Diagnosis of lead-induced tricuspid regurgitation.

Introduction

Clinically important lead-induced tricuspid regurgitation (LITR) is an uncommon complication following cardiac device implantation. Surgical removal and replacement of a lead may improve heart failure caused by LITR. Percutaneous lead extraction and reimplantation may also improve or correct LITR. However, whether severe tricuspid regurgitation (TR) is caused by a lead is often unclear, especially in patients with left ventricular (LV) dysfunction; worsening heart failure in such patients is most often attributed to progression of LV dysfunction.1, 2, 3

Echocardiography may clarify whether worsening heart failure is due to LITR. It is only occasionally obvious that a lead is the culprit.1, 3 However, other findings may still implicate the lead. Right heart failure disproportionate to that expected for the degree of LV dysfunction should suggest possible LITR. In left heart failure, LV end-diastolic pressure (LVEDP) is expected to be greater than right ventricular (RV) end-diastolic pressure (RVEDP): the positive transseptal pressure gradient ( LVEDP − RVEDP) would cause the ventricular septum to be concave toward the LV.4, 5 If the ventricular septum is flattened, the transseptal pressure gradient is close to zero or negative; that is, RVEDP is greater than or equal to LVEDP. This should suggest other possible causes of RV failure, including LITR.

Our experience suggests that the reasoning described above can help determine whether the lead is responsible for, or contributes to, severe TR and that percutaneous lead reimplantation may be beneficial.

Methods

Percutaneous lead replacement for presumed LITR was performed in 6 patients between July 2001 and July 2012. Echocardiograms were reviewed to assess biventricular function, lead relationship to the tricuspid valve (TV), end-diastolic ventricular septal flattening (VSF), and estimated peak systolic pulmonary artery pressure.

Results

Table 1 lists the clinical characteristics of the 6 patients and the devices used. Table 2 summarizes the outcomes. LITR was verified in 4 patients (cases 1, 2, 4, and 6) by substantial clinical improvement. Case 5 needed an open TV repair because a leaflet was torn during lead extraction. In case 3, the cause of heart failure remained unclear. VSF was present in the 5 available echocardiograms.

Table 1

Patient characteristics and devices used

Case no.	Age (y)	Sex	Clinical diagnosis	Device	No. of leads	Lead type	Years from insertion to removal
1	68	M	Ischemic CMP;	CRT-D	2	5076 AF	6.2
			CHB			7122 AF	4.3
2	72	M	A. fib; bradycardia	VVI PPM	1	5076 AF	0.9
3	79	M	A. fib; bradycardia	VVI PPM	1	4088 AF	6.8
4	82	M	Mitral valve repair; VF	DDD ICD	1	0181 AF	4.2
5	70	F	SSS	VVI	2	4082 PF	10.2
				PPM		430-10 PF	6.4
6	24	F	CHB	VDD	2	5038 PF	8.4
				PPM		U	19

AF = active fixation; A. fib = atrial fibrillation; CHB = complete heart block; CMP = cardiomyopathy; CRT-D = cardiac resynchronization therapy with defibrillator; F = female; ICD = implantable cardioverter-defibrillator; M = male; PF = passive fixation; PPM = permanent pacemaker; SSS = sick sinus syndrome; U = unknown lead type; VF = ventricular fibrillation.

Table 2

Echocardiographic findings and clinical results

Case no.	Left heart findings	Lead impinging TV	TA diameter (cm)	RV systolic function	ED septal shape preextraction	Preextraction TR	Postextraction TR	Clinical improvement	ED septal shape postextraction
1	LV dysfunction (EF 0.46)	No	3.8	Mild RV dysfunction	Flattened	Severe	Moderate-severe	Yes	Concave
2	LV dysfunction (EF 0.12)	Yes	4	Mild-moderate RV dysfunction	Flattened	Severe	Moderate	Yes	Concave
3	Moderate-severe MR	No	5	Mild RV dysfunction	Flattened	Severe	Severe	Slight, transient	Mildly flattened
4	Moderate MR; MV repair; moderate LV dysfunction	No	4.9	Moderate RV dysfunction	Flattened	Severe	Mild-moderate	Yes	Concave
5	Normal LV; severe PHTN	Yes	–	Normal RV function	–	Moderate-severe	Mild-moderate	Yes	–
6	Normal LV	Yes	4.2	Normal RV function	Flattened	Severe	Severe	None flail TV leaflet during surgical repair	Flattened

ED = end-diastole; EF = ejection fraction; LV = left ventricular; MR = mitral regurgitation; MV = mitral valve; PHTN = pulmonary hypertension; TA = tricuspid annulus; TR = tricuspid regurgitation; TV = tricuspid valve.

Case 1

A 68-year-old male patient with moderate LV dysfunction and prior coronary artery bypass surgery had a pacemaker implanted in 2006, which was upgraded to a cardiac resynchronization therapy with defibrillator device in 2009. He subsequently developed heart failure resistant to medical therapy.

Echocardiography revealed severe TR, but the effect of the lead was unclear. The estimated peak RV systolic pressure was 33 mm Hg; there was mild RV dysfunction.

Initially, the implantable cardioverter-defibrillator (ICD) lead was removed percutaneously and a defibrillator coil was placed in the azygous vein. The abandoned pace/sense lead was not removed. TR and heart failure remained severe, and 3 months later, the pace/sense lead was replaced percutaneously. TR was improved, his heart failure was easily controlled without diuretics, and he returned to active living. Follow-up echocardiography showed normal ventricular septal shape.

Case 2

A 72-year-old male patient (LV ejection fraction 12%) with prior coronary artery bypass surgery and a pacemaker presented 6 months later with severe right heart failure. There was severe TR with clear lead impingement, an estimated peak RV systolic pressure of 51 mm Hg, mild-to-moderate RV dysfunction, and VSF.

The lead was replaced percutaneously 11 months following the original implantation. He lost 5.6 kg within 4 days. He remains stable 6 years later without diuretics. An echocardiogram recorded 2 years postrevision showed moderate TR and normal ventricular septal shape.

Case 3

A 79-year-old male patient with mitral regurgitation and a pacemaker presented 6 years later with severe heart failure and TR, most likely a ruptured TV chord, moderate-to-severe mitral regurgitation, normal LV systolic function, an estimated peak RV systolic pressure of 54 mm Hg, and mild RV dysfunction. There was VSF.

He underwent percutaneous lead replacement; intraoperative transesophageal echocardiography did not clarify the cause of TR. Subsequently, TR and VSF appeared unchanged, and the patient died several months later. The cause of the persistent heart failure was not clarified.

Case 4

An 82-year-old male patient with a previous mitral valve repair had an ICD implanted after a cardiac arrest. The device was later upgraded to a dual-chamber ICD, and the RV lead was replaced. He developed progressive heart and renal failure requiring frequent hospitalizations. A furosemide infusion (8 mg/h) caused a loss of 24 kg, but severe TR persisted.

LV function was moderately reduced; there was mild-to-moderate mitral regurgitation, an estimated peak RV systolic pressure of 56 mm Hg, moderate RV dysfunction, and VSF.

After percutaneous lead replacement, TR was mild to moderate with normalization of septal shape. A furosemide infusion (2 mg/h) caused loss of another 5.9 kg following the procedure. The serum creatinine level improved from 350 to 140 μmol/L. Subsequently, he required furosemide 20 mg twice daily.

Case 5

A 70-year-old female patient had a pacemaker implanted and a new RV lead was placed 4 years later for lead failure; the old lead was abandoned. She developed severe right heart failure 10 years later.

Echocardiography showed moderate-to-severe aortic and mitral regurgitation with normal LV size and systolic function. There was severe TR, with the lead impinging on the posterior tricuspid leaflet, an estimated peak RV systolic pressure of 70 mm Hg, and normal RV systolic function. Images were not available for review, and septal shape was not described in the report.

After percutaneous lead replacement, TR was mild to moderate and there was spontaneous diuresis in hospital with no alteration in diuretic dose. The follow-up echocardiogram was not available to assess septal shape. She remained asymptomatic 5 years later.

Case 6

A 24-year-old female patient had a pacemaker implanted at the age of 5 years. Eleven years later, the lead failed and she had a passive fixation VDD pacemaker implanted. Severe TR was diagnosed 7 years later. There was no history of congenital or acquired TV disease; there was minimal TR before lead insertion.

LV size and function were normal; there was severe TR, RV dilation (RV basal diameter 6.1 cm) with normal RV function, and estimated pulmonary artery pressure. There was VSF. A lead impinged on the septal leaflet. The chest radiograph suggested that the 2 leads were at opposite sides of the tricuspid annulus, possibly “spreading” the leaflets apart (Figure 1).

Figure 1

Chest radiograph of case 6, with lead position from 2 intracardiac leads suggestive of interaction with valve leaflets (she also had an abandoned lead from an abdominal system seen on the images).

She underwent lead reimplantation of a new DDDR system. However, a leaflet of the valve became flail. She remained well, not requiring any diuretics, but developed erythrocytosis owing to right-to-left shunting across a patent foramen ovale. VSF persisted. She then underwent surgical repair of her TV and patent foramen ovale closure.

Discussion

In this report of 6 patients with a presumed diagnosis of LITR, we made several important observations. We present a novel approach to the diagnosis of LITR, which, although not necessarily diagnostic in each instance, may provide the clinician with sufficient confidence to reimplant the lead. We also show that percutaneous lead reimplantation may be more beneficial than has been suggested recently. Perhaps most importantly, 5 of 6 patients came from a relatively small academic practice where more than 50 cardiologists work. This suggests that LITR is often unrecognized.

Diagnosis of LITR

Echocardiographic evidence of increased TR following device implantation occurs in 7.2%–39% of cases.5, 6 Echocardiography has been disappointing in attributing heart failure to LITR. Impingement of the lead on the TV may be obvious, but the effect of the lead on valve function is frequently unclear.1, 3, 7 Nevertheless, worsening heart failure in a patient with an RV lead and severe TR should still raise suspicion of LITR. If there is no associated structural heart disease, the lead is likely the culprit. Since patients with implantable leads increasingly have other potential causes of heart failure, one should consider the possibility of LITR.

When right heart failure with TR is worse than expected from any associated left-sided heart disease, one should suspect LITR. That diagnosis would be supported by the presence of VSF, which implies that RVEDP is greater than expected if it is secondary to left failure (Figure 2). If there is no other independent cause of RV failure, that is, conditions other than left heart failure causing pulmonary hypertension or RV dysfunction, LITR is likely. If VSF is absent, the effect of the lead on TR is more difficult to determine unless it clearly prevents leaflet coaptation.

Figure 2

Ventricular septal flattening at end diastole. The left image is for case 1, showing ventricular septal flattening at end diastole, and the right image shows an example of normal septal shape at end diastole.

The time from first implantation to lead removal for severe TR varied from 11 months to 18 years in our patients. It is not known how long it took to develop severe TR and how RV remodeling may have contributed to TR over time. There was similar variation in delay from implantation to surgery in a Mayo Clinic series of 41 patients. It seems likely that the development of LITR is frequently time-dependent; studies suggest that there is no or only minimal worsening of TR shortly after implantation.8, 9

Mechanisms of LITR

Four mechanisms of LITR were well documented in confirmed LITR. The lead may impinge on the valve, perforate a leaflet, be entangled in the TV apparatus, or adhere to the valve.1, 10, 11 With time, thrombosis and encapsulation can also occur.12, 13 RV remodeling secondary to TR may contribute to increasing TR.

One of our patients developed a flail tricuspid leaflet during lead extraction, which was apparent on the intraoperative transesophageal echocardiography. The laser sheath had reached past the tricuspid annulus; how the leaflet became damaged is unclear. This has been reported in 9% of percutaneous procedures. Unfortunately, leaflet perforation has not been readily identifiable by 2-dimensional echocardiography1, 3, 7 and the ability to clearly identify other mechanisms is limited.

Lead extraction/reimplantation

It appears that percutaneous lead extraction can be performed with an acceptable risk of complications (given that the occasional need to manage the procedure-related damage of the TV is the same as the alternative open heart surgery). Despite one of our patients not benefiting from the procedure because of the damage of the valve, 4 of 6 patients still derived substantial clinical benefit without an open heart surgery.

The authors of a recent report of a small series of patients suggested that there is limited benefit of percutaneous lead replacement for LITR. We suggest that identifying the lead as the culprit is a critical first step, which too often has been problematic; our approach correctly diagnosed LITR in 4 of our 6 patients who improved and almost certainly in the one who went on to an open heart surgery.

Incidence of LITR

The fact that 5 of our patients were referred by 1 of more than 50 cardiologists suggests that LITR is often unrecognized. Others have reported a 2.8%–7% incidence of LITR at surgery, but the indication for the surgery was only rarely related primarily to TR, which also suggests that LITR may erroneously be attributed to other structural abnormalities.1, 10 Prospective studies will be required to determine the natural history of asymptomatic TR detected by echocardiography and the true incidence and evolution of LITR.

Study limitations

The present study is limited by its small sample size and the fact that it is retrospective and that a systematic approach was not applied to all patients. However, follow-up was complete and those who responded well to lead replacement had clear clinical improvement.

Conclusion

Our limited experience with patients with presumed LITR and severe heart failure suggests that it is possible to diagnose this problem using a novel clinical echocardiographic approach to predict benefits of percutaneous lead reimplantation. This approach needs to be assessed in a larger number of patients to clarify its predictive power.

KEY TEACHING POINTS

• Lead-induced tricuspid regurgitation is underrecognized, and increased vigilance is needed by health care professionals managing patients with cardiac rhythm management devices. • Echocardiography may be a valuable tool for establishing lead-induced tricuspid regurgitation. • Contrary to traditional teaching, patients with lead-induced tricuspid regurgitation, even with leads that are a few years old, may still benefit from removal of the lead.