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Introduction

Acute pulmonary embolism (PE) is a life-threateningdisease, which mostly results from deep venous thrombiof lower extremities. The symptoms and signs are vagueand similar to many other diseases. Here, we describean elderly patient who developed typical symptomsand objective findings of acute coronary syndromeafter a neurologic operation. Despite an initial electro-cardiogram (ECG) suggestive of posterior myocardialinfarction (MI) or unstable angina (UA), his coronaryarteries were patent on coronary angiography. Furtherexaminations showed the presence of acute PE. The

usefulness of bedside echocardiography should be con-sidered to distinguish acute coronary syndrome fromPE in these patients.

Case Report

A 67-year-old man, a current smoker, was admittedbecause of progressive low back pain with gait disabil-ity for at least 1 year. A review of past medical illnessrevealed gout and hypercholesterolemia for the previ-ous 3 months. A series of examinations demonstratedthird to fourth lumbar spondylolisthesis and third tofifth lumbar spinal stenosis. He underwent surgery oflumbar laminectomy, posterior fusion with bone graftand internal fixation 4 days after admission. The courseof operation was smooth. He was advised to ambulate5 days later. However, he developed acute onset ofanterior heaviness-like chest pain, jaw numbness and cold sweating after urination on the same day.

ACUTE PULMONARY EMBOLISM MIMICS ACUTE

CORONARY SYNDROME IN OLDER PATIENT

Chun-Chieh Liu1,2*, Ta-Chuan Hung1,2, Charles Jia-Yin Hou1,2, Cheng-Ho Tsai1,2,3

1Cardiovascular Medicine, Department of Internal Medicine, Mackay Memorial Hospital, 2Mackay Medicine, Nursing and Management College, and 3School of Medicine, Taipei Medical University, Taipei, Taiwan.

SUMMARY

Acute pulmonary embolism is a fatal disease and an often missed diagnosis. There are no specific symptoms orsigns. Accurate diagnosis followed by effective therapy can reduce mortality. We report on a 67-year-old manwho underwent lumbar laminectomy and developed an acute anterior compressive-like chest pain and jawnumbness rather than dyspnea on the fifth postoperative day. Owing to refractory chest pain with suspiciousposterior myocardial infarction or unstable angina on surface electrocardiogram, the patient received emer-gency coronary catheterization, which demonstrated normal coronary arteries. Further investigation provideda final diagnosis of acute pulmonary embolism. Acute pulmonary embolism with simultaneous recent neuro-surgery was a therapeutic dilemma because of the risk of postoperative hemorrhage threatening neurologicfunction. After treatment with enoxaparin and close monitoring of his neurologic condition, his symptoms wereeliminated. Clinicians must keep in mind a differential diagnosis of pulmonary embolism in a postoperativehigh-risk patient. [International Journal of Gerontology 2009; 3(4): 251–255]

Key Words: acute coronary syndrome, laminectomy, pulmonary embolism

■ CASE REPORT

© 2009 Elsevier.

251

*Correspondence to: Dr Chun-Chieh Liu, Cardiovas-cular Medicine, Department of Internal Medicine,Mackay Memorial Hospital, 92, Section 2, Chung-Shan North Road, Taipei 10449, Taiwan.E-mail: jasonliu0528@pchome.com.twAccepted: March 10, 2009

The symptoms could not be relieved by rest. Physicalexamination revealed a heart rate of 106/min, respiratoryrate of 22/min, blood pressure of 100/62 mmHg, androom air oxygen saturation of 93% by pulse oximetry.The breathing sounds were clear, but the heart sounddisplayed a 3/6 grade blowing mid-systolic murmur atthe fifth intercostal space near the sternum. There wasno ankle edema. An ECG taken immediately showedsinus tachycardia with new onset of ST depressionwithout T wave inversion at V1 to V6 (R/S > 1 at V1–2)and a S1Q3T3 pattern (Figure 1A). Initially, acute posteriorMI or UA was suspected. A thrombolytic agent was notindicated owing to his recent major operation. Becauseof refractory chest pain after morphine and sublingualnitroglycerin therapy, primary coronary catheterizationwas planned. Surprisingly, the coronary angiographyshowed normal coronary arteries, and left ventriculog-raphy displayed no wall motion abnormality (Figures2A and 2B). The arterial blood gas analysis presented129 mmHg of PaO2 under 35% oxygen therapy withoutan acid-base imbalance. Because the patient had per-sistent chest pain and jaw numbness, an echocardiog-raphy was performed that demonstrated paradoxicalventricular septal wall motion and D-shaped left ven-tricle in cross section. A peak systolic pulmonary arte-rial pressure of 50 mmHg and a moderate tricuspidregurgitation were also found. It made us highly sus-pect acute PE. Right heart catheterization was plannedimmediately, which revealed a mean pulmonary arte-rial pressure of 45 mmHg. The pulmonary arteriographymanifested multiple large filling defects in bilateral pul-monary arteries (Figure 2C). Acute PE was diagnosed, butemergency thrombolytic therapy was not administeredbecause of relative stable hemodynamics and becausethe patient was recovering from a major operation.Anticoagulant (enoxaparin, 1 mg/kg) was given, and thepatient was admitted to the intensive care unit for closemonitoring of vital signs and neurologic condition.Further examinations included the lung ventilation–perfusion scintigraphy, demonstrating multiple largeperfusion defects in bilateral lobes compatible with a high probability of PE. The D-dimer level was as high as 5,108 ng/mL. The peripheral venous echogramrevealed many thrombi in the bilateral femoral andpopliteal veins. Chest pain/tightness, jaw numbness andtachycardia were relieved 3 days after anticoagulanttherapy. The follow-up ECG showed a remission of theST depression and S1Q3T3 pattern (Figure 1B). Therewas no elevated serum cardiac biomarker during

hospitalization. According to the above-mentionedexaminations, oral warfarin therapy was prescribed for3 months. There was no recurrence of PE after stoppinganticoagulant therapy.

Discussion

Acute PE is a common disease and has a high mortal-ity rate of nearly 30% without therapy. Mortality canbe reduced by accurate diagnosis followed by effectiveanticoagulant therapy. Because of nonspecific manifes-tations of acute PE, it can lead to an erroneous diagno-sis and compromise the patient’s outcome. The mostcommon symptoms are dyspnea with or without exer-tion, pleuritic pain, and cough. The most common signsare tachypnea, tachycardia, and rales1. In addition,the ECG is usually nonspecific, and around one-thirdof patients have normal findings. The common ECGfindings of suspicious PE are sinus tachycardia, T waveinversion in precordial leads V1 through V4, and tran-sient right bundle branch block. The S1Q3T3 pattern alsosuggests PE and is found in around 50% of patients2.Typical chest pain and jaw numbness rather than dys-pnea combined with ECG ST depression (no T waveinversion) in the precordial lead, which mimics acutecoronary syndrome, was rarely reported. We presentan elderly patient who had received lumbar laminec-tomy and developed acute PE on the fifth postopera-tive day with an initial impression of acute posteriorMI or UA. The identifiable risk factors of acute PEinclude immobilization, stroke, paresis, surgery in thepast 3 months, paralysis, malignancy, history of venousthromboembolism, central venous instrumentation inthe past 3 months, and chronic heart disease1,3–5. Inwomen, risk factors such as obesity (body mass index> 29 kg/m2), heavy cigarette smoking (> 25 cigarettes/day), and hypertension have also been identified6.Laminectomies were rarely reported to cause PE7. For our patient, the probable etiologies of acute PEwere immobility during operation and chronic to-bacco use. Interestingly, he experienced typical ante-rior compressive-like chest pain associated with jawnumbness and cold sweating rather than dyspnea thatmade us highly suspect posterior MI or UA on ECGpresentation. Thrombolytic therapy was postponedbecause of a high risk of postoperative hemorrhagethreatening neurologic impairment. Primary coronarycatheterization was only indicated in this emergent

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situation. There were no critical obstructive coronarydiseases on coronary angiogram. Could we have madea more accurate diagnosis before the angiogram wasperformed?

On reviewing the course of management, cardiacultrasound could have contributed to a differential diag-nosis in such patients. Early thrombolysis is a guide-line for saving lives in those with ST elevation during

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A

B

Figure 1. (A) Electrocardiogram (ECG) showing sinus tachycardia with new onset of ST depression without T wave inversion atV1 to V6 (arrow sites) and a S1Q3T3 pattern. (B) Follow-up ECG showing normal sinus rhythm with remission of ST depressionand S1Q3T3 pattern.

MI, but is not recommended in non-high-risk patientsof PE. The common echocardiographic signs of PE arean enlarged right ventricle, paradoxical ventricular sep-tal wall motion, the McConnell sign (right ventricle,free wall hypokinesis with sparing of the apex), andpulmonary hypertension with a tricuspid regurgitantjet velocity > 2.6 m/sec. For our patient, although thepresentation of the McConnell sign was lacking, whichhad been described in instances of massive PE8, para-doxical ventricular septal wall motion made us highlysuspect acute PE. With relatively stable hemodynamics,anticoagulant therapy was the first-priority aim, fol-lowed by closely monitoring the neurologic condition.On the other hand, if massive acute PE with right ven-tricular dysfunction occurred, surgical embolectomyor percutaneous mechanical thrombectomy were con-sidered as therapeutic alternatives9. Pneumatic com-pression stocking prophylaxis is an alternative meansand can effectively decrease the incidence of deep

venous thrombosis and PE in high-risk patients under-going multilevel lumbar laminectomies with instru-mented fusions10. Finally, our patient was stronglyadvised to abstain from smoking and warfarin wasadministered for 3 months according to the guideline11.

Although the initial management of acute coro-nary syndrome and PE may be similar, some criticalconditions are different. For example, thrombolysis isthe first-line therapy in high-risk PE with cardiogenicshock and persistent hypotension. Administration within48 hours of symptom onset is associated with the great-est benefit12, but it can still be effective 6–14 days afteronset of symptoms13. However, thrombolytic therapyis indicated in patients with ST elevation MI within 12 hours of symptoms onset. Besides, low molecularweight heparin only cannot be effective for high-riskPE with unstable hemodynamics11. Those with PE wouldneed anticoagulation therapy for at least 3 months,but it is not a standard therapy with MI.

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A B

C

Figure 2. (A) Left coronary angiography showing normal leftcoronary arteries. (B) Right coronary angiography showing nor-mal right coronary artery. (C) Pulmonary arteriography showingmultiple large filling defects in bilateral pulmonary arteries(arrows).

In conclusion, this case report suggests that acutePE mimicking acute coronary syndrome may developin elderly patients undergoing major operations withmultiple atherosclerotic risk factors. Despite that ECGis unreliable for diagnosis of acute PE, it can show the initial presentation of a right ventricle strain, andfurther investigation is necessary to differentiate thediagnosis. We emphasize that doctors must evaluatePE in all patients suffering from typical chest pain withischemic ECG changes.

References

1. Stein PD, Beemath A, Matta F, et al. Clinical characteris-tics of patients with acute pulmonary embolism: datafrom PIOPED II. Am J Med 2007; 120: 871–9.

2. Ferrari E, Imbert A, Chevalier T, et al. The ECG in pul-monary embolism: predictive value of negative T wavesin precordial leads: 80 case reports. Chest 1997; 111:537–43.

3. The PIOPED investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism: resultsof the prospective investigation of pulmonary embolismdiagnosis (PIOPED). JAMA 1990; 263: 2753–9.

4. Darze ES, Latado AL, Guimaraes AG, et al. Incidence andclinical predictors of pulmonary embolism in severeheart failure patients admitted to a coronary care unit.Chest 2005; 128: 2576–80.

5. Heit JA, O’Fallon WM, Petterson TM, et al. Relative impactof risk factors for deep vein thrombosis and pulmonary

embolism: a population-based study. Arch Intern Med2002; 162: 1245–8.

6. Pulido T, Aranda A, Zevallos MA, et al. Pulmonaryembolism as a cause of death in patients with heart disease: an autopsy study. Chest 2006; 129: 1282–7.

7. Kolilekas L, Gallis P, Liasis N, et al. Unusual case ofpulmonary hypertension. Respiration 2006; 73: 117–9.

8. McConnell MV, Solomon SD, Rayan ME, et al. Regionalright ventricular dysfunction detected by echocardiog-raphy in acute pulmonary embolism. Am J Cardiol 1996;78: 469–73.

9. Eid-Lidt G, Gaspar J, Sandoval J, et al. Combined clotfragmentation and aspiration in patients with acutepulmonary embolism. Chest 2008; 134: 54–60.

10. Epstein NE. Efficacy of pneumatic compression stockingprophylaxis in the prevention of deep venous throm-bosis and pulmonary embolism following 139 lumbarlaminectomies with instrumented fusions. J Spinal DisordTech 2006; 19: 28–31.

11. Torbicki A, Perrier A, Konstantinides S, et al. Guidelineson the diagnosis and management of acute pulmonaryembolism: the Task Force for the Diagnosis andManagement of Acute Pulmonary Embolism of theEuropean Society of Cardiology (ESC). Eur Heart J 2008;29: 2276–315.

12. Ly B, Arnesen H, Eie H, et al. A controlled clinical trial ofstreptokinase and heparin in the treatment of majorpulmonary embolism. Acta Med Scand 1978; 203:465–70.

13. Daniels LB, Parker JA, Patel SR, et al. Relation of durationof symptoms with response to thrombolytic therapy inpulmonary embolism. Am J Cardiol 1997; 80: 184–8.

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