Revascularization after 3 hours of coronary arterial occlusion: Effects on regional cardiac metabolic function and infarct size

Costantini, Costantino; Corday, Eliot; Lang, Tzu-Wang; Meerbaum, Samuel; Brasch, John; Kaplan, Leo; Rubins, Steven; Gold, Herbert; Osher, Jules

doi:10.1016/0002-9149(75)90492-0

Cited by 186 publications

(20 citation statements)

References 26 publications

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“…If only the first occlusion is considered in each dog, the change in mean values remains statistically significant (p < 0.05) for both LVEDV and ejection fraction. For In the second study of five closed-chest dogs that underwent a 48-hour occlusion, 16 echocardiographic short-axis sections were analyzed individually for extent of dyssynergy and compared with infarct size estimated by NBT short-axis sections at levels from base to LV apex. Normal echocardiographic short-axis sections with no dyssynergy were not included in this comparison.…”

Section: Resultsmentioning

confidence: 99%

“…In the third study of six closed-chest dogs that underwent a 3-hour occlusion and 45 hours of reperfusion, 16 echocardiographic short-axis sections were analyzed individually for extent of dyssynergy and compared with NBT analysis of corresponding anatomic sections. Normal echocardiographic shortaxis sections with no dyssynergy were not included in this comparison.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Experimental evaluation of the extent of myocardial dyssynergy and infarct size by two-dimensional echocardiography.

Wyatt¹,

Meerbaum²,

Heng³

et al. 1981

Circulation

124

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SUMMARY The extent of left ventricular (LV) dyssynergy was assessed noninvasively in 19 dogs with twodimensional echocardiographic short-axis sections during myocardial ischemia and infarction. After coronary occlusion, two-dimensional echocardiography uniformly indicated an increase in LV end-diastolic volume and a decrease in LV ejection fraction. Two-dimensional echocardiographic measurements of dyssynergy were evaluated and compared in three subgroups against (1) the extent of LV dyssynergy determined by force-gauge mapping during 10 coronary occlusions of 30-60 minutes' duration in eight open-chest dogs, (2) infarct size delineated by nitroblue tetrazolium (NBT) staining of left ventricular slabs after 48 hours of left anterior descending coronary artery (LAD) occlusion in five closed-chest dogs, and (3) NBT infarct size after 3-hour LAD occlusion followed by 45 hours of reperfusion in six closed-chest dogs. Linear regression analysis of results from these three comparisons gave good correlations (r = 0.89) for groups 1 and 2; in group 2, the extent of dyssynergy by two-dimensional echocardiography was consistently greater than infarct size by NBT. In group 3, the correlation was poor (r = 0.39). These results suggest that an adequate estimate for the extent of LV dyssynergy or infarct size may be obtained with two-dimensional echocardiography during myocardial ischemia or infarction, but not in the presence of coronary reflow, which causes an acute discrepancy between myocardial viability and function.WE recently reported techniques for visualizing the left ventricle in dogs with two-dimensional echocardiography (2-D echo) and for quantifying left ventricular mass and volume.'~" Preliminary studies also showed that quantitative analysis of left ventricular (LV) regional wall motion during myocardial ischemia and infarction by 2-D echo was feasible.6-8 A noninvasive method for estimating the severity and extent of myocardial dyssynergy would be extremely useful for evaluating spontaneous changes during myocardial ischemia and effects of preventive or therapeutic interventions. Meltzer et al.9 reported that estimations of myocardial dyssynergy by 2-D echo correlated well with infarct size measured by another independent technique, even during pharmacologic interventions.In the present study, we analyzed the left ventricle using 2-D echo in both short and long-axis crosssectional views to evaluate the extent of myocardial dyssynergy during coronary artery occlusion and reperfusion in dogs. The ultrasound measurements of dyssynergy were compared with the extent of myocar- From dial dyssynergy estimated by force-gauge mapping and the size of myocardial infarction delineated by histochemical staining with nitroblue tetrazolium (NBT). Methods Experimental ProcedureNineteen dogs that weighed 20-40 kg were anesthetized with morphine (2 mg/kg i.m.) and sodium pentobarbital (30 mg/kg i.v.) and were placed on a Harvard respirator while in the right lateral decubitus position. The dogs were separated into three grou...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Experimental evaluation of the extent of myocardial dyssynergy and infarct size by two-dimensional echocardiography.

Wyatt¹,

Meerbaum²,

Heng³

et al. 1981

Circulation

124

View full text Add to dashboard Cite

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“…Isolated rabbit hearts were perfused by the method of Langendorffat a constant pressure of 80 mmHg with a Krebs-bicarbonate buffered 1. Abbreviations used in this paper: EPR, electron paramagnetic resonance; *°2 superoxide; r-h-SOD, recombinant human superoxide dismutase; SOD, superoxide dismutase.…”

Section: Methodsmentioning

confidence: 99%

“…It has been demonstrated that timely reperfusion of ischemic myocardium can reduce the amount of necrosis after coronary artery occlusion (1)(2)(3)(4)(5). There is evidence, however, that reperfusion while terminating ischemia may also cause further myocardial damage (6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Recombinant superoxide dismutase reduces oxygen free radical concentrations in reperfused myocardium.

et al. 1987

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It has been proposed that oxygen free radicals mediate damage that occurs during postischemic reperfusion. Recombinant human superoxide dismutase (r-h-SOD) has been shown to be effective at reducing reperfusion injury, but it is not known if this infused enzyme actually reduces oxygen free radical concentrations in the myocardial tissue. Electron paramagnetic resonance spectroscopy was used to directly measure the effect of r-h-SOD on free radical concentrations in the postischemic heart. Hearts were freeze clamped at 77°K after 10 min of normothermic global ischemia followed by 10 s of reflow with control perfusate (n = 7) or perfusate containing 60,000 U r-h-SOD (n = 7). The spectra of these hearts exhibited three different signals: signal A isotropic, g = 2.004, identical to the carbon-centered ubiquinone free radical; signal B anisotropic with axial symmetry, g11 = 2.033, gI = 2.005, identical to the oxygen-centered alkyl peroxyl free radical; and the signal C an isotropic triplet, g = 2.000, a. = 24 G, similar to a nitrogencentered free radical such as a peroxyl amine. With r-h-SOD administration the concentration of the oxygen free radical, signal B, was reduced 49% from 6.8±0.3 ,uM to 3.5±0.3 ,M (P < 0.01) and the concentration of the nitrogen free radical, signal C, was reduced 38% from 3.4±0.3 to 2.1±0.3 ;MM (P < 0.01). The concentration of the carbon-centered free radical, signal A, however, was increased 51% from 3.3±0.2 to 5.0±0.2 ,uM (P < 0.01). Identical reperfusion with peroxide-inactivated r-h-SOD did not alter the concentrations of free radicals indicating that the specific enzymatic activity of r-h-SOD is required to decrease the concentrations of reactive oxygen free radicals. Additional measurements performed varying the duration of reflow demonstrate a burst of oxygen free radical generation peaking at 10 s of reperfusion. r-h-SOD entirely abolished this burst. These studies demonstrate that superoxide-derived free radicals are generated during postischemic reperfusion and suggest that the beneficial effect of r-h-SOD is due to its specific enzymatic scavenging of superoxide free radicals.

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“…Histologically, restoration of coronary blood flow by reperfusion within 2 to 3 hours rescues some of the ischemic cells from cell death, [17][18][19] resulting in heterogeneous necrosis in the infarct region. 20 -25 This creates multiple regions of nonuniform anisotropy 26 where the electrical impulse conduction can be significantly delayed.…”

Section: Electroanatomical Correlation During Vtmentioning

confidence: 99%

Magnetic Resonance–Based Anatomical Analysis of Scar-Related Ventricular Tachycardia

Ashikaga

Sasano

Dong

et al. 2007

Circulation Research

190

147

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Abstract-In catheter ablation of scar-related monomorphic ventricular tachycardia (VT), substrate voltage mapping is used to electrically define the scar during sinus rhythm. However, the electrically defined scar may not accurately reflect the anatomical scar. Magnetic resonance-based visualization of the scar may elucidate the 3D anatomical correlation between the fine structural details of the scar and scar-related VT circuits. We registered VT activation sequence with the 3D scar anatomy derived from high-resolution contrast-enhanced MRI in a swine model of chronic myocardial infarction using epicardial sock electrodes (nϭ6, epicardial group), which have direct contact with the myocardium where the electrical signal is recorded. In a separate group of animals (nϭ5, endocardial group), we also assessed the incidence of endocardial reentry in this model using endocardial basket catheters. Ten to 12 weeks after myocardial infarction, sustained monomorphic VT was reproducibly induced in all animals (nϭ11). In the epicardial group, 21 VT morphologies were induced, of which 4 (19.0%) showed epicardial reentry. The reentry isthmus was characterized by a relatively small volume of viable myocardium bound by the scar tissue at the infarct border zone or over the infarct.In the endocardial group (nϭ5), 6 VT morphologies were induced, of which 4 (66.7%) showed endocardial reentry. In conclusion, MRI revealed a scar with spatially complex structures, particularly at the isthmus, with substrate for multiple VT morphologies after a single ischemic episode. Key Words: ventricular tachycardia Ⅲ catheter ablation Ⅲ MRI C atheter ablation of scar-related monomorphic ventricular tachycardia (VT) is a promising therapy that may reduce morbidity and mortality associated with this condition. 1 Substrate voltage mapping allows ablation of scar-related VT during sinus rhythm in patients with hemodynamically unstable VTs where conventional activation mapping is difficult. 2 This electroanatomical mapping technique defines scar in the endocardium or the epicardium during sinus rhythm, and the infarct border zones are ablated.However, scar detection using the voltage-based substrate mapping has several limitations. First, it is essentially 2D because it defines the extent of scar on the surface, either endocardial or epicardial, and does not provide complex 3D anatomy of the scar. Second, spatial resolution of the voltagebased scar definition is limited by the number of points studied by the catheter operator. Lastly, electrically defined scar may not necessarily be identical with anatomical scar. For example, anatomically scarred myocardium with hypertrophy may be electrically defined normal. 3 To elucidate the 3D anatomical correlation between the fine structural details of the scar and scar-related VT circuits, we registered VT activation sequence with the 3D scar anatomy derived from high-resolution contrast-enhanced MRI in a swine model of chronic myocardial infarction (MI). To achieve precise registration between the electrode l...

show abstract

Revascularization after 3 hours of coronary arterial occlusion: Effects on regional cardiac metabolic function and infarct size

Cited by 186 publications

References 26 publications

Experimental evaluation of the extent of myocardial dyssynergy and infarct size by two-dimensional echocardiography.

Experimental evaluation of the extent of myocardial dyssynergy and infarct size by two-dimensional echocardiography.

Recombinant superoxide dismutase reduces oxygen free radical concentrations in reperfused myocardium.

Magnetic Resonance–Based Anatomical Analysis of Scar-Related Ventricular Tachycardia

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