Levels Of Myocardial Injury Research Articles

Effect of extracellular matrix stiffness on efficacy of Dapagliflozin for diabetic cardiomyopathy

BackgroundExtracellular matrix (ECM) stiffness is closely related to the progress of diabetic cardiomyopathy (DCM) and the response of treatment of DCM to anti-diabetic drugs. Dapagliflozin (Dapa) has been proven to have cardio-protective efficacy for diabetes and listed as the first-line drug to treat heart failure. But the regulatory relationship between ECM stiffness and treatment efficacy of Dapa remains elusive.Materials and methodsThis work investigated the effect of ECM stiffness on DCM progression and Dapa efficacy using both in vivo DCM rat model and in vitro myocardial cell model with high glucose injury. First, through DCM rat models with various levels of myocardial injury and administration with Dapa treatment for four weeks, the levels of myocardial injury, myocardial oxidative stress, expressions of AT1R (a mechanical signal protein) and the stiffness of myocardial tissues were obtained. Then for mimicking the stiffness of myocardial tissues at early and late stages of DCM, we constructed cell models through culturing H9c2 myocardial cells on the polyacrylamide gels with two stiffness and exposed to a high glucose level and without/with Dapa intervention. The cell viability, reactive oxygen species (ROS) levels and expressions of mechanical signal sensitive proteins were obtained.ResultsThe DCM progression is accompanied by the increased myocardial tissue stiffness, which can synergistically exacerbate myocardial cell injury with high glucose. Dapa can improve the ECM stiffness-induced DCM progression and its efficacy on DCM is more pronounced on the soft ECM, which is related to the regulation pathway of AT1R-FAK-NOX2. Besides, Dapa can inhibit the expression of the ECM-induced integrin β1, but without significant impact on piezo 1.ConclusionsOur study found the regulation and effect of biomechanics in the DCM progression and on the Dapa efficacy on DCM, providing the new insights for the DCM treatment. Additionally, our work showed the better clinical prognosis of DCM under early Dapa intervention.

Isoflurane Preconditioning Alleviates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting miR-195-3p Expression.

To investigate the role of microRNA-195-3p (miR-195-3p) in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury. AC16 human cardiomyocyte cells were cultured and pretreated with different concentrations of isoflurane (ISO) (1%, 2%, and 3%), followed by 6h each of hypoxia and reoxygenation to construct H/R cell models. The optimum ISO concentration was assessed based on the cell viability. miR-195-3p expression was regulated by in vitro celltransfection. Cell viability was determined by MTT assay, and apoptosis was evaluated by flow cytometry. The levels of myocardial injury and inflammation were determined by enzyme-linked immunosorbent assay. Compared with the control group, the cell viability of the H/R group had significantly decreased and that of ISO pretreatment had increased in a dose-dependent manner. Therefore, we selected a 2% ISO concentration for pretreatment. MiR-195-3p expression had significantly increased in the H/R group and decreased after 2% ISO pretreatment. Additionally, the number of apoptotic cells and the levels of lactate dehydrogenase, creatine kinase-myoglobin binding, cardiactroponin I, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α had increased significantly. ISO preconditioning inhibited H/R-induced AC16 cell damage, whereas miR-195-3p overexpression reversed the protective effects of ISO on cardiomyocytes. The expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was reduced in the H/R-induced AC16 cells, and PTEN is a downstream target gene of miR-195-3p. Preconditioning with 2% ISO plays a protective role in H/R-induced AC16 cell damage by inhibiting miR-195-3p expression.

Propionate alleviates myocardial ischemia-reperfusion injury aggravated by Angiotensin II dependent on caveolin-1/ACE2 axis through GPR41.

Myocardial ischemia/reperfusion (I/R) injury is still a lack of effective therapeutic drugs, and its molecular mechanism is urgently needed. Studies have shown that the intestinal flora plays an important regulatory role in cardiovascular injury, but the specific mechanism has not been fully elucidated. In this study, we found that an increase in Ang II in plasma was accompanied by an increase in the levels of myocardial injury during myocardial reperfusion in patients with cardiopulmonary bypass. Furthermore, Ang II treatment enhanced mice myocardial I/R injury, which was reversed by caveolin-1 (CAV-1)-shRNA or strengthened by angiotensin-converting enzyme 2 (ACE2)-shRNA. The results showed that CAV-1 and ACE2 have protein interactions and inhibit each other's expression. In addition, propionate, a bacterial metabolite, inhibited the elevation of Ang II and myocardial injury, while GPR41-shRNA abolished the protective effects of propionate on myocardial I/R injury. Clinically, the propionate content in the patient's preoperative stool was related to Ang II levels and myocardial I/R injury levels during myocardial reperfusion. Taken together, propionate alleviates myocardial I/R injury aggravated by Ang II dependent on CAV-1/ACE2 axis through GPR41, which provides a new direction that diet to regulate the intestinal flora for treatment of myocardial I/R injury.

Abstract 16895: Interrelation of Exercise Training, Cardiorespiratory Fitness, and Cardiac Biomarkers in Patients Enrolled in the Health Benefits of Aerobic and Resistance Training in Individuals With Type 2 Diabetes Study

Introduction: Low cardiorespiratory fitness (CRF) and elevated biomarker levels of myocardial injury and inflammation are both associated with heart failure (HF) risk. While exercise training (ET) is associated with improvement in CRF, the interrelationships among CRF, cardiac biomarkers, and ET are not well established. Methods: Participants of the Health Benefits of Aerobic and Resistance Training in Individuals with Type 2 Diabetes study were included. High-sensitivity cardiac troponin T (hs-cTnT), growth differentiation factor-15 (GDF-15), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and peak oxygen uptake (VO 2peak ) were assessed at baseline and at 9 months on completion of ET. Longitudinal change in cardiac biomarkers across treatment groups (control versus ET) were assessed using paired t-tests. Multivariable-adjusted linear regression was performed to identify factors associated with follow-up cardiac biomarkers and ΔVO 2peak . Results: This study included 166 participants randomized to control (n = 31) and ET groups (n = 135). There was no significant change in hs-cTnT or NT-proBNP from baseline to follow-up among ET and control group participants. GDF-15 increased among participants randomized to the control (P = 0.01) but not the ET group. In adjusted analysis, each ET regimen was independently associated with lower follow-up GDF-15 but not with change in other biomarkers ( Table ). ΔVO 2peak was not associated with any follow-up biomarker level in adjusted analysis. Among individuals in the ET group, baseline hs-cTnT and GDF-15 were each significantly associated with ΔVO 2peak [per 1-unit higher log(hs-cTnT): β= -0.18 (95% CI = -0.31, -0.05); per 1-unit higher log(GDF-15): β = 0.08 (95% CI = 0.01, 0.15)]. Conclusions: Among patients with type 2 diabetes, ET was associated with reduction in GDF-15 but not with change in other biomarkers. Baseline hs-cTnT and GDF-15 were each independent predictors of CRF change in response to ET.

Are there sex-based differences in myocardial injury in Acute Heart Failure?

Background and Hypothesis: 
 Myocardial injury in acute heart failure (AHF) contributes to worse outcomes. Whether there are sex-based differences in organ injury in AHF is not well known. This study was designed to assess potential sex-based differences in myocardial injury, as defined by high-sensitivity troponin T (hsTnT) levels, in patients presenting in ED with AHF. We hypothesized that men with AHF have higher hsTnT levels. 
 Project Methods: 
 This is a preliminary analysis from the TACIT study, a large, prospective, multi-center, observational, biomarker cohort study. Adult patients diagnosed and treated for AHF, with a systolic blood pressure >100mmHg, and enrolled within 3 hours of first AHF therapy were eligible. Febrile patients, short life-expectancy, ACS, AF with RVR >130bpm, transplant, VAD, or ESRD were excluded. hsTnT were drawn at baseline and 3 hours later. Hemolyzed samples were disregarded as hemolysis falsely lowers hsTnT. A multivariable linear regression model was used to adjust for potential differences in baseline hsTnT using clinically meaningful covariates. 
 Results: 
 Of 527 enrolled, 499 comprised the final analysis set. Of these patients, 413 had a non-hemolyzed baseline hsTnT. Notably, more men than women were enrolled; men had higher mean baseline hsTnT values (48.3ng/mL, SD(74.5)) than women (28.3ng/mL SD(39.9)). After multivariable adjustment, baseline hsTnT differences by sex remained significant (p <0.0001). 
 Conclusion and Potential Impact: 
 Men with AHF have higher baseline levels of myocardial injury than women. These differences may need to be taken into account for risk-stratification as well as management.

Total intravenous versus desflurane-based anesthesia for shunt procedure in pediatric congenital cyanotic heart disease

Background Congenital cyanotic heart disease (CCHD), inclusive of all types of cyanotic heart disease with resulting hypoxemia and hypoxia, has diverse multisystem effects, including erythrocytosis, hyperviscosity, cholelithiasis, cerebral abscess, vascular dysfunction, and hemoptysis. Most, but not all, patients with CCHD, undergo surgical repair in childhood, resulting in either an elimination or reduction in the degree of hypoxemia and its complications. Systemic-to-pulmonary artery shunt is a necessity as a life-saving procedure that is carried out through placement of extracardiac systemic-to-pulmonary artery shunts, using many procedures such as Blalock–Taussig shunt procedure or its modification [modified Blalock–Taussig shunt (MBTS)], which is commonly used nowadays, modified Blalock–Thomas–Taussig shunt (commonly called the MBTS) is a surgical procedure used to increase pulmonary blood flow for palliation in duct-dependent cyanotic heart defects such as pulmonary atresia, which are common causes of blue baby syndrome. In this procedure, there is temporarily direction of the blood flow to the lungs and relieve cyanosis. Traditionally, these surgical procedures are accomplished by either a total intravenous anesthesia (TIVA) or inhalational-based anesthesia. The TIVA technique achieves hemodynamic stability but has many disadvantages such as increases in the period of mechanical ventilation and its associated complications, and increase in ICU stay. Although inhalational anesthetic-based technique may be associated with myocardial depression and dysarrythmias (up to ventricular arrhythmia), but, due to lower blood solubility, facilitates early awakening and endotracheal extubation; this technique decreases the duration of mechanical ventilation, ICU stay, and, therefore, total hospital stay. Patients and methods Forty ASA classes III and IV patients between 18 months and 6 years, scheduled for MBTS procedure for repairing CCHD, were to undergo systemic to pulmonary shunt using cardiopulmonary bypass (CPB) after median sternotomy. They were divided into two groups: patients in the TIVA group (n=20) were administered a combination of midazolam–fentanyl–propofol along with neuromuscular blockade, whereas the desflurane group (n=20) was administered desflurane with 0.6–1 MAC in 100% oxygen with a combination of fentanyl with neuromuscular blockade. Hemodynamic parameters [heart rate (HR), mean blood pressure], duration of elective ventilation, incidence of supraventricular tachycardia and ventricular tachycardia/ventricular fibrillation, and level of myocardial injury were detected by cardiac troponin I as a cardiac biomarker for myocardial injury recorded as primary outcome, whereas duration of inotrope use, ICU and hospital stay, and serum creatinine levels were recorded preoperatively, thereafter, at 24 h postoperatively, they were recorded as secondary outcome. Any serious adverse events, such as acute renal injury, or any other major cardiovascular/neurologic events were recorded. Results Repeated measure analysis was carried out to see the trend in HR from HR1 (at baseline) in both groups, HRs HR2 (just prior to CPB), HR3 (weaning from CPB), and HR4 (arrival at ICU) were significantly higher than HR1 (P<0.001). The mean arterial pressures recorded at time intervals where T2 (just prior to CPB) and T4 (arrival at ICU) were found to be significantly lower in patients included in the TIVA than in the desflurane group (P=0.003 and 0.002, respectively), but mean arterial pressure values at T1 (at baseline) and T3 (weaning from CPB) were insignificant in both the groups (P>0.05). Duration of mechanical ventilation, ICU stay and hospital stay were lower in the desflurane group compared with the TIVA group (P<0.005). While patients in the TIVA group recorded significantly lower inotrope use than those in the desflurane group (P<0.001). Likewise, the creatinine values measured at baseline and 24 h postoperatively were compared in both groups and also, inbetween group itself, were only significantly increased in the TIVA group (P=0.018). For cardiac troponin I levels, at T2 there were significantly higher than those at T1 in the TIVA group (P=0.001) when compared to the desflurane group (P=0.836). Conclusion TIVA has the advantage of hemodynamic stability, but it prolongs the duration of controlled ventilation and length of hospital stay. The current study demonstrated that a desflurane-based anesthetic provides comparable stability, early recovery of myocardial contractility, decreased duration of controlled ventilation, duration of ICU admissions, and total hospital stay.

Are there any effects of chronic carbon monoxide exposure on argyrophilic nucleolar-organizing region-associated protein synthesis in rat myocardium?

The aims of the study are to detect whether there are any possible effects of chronic carbon monoxide (CO) exposure on the argyrophilic nucleolar-organizing region (AgNOR)-associated protein synthesis and evaluate any possible relationship between the amount of AgNOR protein and the level of myocardial injury also and between AgNOR and histopathological evaluation methods. Adult male albino Wistar rats (n = 18) were randomly divided into three groups (groups A, B, and C). Group A served as control, while groups B and C were rats exposed to CO gas chronically (1000 and 3000 ppm CO concentration with a flow rate of 4 L/min for 30 min/day for 7 days, respectively). Total AgNOR area/nuclear area (TAA/NA) and the mean AgNOR numbers for each myocyte nucleus were determined. There were significant differences among all groups for TAA/NA ratio. These differences were not significant for mean AgNOR numbers. According to the histopathological evaluation scores, there were significant differences between the groups. The differences were significant among the groups for loss of sarcomere pattern. A strong positive correlation between histopathological injury scores and TAA/NA ratio was found (Rsq = 0.48; p = 0.002), however, the correlation was not significant for mean AgNOR numbers (Rsq = 0.08; p = 0.25). In conclusion, TAA/NA ratio can be used as an indicator for obtaining information about the level of myocardial damage instead of histopathological evaluation scores.

Clinical and Functional Outcomes Associated With Myocardial Injury After Transfemoral and Transapical Transcatheter Aortic Valve Replacement: A Subanalysis From the PARTNER Trial (Placement of Aortic Transcatheter Valves).

This study sought to clarify the clinical and echocardiographic prognostic implication of myocardial injury after transcatheter aortic valve replacement (TAVR). The clinical significance of cardiac biomarker elevation after TAVR remains unclear. Patients treated with TAVR in the PARTNER (Placement of Aortic Transcatheter Valves) trial were divided into tertiles (T1, T2, T3) based on the difference between the values on post-procedure day 1 and the baseline values of 2 cardiac biomarkers: cardiac troponin I (ΔcTnI); and creatine kinase-myocardial band (ΔCK-MB) fraction. Patients were stratified according to their access route: transfemoral (TF) (n = 1,840) or transapical (TA) (n = 1,173). At 30 days after TF-TAVR, patients in the highest tertile (T3) of cardiac biomarker elevation had a higher rate of all-cause mortality (ΔcTnI: T3: 5.4% vs. T1: 0.5%, p = 0.006; ΔCK-MB: T3: 5.7% vs. T1: 0.9%, p = 0.006) and cardiovascular mortality (ΔcTnI: T3: 4.9% vs. T1: 0.5%, p = 0.01; ΔCK-MB: T3: 3.9% vs. T1: 0.5%, p = 0.02). At 1 year, only patients in the highest CK-MB tertile had higher rates of all-cause (25.4% vs. 16.8%, p = 0.02) and cardiovascular (10.3% vs. 5.0%) mortality. Multivariable analysis demonstrated that greater release of cardiac biomarkers was independently associated with increased mortality in the TF population. After TA-TAVR, being in the highest tertile of cardiac biomarker elevation had no influence on clinical and echocardiographic outcomes at 30 days and 1 year. After TF-TAVR, a greater degree of myocardial injury was associated with higher rates of 30-day all-cause and cardiovascular mortality. At 1 year, being in the highest tertile of ΔCK-MB was correlated with a higher rate of all-cause and cardiac mortality. Finally, the level of myocardial injury after TA-TAVR had no impact on clinical and echocardiographic outcomes.

Endoplasmic Reticulum Is Involved in Myocardial Injury in a Miniature Swine Model of Coronary Artery Stenosis Exposed to Acceleration-Associated Stress.

This study aimed to investigate the effects of myocardial injury in a minimally-invasive miniature swine model with different levels of coronary artery stenosis (CAS) and exposed to maximal tolerated +Gz. Proximal left anterior descending branch was ligated in 20 swine. Five swine underwent a sham operation. A trapezoid acceleration curve was used for +Gz stress. Pathological changes of myocardial tissue were detected by H&E staining. Apoptotic cardiomyocytes were detected by TUNEL. GRP78 and CHOP were investigated by immunohistochemistry and western blot. CAS models were successful in 18 animals.Compared with the sham-operated group (+8.00±0.71 Gz), the maximal tolerated +Gz values of the moderate stenosis (+6.00±0.89 Gz, P<0.05) and severe stenosis groups (+5.20±0.84 Gz, P<0.05) were decreased.Compared with sham animals (12.16±1.25%), after exposure to maximum +Gz, apoptotic cells of the moderate (43.53±8.42%, P<0.05) and severe stenosis group (60.50±9.35%, P<0.05) were increased, MDA content was increased (1.89 and 4.91 folds, respectively, P<0.05), and SOD activity was reduced (-13.66% and -21.71%, respectively). After exposure to maximum +Gz, GRP78 protein expression was low in the sham-operated (0.29±0.05) and mild stenosis groups (0.35±0.04), while expression was high in the moderate (0.72±0.04, P<0.05) and severe stenosis groups (0.65±0.07, P<0.05). CHOP protein expression was not observed in the sham-operated group, while expression was high in the moderate and severe stenosis groups. These results indicated that Under maximum exposure to +Gz stress, different levels of CAS led to different levels of myocardial injury. Endoplasmic reticulum response is involved in the apoptosis of cardiomyocytes after +Gz stress.

Electrocardiography changes in patients with acute myocardial infarction in late hospital phase

One of possibilities to estimate size of myocardial injury during the acute myocardial infarction are electrocardiographic changes, forming of QS formation (ECG signs of scares changes). This investigation which included three groups of patients receiving thrombolytic, nitrates or beta blockers in acute phase of myocardial infarction has aim to analyze 12-chanels electrocardiogram and to establish difference between this therapeutics groups in sum of QRS score, but also to indication frequency of periinfarction heart insufficiency in this therapeutics groups, comparing with observed ECG changes. Analysis shows significant differences between groups in value of QRS score, and also significant lower value of QRS score in patients with acute myocardial infarction treated with thrombolytic therapy. This difference relative to other two groups shows lower level of myocardial injury during acute myocardial infarction in patients treating with thrombolytic therapy.

Periprocedural myocardial damage during percutaneous coronary intervention: a point-of-care platelet testing and intravascular ultrasound/virtual histology study

Recent studies have implied that platelet reactivity as well as certain lesion morphology may be linked to myocardial injury during percutaneous coronary intervention (PCI). However, to date the abovementioned features have not been investigated simultaneously in one population. To determine if and how high on-treatment platelet reactivity, different lesion morphology, and plaque components are associated with increased risk of periprocedural myocardial injury in patients referred for elective coronary stenting. Sixty patients pretreated with aspirin and clopidogrel and undergoing elective PCI with stent(s) implantation were included. On-treatment platelet reactivity was measured with VerifyNow Aspirin and P₂Y₁₂ assays (Accumetrics, USA) before PCI. Grey-scale intravascular ultrasound (IVUS) and virtual histology were performed before stent(s) implantation (Volcano, USA). Two levels of myocardial injury were considered: any elevation of troponin I (periprocedural myocardial damage, PMD) and/or > 3 times the upper normal limit (periprocedural myocardial infarction, PMI). By receiver-operating characteristics analysis, the following factors, ranked from strongest to weakest, were able to distinguish between patients with and without PMD: remodelling index (RI), fibrous tissue, fibro-fatty tissue volume (FFT), plaque and media cross-sectional area, and external elastic membrane cross-sectional area (EEM CSA). Only platelet count and RI could differentiate patients with and without PMI. PMD as well as PMI could not be predicted either by VerifyNow Aspirin or P₂Y₁₂ assay. Likewise, there was no association between necrotic core volume and PMD or PMI. In logistic regression analysis, after adjusting for possible clinical and procedural confounding factors, only EEM CSA > 14.6 mm² (OR 23.7, 95% CI 1.9-302, p = 0.015), RI > 1.044 (OR 12.3, 95% CI 1.2-121.9, p = 0.032) and FFT > 11.2 mm³ (OR 13.6, 95% CI 1.1-160.9, p = 0.038) were independent predictors of PMD. Only RI > 1.044 was identified as an independent predictor of PMI (OR 7.5, 95% CI 1.92-29.6, p = 0.004). Greater total vessel area, positive remodelling at the lesion site, and high volume of FFT in the coronary plaque are independently associated with increased risk of myocardial injury. Only positive RI was an independent predictor of PMI. Simple lesion morphology, rather than more complex VH-IVUS analysis or platelet reactivity, seems to predict myocardial injury after elective PCI.

A rare case of myocardial infarction related to diagnostic intravascular ultrasound

A 71-year-old man underwent intracoronary stent implantation for acute inferior myocardial infarction (MI). Immediately after diagnostic intravascular ultrasound (IVUS) at 8 months' follow-up, an acute occlusion of the sinus node (SN) artery appeared, which developed sinus arrest with junctional escape rhythm. The serum level of high-sensitivity troponin T (TpT) was markedly elevated on the day after the procedure (2.1-32.5 ng/l), which was indicative of MI related to IVUS. Under continuous intravenous infusion of unfractionated heparin, the escape rhythm changed to lower atrial rhythm on the 4th day, and recovered to sinus rhythm on the 14th day. Coronary angiography (CAG) on 15th day showed a recanalization of the SN artery, but optical coherence tomography identified that disrupted plaque and white thrombus still existed in the ostium of the SN artery. The patient was discharged on maintenance anticoagulation therapy. We hypothesized from this case that IVUS-related myocardial injury may exist without clinical problems. Our retrospective investigation showed that the median levels of high-sensitivity TpT in 20 patients who underwent CAG and subsequent diagnostic IVUS significantly increased from 0.6 (interquartile range 0.3-1.1) to 1.6 (0.7-3.6) ng/l (P < 0.05), suggesting that IVUS may induce very low levels of myocardial injury. In conclusion, we experienced a rare case of IVUS-related MI caused by an acute occlusion of the SN artery. This case reaffirms that we should pay more attention to manipulation of IVUS catheters.

Type of desmin expression in cardiomyocytes – a good marker of heart failure development in idiopathic dilated cardiomyopathy

The aim of this study was to determine whether remodelling of the desmin (DES) cytoskeleton affects myocardial function and whether it could be a useful marker of disease progression in patients with idiopathic dilated cardiomyopathy (IDCM). Endomyocardial biopsy was performed in 195 IDCM patients, and five to six specimens were collected from the left ventricle. DES expression was evaluated using tissue immunostaining and Western blotting. The study population was assigned to four groups according to DES expression type: I, normal DES staining at Z-lines giving a regular pattern of cross-striation (n = 57); IIA, increased DES staining with a regular pattern of cross-striation (n = 40); IIB, increased DES staining with an irregular pattern of cross-striation and/or the presence of aggregates (n = 56); and III, decreased/lack of DES staining (n = 42). Fibrosis, cardiomyocyte hypertrophy and ultrastructure were assessed for the four types of DES expression. The pathological types of DES expression (IIB or III) were associated with pathological changes in mitochondria and the contractile apparatus. Cardiomyocyte diameter and level of fibrosis were both significantly affected. DES expression type correlated with NYHA class, left ventricular end-diastolic diameter, left ventricular ejection fraction and the level of N-terminal pro-brain natriuretic protein. The type of immunohistochemical DES expression correlated with the level of myocardial injury at the cellular and organ levels. This correlation was similar to that observed between DES expression and the well-established biochemical, echocardiographic and clinical parameters of heart failure (HF). DES expression type could be used as an important diagnostic feature of HF development.

Validity of elevated interstitial levels of taurine as a predictor of myocardial ischemic injury.

The microdialysis (MD) technique allows for continuous in vivo monitoring of dynamic changes in the interstitial levels of energy-related metabolites. The release of taurine from the myocyte has been suggested as a marker of ischemic injury. The relationship between (interstitial) taurine release and the degree of myocardial ischemic injury was evaluated following a 40 min long ischemia in a porcine heart-infarct-model. Different protocols of ischemia and reperfusion were used in order to achieve a graded level of myocardial injury. Both interstitial peak levels and the area under curve of taurine obtained during ischemia and reperfusion correlated with the degree of ischemic injury (assessed by developed infarct size estimation). The release of taurine in the myocardium measured by the MD-technique correlated with the degree of ischemic injury during ongoing ischemic insult. Hence, taurine determination in the MD-setting represents a powerful tool to follow the development of myocardial ischemic injury over time.