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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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Assessment of ventricular remodeling by echocardiography (A) and LVW/BW ratio. A. Echocardiographic parameters at 1, 3, and 5 weeks after MI (n = 5) and sham groups (n = 5) under isoflurane anesthesia. A progressive increase in LVPWd was seen in MI group compared with sham, but there were no significant differences in LVIDd, %FS, or %Vcf between the two groups. * p < 0.05 vs. sham, # p < 0.05 vs. baseline. MI: myocardial infarction, SH: sham. B. LVW/BW ratio (mg/g) was significantly higher in MI group (n = 5) than in sham group (n = 5) (MI: 5.11 ± 0.32, sham 3.60 ± 0.35; p < 0.05), supporting the echocardiographic finding of LV hypertrophy in MI group. * p < 0.05 vs. sham.
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Figure 2: Assessment of ventricular remodeling by echocardiography (A) and LVW/BW ratio. A. Echocardiographic parameters at 1, 3, and 5 weeks after MI (n = 5) and sham groups (n = 5) under isoflurane anesthesia. A progressive increase in LVPWd was seen in MI group compared with sham, but there were no significant differences in LVIDd, %FS, or %Vcf between the two groups. * p < 0.05 vs. sham, # p < 0.05 vs. baseline. MI: myocardial infarction, SH: sham. B. LVW/BW ratio (mg/g) was significantly higher in MI group (n = 5) than in sham group (n = 5) (MI: 5.11 ± 0.32, sham 3.60 ± 0.35; p < 0.05), supporting the echocardiographic finding of LV hypertrophy in MI group. * p < 0.05 vs. sham.

Mentions: To assess the efficacy of IWS, we examined echocardiographic and hemodynamic changes as well as IWS in post-MI and sham-operated hearts. There was no mortality following small MI throughout the 7 weeks of observation. Echocardiogram was obtained at 0, 1, 3, and 5 weeks after MI under isoflurane anesthesia to assess the temporal changes in LV dilatation [LVID(d)], LV hypertrophy [LVPW(d)], and systolic performance (%FS and %Vcf) in MI (n = 5) and sham (n = 5) groups (Figure 2A). Progressive ventricular hypertrophy was seen in the MI group as indicated by a continuous increase in LVPWd after MI. The LV cavity size remained relatively unchanged in both groups. This experimentally created small MI was restricted to the LV apex [5], and echocardiogram revealed that the majority of the LV appeared symmetrical, and LV myocardium including LV free wall and interventricular septum showed normal symmetric ventricular wall motion without segmental hypokinesia or dyskinesia. LV systolic performance presented by %FS and %Vcf was comparable between the two groups. These results indicate that the small MI procedure induced nearly concentric LV hypertrophy without LV chamber dilatation. The presence of ventricular hypertrophy in the MI group was also confirmed by LV (mg)/body (g) weight ratio, which was significantly higher than in the sham group (MI 5.11 ± 0.32 vs. sham 3.59 ± 0.16, p < 0.05; Figure 2B).


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)

Assessment of ventricular remodeling by echocardiography (A) and LVW/BW ratio. A. Echocardiographic parameters at 1, 3, and 5 weeks after MI (n = 5) and sham groups (n = 5) under isoflurane anesthesia. A progressive increase in LVPWd was seen in MI group compared with sham, but there were no significant differences in LVIDd, %FS, or %Vcf between the two groups. * p < 0.05 vs. sham, # p < 0.05 vs. baseline. MI: myocardial infarction, SH: sham. B. LVW/BW ratio (mg/g) was significantly higher in MI group (n = 5) than in sham group (n = 5) (MI: 5.11 ± 0.32, sham 3.60 ± 0.35; p < 0.05), supporting the echocardiographic finding of LV hypertrophy in MI group. * p < 0.05 vs. sham.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Assessment of ventricular remodeling by echocardiography (A) and LVW/BW ratio. A. Echocardiographic parameters at 1, 3, and 5 weeks after MI (n = 5) and sham groups (n = 5) under isoflurane anesthesia. A progressive increase in LVPWd was seen in MI group compared with sham, but there were no significant differences in LVIDd, %FS, or %Vcf between the two groups. * p < 0.05 vs. sham, # p < 0.05 vs. baseline. MI: myocardial infarction, SH: sham. B. LVW/BW ratio (mg/g) was significantly higher in MI group (n = 5) than in sham group (n = 5) (MI: 5.11 ± 0.32, sham 3.60 ± 0.35; p < 0.05), supporting the echocardiographic finding of LV hypertrophy in MI group. * p < 0.05 vs. sham.
Mentions: To assess the efficacy of IWS, we examined echocardiographic and hemodynamic changes as well as IWS in post-MI and sham-operated hearts. There was no mortality following small MI throughout the 7 weeks of observation. Echocardiogram was obtained at 0, 1, 3, and 5 weeks after MI under isoflurane anesthesia to assess the temporal changes in LV dilatation [LVID(d)], LV hypertrophy [LVPW(d)], and systolic performance (%FS and %Vcf) in MI (n = 5) and sham (n = 5) groups (Figure 2A). Progressive ventricular hypertrophy was seen in the MI group as indicated by a continuous increase in LVPWd after MI. The LV cavity size remained relatively unchanged in both groups. This experimentally created small MI was restricted to the LV apex [5], and echocardiogram revealed that the majority of the LV appeared symmetrical, and LV myocardium including LV free wall and interventricular septum showed normal symmetric ventricular wall motion without segmental hypokinesia or dyskinesia. LV systolic performance presented by %FS and %Vcf was comparable between the two groups. These results indicate that the small MI procedure induced nearly concentric LV hypertrophy without LV chamber dilatation. The presence of ventricular hypertrophy in the MI group was also confirmed by LV (mg)/body (g) weight ratio, which was significantly higher than in the sham group (MI 5.11 ± 0.32 vs. sham 3.59 ± 0.16, p < 0.05; Figure 2B).

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