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Double Trouble: Acute Pulmonary Embolism in a Patient With Acute Inferior Wall Stemi
Pulmonary Vascular Disease SESSION TITLE: Pulmonary Vascular Disease SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM
Double Trouble: Acute Pulmonary Embolism in a Patient With Acute Inferior Wall Stemi Shahniwaz Labana* Marwah Hussein Sandip Saha and Mohammad Khan Wayne State University, Troy, MI
PULMONARY VASCULAR DISEASE
INTRODUCTION: Pulmonary embolism (PE) and myocardial infarction are two of the most feared medical emergencies. Both carry a high mortality, demand radically different interventions, yet are often indistinguishable. Differentiating between a right ventricular myocardial infarction and PE is a challenging clinical scenario; however, correctly ascertaining the pathologic process is imperative, as decision making drastically impacts patient outcome. There have been a few case reports of PE masquerading as a myocardial infarction; however, we report the first ever case of a PE that presented with inferior wall STEMI and how it offered a uniquely difficult clinical dilemma in determining which intervention would confer survivability for our patient. CASE PRESENTATION: This is a 72-year-old male with hypertension, IDDM and recent cholecystectomy who presented with lower extremity edema, dyspnea and hypoxia. An EKG showed ST elevation in leads II, III, and aVF with reciprocal ST depression in aVL and lead I. The troponin was 1.770 with a BNP of 3546. A CT chest angiography demonstrated an acute PE with an RV:LV of 1.32. An echocardiogram demonstrated severe hypokinesis of the base, mid-to-distal-inferior and inferolateral walls. After considerable interdisciplinary debate, a decision was made to perform a coronary angiogram, which demonstrated 99% stenosis of the mid right coronary artery, resulting in drug-eluting stent deployment. Subsequently, the patient underwent successful catheter-directed intra-arterial thrombolysis. A repeat echocardiogram with agitated saline demonstrated a right to left shunt with persistent inferior wall motion abnormalities, suggesting a parodoxical thromboembolism through a pre-existing patent foramen ovale. DISCUSSION: Three proposed mechanisms can possibly explain the co-existing processes. An existing plaque could have ruptured from increased myocardial demand resulting from the PE or profound hypoxia generated a catecholamine surge triggering myocardial ischemia. However, only one mechanism fully accounts for the concurrence of both pathologies: a paradoxical thromboembolism propagating through the patent foramen ovale resulting in acute RCA stenosis. CONCLUSIONS: There have been cases of a PE that have mimicked a STEMI, but yielded negative coronary angiograms for significant obstructive coronary artery disease.1,2 Only Goslar et al. reported a paradoxical thromboembolism from a PE into the conus artery, resulting in an antero-septal myocardial infarction; however, the initial transthoracic echocardiogram findings could not be explained independently by the two processes.3 Therefore, our case demonstrates that a PE and STEMI can occur simultaneously and present identically, resulting in a complicated clinical picture that demands timely decision making. Reference #1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4264717/ Reference #2: https://www.ncbi.nlm.nih.gov/pubmed/25414218 Reference #3: https://cardiovascularultrasound.biomedcentral.com/articles/10.1186/1476-7120-8-50 DISCLOSURE: The following authors have nothing to disclose: Shahniwaz Labana, Marwah Hussein, Sandip Saha, Mohammad Khan No Product/Research Disclosure Information DOI:
http://dx.doi.org/10.1016/j.chest.2017.08.1057
Copyright ª 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.
1024A
[
152#4S CHEST OCTOBER 2017
]
Double Trouble: Acute Pulmonary Embolism in a Patient With Acute Inferior Wall Stemi Shahniwaz Labana* Marwah Hussein Sandip Saha and Mohammad Khan Wayne State University, Troy, MI
PULMONARY VASCULAR DISEASE
INTRODUCTION: Pulmonary embolism (PE) and myocardial infarction are two of the most feared medical emergencies. Both carry a high mortality, demand radically different interventions, yet are often indistinguishable. Differentiating between a right ventricular myocardial infarction and PE is a challenging clinical scenario; however, correctly ascertaining the pathologic process is imperative, as decision making drastically impacts patient outcome. There have been a few case reports of PE masquerading as a myocardial infarction; however, we report the first ever case of a PE that presented with inferior wall STEMI and how it offered a uniquely difficult clinical dilemma in determining which intervention would confer survivability for our patient. CASE PRESENTATION: This is a 72-year-old male with hypertension, IDDM and recent cholecystectomy who presented with lower extremity edema, dyspnea and hypoxia. An EKG showed ST elevation in leads II, III, and aVF with reciprocal ST depression in aVL and lead I. The troponin was 1.770 with a BNP of 3546. A CT chest angiography demonstrated an acute PE with an RV:LV of 1.32. An echocardiogram demonstrated severe hypokinesis of the base, mid-to-distal-inferior and inferolateral walls. After considerable interdisciplinary debate, a decision was made to perform a coronary angiogram, which demonstrated 99% stenosis of the mid right coronary artery, resulting in drug-eluting stent deployment. Subsequently, the patient underwent successful catheter-directed intra-arterial thrombolysis. A repeat echocardiogram with agitated saline demonstrated a right to left shunt with persistent inferior wall motion abnormalities, suggesting a parodoxical thromboembolism through a pre-existing patent foramen ovale. DISCUSSION: Three proposed mechanisms can possibly explain the co-existing processes. An existing plaque could have ruptured from increased myocardial demand resulting from the PE or profound hypoxia generated a catecholamine surge triggering myocardial ischemia. However, only one mechanism fully accounts for the concurrence of both pathologies: a paradoxical thromboembolism propagating through the patent foramen ovale resulting in acute RCA stenosis. CONCLUSIONS: There have been cases of a PE that have mimicked a STEMI, but yielded negative coronary angiograms for significant obstructive coronary artery disease.1,2 Only Goslar et al. reported a paradoxical thromboembolism from a PE into the conus artery, resulting in an antero-septal myocardial infarction; however, the initial transthoracic echocardiogram findings could not be explained independently by the two processes.3 Therefore, our case demonstrates that a PE and STEMI can occur simultaneously and present identically, resulting in a complicated clinical picture that demands timely decision making. Reference #1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4264717/ Reference #2: https://www.ncbi.nlm.nih.gov/pubmed/25414218 Reference #3: https://cardiovascularultrasound.biomedcentral.com/articles/10.1186/1476-7120-8-50 DISCLOSURE: The following authors have nothing to disclose: Shahniwaz Labana, Marwah Hussein, Sandip Saha, Mohammad Khan No Product/Research Disclosure Information DOI:
http://dx.doi.org/10.1016/j.chest.2017.08.1057
Copyright ª 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.
1024A
[
152#4S CHEST OCTOBER 2017
]