Posters
Academic Level (Author 1)
Resident
Discipline/Specialty (Author 1)
Internal Medicine
Discipline Track
Patient Care
Abstract
Background: Interference of device leads with closure of the tricuspid leaflets can cause severe tricuspid regurgitation (TR) and right-sided heart failure, as can heart failure with reduced LV function (HfrEF), and left sided valve disease.
Case Presentation: A 78-year-old male with history of coronary artery disease s/p remote coronary bypass, ischemic cardiomyopathy with left ventricular ejection fraction 35-40%, and inducible ventricular tachycardia status post defibrillator presented with worsening dyspnea on exertion, easy fatigue, lower extremity pitting edema, anasarca, abdominal bloating and new systolic murmurs at the right upper and left lower sternal borders. An Echocardiogram demonstrated severe aortic stenosis with secondary pulmonary hypertension, an RV systolic pressure of 50 mm Hg, severe bi-atrial enlargement, and severe TR in the region of his device lead. A transesophageal echo confirmed mechanical interference by the lead with closure of the septal leaflet. Symptoms initially improved with intravenous furosemide but were ultimately refractory to outpatient therapy with furosemide, and later transitioning to the longer acting torsemide. He was a poor candidate for surgical correction given prior bypass surgery with patent grafts. Transcatheter aortic valve implantation (TAVI) was performed in an effort to reduce pulmonary artery pressures, with concomitant guideline directed medical therapy (GDMT) for HFrEF, in hopes of reducing tricuspid regurgitation from RV pressure overload from left sided heart disease. A repeat echo demonstrated a reduced RV systolic pressure of 42 mm Hg, and improved TR to moderate to severe.
Conclusions: While diuretics are the mainstay of therapy, medical therapies for management of severe TR are limited. Attention should be focused on the underlying etiology of the TR and classification as primary (abnormal valve leaflets--including device lead induced) or secondary (normal valve leaflets). This patient had mixed involvement and management was directed accordingly with TAVI and GDMT for HfrEF, with plans for the higher risk surgical TV repair or replacement should symptoms persist.
Presentation Type
Poster
Recommended Citation
Appareddy, Nina Shyama; Iglesia, Michaela; Khaddam, Ayman; Kwang, Henry; and Flores, Eduardo D., "A Case of Device Lead Induced Severe Tricuspid Regurgitation and Right-Sided Heart Failure" (2023). Research Colloquium. 41.
https://scholarworks.utrgv.edu/colloquium/2022/posters/41
Included in
A Case of Device Lead Induced Severe Tricuspid Regurgitation and Right-Sided Heart Failure
Background: Interference of device leads with closure of the tricuspid leaflets can cause severe tricuspid regurgitation (TR) and right-sided heart failure, as can heart failure with reduced LV function (HfrEF), and left sided valve disease.
Case Presentation: A 78-year-old male with history of coronary artery disease s/p remote coronary bypass, ischemic cardiomyopathy with left ventricular ejection fraction 35-40%, and inducible ventricular tachycardia status post defibrillator presented with worsening dyspnea on exertion, easy fatigue, lower extremity pitting edema, anasarca, abdominal bloating and new systolic murmurs at the right upper and left lower sternal borders. An Echocardiogram demonstrated severe aortic stenosis with secondary pulmonary hypertension, an RV systolic pressure of 50 mm Hg, severe bi-atrial enlargement, and severe TR in the region of his device lead. A transesophageal echo confirmed mechanical interference by the lead with closure of the septal leaflet. Symptoms initially improved with intravenous furosemide but were ultimately refractory to outpatient therapy with furosemide, and later transitioning to the longer acting torsemide. He was a poor candidate for surgical correction given prior bypass surgery with patent grafts. Transcatheter aortic valve implantation (TAVI) was performed in an effort to reduce pulmonary artery pressures, with concomitant guideline directed medical therapy (GDMT) for HFrEF, in hopes of reducing tricuspid regurgitation from RV pressure overload from left sided heart disease. A repeat echo demonstrated a reduced RV systolic pressure of 42 mm Hg, and improved TR to moderate to severe.
Conclusions: While diuretics are the mainstay of therapy, medical therapies for management of severe TR are limited. Attention should be focused on the underlying etiology of the TR and classification as primary (abnormal valve leaflets--including device lead induced) or secondary (normal valve leaflets). This patient had mixed involvement and management was directed accordingly with TAVI and GDMT for HfrEF, with plans for the higher risk surgical TV repair or replacement should symptoms persist.