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      Functional and Bioenergetic Consequences of Postinfarction Left Ventricular Remodeling in a New Porcine Model : MRI and 31 P-MRS Study

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          Abstract

          Background The underlying mechanisms by which left ventricular remodeling (LVR) leads to congestive heart failure (CHF) are unclear. This study examined the functional and bioenergetic abnormalities associated with postinfarction ventricular remodeling in a new, large animal model.

          Methods and Results Remodeling was induced by circumflex coronary artery ligation in young pigs. LV mass, volume, ejection fraction (EF), the ratio of scar surface area to LV surface area, and LV wall stresses were calculated from magnetic resonance imaging anatomic data and simultaneously measured LV pressure. Hemodynamics, transmural blood flow, and high-energy phosphates (spatially localized 31 P–nuclear magnetic resonance) were measured under basal conditions, during hyperperfusion induced by pharmacological vasodilation with adenosine, and during pyruvate infusion (11 mg/kg per minute IV). Six of 18 animals with coronary ligation developed clinical CHF while the remaining 12 animals had LV dilation (LVR) without CHF. The results were compared with 16 normal animals. EF decreased from 55.9±5.6% in normals to 34.6±2.3% in the LVR group ( P <.05) and 24.2±2.8% in the CHF group ( P <.05 versus LVR). The infarct scar was larger in CHF hearts than in LVR hearts ( P <.05). In normals, LV myocardial creatine phosphate (CP)/ATP ratios were 2.10±0.10, 2.06±0.16, and 1.92±0.12 in subepicardium (EPI), mid myocardium (MID), and subendocardium (ENDO), respectively. In LVR hearts, the corresponding ratios were decreased to 1.99±0.13, 1.80±0.14, and 1.57±0.15 (ENDO P <.05 versus normal). In CHF hearts, CP/ATP ratios were 1.41±0.14, 1.33±0.15, and 1.25±0.15; ( P <.05 versus LVR in EPI and MID). The calculated myocardial free ADP levels were significantly increased only in CHF hearts.

          Conclusions Bioenergetic abnormalities in remodeled myocardium are related to the severity of LV dysfunction, which, in turn, is dependent on the severity of the initiating myocardial infarction.

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          Wall stress and patterns of hypertrophy in the human left ventricle.

          R McLaurin, David Hilton, W Grossman (1975)
          It is generally recognized that chronic left ventricular (LV) pressure overload results primarily in wall thickening and concentric hypertrophy, while chronic LV volume overload is characterized by chamber enlargement and an eccentric pattern of hypertrophy. To assess the potential role of the hemodynamic factors which might account for these different patterns of hypertrophy, we measured LV wall stresses throughout the cardiac cycle in 30 patients studied at the time of cardiac catheterization. The study group consisted of 6 subjects with LV pressure overload, 18 with LV volume overload, and 6 with no evidence of heart disease (control). LV pressure, meridional wall stress (sigman), wall thickness (h), and radius (R) were measured in each patient throughout the cardiac cycle. For patients with pressure overload, LV peak systolic and end diastolic pressures were significantly increased (220 plus or minus 6/23 plus or minus 3 mm Hg) compared to control (117 plus or minus 7/10 plus or minus 1 mm Hg, P less than 0.01 for each). However, peak systolic and end diastolic (sigman) were normal (161 plus or minus 24/23 plus or minus 3 times 10-3 dyn/cm-2) compared to control (151 plus or minus 14/17 plus or minus 2 times 10-3 dyn/cm-2, NS), reflecting the fact that the pressure overload was exactly counterbalanced by increased wall thickness (1.5 plus or minus 0.1 cm for pressure overload vs. 0.8 plus or minus 0.1 cm for control, P less than 0.01). For patients with volume overload, peak systolic (sigman) was not significantly different from control, but end diastolic (sigmam) was consistently higher than normal (41 plus or minus 3 times 10-3 dyn/cm-2 for volume overload, 17 plus or minus 2 times 10-3 dyn/cm-2 for control, P less than 0.01). LV pressure overload was associated with concentric hypertrophy, and an increased value for the ratio of wall thickness to radius (h/R ratio). In contrast, LV volume overload was associated with eccentric hypertrophy, and a normal h/R ratio. These data suggest the hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress. We propose that increased systolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolic stress (force per unit cross-sectional area) to normal. In contrast, increased resting or diastolic tension appears to result in gradual fiber elongation or lengthening which improves efficiency of the ventricular chamber but cannot normalize the diastolic wall stress.
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            Altered sarcoplasmic reticulum Ca2(+)-ATPase gene expression in the human ventricle during end-stage heart failure.

            A M Lompré, P Duc-Goiran, Jonathan Allen … (1989)
            A decrease in the myocardial level of the mRNA encoding the Ca2(+)-ATPase of the sarcoplasmic reticulum (SR) has been recently reported during experimental cardiac hypertrophy and failure. To determine if such a deficit occurs in human end-stage heart failure, we compared the SR Ca2(+)-ATPase mRNA levels in left (LV) and right ventricular (RV) specimens from 13 patients undergoing cardiac transplantation (6 idiopathic dilated cardiomyopathies; 4 coronary artery diseases with myocardial infarctions; 3 diverse etiologies) with control heart samples using a rat cardiac SR Ca2(+)-ATPase cDNA probe. We observed a marked decrease in the mRNA for the Ca2(+)-ATPase relative to both the 18S ribosomal RNA and the myosin heavy chain mRNA in LV specimens of patients with heart failure compared to controls (-48%, P less than 0.01 and -47%, P less than 0.05, respectively). The LV ratio of Ca2(+)-ATPase mRNA to 18S RNA positively correlated with cardiac index (P less than 0.02). The RV ratio correlated negatively with systolic, diastolic and mean pulmonary arterial pressures (P less than 0.02, P less than 0.02, and P less than 0.01, respectively). We suggest that a decrease of the SR Ca2(+)-ATPase mRNA in the myocardium plays an important role in alterations of Ca2+ movements and myocardial relaxation reported during human end-stage heart failure.
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              Cineangiography of the heart in a single breath hold with a segmented turboFLASH sequence.

              Elazer Edelman, Mark Atkinson (1991)
              Six healthy volunteers and three patients with cardiac anomalies were studied in a comparison of segmented turboFLASH (fast low-angle shot) cine, a method of magnetic resonance imaging that permits an entire series of high-resolution cine images to be obtained in one breath hold, with standard cine. Segmented turboFLASH uses a gradient-echo sequence designed for short imaging times in combination with a segmented data acquisition method. Presaturation pulses were applied to eliminate the blood pool signal; the signal-to-noise ratio was assessed with a phantom. Standard hardware and image reconstruction methods were used. The breath-hold images consistently showed reduced ghosting and blurring from respiration. Because a very short echo time was used, segmented turboFLASH was relatively insensitive to dephasing caused by local field disturbances or flow. The authors conclude that, by reducing imaging times and eliminating respiratory artifact, segmented turboFLASH can be useful for performing cine studies of the heart and great vessels.
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                Author and article information

                Journal
                Title: Circulation
                Abbreviated Title: Circulation
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 0009-7322
                ISSN (Electronic): 1524-4539
                Publication date Created: September 1996
                Publication date (Print): September 1996
                Volume: 94
                Issue: 5
                Pages: 1089-1100
                Affiliations
                [1 ]the Departments of Biochemistry, Medicine, and Radiology and the Center for Magnetic Resonance Research, University of Minnesota, and the Department of Veterans Affairs Medical Center, Minneapolis, Minn.
                Article
                DOI: 10.1161/01.CIR.94.5.1089
                SO-VID: 964f599f-39eb-41f6-9798-8f85da9ce310
                Copyright © © 1996
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