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Research Article Open Access Barsoum et al., Angiol 2013, 1:1 DOI: 10.4172/2329-9495.1000106 Case Report Open Access Volume 1 • Issue 1 • 1000106 Angiol, an open access journal ISSN: 2329-9495 Angiology: Open Access A n g i o l o g y : O p e n A c c e s s ISSN: 2329-9495 Keywords: Pulmonary Embolism; ACS Introduction Pulmonary Embolism (PE) is a relatively common disease that can be life threatening [1-3]. It occur secondary to occlusion of the pulmonary artery or one of its branches. In spite of, the clinical presentation is variable and sometimes it is difficult to depend on signs and symptoms in diagnosis, early diagnosis and treatment can decrease mortality [4]. Variable Electrocardiogram (EKG) patterns were found in patients with PE [5,6] ST Segment Elevation Myocardial Infarction (STEMI) is extremely rare. In our case report, patient presented with chest pain and EKG finding highly suggestive of Acute Coronary Syndrome (ACS), coronary angiography couldn’t find culprit lesion but there was massive PE on pulmonary angiogram. Case Report 57 year old women smoker with history of hypertension, diabetes, hypercholesterolemia and depression was brought by ambulance to our emergency room for change in mental status aſter suicidal attempt by high dose of vicodin and other pain medications. Patient recently diagnosed as paraspinal abscess in another hospital and she leſt against medical advice one day before her presentation to us. On admission patient was confused, hemodynamic stable with normal heart and chest exam, her EKG revealed sinus rhythm with first degree heart block (Figure 1). On hospital day four patients had sudden retro-sternal chest pain associated with shortness of breath and diaphoresis, patient was tachypneic, hypotensive, tachycardiac with heart rate of 143 beat per minute and hypoxic with oxygen saturation of 76% on room air. EKG was done immediately to reveal sinus tachycardia and ST segment elevation in leads V1 to V3 (Figure 2). Code STEMI was initiated but shortly patient coded with rhythm of ventricular tachycardia that electrically cardioverted to sinus rhythm, Patient was intubated and mechanically ventilated, intravenous vasopressors were started and transferred to cardiac cath. Coronary angiogrqaphy revealed non significant LAD lesion (Figure 3), that didn’t match with the clinical finding so was decision to do pulmonary artery angiogram that showed large saddle embolus in the bifurcation of pulmonary artery. (Figures 4 and 5) Tissue Plasminogen Activator (TPA) started but patient coded again and unfortunately cardiopulmonary resuscitation was unsuccessful. Discussion e most common cause of pulmonary embolism is blood clot that dislodges from peripheral vein and travel through circulation *Corresponding author: Emad A Barsoum, Department of Medicine, Staten Island University Hospital, 475 Seaview Ave, Staten Island New York 10305, USA, Tel: 3476669321; Fax: 7182268695; E-mail: [email protected] Received March 31, 2013; Accepted June 24, 2013; Published June 26, 2013 Citation: Barsoum EA, Bhat T, McCord DA, Lafferty J (2013) Uncommon Presentation of Fatal Pulmonary Embolism. Angiol 1: 106. doi: 10.4172/2329- 9495.1000106 Copyright: © 2013 Barsoum EA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract We are reporting a case of 57 year old lady smoker with history of hypertension, diabetes, hypercholesterolemia and depression that was admitted to hospital for suicidal ideation and paraspinal abscess. Patient had acute retrosternal chest pain associated with shortness of breath, electrocardiogram finding was highly suggestive of STEMI in V1-V3, Patient coded in ventricular tachycardia that cardioverted to sinus rhythm, coronary angiogram didn’t reveal culprit lesion but pulmonary angiogram confirmed the diagnosis of pulmonary embolism. Uncommon Presentation of Fatal Pulmonary Embolism Emad A Barsoum 1 *, Tariq Bhat 2 , Donald A McCord 2 and James Lafferty 2 1 Department of Medicine, Staten Island University Hospital, New York, USA 2 Division of Cardiology, Staten Island University Hospital, New York, USA Figure 1: EKG on admission showing sinus rhythm with prolonged PR interval. Figure 2: EKG showing sinus tachycardia and ST segment elevation in V1-V3.

g y : OpenA g i o A Angiology: Open Access · finding of anteroseptal STEMI, pulmonary embolism could be the underlying cause. References 1. Horlander KT, Mannino DM, Leeper KV (2003)

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Page 1: g y : OpenA g i o A Angiology: Open Access · finding of anteroseptal STEMI, pulmonary embolism could be the underlying cause. References 1. Horlander KT, Mannino DM, Leeper KV (2003)

Research Article Open Access

Barsoum et al., Angiol 2013, 1:1DOI: 10.4172/2329-9495.1000106

Case Report Open Access

Volume 1 • Issue 1 • 1000106Angiol, an open access journalISSN: 2329-9495

Angiology: Open AccessAngio

logy: Open Access

ISSN: 2329-9495

Keywords: Pulmonary Embolism; ACS

IntroductionPulmonary Embolism (PE) is a relatively common disease that

can be life threatening [1-3]. It occur secondary to occlusion of the pulmonary artery or one of its branches. In spite of, the clinical presentation is variable and sometimes it is difficult to depend on signs and symptoms in diagnosis, early diagnosis and treatment can decrease mortality [4].

Variable Electrocardiogram (EKG) patterns were found in patients with PE [5,6] ST Segment Elevation Myocardial Infarction (STEMI) is extremely rare. In our case report, patient presented with chest pain and EKG finding highly suggestive of Acute Coronary Syndrome (ACS), coronary angiography couldn’t find culprit lesion but there was massive PE on pulmonary angiogram.

Case Report57 year old women smoker with history of hypertension, diabetes,

hypercholesterolemia and depression was brought by ambulance to our emergency room for change in mental status after suicidal attempt by high dose of vicodin and other pain medications. Patient recently diagnosed as paraspinal abscess in another hospital and she left against medical advice one day before her presentation to us. On admission patient was confused, hemodynamic stable with normal heart and chest exam, her EKG revealed sinus rhythm with first degree heart block (Figure 1).

On hospital day four patients had sudden retro-sternal chest pain associated with shortness of breath and diaphoresis, patient was tachypneic, hypotensive, tachycardiac with heart rate of 143 beat per

minute and hypoxic with oxygen saturation of 76% on room air. EKG was done immediately to reveal sinus tachycardia and ST segment elevation in leads V1 to V3 (Figure 2).

Code STEMI was initiated but shortly patient coded with rhythm of ventricular tachycardia that electrically cardioverted to sinus rhythm, Patient was intubated and mechanically ventilated, intravenous vasopressors were started and transferred to cardiac cath.

Coronary angiogrqaphy revealed non significant LAD lesion (Figure 3), that didn’t match with the clinical finding so was decision to do pulmonary artery angiogram that showed large saddle embolus in the bifurcation of pulmonary artery. (Figures 4 and 5) Tissue Plasminogen Activator (TPA) started but patient coded again and unfortunately cardiopulmonary resuscitation was unsuccessful.

DiscussionThe most common cause of pulmonary embolism is blood clot

that dislodges from peripheral vein and travel through circulation

*Corresponding author: Emad A Barsoum, Department of Medicine, Staten Island University Hospital, 475 Seaview Ave, Staten Island New York 10305, USA, Tel: 3476669321; Fax: 7182268695; E-mail: [email protected]

Received March 31, 2013; Accepted June 24, 2013; Published June 26, 2013

Citation: Barsoum EA, Bhat T, McCord DA, Lafferty J (2013) Uncommon Presentation of Fatal Pulmonary Embolism. Angiol 1: 106. doi: 10.4172/2329-9495.1000106

Copyright: © 2013 Barsoum EA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

AbstractWe are reporting a case of 57 year old lady smoker with history of hypertension, diabetes, hypercholesterolemia

and depression that was admitted to hospital for suicidal ideation and paraspinal abscess. Patient had acute retrosternal chest pain associated with shortness of breath, electrocardiogram finding was highly suggestive of STEMI in V1-V3, Patient coded in ventricular tachycardia that cardioverted to sinus rhythm, coronary angiogram didn’t reveal culprit lesion but pulmonary angiogram confirmed the diagnosis of pulmonary embolism.

Uncommon Presentation of Fatal Pulmonary Embolism Emad A Barsoum1*, Tariq Bhat2, Donald A McCord2 and James Lafferty2

1Department of Medicine, Staten Island University Hospital, New York, USA2Division of Cardiology, Staten Island University Hospital, New York, USA

Figure 1: EKG on admission showing sinus rhythm with prolonged PR interval.

Figure 2: EKG showing sinus tachycardia and ST segment elevation in V1-V3.

Page 2: g y : OpenA g i o A Angiology: Open Access · finding of anteroseptal STEMI, pulmonary embolism could be the underlying cause. References 1. Horlander KT, Mannino DM, Leeper KV (2003)

Citation: Barsoum EA, Bhat T, McCord DA, Lafferty J (2013) Uncommon Presentation of Fatal Pulmonary Embolism. Angiol 1: 106. doi: 10.4172/2329-9495.1000106

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Volume 1 • Issue 1 • 1000106Angiol, an open access journalISSN: 2329-9495

to pulmonary artery, other causes like air bubbles, fat emboli and amniotic fluid can cause same problem. The diagnosis of PE is based primarily on validated clinical criteria combined with selective testing, shortness of breath and pleauritic chest pain are the most common symptoms experienced by patient with PE, other symptoms include; productive cough, fever, syncope, hemoptysis, palpitation and seizures. In addition, massive PE can present by shock and even sudden death [7-11].

Pulmonary Embolism has been known to be associated with different morphological EkG changes, the predominant rhythm abnormalities is sinus tachycardia, most of PE cases have EKG changes suggestive of acute right ventricular strain like, incomplete or complete right bundle branch block, an S1Q3T3 pattern (defined as an S wave in lead I, a Q wave in lead III, and an amplitude of >1.5 mm associated with inversion of the T wave in lead III), inverted T waves in the second and third precordial leads [12-15].

Although ST segment elevation is not one of the criteria suggestive of PE, few cases were reported to have ST segment elevation in anteroseptal and anterior precordial leads [16,17]. Still the exact

mechanism of ST segment elevation is unclear in patient with PE. In our case, many factors were suggestive of diagnosis as acute coronary syndrome including history of smoking, diabetes, hypertension and hypercholesterolemia, clinical presentation with chest pain, EKG finding in form of significant ST segment elevation anteroseptal leads. In addition patient coded in ventricular tachycardia, this is common with ACS. But, patient didn’t have culprit lesion on coronary angiogram and diagnosis of PE was confirmed by pulmonary artery angiogram.

ConclusionAmong high risk patients that present by chest pain and EKG

finding of anteroseptal STEMI, pulmonary embolism could be the underlying cause.

References

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2. Wiener RS, Schwartz LM, Woloshin S (2011) Time trends in pulmonary embolism in the United States: evidence of overdiagnosis. Arch Intern Med 171: 831-837.

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4. Smith SB, Geske JB, Maguire JM, Zane NA, Carter RE, et al. (2010) Early anticoagulation is associated with reduced mortality for acute pulmonary embolism. Chest 137: 1382-1390.

5. Zhong-Qun Z, Chong-Quan W, Nikus KC, Sclarovsky S, Chao-Rong H (2013) A new electrocardiogram finding for massive pulmonary embolism: ST elevation in lead aVR with ST depression in leads I and V(4) to V(6). Am J Emerg Med 31: 456.

6. Falterman TJ, Jorge A. Martinez, Dayton Daberkow, Weiss LD (2001) Pulmonary Embolism With St Segment Elevation In Leads V1 TO V4: Case report and review of the literature regarding electrocardiographic changes in acute pulmonary embolism. The Journal of Emergency Medicine 21: pp. 255–261.

7. Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, et al. (2007) Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med 120: 871-879.

8. Demircan A, Aygencel G, Keles A, Ozsoylar O, Bildik F (2009) Pulmonary embolism presenting as syncope: a case report. J Med Case Rep 3: 7440.

9. Gaetano Nucifora, Luigi Badano, Fjoralba Hysko, Giuseppe Allocca, Pasquale Gianfagna, et al. (2007) Pulmonary Embolism and Fever. When Should Right-Sided Infective Endocarditis Be Considered? Circulation. 115: e173-e176

10. Lam M, Jammal M, Tiev K, Toledano C, Fardet L, et al. (2012) [Pulmonary embolism revealed by a seizure: a case report and literature review]. Rev Med Interne 33: 457-460.

11. Piazza G, Goldhaber SZ (2006) Acute pulmonary embolism: part II: treatment and prophylaxis. Circulation 114: e42-e47.

12. McGinn S, White PD (1935) Acute cor pulmonale resulting from pulmonary embolism. JAMA 104: 1473–1480.

13. Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, et al. (1997) The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads--80 case reports. Chest 111: 537-543.

14. Cheng AS, Money-Kyrle A (2005) Instructive ECG series in massive bilateral pulmonary embolism. Heart 91: 860-862.

15. Keith Todd, Christopher S Simpson, Damian P Redfearn, Hoshiar Abdollah, Adrian Baranchuk, et al. (2009) ECG For The Diagnosis Of Pulmonary Embolism When Conventional Imaging Cannot Be Utilized: A Case Report And Review Of The Literature. Indian Pacing Electrophysiol J 9: 268–275.

16. Noble J, Singh A (2011) Asymptomatic pulmonary embolus masquerading as acute anteroseptal myocardial infarction. CJEM 13: 62-65.

17. Lin JF, Li YC, Yang PL (2009) A case of massive pulmonary embolism with ST elevation in leads V1-4. Circ J 73: 1157-1159.

Figure 3: Left Coronary angiogram didn’t show culprit lesion.

Figure 4: Pulmonary artery angiogram showing occlusion of right pulmonary artery.

Figure 5: Pulmonary artery angiogram showing occlusion of left pulmonary artery.