By Nestico, Pasquale F Cassimatis, Dimitri C; Sheikh, Fareed; Huber, Michael; Davison, Jonathan; Modlin, Randolph
ABSTRACT Objective: We present a soldier with a pulmonary embolism presenting with syncope during an ischemic stress test, subsequently found to have normal coronary arteries (CA). case: A 49- year-old soldier had 3 months history of exertional chest pain, shortness of breath, syncope, and malaise. He passed out during a stress echocardiogram and had a positive troponin level. A subsequent cardiac catheterization revealed normal CA but with mild hypokinesis of the distal anterior wall with a left ventricular ejection fraction of 44%. A subsequent nuclear ventilation- perfusion scan was consistent with bilateral pulmonary embolism. Results: A Doppler ultrasound revealed thrombosis in the distal superficial femoral vein of the left leg. Hypercoagulable state markers were normal. Conclusion: This case demonstrates that a pulmonary embolism could express itself as an ST depression myocardial ischemic event perhaps by affecting the coronary flow to the left anterior descending CA. INTRODUCTION
Nondiagnosed pulmonary embolism (PE) carries a high mortality rate.1,2 In the International Cooperative Pulmonary Embolism Registry of 2,554 patients, the overall cumulative mortality due to PE was 17.4% at 3 months.1 Acute PE has been reported in a patient with normal coronary arteries (CA).2
The diagnosis of PE is rendered difficult by a clinical presentation that may be subtle and may mimic other cardiopulmonary illnesses.3 In a study of a total of over 135 million passengers from 145 countries, of whom 56 had confirmed severe PE associated with air travel, suspicion of PE was based on the presence of one or more of the following clinical criteria: malaise, dyspnea, syncope, or chest pain.4 Our patient had all four symptoms and pulmonary hypertension by echocardiography, which is a relatively common serious complication of PE.5 He also had an ischemic exercise electrocardiogram (ECG) (Fig. 1) with elevated troponin level. The troponin probably resulted from a severely compromised coronary perfusion as a result of an acute PE.6 In fact, even before he passed out while on the treadmill, his rhythm strip showed ischemia/ injury (Fig. IB). After he passed out, while supine in the recovery phase, his heart rate (HR) increased from a junctional rhythm of 48 beats per minute (bpm) with ventricular and atrial ectopies to a sinus tachycardia of 138 bpm with global ST segment changes (Fig. 1, C-E). Eventually, the tachycardia and all pathologic ECG signs slowly resolved (Fig. 1, F-H). We believe that all these clinical and electrocardiographic events occurred as a result of an acute embolie event superimposed on chronic PE.
CASE REPORT
A 49-year-old Caucasian male soldier, without previous history of cardiovascular problems, was referred to Landstuhl Regional Medical Center (Germany), for evaluation of possible ischemia. An initial clinical work-up revealed a history of malaise, exertional dyspnea, chest pain, and one episode of syncope. He also described left leg swelling. His risks for CA disease included a 3-year history of smoking and an abnormal untreated lipid profile. He then underwent an exercise treadmill test. The study was terminated when the patient began complaining of dyspnea and dizziness which was shortly followed by syncope while on the treadmill. At that point, the ECG showed junctional bradycardia with ventricular and atrial ectopies, followed, seconds later, by sinus tachycardia (HR = 138 bpm), a 1.1- mm ST segment elevation hi leads augmented vector right (aVR), augmented vector left (aVL), Vl, and V2 and a 2.2-mm downsloping ST segment depression in the other leads (Fig. 1). The patient was transferred to the coronary care unit. Under observation, he remained hemodynamically stable. After his cardiac enzyme determinations demonstrated an elevated troponin I level on the third set, he underwent cardiac catheterization which revealed normal coronary circulation with hypokinesis of the distal anterior wall and a mildly reduced left ventricular (LV) ejection fraction (LVEF) of 44%. At this point, antianginal therapy was discontinued. An admission chest x-ray was normal, A prestress test, technically adequate, echocardiogram/ Doppler revealed a normal LV systolic function (LVEF = 68%), mild LV hypertrophy, mild biatrial enlargement, mild mitral regurgitation, bicuspid regurgitation and aortic insufficiency, mild pulmonary hypertension with a right ventricular (RV) systolic pressure of 45 mm Hg. Pulmonary function test was normal but a ventilation perfusion scintigraphy was consistent with bilateral pulmonary emboli (Fig. 2).
A Doppler venous ultrasound of lower extremities revealed thrombosis in the distal superficial femoral vein of the left leg. He was transferred to Walter Reed Army Medical Center (United States) on 90 mg of enoxaparin subcutaneously twice a day and anticipated systemic anticoagulation for a period of 6 months. At WRAMC, a repeat cardiac catheterization was performed to clarify ostium patency of the right CA. It showed normal coronaries and also a normal LV systolic function.
DISCUSSION
At present, more than 30 years after the experimental studies of Mclntyre and Sasahara,7 RV dysfunction and failure is widely accepted to be the single most important determinant of outcome during acute PE. Since then, several carefully designed cohort studies,8″11 prospective randomized therapeutic trials,12,13 and registries1,14,15 have significantly improved understanding of the clinical course and prognosis of this disease. Currently, the accepted diagnostic algorithm is integrated and includes a methodical history and physical examination supplemented by selective laboratory and radiological testing with chest radiography, ventilation perfusion scanning, helical computed tomography, and pulmonary angiography, the gold standard.6 However, it seems fair to say that physicians need to have a higher index of suspicion for PE when confronted with a patient in the proper clinical setting and that dyspnea, chest pain, and/or syncope may not be due to CA disease. In fact, the majority of preventable deaths associated with pulmonary embolie disease can be ascribed to a missed diagnosis, as was the case for our patient rather than to a failure of existing therapies.6,16 Studies over the years have shown the ECG to be both nonspecific and lacking in sensitivity. Different investigators have reported variable parameters as the most frequent pathologic ECG sign of PE (Table I).17-22 Recently, however, ECG has been described as a useful, inexpensive, and readily available tool for assessing the patient’s prognosis and for guiding further diagnostic work-up.23
Our patient is unique in that the diagnosis of PE was ascertained 3 months after he began to have symptoms (malaise, exertional chest pain, dyspnea, and syncope) and a sign (unilateral leg swelling while in Iraq), as well as an exercise treadmill test consistent with ischemia/injury and subsequent normal coronary angiography. As it can be appreciated, Figure 1, A-H, shows-in a vivid way-the sequence of events. These dramatic serial ECG changes raise, in our opinion, several issues.
First, global significant ST changes with ventricular and atrial arrhythmia and junctional bradycardia together with an elevated troponin I level, LV regional wall motion abnormality, and a depressed LVEF suggest that this ominous clinical picture, never described before, was more a result of LV rather than RV ischemia/ infarction.
Second, it can be speculated that PE (acute superimposed on chronic PE since his symptoms began 3 months before) decreased cardiac output which resulted in diminished LV preload, concomitant hypoxemia, and systemic hypotension (his blood pressure was not measured for 4 minutes and 20 seconds, perhaps because the time was spent to get the patient off the treadmill belt and onto the floor). That, in turn, specifically affected coronary flow to the left anterior descending (LAD) CA and reduced oxygen supply even in a patient with normal CA. Impaired flow throughout the left coronary microcirculation could explain a significant decrease of oxygen delivery to the myocardium supplied by the LAD CA, resulting in LV myocardial ischemia/injury.24 Paradoxical embolization of the LAD CA with a thromboembolus via a patent foramen ovale was echocardiographically excluded. Increased concentration of cardiac troponin I was reported to portend an adverse prognosis for patients with acute PE.25
Third, the present case dramatically confirms that PE must be included in the differential diagnosis of acute coronary syndrome. It shows novel pathologic ECG markers of PE, namely global ST segment changes, ventricular ectopic activities, and junctional bradycardia. It also demonstrates that PE can cause LV injury possibly independent of RV infarction. This phenomenon may, perhaps, be called the “ventricular noninterdependency.”
Finally, the role of suspicion in the diagnosis of PE remains today stronger than ever before.
Landstuhl Regional Army Medical Center, Landstuhl, Germany.
This manuscript was received for review in October 2006. The revised manuscript was accepted for publication in April 2008.
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LTC Pasquale F. Nestico, MC USA; MAJ Dimitri C. Cassimatis, MC USA; Capt Fareed Sheikh, USAF MC; MAJ Michael Huber, MC USA; CPT Jonathan Davison, MC USA; COL Randolph Modlin, MC USA
Copyright Association of Military Surgeons of the United States Jul 2008
(c) 2008 Military Medicine. Provided by ProQuest Information and Learning. All rights Reserved.
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