Active-fixation leads have been associated with higher incidence of cardiac perforation. Large series specifically evaluating this complication are lacking. We sought to evaluate the incidence and predictors of clinically relevant cardiac perforation in a consecutive series of patients implanted with active-fixation pacing and defibrillation leads.
We conducted a retrospective observational study including all consecutive patients implanted with an active-fixation pacing/defibrillation lead at our institution from July 2008 to July 2015. The incidence of clinically relevant cardiac perforation and cardiac tamponade was evaluated. Univariate and multivariate analyses were used to identify predictors of cardiac perforation. Acute and long-term management of these patients was also investigated. A total of 3822 active-fixation pacing (n = 3035) and defibrillation (n = 787) leads were implanted in 2200 patients. Seventeen patients (0.8%) had clinically relevant cardiac perforation (13 acute and 4 subacute perforations), and 13 (0.5%) had cardiac tamponade resolved with pericardiocentesis. None of the patients with cardiac perforation required surgical treatment. In multivariate analysis, an age >80 years (OR 3.84, 95% CI 1.14–12.87, P = 0.029), female sex (OR 3.14, 95% CI 1.07–9.22, P = 0.037), and an apical position of the right ventricular lead (OR 3.37, 95% CI 1.17–9.67, P = 0.024) were independent predictors of cardiac perforation.
Implantation of active-fixation leads is associated with a low incidence of clinically relevant cardiac perforation. Older and female patients have a higher risk of perforation as well as those patients receiving the ventricular lead in an apical position.
Previous studies suggest that the incidence of cardiac perforation is higher with active-fixation leads.
Our results demonstrate that systematic use of active-fixation pacing and defibrillation leads is associated with a low incidence of clinically relevant cardiac perforation, comparable with that published for passive-fixation leads.
When occurring, cardiac perforation in this setting can be usually easily managed without the need of cardiac surgery and with complete recovery of the patients without further sequelae.
Introduction
Cardiac perforation is an uncommon complication of pacemaker and implantable cardioverter defibrillator (PM/ICD) implantation with a reported incidence of 0.1–5.2% depending on the series.1–7 Usually occurring at the time of lead insertion, during the past years, different studies have pointed out a non-negligible incidence of subacute or delayed right atrial/ventricular perforation rates.8–10 Different factors have been suggested predisposing to this complication including recent modifications in lead design with reduction of lead diameters and increase in tip stiffness thus resulting in a greater force per unit area.9,11
Active-fixation leads have been traditionally associated with a higher incidence of cardiac perforation.12–16 However, there is paucity of evidence supporting this assertion, and there is little information about the real incidence of cardiac perforation associated with the systematic use of active-fixation leads in large series. Instead, several reports including a limited number of patients or describing a high incidence of cardiac perforation related to specific lead models have been published.9
The aim of our study was to evaluate the incidence and predictors of clinically relevant cardiac perforation associated with the systematic implantation of active-fixation pacing and defibrillation leads in a large cohort of consecutive patients treated in a single tertiary centre during a 7-year period.
Methods
We conducted a retrospective observational study including consecutive patients undergoing implantation of a pacemaker (PM) or an implantable cardioverter defibrillator (ICD) at our institution from July 2008 to July 2015. From 2008, all patients receiving a PM/ICD at our institution are entered into a database prospectively. Relevant clinical information as well as complete data regarding the implantation procedure and clinical follow-up is registered. All patients in our centre are systematically implanted with active-fixation pacing/defibrillator leads from six different manufacturers. The study was carried out following the institutional guidelines of the Hospital Universitari i Politècnic la Fe, and all patients gave informed written consent.
Implant procedure description
Implant procedures were performed in an Electrophysiology Laboratory under conscious sedation obtained with intravenous boluses of midazolam and fentanil. All patients were brought to the laboratory in the fasting state and after prophylactic antibiotics were administered 30–60 min before surgery. Direct puncture of the left or right subclavian vein was used for venous access. The right ventricular lead was implanted first in all patients, and the right ventricular mid-septal area was considered the preferred location for ventricular lead insertion in all cases except in patients with hypertrophic cardiomyopathy in which the ventricular lead was always positioned at the right ventricular apex. Once the ventricular lead was placed at the desired location, the screw was appropriately deployed following the recommendations of each manufacturer. The final location of the ventricular lead was corroborated with two orthogonal fluoroscopic projections, 20–30° right anterior oblique view and 35–40° left anterior oblique view. The atrial lead was preferentially located at the right atrial appendage unless prohibitive sensing or pacing thresholds were present. In that case, alternative sites for atrial pacing were attempted at the discretion of the operator.
Evaluation of cardiac perforation and tamponade
Cardiac perforation was defined as the presence of pericardial effusion unequivocally attributed to lead implantation and in the absence of any other possible aetiological explanation. Acute perforation was considered when symptoms and signs of perforation occurred within the first 24 h after the implant. Perforations occurring within 1–30 days after implantation were considered subacute. Delayed perforation was defined as that occurring ≥30 days after implantation. Cardiac tamponade was defined as the presence of pericardial effusion associating haemodynamic compromise and requiring pericardiocentesis.
No systematic image technique was performed to rule out the presence of pericardial effusion after device implantation. The suspicion of perforation came in all patients from the presence of either clinical symptoms compatible with cardiac perforation during or after the implant, a fluoroscopic image suggesting lead penetration, anomalous electrical data from any lead or an abrupt decrease in blood pressure. In any of these instances, an urgent transthoracic echocardiogram was performed in order to identify the presence of pericardial fluid or cardiac tamponade. If present, the diagnosis of cardiac perforation was established at that moment. If not present, all patients with any of these signs or symptoms underwent additional transthoracic echocardiographic evaluations during the following 24 h and also before hospital discharge in order to completely rule out the presence of pericardial fluid. Thus, only clinically relevant cardiac perforations were investigated.
Clinical follow-up
Routine follow-up of patients included a first visit to the outpatient clinic 7–14 days after implantation where the wound was evaluated and staples were removed. All patients were encouraged to report any symptoms possibly related with cardiac perforation at any moment. In the presence of any of these symptoms, a transthoracic echocardiogram was routinely performed. After the first visit, patients were followed at 3 months after implantation and then in 6–12 months intervals depending on the implanted device (ICD vs. PM).
Endpoints
The main objective of the study was to evaluate the incidence of clinically relevant cardiac perforation associated with the implantation of active-fixation pacing and defibrillation leads in a consecutive series of patients undergoing implantation of a PM/ICD.
The secondary endpoints included the evaluation of the incidence of cardiac tamponade and the identification of predisposing factors favouring the occurrence of cardiac perforation in this setting. We also evaluated the acute and long-term management of these patients.
Statistical analysis
Continuous data are expressed as mean ± SD or range, as appropriate. Categorical variables were compared using the χ2 test, while Student's t-test was used for comparison of continuous variables. Binary logistic regression was used for multivariate analysis including all variables with a P-value of ≤0.1 in the univariate analysis and those variables traditionally associated with cardiac perforation in the literature. A P-value of ≤0.05 was considered statistically significant. All data were analysed using SPSS (IBM SPSS Statistics, Version 22.0, Armonk, New York, USA).
Results
A total of 2200 patients received at least one transvenous active-fixation pacing or defibrillation lead at our institution from July 2008 to July 2015. Patients who underwent implantation of a single left ventricular lead through the coronary sinus during upgrading procedures were excluded from the analysis. The 2200 patients received a total of 4204 leads including 1716 atrial pacing leads, 1319 ventricular pacing leads, 787 defibrillation leads, and 377 left ventricular leads. Baseline characteristics of the patients and leads implanted are represented in Tables 1 and 2.
Baseline characteristics of the patients included in the study
| Parameter | Patients (n = 2200) |
|---|---|
| Age (mean ± SD) | 69 ± 15 |
| Male, n (%) | 1393 (63) |
| Obesity (BMI ≥25), n (%) | 801 (38) |
| Hypertension, n (%) | 1411 (65) |
| Diabetes, n (%) | 669 (31) |
| Dyslipidaemia, n (%) | 927 (43) |
| Renal insufficiency, n (%)a | 257 (12) |
| Structural heart disease, n (%)b | 1191 (54) |
| NYHA class (mean ± SD) | 1.8 ± 0.7 |
| Atrial fibrillation, n (%) | 776 (35) |
| PM, n (%) | 1348 (62) |
| Single chamber | 259 (12) |
| Dual chamber | 1089 (50) |
| ICD, n (%) | 471 (21) |
| CRT, n (%) | 381 (17) |
| Antiplatelet treatment, n (%) | 836 (38) |
| Oral anticoagulation, n (%) | 666 (30) |
| Parameter | Patients (n = 2200) |
|---|---|
| Age (mean ± SD) | 69 ± 15 |
| Male, n (%) | 1393 (63) |
| Obesity (BMI ≥25), n (%) | 801 (38) |
| Hypertension, n (%) | 1411 (65) |
| Diabetes, n (%) | 669 (31) |
| Dyslipidaemia, n (%) | 927 (43) |
| Renal insufficiency, n (%)a | 257 (12) |
| Structural heart disease, n (%)b | 1191 (54) |
| NYHA class (mean ± SD) | 1.8 ± 0.7 |
| Atrial fibrillation, n (%) | 776 (35) |
| PM, n (%) | 1348 (62) |
| Single chamber | 259 (12) |
| Dual chamber | 1089 (50) |
| ICD, n (%) | 471 (21) |
| CRT, n (%) | 381 (17) |
| Antiplatelet treatment, n (%) | 836 (38) |
| Oral anticoagulation, n (%) | 666 (30) |
BMI, body mass index; LVEF, left ventricular ejection fraction; LAA, left atrial arrhythmia; AF, atrial fibrillation.
aRenal insufficiency is defined as a glomerular filtration rate of <60 mL/min/1.73 m2.
bStructural heart disease is defined as left ventricular hypertrophy >15 mm, left ventricular ejection fraction <50%, valvulopathy of at least moderate grade, previous myocardial infarction, significant coronary artery disease, or the presence of a primary myocardial disease.
Baseline characteristics of the patients included in the study
| Parameter | Patients (n = 2200) |
|---|---|
| Age (mean ± SD) | 69 ± 15 |
| Male, n (%) | 1393 (63) |
| Obesity (BMI ≥25), n (%) | 801 (38) |
| Hypertension, n (%) | 1411 (65) |
| Diabetes, n (%) | 669 (31) |
| Dyslipidaemia, n (%) | 927 (43) |
| Renal insufficiency, n (%)a | 257 (12) |
| Structural heart disease, n (%)b | 1191 (54) |
| NYHA class (mean ± SD) | 1.8 ± 0.7 |
| Atrial fibrillation, n (%) | 776 (35) |
| PM, n (%) | 1348 (62) |
| Single chamber | 259 (12) |
| Dual chamber | 1089 (50) |
| ICD, n (%) | 471 (21) |
| CRT, n (%) | 381 (17) |
| Antiplatelet treatment, n (%) | 836 (38) |
| Oral anticoagulation, n (%) | 666 (30) |
| Parameter | Patients (n = 2200) |
|---|---|
| Age (mean ± SD) | 69 ± 15 |
| Male, n (%) | 1393 (63) |
| Obesity (BMI ≥25), n (%) | 801 (38) |
| Hypertension, n (%) | 1411 (65) |
| Diabetes, n (%) | 669 (31) |
| Dyslipidaemia, n (%) | 927 (43) |
| Renal insufficiency, n (%)a | 257 (12) |
| Structural heart disease, n (%)b | 1191 (54) |
| NYHA class (mean ± SD) | 1.8 ± 0.7 |
| Atrial fibrillation, n (%) | 776 (35) |
| PM, n (%) | 1348 (62) |
| Single chamber | 259 (12) |
| Dual chamber | 1089 (50) |
| ICD, n (%) | 471 (21) |
| CRT, n (%) | 381 (17) |
| Antiplatelet treatment, n (%) | 836 (38) |
| Oral anticoagulation, n (%) | 666 (30) |
BMI, body mass index; LVEF, left ventricular ejection fraction; LAA, left atrial arrhythmia; AF, atrial fibrillation.
aRenal insufficiency is defined as a glomerular filtration rate of <60 mL/min/1.73 m2.
bStructural heart disease is defined as left ventricular hypertrophy >15 mm, left ventricular ejection fraction <50%, valvulopathy of at least moderate grade, previous myocardial infarction, significant coronary artery disease, or the presence of a primary myocardial disease.
Lead models implanted
| Atrial leads | n (%) | Ventricular pacing leads | n (%) | Defibrillation leads | n (%) |
|---|---|---|---|---|---|
| Medtronic | Medtronic | Medtronic | |||
| - 5076-52 | 423 (24.7) | - 5076-58 | 310 (23.5) | - 6947-65 | 124 (15.8) |
| - 5086-52 | 13 (0.8) | - 5086-58 | 13 (1) | - 6947M-62 | 87 (11.1) |
| St. Jude Medical | St. Jude Medical | St. Jude Medical | |||
| - 1699TC-52 | 75 (4.4) | - 1699TC-58 | 4 (0.3) | - 7120Q-65 | 116 (14.7) |
| - 1788TC-52 | 158 (9.2) | - 1788TC-58 | 175 (13.3) | - 7120Q-58 | 156 (19.8) |
| - 1888TC-52 | 7 (0.4) | - 1888TC-58 | 10 (0.7) | ||
| - 1999TC-52 OPTISENSE | 128 (7.5) | - 2088TC-58 | 111 (8.4) | ||
| - 2088TC-52 | 117 (6.8) | - LPA1200M-58 | 30 (2.3) | ||
| - LPA1200M-52 | 18 (1) | ||||
| Boston Scientific | Boston Scientific | Boston Scientific | |||
| - 4096-52 | 273 (15.9) | - 4096-59 | 187 (14.2) | - 0185-65 | 37 (4.7) |
| - 7741-52 | 44 (2.6) | - 7741-59 | 47 (3.6) | - 0285-59 | 85 (10.8) |
| - 0695-59 | 43 (5.5) | ||||
| Biotronik | Biotronik | Biotronik | |||
| - Setrox S53 | 50 (2.9) | - Setrox S60 | 47 (3.6) | - Linox SD65/16 | 34 (4.3) |
| - Siello S53 | 33 (1.9) | - Siello S60 | 31 (2.4) | - Linox Smart ProMRI SD 65/16 | 6 (0.8) |
| - Solia S53 | 107 (6.2) | - Solia S60 | 103 (7.8) | - Protego ProMRI SD 65/16 | 31 (3.9) |
| Sorin Group | Sorin Group | Sorin Group | |||
| - Stelix II BRF25D | 12 (0.7) | - Stelix II BRF26D | 2 (0.2) | - Isoline 2CE-6 | 29 (3.7) |
| - Beflex BRF-52 | 91 (5.3) | - Beflex BRF-58 | 92 (7) | - Vigilia 2CR 65/18 | 13 (1.7) |
| - Tilda R53 | 123 (7.2) | - Tilda R60 | 126 (9.6) | - Volta 2CR 65/18 | 26 (3.3) |
| - SonRTIP PS550 | 22 (1.3) | ||||
| Vitatron | Vitatron | ||||
| - ICF09B-52 | 22 (1.3) | - ICF09B-58 | 31 (2.4) |
| Atrial leads | n (%) | Ventricular pacing leads | n (%) | Defibrillation leads | n (%) |
|---|---|---|---|---|---|
| Medtronic | Medtronic | Medtronic | |||
| - 5076-52 | 423 (24.7) | - 5076-58 | 310 (23.5) | - 6947-65 | 124 (15.8) |
| - 5086-52 | 13 (0.8) | - 5086-58 | 13 (1) | - 6947M-62 | 87 (11.1) |
| St. Jude Medical | St. Jude Medical | St. Jude Medical | |||
| - 1699TC-52 | 75 (4.4) | - 1699TC-58 | 4 (0.3) | - 7120Q-65 | 116 (14.7) |
| - 1788TC-52 | 158 (9.2) | - 1788TC-58 | 175 (13.3) | - 7120Q-58 | 156 (19.8) |
| - 1888TC-52 | 7 (0.4) | - 1888TC-58 | 10 (0.7) | ||
| - 1999TC-52 OPTISENSE | 128 (7.5) | - 2088TC-58 | 111 (8.4) | ||
| - 2088TC-52 | 117 (6.8) | - LPA1200M-58 | 30 (2.3) | ||
| - LPA1200M-52 | 18 (1) | ||||
| Boston Scientific | Boston Scientific | Boston Scientific | |||
| - 4096-52 | 273 (15.9) | - 4096-59 | 187 (14.2) | - 0185-65 | 37 (4.7) |
| - 7741-52 | 44 (2.6) | - 7741-59 | 47 (3.6) | - 0285-59 | 85 (10.8) |
| - 0695-59 | 43 (5.5) | ||||
| Biotronik | Biotronik | Biotronik | |||
| - Setrox S53 | 50 (2.9) | - Setrox S60 | 47 (3.6) | - Linox SD65/16 | 34 (4.3) |
| - Siello S53 | 33 (1.9) | - Siello S60 | 31 (2.4) | - Linox Smart ProMRI SD 65/16 | 6 (0.8) |
| - Solia S53 | 107 (6.2) | - Solia S60 | 103 (7.8) | - Protego ProMRI SD 65/16 | 31 (3.9) |
| Sorin Group | Sorin Group | Sorin Group | |||
| - Stelix II BRF25D | 12 (0.7) | - Stelix II BRF26D | 2 (0.2) | - Isoline 2CE-6 | 29 (3.7) |
| - Beflex BRF-52 | 91 (5.3) | - Beflex BRF-58 | 92 (7) | - Vigilia 2CR 65/18 | 13 (1.7) |
| - Tilda R53 | 123 (7.2) | - Tilda R60 | 126 (9.6) | - Volta 2CR 65/18 | 26 (3.3) |
| - SonRTIP PS550 | 22 (1.3) | ||||
| Vitatron | Vitatron | ||||
| - ICF09B-52 | 22 (1.3) | - ICF09B-58 | 31 (2.4) |
Lead models implanted
| Atrial leads | n (%) | Ventricular pacing leads | n (%) | Defibrillation leads | n (%) |
|---|---|---|---|---|---|
| Medtronic | Medtronic | Medtronic | |||
| - 5076-52 | 423 (24.7) | - 5076-58 | 310 (23.5) | - 6947-65 | 124 (15.8) |
| - 5086-52 | 13 (0.8) | - 5086-58 | 13 (1) | - 6947M-62 | 87 (11.1) |
| St. Jude Medical | St. Jude Medical | St. Jude Medical | |||
| - 1699TC-52 | 75 (4.4) | - 1699TC-58 | 4 (0.3) | - 7120Q-65 | 116 (14.7) |
| - 1788TC-52 | 158 (9.2) | - 1788TC-58 | 175 (13.3) | - 7120Q-58 | 156 (19.8) |
| - 1888TC-52 | 7 (0.4) | - 1888TC-58 | 10 (0.7) | ||
| - 1999TC-52 OPTISENSE | 128 (7.5) | - 2088TC-58 | 111 (8.4) | ||
| - 2088TC-52 | 117 (6.8) | - LPA1200M-58 | 30 (2.3) | ||
| - LPA1200M-52 | 18 (1) | ||||
| Boston Scientific | Boston Scientific | Boston Scientific | |||
| - 4096-52 | 273 (15.9) | - 4096-59 | 187 (14.2) | - 0185-65 | 37 (4.7) |
| - 7741-52 | 44 (2.6) | - 7741-59 | 47 (3.6) | - 0285-59 | 85 (10.8) |
| - 0695-59 | 43 (5.5) | ||||
| Biotronik | Biotronik | Biotronik | |||
| - Setrox S53 | 50 (2.9) | - Setrox S60 | 47 (3.6) | - Linox SD65/16 | 34 (4.3) |
| - Siello S53 | 33 (1.9) | - Siello S60 | 31 (2.4) | - Linox Smart ProMRI SD 65/16 | 6 (0.8) |
| - Solia S53 | 107 (6.2) | - Solia S60 | 103 (7.8) | - Protego ProMRI SD 65/16 | 31 (3.9) |
| Sorin Group | Sorin Group | Sorin Group | |||
| - Stelix II BRF25D | 12 (0.7) | - Stelix II BRF26D | 2 (0.2) | - Isoline 2CE-6 | 29 (3.7) |
| - Beflex BRF-52 | 91 (5.3) | - Beflex BRF-58 | 92 (7) | - Vigilia 2CR 65/18 | 13 (1.7) |
| - Tilda R53 | 123 (7.2) | - Tilda R60 | 126 (9.6) | - Volta 2CR 65/18 | 26 (3.3) |
| - SonRTIP PS550 | 22 (1.3) | ||||
| Vitatron | Vitatron | ||||
| - ICF09B-52 | 22 (1.3) | - ICF09B-58 | 31 (2.4) |
| Atrial leads | n (%) | Ventricular pacing leads | n (%) | Defibrillation leads | n (%) |
|---|---|---|---|---|---|
| Medtronic | Medtronic | Medtronic | |||
| - 5076-52 | 423 (24.7) | - 5076-58 | 310 (23.5) | - 6947-65 | 124 (15.8) |
| - 5086-52 | 13 (0.8) | - 5086-58 | 13 (1) | - 6947M-62 | 87 (11.1) |
| St. Jude Medical | St. Jude Medical | St. Jude Medical | |||
| - 1699TC-52 | 75 (4.4) | - 1699TC-58 | 4 (0.3) | - 7120Q-65 | 116 (14.7) |
| - 1788TC-52 | 158 (9.2) | - 1788TC-58 | 175 (13.3) | - 7120Q-58 | 156 (19.8) |
| - 1888TC-52 | 7 (0.4) | - 1888TC-58 | 10 (0.7) | ||
| - 1999TC-52 OPTISENSE | 128 (7.5) | - 2088TC-58 | 111 (8.4) | ||
| - 2088TC-52 | 117 (6.8) | - LPA1200M-58 | 30 (2.3) | ||
| - LPA1200M-52 | 18 (1) | ||||
| Boston Scientific | Boston Scientific | Boston Scientific | |||
| - 4096-52 | 273 (15.9) | - 4096-59 | 187 (14.2) | - 0185-65 | 37 (4.7) |
| - 7741-52 | 44 (2.6) | - 7741-59 | 47 (3.6) | - 0285-59 | 85 (10.8) |
| - 0695-59 | 43 (5.5) | ||||
| Biotronik | Biotronik | Biotronik | |||
| - Setrox S53 | 50 (2.9) | - Setrox S60 | 47 (3.6) | - Linox SD65/16 | 34 (4.3) |
| - Siello S53 | 33 (1.9) | - Siello S60 | 31 (2.4) | - Linox Smart ProMRI SD 65/16 | 6 (0.8) |
| - Solia S53 | 107 (6.2) | - Solia S60 | 103 (7.8) | - Protego ProMRI SD 65/16 | 31 (3.9) |
| Sorin Group | Sorin Group | Sorin Group | |||
| - Stelix II BRF25D | 12 (0.7) | - Stelix II BRF26D | 2 (0.2) | - Isoline 2CE-6 | 29 (3.7) |
| - Beflex BRF-52 | 91 (5.3) | - Beflex BRF-58 | 92 (7) | - Vigilia 2CR 65/18 | 13 (1.7) |
| - Tilda R53 | 123 (7.2) | - Tilda R60 | 126 (9.6) | - Volta 2CR 65/18 | 26 (3.3) |
| - SonRTIP PS550 | 22 (1.3) | ||||
| Vitatron | Vitatron | ||||
| - ICF09B-52 | 22 (1.3) | - ICF09B-58 | 31 (2.4) |
Incidence and clinical characteristics of cardiac perforation and tamponade
Seventeen patients were diagnosed with cardiac perforation related to the implantation of an active-fixation pacing/defibrillation lead (0.8%) (Table 3). An acute perforation occurred in 13 patients, and subacute perforations were diagnosed in 4 patients 7–15 days after device implantation. The ventricular lead was considered responsible of the cardiac perforation in 11/17 cases (64%) because either the pericardial effusion occurred before the atrial lead was implanted or there were unequivocal fluoroscopic and electrical signs of ventricular lead penetration. Only 1/17 cases (6%) was directly related to the atrial pacing lead, and in the remaining 5 cases (30%), there was no certainty about the lead responsible of cardiac perforation.
Clinical and device characteristics of the 17 patients with clinically relevant cardiac perforation
| Patient | Age | Sex | Device | Indication | Time of perforation | Tamponade | Perforation caused by | RV lead location | Lead reposition |
|---|---|---|---|---|---|---|---|---|---|
| Patient 1 | 53 | F | DC-PM | SND | 7 days | No | Uncertain | RV septum | No |
| Patient 2 | 70 | M | DC-PM | AVB | 12 days | No | Uncertain | RV apex | No |
| Patient 3 | 87 | F | DC-PM | CSS | During implant | No | RV lead | RV septum | Yes |
| Patient 4 | 80 | F | DC-PM | AVB | During implant | No | RV lead | RV apex | No |
| Patient 5 | 43 | F | DC-ICD | PP-SCD | 12 days | Yes | Uncertain | RV apex | No |
| Patient 6 | 86 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 7 | 58 | M | DC-ICD | PP-SCD | Within 24 h | Yes | RV lead | RV apex | No |
| Patient 8 | 95 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 9 | 89 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
| Patient 10 | 80 | F | DC-ICD | SP-SCD | During implant | Yes | RV lead | RV apex | No |
| Patient 11 | 71 | F | CRT-D | HF | Within 24 h | Yes | Uncertain | RV apex | No |
| Patient 12 | 81 | M | DC-PM | AVB | During implant | No | RV lead | RV apex | Yes |
| Patient 13 | 78 | M | CRT-D | HF | During implant | Yes | RV lead | RV apex | No |
| Patient 14 | 69 | F | CRT-D | HF | During implant | No | Uncertain | RV septum | No |
| Patient 15 | 77 | F | DC-PM | SND | 15 days | Yes | RA lead | RV septum | No |
| Patient 16 | 83 | F | DC-PM | AVB | During implant | Yes | RV lead | RV septum | Yes |
| Patient 17 | 83 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
| Patient | Age | Sex | Device | Indication | Time of perforation | Tamponade | Perforation caused by | RV lead location | Lead reposition |
|---|---|---|---|---|---|---|---|---|---|
| Patient 1 | 53 | F | DC-PM | SND | 7 days | No | Uncertain | RV septum | No |
| Patient 2 | 70 | M | DC-PM | AVB | 12 days | No | Uncertain | RV apex | No |
| Patient 3 | 87 | F | DC-PM | CSS | During implant | No | RV lead | RV septum | Yes |
| Patient 4 | 80 | F | DC-PM | AVB | During implant | No | RV lead | RV apex | No |
| Patient 5 | 43 | F | DC-ICD | PP-SCD | 12 days | Yes | Uncertain | RV apex | No |
| Patient 6 | 86 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 7 | 58 | M | DC-ICD | PP-SCD | Within 24 h | Yes | RV lead | RV apex | No |
| Patient 8 | 95 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 9 | 89 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
| Patient 10 | 80 | F | DC-ICD | SP-SCD | During implant | Yes | RV lead | RV apex | No |
| Patient 11 | 71 | F | CRT-D | HF | Within 24 h | Yes | Uncertain | RV apex | No |
| Patient 12 | 81 | M | DC-PM | AVB | During implant | No | RV lead | RV apex | Yes |
| Patient 13 | 78 | M | CRT-D | HF | During implant | Yes | RV lead | RV apex | No |
| Patient 14 | 69 | F | CRT-D | HF | During implant | No | Uncertain | RV septum | No |
| Patient 15 | 77 | F | DC-PM | SND | 15 days | Yes | RA lead | RV septum | No |
| Patient 16 | 83 | F | DC-PM | AVB | During implant | Yes | RV lead | RV septum | Yes |
| Patient 17 | 83 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
F, female; M, male; DC-PM, dual-chamber pacemaker; DC-ICD, dual-chamber implantable cardioverter defibrillator; CRT-D, cardiac resynchronization therapy with defibrillation capabilities; SND, sinus node disease; AVB, atrioventricular block; CSS, carotid sinus syndrome; PP-SCD, primary prevention of sudden cardiac death; SP-SCD, secondary prevention of sudden cardiac death; HF, heart failure.
Clinical and device characteristics of the 17 patients with clinically relevant cardiac perforation
| Patient | Age | Sex | Device | Indication | Time of perforation | Tamponade | Perforation caused by | RV lead location | Lead reposition |
|---|---|---|---|---|---|---|---|---|---|
| Patient 1 | 53 | F | DC-PM | SND | 7 days | No | Uncertain | RV septum | No |
| Patient 2 | 70 | M | DC-PM | AVB | 12 days | No | Uncertain | RV apex | No |
| Patient 3 | 87 | F | DC-PM | CSS | During implant | No | RV lead | RV septum | Yes |
| Patient 4 | 80 | F | DC-PM | AVB | During implant | No | RV lead | RV apex | No |
| Patient 5 | 43 | F | DC-ICD | PP-SCD | 12 days | Yes | Uncertain | RV apex | No |
| Patient 6 | 86 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 7 | 58 | M | DC-ICD | PP-SCD | Within 24 h | Yes | RV lead | RV apex | No |
| Patient 8 | 95 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 9 | 89 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
| Patient 10 | 80 | F | DC-ICD | SP-SCD | During implant | Yes | RV lead | RV apex | No |
| Patient 11 | 71 | F | CRT-D | HF | Within 24 h | Yes | Uncertain | RV apex | No |
| Patient 12 | 81 | M | DC-PM | AVB | During implant | No | RV lead | RV apex | Yes |
| Patient 13 | 78 | M | CRT-D | HF | During implant | Yes | RV lead | RV apex | No |
| Patient 14 | 69 | F | CRT-D | HF | During implant | No | Uncertain | RV septum | No |
| Patient 15 | 77 | F | DC-PM | SND | 15 days | Yes | RA lead | RV septum | No |
| Patient 16 | 83 | F | DC-PM | AVB | During implant | Yes | RV lead | RV septum | Yes |
| Patient 17 | 83 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
| Patient | Age | Sex | Device | Indication | Time of perforation | Tamponade | Perforation caused by | RV lead location | Lead reposition |
|---|---|---|---|---|---|---|---|---|---|
| Patient 1 | 53 | F | DC-PM | SND | 7 days | No | Uncertain | RV septum | No |
| Patient 2 | 70 | M | DC-PM | AVB | 12 days | No | Uncertain | RV apex | No |
| Patient 3 | 87 | F | DC-PM | CSS | During implant | No | RV lead | RV septum | Yes |
| Patient 4 | 80 | F | DC-PM | AVB | During implant | No | RV lead | RV apex | No |
| Patient 5 | 43 | F | DC-ICD | PP-SCD | 12 days | Yes | Uncertain | RV apex | No |
| Patient 6 | 86 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 7 | 58 | M | DC-ICD | PP-SCD | Within 24 h | Yes | RV lead | RV apex | No |
| Patient 8 | 95 | M | DC-PM | AVB | During implant | Yes | RV lead | RV apex | Yes |
| Patient 9 | 89 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
| Patient 10 | 80 | F | DC-ICD | SP-SCD | During implant | Yes | RV lead | RV apex | No |
| Patient 11 | 71 | F | CRT-D | HF | Within 24 h | Yes | Uncertain | RV apex | No |
| Patient 12 | 81 | M | DC-PM | AVB | During implant | No | RV lead | RV apex | Yes |
| Patient 13 | 78 | M | CRT-D | HF | During implant | Yes | RV lead | RV apex | No |
| Patient 14 | 69 | F | CRT-D | HF | During implant | No | Uncertain | RV septum | No |
| Patient 15 | 77 | F | DC-PM | SND | 15 days | Yes | RA lead | RV septum | No |
| Patient 16 | 83 | F | DC-PM | AVB | During implant | Yes | RV lead | RV septum | Yes |
| Patient 17 | 83 | F | DC-PM | SND | During implant | Yes | RV lead | RV apex | No |
F, female; M, male; DC-PM, dual-chamber pacemaker; DC-ICD, dual-chamber implantable cardioverter defibrillator; CRT-D, cardiac resynchronization therapy with defibrillation capabilities; SND, sinus node disease; AVB, atrioventricular block; CSS, carotid sinus syndrome; PP-SCD, primary prevention of sudden cardiac death; SP-SCD, secondary prevention of sudden cardiac death; HF, heart failure.
Cardiac tamponade occurred in 11/17 patients with clinically relevant cardiac perforation and required pericardiocentesis. Pericardiocentesis was performed during the implant (n = 7) or within the first 24 h after implant (n = 2) in 9 cases. The other 2 cases were considered subacute perforations as the cardiac tamponade occurred 12 and 15 days after the implant, respectively. All 11 patients with cardiac tamponade had a total recovery without further complications after pericardiocentesis and none of them required surgical treatment.
There were six patients with cardiac perforation but without tamponade in which the diagnosis was made based on the presence of pericardial effusion in a transthoracic echocardiogram performed due to the presence of symptoms suggesting pericardial disease. Four of this patients had signs or symptoms of pericardial effusion during implantation with transient hypotension suggesting the presence of tamponade or reduction of cardiac silhouette excursion in a fluoroscopic left anterior oblique view.17 The other two patients consulted in the outpatient clinic with dyspnoea and chest pain 7 and 12 days after implant and the pericardial effusion was evidenced at that moment by a TTE. Both patients were admitted to the hospital, and the pericardial effusion was monitored with periodic echocardiograms until complete resolution.
Two additional patients had cardiac perforation and tamponade immediately and directly related to removal of a transvenous temporary pacing lead and were not taken into consideration in the absolute estimation of cardiac perforation incidence. In both cases, the pericardial effusion had been previously identified before the implant of the transvenous permanent PM and cardiac perforation was not attributed to the active-fixation pacing lead implantation.
Lead management after cardiac perforation
In 5 of the 17 patients with cardiac perforation in which the ventricular lead was found to be responsible for the perforation during the implant, the lead was repositioned during the same index procedure. In three of these five patients the decision to reposition the lead was based on the presence of unequivocal fluoroscopic evidence of lead penetration. In the remaining two patients, abrupt changes in the electrical parameters compatible with lead penetration were noticed but without a clear fluoroscopic image of macroperforation (Table 3). There were six additional patients with cardiac perforation detected during the initial implant in which none of the implanted leads were repositioned because all the electrical parameters were adequate and there was no fluoroscopic evidence of lead penetration. None of these six patients required further reoperation and routine follow-up in the outpatient clinic revealed completely normal and stable electrical parameters. In one of these six patients there was uncertainty about the lead responsible for perforation. In the remaining five patients, perforation occurred while manipulating the ventricular lead at the RV outflow tract (one patient) and at the RVA in four patients (Table 3). In three patients, the described RV lead position was the first and unique position in which the helix was deployed and symptoms and signs of perforation occurred immediately related to lead deployment. In the other two patients, a previous helix deployment attempt had been performed within the same region (RVA). None of the patients with cardiac perforation diagnosed after the implant procedure required a reintervention. Among the four patients presenting with subacute cardiac perforation no computed tomography (CT) scan was performed in 3/4 patients, so we did not have certainty about the lead responsible for the perforation in these cases. Importantly, all the right atrial and right ventricular leads of these three patients were placed using only one attempt for helix deployment in a single position. The electrical parameters and the X-ray images were normal in all three, and the leads were no repositioned. Therefore, the most plausible cause of perforation in these patients was considered to be a microperforation with the screw tip. In the fourth case (Patient 15 presenting with cardiac tamponade), a CT scan was performed after perforation showing the atrial lead tip protruding into the epicardial fat surrounding the right atrium. Although the electrical parameters were stable and although the patient had total recovery after pericardiocentesis, we recommended a surgical reposition of the atrial lead. However, after a detailed discussion of the potential benefits and risks of the intervention, the patient did not consent to undergo surgery. This patient has been followed for 30 months since cardiac tamponade occurred, and she has remained asymptomatic with stable electrical parameters and completely normal operation of the atrial lead.
Evolution of the electrical parameters at implant, 6 and 12 months of follow-up in the 17 patients who were diagnosed with cardiac perforation.
Predictors of cardiac perforation
Univariate analysis results for cardiac perforation and cardiac tamponade are represented in Table 4. Older patients (age >80 years) had a significantly higher probability of cardiac perforation (1.7% for >80 years vs. 0.5% for <80 years, P = 0.02) and cardiac tamponade (1.1 vs. 0.3%, P = 0.03). An apical location of the right ventricular lead was significantly associated with cardiac perforation when compared with those patients who received the ventricular lead in the septum (1.1 vs. 0.2%, P = 0.009). Of note, active oral anticoagulation at the time of surgery (International Normalized Ratio >2, n = 342) was not associated with perforation as also occurred with active single or dual antiplatelet treatment (n = 791). None of the different lead models were associated with a higher incidence of perforation. In multivariate analysis (Table 5), only an age of >80 years (OR 3.84, 95% CI 1.14–12.87, P = 0.029), female sex (OR 3.14, 95% CI 1.07–9.22, P = 0.037), and an apical position of the right ventricular lead (OR 3.37, 95% CI 1.17–9.67, P = 0.024) were independent predictors of clinically relevant cardiac perforation associated with the implantation of active-fixation pacing/defibrillation leads.
Univariate analysis
| No cardiac perforation (n = 2183) | Cardiac perforation (n = 17) | P-value | |
|---|---|---|---|
| Age >80, n (%) | 536 (25) | 9 (53) | 0.02 |
| Female, n (%) | 795 (36) | 11 (65) | 0.02 |
| Obesity (BMI ≥25), n (%) | 795 (38) | 6 (38) | 1 |
| Hypertension, n (%) | 1401 (65) | 10 (59) | 0.61 |
| Diabetes, n (%) | 666 (31) | 3 (18) | 0.30 |
| Dyslipidemia, n (%) | 924 (43) | 3 (18) | 0.05 |
| Renal insufficiency, n (%) | 254 (12) | 3 (18) | 0.44 |
| Structural heart disease, n (%) | 1183 (54) | 8 (47) | 0.63 |
| NYHA class (mean ± SD) | 1.6 ± 0.8 | 2 ± 0.9 | 0.3 |
| Atrial fibrillation, n (%) | 772 (36) | 3 (18) | 0.30 |
| Device | |||
| PM | 1376 (63) | 11 (65) | 1 |
| ICD | 807 (37) | 6 (35) | |
| RV lead position, n (%) | |||
| Apical | 789 (39) | 12 (71) | 0.01 |
| Septal | 1237 (61) | 5 (29) | |
| Active antiplatelet treatment, n (%) | 785 (56) | 5 (50) | 0.75 |
| Active oral anticoagulation, n (%) | 295 (47) | 3 (75) | 0.35 |
| Procedure, n (%) | |||
| First implant | 1970 (90) | 17 (100) | 0.60 |
| Upgrading | 213 (10) | 0 | |
| Number of leads implanted, n (%) | |||
| 1 | 480 (22) | 0 | 0.09 |
| 2 | 1422 (65) | 14 (82) | |
| 3 | 281 (13) | 3 (18) | |
| EP fellow involved, n (%) | 344 (42) | 2 (33) | 1 |
| Temporary PM, n (%) | 266 (12) | 3 (18) | 0.45 |
| No cardiac perforation (n = 2183) | Cardiac perforation (n = 17) | P-value | |
|---|---|---|---|
| Age >80, n (%) | 536 (25) | 9 (53) | 0.02 |
| Female, n (%) | 795 (36) | 11 (65) | 0.02 |
| Obesity (BMI ≥25), n (%) | 795 (38) | 6 (38) | 1 |
| Hypertension, n (%) | 1401 (65) | 10 (59) | 0.61 |
| Diabetes, n (%) | 666 (31) | 3 (18) | 0.30 |
| Dyslipidemia, n (%) | 924 (43) | 3 (18) | 0.05 |
| Renal insufficiency, n (%) | 254 (12) | 3 (18) | 0.44 |
| Structural heart disease, n (%) | 1183 (54) | 8 (47) | 0.63 |
| NYHA class (mean ± SD) | 1.6 ± 0.8 | 2 ± 0.9 | 0.3 |
| Atrial fibrillation, n (%) | 772 (36) | 3 (18) | 0.30 |
| Device | |||
| PM | 1376 (63) | 11 (65) | 1 |
| ICD | 807 (37) | 6 (35) | |
| RV lead position, n (%) | |||
| Apical | 789 (39) | 12 (71) | 0.01 |
| Septal | 1237 (61) | 5 (29) | |
| Active antiplatelet treatment, n (%) | 785 (56) | 5 (50) | 0.75 |
| Active oral anticoagulation, n (%) | 295 (47) | 3 (75) | 0.35 |
| Procedure, n (%) | |||
| First implant | 1970 (90) | 17 (100) | 0.60 |
| Upgrading | 213 (10) | 0 | |
| Number of leads implanted, n (%) | |||
| 1 | 480 (22) | 0 | 0.09 |
| 2 | 1422 (65) | 14 (82) | |
| 3 | 281 (13) | 3 (18) | |
| EP fellow involved, n (%) | 344 (42) | 2 (33) | 1 |
| Temporary PM, n (%) | 266 (12) | 3 (18) | 0.45 |
Univariate analysis
| No cardiac perforation (n = 2183) | Cardiac perforation (n = 17) | P-value | |
|---|---|---|---|
| Age >80, n (%) | 536 (25) | 9 (53) | 0.02 |
| Female, n (%) | 795 (36) | 11 (65) | 0.02 |
| Obesity (BMI ≥25), n (%) | 795 (38) | 6 (38) | 1 |
| Hypertension, n (%) | 1401 (65) | 10 (59) | 0.61 |
| Diabetes, n (%) | 666 (31) | 3 (18) | 0.30 |
| Dyslipidemia, n (%) | 924 (43) | 3 (18) | 0.05 |
| Renal insufficiency, n (%) | 254 (12) | 3 (18) | 0.44 |
| Structural heart disease, n (%) | 1183 (54) | 8 (47) | 0.63 |
| NYHA class (mean ± SD) | 1.6 ± 0.8 | 2 ± 0.9 | 0.3 |
| Atrial fibrillation, n (%) | 772 (36) | 3 (18) | 0.30 |
| Device | |||
| PM | 1376 (63) | 11 (65) | 1 |
| ICD | 807 (37) | 6 (35) | |
| RV lead position, n (%) | |||
| Apical | 789 (39) | 12 (71) | 0.01 |
| Septal | 1237 (61) | 5 (29) | |
| Active antiplatelet treatment, n (%) | 785 (56) | 5 (50) | 0.75 |
| Active oral anticoagulation, n (%) | 295 (47) | 3 (75) | 0.35 |
| Procedure, n (%) | |||
| First implant | 1970 (90) | 17 (100) | 0.60 |
| Upgrading | 213 (10) | 0 | |
| Number of leads implanted, n (%) | |||
| 1 | 480 (22) | 0 | 0.09 |
| 2 | 1422 (65) | 14 (82) | |
| 3 | 281 (13) | 3 (18) | |
| EP fellow involved, n (%) | 344 (42) | 2 (33) | 1 |
| Temporary PM, n (%) | 266 (12) | 3 (18) | 0.45 |
| No cardiac perforation (n = 2183) | Cardiac perforation (n = 17) | P-value | |
|---|---|---|---|
| Age >80, n (%) | 536 (25) | 9 (53) | 0.02 |
| Female, n (%) | 795 (36) | 11 (65) | 0.02 |
| Obesity (BMI ≥25), n (%) | 795 (38) | 6 (38) | 1 |
| Hypertension, n (%) | 1401 (65) | 10 (59) | 0.61 |
| Diabetes, n (%) | 666 (31) | 3 (18) | 0.30 |
| Dyslipidemia, n (%) | 924 (43) | 3 (18) | 0.05 |
| Renal insufficiency, n (%) | 254 (12) | 3 (18) | 0.44 |
| Structural heart disease, n (%) | 1183 (54) | 8 (47) | 0.63 |
| NYHA class (mean ± SD) | 1.6 ± 0.8 | 2 ± 0.9 | 0.3 |
| Atrial fibrillation, n (%) | 772 (36) | 3 (18) | 0.30 |
| Device | |||
| PM | 1376 (63) | 11 (65) | 1 |
| ICD | 807 (37) | 6 (35) | |
| RV lead position, n (%) | |||
| Apical | 789 (39) | 12 (71) | 0.01 |
| Septal | 1237 (61) | 5 (29) | |
| Active antiplatelet treatment, n (%) | 785 (56) | 5 (50) | 0.75 |
| Active oral anticoagulation, n (%) | 295 (47) | 3 (75) | 0.35 |
| Procedure, n (%) | |||
| First implant | 1970 (90) | 17 (100) | 0.60 |
| Upgrading | 213 (10) | 0 | |
| Number of leads implanted, n (%) | |||
| 1 | 480 (22) | 0 | 0.09 |
| 2 | 1422 (65) | 14 (82) | |
| 3 | 281 (13) | 3 (18) | |
| EP fellow involved, n (%) | 344 (42) | 2 (33) | 1 |
| Temporary PM, n (%) | 266 (12) | 3 (18) | 0.45 |
Multivariate analysis of cardiac perforation predictors
| Variable | Odds ratio | P-value | 95% CI |
|---|---|---|---|
| Age >80 | 3.84 | 0.029 | 1.14–12.87 |
| Female sex | 3.14 | 0.037 | 1.07–9.22 |
| Renal insufficiency | 1.74 | 0.400 | 0.47–6.36 |
| RV lead apical location | 3.37 | 0.024 | 1.17–9.67 |
| Device type (PM vs. ICD) | 2.59 | 0.163 | 0.68–9.88 |
| Temporary PM | 1.33 | 0.673 | 0.35–5.05 |
| Variable | Odds ratio | P-value | 95% CI |
|---|---|---|---|
| Age >80 | 3.84 | 0.029 | 1.14–12.87 |
| Female sex | 3.14 | 0.037 | 1.07–9.22 |
| Renal insufficiency | 1.74 | 0.400 | 0.47–6.36 |
| RV lead apical location | 3.37 | 0.024 | 1.17–9.67 |
| Device type (PM vs. ICD) | 2.59 | 0.163 | 0.68–9.88 |
| Temporary PM | 1.33 | 0.673 | 0.35–5.05 |
Multivariate analysis of cardiac perforation predictors
| Variable | Odds ratio | P-value | 95% CI |
|---|---|---|---|
| Age >80 | 3.84 | 0.029 | 1.14–12.87 |
| Female sex | 3.14 | 0.037 | 1.07–9.22 |
| Renal insufficiency | 1.74 | 0.400 | 0.47–6.36 |
| RV lead apical location | 3.37 | 0.024 | 1.17–9.67 |
| Device type (PM vs. ICD) | 2.59 | 0.163 | 0.68–9.88 |
| Temporary PM | 1.33 | 0.673 | 0.35–5.05 |
| Variable | Odds ratio | P-value | 95% CI |
|---|---|---|---|
| Age >80 | 3.84 | 0.029 | 1.14–12.87 |
| Female sex | 3.14 | 0.037 | 1.07–9.22 |
| Renal insufficiency | 1.74 | 0.400 | 0.47–6.36 |
| RV lead apical location | 3.37 | 0.024 | 1.17–9.67 |
| Device type (PM vs. ICD) | 2.59 | 0.163 | 0.68–9.88 |
| Temporary PM | 1.33 | 0.673 | 0.35–5.05 |
Discussion
We investigated the incidence and predictors of clinically relevant cardiac perforation in patients undergoing implantation of active-fixation pacing leads. Our experience in a large series of consecutive patients over a 7-year period shows that cardiac perforation is a rare complication in this setting (0.8%) and, when occurring, can be easily managed. Cardiac tamponade occurred in 0.5% of patients and was resolved with pericardiocentesis in all cases without the need of cardiac surgery and with complete recovery of the patients. These numbers are comparable with the reported incidences of cardiac perforation and tamponade associated with passive-fixation leads.5–8
Different studies have suggested a possible higher incidence of cardiac perforation associated with the use of active-fixation leads.12–16,18,19 Mahapatra et al. found active-fixation pacing leads as a variable with high risk of cardiac perforation together with the use of temporary PMs and steroid use.5 In the same manner, Sterliński et al. noted an increased incidence of cardiac perforation in patients receiving active-fixation leads.8 They performed a retrospective study including 1200 active-fixation leads and 1047 passive-fixation leads implanted in 1419 patients. Cardiac perforation occurred only in 8 patients (0.5%), but all perforations involved active-fixation leads. However, Hirschl et al. found a comparable incidence of asymptomatic cardiac perforation detected by CT scans in patients receiving active and passive-fixation ventricular leads.10 Of note, in this series, passive-fixation atrial leads had a higher incidence of asymptomatic perforation when compared with active-fixation atrial leads (25 vs. 12%, respectively). In the same manner, a recent nationwide population-based cohort study performed in a Taiwan population has shown no difference in the risk of cardiac perforation between active and passive-fixation pacing leads.19
One of the principal arguments employed in order to explain the supposed higher incidence of cardiac tamponade associated with active-fixation leads is the presence of a small body diameter which is associated with an increase in force per unit area. During the past years, significant technological innovations have been incorporated into active-fixation leads and progressive reduction of lead diameter is one of the most remarkable ones, especially among defibrillation leads. This has been related with an increased risk of perforation with some specific lead models.9 The overtorquing of active-fixation leads is another factor that has been associated with cardiac perforation.11 Experimental animal models have shown that overtorquing is associated with an increased tissue distortion that might result in cardiac perforation. The final mechanism responsible for perforation would be the abrasion of the visceral pericardial layer caused by the protruding helix of the lead.12,21,22
Of note, the clinical course of patients with cardiac perforation was favourable. All patients with cardiac tamponade were successfully treated with urgent pericardiocentesis and none of them required surgical treatment. Complete recovery without further complications was achieved in all these patients. The traditional approach for management of patients with lead perforation has been an urgent pericardiocentesis in the case of cardiac tamponade and, after hemodynamic stabilization, percutaneous reposition of the lead either in the electrophysiology laboratory or in the operating room but with surgical backup in any case. Geyfman et al. proposed to reposition the perforated leads in the electrophysiology laboratory considering that the perforation caused by the helix or the lead body is very small and will spontaneously close without the need of surgical repair in the majority of cases.22 Our results are in concordance with these observations. Moreover, in a high percentage of cases we did not reposition the perforated leads based on the presence of normal electrical parameters and in the absence of fluoroscopic images of lead penetration. These findings would suggest that the pericardial abrasion or the gap created by the lead in the right atrial or right ventricle wall is of very small entity and usually heals without any sequelae. Indeed, only two patients with cardiac perforation occurring at implantation showed abnormal electrical parameters requiring lead reposition during the same procedure. The remaining nine patients with cardiac perforation evidenced during the implant showed absolutely normal electrical parameters including pacing, sensing, and impedance values, and no lead repositioning was then performed. The electrical parameters in this last subgroup of patients remained stable at follow-up.
With respect to the timing of perforations, almost 76% of all cases were considered acute perforations and occurred during the first 24 h after surgery, and most of them were identified during the implant procedure. Subacute perforations were less frequent (4 cases, 24%) and no single case of late perforation was registered in our series. As other authors have previously reported, active-fixation defibrillator leads were not associated with an increased risk of perforation when compared with pacing leads. Interestingly, the position of the right ventricular lead in the right ventricular septal area was rarely associated with cardiac perforation, while an apical location was an independent predictor of cardiac perforation. This observation could be of significant clinical relevance and could lead to recommend the systematic implantation of active-fixation right ventricular leads in a septal area. The presence of an increased myocardial thickness in the septal region could prevent or make more difficult the occurrence of cardiac perforation associated with active-fixation leads.
Limitations
This is a retrospective study and inherent limitations associated with this kind of design should be taken into consideration. We did not perform a systematic evaluation of the presence of pericardial effusion in every patient. Only those with clinical suspicion, with abnormal electrical parameters or with radiologic evidence of lead penetration underwent transthoracic echocardiography. Thus, eventual asymptomatic perforations could not have been identified.
Conclusions
The incidence of clinically relevant cardiac perforation associated with systematic implantation of active-fixation leads is low and comparable with that reported with the use of passive-fixation leads. When occurring, cardiac perforation can be usually managed without the need of cardiac surgery with total recovery in the majority of cases.
Conflict of interest: none declared.
