Impact of Transapical Aortic Valve Replacement on Apical Wall Motion


Recent reports indicate that the transapical approach for transcatheter aortic valve replacement may be associated with elevated cardiac enzymes, poor recovery of left ventricular function, and poor outcomes. The aim of this study was to evaluate whether transapical access is associated with apical dysfunction and to assess consequences on patient outcomes.


In patients undergoing transapical aortic valve replacement, apical regional function was retrospectively assessed using the three standard echocardiographic long-axis views. Patients with abnormal baseline apical motion were excluded. Apical regional wall motion abnormality was assessed on preprocedural (baseline), immediate postprocedural (early [6 ± 2 days]), and late postprocedural (late [95 ± 76 days]) examinations. Apical regional wall motion abnormalities were categorized as normal, hypokinesis, or akinesis.


A total of 58 patients undergoing transapical aortic valve replacement were included in the present analysis. Of those, 16 (28%) developed early apical dysfunction. There were no differences in baseline characteristics between the patients who developed early apical dysfunction and those who did not. Patients who received 26-mm valves were more likely to develop apical dysfunction (40% vs 69%, P = .05). In total, 50% of patients with apical dysfunction (eight of 16) had complete recovery of apical function but tended to have lower ejection fractions (50% vs 60%, P = .045) at long-term follow-up. No difference in short-term or long-term mortality was detected in these small patient cohorts.


Myocardial injury during transapical access resulted in apical dysfunction early after the procedure in 28% of patients. This apical dysfunction was transient in half of the patients and was associated with a decrease in left ventricular function but did not affect mortality.

Patients selected for the transapical (vs transfemoral) approach for transcatheter aortic valve replacement (AVR) generally represent a sicker population, especially in terms of prior cardiac surgery and peripheral vascular and cerebrovascular disease. Nonrandomized, retrospective studies have indicated that patients undergoing transapical AVR have outcomes comparable with those of patients undergoing transfemoral AVR, especially after adjusting for baseline characteristics. Recent publications, however, have raised concerns regarding the safety, quality-of-life implications, and cost-effectiveness of the transapical approach compared with surgical AVR.

Direct transapical access to the left ventricle involves the placement of two circular purse-string sutures with an internal diameter of approximately 1 to 2 cm at the left ventricular access site, followed by the insertion of a large sheath through the myocardium. The transapical approach was found to be associated with higher levels of myocardial enzyme leakage compared with the transfemoral approach; this leakage was demonstrated to be independently associated with poor outcomes. Likewise, data derived from patients undergoing coronary bypass surgery indicate that patients who develop myocardial enzyme elevation have worse outcomes.

Thus, the aim of the present study was to assess whether the myocardial injury associated with transapical valve implantation translates into wall motion abnormalities.


This retrospective study was approved by the institutional review board of the MedStar Health Research Institute.


A retrospective analysis of consecutive patients with symptomatic severe aortic stenosis who underwent transapical transcatheter AVR from January 2009 to April 2011 was performed. Patients with abnormal apical function at baseline were excluded from the present analysis. Patients who died during the procedure or during the immediate periprocedural period were also excluded.

Patients were divided into two groups on the basis of the results of early postprocedural echocardiography: those who developed regional apical dysfunction (apical dysfunction group) and those who did not have any new apical motion abnormality or deterioration from baseline (no apical dysfunction group). Prespecified clinical data were prospectively collected for all patients on admission, immediately after transcatheter AVR, and during long-term follow-up. Collected data included medical history, medications on admission, procedural data, amount of contrast used, procedural length, success, and complications.

Transapical Procedure

For transapical procedures, a left minithoracotomy was performed, and two intramural pledgeted purse-string apical sutures were placed before apical puncture. After puncture and stiff wire positioning in the descending aorta, a 26-Fr or 22-Fr sheath was inserted, and an Edwards SAPIEN or SAPIEN XT transcatheter heart valve was implanted using the Ascendra delivery system (Edwards Lifesciences, Irvine, CA) following balloon aortic valvuloplasty. Upon completion of the procedure, the sheath was removed and the purse-string sutures were closed under rapid pacing. A drain was retained in the pericardial space and the chest incision was closed.


Transthoracic echocardiograms of all patients who underwent transapical transcatheter AVR were retrospectively reviewed at three time points: before transcatheter AVR (baseline), before discharge from the index hospitalization (short-term follow-up), and ≥1 month after the procedure (long-term follow-up). For the assessment of apical regional wall motion abnormalities, all long-axis views of the left ventricle were assessed and graded as normal, hypokinetic, akinetic, dyskinetic, or scarred. Echocardiographic studies were reviewed by two independent cardiologists (I.M.B. and D.D.). Valvuloarterial impedance was calculated as a surrogate for global left ventricular hemodynamic load at baseline and early after the procedure.

Periprocedural complications included atrial fibrillation, pulmonary complications defined as the need for prolonged ventilation and pleural effusion requiring drainage, prolonged periprocedural hypotension requiring inotropic support, and dialysis. Creatine kinase–MB fraction and troponin I levels were measured routinely after the procedure, and the cardiac biomarker peak levels are reported. On the basis of the 99th percentile in a healthy population and the requirement of a ≤10% coefficient variation, the upper normal limit for creatine kinase–MB fraction was 3.6 ng/mL and for cardiac troponin I was 0.045 ng/mL at our institution.

Statistical Analysis

Statistical analysis was performed using SAS version 8.2 (SAS Institute Inc., Cary, NC). Continuous variables are expressed as mean ± SD or as median (interquartile range [IQR]) as appropriate, according to variable distribution. Categorical variables are expressed as percentages. Two-sided Wilcoxon’s tests were used to compare continuous variables, and χ 2 or Fisher’s exact tests were used to compare categorical variables. P values < .05 were considered statistically significant. Intraobserver and interobserver agreement was assessed and interpreted using Cohen’s κ coefficient for categorical variables.


A total of 81 patients underwent AVR with transapical access ( Figure 1 ). Of these, seven patients who died before the acquisition of follow-up echocardiography, 14 patients who had baseline abnormal apical function, and two patients who were lost to follow-up were excluded. Thus, 58 patients were included in the final analysis. The median age of patients undergoing transapical AVR was 86 years (IQR, 83–89 years), and 47% were men. The median Society of Thoracic Surgeons risk score was 12% (IQR, 10%–13%); 94% of the patients had hypertension, 32% had diabetes mellitus, and 56% had peripheral vascular disease.

Figure 1

Flowchart. TA , Transapical; TAVR , transcatheter AVR.

As presented in Figure 1 , of the 58 patients, 16 (28%) developed new apical regional motion abnormalities on early follow-up echocardiography (6 ± 2 days after the procedure; apical dysfunction group). None of the patients developed apical dyskinesis early after the procedure. Forty-two patients (72%) did not develop any new apical regional motion abnormalities (no apical dysfunction group). Intraobserver (κ = 0.60, P < .001) and interobserver (κ = 0.67, P < .001) variability in the assessment of apical motion abnormality was assessed using Cohen’s κ coefficient.

The baseline characteristics of patients with and without apical dysfunction were generally similar; however, the apical dysfunction group included more men (75% vs 36%, P = .07) and tended to have a higher prevalence of atrial fibrillation at baseline (31% vs 7%, P = .08) ( Table 1 ). Median age (83 vs 85 years, P = .30), Society of Thoracic Surgeons risk score (11% vs 11%, P = .98), and systemic hypertension (93% vs 95%, P = 1.00) were comparable between the apical dysfunction and no apical dysfunction groups, respectively. Baseline echocardiographic parameters were generally comparable between those with and those without apical dysfunction, respectively, including left ventricular ejection fraction (55 ± 7% vs 58 ± 10%, P = .17), right ventricular function, aortic valve area, and baseline valvuloarterial impedance. However, patients with apical dysfunction had larger ventricles, as indicated by higher median left ventricular end-diastolic diameters compared with the no apical dysfunction group (4.7 vs 4.3 mm, P = .03; Table 2 ).

Table 1

Baseline characteristics

Variable No apical dysfunction ( n = 42) Apical dysfunction ( n = 16) P
Age (y) 85 (83–89) 83 (81–89) .33
Men 15 (36%) 12 (75%) .07
Body mass index (kg/m 2 ) 25 (21–28) 27 (25–28) .27
Society of Thoracic Surgeons risk score (%) 11 (10–13) 11 (9–13) .98
Systemic hypertension 37 (95%) 14 (93%) 1.00
Diabetes mellitus 12 (31%) 5 (33%) 1.00
Hypercholesterolemia 30 (79%) 11 (73%) .72
Atrial fibrillation 12 (31%) 1 (7%) .08
Coronary artery disease 27 (64%) 12 (80%) .34
Prior percutaneous coronary intervention 7 (20%) 6 (40%) .17
Prior coronary bypass surgery 15 (40%) 7 (47%) .60
Peripheral vascular disease 18 (53%) 9 (64%) .47
Aspirin 36 (88%) 15 (94%) .67
Angiotensin-converting enzyme inhibitors 18 (44%) 6 (38%) .66
Diuretics 15 (37%) 9 (56%) .18

Data are expressed as median (IQR) or as number (percentage).

Table 2

Baseline echocardiographic data

Variable No apical dysfunction ( n = 42) Apical dysfunction ( n = 16) P
Ejection fraction (%) 61 (56–65) 54 (50–64) .32
Aortic valve area (mm 2 ) 0.6 (0.5–0.7) 0.6 (0.6–0.8) .40
LV end-diastolic diameter (mm) 4.3 (4–4.6) 4.7 (4.3–5) .03
LV end-systolic diameter (mm) 2.7 (2.2–3.1) 3.0 (2.6–3.5) .11
Pulmonary pressure (mm Hg) 46 (40–60) 41 (40–47) .34
Right ventricular dysfunction 8 (21%) 2 (13%) .70
Valvuloarterial impedance 4 (3.6–5.3) 4.3 (3.8–5.3) .48

LV , Left ventricular.

Data are expressed as median (IQR) or as number (percentage).

Procedural characteristics were generally comparable between the two groups, save for valve size. Patients with early apical dysfunction were more likely to receive 26-mm valves compared to those without apical dysfunction (69% vs 40%, P = .05; Table 3 ).

Table 3

Procedural data and clinical outcomes

Variable No apical dysfunction ( n = 42) Apical dysfunction ( n = 16) P
Procedural characteristics
23-mm valve 28 (60%) 5 (31%) .05
26-mm valve 19 (40%) 11 (69%) .05
Fluoroscopy time (min) 10.4 (8.8–14.2) 9.4 (8.2–15.1) .44
Myocardial enzyme leak
Peak creatine kinase–MB (ng/mL) 26.8 (15.4–36.8) 24.4 (17.7–63.5) .56
Peak cardiac troponin (ng/mL) 10.1 (5.1–19.9) 11 (7.6–16.7) .42
In-hospital complications
Intensive care unit stay (h) 44.7 (29–168) 30.5 (27.5–97.5) .42
Blood transfusion (mL) 250 (0–500) 250 (0–563) .90
Hemodynamic instability 9 (27%) 1 (9%) .41
Respiratory complications 7 (21%) 3 (27%) .69
Postoperative atrial fibrillation 19 (45%) 6 (38%) .60
Permanent pacemaker 2 (4.8%) 1 (6.3%) 1.00
New left bundle branch block 2 (5.1%) 2 (17%) .19
30 d 5 (12%) 0 .31
1 y 9 (21%) 3 (19%) 1.00

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Jun 2, 2018 | Posted by in CARDIOLOGY | Comments Off on Impact of Transapical Aortic Valve Replacement on Apical Wall Motion

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