Case Report
A 69 year old Hispanic male patient with a history of non-ischemic cardiomyopathy, normal coronary arteries by cardiac catheterization in 2011 and compensated combined congestive heart failure (EF 47% on therapy) presented in October of 2019 with shortness of breath and lightheadedness. Initial ECG showed high grade AV block and a ventricular escape rate of 30 bpm with a wide QRS of 120 ms exhibiting a right bundle branch block/left posterior fascicular block morphology (Figure 1A). His home medications included Losartan 100 mg a day, long-acting Metoprolol 100 mg a day and Spironolactone 25 mg a day.
A dual chamber pacemaker (Azure™ S DR MRI SureScan, Medtronic PLC, Dublin, Ireland) was implanted with insertion of a SelectSecure™ 3830 lead, (Medtronic PLC) intraseptally while a CapSureFix Novus™ 4076 lead, (Medtronic PLC) was inserted into the right atrial appendage. The 3830 lead was implanted using a stepwise approach in accordance with recently published recommendations4. The key steps included recording of a “W” shaped paced QRS complex, observation of appropriate changes in pacing impedance during advancement of the lead and ventricular activation time of 82 ms with both high (5.0V) and low output (2.0V). The intra-septal depth of the lead tip including the screw was measured at 13 mm with contrast injection.
A 12-lead ECG recorded after the implant was consistent with direct conduction system capture, possibly via the left posterior fascicle as shown in Figure 1B. The patient was discharged home on the previously mentioned medical regimen. Almost immediately he developed progressive heart failure symptoms prompting re-admission 1 month later for intravenous diuresis. Following discharge, the patient’s heart failure symptoms remained refractory despite escalating doses of oral diuretics. He was re-hospitalized in February of 2020 for recalcitrant decompensated systolic heart failure. Lower extremity DVT and a small, sub-segmental pulmonary embolism were concomitantly diagnosed and required the addition of anticoagulation. An echocardiogram was performed revealing a striking drop in his ejection fraction to 21% with severe wall motion abnormalities and dyssynchrony on strain imaging (Figure 2A). A right heart catheterization showed pulmonary capillary wedge pressure of 22 mmHg and a cardiac index of 2.4 L/min/m2. The patient was treated with intravenous diuresis and afterload reduction with some symptomatic improvement but eventual worsening of his pre-renal state. He was given intravenous amiodarone to suppress frequent PVCs with improvement in this new arrhythmia burden but persistence of his symptoms. Multiple causes for worsening cardiomyopathy were considered and excluded by noninvasive and invasive testing.
The possibility of direct left bundle branch pacing as the cause for this patient’s substrate and clinical decompensation was considered. In the absence of other explainable causes and given the patient’s failure to respond to aggressive medical therapy a decision was made to upgrade the device to a biventricular defibrillator. A left sided pacing lead (4598, Attain Performa™, Medtronic PLC) was placed into the postero-lateral branch of the coronary sinus while an RV defibrillator lead (6935, Quattro Secure™, Medtronic PLC) was added to the configuration and inserted at the RV apex. The direct left bundle branch lead (3830) was used as the RV pace/sense lead. The device (Amplia MRI Quad™ CRT-D, Medtronic PLC) was programmed to DDD mode with a lower rate limit of 60 beats per minute (bpm) with biventricular pacing at an LV to RV delay of 30 ms. Twelve-lead ECG with pacing in this configuration is shown in Figure 1C. Paced QRS morphology is similar to direct left bundle branch pacing with some changes in terminal forces in lead I and lateral precordial leads. The chest X-ray of the final lead positioning is shown in Figure 3. A subsequent device interrogation confirmed 97% biventricular pacing.
The patient was followed after discharge and reported an immediate significant improvement in his symptoms with resolution of cough, orthopnea and improved exercise tolerance over a course of one month. An echocardiogram performed 1 month after the CRT-D upgrade showed an improvement in EF back to baseline (46%). Strain imaging demonstrated a much more synchronous left ventricular contraction pattern (Figure 2B).