Vol 82, No 1 (2024)
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Impact of lead position on tricuspid regurgitation, ventricular function, and heart failure exacerbation and mortality after cardiac implantable electronic device implantation. Preliminary results from the PACE-RVTR Registry

Karolina Chodór-Rozwadowska12, Magdalena Sawicka3, Stanisław Morawski4, Zbigniew Kalarus5, Tomasz Kukulski2
Pubmed: 38319145
Pol Heart J 2024;82(1):53-62.

Abstract

Background: The most frequent mechanism of lead-related tricuspid regurgitation (LRTR), which occurs in 7.2% to 44.7% of patients implanted with a cardiac implantable electronic device (CIED), is leaflet impingement or the restriction of its movement by a ventricular lead. It is unclear if the position of the lead tip — in the right ventricular apex (RVA) or other location (non-RVA) — has any influence on the development of LRTR. The study aimed to determine the impact of the CIED lead tip position on the development or progression of tricuspid regurgitation (TR) and its potential impact on heart failure exacerbation and mortality.
Methods: One hundred and two consecutive patients who received CIEDs between March 2020 and October 2021 were included in the prospective registry (PACE-RVTR). Patients were assigned to two groups depending on the lead position — the RVA group and the non-RVA group. All patients underwent echocardiographic evaluation before implantation and one year later.
Results: In terms of baseline clinical characteristics, the two groups did not differ. Before CIED implantation, patients in the non-RVA group had better left ventricular systolic function (P = 0.004). Pacemakers were implanted more often in the non-RVA group (P = 0.001) while implantable cardioverter-defibrillators in the RVA group (P = 0.008). Progression to severe or massive TR was more common in the non-RVA group (P = 0.005).
Conclusion: Severe and massive TR occurred more often in patients with the non-RVA position of the lead. The right ventricular lead position did not impact heart failure progression or all-cause mortality at two-year follow-up.

ORIGINAL ARTICLE

Impact of lead position on tricuspid regurgitation, ventricular function, and heart failure exacerbation and mortality after cardiac implantable electronic device implantation. Preliminary results from the PACE-RVTR Registry

Karolina Chodór-Rozwadowska12Magdalena Sawicka3Stanisław Morawski4Zbigniew Kalarus5Tomasz Kukulski2
1Doctoral School, Department of Cardiology, Congenital Heart Diseases and Electrotherapy, Silesian Centre for Heart Diseases, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, Katowice, Poland
22nd Department of Cardiology, Medical University of Silesia, Katowice, Specialist Hospital, Zabrze, Poland
3Department of Cardiac Transplantation and Mechanical Circulatory Support, Silesian Centre for Heart Diseases, Zabrze, Poland
4Department of Cardiology, Silesian Centre for Heart Diseases, Zabrze, Poland
5Department of Cardiology, Congenital Heart Diseases and Electrotherapy, Medical University of Silesia, Katowice, Poland

Correspondence to:

Karolina Chodór-Rozwadowska, MD,

Doctoral School, Department of Cardiology, Congenital Heart Diseases and Electrotherapy,

Silesian Centre for Heart Diseases,

Faculty of Medical Sciences in Zabrze,

Medical University of Silesia,

M. Curie-Skłodowskiej 9, 41–800 Zabrze, Poland,

phone: +48 32 373 23 00,

e-mail: d201040@365.sum.edu.pl

Copyright by the Author(s), 2024

DOI: 10.33963/v.kp.98740

Received: September 9, 2023

Accepted: December 29, 2023

Early publication date: January 31, 2024

ABSTRACT
Background: The most frequent mechanism of lead-related tricuspid regurgitation (LRTR), which occurs in 7.2% to 44.7% of patients implanted with a cardiac implantable electronic device (CIED), is leaflet impingement or the restriction of its movement by a ventricular lead. It is unclear if the position of the lead tip in the right ventricular apex (RVA) or other location (non-RVA) has any influence on the development of LRTR.
Aims: The study aimed to determine the impact of the CIED lead tip position on the development or progression of tricuspid regurgitation (TR) and its potential impact on heart failure exacerbation and mortality.
Methods: One hundred and two consecutive patients who received CIEDs between March 2020 and October 2021 were included in the prospective registry (PACE-RVTR). Patients were assigned to two groups depending on the lead position the RVA group and the non-RVA group. All patients underwent echocardiographic evaluation before implantation and one year later.
Results: In terms of baseline clinical characteristics, the two groups did not differ. Before CIED implantation, patients in the non-RVA group had better left ventricular systolic function (P = 0.004). Pacemakers were implanted more often in the non-RVA group (P = 0.001) while implantable cardioverter-defibrillators in the RVA group (P = 0.008). Progression to severe or massive TR was more common in the non-RVA group (P = 0.005).
Conclusion: Severe and massive TR occurred more often in patients with the non-RVA position of the lead. The right ventricular lead position did not impact heart failure progression or all-cause mortality at two-year follow-up.
Key words: cardiac implantable electronic device, heart failure, right ventricle, tricuspid regurgitation, valve disease

WHAT’S NEW?

Severe and massive tricuspid regurgitation occurred more often in patients with the non-right ventricular apex position of the lead. The position of the right ventricular lead did not affect the progression of heart failure and all-cause mortality at one-year follow-up. Tricuspid regurgitation progression by one grade was unaffected by the type of the implanted device.

INTRODUCTION

The development or progression of tricuspid regurgitation (TR) after implantation of cardiac implantable electronic devices (CIEDs) is a growing concern [1–4]. This complication occurs in 7.2% to 44.7% of patients who received CIEDs [1, 2, 5–24]. It may result from ventricular remodeling in the natural course of heart failure (HF) or from a direct interaction between the lead and the tricuspid leaflets. The most frequent mechanism is leaflet impingement or leaflet movement restriction by a ventricular lead [11, 15, 21, 25–28]. Many authors reported that the posterior and septal leaflets are most often affected [10, 11, 15, 17, 21, 23, 26]. The most favorable position of the lead is the center of the valve orifice or one of the commissures [15, 17, 21, 23, 26, 29, 30]. It seems that placement of the lead in the right ventricular apex (RVA) more often causes TR than other locations [27]. The reason for this may be the placement of the lead closer to the posterior leaflet and its impingement [27]. Targeting a non-RVA location for the lead usually results in a central position of the tricuspid orifice [5, 27, 31, 32]. On the other hand, Cheng et al. [26] reported that significant progression of TR after CIED implantation occurred more often when the lead tip was placed in the interventricular septum (IVS). Polewczyk et al. [28] reported that in patients with lead-related tricuspid regurgitation (LRTR), the non-apical location of the lead was more frequent. Some authors claim that the position of the lead is irrelevant to TR development [17, 33, 34]. Nevertheless, coexisting TR in patients with CIEDs is associated with increased mortality [2, 7, 8, 22, 28, 35] and right ventricular failure more often than in patients without TR [6, 8, 11, 12, 22, 23]. Thus, our study aimed to determine the impact of the CIED lead tip position on TR development and progression as well as on the function of the right and left ventricles and decompensated HF-free and survival.

METHODS

Design of the study

One hundred and two consecutive patients who received a CIED pacemaker (PM), implantable cardioverter-defibrillator (ICD), cardiac resynchronization therapy defibrillator (CRT-D), or pacemaker (CRT-P) between March 2020 and October 2021 were involved in the single-center PACE-RVTR registry. Patients were assigned to two groups depending on the lead position the RVA group and the non-RVA group, including the upper lower parts of the IVS, the right ventricular outflow tract (RVOT), and His bundle. The position of the lead was determined on the basis of the description of the implantation procedure and chest radiography in the posteroanterior view, performed routinely after surgery (Figure 1).

Figure 1. Position of the lead. A. Non-right ventricular apex. B. Right ventricular apex

All patients underwent echocardiographic evaluation directly before and one year after CIED implantation (15.2 [12.016.0] months). Clinical data, including mortality and hospital admissions, were retrieved from the electronic medical records. HF-free survival was defined as hospitalization for HF exacerbation or an increase in diuretic doses up to the last check-up of the medical records in July 2023 (25.5 [17.034.0] months). LRTR was defined as an increase in TR severity by at least one grade. The percentage of ventricular pacing was checked one year after implantation.

Echocardiographic examination

Two-dimensional transthoracic echocardiography was performed before CIED implantation and one year later by Vivid 7 GE Healthcare (Chicago, IL, US). TR grade (trivial/none 0, mild 1, moderate 2, severe 3, massive 4), other valvular insufficiencies, dimensions, and function of the right ventricle (RV) and the left ventricle (LV) were evaluated in accordance with the guidelines of the European Association of Cardiovascular Imaging [36, 37]. In the case of the RV, the evaluated parameters included RV and tricuspid valve (TV) diameters in the four-chamber view, RV area, fractional area change, tricuspid annular plane systolic excursion (TAPSE), TAPSE/tricuspid regurgitation peak gradient, and right ventricular systolic pressure; in the case of the left ventricle, these were diastolic and systolic volume and ejection fraction (EF) measured by the Simpson method. The analysis of dyssynchrony was performed according to a review by Galderisi et al. [38], and the main focus was on interventricular dyssynchrony and measured interventricular mechanical delay. According to that article, interventricular mechanical delay >40 ms was considered dyssynchrony.

Data analysis

The Kolmogorov-Smirnov test was used for the evaluation of data distribution. The numerical variables were presented as mean value and standard deviation or median and percentile distribution, depending on the result of the KolmogorovSmirnov test. For normally distributed independent and dependent variables, Student’s t-test and paired Student’s test were used, respectively. The MannWhitney U test was used for comparing the nonparametric independent variables, and the Wilcoxon test for dependent variables. Differences in categorical parameters were checked using Yates’s χ2 and Fisher’s exact tests or McNemar’s test in the case of dependent variables. P <0.05 was adopted as statistically significant. HF-free survival and overall survival were analyzed using the log-rank test and the Kaplan-Meier estimator. Calculations were performed using Statistica 10 software (TIBCO Software Inc., Palo Alto, CA, US).

RESULTS

Baseline characteristics

The average period from CIED implantation to echocardio­graphic examination was 15 (6) months. The RVA group included 24 patients (17 men) and the non-RVA group 78 patients (40 men). In the non-RVA group, 65.7% of patients had the lead in the upper part of the IVS, 5.9% in the lower part, 1.9% in the RVOT, and 2.9% in the His bundle. Median age was 67.9 (60.077.0) years old and was similar in both groups (P = 0.39). The groups did not differ in the prevalence of atrial fibrillation (P = 1.0), coronary heart disease (P = 0.24), diabetes mellitus (P = 0.61), or chronic obstructive pulmonary disease (P = 1.0) (Table 1).

Table 1. Patient characteristics

All

(n = 102)

RVA

(n = 24)

Non-RVA

(n = 78)

P-value

Men, n (%)

57 (55.9)

17 (70.8)

40 (51.3)

0.10

Age, years, median (Q1–Q3)

67.9 (60.0–77.0)

66.5 (58.0–77.0)

68.4 (61.0–76.0)

0.39

Weigh, kg, median (Q1–Q3)

83.7 (73.0–91.5)

84.0 (71.5–92.0)

83.6 (74.0–91.5)

0.68

Height, m, median (Q1–Q3)

1.70 (1.64–1.76)

1.73 (1.67–1.78)

1.69 (1.64–1.76)

0.25

Coronary artery disease, n (%)

52 (50.9)

15 (62.5)

37 (47.4)

0.24

Diabetes mellitus, n (%)

29 (28.4)

8 (33.3)

21 (26.9)

0.61

Pulmonary disease, n (%)

7 (6.9)

1 (4.2)

5 (6.4)

1.00

Atrial fibrillation, n (%)

38 (3.2)

9 (37.5)

29 (37.2)

1.00

NYHA class, n (%)

I

60 (58.8)

8 (33.3)

52 (66.7)

0.03

II

34 (33.3)

14 (58.3)

20 (25.6)

III

5 (4.9)

1 (4.2)

4 (5.1)

IV

3 (2.9)

1 (4.2)

2 (2.6)

Bilirubin, µmol/l, median (Q1-Q3)

12.8 (7.2–14.6)

11.3 (7.1–12.4)

13.3 (7.2–17.5)

0.33

INR, median (Q1–Q3)

1.6 (0.9–1.2)

1.2 (0.9–1.1)

1.7 (0.9–1.2)

0.49

Creatinine, µmol/l, median (Q1–Q3)

89.9 (75.0–103.0)

100.9 (81.5–114.5)

86.5 (69.0–101.0)

0.008

Time since CIED implantation, months, median (Q1–Q3)

15.2 (12.0–16.0)

15.7 (12.0–15.0)

15.1 (12.0–16.0)

0.97

Before CIED implantation, patients in the non-RVA group showed better LV systolic function 52.5% (33.057.0%) vs. 32.5% (23.549.5%); P = 0.004; they also a lower New York Heart Association (NYHA) classification grade (P = 0.03). They exhibited lower LV end-diastolic volume (113.0 [81.5157.0] ml vs. 175.5 [149.0219.0] ml; P = 0.001) and systolic volume (45.5 [33.095.0] ml vs. 129.0 [92.0154.0] ml; P = 0.001); the same relation persisted after CIED implantation. The groups did not differ in terms of the right ventricular dimension and function or TR and other valvular diseases (Table 2).

Table 2. Results of echocardiographic examination before cardiac implantable electronic device implantation

All

(n = 102)

RVA

(n = 24)

Non-RVA

(n = 78)

P-value

RV dimension in four-chamber view, mm, median (Q1–Q3)

37.0 (35.0–40.0)

38.0 (35.0–40.0)

37.0 (35.0–41.0)

0.86

Area of RA in diastole, cm2, median (Q1–Q3)

17.4 (15.0–21.7)

16.9 (14.3–21.0)

17.7 (15.4–21.9)

0.33

Area of RA in systole, cm2, median (Q1–Q3)

12.0 (10.4–16.3)

12.0 (11.0–14.9)

12.2 (10.3–16.5)

0.87

TV diameter, mm, median (Q1–Q3)

32.0 (29.0–38.0)

31.0 (29.0–35.0)

33.0 (29.0–38.0)

0.67

FAC, %, mean (SD)

38.4 (10.6)

38.1 (11.0)

38.5 (10.5)

0.89

TAPSE, mm, median (Q1–Q3)

20.0 (17.0–23.0)

18.0 (16.0–21.0)

20.0 (17.0–25.0)

0.15

RVSP, mm Hg, mean (SD)

33.8 (15.8)

33.5 (19.3)

33.9 (14.9)

0.94

TAPSE/TRPG, mm/mm Hg, median (Q1–Q3)

0.5 (0.4–0.9)

0.5 (0.3–0.9)

0.5 (0.4–0.9)

0.84

LV EDV, ml, median (Q1–Q3)

127.5 (86.0–169.0)

175.5 (149.0–219.0)

113.0 (81.5–157.0)

0.001

LV ESV, ml, median (Q1–Q3)

58.0 (36.0–120.0)

129.0 (92.0–154.0)

45.5 (33.0–95.0)

0.001

LVEF, %, median (Q1–Q3)

50.0 (30.0–55.0)

32.5 (23.5–49.5)

52.5 (33.0–57.0)

0.004

TR, n (%)

None/trace

59 (57.8)

11 (45.8)

48 (61.5)

0.50

Mild

32 (31.4)

10 (41.7)

22 (28.2)

Medium

10 (9.8)

3 (12.5)

7 (8.9)

Severe

1 (0.9)

0 (0.0)

1 (1.3)

Massive

0 (0.0)

0 (0.0)

0 (0.0)

Aortic stenosis, n (%)

None

88 (86.3)

23 (96.0)

65 (83)

0.13

Mild

10 (9.8)

0 (0.0)

10 (12.8)

Medium

3 (2.9)

0 (0.0)

3 (3.8)

Severe

1 (0.9)

1 (4.2)

0 (0.0)

Aortic regurgitation, n (%)

None

88 (86.3)

18 (75.0)

70 (90.0)

0.1

Mild

11 (10.8)

4 (16.7)

7 (8.9)

Medium

3 (2.9)

2 (8.3)

1 (1.3)

Severe

0 (0.0)

0 (0.0)

0 (0.0)

Mitral stenosis, n (%)

Mild

0 (0.0)

0 (0.0)

0 (0.0)

1.0

Medium

0 (0.0)

0 (0.0)

0 (0.0)

Severe

0 (0.0)

0 (0.0)

0 (0.0)

Mitral regurgitation, n (%)

None

58 (56.8)

11 (54.2)

47 (60.3)

0.43

Mild

30 (29.4)

7 (29.2)

23 (29.5)

Medium

9 (8.8)

4 (16.7)

5 (6.4)

Severe

5 (4.9)

2 (8.3)

3 (3.8)

Pacemakers were implanted more often in the non-RVA group and ICDs in the RVA group (P = 0.003). CRT devices were implanted in both groups with the same frequency. The groups did not differ in terms of the pacing mode (P = 0.11) and ventricular pacing percentage (group 1: 37.5% [1.099.0%] vs. group 2: 19.1 [1.091.0%]; P = 0.81) (Table 3).

Table 3. Results of cardiac implantable electronic device implantation (CIED) controls and echocardiographic examinations after one year of follow-up

All

(n = 102)

RVA

(n = 24)

Non-RVA

(n = 78)

P-value

CIED type and parameters

Type of device, n (%)

PM

58 (56.9)

6 (25.0)

52 (66.7)

0.003

ICD

28 (27.5)

12 (50.0)

16 (20.5)

CRT-P/CRT-D

16 (15.6)

6 (25.0)

10 (12.8)

Pacing mode, n (%)

AAI

0 (0.0)

0 (0.0)

0 (0.0)

0.11

VVI

27 (26.5)

8 ( 33.3)

19 (24.4)

DDD

60 (58.8)

10 (41.7)

50 (64.1)

BiV

15 (14.7)

6 (25.0)

9 (11.5)

Percentage of ventricular pacing, %, median (Q1–Q3)

20.0 (1.0–93.0)

37.5 (1.0–99.0)

19.1 (1.0–91.0)

0.81

Echocardiographic parameters

TV diameter, mm, median (Q1–Q3)

33.0 (30.0–38.0)

33.5 (29.0–38.0)

33.0 (36.0–42.0)

0.98

FAC, %, mean (SD)

41.7 (11.2)

37.4 (10.6)

43.1 (.11.1)

0.03

TAPSE, mm, mean (SD)

19.5 (4.7)

17.9 (4.2)

20.0 (4.8)

0.06

RVSP, mm Hg, mean (SD)

30.2 (14.2)

29.3 (17.5)

30.4 (13.4)

0.79

TAPSE/TRPG, mm/mm Hg, median (Q1–Q3)

0.62 (0.46–0.94)

0.53 (0.45–1.2)

0.65 (0.47–0.93)

0.57

LV EDV, ml, median (Q1–Q3)

114.8 (86.0–166.0)

149.5 (119.0–236.0)

108.2 (85.3–194.0)

0.003

LV ESV, ml, median (Q1–Q3)

59.0 (38.0–103.0)

93.0 (49.5–146.0)

55.5 (32.5–80.5)

0.003

LVEF, %, median (Q1–Q3)

49.0 (31.0–58.0)

30.0 (26.5–51.5)

53.0 (38.0–59.0)

0.003

TR, n (%)

None/trace

28 (27.4)

9 (37.5)

19 (24.4)

0.33

Mild

43 (42.2)

8 (33.3)

35 (44.9)

Medium

17 (16.7)

6 (25.0)

11 (14.1)

Severe

10 (9.8)

1 (4.2)

9 (11.5)

Massive

2 (1.9)

0 (0.0)

2 (2.6)

Aortic stenosis, n (%)

None

92 (90.2)

23 (96.8)

69 (88.5)

0.051

Mild

7 (6.9)

1 (4.2)

6 (7.7)

Medium

3 (2.9)

0 (0.0)

3 (3.8)

Severe

0 (0.0)

0 (0.0)

0 (0.0)

Aortic regurgitation, n (%)

None

88 (86.2)

16 (66.7)

72 (92.3)

0.1

Mild

11 (10.8)

5 (20.8)

6 (7.7)

Medium

3 (2.9)

3 (12.5)

0 (0.0)

Severe

0 (0.0)

0 (0.0)

0 (0.0)

Mitral stenosis, n (%)

None

97 (95)

22 (91.7)

75 (96.2)

0.19

Mild

4 (3.9)

1 (4.2)

3 (3.8)

Medium

1 (0.9)

1 (4.2)

0 (0.0)

Severe

0 (0.0)

0 (0.0)

0 (0.0)

Mitral regurgitation, n (%)

None

54 (52. 9)

9 (37.5)

45 (57.7)

0.09

Mild

30 (29.4)

10 (41.7)

20 (25.6)

Medium

16 (15.7)

5 (20.8)

11 (14.1)

Severe

2 (1.9)

0 (0.0)

2 (2.6)

Interventricular dyssynchrony, n (%)

IVMD >40 ms

13 (12.7)

2 (8.3)

11 (14.1)

0.719

Tricuspid valve and right ventricle at one-year follow-up

Tricuspid regurgitation progression in both groups was similar (by one grade P = 0.33; by two or more grades P = 0.35) (Table 4). Comparison of particular TR degrees before and after CIED implantation, respectively, is as follows (Table 5):

Table 4. Level of progression of tricuspid regurgitation (TR) after cardiac implantable electric device (CIED) implantation and the position of the lead

All

(n = 102)

RVA

(n = 24)

Non-RVA

(n = 78)

P-value

TR progression

No progression, n (%)

42 (41.2)

13 (54.2)

29 (37.2)

0.16

TR progression by 1 grade n (%)

35 (34.3)

6 (25.0)

29 (37.2)

0.33

None/trace to mild

25 (24.5)

3 (12.5)

22 (28.2)

Mild to moderate

5 (4.9)

2 (8.3)

3 (3.8)

Moderate to severe

4 (3.9)

1 (4.2)

3 (3.8)

Severe to massive

1 (0.9)

0 (0.0)

1 (1.3)

TR progression by ≥2 grade, n (%)

16 (15.7)

2 (8.3)

14 (17.9)

0.35

None/trace to medium

9 (8.8)

2 (8.3)

7 (8.9)

None/trace to severe

2 (1.9)

0 (0.0)

2 (2.6)

Mild to severe

5 (4.9)

0 (0.0)

5 (6.4)

Moderate to massive

0 (0.0)

0 (0.0)

0 (0.0)

Regression, n (%)

10 (9.8)

3 (125)

7 (8.9)

0.69

All

(n = 102)

RVA

(n = 24)

Non-RVA

(n = 78)

P-value

(Group 1 vs. Group 2)

PM

(n = 58)

ICD/

CRT-D/

CRT-P

(n = 44)

P-value

PM

(n = 6)

ICD/

CRT-D/

CRT-P

(n = 18)

P-value

PM

(n = 52)

ICD/

CRT-D/

CRT-P

(n = 26)

P-value

PM

ICD/

CRT-D/

CRT-P

TR progression due to CIED type

No progression, n (%)

22 (37.9)

19 (43.2)

0.68

4 (66.7)

9 (50.0)

0.65

18 (34.6)

10 (38.5)

0.80

0.187

0.54

Progression by 1 grade, n (%)

24 (41.4)

11 (25.0)

0.09

1 (16.7)

5 (27.8)

1.00

23 (44.2)

6 (23.1)

0.09

0.384

0.74

Progression by ≥2 grades, n (%)

6 (10.3)

10 (22.7)

0.10

0 (0.0)

2 (11.1)

1.00

6 (11.5)

8 (30.8)

0.06

1.000

0.16

Regression, n (%)

6 (10.3)

4 (9.1)

1.00

1 (16.7)

2 (11.1)

1.00

5 (9.6)

2 (7.7)

1.00

0.497

1.00

Table 5. Comparison of changes in echocardiographic parameters before and after implantation of cardiac implantable electric devices

Parameter

All

(n = 102)

RVA

(n = 24)

Non-RVA

(n = 78)

Before implantation

After implantation

P-value

Before implantation

After implantation

P-value

Before implantation

After implantation

P-value

TR grade, n (%)

None

59 (57.8)

28 (27.4)

0.001

11 (45.8)

9 (37.5)

0.77

48 (61.5)

19 (24.4)

0.001

Mild

32 (31.4)

43 (42.2)

0.15

10 (41.7)

8 (33.3)

0.76

22 (28.2)

35 (44.9)

0.045

Medium

10 (9.8)

17 (16.7)

0.21

3 (12.5)

6 (25.0)

0.46

7 (8.9)

11 (14.1)

0.45

≥Severe

1 (0.9)

12 (11.7)

0.002

0 (0.0)

1 (4.2)

1.00

1 (1.3)

11 (14.1)

0.005

RA in diastole, cm2, median (Q1–Q3)

17.4 (15.0–21.7)

19.4 (16.3–24.0)

0.12

16.9 (14.3–21.0)

18.5 (15.4–21.3)

0.74

17.7 (15.4–21.9)

19.8 (16.6–24.2)

0.11

RA in systole, cm2, median (Q1–Q3)

12.0 (10.4–16.3)

13.0 (11.3–16.9)

0.33

12.0 (11.0–14.9)

12.2 (10.1–15.5)

0.79

12.2 (10.3–16.5)

13.2 (11.5–18.1)

0.37

TV diameter, mm, median (Q1–Q3)

32.0 (29.0–38.0)

33.0 (30.0–38.0)

0.39

31.0 (29.0-35.0)

33.5 (29.0–38.0)

0.11

33.0 (29.0–38.0)

33.0 (36.0–42.0)

0.82

RV in 4 chambers, mm, median (Q1–Q3)

37.0 (35.0–40.0)

38.0 (36.0–42.0)

0.15

38.0 (35.0–40.0)

37.0 (34.0–42.0)

0.79

37.0 (35.0–41.0)

38.0 (36.0–42.0)

0.07

RV in diastole, cm2, mean (SD)

18.9 (5.4)

20.5 (5.9)

0.004

18.3 (4.3)

21.0 (6.1)

0.06

19.2 (5.8)

20.3 (5.8)

0.03

RVSP, mm Hg, mean (SD)

33.8 (15.8)

30.2 (14.2)

0.06

33.5 (19.3)

29.3 (17.5)

0.39

33.9 (14.9)

30.4 (13.4)

0.08

FAC RV, %, mean (SD)

38.4 (10.6)

41.7 (11.2)

0.28

38.1 (11.0)

37.4 (10.6)

0.88

38.5 (10.5)

43.1 (11.1)

0.17

TAPSE, mm, median (Q1–Q3)

20.0 (17.0–23.0)

19.5 (4.7)

0.32

18.0 (16.0–21.0)

17.9 (4.2)

0.29

20.0 (17.0–25.0)

20.0 (4.8)

0.57

TAPSE/TRPG, mm/mm Hg, median (Q1–Q3)

0.5 (0.4–0.9)

0.62 (0.46–0.94)

0.12

0.5 (0.3–0.9)

0.53 (0.45–1.2)

1.00

0.5 (0.4–0.9)

0.65 (047–0.93)

0.10

LV EDV, ml, median (Q1–Q3)

127.5 (86.0–169.0)

114.8 (86.0–166.0)

0.38

175.5 (149.0–219.0)

149.5 (119.0–236.0)

0.72

113.0 (81.5–157.0)

108.2 (85.3–194.0)

0.51

LV ESV, ml, median (Q1–Q3)

58.0 (36.0–120.0)

59.0 (38.0–103.0)

0.36

129.0 (92.0–154.0)

93.0 (49.5–146.0)

0.49

45.5 (33.0–95.0)

55.5 (32.5–80.5)

0.69

LVEF, %, median (Q1–Q3)

50.0 (30.0–55.0)

49.0 (31.0–58.0)

0.003

32.5 (23.5–49.5)

30.0 (26.5–51.5)

0.24

52.5 (33.0–57.0)

53.0 (38.0–59.0)

0.006

  • The non-RVA group: none/trivial TR (61.5% vs. 24.4%; P = 0.001), mild TR (28.3% vs. 44.9%; P = 0.04), moderate TR (8.9% vs. 14.1%; P = 0.45), severe and massive TR (1.3% vs. 14.1%; P = 0.005);
  • The RVA group: none/trivial TR (45.8% vs. 37.5%; P = 0.77), mild TR (41.7% vs. 33.3%; P = 0.76), moderate TR (12.5% vs. 25.0%; P = 0.46), severe and massive TR (0.0% vs. 4.2%; P = 1.00).

In the non-RVA group, TR progression by at least one grade was related to the position of the lead in the upper part of the IVS. Moreover, interventricular dyssynchrony did not affect TR progression in all patients (P = 0.55) (Table 6).

Table 6. Progression of tricuspid regurgitation in relation to the position of the lead within the right ventricle and interventricular dyssynchrony

All

(n = 102)

No progression or decrease in TR

(n = 51)

Progression of TR by at least 1 degree

(n = 51)

P-value

Upper part of IVS, n (%)

67 (65.7)

28 (54.9)

39 (76.5)

0.04

Lower part of IVS, n (%)

6 (5.9)

5 (9.8)

1 (1.9)

0.20

RVOT, n (%)

2 (1.9)

1 (1.9)

1 (1.9)

1.00

His bundle, n (%)

3 (2.9)

1 (1.9)

2 (3.9)

1.00

Apex, n (%)

24 (23.5)

16 (31.4)

8 (15.7)

0.10

Dyssynchrony, n (%)

13 (12.7)

5 (9.8)

8 (15.7)

0.55

Tricuspid regression progression by one grade was independent of the type of the implanted device (patients with PM: non-RVA 34.6% vs. RVA 66.7%; P = 0.19 and with ICD/CRT-D/CRT-P: non-RVA 23.1% vs. RVA 27.8%; P = 0.74). Moreover, in patients in the non-RVA group with ICDs and CRT-Ds, there was a tendency for TR progression by 2 or more grades in comparison to patients with PMs (P = 0.06) (Table 4).

Fractional area change was higher in the non-RVA group than in the RVA group (43.1% [mean SD 11.1%] vs. 37.4 [mean SD 10.6%]; P = 0.03); however, other parameters of the right ventricular function and dimensions were comparable in both groups (Table 5).

In the non-RVA group, the RV area was larger than before implantation (20.3 [mean SD 5.8] cm2 vs. 19.2 [mean SD 5.8] cm2 before implantation; P = 0.03), and EF increased to 53.0 (38.059.0)% from 52.5 (33.057.0)%; P = 0.006 (Table 5).

Mortality and heart failure exacerbation at two-year follow-up

The two groups did not differ in terms of the HF decompensation rate (RVA group 25.0% vs. non-RVA group 25.6%; P = 0.64) and deaths (RVA group 4.2% vs. non-RVA group 5.1%; P = 0.58) (Figure 2).

Figure 2. Overall survival and heart failure decompensation
Abbreviations: see Table 1

DISCUSSION

This study aimed to determine the impact of the CIED lead tip position on TR development and progression as well as on the RV and LV function and decompensated HF-free and overall survival.

The non-RVA group was more numerous, as it is believed that non-apical pacing is more physiological and ensures better function of the right and left ventricles; therefore, this position is preferable [39, 40]. At the beginning of the study, the group included healthier patients with higher EF and lower NYHA grades who could tolerate CIED implantation better and usually could bear longer attempts to place the lead in a position other than the RV apex. TR progression was more pronounced in the non-RVA group, with a significantly higher number of severe and massive TR. As TR progression was mainly related to the position of the lead in the upper part of the IVS, this may have resulted from damaging the TV apparatus when attempting to obtain the target position of the lead in the IVS, as the chordae tendineae of the TV are densely distributed in the RV and some of them are directly connected to the IVS [41]. This finding is consistent with the observations of Cheng et al. [26] and Polewczyk et al. [28]. On the other hand, in the study of Yu et al. [27], including only patients with pacemakers, targeting the lead to a non-RVA position resulted in placing it in the middle of the TV with the lowest chance of the leaflet impingement, while RVA placement was associated with TR progression. According to Saito et al. [33], the RV pacing site is not associated with TR worsening and did not directly affect RV function at a 2-year follow-up. Rothschild, Schleifer, and Poorzand drew a similar conclusion [17, 34, 42], and Anvardeen et al. [43] suggested that only tricuspid leaflet interference by the endocardial lead is a predictor of TR development or progression, which in turn, in studies by other authors, is more often found in the case of the RVA lead position [27].

The question arises which option is safer for the patient the non-RVA position with more physiological pacing and location in the middle of the TV (provided that the TV apparatus is not damaged during the attempts to achieve that position), or RVA placement with higher risk of the lead restricting movements of the posterior leaflet.

As non-RVA pacing prevents the RV and LV negative remodeling [40, 44], which is consistent with the results of our study, and, consequently, secondary TR, non-RVA lead placement seems to be a better solution if surgery is performed by an experienced electrophysiologist who can place the lead in the desired location without unnecessary manipulation and risk of entanglement and damage to the chordae tendinae. Three-D echocardiographic examination performed during the procedure and directly after lead implantation may help prevent severe TR development because it enables lead replacement if its position is not optimal for TV functioning.

The importance of pacing the heart as physiologically as possible led to the development of the idea of His bundle pacing. Zaidi et al. reported that patients with His bundle pacing had a lower risk of developing LRTR; they also had decreased severity of existing TR and improved LVEF [45].

According to Xin et al. [46], who conducted an almost 10-year follow-up of RVA pacing in patients with normal LV function, long-term RVA pacing significantly increased ventricular dyssynchrony and TR degree. In our study, which had a shorter follow-up period, we did not observe any difference in the occurrence of dyssynchrony between both groups or any impact on the progression of TR.

The impact of the lead position on heart function, decompensated HF, or mortality was not demonstrated in this study. The most significant limitation of our study is a relatively short follow-up period, while RV remodeling and TR development may occur after a longer period, as presented in a meta-analysis from 2022 [2]. In our study, none of the patients with severe or more advanced tricuspid regurgitation experienced deterioration of right ventricular function, which, in the light of the current ESC guidelines for the management of valvular heart disease [47], provided an argument for the Heart Team to forego both tricuspid valve correction and lead replacement. In fact, further observation is needed to determine whether early replacement of the right ventricular lead would be a better solution than waiting for the occurrence of the right ventricular enlargement or dysfunction, especially since it is safer to remove the lead soon after implantation before it adheres to the structures of the tricuspid valve apparatus and the right ventricle. The study participants are still followed up with periodical assessments of their symptoms and changes in parameters of the right ventricular function. If their condition worsens, they will be re-qualified for intervention. Rdzanek et al. suggested in their study [48] that the presence of PM leads, when they collide with the valve leaflets, decreases the chances of a successful percutaneous tricuspid edge-to-edge procedure. However, they did not consider the presence of CIED leads as an echocardiographic exclusion criterion and indicated that the commissural position is preferable for edge-to-edge repair [48]. An often-studied aspect is the impact of CIED type on TR progression. Some authors suggest that ICDs predispose to TR because defibrillator leads are thicker and more rigid than pacing leads, which makes it more difficult to maneuver them into the target position, and damaging the tricuspid valve apparatus is more likely [6, 18, 22, 26, 49, 50]. In our study, in patients in the non-RVA groups with ICD/CRT-D devices, there was a tendency for TR progression by two or more grades (P = 0.06) (Table 4).

Limitations of the study

The most significant limitations of the study are the small number of patients and the relatively short follow-up period. Moreover, the difference between both groups in terms of LVEF, LV end-diastolic volume, LV ESV, creatine level, and NYHA class is the major drawback of our study. We did not perform systematic imaging of the tricuspid valve using a three-dimensional probe, which precluded the determination of the RV lead position within the tricuspid orifice.

CONCLUSION

Severe and massive TR occurred in patients with the non-RVA position of the lead. The position of the lead did not impact HF exacerbation or mortality at two years of follow-up.

Article information

Conflict of interest: None declared.

Funding: None.

Open access: This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, which allows downloading and sharing articles with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially. For commercial use, please contact the journal office at kardiologiapolska@ptkardio.pl

REFERENCES

  1. Tatum R, Maynes EJ, Wood CT, et al. Tricuspid regurgitation associated with implantable electrical device insertion: A systematic review and meta-analysis. Pacing Clin Electrophysiol. 2021; 44(8): 12971302, doi: 10.1111/pace.14287, indexed in Pubmed: 34081789.
  2. Zhang XX, Wei M, Xiang R, et al. Incidence, risk factors, and prognosis of tricuspid regurgitation after cardiac implantable electronic device implantation: a systematic review and meta-analysis. J Cardiothorac Vasc Anesth. 2022; 36(6): 17411755, doi: 10.1053/j.jvca.2021.06.025, indexed in Pubmed: 34389210.
  3. Gelves-Meza J, Lang RM, Valderrama-Achury MD, et al. Tricuspid regurgitation related to cardiac implantable electronic devices: an integrative review. J Am Soc Echocardiogr. 2022; 35(11): 11071122, doi: 10.1016/j.echo.2022.08.004, indexed in Pubmed: 35964911.
  4. Wang N, Fulcher J, Abeysuriya N, et al. Tricuspid regurgitation is associated with increased mortality independent of pulmonary pressures and right heart failure: a systematic review and meta-analysis. Eur Heart J. 2019; 40(5): 476484, doi: 10.1093/eurheartj/ehy641, indexed in Pub­med: 30351406.
  5. Lee RC, Friedman SE, Kono AT, et al. Tricuspid regurgitation following implantation of endocardial leads: incidence and predictors. Pacing Clin Electrophysiol. 2015; 38(11): 12671274, doi: 10.1111/pace.12701, indexed in Pubmed: 26234305.
  6. Arabi P, Özer N, Ateş AH, et al. Effects of pacemaker and implantable cardioverter defibrillator electrodes on tricuspid regurgitation and right sided heart functions. Cardiol J. 2015; 22(6): 637644, doi: 10.5603/CJ.a2015.0060, indexed in Pubmed: 26412607.
  7. Al-Bawardy R, Krishnaswamy A, Rajeswaran J, et al. Tricuspid regurgitation and implantable devices. Pacing Clin Electrophysiol. 2015; 38(2): 259266, doi: 10.1111/pace.12530, indexed in Pubmed: 25377489.
  8. Delling FN, Hassan ZK, Piatkowski G, et al. Tricuspid regurgitation and mortality in patients with transvenous permanent pacemaker leads. Am J Cardiol. 2016; 117(6): 988992, doi: 10.1016/j.amjcard.2015.12.038, indexed in Pubmed: 26833208.
  9. Rydlewska A, Ząbek A, Boczar K, et al. Tricuspid valve regurgitation in the presence of endocardial leads - an underestimated problem. Postepy Kardiol Interwencyjnej. 2017; 13(2): 165169, doi: 10.5114/pwki.2017.68073, indexed in Pubmed: 28798789.
  10. Nakajima H, Seo Y, Ishizu T, et al. Features of lead-induced tricuspid regurgitation in patients with heart failure events after cardiac implantation of electronic devices a three-dimensional echocardiographic study. Circ J. 2020; 84(12): 23022311, doi: 10.1253/circj.CJ-20-0620, indexed in Pubmed: 33071243.
  11. Seo Y, Nakajima H, Ishizu T, et al. Comparison of outcomes in patients with heart failure with versus without lead-induced tricuspid regurgitation after cardiac implantable electronic devices implantations. Am J Cardiol. 2020; 130: 8593, doi: 10.1016/j.amjcard.2020.05.039, indexed in Pubmed: 32622503.
  12. Papageorgiou N, Falconer D, Wyeth N, et al. Effect of tricuspid regurgitation and right ventricular dysfunction on long-term mortality in patients undergoing cardiac devices implantation: >10-year follow-up study. Int J Cardiol. 2020; 319: 5256, doi: 10.1016/j.ijcard.2020.05.062, indexed in Pubmed: 32470533.
  13. Lee WC, Fang HY, Chen HC, et al. Progressive tricuspid regurgitation and elevated pressure gradient after transvenous permanent pacemaker implantation. Clin Cardiol. 2021; 44(8): 10981105, doi: 10.1002/clc.23656, indexed in Pubmed: 34036612.
  14. Riesenhuber M, Spannbauer A, Gwechenberger M, et al. Pacemaker lead-associated tricuspid regurgitation in patients with or without pre-existing right ventricular dilatation. Clin Res Cardiol. 2021; 110(6): 884894, doi: 10.1007/s00392-021-01812-3, indexed in Pubmed: 33566185.
  15. Seo Y, Ishizu T, Nakajima H, et al. Clinical utility of 3-dimensional echocardiography in the evaluation of tricuspid regurgitation caused by pacemaker leads. Circ J. 2008; 72(9): 14651470, doi: 10.1253/circj.cj-08-0227, indexed in Pubmed: 18724023.
  16. Kanawati J, Ng AC, Khan H, et al. Long-Term follow-up of mortality and heart failure hospitalisation in patients with intracardiac device-related tricuspid regurgitation. Heart Lung Circ. 2021; 30(5): 692697, doi: 10.1016/j.hlc.2020.08.028, indexed in Pubmed: 33132050.
  17. Poorzand H, Tayyebi M, Hosseini S, et al. Predictors of worsening TR severity after right ventricular lead placement: any added value by post-procedural fluoroscopy versus three-dimensional echocardiography? Cardiovasc Ultrasound. 2021; 19(1): 37, doi: 10.1186/s12947-021-00267-w, indexed in Pubmed: 34802441.
  18. Kim JB, Spevack DM, Tunick PA, et al. The effect of transvenous pacemaker and implantable cardioverter defibrillator lead placement on tricuspid valve function: an observational study. J Am Soc Echocardiogr. 2008; 21(3): 284287, doi: 10.1016/j.echo.2007.05.022, indexed in Pubmed: 17604958.
  19. Klutstein M, Balkin J, Butnaru A, et al. Tricuspid incompetence following permanent pacemaker implantation. Pacing Clin Electrophysiol. 2009; 32(Suppl 1): S135S137, doi: 10.1111/j.1540-8159.2008.02269.x, indexed in Pubmed: 19250077.
  20. Alizadeh A, Sanati HR, Haji-Karimi M, et al. Induction and aggravation of atrioventricular valve regurgitation in the course of chronic right ventricular apical pacing. Europace. 2011; 13(11): 15871590, doi: 10.1093/europace/eur198, indexed in Pubmed: 21742681.
  21. Addetia K, Maffessanti F, Mediratta A, et al. Impact of implantable transvenous device lead location on severity of tricuspid regurgitation. J Am Soc Echocardiogr. 2014; 27(11): 11641175, doi: 10.1016/j.echo.2014.07.004, indexed in Pubmed: 25129393.
  22. Höke U, Auger D, Thijssen J, et al. Significant lead-induced tricuspid regurgitation is associated with poor prognosis at long-term follow-up. Heart. 2014; 100(12): 960968, doi: 10.1136/heartjnl-2013-304673, indexed in Pubmed: 24449717.
  23. Mediratta A, Addetia K, Yamat M, et al. 3D echocardiographic location of implantable device leads and mechanism of associated tricuspid regurgitation. JACC Cardiovasc Imaging. 2014; 7(4): 337347, doi: 10.1016/j.jcmg.2013.11.007, indexed in Pubmed: 24631508.
  24. Fanari Z, Hammami S, Hammami MB, et al. The effects of right ventricular apical pacing with transvenous pacemaker and implantable cardioverter defibrillator on mitral and tricuspid regurgitation. J Electrocardiol. 2015; 48(5): 791797, doi: 10.1016/j.jelectrocard.2015.07.002, indexed in Pubmed: 26216371.
  25. Polewczyk A, Kutarski A, Tomaszewski A, et al. Lead dependent tricuspid dysfunction: Analysis of the mechanism and management in patients referred for transvenous lead extraction. Cardiol J. 2013; 20(4): 402410, doi: 10.5603/CJ.2013.0099, indexed in Pubmed: 23913459.
  26. Cheng Y, Gao H, Tang L, et al. Clinical utility of three-dimensional echocardiography in the evaluation of tricuspid regurgitation induced by implantable device leads. Echocardiography. 2016; 33(11): 16891696, doi: 10.1111/echo.13314, indexed in Pubmed: 27539645.
  27. Yu YJ, Chen Y, Lau CP, et al. Nonapical right ventricular pacing is associated with less tricuspid valve interference and long-term progress of tricuspid regurgitation. J Am Soc Echocardiogr. 2020; 33(11): 13751383, doi: 10.1016/j.echo.2020.06.014, indexed in Pubmed: 32828623.
  28. Polewczyk A, Jacheć W, Nowosielecka D, et al. Lead dependent tricuspid valve dysfunction-risk factors, improvement after transvenous lead extraction and long-term prognosis. J Clin Med. 2021; 11(1), doi: 10.3390/jcm11010089, indexed in Pubmed: 35011829.
  29. Addetia K, Harb S, Hahn R, et al. Cardiac implantable electronic device lead-induced tricuspid regurgitation. JACC: Cardiovascular Imaging. 2019; 12(4): 622636, doi: 10.1016/j.jcmg.2018.09.028, indexed in Pub­med: 30947905.
  30. Orban M, Orban M, Hausleiter J, et al. Tricuspid regurgitation and right ventricular dysfunction after cardiac device implantation Is it time for intra-procedural TEE-guided lead implantation? Int J Cardiol. 2020; 321: 131132, doi: 10.1016/j.ijcard.2020.07.010, indexed in Pubmed: 32673696.
  31. Zhang HX, Qian J, Hou FaQ, et al. Comparison of right ventricular apex and right ventricular outflow tract septum pacing in the elderly with normal left ventricular ejection fraction: long-term follow-up. Kardiol Pol. 2012; 70(11): 11301139, indexed in Pubmed: 23180520.
  32. Occhetta E, Bortnik M, Magnani A, et al. Prevention of ventricular desynchronization by permanent para-Hisian pacing after atrioventricular node ablation in chronic atrial fibrillation: a crossover, blinded, randomized study versus apical right ventricular pacing. J Am Coll Cardiol. 2006; 47(10): 19381945, doi: 10.1016/j.jacc.2006.01.056, indexed in Pubmed: 16697308.
  33. Saito M, Iannaccone A, Kaye G, et al. Effect of right ventricular pacing on right ventricular mechanics and tricuspid regurgitation in patients with high-grade atrioventricular block and sinus rhythm (from the protection of left ventricular function during right ventricular pacing study). Am J Cardiol. 2015; 116(12): 18751882, doi: 10.1016/j.amjcard.2015.09.041, indexed in Pubmed: 26517949.
  34. Schleifer JW, Pislaru SV, Lin G, et al. Effect of ventricular pacing lead position on tricuspid regurgitation: A randomized prospective trial. Heart Rhythm. 2018; 15(7): 10091016, doi: 10.1016/j.hrthm.2018.02.026, indexed in Pubmed: 29496605.
  35. Di Mauro M, Bezante GP, Di Baldassarre A, et al. Functional tricuspid regurgitation: an underestimated issue. Int J Cardiol. 2013; 168(2): 707715, doi: 10.1016/j.ijcard.2013.04.043, indexed in Pubmed: 23647591.
  36. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2015; 16(3): 233270, doi: 10.1093/ehjci/jev014, indexed in Pubmed: 25712077.
  37. Lancellotti P, Tribouilloy C, Hagendorff A, et al. Recommendations for the echocardiographic assessment of native valvular regurgitation: an executive summary from the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2013; 14(7): 611644, doi: 10.1093/ehjci/jet105, indexed in Pubmed: 23733442.
  38. Galderisi M, Cattaneo F, Mondillo S. Doppler echocardiography and myocardial dyssynchrony: a practical update of old and new ultrasound technologies. Cardiovasc Ultrasound. 2007; 5: 28, doi: 10.1186/1476-7120-5-28, indexed in Pubmed: 17822551.
  39. Arora V, Suri P. Physiological pacing: a new road to future. Indian J Clin Cardiol. 2021; 2(1): 3243, doi: 10.1177/2632463620978045.
  40. Grieco D, Bressi E, Curila K, et al. Impact of His bundle pacing on right ventricular performance in patients undergoing permanent pacemaker implantation. Pacing Clin Electrophysiol. 2021; 44(6): 986994, doi: 10.1111/pace.14249, indexed in Pubmed: 33890685.
  41. Hahn RT. State-of-the-art review of echocardiographic imaging in the evaluation and treatment of functional tricuspid regurgitation. Circ Cardiovasc Imaging. 2016; 9(12): e005332, doi: 10.1161/CIRCIMAGING.116.005332, indexed in Pubmed: 27974407.
  42. Rothschild DP, Goldstein JA, Kerner N, et al. Pacemaker-induced tricuspid regurgitation is uncommon immediately post-implantation. J Interv Card Electrophysiol. 2017; 49(3): 281287, doi: 10.1007/s10840-017-0266-2, indexed in Pubmed: 28685199.
  43. Anvardeen K, Rao R, Hazra S, et al. Lead-specific features predisposing to the development of tricuspid regurgitation after endocardial lead implantation. CJC Open. 2019; 1(6): 316323, doi: 10.1016/j.cjco.2019.10.002, indexed in Pubmed: 32159126.
  44. Khurwolah MR, Yao J, Kong XQ. Adverse consequences of right ventricular apical pacing and novel strategies to optimize left ventricular systolic and diastolic function. Curr Cardiol Rev. 2019; 15(2): 145155, doi: 10.2174/1573403X15666181129161839, indexed in Pubmed: 30499419.
  45. Zaidi SM, Sohail H, Satti DI, et al. Tricuspid regurgitation in His bundle pacing: A systematic review. Ann Noninvasive Electrocardiol. 2022; 27(6): e12986, doi: 10.1111/anec.12986, indexed in Pubmed: 35763445.
  46. Xin MK, Gao P, Zhang SY. Effects of long-term right ventricular apex pacing on left ventricular dyssynchrony, morphology and systolic function. Int J Cardiol. 2021; 331: 9199, doi: 10.1016/j.ijcard.2021.01.042, indexed in Pubmed: 33529668.
  47. Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease: Developed by the Task Force for the management of valvular heart disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Rev Esp Cardiol (Engl Ed). 2022; 75(6): 524, doi: 10.1016/j.rec.2022.05.006, indexed in Pubmed: 35636831.
  48. Rdzanek A, Szymański P, Gackowski A, et al. Percutaneous tricuspid edge-to-edge repair - patient selection, imaging considerations, and the procedural technique. Expert opinion of the Working Group on Echocardiography and Association of CardioVascular Interventions of the Polish Cardiac Society. Kardiol Pol. 2021; 79(10): 11781191, doi: 10.33963/KP.a2021.0125, indexed in Pubmed: 34611879.
  49. Van De Heyning CM, Elbarasi E, Masiero S, et al. Prospective study of tricuspid regurgitation associated with permanent leads after cardiac rhythm device implantation. Can J Cardiol. 2019; 35(4): 389395, doi: 10.1016/j.cjca.2018.11.014, indexed in Pubmed: 30852048.
  50. Seo J, Kim DY, Cho I, et al. Prevalence, predictors, and prognosis of tricuspid regurgitation following permanent pacemaker implantation. PLoS One. 2020; 15(6): e0235230, doi: 10.1371/journal.pone.0235230, indexed in Pubmed: 32589674.



Polish Heart Journal (Kardiologia Polska)