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Clinical decision-making in patients with ST-segment elevation myocardial infarction (STEMI) presenting beyond 12 h of symptom onset (late presenters) is challenging. However, the electrocardiogram (ECG) may provide helpful information. We investigated the association between three ECG-scores and myocardial salvage and infarct size in late presenters treated with primary percutaneous coronary intervention (primary PCI).Sixty-six patients with STEMI and ongoing symptoms presenting 12-72 h after symptom onset were included. Cardiac magnetic resonance was performed at day 1 (interquartile range [IQR], 1-1) and at follow-up at day 93 (IQR, 90-98). The pre-PCI ECG was analyzed for the presence of pathological QW (early QW) as well as Anderson-Wilkins acuteness score (AW-score), the classic Sclarovsky-Birnbaum Ischemia Grading System (classic SB-IG-score) and a modified SB-IG-score including any T-wave morphologies.Early QW was associated with a larger myocardium at risk (39 ± 12 versus 33 ± 12; p = 0.030) and final infarct size (20 ± 11 versus 14 ± 9; p = 0.021) as well as a numerical lower final myocardial salvage (0.52 ± 0.19 versus 0.61 ± 0.23; p = 0.09). The association with final infarct size disappeared after adjusting for myocardium at risk. An AW-score 3 showed a trend towards a larger final infarct size (18 ± 11 versus 11 ± 11; p = 0.08) and was not associated with salvage index (0.55 ± 0.20 versus 0.65 ± 0.30; p = 0.23). The classic and modified SB-IG-score were not associated with final infarct size (modified SB-IG-score, 17 ± 10 versus 21 ± 13; p = 0.28) or final myocardial salvage (0.53 ± 0.20 versus 0.53 ± 0.26; p = 0.96).Of three well-established ECG-scores only early QW and AW-score 3 showed association with myocardium at risk and infarct size to some extent, but the association with myocardial salvage was weak. Hence, neither of the three investigated ECG-scores are sufficient to guide clinical decision-making in patients with STEMI and ongoing symptoms presenting beyond 12 h of symptom onset.

Background The diagnosis of ST elevation myocardial infarction (STEMI) is challenging when the culprit is in the left circumflex coronary artery (CX) territory because ST elevations are often not captured by the standard 12-lead electrocardiogram (ECG). Although, guidelines recommend the acquisition of the additional posterior leads V7-V9 (pECG) when the suspicion of acute coronary syndrome (ACS) is high and the ECG non-diagnostic, this is not routinely done. Purpose The purpose of the FLAWLESS trial, was to improve the prehospital CX STEMI diagnostic. The study consisted of 2 parts: a) a training and implementation study, and b) an outcomes study after implementation. In the implementation study we evaluated the FLAWLESS process from the paramedic's point of view on experiences, implementation of pECG lead recordings and its barriers. Methods Before initiating the trial, all active paramedics in 2 health care regions were educated via a specifically designed and mandatory online 30 min course and all 250 ambulances equipped with a SMART-CARD (instructing how to record pECG leads) and FAQ-sheet. All paramedics were invited by email to anonymously answer an online questionnaire (OQ) designed in REDCap® and interviewed. Utility-score and difficulty-score, ranging from 0 (not useful at all/very easy) to 100 (very useful/very difficult), were introduced for quantitative assessments. Results A total of 1268 paramedics were invited to answer the OQ. The response rate was intermediate at 35%. Among responders, 89% had completed the OEP. On duty 80% had used FAQ-sheet and 74% SMART-CARD in the field. The median utility scores were 80 (25th and 75th quartiles 67–90) for OEP, 79 (61–90) for FAQ-sheet and 85 (75–97) for SMART-CARD, respectively. The implementation of pECG leads recordings was fairly high – 54% reported always recording V7-V9 in ACS patients and 36% reported doing it frequently. Difficulty-score for recording V7-V9 leads in the prehospital setting was 50 (19–70). Finally, 43% reported difficulties that were related to technicalities i.e. defibrillators not having dedicated V7, V8 and V9 cables, hence ambulance staff is forced to record and transmit a second ECG after moving the V4, V5 and V6 cables to the V7-V9 positioned electrodes. Conclusion We demonstrated that large-scale online training of paramedics in the recording of prehospital 15-lead ECG is feasible. The evaluation was positive regarding training and support tools in the ambulances but almost 50% of paramedics found the recording very difficult in the field. Future ECG machines used in emergency settings should be constructed with 13 instead of 10 cables to allow simultaneously recording of 15 leads (standard, precordial and the V7-V9 posterior). This would ease acquisition, facilitate implementation of guideline recommendation. Funding Acknowledgement Type of funding sources: None.

Background Early and correct diagnosis of ST-segment elevation myocardial infarction (STEMI) is crucial for providing timely reperfusion therapy. Patients with ischemic symptoms presenting with ST-segment elevation on the electrocardiogram (ECG) are preferably transported directly to a catheterization laboratory (Cath-lab) for primary percutaneous coronary intervention (PPCI). However, the ECG often contains confounding factors making the STEMI diagnosis challenging leading to false positive Cath-lab activation. The objective of this study was to test the performance of a standard automated algorithm against an additional high specificity setting developed for reducing the false positive STEMI calls. Methods We included consecutive patients with an available digital prehospital ECG triaged directly to Cath-lab for acute coronary angiography between 2009 and 2012. An adjudicated discharge diagnosis of STEMI or no myocardial infarction (no-MI) was assigned for each patient. The new automatic algorithm contains a feature to reduce false positive STEMI interpretation. The STEMI performance with the standard setting (STD) and the high specificity setting (HiSpec) was tested against the adjudicated discharge diagnosis in a retrospective manner. Results In total, 2256 patients with an available digital prehospital ECG (mean age 63 ± 13 years, male gender 71%) were included in the analysis. The discharge diagnosis of STEMI was assigned in 1885 (84%) patients. The STD identified 165 true negative and 1457 true positive (206 false positive and 428 false negative) cases (77.3%, 44.5%, 87.6% and 17.3% for sensitivity, specificity, PPV and NPV, respectively). The HiSpec identified 191 true negative and 1316 true positive (180 false positive and 569 false negative) cases (69.8%, 51.5%, 88.0% and 25.1% for sensitivity, specificity, PPV and NPV, respectively). From STD to HiSpec, false positive cases were reduced by 26 (12,6%), but false negative results were increased by 33%. Conclusions Implementing an automated ECG algorithm with a high specificity setting was able to reduce the number of false positive STEMI cases. However, the predictive values for both positive and negative STEMI identification were moderate in this highly selected STEMI population. Finally, due the reduced sensitivity/increased false negatives, a negative AMI statement should not be solely based on the automated ECG statement.

Background Anteroseptal ST elevation myocardial infarction (STEMI) is traditionally defined on the electrocardiogram (ECG) by ST elevation (STE) in leads V1-V3, with or without involvement of lead V4. It is commonly taught that such infarcts affect the basal anteroseptal myocardial segment. While there are suggestions in the literature that Q waves limited to V1-V4 represent predominantly apical infarction, none have evaluated anteroseptal ST elevation territories. We compared the distribution of the myocardium at risk (MaR) in STEMI patients presenting with STE limited to V1-V4 and those with more extensive STE (V1-V6). Methods We identified patients in the MITOCARE study presenting with a first acute STEMI and new STE in at least two contiguous anterior leads from V1 to V6. Patients underwent cardiac magnetic resonance (CMR) imaging three to five days after acute infarction. Results Thirty-two patients met inclusion criteria. In patients with STE in V1-V4 (n = 20), myocardium at risk (MaR) > 50% was seen in 0%, 85%, 75%, 100%, and 90% in the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. The group with STE in V1-V6 (n = 12), MaR > 50% was seen in 8%, 83%, 83%, 92%, and 83% of the same segments. Conclusions Patients with acute STEMI and STE in leads V1-V4, exhibit MaR in predominantly apical territories and rarely in the basal anteroseptum. We found no evidence to support existence of isolated basal anteroseptal or septal STEMI. “Anteroapical” infarction is a more precise description than “anteroseptal” infarction for acute STEMI patients exhibiting STE in V1-V4.

Introduction: The myocardium at risk (MaR) represents the quantitative ischemic area destined to myocardial infarction (MI) if no reperfusion therapy is initiated. Different ECG scores for MaR have been developed, but there is no consensus as to which should be preferred. Objective: Comparisons of ECG scores and Cardiac Magnetic Resonance (CMR) for determining MaR. Methods: MaR was determined by 3 different ECG scores, and by CMR in ST-segment elevation MI (STEMI) patients from the MITOCARE cardioprotection trial. The Aldrich score (AL) is based on the number of leads with ST-elevation for anterior MI and the sum of ST-segment elevation for inferior MI on the admission ECG. The van Hellemond score (VH) considers both the ischemic and infarcted component of the MaR by adding the AL and the QRS score, which is an estimate of final infarct size. The Hasche score is based on the maximal possible infarct size determined from the QRS score on the baseline ECG. Results: Ninety-eight patients (85% male, mean age 61. years) met STEMI criteria on their admission ECG and underwent CMR within 3-5. days after STEMI. Mean MaR by CMR was 41.2. ±. 10.2 and 30.3. ±. 7.2 for anterior and inferior infarcts, respectively. For both anterior and inferior infarcts the Aldrich (18.2. ±. 5.1 and 18.6. ±. 6.0) and Hasche (25.3. ±. 9.8 and 26.4. ±. 8.8) scores significantly underestimated MaR compared to MaR measured by CMR. In contrast, MaR by the van Hellemond score (37.0. ±. 14.2 and 31.7. ±. 12.8) was comparable to CMR. Conclusion: We tested the performance of the electrocardiographic estimation of myocardium area at risk by Aldrich, Hasche and van Hellemond ECG scores in comparison to MaR measured by CMR in STEMI patients. MaR by the van Hellemond score and CMR were comparable, while Aldrich and Hasche underestimated MaR.

BACKGROUND: The acuteness score (based on the modified Anderson-Wilkins score) estimates the acuteness of ischemia based on ST-segment, Q-wave and T-wave measurements obtained from the electrocardiogram (ECG) in patients with ST Elevation Myocardial Infarction (STEMI). The score (range 1 (least acute) to 4 (most acute)) identifies patients with substantial myocardial salvage potential regardless of patient reported symptom duration. However, due to the complexity of the score, it is not used in clinical practice. Therefore, we aimed to develop a reliable algorithm that automatically computes the acuteness score.METHODS: We scored 50 pre-hospital ECGs from STEMI patients, manually and by the automated algorithm. We assessed the reliability test between the manual and automated algorithm by interclass correlation coefficient (ICC) and Bland-Altman plot.RESULTS: The ICC was 0.84 (95% CI 0.72-0.91), PCONCLUSION: In conclusion, we have developed an automated algorithm for measurement of the modified Anderson-Wilkins ECG acuteness score from the pre-hospital ECG in STEMI patients. This automated algorithm is highly reliable, can be applied in daily practice for research purposes and may be implemented in commercial automated ECG analysis programs to achieve practical use for decision support in the acute phase of STEMI.

Background Pathological Q-wave (QW) in the electrocardiogram (ECG) before primary percutaneous coronary intervention (primary PCI) is a strong prognostic marker in patients with ST-segment elevation myocardial infarction (STEMI). However, current binary QW criteria are either not clinically applicable or have a lack of diagnostic performance. Accordingly, we evaluated the association between duration, depth and area of QW and markers of the effect of reperfusion (reperfusion success). Methods A total of 516 patients with their first STEMI had obtained an ECG before primary PCI and an acute cardiac magnetic resonance imaging (CMR) at day 1 (interquartile range [IQR], 1–1) and at follow-up at day 92 (IQR, 89–96). The largest measurable QW in ECG was used for analysis of duration, depth and area of QW (QW morphology). The QW morphology was evaluated as a continuous variable in linear regression models and as a variable divided in four equally large groups. Results The QW morphology as four equally large groups was significantly associated with all CMR endpoints (p ≤ 0.001) and showed a linear relationship (p ≤ 0.001) with final infarct size (for QW duration, β = 0.47; QW depth, β = 0.41 and QW area, β = 0.39), final infarct transmurality (for QW duration, β = 0.36; QW depth, β = 0.26 and QW area, β = 0.23) and final myocardial salvage index (for QW duration, β = −0.34; QW depth, β = −0.26 and QW area, β = −0.24). Conclusion Although modest, the QW morphology in STEMI patients showed significant linear association with markers of reperfusion success. Hence, it is suggested that the term pathological is not used as a dichotomous parameter in patients with STEMI but rather evaluated on the basis of extent.

Objectives System delay (time from first medical contact to primary percutaneous coronary intervention) is associated with heart failure and mortality in patients with ST segment elevation myocardial infarction (STEMI). We evaluated the impact of system delay on left ventricular function (LVF) according to the combination of ischemia severity (Sclarovsky–Birnbaum grades) and acuteness (Anderson–Wilkins scores) in the pre-hospital electrocardiogram (ECG). Methods In a predefined secondary analysis of a prospective study, the severity and acuteness scores were performed on the pre-hospital ECG. Patients were assessed with respect to 4 classifications which were not mutually exclusive: severe ischemia (+ SI) or non-severe ischemia (− SI) and acute ischemia (+ AI) or non-acute ischemia (− AI). LVF was assessed by global longitudinal strain (GLS) within 48 hours of admission. Adjusted linear regression investigated the association of system delay with GLS in each group. Results In total 262 patients were eligible for analysis of the ECG, which resulted in 42 (16%) with (+ SI, − AI), 110 (42%) with (− SI, − AI), 90 (34%) with (− SI, + AI), and 20 (8%) patients with (+ SI, + AI). Although system delay did not differ between groups, patients with severe and non-acute ischemia had the most impaired LVF. System delay correlated weakly with GLS in the entire population (r = 0.133, p = 0.031), and well with GLS in the (+ SI, + AI) group (r = 0.456, p = 0.04), while there was no correlation in the other groups. By adjusted analysis, system delay predicted impaired GLS only in the (+ SI, + AI) group (β = 0.578, p = 0.002). Conclusion Pre-hospital risk stratification by ECG identifies patients with acute and severe ischemia who are at increased risk for reduced ventricular function (assessed by GLS) after STEMI. Optimizing reperfusion delays in these patients can therefore be of particular benefit in improving clinical outcome after STEMI.

Background: Anterolateral myocardial infarction (MI) is traditionally defined on the electrocardiogram by ST-elevation (STE) in I, aVL, and the precordial leads. Traditional literature holds STE in lead aVL to be associated with occlusion proximal to the first diagonal branch of the left anterior descending coronary artery. However, concomitant ischemia of the inferior myocardium may theoretically lead to attenuation of STE in aVL. We compared segmental distribution of myocardial area at risk (MaR) in patients with and without STE in aVL. Methods: We identified patients in the MITOCARE study presenting with a first acute MI and new STE in two contiguous anterior leads from V1 to V6, with or without aVL STE. Patients underwent cardiac magnetic resonance imaging 3-5 days after acute infarction for quantitative assessment of MaR. Results: A total of 32 patients met inclusion criteria; 13 patients with and 19 without STE in lead aVL. MaR > 20% at the basal anterior segment was seen in 54% of patients with aVL STE, and 11% of those without (p = 0.011). MaR > 20% at the apical inferior segment was seen in 62% and 95% of patients with and without aVL STE, respectively (p = 0.029). The total MaR was not different between groups (44% ± 10% and 39% ± 8.3% respectively, p = 0.15). Conclusion: Patients with anterior STEMI and concomitant STE in aVL have less MaR in the apical inferior segment and more MaR in the basal anterior segment.

Background Terminal “QRS distortion” on the electrocardiogram (ECG) (based on Sclarovsky-Birnbaum's Grades of Ischemia Score) is a sign of severe ischemia, associated with adverse cardiovascular outcome in ST-segment elevation myocardial infarction (STEMI). In addition, ECG indices of the acuteness of ischemia (based on Anderson-Wilkins Acuteness Score) indicate myocardial salvage potential. We assessed whether severe ischemia with or without acute ischemia is predictive of infarct size (IS), myocardial salvage index (MSI) and left ventricular ejection fraction (LVEF) in anterior versus inferior infarct locations. Methods In STEMI patients, the severity and acuteness scores were obtained from the admission ECG. Based on the ECG patients were assigned with severe or non-severe ischemia and acute or non-acute ischemia. Cardiac magnetic resonance (CMR) was performed 2–6 days after primary percutaneous coronary intervention (pPCI). LVEF was measured by echocardiography 30 days after pPCI. Results ECG analysis of 85 patients with available CMR resulted in 20 (23%) cases with severe and non-acute ischemia, 43 (51%) with non-severe and non-acute ischemia, 17 (20%) with non-severe and acute ischemia, and 5 (6%) patients with severe and acute ischemia. In patients with anterior STEMI (n = 35), ECG measures of severity and acuteness of ischemia identified significant and stepwise differences in myocardial damage and function. Patients with severe and non-acute ischemia had the largest IS, smallest MSI and lowest LVEF. In contrast, no difference was observed in patients with inferior STEMI (n = 50). Conclusions The applicability of ECG indices of severity and acuteness of myocardial ischemia to estimate myocardial damage and salvage potential in STEMI patients treated with pPCI, is confined to anterior myocardial infarction.

BACKGROUND: Terminal QRS distortion on the electrocardiogram (ECG) is a sign of severe ischemia in patients with STEMI and can be quantified by the Sclarovsky-Birnbaum Severity of Ischemia. Due to score complexity, it has not been applied in clinical practice. Automatic scoring of digitally recorded ECGs could facilitate clinical application. We aimed to develop an automatic algorithm for the severity of ischemia.METHODS: Development set: 50 STEMI ECGs were manually (Manual-score) and automatically (Auto-score) scored by our designed algorithm. The agreement between Manual- and Auto-score was assessed by kappa statistics. Test set: ECGs from 199 STEMI patients were assigned a severity grade (severe or non-severe ischemia) by the Auto-score. Infarct size estimated by median peak Troponin T (TnT) and Creatinine Kinase Myocardial Band (CKMB) was tested between the groups.RESULTS: The agreement between Manual- and Auto-score was 0.83 ((95% CI 0.55-1.00), p CONCLUSION: The automatic ECG algorithm for severity of ischemia in STEMI performs adequately for clinical use. Severe ischemia obtained by the Auto-score was associated with biomarker estimated larger infarct size.

BACKGROUND: In traditional literature, it appears that "anteroseptal" MIs with Q waves in V1-V3 involve basal anteroseptal segments although studies have questioned this belief.METHODS: We studied patients with first acute anterior Q-wave (>30ms) MI. All underwent late gadolinium enhancement (LGE) cardiac magnetic resonance imaging (MRI).RESULTS: Those with Q waves in V1-V2 (n=7) evidenced LGE >50% in 0%, 43%, 43%, 57%, and 29% of the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. Patients with Q waves in V1-V3 (n=14), evidenced involvement was 14%, 43%, 43%, 50%, and 7% of the same respective segments. In those with extensive anterior Q waves (n=7), involvement was 0%, 71%, 57%, 86%, and 86%.CONCLUSIONS: Q-wave MI in V1-V2/V3 primarily involves mid- and apical anterior and anteroseptal segments rather than basal segments. Data do not support existence of isolated basal anteroseptal or septal infarction. "Anteroapical infarction" is a more appropriate term than "anteroseptal infarction."

BACKGROUND: Terminal "QRS distortion" on the electrocardiogram (ECG) (based on Sclarovsky-Birnbaum's Grades of Ischemia Score) is a sign of severe ischemia, associated with adverse cardiovascular outcome in ST-segment elevation myocardial infarction (STEMI). In addition, ECG indices of the acuteness of ischemia (based on Anderson-Wilkins Acuteness Score) indicate myocardial salvage potential. We assessed whether severe ischemia with or without acute ischemia is predictive of infarct size (IS), myocardial salvage index (MSI) and left ventricular ejection fraction (LVEF) in anterior versus inferior infarct locations.METHODS: In STEMI patients, the severity and acuteness scores were obtained from the admission ECG. Based on the ECG patients were assigned with severe or non-severe ischemia and acute or non-acute ischemia. Cardiac magnetic resonance (CMR) was performed 2-6days after primary percutaneous coronary intervention (pPCI). LVEF was measured by echocardiography 30days after pPCI.RESULTS: ECG analysis of 85 patients with available CMR resulted in 20 (23%) cases with severe and non-acute ischemia, 43 (51%) with non-severe and non-acute ischemia, 17 (20%) with non-severe and acute ischemia, and 5 (6%) patients with severe and acute ischemia. In patients with anterior STEMI (n=35), ECG measures of severity and acuteness of ischemia identified significant and stepwise differences in myocardial damage and function. Patients with severe and non-acute ischemia had the largest IS, smallest MSI and lowest LVEF. In contrast, no difference was observed in patients with inferior STEMI (n=50).CONCLUSIONS: The applicability of ECG indices of severity and acuteness of myocardial ischemia to estimate myocardial damage and salvage potential in STEMI patients treated with pPCI, is confined to anterior myocardial infarction.

Background Elevated levels of N-terminal pro brain natriuretic peptide (NT-proBNP) are associated with adverse cardiovascular outcome after ST elevation myocardial infarction (STEMI). We hypothesized that decreasing acuteness-score (based on the electrocardiographic score by Anderson-Wilkins acuteness score of myocardial ischemia) is associated with increasing NT-proBNP levels and the impact of decreasing acuteness-score on NT-proBNP levels is substantial in STEMI patients with severe ischemia. Methods In 186 STEMI patients treated with primary percutaneous coronary intervention (pPCI), the severity of ischemia (according to Sclarovsky-Birnbaum severity grades of ischemia) and the acuteness-score were obtained from prehospital ECG. Patients were classified according to the presence of severe ischemia or non-severe ischemia and acute ischemia or non-acute ischemia. Plasma NT-proBNP (pmol/L) was obtained after pPCI within 24 hours of admission and was correlated with the acuteness-score. Results NT-proBNP levels were median (25th–75th interquartile) 112 (51–219) pmol/L in patients with non-severe ischemia (71.5%) and 145 (79–339) in patients with severe ischemia (28.5%) (p = 0.074). NT-proBNP levels were highest in patients with severe and non-acute ischemia compared to those with severe and acute ischemia (182 (98–339) pmol/L vs 105 (28–324) pmol/L, p = 0.012). There was a negative correlation between acuteness-score and log(NT-proBNP) in patients with severe ischemia (r = 0.395, p = 0.003), which remained significant in multilinear regression analysis (β = −0.155, p = 0.007). No correlation was observed between the acuteness-score and log(NT-proBNP) in patients with non-severe ischemia (p = 0.529) or in the entire population (p = 0.187). Conclusion In STEMI patients with severe ischemia, neurohormonal activation is inversely associated with ECG patterns of acute myocardial ischemia.

A 69-year-old woman presented with arterial hypotension, pulmonary oedema and a severely depressed left ventricular ejection fraction (LVEF) of 25% only 3 days after having received her first treatment for colorectal cancer with 5-fluorouracil (5-FU)-based therapy. The ECG demonstrated widespread ST-segment depression and echocardiography showed uniform hypokinesia of all left ventricular (LV) myocardial segments without signs of regional LV ballooning. Coronary angiography was normal and the patient gained full recovery after receiving treatment with heart failure medication. Interestingly, cardiac MRI scan 9 days later showed a normal LVEF with signs of neither myocardial oedema nor necrosis. Despite the high therapeutic efficacy of 5-FU in treatment of colorectal cancer, it is associated with undesired cardiac toxicities including coronary spasms, toxic inflammation and takotsubo cardiomyopathy. However, our patient did not fulfil the diagnostic criteria for the aforementioned complications. Based on this case report, we discuss alternative mechanisms including myocardial adenosine triphosphate depletion suggested from animal experiments.

BACKGROUND: Primary percutaneous coronary intervention (pPCI) is recommended in patients with ST Elevation Myocardial Infarction (STEMI) and symptom duration 12hours (late-presenters). The Anderson-Wilkin's score (AW-score) estimates the acuteness of myocardial ischemia from the electrocardiogram (ECG) in STEMI patients. We hypothesized that the AW-score is superior to symptom duration in identifying substantial salvage potential in late-presenters.METHODS: The AW-score (range 1-4) was obtained from the pre-pPCI ECG in 55 late-presenters and symptoms 12-72 hours. Myocardial perfusion imaging was performed to assess area at risk before pPCI and after 30days to assess myocardial salvage index (MSI). We correlated both the AW-score and pain-to-balloon with MSI and determined the salvage potential (MSI) according to AW-score ≥3 (acute ischemia) and AW-score RESULTS: Late-presenters had median MSI 53% (inter quartile range (IQR) 27-89). The AW-score strongly correlated with MSI (β=0.60, R(2)=0.36, pmedian was observed in 79% in patients with AW-score ≥3 vs 32% in patients with AW-score CONCLUSION: AW-score was strongly associated with myocardial salvage while pain-to-balloon time was not. STEMI patients with symptom duration between 12 -72hours and AW-score ≥3 achieved substantial salvage after pPCI.

Anteroseptal myocardial infarction (MI) is traditionally defined on the electrocardiogram (ECG) by ST elevations (STE) in leads V1-V3, with or without involvement of lead V4. While existing pedagogy depicts such MIs as affecting the basal anteroseptal myocardial segment, there are reports that the

This review summarizes the electrocardiographic changes during an evolving ST segment elevation myocardial infarction and discusses associated electrocardiographic scores and the potential use of these indices in clinical practice, in particular the ECG scores developed by Anderson and Wilkins estimating the acuteness of myocardial ischemia and Sclarovsky-Birnbaum's grades of ischemia evaluating the severity of ongoing ischemia.

ventricle not only on the QRS complex, but also on the ST segment. In myocardial infarction a localized slowing of impulse propagation—the periinfarction block refers to an electrocardiographic abnormality caused by delayed activation of the myocardium in the affected region. In this study we simulated the effects of localized changes in impulse propagation on the QRS and ST-segment patterns, using computer modeling. Material and methods: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows to change the velocity of impulse propagation in the myocardium. The following changes were introduced in anteroseptal and posterolateral locations: intramural electrically inactive area (infarct), encircled by a transmural area with slowed impulse propagation velocity (peri-infarction block). The effects of sole infarct and peri-infarction blocks, as well the effects of their combinations on the QRS complex and the ST segment are presented. Results: A sole intramural infarct caused QRS changes typical for corresponding locations which were further considerably modified by slowed impulse propagation velocity in the surrounding area. Additionally, the areas of slowed impulse propagation velocity in both locations caused ST-segment deviations, shifting the ST segment toward the affected areas. Conclusion: Using computer modeling we showed that the localized slowing in impulse propagation (peri-infarction block) not only modified the QRS complex, but produced also changes in the ST segment that are consistent with changes that are usually interpreted as effect of the “injury current.”