Nonoperative Treatment of Acute Pulmonary Embolism



Nonoperative Treatment of Acute Pulmonary Embolism



Tod C. Engelhardt


Pulmonary embolism (PE) is a serious and potentially life-threatening condition afflicting a broad spectrum of the population. It has been reported that approximately 600,000 patients experience a PE episode each year in the United States. Mortality rate exceeds 15% in the first 3 months after diagnosis, surpassing that of myocardial infarction. The majority of deaths from acute PE result from right ventricular (RV) pressure overload and subsequent RV failure. As long as their RV dysfunction persists, these patients are at risk for proceeding into hemodynamic compromise, cardiogenic shock, and death. Acute PE represents a spectrum of clinical syndromes with a variety of prognostic implications based on three distinct categories: minor, submassive, and massive.



Risk Stratification


Patients with minor PE present with small clots in the distal pulmonary vessels, pleuritic chest pain, mild tachycardia, and possibly hemoptysis, with normal systemic arterial blood pressure and no evidence of right heart dysfunction. These patients have an excellent prognosis with therapeutic anticoagulation alone.


Patients with submassive PE present with thrombosis usually in one or both of the left and right pulmonary arteries, hemodynamic compensation, and maintenance of adequate systolic arterial blood pressure, albeit with of right RV dysfunction identified by one or more clinical signs detectable on physical examination, electrocardiography, biomarker tests, echocardiography, and chest computed tomography (Box 1). These patients carry an increased risk for adverse events and early mortality.



BOX 1   Clinical Signs of Right Ventricular Dysfunction






Massive PE characterizes patients who present with severe right heart dysfunction, syncope, systemic arterial hypotension, cardiogenic shock, or cardiac arrest. Consequently, they have the highest mortality rate.


Minor PE represents 55% of occurrences and submassive and massive PEs represent 40% and 5% of occurrences, respectively. In the International Cooperative Pulmonary Embolism Registry (ICOPER), the 90-day mortality rate was 15%, 22%, and 58% for minor, submassive, and massive PE, respectively. Patients with massive PE are routinely treated using aggressive strategies, and those with submassive PE are treated conservatively. However, data have shown poor prognosis associated with RV dysfunction (characteristic of submassive PE), thus prompting the need to consider advanced treatment strategies for this group of patients.



Treatment Strategies


Therapeutic anticoagulation with immediate parenteral anticoagulants followed by oral agents is the cornerstone of therapy for acute PE. However, although the majority of acute PE patients have a benign clinical course with standard therapeutic anticoagulation alone, patients with massive and submassive PE remain at increased risk for adverse clinical events, including RV failure and hemodynamic collapse.


The major limitation associated with systemic anticoagulation is that endogenous fibrinolysis may often be incomplete; up to 33% of the patients have ongoing RV dysfunction at 7 days after onset of treatment.


In patients with submassive PE and patients in extremis from massive PE, more aggressive treatment including thrombolysis and mechanical thrombectomy may be warranted to rapidly restore pulmonary blood flow and prevent death. An added benefit of advanced therapy is to prevent long-term sequelae (chronic pulmonary hypertension and RV failure). Options for advanced therapy include peripherally administered systemic fibrinolysis, catheter-directed local fibrinolysis, catheter-directed (mechanical or pharmacomechanical) thrombectomy, and inferior vena cava (IVC) filter insertion. An IVC filter, of course, is inserted to prevent further embolization of thrombotic material into the pulmonary circulation and not to remove the existing embolus.



Systemic Fibrinolysis


In 1987, recombinant tissue plasminogen inhibitor (rt-PA) was first approved by the U.S. Food and Drug Administration (FDA) for treatment of acute myocardial infarction, followed by approvals in 1990 and 1996 for treatment of massive pulmonary embolism and ischemic stroke, respectively. Specifically, the FDA has approved a dosage of 100 mg alteplase (Activase, Genentech, Inc., South San Francisco, CA) infused continuously over 2 hours for fibrinolysis of acute massive PE. The 2008 American College of Chest Physicians (ACCP) Evidence-Based Clinical Practice Guidelines recommend fibrinolysis for patients with evidence of hemodynamic compromise unless there are major contraindications related to bleeding risk (Grade 1B). The Guidelines caution against delays in administration of fibrinolysis in massive PE patients and warn that procrastination can result in irreversible cardiogenic shock. Fibrinolysis for submassive PE remains controversial because of a lack of conclusive randomized, controlled trials. The guidelines include fibrinolysis as an option for submassive PE patients with a low risk of bleeding (Grade 2B).


Optimal administration of fibrinolytic therapy requires careful consideration of indications and contraindications to maximize benefit and minimize risk. Numerous contraindications to fibrinolytic administration and concerns for major bleeding complications, particularly intracranial hemorrhage, contribute to low utilization of fibrinolysis for acute PE. An analysis from the ICOPER showed a 22% risk of major bleeding complications and a 3% risk of intracranial hemorrhage. These findings prompted the need for development of advanced therapeutic options that will effectively reduce the clot burden and relieve clinical symptoms with a minimized risk of bleeding.

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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Nonoperative Treatment of Acute Pulmonary Embolism

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