March 20th, 2014
Pulmonary Embolism in a Patient with Acute Decompensated Systolic Heart Failure
Ian Neeland, MD and James Fang, MD
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.
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 gallop, elevated jugular venous pressure, diminished breath sounds at the right lung base, and 2+ pitting edema to the knees.
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%.
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.
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.
Questions:
1. What would be your next step in managing this patient?
2. What factors would you consider in deciding how best to manage the pulmonary embolism?
3. Is there an appropriate role of advanced therapies, such as systemic or catheter-directed thrombectomy/thrombolysis, for this patient?
4. What treatment options are available to prevent further episodes?
Response:
March 27, 2014
1. What would be your next step in managing this patient?
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 “stable,” 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.
2. What factors would you consider in deciding how best to manage the pulmonary embolism?
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 — not hypoxemia — generally define the PE’s 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 “baseline” severe biventricular heart failure suggest that a more aggressive approach than simple heparin should be entertained. The “baseline” RV enlargement and dysfunction may, in fact, have reflected the severity of the patient’s presenting PE.
3. Is there an appropriate role of advanced therapies, such as systemic or catheter-directed thrombectomy/thrombolysis, for this patient?
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 Lancet 1993; 341:507; N Engl J Med 2002; 347:1143;Circulation 2004; 110:744), 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 Lancet trial); contemporary studies have shortened this window to <1 week. This patient’s 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., ULTIMATE) are promising. In the case of massive PE, surgical thrombectomy may be appropriate.
4. What treatment options are available to prevent further episodes?
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.
Follow-Up:
April 3, 2014
The patient was transferred to the ICU, and vasodilator and diuretic medications were withheld. Lower-extremity venous Doppler imaging showed no evidence of deep-vein thrombosis. Pulmonary specialty consultation was ordered, to help assess the risks and benefits of systemic or catheter-directed thrombolysis. Given the patient’s hemodynamic stability (despite persistent tachycardia) and the presence of pulmonary infarction, the decision was made to continue intravenous heparin but not pursue further thrombolytic therapy. An inferior vena cava filter was not placed because the patient was able to receive full anticoagulation. Repeat echocardiogram 2 days later did not show any significant changes.
During the next few days, the patient’s tachycardia resolved and his oxygen requirements lessened. He was transferred from the ICU to a monitored bed, and warfarin was started with a plan to bridge with heparin until a therapeutic INR was reached. His vasodilator and diuretic heart failure medications were slowly restarted and titrated up, as tolerated. He also underwent physical and occupational therapy to improve his functional status.
Ultimately, 2 weeks after initial diagnosis, the patient was well enough to return home. His discharge medications included furosemide, hydralazine/isosorbide dinitrate, lisinopril, and warfarin. He plans to follow up in the heart failure and pulmonary medicine clinics.
8 Responses to “Pulmonary Embolism in a Patient with Acute Decompensated Systolic Heart Failure”
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Thanks for sharing this case, Ian. This is particularly challenging because the main method we assess the need for thrombolytics is based on signs of shock (hypotension etc) or right ventricular failure (and possibly overload). In this setting the right ventricle is already failing and therefore clinical and echocardiographic assessment of RV function is going to be of little added value. Therefore, in my opinion, the option for advanced therapies, beit systemic lytics or catheter directed lytics depends on hemodynamic status- if the patient is hypotensive and requiring pressors, then I would opt for lytics. If the patient is not hypotensive, then I would recommend waiting- considering the detrimental effects of intracranial bleed from lytics. In my mind the use of catheter directed lytics is potentially useful if the RV is in complete failure and you need to recover RV function ASAP. This is supported by recently published work by Kucher et al out of Germany and Switzerland (Circulation. 2014 Jan 28;129(4):479-86). I have been underwhelmed by the data on catheter directed thrombectomy and remain of the opinion that if you are considering thrombectomy, the best results are obtained with a surgical approach.
I agree with Dr Rayan. I have a few ideas I want to present. In this case it is very important the heart failure and pulmonary thrombosis etiologies and the severity of the RV disfunction. First the etiology of the hearth failure because you must be sure the right chambers dilatations are not a new event, if this is the case this is a very important factor, because is a sign of RV dysfunction (overload), and in consecuence to consider thrombolysis or more advance treatments. Don’t forget the pulmonary infarction is an important factor in this case, is a marker of severity and open the possibilities for important complications. About the etiology of the thrombosis, if is from stasis, factor like the heart failure and the ventricular interdependence are very important and need to be resolved, but if hypercoagulability is the main precursor this could change the treatment and prognosis. So you need more information about the etiology and previous condition of the heart failure and be sure about the origin of the thrombosis.
I would seriously consider thrombolytic therapy. The patient has several high risk features:pulmonary infarction (as per Enrique), elevated biomarkers, and newly documented biventricular systolic dysfunction ( irrespective of cause).His thromboembolic process has been untreated “a few days” into the hospitalization, at which point his oxygenation declines (after relief of pulmonary congestion). Along with his presumed low risk of bleeding (using age only), I would likely elect for thrombolytic or CDT (we have a trial using ultrasound to assist thrombectomy)
Curious aspects of this case include the history of HFNEF in this 42 yo… Does he have hypertension, obesity, and/or OSA? Then newly documented biventricular systolic failure? Myocarditis? Was there a McConnell’s sign? Did a progressively cardiomyopathic process lead to venous stasis and subsequent DVT and PE? Or was the initial insult a PE with RV dysfunction, and subsequent LV dysfunction from an unknown cause (ischemia/stunning)?
If I am at my more “community hospital”, I might transfer and/or elicit support from a heart failure team, as BiVAD or ECHMO may be considerations if the clinical course is not reversed expeditiously. “Increasing oxygen requirements” seems ominous.
Was PE prevalent(present on admission) or incident(after admission) and was DVT/PE prophylaxis started on admission? Imaging of legs would be of benefit- if high thrombus burden, then low threshold for IVC filter should clinical recurrence of PE develop.
Agree with Dr. Ryan- if failed initial medical therapy , then surgical thrombectomy appears superior to CDT- although I
remain concerned about the extent of distal subsegmental involvement, that which will require anticoagulaion/lysis for resolution.
Thanks Dr/Neeland & Dr/Fang for that interesting case I would like to talk about some points. PE is a well known precipitating cause of heart failure but it is not known to be a reason for global hypokinesia which means that half of the case diagnosis is still unsolved and require further assessment (viral/toxic myocarditis) .
In the setting of hemodynamic instability in PE patient(Massive PE) thrombolytic therapy is indicated if other causes of hemodynamic instability are excluded(the severe LV systolic dysfunction might be the reason in this patient) which makes decision even if he develops HD instability unclear.
The clear indications for IVC filter include contraindication of anticoagulation or failure of anticoagulation which are not the problem in this patient. A weaker indication might be its benifit in those with poor cardiorespiratory reserve (like the presented case) although the definition of poor cardiorespiratory reserve is unclear.
Thank you for this very interesting and unusual story.
Which is surprising is the initial missing diagnosis of Pulmonary Embolism and the subsequent delay of an efficient anticoagulation. Symptoms and signs of PE (with pulmonary infarct!) seem to be evident on admission. Acute pneumonitis does not appear likely (no fever reported)
The possibility of acute myocarditis is ruled out by normal TnT at admission and moderatly high level “few days” after.
So how this young (very)patient can suffer from a so severe cardiomyopathy (EF=15% my good how do you live without previous symptoms and medical seek?) This important question has to be answered by the authors.
Considering systemic thrombolytic therapy the existence of pulmonary infarct and hemoptysis will make me very cautious. I will stay simple in this complicated case initially starting with heparin or better LWMH probably more reliable for un stable anticoagulation.
Checking the lower limbs and IVC for the presence of a thrombus is as suggested by my colleagues important.
I would not consider LVAD or ECMO at this moment. I would stay on a classical treatment anticoagulation, diuretics oxygen…
But I really want to know about medical history.
Best regards
the factors which i would consider for aggresive treatment of this patient are, age 42 – history of previous well preserved EF. No associated co-morbidities like DM, Dyslipidemia.
because the thrombus is few days old therefore i do not see role of systemic thrombolysis. i would like to go for catheter based thrombectomy.
for prevention of further such events, an IVC filter or lifelong prophylactic anticoagulation viz. Warfarin or Acenocoumarin based will be my best option.
thanks for the interesting and informative case.
i will just add my oppinions about the ecg. if there is atrial fibrillation , i would not check for the etiology for thrombosis. regardless of the etiology, i will continue warfarin for the patient.
best regards,