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Rapid Ventricular Remodeling with Left Ventricular Unloading Postventricular Assist Device Placement: New Insights with Strain Imaging
Rapid Ventricular Remodeling with Left Ventricular Unloading Postventricular Assist Device Placement: New Insights with Strain Imaging Luke Havemann, RDCS, Colin J. McMahon, MB, Javier Ganame, MD, Jack Price, MD, Charles D. Fraser, MD, Benjamin W. Eidem, MD, and Ricardo H. Pignatelli, MD, Houston, Texas; Dublin, Ireland; and Leuven, Belgium
We report the case of a 6-year old girl who presented with severe dilated cardiomyopathy. Cross-sectional echocardiography demonstrated a severely dilated hypokinetic left ventricle with an ejection fraction less than 10%. She developed intractable ventricular tachyarrhythmias and subsequently had a left ventricular assist device implanted. Within 1 week of
CASE REPORT
A 6-year-old girl presented to a local hospital with lethargy and tachypnea after a viral gastrointestinal illness. She was resuscitated with intravenous volume and was subsequently noted to have a gallop rhythm and prominent cardiomegaly on chest radiograph. She was referred to our institution where echocardiography demonstrated dilated cardiomyopathy with a markedly dilated and hypokinetic left ventricle (LV) with a LV ejection fraction less than 10% and extremely thin myocardial walls (Figure 1). After admission to the cardiac intensive care department, she received intravenous immunoglobulin and low-dose intravenous dopamine (5 g/kg/min) and milrinone (0.25 g/kg/min) infusions were started. Over the subsequent week of hospitalization, she demonstrated improvement in her cardiac output; however, she later developed intractable ventricular tachyarrhythmias with persistently depressed LV contractility. Cardiac hemodynamics necessitated placement on mechanical support to rest her myocardium and a Biomedicus LV assist device (LVAD; Medtronics BioMed, Inc., Eden Prairie, MN) was placed 12 From the Lillie Frank Abercrombie Section of Pediatric Cardiology, Texas Children’s Hospital and Baylor College of Medicine; Our Lady’s Hospital for Sick Children, Dublin, Ireland (C.J.M.); and Pediatric Cardiology, University Hospital Leuven, Belgium (J.G.). Reprint requests: Ricardo H. Pignatelli, MD, Lillie Frank Abercrombie Section of Pediatric Cardiology, Texas Children’s Hospital and Baylor College of Medicine, 6621 Fannin, Houston, TX 77030 (E-mail: [email protected]). 0894-7317/$32.00 Copyright 2006 by the American Society of Echocardiography. doi:10.1016/j.echo.2005.11.010
mechanical support, echocardiography demonstrated dramatic reverse remodeling of the left ventricle with marked improvement in myocardial deformation using strain rate imaging. This report further highlights the potential for rapid remodeling after mechanical support of the failing myocardium. (J Am Soc Echocardiogr 2006;19:355.e9-355.e11.)
days after hospital admission. She tolerated the initial procedure well but developed significant mediastinal bleeding and thereafter underwent replacement of the Biomedicus LVAD with an implantable DeBakey VAD (Micro Med Technology, Houston, TX). After institution of LVAD support her LV ejection fraction demonstrated steady improvement with clear evidence of ejection through the aortic valve. Within 1 week of instituting mechanical support her LV myocardium demonstrated significant reverse remodeling (Figure 2), which was accompanied by prominent improvement in myocardial deformation as assessed by strain and strain rate imaging (Speqle, Leuven, Belgium) (Figure 3). The child developed persistent bleeding complications in the postoperative period and subsequently developed further intractable arrhythmias, which degenerated to asystole despite aggressive resuscitative measures. Our patient’s ventricular function improved slightly after initiation of inotropic agents and intravenous immunoglobulin. However, the greatest improvement in contractility was observed 2 weeks after admission when she was placed on mechanical support. We speculate that the resultant cardiac reverse remodeling was caused, in part, by unloading of the ventricular myocardium. Structural and functional remodeling has been demonstrated to occur in the failing myocardium during LVAD support, including favorable changes in myocyte size, collagen content, and proinflammatory cytokine levels.1-5 Recently it has been demonstrated that resting the myocardium reverses disruption of the dystrophinsarcoglycan complex, which results from end-stage congestive heart failure.6 It has also been shown that the beneficial effects of ventricular unloading may be mediated by increased endothelial nitric oxide synthase (eNOS)
355.e9
Journal of the American Society of Echocardiography March 2006
355.e10 Havemann et al
A
B
Strain Pre Device
C 30
Strain (%)
25 20 15 10 5 0 0
200
400
600 800 1000 Time (ms)
A
1200
1400
Figure 1 Patient with echocardiographic evidence of severe cardiac heart failure. A, Color M-mode with evidence of left ventricular dilation and poor ventricular function. B, Strain rate acquisition with abnormal deformation pattern. C, Circumferential strain before initiation of mechanical support.
B
Strain Post Device
40
C
35
Strain (%)
30 25 20 15 10 5 0 -5
0
0.2
0.4
0.6
0.8
1
Figure 2 Same patient during unloading. A, Concentric hypertrophy by color M-mode. B, Improved strain rate post-left ventricular assist device support. C, Improved deformation by strain imaging.
Journal of the American Society of Echocardiography Volume 19 Number 3
Post Wall Short Axis -1
12-Mar 26-Mar 27-Mar 31-Mar 2-Apr
Septum A4C
Strain (%)/10 1.057 1.144 1.832 3.455 5.25
Strain Rate (s ) 1.05 1.72 1.99 2.21 4.17
-1
Strain Rate (s ) 1 1 2 2.1 2.91
Strain (%)/10 0 1.22 1.427 2.215 2.967
Strain/Strain Rate
Havemann et al 355.e11
Strain and strain rate imaging could potentially help by providing novel information regarding the condition of the resting myocardium and its changes during ventricular volume manipulations. Mechanical support, particularly in children with reversible causes of failing myocardium, may allow significant improvement in systolic performance. These devices should be considered in most children with acute decompensated heart failure.
6 5
REFERENCES
4
Strain Rate Post wall Strain Post Wall Strain Rate Septum Strain Septum
3 2 1 0
Strain Rate Post wall
1
2
3
4
5
1.05
1.72
1.99
2.21
4.17
Strain Post 1.057 1.144 1.832 3.455 5.25 Wall 1 1 2 2.1 2.91 Strain Rate Septum 0 1.22 1.427 2.215 2.967 Strain Septum
Figure 3 Change in strain and strain rate imaging values over period of time of mechanical support demonstrating continuous improvement of deformation values for both circumferential (posterior wall short axis) and longitudinal fibers (septum apical 4-chamber [A4C]). and dimethylarginine dimethylaminohydrolase 1 (DDAH1) expression resulting in improvements in endothelial function.7 Although there are limited data regarding the time course of these events, this report serves to highlight the rapidity of some of these changes often occurring within days to weeks as was the case in this patient.
1. Barbone A, Holmes JW, Heerdt PM, et al. Comparison of right and left ventricular responses to left ventricular assist device support in patients with severe heart failure: a primary role of mechanical unloading underlying reverse remodeling. Circulation 2001;104:670-5. 2. Bruckner BA, Stetson SJ, Perez-Verdia A, et al. Regression of fibrosis and hypertrophy in failing myocardium following mechanical circulatory support. J Heart Lung Transplant 2001;20: 457-64. 3. Khan T, Delgado RM, Radovancevic B, et al. Dobutamine stress echocardiography predicts myocardial improvement in patients supported by left ventricular assist devices (LVADs): hemodynamic and histologic evidence of improvement before LVAD explanation. J Heart Lung Transplant 2003;22:137-46. 4. Torre-Amione G, Stetson SJ, Youker KA, et al. Decreased expression of tumor necrosis factor-alpha in failing human myocardium after mechanical circulatory support: a potential mechanism for cardiac recovery. Circulation 1999;100:1189-93. 5. Goldstein DJ, Moazami N. Seldomridge JA, et al. Circulatory resuscitation with left ventricular assist device support reduces interleukins 6 and 8 levels. Ann Thorac Surg 1997;63:971-4. 6. Vatta M, Stetson SJ, Entman ML, et al. Molecular normalization of dystrophin in the failing left and right ventricle of patients treated with either pulsatile or continuous flow-type ventricular assist devices. J Am Coll Cardiol 2004;43:811-7. 7. Chen Y, Park S, Li Y, et al. Alterations of gene expression in failing myocardium following left ventricular assist device support. Physiol Genomics 2003;14:251-60.
We report the case of a 6-year old girl who presented with severe dilated cardiomyopathy. Cross-sectional echocardiography demonstrated a severely dilated hypokinetic left ventricle with an ejection fraction less than 10%. She developed intractable ventricular tachyarrhythmias and subsequently had a left ventricular assist device implanted. Within 1 week of
CASE REPORT
A 6-year-old girl presented to a local hospital with lethargy and tachypnea after a viral gastrointestinal illness. She was resuscitated with intravenous volume and was subsequently noted to have a gallop rhythm and prominent cardiomegaly on chest radiograph. She was referred to our institution where echocardiography demonstrated dilated cardiomyopathy with a markedly dilated and hypokinetic left ventricle (LV) with a LV ejection fraction less than 10% and extremely thin myocardial walls (Figure 1). After admission to the cardiac intensive care department, she received intravenous immunoglobulin and low-dose intravenous dopamine (5 g/kg/min) and milrinone (0.25 g/kg/min) infusions were started. Over the subsequent week of hospitalization, she demonstrated improvement in her cardiac output; however, she later developed intractable ventricular tachyarrhythmias with persistently depressed LV contractility. Cardiac hemodynamics necessitated placement on mechanical support to rest her myocardium and a Biomedicus LV assist device (LVAD; Medtronics BioMed, Inc., Eden Prairie, MN) was placed 12 From the Lillie Frank Abercrombie Section of Pediatric Cardiology, Texas Children’s Hospital and Baylor College of Medicine; Our Lady’s Hospital for Sick Children, Dublin, Ireland (C.J.M.); and Pediatric Cardiology, University Hospital Leuven, Belgium (J.G.). Reprint requests: Ricardo H. Pignatelli, MD, Lillie Frank Abercrombie Section of Pediatric Cardiology, Texas Children’s Hospital and Baylor College of Medicine, 6621 Fannin, Houston, TX 77030 (E-mail: [email protected]). 0894-7317/$32.00 Copyright 2006 by the American Society of Echocardiography. doi:10.1016/j.echo.2005.11.010
mechanical support, echocardiography demonstrated dramatic reverse remodeling of the left ventricle with marked improvement in myocardial deformation using strain rate imaging. This report further highlights the potential for rapid remodeling after mechanical support of the failing myocardium. (J Am Soc Echocardiogr 2006;19:355.e9-355.e11.)
days after hospital admission. She tolerated the initial procedure well but developed significant mediastinal bleeding and thereafter underwent replacement of the Biomedicus LVAD with an implantable DeBakey VAD (Micro Med Technology, Houston, TX). After institution of LVAD support her LV ejection fraction demonstrated steady improvement with clear evidence of ejection through the aortic valve. Within 1 week of instituting mechanical support her LV myocardium demonstrated significant reverse remodeling (Figure 2), which was accompanied by prominent improvement in myocardial deformation as assessed by strain and strain rate imaging (Speqle, Leuven, Belgium) (Figure 3). The child developed persistent bleeding complications in the postoperative period and subsequently developed further intractable arrhythmias, which degenerated to asystole despite aggressive resuscitative measures. Our patient’s ventricular function improved slightly after initiation of inotropic agents and intravenous immunoglobulin. However, the greatest improvement in contractility was observed 2 weeks after admission when she was placed on mechanical support. We speculate that the resultant cardiac reverse remodeling was caused, in part, by unloading of the ventricular myocardium. Structural and functional remodeling has been demonstrated to occur in the failing myocardium during LVAD support, including favorable changes in myocyte size, collagen content, and proinflammatory cytokine levels.1-5 Recently it has been demonstrated that resting the myocardium reverses disruption of the dystrophinsarcoglycan complex, which results from end-stage congestive heart failure.6 It has also been shown that the beneficial effects of ventricular unloading may be mediated by increased endothelial nitric oxide synthase (eNOS)
355.e9
Journal of the American Society of Echocardiography March 2006
355.e10 Havemann et al
A
B
Strain Pre Device
C 30
Strain (%)
25 20 15 10 5 0 0
200
400
600 800 1000 Time (ms)
A
1200
1400
Figure 1 Patient with echocardiographic evidence of severe cardiac heart failure. A, Color M-mode with evidence of left ventricular dilation and poor ventricular function. B, Strain rate acquisition with abnormal deformation pattern. C, Circumferential strain before initiation of mechanical support.
B
Strain Post Device
40
C
35
Strain (%)
30 25 20 15 10 5 0 -5
0
0.2
0.4
0.6
0.8
1
Figure 2 Same patient during unloading. A, Concentric hypertrophy by color M-mode. B, Improved strain rate post-left ventricular assist device support. C, Improved deformation by strain imaging.
Journal of the American Society of Echocardiography Volume 19 Number 3
Post Wall Short Axis -1
12-Mar 26-Mar 27-Mar 31-Mar 2-Apr
Septum A4C
Strain (%)/10 1.057 1.144 1.832 3.455 5.25
Strain Rate (s ) 1.05 1.72 1.99 2.21 4.17
-1
Strain Rate (s ) 1 1 2 2.1 2.91
Strain (%)/10 0 1.22 1.427 2.215 2.967
Strain/Strain Rate
Havemann et al 355.e11
Strain and strain rate imaging could potentially help by providing novel information regarding the condition of the resting myocardium and its changes during ventricular volume manipulations. Mechanical support, particularly in children with reversible causes of failing myocardium, may allow significant improvement in systolic performance. These devices should be considered in most children with acute decompensated heart failure.
6 5
REFERENCES
4
Strain Rate Post wall Strain Post Wall Strain Rate Septum Strain Septum
3 2 1 0
Strain Rate Post wall
1
2
3
4
5
1.05
1.72
1.99
2.21
4.17
Strain Post 1.057 1.144 1.832 3.455 5.25 Wall 1 1 2 2.1 2.91 Strain Rate Septum 0 1.22 1.427 2.215 2.967 Strain Septum
Figure 3 Change in strain and strain rate imaging values over period of time of mechanical support demonstrating continuous improvement of deformation values for both circumferential (posterior wall short axis) and longitudinal fibers (septum apical 4-chamber [A4C]). and dimethylarginine dimethylaminohydrolase 1 (DDAH1) expression resulting in improvements in endothelial function.7 Although there are limited data regarding the time course of these events, this report serves to highlight the rapidity of some of these changes often occurring within days to weeks as was the case in this patient.
1. Barbone A, Holmes JW, Heerdt PM, et al. Comparison of right and left ventricular responses to left ventricular assist device support in patients with severe heart failure: a primary role of mechanical unloading underlying reverse remodeling. Circulation 2001;104:670-5. 2. Bruckner BA, Stetson SJ, Perez-Verdia A, et al. Regression of fibrosis and hypertrophy in failing myocardium following mechanical circulatory support. J Heart Lung Transplant 2001;20: 457-64. 3. Khan T, Delgado RM, Radovancevic B, et al. Dobutamine stress echocardiography predicts myocardial improvement in patients supported by left ventricular assist devices (LVADs): hemodynamic and histologic evidence of improvement before LVAD explanation. J Heart Lung Transplant 2003;22:137-46. 4. Torre-Amione G, Stetson SJ, Youker KA, et al. Decreased expression of tumor necrosis factor-alpha in failing human myocardium after mechanical circulatory support: a potential mechanism for cardiac recovery. Circulation 1999;100:1189-93. 5. Goldstein DJ, Moazami N. Seldomridge JA, et al. Circulatory resuscitation with left ventricular assist device support reduces interleukins 6 and 8 levels. Ann Thorac Surg 1997;63:971-4. 6. Vatta M, Stetson SJ, Entman ML, et al. Molecular normalization of dystrophin in the failing left and right ventricle of patients treated with either pulsatile or continuous flow-type ventricular assist devices. J Am Coll Cardiol 2004;43:811-7. 7. Chen Y, Park S, Li Y, et al. Alterations of gene expression in failing myocardium following left ventricular assist device support. Physiol Genomics 2003;14:251-60.