Regional systolic and remodeling strain differences during cardiac remodeling
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CONCLUSIONS: Patients undergoing VATS lobectomy for clinical stage I NSCLC, despite more comorbidities, had fewer postoperative complications. The approaches have equivalent operative time, blood loss, length of stay, and survival. Compared to OT, VATS lobectomy for clinical stage I NSCLC appears to be a less morbid operation. Deficiency of TNFR1 protects myocardium through STAT3, SOCS3, and IL-6, but not p38 MAPK or IL-1 beta MeijingWang MD, MS, Paul Crisostomo MD, Keith Lillemoe MD, Daniel Meldrum MD Indiana University Medical Center, Indianapolis, IN INTRODUCTION: Suppressor of cytokine signaling (SOCS) pro- teins are major inhibitors of cytokine signaling via the JAK/STAT pathway. TNF plays an important role in the development of heart failure. There is a direct correlation between myocardial function and myocardial TNF levels in humans. However, it is unknown whether TNF mediates myocardial inflammation via STAT3/SOCS3 signal- ing in the heart, and if so, whether this effect is through the type 1 55-kDa TNF receptor (TNFR1). We hypothesized that TNFR1 de- ficiency protects myocardial function and decreases myocardial IL-6 production via the STAT3/SOCS3 pathway in response toTNF. METHODS: Isolated male mouse hearts (n4/group) from wild type (WT), TNFR1 knockout (TNFR1KO) were subjected to direct TNF infusion (500 pg/ml/min x 30 min) and LVDP, dP/dT, dP/dT were continuously recorded. Heart tissue was performed for active forms of STAT3, p38, SOCS3 (Western blot) and IL-6, IL- 1beta (ELISA). p0.05statistically significant. RESULTS: TNFR1KO had significantly better myocardial func- tion (LVDP: 37.9/4.4 vs. WT 20.6/3.2mmHg; dP/dt: 1176.4/159.1 vs. WT 589.1/85.6 mmHg/s; dP/dt: 877.2/115.4 vs. WT 448.6/61.8mmHg/s) and greater expression of SOCS3 after TNF(% of SOCS3/GAPDH: 45/ 4.5% vs. WT 22/6.5%).TNFR1 deficiency decreased STAT3 activation (% p-STAT3/STAT3: 29/6.4% vs. WT 45/ 8.8%). IL-6 decreased in TNFR1KO (150.2/3.65 pg/mg pro- tein) vs. WT (211.4/26.08). TNFR1 deficiency did not change expression of p38 and IL-1 beta following TNF infusion. CONCLUSIONS: Deficiency of TNFR1 protects myocardium through STAT3, SOCS3, and IL-6, but not p38 MAPK or IL-1 beta. Regional systolic and remodeling strain differences during cardiac remodeling Ahmet Kilic MD, G KwameYankey MD, Tim Nolan MS, Tieluo Li MD, Jennifer Nash MS, Guangming Cheng MD, Zhongjun Wu PhD, Bartley Griffith MD University of Maryland, Baltimore, MD INTRODUCTION: The purpose of this study is to investigate differ- ences in systolic and remodeling strains in the infarct, adjacent and remote regions of the left ventricular (LV) myocardium in an ovine postinfarction model. METHODS: Sixteen sonomicrometry transducers were placed into the LV free wall to assess regional contractile function by systolic strain and structural alteration by remodeling strain. All animals underwent daily hemodynamic and strain measurements. RESULTS: Systolic function of the remote zone was preserved with strain of 21.2 3.8, 22.2 1.6, 26.0 0.2, 28.6 3.2 and 27.6 1.2 (%) at pre-, post-, 2 weeks, 6 weeks and 8 weeks postinfarction. The adjacent zone showed progressive dysfunction with strain of 18.6 6.9, 15.4 4.3, 10.3 9.6, 7.8 13.9, 7.7 10.2. The infarct zone became non-contractile imme- diately postinfarction with strain of 14.0 1.5, 6.6 11.8, 3.1 1.5, 2.1 1.2, 1.4 0.8. Using pre-infarction end diastolic geometry as reference, the remote zone had a progressive increase in remodeling areal strain of 7.2 2.3, 1.5 3.4, 7.5 3.5 and 16.0 6.9; the adjacent zone had values of 2.0 1.3, 12.3 3.9, 29.6 6.7 and 33.4 9.8; and the infarct zone with 6.0 4.5, 13.0 5.6, 21.5 6.7, 60.1 8.7. CONCLUSIONS: Regional function strain and geometrical struc- tural analysis can be used to illustrate the dynamics and progression of cardiac remodeling. Finite element analysis of transmural stress in left ventricular aneurysm Amod P Tendulkar MD, JosephWalker PhD, Julius Guccione PhD, Mark Ratcliffe MD University of California, San Francisco, Oakland, CA INTRODUCTION: Normally, there is a transmural variation in stress that is related to myofiber orientation. Finite element analysis (FEA) is a computational tool used to calculate stress. In REA, infinitesimal deformation method (IDM) uses stiff linear material properties and does not account for myofiber orientation whereas finite deforma- tion method (FDM) uses non-linear physiologic material properties based on myofiber orientation to compute stress. We hypothesized that FDM will demonstrate better transmural variation in stress than IDM. METHODS: A FE mesh was created from MRI of sheep hearts (n3) with left ventricular aneurysm (LVA). Aneurysm, border-zone and remote regions were identified. Validated material properties were used for FDM. Stiff,isotropic material properties were used for IDM. Endocardial surface was pressurized to 78.7mmHg. End sys- tolic stresses (circumferential(CS) and longitudinal(LS)) were calcu- lated for every element and then grouped by region and transmural location. ANOVA and post-hoc analysis with p0.05 was deter- mined significant. RESULTS: Transmural variation was observed in CS calculated by FDM in the endocardium versus midwall and epicardium (p0.0001) in aneurysm and remote regions. Only remote region had transmural variation in calculated CS for IDM (p0.01). LS was different in endocardium versus epicardium in aneurysm and remote regions and endocardium versus midwall in aneurysm region (p0.0001) for FDM. IDM demonstrated a difference between midwall and epicardium in remote only (p0.04). Finally, the two methods were also different (p0.03). S21 Vol. 203, No. 3S, September 2006 Cardiothoracic Surgery
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Transcript of Regional systolic and remodeling strain differences during cardiac remodeling
CONCLUSIONS: Patients undergoing VATS lobectomy for clinicalstage I NSCLC, despite more comorbidities, had fewer postoperativecomplications. The approaches have equivalent operative time,blood loss, length of stay, and survival. Compared to OT, VATSlobectomy for clinical stage I NSCLC appears to be a less morbidoperation.
Deficiency of TNFR1 protects myocardium throughSTAT3, SOCS3, and IL-6, but not p38 MAPK or IL-1betaMeijing Wang MD, MS, Paul Crisostomo MD, Keith Lillemoe MD,Daniel Meldrum MDIndiana University Medical Center, Indianapolis, IN
INTRODUCTION: Suppressor of cytokine signaling (SOCS) pro-teins are major inhibitors of cytokine signaling via the JAK/STATpathway. TNF plays an important role in the development of heartfailure. There is a direct correlation between myocardial function andmyocardial TNF levels in humans. However, it is unknown whetherTNF mediates myocardial inflammation via STAT3/SOCS3 signal-ing in the heart, and if so, whether this effect is through the type 155-kDa TNF receptor (TNFR1). We hypothesized that TNFR1 de-ficiency protects myocardial function and decreases myocardial IL-6production via the STAT3/SOCS3 pathway in response to TNF.
METHODS: Isolated male mouse hearts (n�4/group) from wildtype (WT), TNFR1 knockout (TNFR1KO) were subjected to directTNF infusion (500 pg/ml/min x 30 min) and LVDP, �dP/dT,�dP/dT were continuously recorded. Heart tissue was performed foractive forms of STAT3, p38, SOCS3 (Western blot) and IL-6, IL-1beta (ELISA). p�0.05�statistically significant.
RESULTS: TNFR1KO had significantly better myocardial func-tion (LVDP: 37.9�/�4.4 vs. WT 20.6�/�3.2mmHg; �dP/dt:1176.4�/�159.1 vs. WT 589.1�/�85.6 mmHg/s; �dP/dt:�877.2�/�115.4 vs. WT �448.6�/�61.8mmHg/s) and greaterexpression of SOCS3 after TNF(% of SOCS3/GAPDH: 45�/�4.5% vs. WT 22�/�6.5%). TNFR1 deficiency decreased STAT3activation (% p-STAT3/STAT3: 29�/�6.4% vs. WT 45�/�8.8%). IL-6 decreased in TNFR1KO (150.2�/�3.65 pg/mg pro-tein) vs. WT (211.4�/�26.08). TNFR1 deficiency did not changeexpression of p38 and IL-1 beta following TNF infusion.
CONCLUSIONS: Deficiency of TNFR1 protects myocardiumthrough STAT3, SOCS3, and IL-6, but not p38 MAPK or IL-1 beta.
Regional systolic and remodeling strain differencesduring cardiac remodelingAhmet Kilic MD, G Kwame Yankey MD, Tim Nolan MS,Tieluo Li MD, Jennifer Nash MS, Guangming Cheng MD,Zhongjun Wu PhD, Bartley Griffith MDUniversity of Maryland, Baltimore, MD
INTRODUCTION: The purpose of this study is to investigate differ-ences in systolic and remodeling strains in the infarct, adjacent andremote regions of the left ventricular (LV) myocardium in an ovinepostinfarction model.
METHODS: Sixteen sonomicrometry transducers were placed intothe LV free wall to assess regional contractile function by systolicstrain and structural alteration by remodeling strain. All animalsunderwent daily hemodynamic and strain measurements.
RESULTS: Systolic function of the remote zone was preserved withstrain of �21.2 �3.8, �22.2 � 1.6, �26.0 � 0.2, �28.6 � 3.2 and�27.6 � 1.2 (%) at pre-, post-, 2 weeks, 6 weeks and 8 weekspostinfarction. The adjacent zone showed progressive dysfunctionwith strain of �18.6 � 6.9, �15.4 � 4.3, �10.3 � 9.6, �7.8 �13.9, �7.7 � 10.2. The infarct zone became non-contractile imme-diately postinfarction with strain of �14.0 � 1.5, �6.6 � 11.8,3.1 � 1.5, 2.1 �1.2, 1.4 � 0.8. Using pre-infarction end diastolicgeometry as reference, the remote zone had a progressive increase inremodeling areal strain of 7.2 � 2.3, 1.5 � 3.4, 7.5 � 3.5 and16.0 � 6.9; the adjacent zone had values of 2.0 � 1.3, 12.3 � 3.9,29.6 � 6.7 and 33.4 � 9.8; and the infarct zone with 6.0 � 4.5,13.0 � 5.6, 21.5 � 6.7, 60.1 � 8.7.
CONCLUSIONS: Regional function strain and geometrical struc-tural analysis can be used to illustrate the dynamics and progressionof cardiac remodeling.
Finite element analysis of transmural stress in leftventricular aneurysmAmod P Tendulkar MD, Joseph Walker PhD, Julius Guccione PhD,Mark Ratcliffe MDUniversity of California, San Francisco, Oakland, CA
INTRODUCTION: Normally, there is a transmural variation in stressthat is related to myofiber orientation. Finite element analysis (FEA)is a computational tool used to calculate stress. In REA, infinitesimaldeformation method (IDM) uses stiff linear material properties anddoes not account for myofiber orientation whereas finite deforma-tion method (FDM) uses non-linear physiologic material propertiesbased on myofiber orientation to compute stress. We hypothesizedthat FDM will demonstrate better transmural variation in stress thanIDM.
METHODS: A FE mesh was created from MRI of sheep hearts(n�3) with left ventricular aneurysm (LVA). Aneurysm, border-zoneand remote regions were identified. Validated material propertieswere used for FDM. Stiff,isotropic material properties were used forIDM. Endocardial surface was pressurized to 78.7mmHg. End sys-tolic stresses (circumferential(CS) and longitudinal(LS)) were calcu-lated for every element and then grouped by region and transmurallocation. ANOVA and post-hoc analysis with p�0.05 was deter-mined significant.
RESULTS: Transmural variation was observed in CS calculated byFDM in the endocardium versus midwall and epicardium(p�0.0001) in aneurysm and remote regions. Only remote regionhad transmural variation in calculated CS for IDM (p�0.01). LS wasdifferent in endocardium versus epicardium in aneurysm and remoteregions and endocardium versus midwall in aneurysm region(p�0.0001) for FDM. IDM demonstrated a difference betweenmidwall and epicardium in remote only (p�0.04). Finally, the twomethods were also different (p�0.03).
S21Vol. 203, No. 3S, September 2006 Cardiothoracic Surgery
