Decreased expression of Na+/H+ exchanger isoform 1 (NHE1) in non-infarcted myocardium after acute myocardial infarction

Although cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in non-infarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury.     

A novel activation process of protein kinase C in the remote, non-ischemic area of an infarcted heart is mediated by angiotensin-AT1 receptors

BACKGROUND: Translocation and activation of protein kinase C (PKC) has been shown to occur in the ischemic heart. It is, however, controversial if this activation process occurs also in the non-ischemic, remote area of an infarcted heart early after infarction. Furthermore, the mechanisms contributing to the translocation process induced by acute myocardial ischemia in both areas are not fully elucidated. METHODS: Regional myocardial infarction was induced by left anterior descending coronary artery (LAD-) ligation in situ for 2.5 min in rats or in pigs. To evaluate the influence of angiotensin and bradykinin signaling, ramiprilat, candesartan, or the bradykinin-receptor antagonist HOE 140 was given. In biopsies from the ischemic and the non-ischemic remote area, PKC activity and intracellular isozyme distribution were determined. RESULTS: Translocation and activation of PKC could be demonstrated for the first time in the myocardium remote from the infarcted area. This activation was conserved both in pigs and in rats. All major cardiac isozymes of PKC were involved. Whereas bradykinin-receptor blockade had no effect, both angiotensin-converting enzyme inhibition (ACEI) and angiotensin receptor could effectively block this activation process of PKC. CONCLUSION: In the area remote from a myocardial infarction, the activation of PKC could be detected for the first time as early as 2.5 min after LAD ligation. This newly characterized activation in the non-infarcted area can be prevented by ACEI via an angiotensin-AT1-receptor-dependent mechanism. It is supposed that this newly characterized activation process of PKC plays an important role in the signal transduction in the remote myocardium in acute myocardial infarction as a trigger for the late development of hypertrophy and heart failure.     

Beta-adrenoceptor density in chronic infarcted myocardium: a subtype specific decrease of beta1-adrenoceptor density

Beta-adrenoceptor density is altered in different cardiac diseases. In heart failure beta-adrenoceptor density is down regulated but in acute myocardial ischemia beta-adrenoceptor density is up regulated. In hearts with myocardial infarction total beta-adrenoceptor density is decreased shortly after myocardial infarction. AIMS AND METHODS: To investigate whether total beta-adrenoceptor number is altered in the chronic phase after myocardial infarction, and to identify the specificity of alteration, we studied male Wistar rats (n = 18) which underwent a ligation of the left coronary artery or a sham operation. Twelve weeks after coronary ligation, rats were sacrificed and hearts were excised, perfused to obtain blood-free myocardium and frozen in liquid nitrogen. Infarcted myocardium was identified visually and separated from non-infarcted myocardium. Total beta-adrenoceptor number was calculated in fmol (-)-[125I]iodocyanopindolol specifically bound/mg protein and the relative amount of beta1- and beta2-adrenoceptor density was measured by inhibition of (-)-[125I]iodocyanopindolol binding with CGP 20712 A. RESULTS: Total beta-adrenoceptor number in infarcted myocardium was significantly decreased (25.7+/-1.4 vs. 24.9+/-2.2 vs. 20.1+/-3.2 fmol/mg protein (P=0.03) resp. Sham vs. Non-infarcted vs. Infarcted myocardium), due to a decrease of only beta1-adrenoceptor density (14.7+/-0.61 vs. 12.7+/-1.09 vs. 4.84+/-0.96 fmol/mg protein (P=0.004) resp.), whereas the beta2-adrenoceptor density and the dissociation constant (Kd) were not significantly decreased. CONCLUSION: In the infarcted myocardium total beta-adrenoceptor density is decreased due to a decreased beta1-adrenoceptor density at 12 weeks after myocardial infarction.     

Tritiated digoxin. XX. Tissue distribution in experimental myocardial infarction

The role and potential hazards of digitalis glycoside administration in acute myocardial infarction remain controversial. We investigated the concentration of tritiated digoxin in normal, ischemic, and infarcted left ventricular myocardium of the dog after ligation of the anterior interventricular coronary artery. The normal homogeneous distribution of tritiated digoxin in the normal canine left ventricle was altered following acute myocardial infarction. The ischemic and infarcted zones exhibited a marked diminution in digoxin concentration. Oxidative phosphorylation determinations confirmed tissue hypoxia in the infarcted zone. The gradient of digoxin concentration between normal, ischemic, and infarcted zones of myocardium may potentiate the development of an arrhythmia in the electrically unstable infarcted myocardium.     

PCI术后AMI患者非梗死区冠脉血流储备的变化及其对左室功能的影响

目的 观察和分析急性心肌梗死（AMI）患者PCI术后非梗死区冠脉血流储备（CFR）的变化及其对左室功能的影响。方法 22名AMI患者PCI术后1周行二维超声心动图和多巴酚丁胺负荷实时心肌声学造影（MCE）检查,测量左室功能和梗死区、非梗死区CFR,比较非梗死区CFR与梗死区及正常对照组CFR;根据非梗死区CFR值将患者分为两组,比较两组远期左室功能的变化。结果 非梗死区CFR值与正常对照组相比明显下降,非梗死区CFR与左室舒张末期容积呈负相关。结论 AMI后非梗死区心肌同样存在微循环功能障碍,非梗死区CFR值能预测AMI后远期左室功能。     

Basic fibroblast growth factor increases regional myocardial blood flow and salvages myocardium in the infarct border zone in a rabbit model of acute myocardial infarction.

Basic fibroblast growth factor (bFGF) has been shown by some to promote angiogenesis and myocardial salvage in experimentally induced acute myocardial infarction. Although these findings have spurred much clinical interest, they are not universally observed, and the true efficacy of bFGF remains unclear. The authors used a rabbit model of acute myocardial infarction to further elucidate the effects of bFGF on acutely infarcted myocardium containing few collaterals. Myocardial infarction was evoked by ligation of the left coronary artery. Prior to ligation, either 100 microg of bFGF (bFGF group; n = 15) or physiological saline (control group; n = 22) was injected into the myocardium supplied by the ligated artery. With use of nonradioactive colored microspheres, regional blood flow (Qm) was measured before, immediately after, and 4 weeks after coronary artery ligation. Infarct and border zone sizes were measured in cross-sectional slices of the resected hearts, and the amount of viable myocardium (myocardium score) and the extent of fibrosis were histologically determined in each area. Four weeks after ligation, Qm values in the infarcted area did not significantly differ between the bFGF and control groups (0.54 +/- 0.36 vs 0.48 +/- 0.30 mL/min/g); in the border zone, Qm tended to be higher in the bFGF group (3.39 +/- 2.68 vs 1.47 +/- 0.80 mL/min/g), but the difference was not significant; finally in the noninfarcted area, Qm was significantly (p < 0.05) higher in the bFGF group (6.06 +/- 3.85 vs 2.09 +/- 0.82 mL/min/g). There was no significant difference in the amount of viable myocardium or the extent of fibrosis in the infarcted areas of the two groups. In the border zone, however, the amount of viable myocardium was significantly (p < 0.005) larger in the bFGF group (61.8 +/- 8.5% vs 35.8 +/- 20.3% of the visual field). Likewise, as graded on a scale from 0 to 5, the extent of fibrosis was significantly (p < 0.005) less in the bFGF group (2.1 +/- 0.5 vs 3.3 +/- 0.8). In conclusion, injection of bFGF into acutely infarcted myocardium increased blood flow to the noninfarcted area and salvaged the myocardium in the border zone.     

Myocardial contractility, haemodynamics, and metabolism in acute myocardial infarction. Experimental and clinical study

In order to investigate the systemic and central haemodynamics, blood perfusion, and metabolism of the myocardium in acute myocardial infarction (AMI), experiments were carried out in 80 mongrel dogs with experimental AMI, induced by ligation of the descending branch of the left coronary artery, and 183 patients with transmural AMI were clinically followed-up. It was found that after coronary artery ligation the blood flow in the intact myocardial parts increased, whereas in the infarcted zone it decreased. These shifts persisted fairly long after the induction of AMI. Simultaneously the cardiac output markedly tended to decrease in all animals, and this tendency also persisted for the next two days. It was proved that the haemodynamic shifts in question were associated with a decrease in the myocardial biosynthesis of individual fractions of RNA after the coronary artery ligation. The clinical observations confirmed that AMI was accompanied by a decrease in myocardial contractility. The degree of the decrease was directly proportional to the infarct size. The dependence of the changes on the localization of AMI was less marked.     

Scintigraphic assessment of sympathetic innervation after transmural versus nontransmural myocardial infarction

To evaluate the feasibility of detecting denervated myocardium in the infarcted canine heart, the distribution of sympathetic nerve endings using I-123 metaiodobenzylguanidine (MIBG) was compared with the distribution of perfusion using thallium-201, with the aid of color-coded computer functional map in 16 dogs. Twelve dogs underwent myocardial infarction by injection of vinyl latex into the left anterior descending coronary artery (transmural myocardial infarction, n = 6), or ligation of the left anterior descending coronary artery (nontransmural myocardial infarction, n = 6). Four dogs served as sham-operated controls. Image patterns were compared with tissue norepinephrine content and with histofluorescence microscopic findings in biopsy specimens. Hearts with transmural infarction showed zones of absent MIBG and thallium, indicating scar. Adjacent and distal regions showed reduced MIBG but normal thallium uptake, indicating viable but denervated myocardium. Denervation distal to infarction was confirmed by reduced norepinephrine content and absence of nerve fluorescence. Nontransmural myocardial infarction showed zones of wall thinning with decreased thallium uptake and a greater reduction or absence of MIBG localized to the region of the infarct, with minimal extension of denervation beyond the infarct. Norepinephrine content was significantly reduced in the infarct zone, and nerve fluorescence was absent. These findings suggest that 1) MIBG imaging can detect viable and perfused but denervated myocardium after infarction; and 2) as opposed to the distal denervation produced by transmural infarction, nontransmural infarction may lead to regional ischemic damage of sympathetic nerves, but may spare subepicardial nerve trunks that course through the region of infarction to provide a source of innervation to distal areas of myocardium.     

The impaired tolerance of the recently infarcted rat heart to cardioplegic arrest: the protective effect of orotic acid

After myocardial infarction, a reduced mass of non-infarcted myocardium remains to maintain cardiac output. This acutely stressed, non-infarcted myocardium exhibits many metabolic disturbances, and undergoes a process of acute hypertrophy. These stress-induced disturbances may reduce the tolerance of the heart to the global ischaemia of cardioplegic arrest and may explain the increased mortality and morbidity associated with cardiac surgery in patients with recent myocardial infarction. We postulated that orotic acid, a pyrimidine precursor which augments the rate of protein synthesis during hypertrophy, might improve the response of the recently infarcted heart to cardioplegic arrest. Myocardial infarction was induced in rats by coronary ligation, and after 2 days or 3 days the hearts were excised and perfused on the working heart apparatus. After measurement of work capacity, the hearts underwent 1 hour of hypothermic cardioplegic arrest. Post-arrest function was then measured and expressed as a percentage of the pre-arrest value. A group of sham-operated, non-infarcted hearts served as controls. There were two distinct findings: (1) when subjected to hypothermic cardioplegic arrest 2 days after myocardial infarction, hearts recovered only 49% of pre-arrest function, compared with 80% recovery in non-infarcted controls (P less than 0.001). Three days after infarction, recovery had improved to 68% (P less than 0.01 vs. 2 days, P less than 0.05 vs. non-infarcted). (2) Treatment with oral orotic acid following infarction augmented recovery from cardioplegic arrest to 83%, 2 days after infarction (P less than 0.001 vs. untreated) and to 87%, 3 days after infarction (P less than 0.01 vs. untreated).(ABSTRACT TRUNCATED AT 250 WORDS)     

President lecture. Observations on myocardial ischemia

Several problems in myocardial ischemia are discussed based on our experimental and clinical studies. Histochemical changes of the myocardium of adult mongrel dogs with a coronary artery ligation were as follows: The most noticeable findings were a decrease of phosphorylase activity in the pericapillary region of the infarcted area and an enlargement of the discoloration area due to fusion according to the prolongation of the ligation period. This may be explained by the fact that ischemic process takes place around the pericapillary zone in the early stage due to an arborescent distribution of the vascular system in the myocardium. This is presumed as one of the factors which induces heterogeneity of the ischemic myocardium. The reversibility of the injured myocardium due to ischemia was investigated electron-microscopically. The time limit of the myocardial reversibility from ischemic damage was 30 to 50 min. Characteristic changes of LDH isoenzymes and the pathohistological changes of the myocardium after ligation and reperfusion of the coronary artery were as follows: a) A decrease of the LD5 (H subunit) fraction degeneration of the myocardial fibers, fibrosis of the connective tissue and scar formation took place. b) The minimum value of LD5 (H subunit) was observed in cases with a 7-day ligation in the ligation group and in cases with a 12-hour ligation which was followed by a 7-day reperfusion in the reperfusion group. c) The time to reach the minimum LD5 value differed between these 2 groups. The most probable cause of this difference is the protection of the myocardium by reperfusion. 4) In 24 dogs 20 mCi 99mTc-PYP was injected intravenously one and a half hours before the reopening of the chest. Then, Tc-PYP images were obtained at frontal and left lateral views. Tc-PYP images of each cross-sectional surface were also obtained. In the ligation group, 99mTc-PYP uptake in the ischemic myocardium was demarcated clearly in cases with a 1-7 day ligation. In the reperfusion group, 99mTc-PYP uptake in the ischemic area was clearly noticed in cases with a 12-hour to 6-day ligation, which was followed by a 1- to 7-day reperfusion. When the period of the reperfusion was prolonged, it became more difficult to obtain a positive image. In 14 patients with acute myocardial infarction Tc-PYP scintigrams were studied with reference to their ECG.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of oxygen on acute myocardial infarction: a thermographic study in the dog

An acute myocardial infarction was created in a series of dogs by ligation of a branch from the left anterior descending coronary artery. The effects on the infarction with 100% oxygen were studied by thermography in 23 animals. The changes in the infarction size were registered on polaroid photographs. In 10 dogs the infarction showed a uniform cool area, permitting accurate measurement by cutting out and weighing the black, infarcted area from the photographs. During oxygen administration 2 dogs showed a considerable increase in the cool area and 6 other dogs a moderate but significant increase. The remaining 2 dogs in this group showed non-significant change in the infarcted area. In the other 13 animals the cool area was not sufficiently uniform to allow accurate measurement. However, all the dogs in this group, except one, presented a visable increase of the cool area of varying degree. High oxygen supply does not seem to have a favourable effect on an experimentally induced acute myocardial infarction. It is known to promote a lowering of the coronary artery perfusion pressure. In addition to this, it may somehow decrease the arterial supply from the vascular bed round the ischaemic area.     

Differences in time course of myocardial mRNA expression in non-infarcted myocardium after myocardial infarction

In non-infarcted myocardium after myocardial infarction, the change of cardiac phenotypic modulation of contractile protein, extracellular matrix and intracellular Ca²⁺ transport protein, such as sarcoplasmic reticulum Ca²⁺(SR-Ca²⁺)-ATPase, Na⁺-Ca²⁺ exchanger, have a important role during cardiac remodeling. However, the time course in this gene expression in the adjacent and remote left ventricular, or right ventricular myocardium after myocardial infarction has not been well examined. The purpose of this study was to examine the left ventricular function and regional cardiac gene expression after myocardial infarction. Myocardial infarction was produced in Wistar rats by the ligation of the left anterior descending coronary artery. After 3 weeks, 2 months and 4 months from myocardial infarction, we performed Doppler echocardiography and measured the systolic and diastolic function. Then, we analyzed the contractile protein, extracellular matrix and intracellular Ca ²⁺ transport protein mRNAs of cardiac tissues in the adjacent and the remote noninfarcted myocardium, and right ventricular myocardium by Northern blot hybridization. Fractional shortening of infarcted heart progressively decreased. Peak early diastolic filling wave (E wave) velocity increased, and the deceleration rate of the E wave velocity was more rapid in myocardial infarction areas. Atrial filling wave (A wave) velocity decreased, resulting in a marked increase in the ration of E wave to A wave velocity. Expression of myocardial α-skeletal actin, β-MHC and ANP mRNA, or collagen I and III mRNA were higher at 3 weeks after myocardial infarction. SR Ca²⁺-ATPase mRNA in the adjacent non-infarcted myocardium was decreased at 2 months, and that in remote myocardium was decreased at 4 months after infarction. Na⁺-Ca²⁺ exchanger mRNA levels were increased at 3 weeks, but was decreased at 2 months in the adjacent non-infarcted myocardium and at 4 months in the remote myocardium. These findings suggest that the compensation for myocardial infarction by myocardial gene expression in non-infarcted myocardium may occur at an early phase after myocardial infarction, and myocardial dysfunction may begin from adjacent to remote non-infarcted myocardium during progressive cardiac remodeling. Received: 9 August 1999, Returned for revision: 16 September 1999, Revision received: 5 January 2000, Accepted: 26 January 2000     

Contractility of the surviving myocardium following experimental infarct]

The contractile function of the non-infarcted myocardium was examined in adult cats following myocardial infarction produced by ligation of several branches of the LAD and circumflex coronary artery. Two and seven days following infarction, after determination of intracardiac pressures, papillary muscles were excised from the non-infarcted portion of the right ventricle and transferred into a myograph for analysis of contractile function. One week following infarction, force-velocity relations of the surviving myocardium showed a shift downward and to the left in comparison to sham-operated controls. At the same time, there was a decline in actively developed force at Lmax to be deserved, which appeared to be caused by a decrease in the rate of force development. Two days following infarction, similar changes were to be observed, although to a lesser extent. There appears to be a distinct loss of contractility in the remaining viable myocardium following experimental infarction.     

High cardiac angiotensin-II-forming activity in infarcted and non-infarcted human myocardium

The aims of this study were to compare human cardiac angiotensin-II-forming activity (AIIFA) between the intact area of control autopsy hearts without cardiac disease (n = 10) and the infarcted or non-infarcted area of autopsy hearts with myocardial infarction (MI, n = 7) and to determine responsible angiotensin-II-forming enzymes. Cardiac total and chymase-dependent AIIFAs were significantly higher in the infarcted and non-infarcted myocardium than those in non-MI heart, while angiotensin-converting enzyme-dependent AIIFA increased only in the infarcted myocardium. The density of chymase antibody-positive mast cells in the non-infarcted area of MI heart correlated positively with total or chymase-dependent AIIFA. Augmented AIIFA was also detected in the left atrium of post-MI hearts. Our results indicated that cardiac angiotensin II formation could be activated in the infarcted as well as in non-infarcted myocardium of the post-MI human heart.     

Creatine kinase MM isoenzyme subforms in myocardium, cardiac lymph and blood after coronary artery occlusion in dogs

A time-varying pattern of creatine kinase MM (CK-MM) isoenzyme subforms has been found in the blood of patients after acute myocardial infarction, but the site of enzyme modification has not been identified. Therefore, we studied the CK-MM subform patterns in myocardium, cardiac lymph and blood of dogs after coronary artery occlusion. In five conscious dogs, serial blood samples were taken for 72 h after occlusion of the left anterior descending coronary artery. Samples of non-infarcted and infarcted myocardium were taken after 72 h. In five other anaesthetised, open-chest dogs, cardiac lymph and blood samples were taken for 6 h after coronary artery occlusion. CK-MM subforms were quantitated by an isoelectric focusing method. Before coronary occlusion, 64% of the total CK activity in blood appeared as the anodal subform CK-MM 1 (pI 6.3); 20% and 9% as the cathodal subforms CK-MM 2 (pI 6.6) and CK-MM 3 (pI 6.9), respectively. However, after 2 h of coronary occlusion CK-MM 2 and CK-MM 3 were increased (38% and 17% of total activity respectively) compared with CK-MM 1. Between 4 h and 10 h, CK-MM 2 and CK-MM 3 decreased as CK-MM 1 increased restoring the control relative activities of subforms. In contrast to the subform changes in blood, CK-MM 3 was the predominant subform in both non-infarcted and infarcted myocardium after 72 h of coronary occlusion and in cardiac lymph during 6 h of coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of intraaortic balloon counterpulsation on regional coronary blood flow in experimental myocardial infarction

Intraaortic balloon Counterpulsation was carried out in 10 anesthetized normotensive dogs after ligation of the left anterior descending coronary artery. The distribution of myocardial blood flow was determined in these animals by the radioactive microsphere technique. Counterpulsation resulted in a significant decrease in mean arterial pressure of 29 mm Hg (P < 0.001) and an increase of 20 mm Hg in peak and 10 mm Hg in mean aortic diastolic pressure (P < 0.005). There was no direct relation between the hemodynamic effects of counterpulsation and improvement in the distribution of myocardial blood flow to the infarcted area of myocardium. Analysis of data from individual experiments suggests that improvement in myocardial blood flow to the infarcted region is dependent upon the presence of preexisting collateral vessels, since animals with the highest rates of flow to the infarcted region after ligation of the left anterior descending coronary artery had the greatest increase in myocardial blood flow after intraaortic balloon counterpulsation. Despite the failure of any overall improvement in myocardial blood flow to the infarcted area after Counterpulsation, there was a small but significant relative increase in endocardial flow to the normal and border zones of myocardium surrounding the infarcted region.     

Left ventricular contractility related to the state of the coronary bed

The authors studied total and segmental contractility of the left ventricular (LV) myocardium in patients with acute myocardial infarction with single and multiple coronary artery (CA) disease. The group included 75 patients with acute transmural myocardial infarction; coronary arteriography was performed in 56 of them. All patients underwent echocardiography (sector scanning), on the basis of which total (ejection fraction) and segmental parameters (segmental ejection fraction, fraction of segmental wall shortening, velocity of change of segmental area, velocity of change in segmental wall thickness) of LV contractility were calculated. Patients with single CA affection display only a moderate decrease in total ejection fraction, and an insignificant number of complications of myocardial infarction. Segmental contractility data showed severe hyperkinesis of the intact segments of the left ventricle. Multiple CA disease is associated with a marked decrease in both total and segmental contractility of the LV myocardium, and there is no hyperkinesis of the intact segments of the heart.     

Altered expression of proteins of metabolic regulation during remodeling of the left ventricle after myocardial infarction

Non-infarcted myocardium after coronary occlusion undergoes progressive morphological and functional changes. The purpose of this study was to determine whether non-infarcted myocardium exhibits (1) alteration of the substrate pattern of myocardial metabolism and (2) concomitant changes in the expression of regulatory proteins of glucose and fatty acid metabolism. Myocardial infarction was induced in rats by ligation of the left coronary artery. One day and eight weeks after coronary occlusion, glucose and palmitate oxidation were measured. Expression of selected proteins of metabolism were determined one day to 12 weeks after infarction. One day after coronary occlusion no difference of glucose and palmitate oxidation was detectable, whereas after eight weeks, glucose oxidation was increased (+84%, P<0.05) and palmitate oxidation did not change significantly (-19%, P=0.07) in infarct-containing hearts, compared with hearts from sham-operated rats. One day after coronary occlusion, myocardial mRNA expression of the glucose transporter GLUT-1 was increased (+86%, P<0.05) and the expression of GLUT-4 was decreased (-28%, P<0.05) in surviving myocardium of infarct-containing hearts. Protein level of GLUT-1 was increased (+81%, P<0.05) and that of GLUT-4 slightly, but not significantly, decreased (-16%, P=NS). mRNA expressions of heart fatty acid binding protein (H-FABP), and of medium chain acyl-CoA dehydrogenase (MCAD), were decreased by 36% (P<0.05) and 35% (P=0. 07), respectively. Eight weeks after acute infarction, the left ventricle was hypertrophied and, at this time-point, there was no difference in the expression of GLUT-1 and GLUT-4 between infarcted and sham-operated hearts. However, myocardial mRNA and protein content of MCAD were decreased by 30% (P<0.01) and 27% (P<0.05), respectively. In summary, in surviving myocardium, glucose oxidation was increased eight weeks after coronary occlusion. Concomitantly, mRNA and protein expression of MCAD were decreased, compatible with a role of altered expression of regulatory proteins of metabolism in post-infarction modification of myocardial metabolism.