A 42-year-old man with a history of heart failure with preserved ejection fraction reports a one-day history of scant hemoptysis, cough, and right-sided pleuritic chest pain. During the past month, he has noted increasing exertional dyspnea, paroxysmal nocturnal dyspnea, lower-extremity swelling, and abdominal girth.<\/p>\n
On examination, his blood pressure is 130\/70 mm Hg, his heart rate is 110 beats per minute, and his oxygen saturation is 95% on room air. He has an S3<\/sub> gallop, elevated jugular venous pressure, diminished breath sounds at the right lung base, and 2+ pitting edema to the knees.<\/p>\n Chest radiograph shows an enlarged cardiac silhouette and small right pleural effusion. His NT-proBNP level is 6328 pg\/mL. Troponin T (TnT) is normal. Transthoracic echocardiography shows four-chamber enlargement, severe global hypokinesis, and severe biventricular systolic dysfunction with an LV ejection fraction of 15%.<\/p>\n The patient is hospitalized for further evaluation and treatment. Pharmacologic treatment is initiated for acute decompensated systolic heart failure. During the next few days, he has good diuresis and his lower-extremity swelling and abdominal distention improve; however, his chest pain is not relieved by analgesia, and his cough persists. He develops increased oxygen demands.<\/p>\n A CT scan of the chest reveals a large pulmonary embolus in the right pulmonary artery extending into all segmental and subsegmental branches, with pulmonary infarction in the right lower lobe. A repeat TnT test shows a concentration of 0.29 ng\/mL. Blood pressure remains stable, exam results are not significantly changed, and a repeat echocardiogram is also unchanged. The patient is transferred to the intensive care unit, where a heparin infusion is begun.<\/p>\n Questions:<\/b><\/p>\n 1.\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/span><\/span><\/span>What would be your next step in managing this patient?<\/p>\n 2.\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/span><\/span><\/span>What factors would you consider in deciding how best to manage the pulmonary embolism?<\/p>\n 3.\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/span><\/span><\/span>Is there an appropriate role of advanced therapies, such as systemic or catheter-directed thrombectomy\/thrombolysis, for this patient?<\/p>\n 4.\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/span><\/span><\/span>What treatment options are available to prevent further episodes?<\/p>\n <\/p>\n Response:<\/b><\/p>\n James Fang, MD<\/a><\/p>\n March 27, 2014<\/i><\/p>\n 1. What would be your next step in managing this patient?<\/i><\/p>\n Managing the PE is the most pressing issue, and moving the patient to the ICU is appropriate in light of the background severe biventricular heart failure. The patient likely had a PE on admission and another event during his hospitalization. Although blood pressure is \u201cstable,\u201d I suspect that the patient has become more tachycardic, reflecting the hemodynamic consequences of the PE, and that he may become more unstable despite anticoagulation. Heart failure is known to be a hypercoaguable state, so a search for a thrombophilia is probably unnecessary. Risk stratification of this PE is prudent at this point. I wonder if the patient had received DVT prophylaxis on admission. Lower-extremity noninvasive testing should also be considered to assess further thrombus burden. Acutely holding vasodilators and diuretics is appropriate as well.<\/p>\n 2. What factors would you consider in deciding how best to manage the pulmonary embolism?<\/i><\/p>\n The approach to PE should generally entail risk stratification in order to match the appropriate aggressiveness of therapy to the risk of immediate- and long-term sequelae. The cornerstone of PE risk assessment is the impact of the thrombus burden on RV function. In general, when there is significant RV dysfunction, the PE by definition becomes either submassive or massive. The hemodynamic consequences of RV dysfunction \u2014 not hypoxemia \u2014 generally define the PE\u2019s acute risk to the patient. RV dysfunction can be assessed on physical examination (e.g., new tricuspid regulgitation, RV heave, jugular venous distention, RV S3), imaging (e.g., RV\/LV size >1 on echocardiogram or CT), or elevated biomarkers (TnI, BNP). The newly positive TnT, progressive hypoxemia, and long-term sequelae of RV dysfunction in a young patient with \u201cbaseline\u201d severe biventricular heart failure suggest that a more aggressive approach than simple heparin should be entertained. The \u201cbaseline\u201d RV enlargement and dysfunction may, in fact, have reflected the severity of the patient\u2019s presenting PE.<\/p>\n 3. Is there an appropriate role of advanced therapies, such as systemic or catheter-directed thrombectomy\/thrombolysis, for this patient?<\/i><\/p>\n Other therapeutic strategies, in addition to heparin, should always be at least entertained once a PE is considered massive or submassive. Randomized evidence has been equivocal (Goldhaber\u00a0Lancet\u00a0<\/i>1993; 341:507<\/a>;\u00a0N Engl J Med\u00a0<\/a><\/i>2002; 347:1143<\/a>;Circulation\u00a0<\/a><\/i>2004; 110:744<\/a>), but carefully selected patients may benefit (e.g., those with low risk for intracranial bleeding). The window for treatment may be as long as 2 weeks from symptom onset (Goldhaber\u00a0Lancet<\/i>\u00a0trial); contemporary studies have shortened this window to <1 week. This patient\u2019s recent hemoptysis and pulmonary infarction may temper the enthusiasm for systemic lytics; as an alternative, catheter-directed thrombolysis could be considered, and early studies (e.g.,\u00a0ULTIMATE<\/a>) are promising. In the case of massive PE, surgical thrombectomy may be appropriate.<\/p>\n 4. What treatment options are available to prevent further episodes?<\/i><\/p>\n Chronic anticoagulation with warfarin is the most appropriate therapy to prevent future events. Novel oral anticoagulants could be considered, but the evidence base to date is limited. I would not favor an inferior vena cava filter, as it has become increasingly clear that these devices can have significant long-term sequelae that are not outweighed by the acute benefits. The exception are the retrievable filters that can be placed until the risk for recurrent PE and\/or bleeding risk has passed.<\/p>\n <\/p>\n Follow-Up:<\/b><\/p>\n