Impella RP

Abstract

Due to the scarcity of data, Impella RP is not approved for acute right ventricular failure caused by massive pulmonary embolism. We describe here the successful use of Impella RP in acute right ventricular failure caused by massive pulmonary embolism to highlight its promising outcome in such an indication. (Level of Difficulty: Advanced.)

Graphical abstract

Due to the scarcity of data, Impella RP is not approved for acute right ventricular failure caused by massive pulmonary embolism. We describe here the…

History of Presentation

An 83-year-old woman presented with acute shortness of breath for 4 h. She had no associated chest pain, cough, or fever. Her home medications include spironolactone, aspirin, and furosemide. On examination, her blood pressure was 145/90 mm Hg, pulse rate was 102 beats/min and regular, respiratory rate was 26 breaths/min, oxygen saturation was 88% on 3 L oxygen nasal cannula, and her temperature was 98.6^oF. She was confused and had cold extremities. Cardiovascular examination revealed normal heart sounds and jugular venous distention. Lungs were clear with good air movement bilaterally, and the rest of the physical examination was unremarkable.

Learning Objectives

• •Diagnose massive PE by using hemodynamic parameters rather than the anatomical findings.
• •Consider the use of Impella RP in acute RV failure due to massive PE.

Medical History

The patient’s medical history included essential hypertension, diabetes mellitus, and mild dementia.

Differential Diagnosis

The differential diagnosis of acute dyspnea with hypoxia in such an 83-year-old women is broad. An atypical presentation of acute coronary syndrome was a major concern. Other differential diagnoses included acute pulmonary embolism (PE), acute heart failure, and spontaneous pneumothorax.

Investigations

Results of the patient’s laboratory tests were as follows: total white blood cell count, 15,800/mm³ and 82% neutrophils; hemoglobin, 13.8 g/dl; platelet count, 140,000/mm³; serum creatinine, 1.9 mg/dl (baseline creatinine level, 0.6 mg/dl); troponin I, 0.82 ng/ml (normal, <0.05 ng/ml); and B-type natriuretic peptide, 368 pg/ml (normal, <100 pg/ml). An electrocardiogram showed T-wave inversion in V₁ to V₃, and a chest radiograph was unremarkable. A transthoracic echocardiogram showed severe right ventricular (RV) dysfunction, RV systolic pressure 56 mm Hg, and normal left ventricular (LV) function. Computed tomography pulmonary angiography (CTPA) revealed bilateral occlusive emboli in the right and left main pulmonary arteries (right ventricle:left ventricle = 1.9) (Figure 1).

Figure 1.

CTPA Showing Bilateral PE and RV Strain

Computed tomography pulmonary angiography (CTPA) showing (A) acute pulmonary embolism (PE) in the main right and left pulmonary arteries (arrows) and (B) acute right ventricular (RV) strain with dilated right ventricle. Right ventricle:left ventricle = 1.9 with relative bowing of the interventricular septum.

Management

Based on the clinical presentation and radiological findings, the diagnosis of intermediate- to high-risk PE was made. Due to acute kidney injury, a bolus, followed by an infusion, of unfractionated heparin was administered. A few hours later, the patient became hypotensive (systolic blood pressure dropped to 80 mm Hg); the activated partial thromboplastin time was therapeutic (82 s) at the time of decompensation. Cautious fluid resuscitation and inotropic support with dopamine were immediately initiated, and she was taken to the catheterization laboratory. Ultrasound-assisted catheter-directed thrombolysis (UCDT) through an EndoWave Infusion Catheter System (EkoSonic Endovascular System, EKOS Corporation, Bothell, Washington) was inserted into each pulmonary artery. The patient’s blood pressure continued to drop after the insertion of the EKOS device, and Impella RP (Abiomed, Inc., Danvers, Massachusetts) was deployed 25 min after the insertion of the EKOS device due to the profound and persistent shock state. The device’s inflow sat in the proximal inferior vena cava, and the outflow was to the left pulmonary artery (Figure 2).

Figure 2.

Fluoroscopic Image of Impella RP and Bilateral EKOS

The Impella RP inflow is located in the inferior vena cava, and the outflow is in the left main pulmonary artery; bilateral EKOS catheters are located in the main right and left pulmonary arteries.

Discussion

About 5% of patients with acute PE develop cardiogenic shock due to acute RV failure. The prognosis in such patients is grave, and the mortality rate may exceed 50% (1). UCDT has emerged as an appealing treatment modality for intermediate- to high-risk PE. Compared with systemic thrombolysis, it is safe and effective at rapidly decreasing RV strain and reduction in pulmonary arterial pressure, with a potentially lower risk of bleeding complications (2). Due to the prohibitive risk of systemic thrombolysis that puts the patient at 2% to 3% risk of intracranial hemorrhage (advanced age), the authors elected to proceed with UCDT. She received 24 mg of alteplase in 24 h (0.5 mg/h on each side) through the bilateral EKOS device.

It is also imperative to recognize acute PE as a dynamic pathology based on the hemodynamic data, as the treatment modalities could vary accordingly. Massive PE is typically defined by hemodynamic parameters rather than according to the anatomical findings in CTPA (3). Vedovati et al. (4) found no association between central obstruction and death or clinical deterioration in 579 patients with pulmonary embolus. However, when a subset of 516 patients who were hemodynamically stable was assessed, central localization of emboli was found to be an independent risk factor for increased mortality. Thus, anatomical findings in CTPA should not be used as a defining criterion for PE but may be important in assessing the risk in otherwise hemodynamically stable patients with PE (4).

The study patient was initially hemodynamically stable; hence the diagnosis was intermediate- to high-risk PE, and she received systemic anticoagulation. However, when she developed cardiogenic shock, the working diagnosis was shifted to massive PE, and thrombolysis was then considered. To achieve better clinical outcomes, patients with PE should be under close observation, preferably in an intensive care setting, with prompt consideration of mechanical ventilation and circulatory support.

The current American College of Cardiology/American Heart Association guidelines in the management of acute RV failure recommend judicious fluid resuscitation, as liberal fluid resuscitation could increase RV filling pressure, thereby worsening the RV failure, followed by inotropic support to increase RV cardiac output by increasing RV contractility and heart rate (5). If volume expansion and inotropic support are not successful, then Impella RP comes into play. Impella RP is approved by the U.S. Food and Drug Administration to provide circulatory support in acute RV failure after LV assist device implantation, myocardial infarction, heart transplant, or open-heart surgery (6). However, the evidence supporting Impella RP use in cardiogenic shock due to acute RV failure after a massive PE is still lacking.

Despite the lack of evidence, the authors elected to proceed with Impella RP implantation because the patient received guideline-based treatment with anticoagulation, UCDT, volume expansion, and inotropic support, and she had remained in refractory cardiogenic shock.

In 1 series, Elder et al. (7) described 5 cases with cardiogenic shock due to massive or submassive PE who received Impella RP and UCDT. To the authors’ knowledge, these are the only cases published in the literature to date. In this series by Elder et al. (7), cardiac index was improved from a mean of 1.69 to 2.5 l/min/m² 24 h after treatment; no significant changes were recorded in kidney function or levels of hemoglobin or platelets, and all patients survived to discharge. Similar to the current case, LV function was preserved in all 5 patients in this series by Elder et al. (7), and 4 of their patients presented with submassive PE, which was complicated with shock after admission. However, and in contrast to this case that represents an 83-year-old patient, 4 cases in the series of Elder et al. (7) were <55 years of age. The current report could thus uniquely represent the benefit of Impella RP in the elderly population.

Follow-Up

Shortly after the Impella RP implantation, rapid improvement of hemodynamics and organ function was achieved in the study patient. Dopamine was weaned off in <24 h, and the Impella RP and EKOS catheters were removed in <48 h (Table 1).

Table 1.

Risk Stratification Before and After Impella RP

Impella RP	Trop I (ng/ml)	BNP (pg/ml)	EKOS	PESI	sPESI (%)	PAPI	Heart Rate (beats/min)		Blood Pressure (mm Hg)
							Before	After	At Admission	Before	After
2 days	0.884	368	1	213	8.9	3.0	88	69	145/94	85/67	130/84

BNP = B-type natriuretic peptide; PAPI = pulmonary artery pulsatility index; PESI = Pulmonary Embolism Severity Index; sPESI = simplified Pulmonary Embolism Severity Index; Trop I = peak troponin I.

The patient was discharged home in stable condition. A repeat transthoracic echocardiogram showed normalization of the RV function (Table 2).

Table 2.

Right Heart Hemodynamics According to Transthoracic Echocardiogram Before and After Treatment With Impella RP

RAP (mm Hg)		RVP (mm Hg)		PA (mm Hg)		Cardiac Index (l/min/m2)		TAPSE (mm)
Before	After	Before	After	Before	After	Before	After	Before	After
8	8	56.5	50.8	44	NA	1.05	1.01	15	24

Pressure values are described as systolic pressures.

NA = not available; PA = pulmonary artery pressure; RAP = right atrial pressure; RVP = right ventricular pressure; TAPSE = tricuspid annulus plane systolic excursion.

Conclusions

Impella RP is a promising intervention in acute RV failure due to PE, particularly if the guideline-based treatment with anticoagulation, UCDT, volume expansion, and inotropic support fail. This report highlights the promising clinical outcome of Impella RP use in cardiogenic shock due to acute RV failure secondary to massive PE; however, further studies are required to validate these findings and to establish the causes of these observations.