A 67-year-old man with a history of relapsing heart failure (left ventricular ejection fraction 25%-30%), hypertension, and dyslipidemia presents to the emergency department with a 1-week history of spontaneous pain and swelling within the left calf. His chronic dyspnea on exertion is unchanged and he denies pleuritic chest pain or cough.
On physical examination the patient is alert and in no acute distress with normal vital signs. Pulse oximetry obtained on room air is 95%. On physical examination the patient appears euvolemic with a murmur of aortic sclerosis, an S4 gallop, and no adventitial lung sounds. His left calf is swollen, tender, and slightly warmer than the right calf. The muscle compartments are soft and distal pulses are intact bilaterally.
Duplex ultrasonography of the left leg documents an acute deep venous thrombosis within the gastrocnemius and popliteal veins (Figure 18-1). A complete blood count, chemistry profile, as well as prothrombin time/international normalized ratio (INR) and partial thromboplastin times are within normal limits. Anticoagulation is begun with therapeutic doses of apixaban and he is discharged to home with instructions to see his primary care provider in 1 week.
Venous duplex ultrasonography of the popliteal fossa demonstrating acute occlusive deep venous thrombosis within a dilated left gastrocnemius vein that has propagated into the juxtaposed popliteal vein.
Heart failure (HF) is a major risk factor for venous thromboembolism (VTE) that is independent of concurrent coronary events or atrial fibrillation.
Although classically listed as a risk factor for decompensated hospitalized patients, HF increases the risk of VTE in stable outpatients as well.
In the absence of thromboprophylaxis, the prevalence of deep venous thrombosis (DVT) in patients hospitalized with HF traditionally ranges from 4% to 26%.1 However, in a more contemporary 2014 prospective study of Japanese patients hospitalized for HF, DVT was remarkably detected in 34% despite the use of mechanical prophylaxis and/or antiplatelet therapy.2
In the Worcester Venous thromboembolism study of 1822 patients, the concurrence of HF in subjects with VTE yielded a 3-fold higher risk of in-hospital death and approximately 2.5-fold increased risk of dying within 30 days of the thrombotic diagnosis.3
In the U.S. National Hospital Discharge Survey (NHDS), a patient with HF was 2.2 times more likely to incur a pulmonary embolism (PE) when compared to patients without HF.4 PE was documented in 9% of patients with decompensated HF admitted to an intensive care unit,5 and 10% of the symptomatic PE patients enrolled in the RIETE registry had underlying HF.6
HF is a potent risk factor for VTE in young patients. For instance, in the NHDS the relative risk (RR) for PE in octogenarian congestive ...