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Global and Regional Left Ventricular Function in Patients Undergoing Transcatheter Closure of Secundum Atrial Septal Defect
Global and Regional Left Ventricular Function in Patients Undergoing Transcatheter Closure of Secundum Atrial Septal Defect Marco Pascotto, MDa,*, Giuseppe Santoro, MDa, Pio Caso, MDb, Fabiana Cerrato, MDa, Ilaria Caso, MDa, Salvatore Caputo, MDa, Maurizio Cappelli Bigazzi, MDa, Antonello D’Andrea, MDa, Maria Giovanna Russo, MDa, and Raffaele Calabrò, MDa This study sought to evaluate global and regional left ventricular (LV) function before and early after device closure of atrial septal defects (ASDs) in patients with normal pulmonary pressure. Global LV diastolic function was unaffected by ASD closure. An improvement in global LV systolic function at rest resulted in an increase in stroke volume at rest. Nevertheless, total cardiac output did not change after the procedure, because of a decrease in heart rate at rest counterbalancing the increase in stroke volume. Thus, lateral and inferior LV regional systolic function were preserved after device implantation. Moreover, no changes in regional LV diastolic function were highlighted during the study. © 2005 Elsevier Inc. All rights reserved. (Am J Cardiol 2005;96:439 – 442) Recently, percutaneous atrial septal defect (ASD) closure has become a standard procedure.1,2 However, discordant data are available on the impact of device implantation and overload relief on left ventricular (LV) function. Because the ASD occluder is a relatively rigid device, some concern has been raised regarding its potentially negative impact on LV regional performance as well as on left atrial contraction early after the procedure.3 In contrast, LV function and exercise tolerance have been shown to improve in patients who undergo percutaneous ASD closure.4 – 6 The aim of this study was to describe systolic and diastolic global and regional LV function in a large cohort of patients who underwent the device closure of ASDs. •••
Seventy consecutive patients who underwent the device closure of ASDs at Monaldi Hospital, Naples, Italy, were enrolled in the study. Demographic and hemodynamic data are listed in Table 1. In all patients, an Amplatzer septal occluder device (AGA Medical Corporation, Golden Valley, Minnesota) was implanted. Two days after ASD closure, patients were discharged and received aspirin 100 mg/day for 6 months. All echocardiographic studies were performed using an Acuson Sequoia C256 system (Siemens Medical Solutions USA, Inc., Mountain View, California). Monodimensional (M-mode) left-sided cardiac dimensions were recorded according to the criteria of the American Society of Echocardiography.7 LV volumes were analyzed according to the Teichholz formula.8 Pulse-wave Doppler flow analysis was
a
Pediatric Cardiology, Second University of Naples, and bDivision of Cardiology, Monaldi Hospital, Naples, Italy. Manuscript received December 30, 2004; revised manuscript received and accepted March 25, 2005. *Corresponding author. Tel.: 39-081-5754332; fax: 39-081-7062683. E-mail address: [email protected] (M. Pascotto). 0002-9149/05/$ – see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.amjcard.2005.03.096
performed at the levels of the mitral valve and of the LV outflow tract according to the criteria of the American Society of Echocardiography.9 Mitral Doppler was performed to analyze LV diastolic function. Early (E) and late (A) diastolic peak velocities, the E/A ratio, and mitral deceleration time and isovolumetric relaxation time were recorded. Again, pulse-wave Doppler of the LV outflow tract (5-chamber apical view) was performed to obtain the corresponding velocity–time integrals (VTIao). VTIao was used as surrogate of stroke volume, and VTIao ⫻ heart rate was used as surrogate of cardiac output. Pulsed Doppler tissue imaging (DTI) was performed by spectral pulsed Doppler signal filters from the apical view to minimize the incidence angle between the Doppler beam and longitudinal wall motion. The basal lateral and inferior LV borders were sampled. The Doppler spectrum was recorded at a velocity of 50 mm/s. The myocardial peak velocity of S= (centimeters per second), myocardial precontraction time (from the onset of the QRS complex to the beginning of S=), and time to peak systolic velocities (from the onset of the QRS complex to the S= peak) were calculated as systolic indexes. Myocardial E= and A= peak velocTable 1 Demographic and hemodynamic data Variable
Study Population (n ⫽ 70)
Age (yrs) Women/men Body mass index (kg/m2) ASD diameter (mm) Device diameter (mm) Systolic pulmonary pressure (mm Hg) Diastolic pulmonary pressure (mm Hg) Mean pulmonary pressure (mm Hg) Qp/Qs (pulmonary-to-systemic flow ratio)
18 ⫾ 16 (4–66) 1.8/1 20.0 ⫾ 4.8 (12.2–34.6) 13 ⫾ 7 (3–29) 18 ⫾ 8 (5–38) 30 ⫾ 9 (16–46) 15 ⫾ 5 (8–29) 22 ⫾ 6 1.9 ⫾ 0.8 (1–5) www.AJConline.org
440
The American Journal of Cardiology (www.AJConline.org)
Table 2 Clinical and echocardiographic data before and after ASD closure Variable
Before Closure
After 24 Hours
After 1 Month
Heart rate (beats/min) Systolic blood pressure (mm Hg) LV end-diastolic diameter (mm) LV end-systolic diameter (mm) Fractional shortening (%) LV end-diastolic volume (ml) LV end-systolic volume (ml) Ejection fraction (%) Mitral annular plane systolic excursion (mm) VTIao (m) VTIao ⫻ heart rate (m/min) E mitral (cm/s) A mitral (cm/s) E/A mitral Isovolumetric relaxation time (ms) Deceleration time (ms)
86 ⫾ 14 110 ⫾ 17 37 ⫾ 6 25 ⫾ 6 32 ⫾ 10 62 ⫾ 26 25 ⫾ 15 60 ⫾ 14 14 ⫾ 3 0.20 ⫾ 0.04 16.8 ⫾ 3.5 90 ⫾ 20 53 ⫾ 15 1.9 ⫾ 0.8 58 ⫾ 16 182 ⫾ 41
85 ⫾ 15 108 ⫾ 14 39 ⫾ 7† 24 ⫾ 6 38 ⫾ 11† 69 ⫾ 29† 25 ⫾ 14 64 ⫾ 11† 13 ⫾ 3 0.21 ⫾ 0.04 17.7 ⫾ 3.5 94 ⫾ 21 53 ⫾ 13 1.9 ⫾ 0.7 54 ⫾ 16 188 ⫾ 44
79 ⫾ 16* 111 ⫾ 15 42 ⫾ 7† 26 ⫾ 6 38 ⫾ 6† 79 ⫾ 30† 26 ⫾ 13 68 ⫾ 8† 13 ⫾ 3 0.23 ⫾ 0.05† 17.6 ⫾ 3.8 97 ⫾ 20 53 ⫾ 13 1.9 ⫾ 0.7 49 ⫾ 15* 184 ⫾ 37
* p ⬍0.03;
†
p ⬍0.001.
ities, the E=/A= ratio, and regional relaxation time (the time interval between the end of S= and the onset of E=) were determined as diastolic measurements. Mitral flow and myocardial Doppler measurements were digitally stored and analyzed offline as the average of 3 consecutive beats. The study protocol consisted of clinical, electrocardiographic, and echocardiographic evaluation before as well as 24 hours and 1 month after device implantation. Statistical analysis was performed using SPSS for Windows version 11.0 (SPSS, Inc., Chicago, Illinois). Variables
are presented as mean ⫾ SD. Comparisons between stages were made by repeated-measures analysis of variance. When differences were found between stages, Student’s paired t test was performed to determine interstage differences. Linear regression analyses and partial correlation test by Pearson’s method were done to assess univariate relations. ASD closure was successfully performed in all patients. Clinical, M-mode and Doppler flow data are listed in Table 2. Heart rate significantly reduced after device im-
Figure 1. In the presence of normal pulmonary pressures, ASD size is the major contributor to right ventricular volume overload. The greater the right ventricular volume overload, the greater the impact on LV end-diastolic (LVED) volume. These 2 graphs show how the increase in LVED volume (A) and stroke volume (B) correlate with ASD maximal diameter. LVED volume change after 1 month ⫽ (LVED volume1 month ⫺ LVED volumepreclosure)/LVED volumepreclosure. VTIao change after 1 month ⫽ (VTIao 1 month ⫺ VTIao preclosure) / VTIao preclosure.
Congenital Heart Disease/ASD Closure and LV Function
441
Figure 2. DTI velocities. Regional velocities were recorded at lateral (lat) and inferior (inf) mitral annulus. No differences were found between preclosure and postclosure velocities. (A) Systolic velocities (S=). (B) Early diastolic velocities (E=). (C) End-diastolic velocities (A=).
plantation. Unlike heart rate, systolic blood pressure did not change over time. An increase in LV end-diastolic volume was recorded, whereas end-systolic volume was unchanged. Overall, the ejection fraction significantly increased over time. At follow-up, no significant differences in either E, A, the E/A ratio, or deceleration time were found compared with baseline. A mild reduction in isovolumetric relaxation time was recorded 1 month after the intervention. Overall, diastolic function parameters were in the normal range before and did not change in the first month after ASD closure. A progressive increase in VTIao was found at follow-up. Thus, in agreement with ejection fraction data, LV stroke volume tended to increase after closure. This increase was counterbalanced by a decrease in heart rate. Overall, cardiac output did not change compared with preclosure values. Again, 1 month after the procedure, the percentage increase in LV end-diastolic volume and VTIao correlated positively with ASD maximal diameter (Figure 1), suggesting a direct effect of the overload relief on the stroke volume increase. DTI velocities are shown in Figure 2. No significant differences were highlighted in regional systolic and diastolic function over time. Again, the regional E=/A= ratio
Table 3 DTI velocity analysis Variable Lateral wall E=/A= ratio E/E= ratio Inferior wall E=/A= ratio E/E= ratio
Before Closure
After 24 Hours
After 1 Month
1.9 ⫾ 0.7 5⫾1
1.9 ⫾ 0.8 5⫾2
2.1 ⫾ 0.9 5⫾2
1.8 ⫾ 0.6 5⫾2
1.7 ⫾ 0.6 6⫾2
1.8 ⫾ 0.6 6⫾2
p ⫽ NS. No changes were recorded before and after ASD closure. E/E= ⬍8 is considered an expression of normal LV end-diastolic pressure A= ⫽ end-diastolic myocardial velocity; E ⫽ early diastolic mitral inflow peak velocity; E= ⫽ early diastolic myocardial velocity.
and the E/E= ratio were normal before and did not change after device implantation (Table 3), suggesting preserved LV diastolic function and end-diastolic pressure. Overall, myocardial velocities were in the normal range before and after the procedure.10 DTI time analysis is listed in Table 4. All time-analysis data were unaffected by the intervention. •••
This is the first study evaluating global and regional LV function in a large series of patients before and after the device closure of ASDs. It is well established that chronic right ventricular overload is associated with an impairment of LV performance over time.11,12 This is mainly due to the mechanical disadvantage of a noncircular short-axis configuration over radial function.4 In our study, DTI analysis of the lateral and inferior LV wall showed normal diastolic and systolic regional velocities. These findings highlight that, unlike radial function, LV longitudinal function does not seem to be affected by right ventricular overload in children and young adults with ASDs. A potential impairment of regional function is more likely to ensue in older patients with long-lasting cardiac remodeling due to volume overload. Overload relief determines striking geometric changes of the cardiac chambers early after transcatheter ASD closure.13–16 Although remodeling of the cardiac chambers has been evaluated, few data are available concerning global and regional LV function before and after device implantation. Although cardiac overload relief may positively affect LV function,4 the implantation of a relatively rigid device in a remodeling heart may potentially have a negative impact on cardiac performance, at least in the first month, when most of the geometric changes ensue.3 Recently, global LV function has been shown to improve after percutaneous ASD closure.4 – 6,13 Our data confirm that global systolic function at rest improves after the procedure, even in young patients with normal pulmonary pressures. In accordance with previous studies,4,6 the increase in the LV
442
The American Journal of Cardiology (www.AJConline.org)
Table 4 DTI time analysis before and after ASD closure Variable Lateral wall Precontraction time (ms) Time to peak S= (ms) Isometric relaxation time (ms) Inferior wall Precontraction time (ms) Time to peak S= (ms) Isometric relaxation time (ms)
Before Closure
After 24 Hours
After 1 Month
64 ⫾ 25 118 ⫾ 30 63 ⫾ 23
65 ⫾ 25 126 ⫾ 45 57 ⫾ 20
60 ⫾ 25 127 ⫾ 45 56 ⫾ 21
70 ⫾ 25 139 ⫾ 49 63 ⫾ 27
70 ⫾ 26 141 ⫾ 38 62 ⫾ 28
63 ⫾ 23 150 ⫾ 48 60 ⫾ 18
p ⫽ NS. S= ⫽ systolic myocardial peak velocity.
ejection fraction was mostly due to an increase in LV end-diastolic volume. This was further validated by Doppler flussimetry of the LV outflow tract, suggesting an increase in cardiac stroke volume. Total cardiac output at rest did not seem to change, because of a mild but significant decrease in heart rate counterbalancing the increase in stroke volume. A lower heart rate at rest may favor a better chronotropic reserve with exercise, which is in accordance with the improvement in the cardiopulmonary exercise tolerance after ASD closure.5,6 Pathophysiologically, regional dysfunction may ensue even in the presence of preserved global function. Thus, the absence of significant changes in DTI velocities and time-analysis data underscores how regional myocardial systolic function is unaffected by device implantation. Moreover, we did not find a significant difference in either geometric remodeling or in regional and global function even after dividing patients into 2 age groups (data not shown). However, most of the patients in our study population were ⬍45 years of age (90%), so we did not have enough statistical power to address age dependence in older patients. Further studies are needed to address this issue.16 1. Chessa M, Carminati M, Butera G, Bini MR, Drago M, Rosti L, Giamberti A, Pomè G, Bossone E, Frigiola A. Early and late complications associated with transcatheter occlusion of secundum atrial septal defect. J Am Coll Cardiol 2002;39:1061–1065. 2. Du ZD, Hijazi ZM, Kleinman CS, Silverman NH, Larntz K, Amplatzer Investigators. Comparison between transcatheter and surgical closure of secundum atrial septal defect in children and adults: results of a multicenter non randomized trial. J Am Coll Cardiol 2002;39:1836 –1844. 3. Lange A, Coleman DM, Palka P, Burstow DJ, Wilkinson JL, Godman MJ. Effect of catheter device closure of atrial septal defect on diastolic mitral annular closure. Am J Cardiol 2003;91:104 –108. 4. Walker RE, Moran AM, Gauvreau K, Colan SD. Evidence of adverse ventricular interdependence in patients with atrial septal defect. Am J Cardiol 2004;93:1374 –1377. 5. Brochu MC, Baril JF, Dore A, Juneau M, De Guise P, Mercier LA. Improvement in exercise capacity in asymptomatic and mildly symptomatic adults after atrial septal defect percutaneous closure. Circulation 2002;106:1821–1826.
6. Giardini A, Donti A, Formigari M, Specchia S, Prandstraller D, Bronzetti G, Bonvicini M, Picchio FM. Determinants of cardiopulmonary functional improvement after transcatheter atrial septal defect closure in asymptomatic adults. J Am Coll Cardiol 2004;43:1886 –1891. 7. American Society of Echocardiography, Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiography. Recommendation for quantitation of the left ventricular by twodimensional echocardiography. J Am Soc Echocardiogr 1989;2:358 – 367. 8. Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence or absence of asynergy. Am J Cardiol 1976;37:7–11. 9. American Society of Echocardiography. A report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography. Recommendation for quantitation of Doppler echocardiography. J Am Soc Echocardiogr 2002;15:167–184. 10. Eidem BW, McMahon CJ, Cohen RR, Wu J, Finkelshteyn I, Kovalchin JP, Ayres NA, Bezold LI, O’Brian Smith E, Pignatelli RH. Impact of growth on Doppler tissue imaging velocities: a study in healthy children. J Am Soc Echocardiogr 2004;17:212–221. 11. Flamm MD, Cohn KE, Hancock EW. Ventricular function in atrial septal defect. Am J Med 1970;48:286 –294. 12. Popio KA, Gorlin R, Teichholz LE, Cohn PF, Bechtel D, Herman MV. Abnormalities of left ventricular and geometry in adults with an atrial septal defect. Ventriculographic, hemodynamic and echocardiographic studies. Am J Cardiol 1975;36:302–308. 13. Du ZD, Cao QL, Koenig P, Heitschmidt M, Hijazi ZM. Speed of normalization of right ventricular volume overload after transcatheter closure of atrial septal defect in children and adults. Am J Cardiol 2001;88:1450 –1453. 14. Veldtman GR, Razack V, Siu S, El-Hajj H, Walker F, Webb GD, Benson LN, McLaughlin PR. Right ventricular form and function after percutaneous atrial septal defect device closure. J Am Coll Cardiol 2001;37:2108 –2113. 15. Santoro G, Pascotto M, Sarubbi B, Cappelli Bigazzi M, Calvanese R, Iacono C, Pisacane C, Palladino MT, Pacileo G, Russo MG, et al. Early electrical and geometric changes after percutaneous closure of large atrial septal defect. Am J Cardiol 2004;93:876 – 880. 16. Pascotto M, Caso P, Santoro G, Caso I, Cerrato F, Pisacane C, D’Andrea A, Severino S, Russo MG, Calabrò R. Analysis of right ventricular Doppler tissue imaging and load dependence in patients undergoing percutaneous closure of atrial septal defect. Am J Cardiol 2004;9:115–119.
Seventy consecutive patients who underwent the device closure of ASDs at Monaldi Hospital, Naples, Italy, were enrolled in the study. Demographic and hemodynamic data are listed in Table 1. In all patients, an Amplatzer septal occluder device (AGA Medical Corporation, Golden Valley, Minnesota) was implanted. Two days after ASD closure, patients were discharged and received aspirin 100 mg/day for 6 months. All echocardiographic studies were performed using an Acuson Sequoia C256 system (Siemens Medical Solutions USA, Inc., Mountain View, California). Monodimensional (M-mode) left-sided cardiac dimensions were recorded according to the criteria of the American Society of Echocardiography.7 LV volumes were analyzed according to the Teichholz formula.8 Pulse-wave Doppler flow analysis was
a
Pediatric Cardiology, Second University of Naples, and bDivision of Cardiology, Monaldi Hospital, Naples, Italy. Manuscript received December 30, 2004; revised manuscript received and accepted March 25, 2005. *Corresponding author. Tel.: 39-081-5754332; fax: 39-081-7062683. E-mail address: [email protected] (M. Pascotto). 0002-9149/05/$ – see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.amjcard.2005.03.096
performed at the levels of the mitral valve and of the LV outflow tract according to the criteria of the American Society of Echocardiography.9 Mitral Doppler was performed to analyze LV diastolic function. Early (E) and late (A) diastolic peak velocities, the E/A ratio, and mitral deceleration time and isovolumetric relaxation time were recorded. Again, pulse-wave Doppler of the LV outflow tract (5-chamber apical view) was performed to obtain the corresponding velocity–time integrals (VTIao). VTIao was used as surrogate of stroke volume, and VTIao ⫻ heart rate was used as surrogate of cardiac output. Pulsed Doppler tissue imaging (DTI) was performed by spectral pulsed Doppler signal filters from the apical view to minimize the incidence angle between the Doppler beam and longitudinal wall motion. The basal lateral and inferior LV borders were sampled. The Doppler spectrum was recorded at a velocity of 50 mm/s. The myocardial peak velocity of S= (centimeters per second), myocardial precontraction time (from the onset of the QRS complex to the beginning of S=), and time to peak systolic velocities (from the onset of the QRS complex to the S= peak) were calculated as systolic indexes. Myocardial E= and A= peak velocTable 1 Demographic and hemodynamic data Variable
Study Population (n ⫽ 70)
Age (yrs) Women/men Body mass index (kg/m2) ASD diameter (mm) Device diameter (mm) Systolic pulmonary pressure (mm Hg) Diastolic pulmonary pressure (mm Hg) Mean pulmonary pressure (mm Hg) Qp/Qs (pulmonary-to-systemic flow ratio)
18 ⫾ 16 (4–66) 1.8/1 20.0 ⫾ 4.8 (12.2–34.6) 13 ⫾ 7 (3–29) 18 ⫾ 8 (5–38) 30 ⫾ 9 (16–46) 15 ⫾ 5 (8–29) 22 ⫾ 6 1.9 ⫾ 0.8 (1–5) www.AJConline.org
440
The American Journal of Cardiology (www.AJConline.org)
Table 2 Clinical and echocardiographic data before and after ASD closure Variable
Before Closure
After 24 Hours
After 1 Month
Heart rate (beats/min) Systolic blood pressure (mm Hg) LV end-diastolic diameter (mm) LV end-systolic diameter (mm) Fractional shortening (%) LV end-diastolic volume (ml) LV end-systolic volume (ml) Ejection fraction (%) Mitral annular plane systolic excursion (mm) VTIao (m) VTIao ⫻ heart rate (m/min) E mitral (cm/s) A mitral (cm/s) E/A mitral Isovolumetric relaxation time (ms) Deceleration time (ms)
86 ⫾ 14 110 ⫾ 17 37 ⫾ 6 25 ⫾ 6 32 ⫾ 10 62 ⫾ 26 25 ⫾ 15 60 ⫾ 14 14 ⫾ 3 0.20 ⫾ 0.04 16.8 ⫾ 3.5 90 ⫾ 20 53 ⫾ 15 1.9 ⫾ 0.8 58 ⫾ 16 182 ⫾ 41
85 ⫾ 15 108 ⫾ 14 39 ⫾ 7† 24 ⫾ 6 38 ⫾ 11† 69 ⫾ 29† 25 ⫾ 14 64 ⫾ 11† 13 ⫾ 3 0.21 ⫾ 0.04 17.7 ⫾ 3.5 94 ⫾ 21 53 ⫾ 13 1.9 ⫾ 0.7 54 ⫾ 16 188 ⫾ 44
79 ⫾ 16* 111 ⫾ 15 42 ⫾ 7† 26 ⫾ 6 38 ⫾ 6† 79 ⫾ 30† 26 ⫾ 13 68 ⫾ 8† 13 ⫾ 3 0.23 ⫾ 0.05† 17.6 ⫾ 3.8 97 ⫾ 20 53 ⫾ 13 1.9 ⫾ 0.7 49 ⫾ 15* 184 ⫾ 37
* p ⬍0.03;
†
p ⬍0.001.
ities, the E=/A= ratio, and regional relaxation time (the time interval between the end of S= and the onset of E=) were determined as diastolic measurements. Mitral flow and myocardial Doppler measurements were digitally stored and analyzed offline as the average of 3 consecutive beats. The study protocol consisted of clinical, electrocardiographic, and echocardiographic evaluation before as well as 24 hours and 1 month after device implantation. Statistical analysis was performed using SPSS for Windows version 11.0 (SPSS, Inc., Chicago, Illinois). Variables
are presented as mean ⫾ SD. Comparisons between stages were made by repeated-measures analysis of variance. When differences were found between stages, Student’s paired t test was performed to determine interstage differences. Linear regression analyses and partial correlation test by Pearson’s method were done to assess univariate relations. ASD closure was successfully performed in all patients. Clinical, M-mode and Doppler flow data are listed in Table 2. Heart rate significantly reduced after device im-
Figure 1. In the presence of normal pulmonary pressures, ASD size is the major contributor to right ventricular volume overload. The greater the right ventricular volume overload, the greater the impact on LV end-diastolic (LVED) volume. These 2 graphs show how the increase in LVED volume (A) and stroke volume (B) correlate with ASD maximal diameter. LVED volume change after 1 month ⫽ (LVED volume1 month ⫺ LVED volumepreclosure)/LVED volumepreclosure. VTIao change after 1 month ⫽ (VTIao 1 month ⫺ VTIao preclosure) / VTIao preclosure.
Congenital Heart Disease/ASD Closure and LV Function
441
Figure 2. DTI velocities. Regional velocities were recorded at lateral (lat) and inferior (inf) mitral annulus. No differences were found between preclosure and postclosure velocities. (A) Systolic velocities (S=). (B) Early diastolic velocities (E=). (C) End-diastolic velocities (A=).
plantation. Unlike heart rate, systolic blood pressure did not change over time. An increase in LV end-diastolic volume was recorded, whereas end-systolic volume was unchanged. Overall, the ejection fraction significantly increased over time. At follow-up, no significant differences in either E, A, the E/A ratio, or deceleration time were found compared with baseline. A mild reduction in isovolumetric relaxation time was recorded 1 month after the intervention. Overall, diastolic function parameters were in the normal range before and did not change in the first month after ASD closure. A progressive increase in VTIao was found at follow-up. Thus, in agreement with ejection fraction data, LV stroke volume tended to increase after closure. This increase was counterbalanced by a decrease in heart rate. Overall, cardiac output did not change compared with preclosure values. Again, 1 month after the procedure, the percentage increase in LV end-diastolic volume and VTIao correlated positively with ASD maximal diameter (Figure 1), suggesting a direct effect of the overload relief on the stroke volume increase. DTI velocities are shown in Figure 2. No significant differences were highlighted in regional systolic and diastolic function over time. Again, the regional E=/A= ratio
Table 3 DTI velocity analysis Variable Lateral wall E=/A= ratio E/E= ratio Inferior wall E=/A= ratio E/E= ratio
Before Closure
After 24 Hours
After 1 Month
1.9 ⫾ 0.7 5⫾1
1.9 ⫾ 0.8 5⫾2
2.1 ⫾ 0.9 5⫾2
1.8 ⫾ 0.6 5⫾2
1.7 ⫾ 0.6 6⫾2
1.8 ⫾ 0.6 6⫾2
p ⫽ NS. No changes were recorded before and after ASD closure. E/E= ⬍8 is considered an expression of normal LV end-diastolic pressure A= ⫽ end-diastolic myocardial velocity; E ⫽ early diastolic mitral inflow peak velocity; E= ⫽ early diastolic myocardial velocity.
and the E/E= ratio were normal before and did not change after device implantation (Table 3), suggesting preserved LV diastolic function and end-diastolic pressure. Overall, myocardial velocities were in the normal range before and after the procedure.10 DTI time analysis is listed in Table 4. All time-analysis data were unaffected by the intervention. •••
This is the first study evaluating global and regional LV function in a large series of patients before and after the device closure of ASDs. It is well established that chronic right ventricular overload is associated with an impairment of LV performance over time.11,12 This is mainly due to the mechanical disadvantage of a noncircular short-axis configuration over radial function.4 In our study, DTI analysis of the lateral and inferior LV wall showed normal diastolic and systolic regional velocities. These findings highlight that, unlike radial function, LV longitudinal function does not seem to be affected by right ventricular overload in children and young adults with ASDs. A potential impairment of regional function is more likely to ensue in older patients with long-lasting cardiac remodeling due to volume overload. Overload relief determines striking geometric changes of the cardiac chambers early after transcatheter ASD closure.13–16 Although remodeling of the cardiac chambers has been evaluated, few data are available concerning global and regional LV function before and after device implantation. Although cardiac overload relief may positively affect LV function,4 the implantation of a relatively rigid device in a remodeling heart may potentially have a negative impact on cardiac performance, at least in the first month, when most of the geometric changes ensue.3 Recently, global LV function has been shown to improve after percutaneous ASD closure.4 – 6,13 Our data confirm that global systolic function at rest improves after the procedure, even in young patients with normal pulmonary pressures. In accordance with previous studies,4,6 the increase in the LV
442
The American Journal of Cardiology (www.AJConline.org)
Table 4 DTI time analysis before and after ASD closure Variable Lateral wall Precontraction time (ms) Time to peak S= (ms) Isometric relaxation time (ms) Inferior wall Precontraction time (ms) Time to peak S= (ms) Isometric relaxation time (ms)
Before Closure
After 24 Hours
After 1 Month
64 ⫾ 25 118 ⫾ 30 63 ⫾ 23
65 ⫾ 25 126 ⫾ 45 57 ⫾ 20
60 ⫾ 25 127 ⫾ 45 56 ⫾ 21
70 ⫾ 25 139 ⫾ 49 63 ⫾ 27
70 ⫾ 26 141 ⫾ 38 62 ⫾ 28
63 ⫾ 23 150 ⫾ 48 60 ⫾ 18
p ⫽ NS. S= ⫽ systolic myocardial peak velocity.
ejection fraction was mostly due to an increase in LV end-diastolic volume. This was further validated by Doppler flussimetry of the LV outflow tract, suggesting an increase in cardiac stroke volume. Total cardiac output at rest did not seem to change, because of a mild but significant decrease in heart rate counterbalancing the increase in stroke volume. A lower heart rate at rest may favor a better chronotropic reserve with exercise, which is in accordance with the improvement in the cardiopulmonary exercise tolerance after ASD closure.5,6 Pathophysiologically, regional dysfunction may ensue even in the presence of preserved global function. Thus, the absence of significant changes in DTI velocities and time-analysis data underscores how regional myocardial systolic function is unaffected by device implantation. Moreover, we did not find a significant difference in either geometric remodeling or in regional and global function even after dividing patients into 2 age groups (data not shown). However, most of the patients in our study population were ⬍45 years of age (90%), so we did not have enough statistical power to address age dependence in older patients. Further studies are needed to address this issue.16 1. Chessa M, Carminati M, Butera G, Bini MR, Drago M, Rosti L, Giamberti A, Pomè G, Bossone E, Frigiola A. Early and late complications associated with transcatheter occlusion of secundum atrial septal defect. J Am Coll Cardiol 2002;39:1061–1065. 2. Du ZD, Hijazi ZM, Kleinman CS, Silverman NH, Larntz K, Amplatzer Investigators. Comparison between transcatheter and surgical closure of secundum atrial septal defect in children and adults: results of a multicenter non randomized trial. J Am Coll Cardiol 2002;39:1836 –1844. 3. Lange A, Coleman DM, Palka P, Burstow DJ, Wilkinson JL, Godman MJ. Effect of catheter device closure of atrial septal defect on diastolic mitral annular closure. Am J Cardiol 2003;91:104 –108. 4. Walker RE, Moran AM, Gauvreau K, Colan SD. Evidence of adverse ventricular interdependence in patients with atrial septal defect. Am J Cardiol 2004;93:1374 –1377. 5. Brochu MC, Baril JF, Dore A, Juneau M, De Guise P, Mercier LA. Improvement in exercise capacity in asymptomatic and mildly symptomatic adults after atrial septal defect percutaneous closure. Circulation 2002;106:1821–1826.
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