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Myocardial reperfusion decreases glucose oxidation and uncouples glucose oxidation from glycolysis. Therapies that increase glucose oxidation lessen myocardial ischemia-reperfusion (I/R) injury. However, the regulation of glucose uptake during reperfusion remains poorly understood. We found that glucose uptake was remarkably diminished in the myocardium following reperfusion in Sprague-Dawley rats as detected by 18 F-labeled and fluorescent-labeled glucose analogs, even though GLUT1 was upregulated by threefold and GLUT4 translocation remained unchanged compared with those of sham-treated rats. The decreased glucose uptake was accompanied by suppressed glucose oxidation. Interestingly, stimulating glucose oxidation by inhibition of pyruvate dehydrogenase kinase 4 (PDK4), a rate-limiting enzyme for glucose oxidation, increased glucose uptake and alleviated I/R injury. In vitro data in neonatal myocytes showed that PDK4 overexpression decreased glucose uptake, whereas its knockdown increased glucose uptake, suggesting that PDK4 has a role in regulating glucose uptake. Moreover, inhibition of PDK4 increased myocardial glucose uptake with concomitant enhancement of cardiac insulin sensitivity following myocardial I/R. These results showed that the suppressed glucose oxidation mediated by PDK4 contributes to the reduced glucose uptake in the myocardium following reperfusion, and enhancement of glucose uptake exerts cardioprotection. The findings suggest that stimulating glucose oxidation via PDK4 could be an efficient approach to improve recovery from myocardial I/R injury., (Copyright © 2017 the American Physiological Society.)

Objective: To investigate the evolution of left ventricular global strain in anterior myocardial infarction patients treated with emergency percutaneous coronary intervention (PCI).
 Methods: A total of 54 patients with PCI were enrolled as a PCI group. Forty healthy subjects were enrolled as a control group. Dynamic cardiac images were collected. All of these images were analyzed off-line by velocity vector imaging (VVI) software. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was measured with an electrochemiluminescence immunoassay through the Elecsys 1010/2010 system. Correlation analysis were undertaken between VVI and NT-proBNP levels in blood.
 Results: In PCI group, only globle longitudinal strain (GLS) was significantly increased 3 day after operation (P<0.05). GLS and globle circumferencial strain (GCS) were markedly increased 6 months after operation (P<0.05). In PCI group, left ventricular GLS 1 d to 6 months after PCI shows positive correlation with lgNT-proBNP levels (r=0.66, P<0.001). GLS value was -12.50% at the 3rd day after operation, indicating the improvment of cardiac function in the first and sixth month after PCI.
 Conclusion: The change of Left ventricular globle longitudinal systolic function after emergency PCI may be more sensitive to the improvement of myocardial stunning after STEMI reperfusion; GLS value (-12.50%) at the 3rd day after operation predict the improvment of cardiac function in the first and sixth months after PCI.

Objective: This retrospective study aimed to investigate the relationship between admission levels of serum y-glutamyltransferase and poor myocardial perfusion after primary percutaneous coronary intervention in patients with acute myocardial infarction., Introduction: Reperfusion injury caused by free radical release and increased oxidative stress is responsible for the pathophysiology of the no-reflow phenomenon in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. Serum γ-glutamyltransferase is an established marker of increased oxidative stress., Methods: The study population consisted of 80 patients (64 men and 16 women, mean age = 67.5 + 6.6 years) with thrombolysis in myocardial infarction 0/1 flow pre-procedurally. The patients were divided into two groups according to thrombolysis in myocardial perfusion grades that were assessed immediately following primary percutaneous coronary intervention. The two groups (group 1 and group 2) each consisted of 40 patients with thrombolysis in myocardial perfusion grades 0-1 and thrombolysis in myocardial perfusion grades 2-3, respectively., Results: Admission pain to balloon time, γ-glutamyltransferase and creatine kinase-MB isoenzyme levels of group 1 patients were significantly higher than those of group 2 patients. Pain to balloon time, γ-glutamyltransferase, peak creatine kinase-MB isoenzyme, low left ventricular ejection fraction and poor pre-procedural thrombolysis in myocardial infarction grade were significantly associated with poor myocardial perfusion by univariate analysis. However, only pain to balloon time and γ-glutamyltransferase levels showed a significant independent association with poor myocardial perfusion by backward logistic regression analysis. Adjusted odds ratios were calculated as 4.92 for pain to balloon time and 1.13 for γ-glutamyltransferase., Conclusion: High admission γ-glutamyltransferase levels are associated with poor myocardial perfusion in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention, particularly in patients with prolonged pain to balloon time.

The aim of this work is to evaluate the relationship between improvement of regional myocardial function and visual analysis of contrast-enhanced (CE) MRI in patients after acute myocardial infarction. MRI was performed on 19 patients 1 and 11 weeks after a reperfused acute myocardial infarction. Perfusion data (first-pass images [FPI] and delayed CE images) were acquired after an intravenous bolus of gadolinium-DTPA and visually analyzed using a 17 segment model. Each segment was then classified in 3 groups, according to the presence or absence of FPI and CE patterns at baseline study: group 0: normal-appearing segments; group 1: segments with delayed hyper-enhancement but no early hypo-enhancement; group 2: segments with early hypoenhancement. Relative Wall thickening (RWT) was analyzed in each segment and its improvement evaluated in each group. Between first MRI and follow-up study, a significant improvement of RWT occurred in group 1 (mean +/- SD) [from 43.43 +/- 26.59% to 76.71 +/- 47.38%; p = 0.001] but not in group 2 (from 32.73 +/- 25.58% to 39.57 +/- 30.57%; p = NS). In group 0, RWT despite normal value at baseline study exhibited a significant improvement at follow-up (from 65.23 +/- 46.52% to 79.73 +/- 48.46%; p = 0.0015). In conclusion, the combined analysis of early and delayed perfusion abnormalities in MRI in the week following myocardial infarction can predict myocardial viability and allows in the future an evaluation of the efficacy of perfusion therapy.

Background: We have observed 3 abnormal patterns on contrast-enhanced MRI early after reperfused myocardial infarction (MI): (1) absence of normal first-pass signal enhancement (HYPO), (2) normal first pass signal followed by hyperenhanced signal on delayed images (HYPER), or (3) both absence of normal first-pass enhancement and delayed hyperenhancement (COMB). This study examines the association between these patterns in the first week after MI and late recovery of myocardial contractile function by use of magnetic resonance myocardial tissue tagging., Methods and Results: Seventeen patients (14 men) with a mean age of 53+/-12 years were studied after a reperfused first MI. Contrast-enhanced images were acquired immediately after bolus administration of gadolinium and 7+/-2 minutes later. Tagged images were acquired at weeks 1 and 7. Circumferential segment shortening (%S) was measured in regions displaying HYPER, COMB, or HYPO contrast patterns and in remote regions (REMOTE) at weeks 1 and 7. At week 1, %S was depressed in HYPER, COMB, and HYPO (9+/-8%, 7+/-6%, and 5+/-4%, respectively) and were less than REMOTE (18+/-6%, P<0.003). However, in HYPER, %S improved at week 7 from 9+/-8% to 18+/-5% (P<0.001 versus week 1). In contrast, HYPO did not improve significantly (5+/-4% to 6+/-3%, P=NS) and COMB tended to improve 7+/-6% to 11+/-6% (P=0.06)., Conclusions: HYPER has partially reversible dysfunction and represents predominantly viable myocardium. COMB shows borderline improvement and likely contains an admixture of viable and necrotic myocardium. HYPO shows little functional improvement at 7 weeks, presumably because of irreversible myocardial damage.

The present study was designed to assess the possibility of maximizing the effects of reperfusion by the association of the calcium channel blocker, verapamil and the iron chelator deferoxamine, to delay necrosis and avoid reperfusion injury. Sixty-four mongrel dogs (15 +/- 1.1 (SD) kg) were successfully subjected to 24 h of reperfusion following 90-min occlusion of the left anterior coronary artery. ECG and arterial pressure were monitored. The risk area (RA; % left ventricle (LV)) was determined by the infusion of Evans blue into the aortic root and the area of necrosis (AN; %RA) by triphenyltetrazolium chloride staining. Myocardial preservation was defined as %RA not necrosed calculated as (RA-AN)/RA x 100. RA was similar in all dogs, i.e., 33 +/- 2% LV (SD). There were no differences in arterial pressure, heart rate or double product among groups. Myocardial preservation was 60 +/- 13% RA in 9 control dogs submitted to reperfusion only (group C), and 58 +/- 18% RA in 17 dogs treated with deferoxamine (500 mg, iv), 30 min before reperfusion (group DF). Verapamil (0.2 mg/kg, iv) was given alone 15 min after occlusion to 15 dogs (group VP), followed by prereperfusion deferoxamine to 16 dogs (group VP+DF) and in two doses after occlusion and 15 min before reperfusion in 7 dogs (group VP+VP). Myocardial preservation was greater in the latter groups when compared to controls, namely 76 +/- 13% RA in group VP, 74 +/- 11% in group VP+DF and 73 +/- 9% in group VP+VP (P = 0.04 vs group C, ANOVA). The data suggest that the mechanism underlying this beneficial effect is mainly related to the retardation of necrosis progression. O2 free radicals or Ca(2+)-induced reperfusion injury do not play a major role.