SESSION TITLE: Critical Care Case Report Posters II
SESSION TYPE: Affiliate Case Report Poster
PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM
INTRODUCTION: Severe pulmonary hypertension can result in pulmonary artery (PA) dilatation with resultant mechanical complications, such as pulmonary valve insufficiency, PA rupture and, rarely, compression of nearby anatomical structures.
CASE PRESENTATION: A 53-year-old male with a known history of severe, inoperable, chronic thromboembolic pulmonary hypertension (CTEPH), presented with hypotension and hypoxic respiratory failure. He had recently been treated for a right lower lobe pneumonia with levofloxacin and described pleuritic chest pain in that area, as well as dull chest discomfort in his left chest. Laboratory examinations were significant for leukocytosis (41 k/uL), international normalized ratio (INR) of 3.9, elevated D-dimer, central venous oxygen saturation of 43%, troponin I of 4ng/mL and a creatinine kinase-MB fraction of 39 ng/mL. EKG showed a prior right bundle branch block and new inferolateral ST depressions and ST elevation in aVR. Echocardiogram was significant for new left ventricular systolic dysfunction with an ejection fraction of 30%, worsened right ventricular function with 3+ pulmonic valve regurgitation, dilatation of the main PA to 7 cm and a visible mobile thrombus in the right main PA. An intra-aortic balloon pump was inserted and an emergent coronary angiography revealed 95% ostial left main coronary artery stenosis secondary to extrinsic compression from the dilated PA,which was successfully treated with placement of a bare metal stent. Therapy with aspirin and ticagrelor was initiated in addition to IV heparin and inhaled epoprostenol. Once he was hemodynamically stable, warfarin and sildenafil were resumed and he was discharged to a rehabilitation facility on home oxygen.
DISCUSSION: The patient's chest pain and hypoxia was likely multifactorial, including a necrotizing pneumonia, pulmonary embolism (PE) and MI. We suspect that his PE occurred due to subtherapeutic warfarin levels secondary to his recent hospitalization and possible dosing changes due to the initiation of levofloxacin. The PE and pneumonia contributed to worsened PA dilation and subsequent compression of the left main coronary artery.
CONCLUSIONS: Severe dilatation of the PA trunk can compress adjacent anatomical structures, including the left main coronary artery, leading to myocardial infarction for which stenting can be a life-saving intervention.
Reference #1: Vaseghi et al. Acute myocardial infarction secondary to left main coronary compression by pulmonary artery aneurysm. J Invasive Cardiol 2007;19:375-7.
DISCLOSURE: The following authors have nothing to disclose: Jonathan Wiesen, Gustavo Heresi, Wayne Tsuang
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