A pulmonary embolism (PE) is a sudden blockage in a lung artery, typically caused by a blood clot that has traveled from elsewhere, often originating as a deep vein thrombosis (DVT) in the legs. Anticoagulants, or blood thinners, are prescribed to prevent the formation of these clots. For those who have experienced a PE or DVT, these drugs are standard long-term therapy to prevent recurrence. This article addresses the function and limitations of these medications and the risks of recurrence while on treatment.
How Anticoagulants Work
Anticoagulant medications function by interrupting the complex chain of chemical reactions in the blood known as the coagulation cascade. These drugs do not quickly dissolve existing clots; that is the role of specialized “clot-busting” drugs called thrombolytics. Instead, anticoagulants stabilize existing clots, preventing them from growing larger, and stop new clots from forming. This provides the body’s natural processes time to slowly reabsorb the existing clot material.
The two main categories of oral anticoagulants include Warfarin, a Vitamin K antagonist (VKA), and the Direct Oral Anticoagulants (DOACs), which include Factor Xa inhibitors and direct thrombin inhibitors. Warfarin acts indirectly by interfering with the liver’s production of several clotting factors that depend on Vitamin K. DOACs, such as rivaroxaban and apixaban, work more directly by targeting and inhibiting specific coagulation proteins like Factor Xa.
Why Breakthrough PEs Occur
It is possible to experience a new PE or DVT, often termed a “breakthrough” event, even while receiving therapeutic doses of anticoagulants. While these medications significantly reduce the risk of recurrence, the risk is not entirely eliminated. Studies indicate the recurrence risk on well-managed oral anticoagulation is approximately 2 per 100 patient-years. These breakthrough events often relate to issues with drug effectiveness or the underlying disease state.
Suboptimal drug levels are a major contributing factor to recurrence, stemming from several possibilities. A patient may have poor adherence to the prescribed regimen, or the medication dosage may be inappropriate for their body weight or kidney function. Warfarin levels, in particular, can be affected by drug-drug interactions, dietary changes, or inconsistent monitoring, leading to subtherapeutic blood levels that are too low to prevent clotting.
Underlying medical conditions can also overwhelm the protective effect of standard anticoagulation. The patient may have an aggressive, severe hypercoagulable state that promotes clotting despite the drug’s presence. Active cancer, for example, is a known cause of increased clotting risk that can make the standard anticoagulant dose insufficient. Certain genetic clotting disorders, like antiphospholipid syndrome, can similarly lead to recurrence even with compliant treatment.
Recognizing Symptoms of a Recurrence
Individuals on anticoagulant therapy who have a history of PE or DVT must be aware of the signs of a potential recurrence. Symptoms of a new PE are typically sudden in onset and require immediate medical attention. The most common symptom is sudden and unexplained shortness of breath, which may be mild or severe.
Chest pain is frequently experienced, often described as a sharp, stabbing sensation that worsens when taking a deep breath, known as pleuritic chest pain. Other symptoms that can indicate a PE include a rapid heart rate, lightheadedness, or fainting. A cough, sometimes producing blood, may also occur.
Recurrent DVT may present with a return of symptoms in the leg, such as swelling, pain, warmth, or tenderness. Because a recurrent PE can be fatal, it is imperative to seek emergency medical care immediately if any of these warning signs appear. Do not wait for symptoms to improve or try to manage them at home.
Adjusting Treatment After a Breakthrough Event
When a PE or DVT occurs despite therapeutic anticoagulation, the medical team will typically intensify the treatment strategy. The first step often involves a thorough investigation to determine the reason for the failure, including reviewing medication adherence, checking for drug interactions, and screening for underlying conditions like active cancer. Once the cause is identified, the anticoagulant regimen usually undergoes a change to provide stronger protection.
This adjustment may involve switching to a different type of anticoagulant, such as moving from a DOAC to an injectable low-molecular-weight heparin (LMWH). Alternatively, the dose of the current medication may be increased to achieve a more potent therapeutic effect. In rare or severe cases where the PE is life-threatening despite optimized drug therapy, mechanical intervention may be considered. This includes the placement of an inferior vena cava (IVC) filter or a catheter-directed thrombectomy to remove the clot. Consistent communication with a hematologist or cardiologist is necessary to customize the treatment plan and balance clot prevention against the associated risk of bleeding.