Bilateral Venous Access for Cardiac Resynchronization Therapy in a Hemodialysis Patient With Cabozantinib-associated Heart Failure

Case Report

A 63-year-old male patient was referred to the cardiovascular department for evaluation of dyspnea attributed to HF, which had developed one week prior. His medical history includes left-sided clear cell renal cell carcinoma (ccRCC), treated with radical nephrectomy 27 years ago. Due to metastatic recurrence of ccRCC, he underwent multiple chemotherapy regimens, including interferon-alpha, various tyrosine kinase inhibitors such as sorafenib and axitinib, and the immune checkpoint inhibitor nivolumab. However, all treatments were discontinued due to adverse events or disease progression. Three years ago, cabozantinib was initiated as fifth-line therapy, resulting in moderate tumor shrinkage. Hemodialysis was started two years ago due to worsening renal function.

During his visit, an electrocardiogram (ECG) revealed a complete left bundle branch block (CLBBB) (Figure 1A), although his QRS complex had been narrow prior to chemotherapy (four years ago). A chest X-ray showed cardiomegaly with a cardio-thoracic ratio of 57.7% (Figure 2A). Transthoracic echocardiography revealed a dilated left ventricle (left ventricular end-diastolic diameter: 61.9 mm) with a reduced EF of 34% (Figure 3A). Additional findings included apical shuffling, a septal flash, moderate aortic stenosis, and mild-to-moderate functional mitral regurgitation. Three months later, coronary angiography was performed to evaluate ischemic etiology, revealing no significant stenosis. Cardiac magnetic resonance imaging was contraindicated due to impaired renal function, and a myocardial biopsy was avoided to minimize procedural risk. While cabozantinib-induced CTRCD was suspected to be a potential cause of the reduced cardiac function, the urology department recommended continuing cabozantinib due to the limited availability of alternative anticancer treatments (a decision also supported by the patient). Subsequently, medical therapy with an angiotensin receptor-neprilysin inhibitor and carvedilol was initiated. Despite this, the patient’s symptoms, classified as NYHA Class III, showed no improvement over six months of cardioprotective treatment. Approximately one year after the initial cardiology visit, the patient was admitted for implantation of a cardiac resynchronization therapy-defibrillator (CRT-D) device to manage wide QRS heart failure with reduced ejection fraction (HFrEF).

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Figure 1.

Electrocardiogram (ECG) before and after cardiac resynchronization therapy (CRT). A) ECG showing complete left bundle branch block (CLBBB) with a QRS duration of 154 ms at the initial cardiology visit. B) ECG taken at the follow-up visit after CRT, showing a reduced QRS duration of 124 ms. Left ventricular pacing, rather than biventricular pacing, was employed based on echocardiography-guided optimization.

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Figure 2.

Chest X-rays before and after cardiac resynchronization therapy (CRT). A) Chest radiograph from the initial cardiology visit, demonstrating cardiomegaly with a cardiothoracic ratio of 57.7%. B) Follow-up chest radiograph after CRT, showing a reduction in the cardiothoracic ratio to 54.6%. The CRT generator is implanted in the right chest, with the left ventricular lead positioned via the left subclavian vein (arrow).

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Figure 3.

Apical four chamber views of echocardiography before and after cardiac resynchronization therapy (CRT). A) Transthoracic echocardiography (TTE) at the initial cardiology visit, showing a dilated left ventricle (left ventricular end-diastolic diameter [LVEDD]: 61.9 mm) and a reduced ejection fraction (EF) of 34%, with apical shuffling and a septal flash. B) TTE at the follow-up visit after CRT, demonstrating reverse remodeling with an improved EF of 53% and a reduced LVEDD of 57.3 mm.

Upon admission, the patient’s blood pressure was 103/51 mmHg, and his heart rate was 76 beats per minute. A physical examination revealed a Levine grade 2/6 systolic murmur. Laboratory findings indicated anemia, with a hemoglobin level of 9.4 g/dl, and impaired renal function, evidenced by a creatinine level of 5.9 mg/dl. Additionally, BNP was elevated at 398.7 pg/ml, and N-terminal pro b-type natriuretic peptide (NT pro-BNP) was markedly elevated at 12,468 pg/ml.

On the fifth day of hospitalization, a CRT-D implantation procedure was performed. Due to the presence of a dialysis shunt in the patient’s left arm, the right subclavian vein was chosen for venous access to minimize the risk of lead-related complications. The right ventricular and atrial leads were successfully placed via the right subclavian vein; however, placement of the left ventricular lead proved challenging due to insufficient backup support from the guiding catheter. After several unsuccessful attempts, the right-sided approach was abandoned. Subsequently, the left subclavian vein was punctured, and a sheath was inserted. This allowed for smooth catheter advancement and successful placement of the left ventricular lead into the postero-lateral branch of the coronary sinus. A tunneling tool was then used to route the left ventricular lead subcutaneously from the left anterior chest to the right-sided pocket, where it was connected to the device (Figure 4A). Using this bilateral approach, the CRT procedure was completed successfully (Figure 4B and C). Guided by echocardiographic optimization, left ventricular pacing was chosen over biventricular pacing.

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Figure 4.

Bilateral venous approach for cardiac resynchronization therapy (CRT). A) A tunneled lead from the contralateral vasculature to the ipsilateral pulse generator. B) Final view of CRT implantation in the right anterior oblique (RAO) projection. C) Left anterior oblique (LAO) view following CRT completion.

Six months post-CRT-D implantation, echocardiography demonstrated reverse remodeling, with an improved EF of 53% and a reduced left ventricular end-diastolic diameter of 57.3 mm (Figure 3B). The QRS duration improved to 124 ms under left ventricular pacing (Figure 1B). A chest X-ray revealed no signs of pulmonary congestion, and the cardiothoracic ratio had decreased to 54.6% (Figure 2B).