Transcatheter aortic valve implantation (TAVI) frequently requires postprocedural permanent pacemaker (PPM) implantation. We evaluated clinical and hemodynamic impact of PPM after TAVI. Clinical and echocardiographic data were retrospectively analyzed in 230 consecutive patients who underwent TAVI and echocardiography at baseline and after 6 months. Echocardiographic parameters included left ventricular ejection fraction (LVEF), left ventricular (LV) stroke volume, early mitral velocity/annulus velocity ratio (E/e′), right ventricular index of myocardial performance, systolic pulmonary artery pressure (SPAP), and aortic, mitral, and tricuspid regurgitation grades. Clinical outcomes included 2-year survival and cardiovascular and PPM-related event-free survival. The Medtronic CoreValve and Edwards Sapien prosthesis were used in 201 and 29 patients, respectively. PPM was required in 58 patients (25.4%). Two-year and event-free survival rates were similar between patients with and without PPM. At 6 months, patients with PPM demonstrated attenuated improvement in LVEF (−0.9 ± 8.7% vs 2.3 ± 10.8%, respectively, p = 0.03) and LV stroke volume (−2 ± 16 vs 4 ± 10 ml/m 2 , respectively, p = 0.015), a trend toward smaller reduction in systolic pulmonary artery pressure (−1 ± 12 vs −6 ± 10 mm Hg, respectively, p = 0.09), and deterioration of right ventricular index of myocardial performance (−3 ± 17% vs 5 ± 26%, respectively, p = 0.05). The differences in post-TAVI aortic, mitral, and tricuspid regurgitation grades were insignificant. In conclusion, PPM implantation after TAVI is associated with reduced LVEF and impaired LV unloading. However, this unfavorable hemodynamic response does not affect the 2-year clinical outcome. The maintenance of clinical benefit appears to be driven by TAVI-related recovery of LV and right ventricular performance that mitigates unfavorable impact of PPM.
The close anatomical relation between the aortic valve and the branching atrioventricular (AV) bundle may lead to conduction system abnormalities during transcatheter aortic valve implantation (TAVI). Up to 40% of patients undergoing TAVI, particularly those using a self-expanding prosthesis, require permanent pacemaker (PPM) implantation. Right ventricular (RV) pacing results in desynchronization of left ventricular (LV) contraction, which in turn may lead to LV remodeling and reduced LV ejection fraction (LVEF). Numerous randomized clinical trials have demonstrated deleterious effects of RV pacing including increased risk of atrial fibrillation, ventricular arrhythmia, and heart failure. These studies evaluated patients with primary conduction system abnormalities with or without LV systolic dysfunction unrelated to aortic stenosis and TAVI. Furthermore, TAVI-related left bundle branch block (LBBB) or need of PPM was shown to adversely affect LV improvement. However, a recent study evaluating clinical outcomes among patients with or without PPM implantation after TAVI showed similar mortality rates in both groups, along with similar cardiac and cerebrovascular morbidity rates. The mechanism of maintenance of clinical benefit of TAVI despite adverse hemodynamic effect of PPM in this subgroup of patients is unclear. Therefore, the purpose of the present study was to evaluate the hemodynamic consequences of permanent pacing in patients undergoing TAVI and further define its relation to clinical outcome.
Methods
Our study population consisted of consecutive patients undergoing percutaneous transfemoral TAVI for treatment of symptomatic aortic valve stenosis using the Edwards Sapien/Sapien XT prosthesis (Edwards Lifesciences, Irvine, California) or the Medtronic CoreValve prosthesis (MCV; Medtronic, Minneapolis, Minnesota) at a tertiary university hospital. The institutional ethics committee approved the study.
Inclusion criteria were logistic EuroSCORE >20, porcelain aorta, previous chest radiation, logistic EuroSCORE >10%, and 1 of the following: cachexia, need for assistance in basic daily activities, or previous open heart surgery. The Institutional Heart Team including an interventional cardiologist, echocardiologists, and a cardiothoracic surgeon determined eligibility for TAVI.
Temporary pacemakers were implanted in all patients unless they were already carrying PPM. For the immediate 36 hours after procedure interval, the patients were monitored in the intensive care unit; the temporary pacemaker was extracted after 24 hours unless AV conduction disturbances were detected. The criteria for PPM implantation included pre-TAVI right bundle branch block (BBB), post-TAVI complete AV block (AVB), type II second-degree AV block, alternating BBB, or new-onset LBBB with PR-interval prolongation ≥280 ms.
Patients undergoing TAVI have been enrolled in a prospective registry recording procedural information as well as clinical, echocardiographic, and pacemaker data collected at baseline 30 days, 6 months, 12 months, and then at regular 6- to 12-month intervals. Clinical end points were overall survival and cardiovascular event-free survival. Cardiovascular events included hospitalization for heart failure, stroke, myocardial infarction, new-onset atrial fibrillation, and AVB occurring after discharge.
At each follow-up visit, we recorded pacemaker pacing mode, battery and electrode status, capture threshold, impedance and sensing as well as cumulative percentage of RV pacing. Devices were programed to minimize ventricular pacing by activating ventricular pacing suppression algorithms, increasing AV delay, or lowering pacing rate.
Transthoracic echocardiographic data were obtained with a standardized protocol. LV linear dimensions were obtained on the parasternal long-axis view. LV mass was estimated based on LV modeling as a prolate ellipse. LV end-diastolic volume, LV end-systolic volume, and LVEF were calculated using the Simpson rule or Quinones method. LV stroke volume (LVSV) was calculated as previously described. Early (E) transmitral filling peak velocity was obtained with pulsed wave Doppler sample at the tip of the mitral valve leaflets. Early velocity of the septal and lateral aspects of the mitral annulus was measured using tissue Doppler imaging. Mitral annulus velocity (e′) was defined as the average of septal and lateral velocities. Left atrial volume was determined using the biplane area-length or dimension-length methods. RV index of myocardial performance (RIMP) was used for global estimates of RV systolic and diastolic functions. RIMP was defined as the ratio of isovolumic time and ejection time. RV ejection time was measured using pulsed wave Doppler of the RV outflow. The isovolumetric time was calculated as the difference between the duration of flow of the tricuspid regurgitant jet and the ejection time. Systolic pulmonary artery pressure (SPAP) and right atrial pressure were estimated as previously described. Echo Doppler indexes of aortic stenosis severity included the maximal velocity across the aortic valve, the mean pressure gradient, and the aortic valve area (AVA) calculated using the standard continuity equation. Severe aortic stenosis was defined as an AVA <1.0 cm 2 and a mean pressure gradient of >40 mm Hg. Aortic, mitral, and tricuspid regurgitation grades were classified semiquantitatively on a scale of 0 to 4 according to established criteria. AVA, left atrial volume, LV end-diastolic volume, LV end-systolic volume, and LVSV were indexed by body surface area.
The implantation depth of the bioprosthesis was assessed using aortography immediately after TAVI. For each patient, the distance between lower edges of the noncoronary cusp and ventricular end of prosthesis frame were obtained twice. Implantation depth was defined as an average of these 2 measurements.
Continuous normally distributed parameters are presented as the mean ± SD and were compared using the Student or paired t test, as appropriate. Ordinal and/or non-normally distributed data are presented by the median and the first and third quartiles and were compared using the Wilcoxon rank sum or Wilcoxon signed-rank test. Categorical data were analyzed using the Fisher’s exact test. Event distributions were calculated according to the Kaplan-Meier method and were compared using the log-rank test. All p values were 2-sided, and values of <0.05 were considered statistically significant. All data were analyzed with the JMP System software version 8.0 (SAS Institute, Inc, Cary, North Carolina).
Results
Of 249 consecutive patients undergoing TAVI, 19 were excluded because of the presence of preexisting PPM. Thus, the study population consisted of 230 patients, including 201 (87%) with MCV and 29 (13%) with Edwards Sapien prosthesis. Fifty-eight patients (25%) required PPM implantation, 55 (27%) with MCV and 3 (10%) with Edwards Sapien prosthesis. Relative risk of PPM implantation for MCV was 2.52 (0.84 to 7.53, p = 0.09). In patients with MCV, the depth of the implantation was greater in patients with PPM compared with those without PPM (6.6 ± 2.8 vs 4.4 ± 2.6 mm, respectively, p <0.001). Indications for PPM implantation included complete AVB in 36 patients (62%), LBBB associated with prolonged PR in 19 patients (32.3%), alternating BBB in 2 patients (3.4%), and right BBB before TAVI in 1 patient (1.7%). The cumulative percentage of RV pacing among patients with PPM was 50 ± 42%. Percent pacing was greater among patients with complete AVB compared with other indications (66 ± 38% and 26 ± 36%, respectively, p = 0.0003). Two patients had PPM-related complications. One subsequently required ventricular electrode reposition because of dislodgement and the other with atrial lead dislodgement was programed to ventricular sensing and pacing mode (VVI).
Table 1 demonstrates baseline demographic and clinical characteristics of the entire cohort and subgroups with and without PPM implantation. No significant differences were observed in any of the baseline parameters. Male gender tended to be more prevalent in the PPM group (p = 0.086).
| Variable | Total (n = 230), % | Pacemaker Implanted, % | p | |
|---|---|---|---|---|
| No (n = 172) | Yes (n = 58) | |||
| Age (yrs) | 83 ± 5 | 83 ± 6 | 83 ± 5 | 0.91 |
| Men | 38.3 | 34.9 | 48.3 | 0.086 |
| Height (cm) | 162 ± 9 | 162 ± 9 | 163 ± 10 | 0.61 |
| Weight (kg) | 72 ± 15 | 71 ± 15 | 75 ± 15 | 0.15 |
| Body surface area (m²) | 1.64 ± 0.4 | 1.62 ± 0.4 | 1.7 ± 0.4 | 0.18 |
| Diabetes mellitus | 32.6 | 30.2 | 39.7 | 0.198 |
| Dyslipidemia | 78.3 | 79.7 | 74.1 | 0.462 |
| Hypertension | 84.8 | 86 | 81 | 0.399 |
| Peripheral vascular disease | 11.3 | 12.8 | 9 | 0.337 |
| Past stroke | 7.8 | 7.6 | 8.6 | 0.781 |
| Heart failure | 34.8 | 37.8 | 25.9 | 0.112 |
| Previous coronary bypass grafting | 18.3 | 19.8 | 13.8 | 0.432 |
| Atrial fibrillation | 18.7 | 19.8 | 15.5 | 0.562 |
| Logistic EuroSCORE | 26 ± 14 | 26 ± 13 | 26 ± 13 | 0.9 |
Baseline echo Doppler characteristics are listed in Table 2 . AVA was smaller in patients with no PPM compared with those with PPM implantation (p = 0.01). No difference existed when body surface area was used to index AVA. The rate of mitral regurgitation was higher in no PPM group (p = 0.054); no significant difference was observed in the rates of aortic or tricuspid regurgitation of grade ≥2.
| Variable | Total | Pacemaker Implanted | p | |
|---|---|---|---|---|
| No | Yes | |||
| Aortic valve V max (cm/s) | 428 ± 66 | 439 ± 66 | 428 ± 66 | 0.26 |
| Aortic valve mean gradient (mm Hg) | 47 ± 15 | 47 ± 66 | 46 ± 15 | 0.86 |
| AVA index (cm²/m²) | 0.43 ± 0.12 | 0.42 ± 0.12 | 0.44 ± 0.15 | 0.4 |
| Left atrial volume index (ml/m²) | 47 ± 17 | 48 ± 18 | 45 ± 21 | 0.50 |
| LV mass index (g/m²) | 139 ± 56 | 134 ± 65 | 137 ± 32 | 0.77 |
| LV end-diastolic volume index (ml/m²) | 63 ± 20 | 63 ± 24 | 65 ± 26 | 0.7 |
| LV end-systolic volume index (ml/m²) | 28 ± 10 | 28 ± 16 | 28 ± 15 | 0.74 |
| SV index (ml/m²) | 33 ± 12 | 33 ± 15 | 34 ± 18 | 0.67 |
| LVEF (%) | 58 ± 10 | 58 ± 11 | 58 ± 10 | 0.54 |
| E wave (cm/s) | 99 ± 31 | 100 ± 32 | 98 ± 30 | 0.67 |
| e′ (cm/s) | 5.1 ± 1.6 | 5 ± 1.7 | 5.2 ± 1.4 | 0.59 |
| E/e′ | 21 ± 8 | 21 ± 8 | 20 ± 8 | 0.64 |
| SPAP (mm Hg) | 44 ± 15 | 45 ± 15 | 41 ± 13 | 0.12 |
| Tricuspid regurgitation time (ms) | 402 ± 45 | 401 ± 50 | 404 ± 45 | 0.66 |
| RV ejection time (ms) | 306 ± 41 | 305 ± 32 | 308 ± 40 | 0.55 |
| RIMP | 0.32 ± 0.15 | 0.32 ± 0.15 | 0.32 ± 0.15 | 0.99 |
| Mitral regurgitation grade ≥2 (%) | 44 (19) | 38 (22) | 6 (10) | 0.054 |
| Tricuspid regurgitation grade ≥2 (%) | 23 (10) | 18 (10) | 5 (9) | 0.76 |
| Aortic regurgitation grade ≥2 (%) | 18 (8) | 15 (9) | 3 (5) | 0.57 |
Median (minimum, maximum) follow-up was 19.5 months (6, 43). Eight patients died within 30 days of undergoing TAVI, 2 from the PPM group and 6 from the no PPM group. There was no significant difference in early mortality between patients with and without PPM (3.5% vs 3.4%, respectively, p = 1.0). A total of 41 patients died, and 58 patients were rehospitalized for cardiovascular events. No difference in mortality was found between patients with and without PPM with both groups having similar 1-year (89.2 ± 4.2% vs 89.8 ± 2.3%, respectively) and 2-year event-free survival rates (80.8 ± 7.4% vs 84.5 ± 3.4%, respectively). The hazard ratio of PPM for all-cause mortality was 1.02 (95% confidence interval 0.46 to 2.1, p = 0.94). Cardiovascular event-free survival rate was not significantly different between the 2 groups at 1 year (59.4 ± 4.0% vs 65 ± 3.7%) or 2 years (59.4 ± 6.6% vs 47.8 ± 4.7%). The combined hazard ratio of post-TAVI PPM implantation for mortality and cardiovascular events was 0.89 (95% confidence interval 0.55 to 1.39, p = 0.62).
At 6 months, 54 patients with PPM and 158 patients without PPM were alive. The changes in echo Doppler parameters between baseline and the 6-month follow-up are presented in Table 3 . Patients with PPM demonstrated less favorable changes in LVSV, LVEF, and E/e′ ratio. In addition, these patients demonstrated a trend toward a lesser decrease in SPAP (p = 0.09) and worsening of RIMP (p = 0.05).
| Variable | Total | Pacemaker Implanted | p | |
|---|---|---|---|---|
| No | Yes | |||
| Aortic valve V max (cm/s) | −235 ± 118 | −241 ± 120 | −240 ± 106 | 0.67 |
| Aortic valve mean gradient (mm Hg) | −38 ± 15 | −38 ± 16 | −40 ± 15 | 0.46 |
| Left atrial volume index (ml/m²) | −2 ± 12 | −3 ± 12 | −2 ± 10 | 0.85 |
| LV mass index (g/m²) | −6 ± 32 | −7 ± 35 | −6 ± 27 | 0.92 |
| LV end-diastolic volume index (ml/m²) | 4 ± 14 | 4 ± 16 | 1 ± 14 | 0.21 |
| LV end-systolic volume index (ml/m²) | 1 ± 10 | 0.4 ± 12 | 2 ± 11 | 0.42 |
| SV index (ml/m²) | 2 ± 8 | 4 ± 10 | −2 ± 16 | 0.015 |
| LVEF (%) | 1 ± 8 | 2 ± 10 | −3 ± 14 | 0.02 |
| E wave (cm/s) | 4.2 ± 30 | −1.2 ± 29 | 14 ± 28 | 0.002 |
| e′ (cm/s) | 0.5 ± 1.8 | 0.6 ± 1.7 | 0.3 ± 1.5 | 0.5 |
| E/e′ | −0.14 ± 7.7 | −1.8 ± 7.6 | 2.5 ± 7.7 | 0.01 |
| SPAP (mm Hg) | −4 ± 10 | −6 ± 10 | −1 ± 12 | 0.09 |
| Tricuspid regurgitation time (ms) | −9 ± 50 | −5 ± 52 | −19 ± 55 | 0.16 |
| RV ejection time (ms) | −7 ± 35 | 1 ± 36 | −26 ± 50 | 0.002 |
| RIMP | 0.01 ± 0.13 | −0.02 ± 0.16 | 0.09 ± 0.33 | 0.05 |
| Mitral regurgitation grade reduced from ≥2 to ≤1 (%) | 28 (56) | 26 (63) | 2 (33) | 0.19 |
| Tricuspid regurgitation grade reduced from ≥2 to ≤1 (%) | 8 (35) | 5 (28) | 3 (60) | 0.29 |
| Aortic regurgitation grade ≥2 (%) | 18 (8) | 16 (9) | 3 (5) | 0.57 |
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