ACUTE PULMONARY EMBOLISM MIMICS ACUTE CORONARY SYNDROME IN OLDER PATIENT

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1 CASE REPORT ACUTE PULMONARY EMBOLISM MIMICS ACUTE CORONARY SYNDROME IN OLDER PATIENT Chun-Chieh Liu 1,2 *, Ta-Chuan Hung 1,2, Charles Jia-Yin Hou 1,2, Cheng-Ho Tsai 1,2,3 1 Cardiovascular Medicine, Department of Internal Medicine, Mackay Memorial Hospital, 2 Mackay Medicine, Nursing and Management College, and 3 School 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 or signs. Accurate diagnosis followed by effective therapy can reduce mortality. We report on a 67-year-old man who underwent lumbar laminectomy and developed an acute anterior compressive-like chest pain and jaw numbness rather than dyspnea on the fifth postoperative day. Owing to refractory chest pain with suspicious posterior myocardial infarction or unstable angina on surface electrocardiogram, the patient received emergency coronary catheterization, which demonstrated normal coronary arteries. Further investigation provided a final diagnosis of acute pulmonary embolism. Acute pulmonary embolism with simultaneous recent neurosurgery was a therapeutic dilemma because of the risk of postoperative hemorrhage threatening neurologic function. After treatment with enoxaparin and close monitoring of his neurologic condition, his symptoms were eliminated. Clinicians must keep in mind a differential diagnosis of pulmonary embolism in a postoperative high-risk patient. [International Journal of Gerontology 2009; 3(4): ] Key Words: acute coronary syndrome, laminectomy, pulmonary embolism Introduction Acute pulmonary embolism (PE) is a life-threatening disease, which mostly results from deep venous thrombi of lower extremities. The symptoms and signs are vague and similar to many other diseases. Here, we describe an elderly patient who developed typical symptoms and objective findings of acute coronary syndrome after a neurologic operation. Despite an initial electrocardiogram (ECG) suggestive of posterior myocardial infarction (MI) or unstable angina (UA), his coronary arteries were patent on coronary angiography. Further examinations showed the presence of acute PE. The *Correspondence to: Dr Chun-Chieh Liu, Cardiovascular Medicine, Department of Internal Medicine, Mackay Memorial Hospital, 92, Section 2, Chung- Shan North Road, Taipei 10449, Taiwan. jasonliu0528@pchome.com.tw Accepted: March 10, 2009 usefulness of bedside echocardiography should be considered to distinguish acute coronary syndrome from PE in these patients. Case Report A 67-year-old man, a current smoker, was admitted because of progressive low back pain with gait disability for at least 1 year. A review of past medical illness revealed gout and hypercholesterolemia for the previous 3 months. A series of examinations demonstrated third to fourth lumbar spondylolisthesis and third to fifth lumbar spinal stenosis. He underwent surgery of lumbar laminectomy, posterior fusion with bone graft and internal fixation 4 days after admission. The course of operation was smooth. He was advised to ambulate 5 days later. However, he developed acute onset of anterior heaviness-like chest pain, jaw numbness and cold sweating after urination on the same day. International Journal of Gerontology December 2009 Vol 3 No Elsevier.

2 C.C. Liu et al The symptoms could not be relieved by rest. Physical examination revealed a heart rate of 106/min, respiratory rate of 22/min, blood pressure of 100/62 mmhg, and room air oxygen saturation of 93% by pulse oximetry. The breathing sounds were clear, but the heart sound displayed a 3/6 grade blowing mid-systolic murmur at the fifth intercostal space near the sternum. There was no ankle edema. An ECG taken immediately showed sinus tachycardia with new onset of ST depression without T wave inversion at V1 to V6 (R/S > 1 at V1 2) and a S 1 Q 3 T 3 pattern (Figure 1A). Initially, acute posterior MI or UA was suspected. A thrombolytic agent was not indicated owing to his recent major operation. Because of refractory chest pain after morphine and sublingual nitroglycerin therapy, primary coronary catheterization was planned. Surprisingly, the coronary angiography showed normal coronary arteries, and left ventriculography displayed no wall motion abnormality (Figures 2A and 2B). The arterial blood gas analysis presented 129 mmhg of PaO 2 under 35% oxygen therapy without an acid-base imbalance. Because the patient had persistent chest pain and jaw numbness, an echocardiography was performed that demonstrated paradoxical ventricular septal wall motion and D-shaped left ventricle in cross section. A peak systolic pulmonary arterial pressure of 50 mmhg and a moderate tricuspid regurgitation were also found. It made us highly suspect acute PE. Right heart catheterization was planned immediately, which revealed a mean pulmonary arterial pressure of 45 mmhg. The pulmonary arteriography manifested multiple large filling defects in bilateral pulmonary arteries (Figure 2C). Acute PE was diagnosed, but emergency thrombolytic therapy was not administered because of relative stable hemodynamics and because the patient was recovering from a major operation. Anticoagulant (enoxaparin, 1 mg/kg) was given, and the patient was admitted to the intensive care unit for close monitoring of vital signs and neurologic condition. Further examinations included the lung ventilation perfusion scintigraphy, demonstrating multiple large perfusion 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 echogram revealed many thrombi in the bilateral femoral and popliteal veins. Chest pain/tightness, jaw numbness and tachycardia were relieved 3 days after anticoagulant therapy. The follow-up ECG showed a remission of the ST depression and S 1 Q 3 T 3 pattern (Figure 1B). There was no elevated serum cardiac biomarker during hospitalization. According to the above-mentioned examinations, oral warfarin therapy was prescribed for 3 months. There was no recurrence of PE after stopping anticoagulant therapy. Discussion Acute PE is a common disease and has a high mortality rate of nearly 30% without therapy. Mortality can be reduced by accurate diagnosis followed by effective anticoagulant therapy. Because of nonspecific manifestations of acute PE, it can lead to an erroneous diagnosis and compromise the patient s outcome. The most common symptoms are dyspnea with or without exertion, pleuritic pain, and cough. The most common signs are tachypnea, tachycardia, and rales 1. In addition, the ECG is usually nonspecific, and around one-third of patients have normal findings. The common ECG findings of suspicious PE are sinus tachycardia, T wave inversion in precordial leads V1 through V4, and transient right bundle branch block. The S 1 Q 3 T 3 pattern also suggests PE and is found in around 50% of patients 2. Typical chest pain and jaw numbness rather than dyspnea combined with ECG ST depression (no T wave inversion) in the precordial lead, which mimics acute coronary syndrome, was rarely reported. We present an elderly patient who had received lumbar laminectomy and developed acute PE on the fifth postoperative day with an initial impression of acute posterior MI or UA. The identifiable risk factors of acute PE include immobilization, stroke, paresis, surgery in the past 3 months, paralysis, malignancy, history of venous thromboembolism, central venous instrumentation in the past 3 months, and chronic heart disease 1,3 5. In women, risk factors such as obesity (body mass index > 29 kg/m 2 ), heavy cigarette smoking (> 25 cigarettes/ day), and hypertension have also been identified 6. Laminectomies were rarely reported to cause PE 7. For our patient, the probable etiologies of acute PE were immobility during operation and chronic tobacco use. Interestingly, he experienced typical anterior compressive-like chest pain associated with jaw numbness and cold sweating rather than dyspnea that made us highly suspect posterior MI or UA on ECG presentation. Thrombolytic therapy was postponed because of a high risk of postoperative hemorrhage threatening neurologic impairment. Primary coronary catheterization was only indicated in this emergent 252 International Journal of Gerontology December 2009 Vol 3 No 4

(B) Follow-up ECG showing normal sinus rhythm with remission of ST depression and S 1 Q 3 T 3 pattern. situation. There were no critical obstructive coronary diseases on coronary angiogram.

3 Acute PE Mimicking Acute Coronary Syndrome A B Figure 1. (A) Electrocardiogram (ECG) showing sinus tachycardia with new onset of ST depression without T wave inversion at V1 to V6 (arrow sites) and a S 1 Q 3 T 3 pattern. (B) Follow-up ECG showing normal sinus rhythm with remission of ST depression and S 1 Q 3 T 3 pattern. situation. There were no critical obstructive coronary diseases on coronary angiogram. Could we have made a more accurate diagnosis before the angiogram was performed? On reviewing the course of management, cardiac ultrasound could have contributed to a differential diagnosis in such patients. Early thrombolysis is a guideline for saving lives in those with ST elevation during International Journal of Gerontology December 2009 Vol 3 No 4 253

C.C. Liu et al A B C Figure 2. (A) Left coronary angiography showing normal left coronary arteries. (B) Right coronary angiography showing normal right coronary artery.

The common echocardiographic signs of PE are an enlarged right ventricle, paradoxical ventricular septal wall motion, the McConnell sign (right ventricle, free wall hypokinesis with sparing of the

For our patient, although the presentation of the McConnell sign was lacking, which had been described in instances of massive PE 8, paradoxical ventricular septal wall motion made us highly suspect

4 C.C. Liu et al A B C Figure 2. (A) Left coronary angiography showing normal left coronary arteries. (B) Right coronary angiography showing normal right coronary artery. (C) Pulmonary arteriography showing multiple large filling defects in bilateral pulmonary arteries (arrows). MI, but is not recommended in non-high-risk patients of PE. The common echocardiographic signs of PE are an enlarged right ventricle, paradoxical ventricular septal wall motion, the McConnell sign (right ventricle, free wall hypokinesis with sparing of the apex), and pulmonary hypertension with a tricuspid regurgitant jet velocity > 2.6 m/sec. For our patient, although the presentation of the McConnell sign was lacking, which had been described in instances of massive PE 8, paradoxical ventricular septal wall motion made us highly suspect acute PE. With relatively stable hemodynamics, anticoagulant therapy was the first-priority aim, followed by closely monitoring the neurologic condition. On the other hand, if massive acute PE with right ventricular dysfunction occurred, surgical embolectomy or percutaneous mechanical thrombectomy were considered as therapeutic alternatives 9. Pneumatic compression stocking prophylaxis is an alternative means and can effectively decrease the incidence of deep venous thrombosis and PE in high-risk patients undergoing multilevel lumbar laminectomies with instrumented fusions 10. Finally, our patient was strongly advised to abstain from smoking and warfarin was administered for 3 months according to the guideline 11. Although the initial management of acute coronary syndrome and PE may be similar, some critical conditions are different. For example, thrombolysis is the first-line therapy in high-risk PE with cardiogenic shock and persistent hypotension. Administration within 48 hours of symptom onset is associated with the greatest benefit 12, but it can still be effective 6 14 days after onset of symptoms 13. However, thrombolytic therapy is indicated in patients with ST elevation MI within 12 hours of symptoms onset. Besides, low molecular weight heparin only cannot be effective for high-risk PE with unstable hemodynamics 11. Those with PE would need anticoagulation therapy for at least 3 months, but it is not a standard therapy with MI. 254 International Journal of Gerontology December 2009 Vol 3 No 4

5 Acute PE Mimicking Acute Coronary Syndrome In conclusion, this case report suggests that acute PE mimicking acute coronary syndrome may develop in elderly patients undergoing major operations with multiple atherosclerotic risk factors. Despite that ECG is unreliable for diagnosis of acute PE, it can show the initial presentation of a right ventricle strain, and further investigation is necessary to differentiate the diagnosis. We emphasize that doctors must evaluate PE in all patients suffering from typical chest pain with ischemic ECG changes. References 1. Stein PD, Beemath A, Matta F, et al. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med 2007; 120: Ferrari E, Imbert A, Chevalier T, et al. The ECG in pulmonary embolism: predictive value of negative T waves in precordial leads: 80 case reports. Chest 1997; 111: The PIOPED investigators. Value of the ventilation/ perfusion scan in acute pulmonary embolism: results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA 1990; 263: Darze ES, Latado AL, Guimaraes AG, et al. Incidence and clinical predictors of pulmonary embolism in severe heart failure patients admitted to a coronary care unit. Chest 2005; 128: Heit JA, O Fallon WM, Petterson TM, et al. Relative impact of risk factors for deep vein thrombosis and pulmonary embolism: a population-based study. Arch Intern Med 2002; 162: Pulido T, Aranda A, Zevallos MA, et al. Pulmonary embolism as a cause of death in patients with heart disease: an autopsy study. Chest 2006; 129: Kolilekas L, Gallis P, Liasis N, et al. Unusual case of pulmonary hypertension. Respiration 2006; 73: McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol 1996; 78: Eid-Lidt G, Gaspar J, Sandoval J, et al. Combined clot fragmentation and aspiration in patients with acute pulmonary embolism. Chest 2008; 134: Epstein NE. Efficacy of pneumatic compression stocking prophylaxis in the prevention of deep venous thrombosis and pulmonary embolism following 139 lumbar laminectomies with instrumented fusions. J Spinal Disord Tech 2006; 19: Torbicki A, Perrier A, Konstantinides S, et al. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J 2008; 29: Ly B, Arnesen H, Eie H, et al. A controlled clinical trial of streptokinase and heparin in the treatment of major pulmonary embolism. Acta Med Scand 1978; 203: Daniels LB, Parker JA, Patel SR, et al. Relation of duration of symptoms with response to thrombolytic therapy in pulmonary embolism. Am J Cardiol 1997; 80: International Journal of Gerontology December 2009 Vol 3 No 4 255

Dr. Rami M. Adil Al-Hayali Assistant Professor in Medicine

Dr. Rami M. Adil Al-Hayali Assistant Professor in Medicine Venous thromboembolism: pulmonary embolism (PE) deep vein thrombosis (DVT) 1% of all patients admitted to hospital 5% of in-hospital mortality