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Integrated wall stress: a new methodological approach to assess ventricular workload and myocardial contractile reserve.

Dong H, Mosca H, Gao E, Akins RE, Gidding SS, Tsuda T - J Transl Med (2013)

Bottom Line: IWS was calculated over one minute through simultaneous measurement of LV internal diameter and wall thickness by echocardiography and LV pressure by LV catheterization.At rest, the MI group showed concentric LV hypertrophy pattern with preserved LV cavity size, LV systolic function, and IWS comparable with the sham group.IWS showed good correlation with a product of peak-systolic wall stress and heart rate.

View Article: PubMed Central - HTML - PubMed

Affiliation: Nemours Cardiac Center and Nemours Biomedical Research, Alfred I, duPont Hospital for Children, 1600 Rockland Rd, Wilmington, DE 19103, USA.

ABSTRACT

Background: Wall stress is a useful concept to understand the progression of ventricular remodeling. We measured cumulative LV wall stress throughout the cardiac cycle over unit time and tested whether this "integrated wall stress (IWS)" would provide a reliable marker of total ventricular workload.

Methods and results: We applied IWS to mice after experimental myocardial infarction (MI) and sham-operated mice, both at rest and under dobutamine stimulation. Small infarcts were created so as not to cause subsequent overt hemodynamic decompensation. IWS was calculated over one minute through simultaneous measurement of LV internal diameter and wall thickness by echocardiography and LV pressure by LV catheterization. At rest, the MI group showed concentric LV hypertrophy pattern with preserved LV cavity size, LV systolic function, and IWS comparable with the sham group. Dobutamine stimulation induced a dose-dependent increase in IWS in MI mice, but not in sham mice; MI mice mainly increased heart rate, whereas sham mice increased LV systolic and diastolic function. IWS showed good correlation with a product of peak-systolic wall stress and heart rate. We postulate that this increase in IWS in post-MI mice represents limited myocardial contractile reserve.

Conclusion: We hereby propose that IWS provides a useful estimate of total ventricular workload in the mouse model and that increased IWS indicates limited LV myocardial contractile reserve.

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Molecular expression and histological changes in non-ischemic myocardium in sham and MI mice. Upper: The mRNA levels of ANP, BNP, and collagens type I and III in the non-ischemic myocardium of MI (n = 5) and sham (n = 5) groups by real-time RT-PCR to assess the molecular aspects of myocardial hypertrophy and fibrosis. ANP, BNP, and collagens type I and III were all significantly up-regulated in MI myocardium compared with sham myocardium. * p < 0.05 vs. sham. Lower: Myocardial fibrosis in the remote non-ischemic myocardium after MI. Histological assessment of remote non-ischemic myocardium with H&E (left column; A and C) and Masson’s Trichrome staining (right column; B and D. Collagen stains as blue color) in sham (A, B) and MI (C, D) hearts. In MI hearts, there is an increase deposition of collagen in the interstitial space (arrows) in the remote non-ischemic myocardium suggesting the development of myocardial fibrosis. Magnification bar = 100 μm.
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Figure 3: Molecular expression and histological changes in non-ischemic myocardium in sham and MI mice. Upper: The mRNA levels of ANP, BNP, and collagens type I and III in the non-ischemic myocardium of MI (n = 5) and sham (n = 5) groups by real-time RT-PCR to assess the molecular aspects of myocardial hypertrophy and fibrosis. ANP, BNP, and collagens type I and III were all significantly up-regulated in MI myocardium compared with sham myocardium. * p < 0.05 vs. sham. Lower: Myocardial fibrosis in the remote non-ischemic myocardium after MI. Histological assessment of remote non-ischemic myocardium with H&E (left column; A and C) and Masson’s Trichrome staining (right column; B and D. Collagen stains as blue color) in sham (A, B) and MI (C, D) hearts. In MI hearts, there is an increase deposition of collagen in the interstitial space (arrows) in the remote non-ischemic myocardium suggesting the development of myocardial fibrosis. Magnification bar = 100 μm.

Mentions: This small MI model was previously reported by us as an experimental model to induce ventricular remodeling without initial hemodynamic deterioration [5]. After 7 weeks, a significant increase in the mRNA of hypertrophic markers, including ANP and BNP, was seen in the non-ischemic hypertrophied myocardium of the MI group, when compared with that of sham animals (Figure 3). In addition, mRNA levels of collagens type I and type III were also significantly elevated compared with that of the sham group, consistent with histological findings of increased interstitial fibrosis in the remote non-ischemic myocardium in the MI group (Figure 3). Molecular and histological findings of ventricular remodeling were seen in non-ischemic myocardium after small MI but without ventricular dilatation (Figure 2A).


Integrated wall stress: a new methodological approach to assess ventricular workload and myocardial contractile reserve.

Dong H, Mosca H, Gao E, Akins RE, Gidding SS, Tsuda T - J Transl Med (2013)

Molecular expression and histological changes in non-ischemic myocardium in sham and MI mice. Upper: The mRNA levels of ANP, BNP, and collagens type I and III in the non-ischemic myocardium of MI (n = 5) and sham (n = 5) groups by real-time RT-PCR to assess the molecular aspects of myocardial hypertrophy and fibrosis. ANP, BNP, and collagens type I and III were all significantly up-regulated in MI myocardium compared with sham myocardium. * p < 0.05 vs. sham. Lower: Myocardial fibrosis in the remote non-ischemic myocardium after MI. Histological assessment of remote non-ischemic myocardium with H&E (left column; A and C) and Masson’s Trichrome staining (right column; B and D. Collagen stains as blue color) in sham (A, B) and MI (C, D) hearts. In MI hearts, there is an increase deposition of collagen in the interstitial space (arrows) in the remote non-ischemic myocardium suggesting the development of myocardial fibrosis. Magnification bar = 100 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750700&req=5

Figure 3: Molecular expression and histological changes in non-ischemic myocardium in sham and MI mice. Upper: The mRNA levels of ANP, BNP, and collagens type I and III in the non-ischemic myocardium of MI (n = 5) and sham (n = 5) groups by real-time RT-PCR to assess the molecular aspects of myocardial hypertrophy and fibrosis. ANP, BNP, and collagens type I and III were all significantly up-regulated in MI myocardium compared with sham myocardium. * p < 0.05 vs. sham. Lower: Myocardial fibrosis in the remote non-ischemic myocardium after MI. Histological assessment of remote non-ischemic myocardium with H&E (left column; A and C) and Masson’s Trichrome staining (right column; B and D. Collagen stains as blue color) in sham (A, B) and MI (C, D) hearts. In MI hearts, there is an increase deposition of collagen in the interstitial space (arrows) in the remote non-ischemic myocardium suggesting the development of myocardial fibrosis. Magnification bar = 100 μm.
Mentions: This small MI model was previously reported by us as an experimental model to induce ventricular remodeling without initial hemodynamic deterioration [5]. After 7 weeks, a significant increase in the mRNA of hypertrophic markers, including ANP and BNP, was seen in the non-ischemic hypertrophied myocardium of the MI group, when compared with that of sham animals (Figure 3). In addition, mRNA levels of collagens type I and type III were also significantly elevated compared with that of the sham group, consistent with histological findings of increased interstitial fibrosis in the remote non-ischemic myocardium in the MI group (Figure 3). Molecular and histological findings of ventricular remodeling were seen in non-ischemic myocardium after small MI but without ventricular dilatation (Figure 2A).

Bottom Line: IWS was calculated over one minute through simultaneous measurement of LV internal diameter and wall thickness by echocardiography and LV pressure by LV catheterization.At rest, the MI group showed concentric LV hypertrophy pattern with preserved LV cavity size, LV systolic function, and IWS comparable with the sham group.IWS showed good correlation with a product of peak-systolic wall stress and heart rate.

View Article: PubMed Central - HTML - PubMed

Affiliation: Nemours Cardiac Center and Nemours Biomedical Research, Alfred I, duPont Hospital for Children, 1600 Rockland Rd, Wilmington, DE 19103, USA.

ABSTRACT

Background: Wall stress is a useful concept to understand the progression of ventricular remodeling. We measured cumulative LV wall stress throughout the cardiac cycle over unit time and tested whether this "integrated wall stress (IWS)" would provide a reliable marker of total ventricular workload.

Methods and results: We applied IWS to mice after experimental myocardial infarction (MI) and sham-operated mice, both at rest and under dobutamine stimulation. Small infarcts were created so as not to cause subsequent overt hemodynamic decompensation. IWS was calculated over one minute through simultaneous measurement of LV internal diameter and wall thickness by echocardiography and LV pressure by LV catheterization. At rest, the MI group showed concentric LV hypertrophy pattern with preserved LV cavity size, LV systolic function, and IWS comparable with the sham group. Dobutamine stimulation induced a dose-dependent increase in IWS in MI mice, but not in sham mice; MI mice mainly increased heart rate, whereas sham mice increased LV systolic and diastolic function. IWS showed good correlation with a product of peak-systolic wall stress and heart rate. We postulate that this increase in IWS in post-MI mice represents limited myocardial contractile reserve.

Conclusion: We hereby propose that IWS provides a useful estimate of total ventricular workload in the mouse model and that increased IWS indicates limited LV myocardial contractile reserve.

Show MeSH
Related in: MedlinePlus