT shows pulmonary embolism in the right pulmonary artery (red arrows indicate the pulmonary embolus); (b) Right chamber sized were normal in the CCTA (Right ventricle: 45 mm, Left ventricle: 56 mm; RV/LV < 0,9); (c) The pulmonary computed tomography angiography was normal at the 3-month follow-up

DISCUSSION

PE is a common and potentially life-threatening condition. Despite the advances in diagnostic modalities, diagnosis of PE still remains a challenge. The presentation can vary widely. Although the “classical” presentation is abrupt onset of pleuritic chest pain, dyspnea, and hypoxia, clinical manifestation is not sensitive and specific in most patients and the combination of these findings are seen in less than 20% of the cases.[3] In fact, previous studies showed delay and misdiagnosis in up to 50% of the PE cases.[4]

ECG is one of the indispensable diagnostic tools in evaluating the patients with chest pain and dyspnea. Patients with PE may demonstrate a variety of electrocardiographic changes, including alterations in rate, rhythm, conduction, axis, and morphology[5]; however, most of these alterations are non-specific, thus, their diagnostic value is limited. These alterations may be because of right ventricular overload, dilation, ischemia, and/or increased sympathetic activity.[6] Most common finding on the ECG is sinus tachycardia. Other possible changes include, but not limited to, T-wave inversion in the right pre-cordial leads; an S1Q3T3 pattern; q waves in the inferior leads, complete, or incomplete right bundle-branch block.[6,7] ST elevations are rarely present,[5,8] however, if present, they are mostly seen in anteroseptal leads.[9] The mechanism of ST-segment elevations are not clear, but suggested mechanisms include paradoxical coronary artery embolism via atrial sepal defect or patent foramen ovale[8] and right ventricular ischemia because of hypotension, hypoxemia, pulmonary artery hypertension, or catecholamine surge.[10] Nevertheless, our patient demonstrated ST-elevations without clinical distress, hypoxia, or right heart dilatation. In addition, CCTA also excluded any thromboembolic obstruction.

In most cases, patients with acute pericarditis present with pleuritic chest pain. ECG usually shows widespread concave ST elevations, however, it can also cause localized ST elevations. Increased troponins suggests associated myocarditis. Guidelines for the diagnosis and management of pericardial diseases recommends coronary angiography in order to rule out acute coronary syndromes, in cases of pericarditis with suspected associated myocarditis.[11] Although increasing troponins in this patient mandated coronary evaluation, the low probability of the coronary artery disease precluded us from performing an invasive angiogram. We proceeded with CCTA relying on its high negative predictive value, and to our surprise, a diagnosis of PE was made.

Most common wrong diagnosis for PE include pneumonia, bronchitis, exacerbation of chronic obstructive pulmonary disease, and heart failure. However, this patient was initially diagnosed as peri/myocarditis. The diagnosis of PE starts with suspicion based on the symptoms and signs. The patient here presented with chest pain; nevertheless, the lack of risk factors for PE and a recent history of URTI together with concave ST-elevations misled the clinician to a diagnosis of pericarditis. Moreover, there was no sign of dilatation in the right heart in echocardiography or CCTA [Figure 3b]. The take-home messages from this case are twofolds. First, CCTA allows evaluations extracardiac structures, such as portions of lungs and aorta unlike conventional angiography, thus providing a broader diagnostic approach and offering the opportunity to detect clinically significant pathologies or underlying etiology,[12] including PE and even myocarditis.[13] Therefore, CCTA can be the modality of choice to exclude CAD in younger patients without a clear diagnosis. Second, ST-elevations can occur in PE, and it should be kept in in mind for the differential diagnosis, when the presentation is not typical for ACS.

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Conflicts of interest

There are no conflicts of interest.