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A woman in her 70s was referred to our centralized heart failure management program because of New York Heart Association functional class III heart failure with preserved left ventricular systolic function and recurrent hospitalizations for heart failure. Her medical history was remarkable for coronary artery disease after coronary artery bypass grafting, chronic stable angina, severe tricuspid regurgitation, atrial fibrillation, and obesity with a body mass index of 39 (calculated as weight in kilograms divided by height in meters squared). After screening and medication optimization, she underwent successful implantation of a small sensor-pressure device (CardioMEMS; Abbott) into her pulmonary artery without complication. Her home medications included torsemide, metolazone, metoprolol succinate, spironolactone, isosorbide mononitrate, diltiazem, and ranolazine. Her initial postimplantation sensor readings and waveforms are shown in Figure 1A.
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Migration of CardioMEMS sensor
D. Obtain a chest radiograph
In managing patients with implanted CardioMEMS sensors, it is not unusual to have to troubleshoot pulmonary artery pressure readings, connectivity challenges, or abnormal readings suggestive of electromechanical interference. This case presented a different challenge in that after positional adjustment a tracing was recorded, but the waveform recorded in the prone position showed loss of the dicrotic notch, suggesting late device migration to the right ventricle, as confirmed on chest radiography (Figure 2).
The CardioMEMS heart failure system allows for ambulatory heart failure management by targeting pulmonary artery pressures to maintain euvolemia. The device is approved for use in patients with New York Heart Association class III heart failure who have been previously hospitalized for heart failure.1 The device is implanted percutaneously in a segmental pulmonary artery, calibrated in real time with a pulmonary artery catheter, and interrogated remotely at home using an electromagnetic receiver that transmits centrally to a cloud storage platform. Meticulous attention to vessel sizing and device placement is required to ensure that the distal nitinol loop is adequately secured within a segmental pulmonary artery, but not too deep so that the sensor itself becomes overendothelialized, which can lead to late signal loss or signal dampening.
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Corresponding Author: Kelly Axsom, MD, Division of Cardiology, Center for Advanced Cardiac Care, Columbia University Irving Medical Center, 622 W 168th St, PH1266, New York, NY 10032 (firstname.lastname@example.org).
Published Online: June 16, 2021. doi:10.1001/jamacardio.2021.1820
Conflict of Interest Disclosures: Dr Kirtane reported receiving Institutional funding to Columbia University and/or the Cardiovascular Research Foundation from Abbott Vascular, Abiomed, Boston Scientific, CathWorks, CSI, Medtronic, Philips, ReCor Medical, and Siemens. In addition to research grants, institutional funding included fees paid to Columbia University and/or the Cardiovascular Research Foundation for speaking engagements and/or consulting. Dr Kirtane also reported receiving personal, consulting, neurotronic, and travel expenses and meals from Abbott Vascular, Abiomed, Boston Scientific, CathWorks, Chiesi, CSI, Medtronic, OpSens, Philips, ReCor Medical, Regeneron, Siemens, and Zoll. Dr Axsom reported being a paid consultant to Abbott and Medtronic. No other disclosures were reported.
Additional Contributions: We thank the patient for granting permission to publish this information.
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