Impella to Resist the Storm


A 69-year-old woman was admitted with a non–ST-segment–elevation myocardial infarction. Despite successful percutaneous coronary intervention, echocardiogram post-non–ST-segment–elevation myocardial infarction showed left ventricular ejection failure (15%, Interagency Registry for Mechanically Assisted Circulatory Support 3). The patient developed recurrent ventricular tachycardia and deteriorated to cardiogenic shock, characterized by a decreasing pulse pressure (Figure [A]).

Figure.

Figure. Cardiac output during supported vs unsupported sustained ventricular tachycardia (VT). A and C, Electrocardiography (top) and ventricular (green)-arterial (red) curve (bottom): illustrating (A) loss of pulse pressure (#) and cardiac output in unsupported sustained VT vs (C) ventriculo-arterial uncoupling with sustained output, generated by nonpulsatile 4.8 L/min output by the Impella-5.0 support and resulting in a systemic pressure of 65 mm Hg. B, Fluoroscopy (right anterior oblique) during Impella-5.0–supported VT ablation (*electrophysiology catheters). D, Voltage map delineating infarct zone (red) and scar border zone (yellow-green).

To preserve adequate systemic perfusion, a percutaneous mechanical circulatory support (pMCS) device (Impella-5.0; Abiomed) was inserted (Figure [B]). pMCS offers continuous forward flow of blood from the left ventricle into the aorta. This flow is both afterload sensitive, with end-organ perfusion increasing with lower systemic vascular resistance, and preload dependent, requiring sufficient volume from the right ventricle to operate effectively.

If the failing left ventricular is no longer able to overcome afterload in the new equilibrium of increased mean arterial pressure and reduced preload created by the continuous flow of the pMCS device, the arterial trace will flatten. This process is called ventriculo-arterial uncoupling.1 In our patient, at a flow of 4.8 L/min, the pump preserved a mean arterial pressure of 65 mm Hg and end-organ perfusion (normalized lactate levels), despite the heart continuing in a low output state (Figure [C]). If pump flow is prematurely lowered during a prolonged low output state, ventriculo-arterial recoupling may occur but with a resultant lower mean arterial pressure, increasing the risk of insufficient end-organ perfusion (Figure [C], dotted line).

For patients in cardiogenic shock, pMCS during interventional cardiac procedures confers 2 main benefits. First, it provides hemodynamic stability, allowing for lengthy therapeutic interventions (such as mapping and ablation of ventricular tachycardia in our case, Figure [D]) to take place. Second, pMCS protects the myocardium through both a direct increase in coronary flow and a reduction in end-diastolic pressure (ventricular unloading). As such, when cardiogenic shock is caused by left ventricular failure secondary to electric instability from ventricular tachycardia, pMCS may be considered.2,3

Footnotes

For Disclosures, see page 1.

Correspondence to: Christophe Vandenbriele, MD, PhD, Department of Cardiovascular Diseases, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium. Email

References

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