A 60-year-old woman with a history of hypertension and tobacco use presents to the emergency room with complaints of shortness of breath for the last two hours. She has no history of heart disease and denies any recent chest pain. On arrival to the emergency room, her vital signs and pertinent physical exam are noted to be:
Respiratory Rate: 18 breaths per minute
Heart rate: 98 beats per minute
Blood pressure: 115/60 mmHg
O2 sat: 88% on room air
Physical exam:
General: Appears well, in no acute distress
CV: Regular rate and rhythm, Normally split S1, S2, No murmur or S3. JVP normal. Normal peripheral pulses. No carotid or abdominal bruits.
Pulmonary: Mildly labored breathing. Breath sounds throughout. No wheezes, rales or rhonchi.
Imaging:
EKG: Sinus rhythm, normal axis, no acute ST changes
Chest X-ray: no acute cardiopulmonary process.
CT pulmonary angiogram: Multiple scattered thrombi seen in the intermediate pulmonary arteries. No thrombus is seen in the main pulmonary arteries or right and left trunk. RV dimension appears larger in size compared to left.
She is started on a heparin drip, and you are contacted to further address the significance of the elevated troponin and BNP.
How would you advise the primary team?
Show Answer
The correct answer is: 2. The elevated biomarkers indicate that she is at increased risk of adverse outcomes and further monitoring is warranted
Discussion
Venous thromboembolism (VTE) is a common cardiovascular disease process that is responsible for over 250,000 hospitalizations annually in the United States.1 Acute pulmonary embolism (PE) is an entity of VTE that carries a high risk of morbidity and mortality. Previous literature characterized pulmonary embolism as massive, submassive, or low-risk based on angiographic burden and presence or lack of hemodynamic compromise. This approach, however, has fallen out of favor as a subset of hemodynamically stable patients previously identified as low-risk were found to have high adverse event rates.2-4
In 2011, an American Heart Association (AHA) committee released a consensus statement to provide standardized definitions and management of an acute PE.5 They found that biomarkers such as elevated troponins and BNP were often elevated in hemodynamically stable patients that were at increased for adverse outcomes from PEs.6-7 Elevated troponins can be seen in up to one-third of stable patients diagnosed with a pulmonary embolism and were an independent predictor of adverse outcomes, such as need for inotrope support, cardiopulmonary resuscitation, and 30-day mortality [OR, 24.1; 95% CI, 2.9 to 200].8-9 Similarly, elevated BNPs were a predictor of adverse outcomes, such as recurrent thromboembolic events and death from the PE, in hemodynamically stable patients.
10 With this information, the AHA committee re-categorized patients from low-risk to sub-massive pulmonary embolism based on the presence of abnormal biomarkers (BNP > 90 pg/ml, N-terminal pr-BNP > 500 pg/ml, troponin I > 0.4 ng/mL, or troponin T > 0.1 ng.mL).
The use of systemic thrombolytics remains a mainstay of therapy for patients with a massive pulmonary embolism despite a lack of evidence that thrombolytics provide a mortality benefit. More controversy exists over the use of systemic thrombolytics, and more recently catheter-directed thrombolytics, in the management of patients with submassive pulmonary embolism. The current guidelines do not advocate the upfront use of thrombolytics in patients with submassive pulmonary embolisms based only on elevated biomarkers. They do recommend close monitoring and using clinical acumen on when to use thrombolytics based on the overall clinical presentation of the patient with supporting imaging and biomarker data.
Our patient has a pulmonary embolism with elevated biomarkers and dilated right ventricle, but without hemodynamic compromise. She should be considered to have a sub-massive pulmonary embolism per the current guidelines and initial treatment with heparin is appropriate. Her elevated troponins and BNP, however, signify that she is at increased risk for an acute adverse outcome and further judicious monitoring is warranted.
References
Lloyd-Jones D, et al. Heart disease and stroke characteristics: 2010 update: a report from the American Heart Association. Circulation 2010;121:e46-e215.
Aujesky D, Obrosky DS, Stone RA, Auble TE, Perrier A, Cornuz J, Roy PM, Fine MJ. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med 2005;172:1041-1046.
Miller GA, Sutton GC, Kerr IH, Gibson RV, Honey M. Comparison of streptokinase and heparin in treatment of isolated acute massive pulmonary embolism. Br Med J 1971;2:681-684.
Kucher N, Rossi E, De Rosa M, Goldhaber SZ. Massive pulmonary embolism. Circulation 2006;113:577-582.
Jaff MR, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2011;123:1788-1830.
Becattini C, Vedovati MC, Agnelli G. Prognostic value of troponins in acute pulmonary embolism: a meta-analysis. Circulation 2007;116:427-433
Sanchez O, Trinquart L, Colombet I, Durieux P, Huisman MV, Chatellier G, Meyer G. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: a systematic review. Eur Heart J 2008;29:1569-1577
Meyer T, Binder L, Hruska N, Luthe H, Buchawlad AB. Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular strain. J Am Coll Cardiol 2000;36(5):1632
Pruszczyk P, et al. Cardiac troponin T monitoring identifies high-risk group of normotensive patients with acute pulmonary embolism. Chest 2003;123(6):1947
Sohne M, et al. Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism. J Thromb Haemost 2006;4(3):552.
Log in to MyACC
