Evolution Of Electrocardiogram Research Articles

Electrocardiogram evolution in Anderson-Fabry disease patients during follow-up

Abstract Background Anderson-Fabry disease (AFD) is a rare and progressive X-linked metabolic disorder caused by mutations in alfa galactosidase A gene, which leads to a pathologic, multiorgan, accumulation of ceramides with cytotoxic, proinflammatory and fibrotic effects. Cardiovascular involvement represents one of the main causes of death. Although ECG has proven to be useful for early AFD recognition, little evidence is available on the evolution of ECG alterations during follow-up. Purpose and Methods The aims of the study were to describe ECG changes during a long-term follow up, and to evaluate their association with the progression of cardiac involvement. The presence of interactions between ECG changes and specific AFD therapy (treatment status) were also evaluated. 219 AFD patients from a multicentre cohort underwent 12-lead ECG extensive analysis, transthoracic echocardiography, and complete clinical evaluation. Results After the exclusion of 3 patients with a permanent pacemaker, 5 with poor ECG quality, 2 with only one ECG, and 18 ≤18 years old, 181 AFD patients composed the final cohort (age 46 [IQR 35-58], 36% male, 67% classic phenotype). Treatment status (either enzyme replacement or chaperone molecules) was distributed as follows: chronic therapy for at least one year (24%), specific therapy started during the follow up (39%), no specific therapy (37%). During a median follow up of 62 months (IQR 33-83 months), several ECG parameters showed significant changes: atrial fibrillation detection (p<0.001), PQ interval (p=0.004), left atrial enlargement (p=0.001), a new right bundle branch block (RBBB, p<0.001), QRS interval (p<0.001) and QRS fragmentation (p=0.022), QTcB interval (p=0.001), and negative T waves development (p=0.001) mostly lateral and symmetric (p=0.016). Among these, PQ interval showed a significant interaction with treatment status being significantly altered only in patients in the chronic therapy and no specific therapy groups, being stable in patients who started the specific therapy during the follow up (p for interaction=0.048). In addition, PQ, QRS interval duration, a new RBBB, and a new pathologic QT interval were associated with the evolution of the echocardiographic maximal left ventricular (LV) wall thickness during the follow up on univariable analysis, with the QRS duration losing the statistical significance on multivariable analysis but still showing a trend (p=0.089) toward an association with an increased LV wall thickness. Conclusions In this multicentric cohort of AFD patients, different ECG parameters underwent significant changes during follow-up. Of these, PQ interval duration showed a significant interaction with the specific therapy status in that it did not increase in patients who started the therapy at the begin of the follow up. PQ interval, a new RBBB and pathologic QTc development were also significantly associated with the progression of LV hypertrophy on multivariable analysis.Table 1 and Table 2Figure 1

Evolution of surface and endocavitary signals in patients with arrhythmogenic cardiomyopathy at 1 and 5 years

Abstract Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): Small fee from Boston Scientific. Background The use of subcutaneous defibrillator (S-ICD) is a viable alternative to transvenous ICD in patients with Arrhythmogenic Cardiomyopathy (ACM). In transvenous ICD recipients low sensing values may exist at the time of implantation and a progressive decline of signal amplitude may occur later on due to the progressive myocardial fibrofatty replacement. Similarly to what happens at the intracavitary level, in patients with ACM there is a progressive modification of the surface ECG over time. Data on the impact of ECG evolution on S-ICD sensing are still lacking, particularly for different ACM phenotypes. Purpose This study aims to analyze the evolution of surface electrocardiogram (ECG), focusing on R-wave amplitude variation, and intracavitary electrograms (EGMs) in ACM different phenotypes during a 1-year and a 5 five-year follow-up. Methods This study is a retrospective analysis of the data of consecutive patients with ACM who were referred to our centre from January 1992 to October 2021. Using a dedicated software, the ECG analysis was performed in 7 leads: DI, DII, aVF (in view of the similar orientation with the three S-ICD vectors) and V1, V2, V3 and V5. Results We included 69 ACM patients: 28 patients (41%) had a right ventricular involvement (ARVC), 19 (27%) had a dominant LV involvement (ALVC) and 22 (32%) had biventricular involvement. 58 patients (84%) were ICD recipients; 45/58 patients (78%) had a transvenous ICD, and 13/58 (22%) had an S-ICD. During 5-year follow-up, in the whole ACM population, there were no significant changes in the amplitude of the R-wave, S-wave and T-wave. Phenotypic subgroups showed a different R-wave amplitude at baseline: biventricular ACM and ALVC patients had a lower R-wave amplitude in DII (p=0.04; p=0.05) and aVF (p=0.01; p=0.01) compared to ARVC patients. However, within each group, no difference was observed in R-wave amplitude at 1 and 5 years compared to baseline ECG (Figure 1). In the transvenous ICD recipients (45/69 patients) mean sensing decreased progressively over time (9,38 ± 4,24 mV at baseline, 7,70 ± 2,91 mV at 1 year, 1,85 ± 6,86 mV at 5 years). The reduction was not statistically significant at the first year of follow-up (p=0.239) but it reached significance at 5 years (p<0.001). Patients with biventricular ACM had lower sensing values at baseline than ARVC and ALVC (p<0,001). Sensing values in the biventricular patients did not decrease significantly during the 5-year follow-up (p=0.21), whereas in the ARVC and ALVC groups a reduction in sensing values was observed albeit not statistically significant in ALVC (p=0.01 in ARVC and p =0.06 in ALVC) (Figure2). Conclusions These data suggest that surface ECG may be more stable over time compared to EGM, therefore if a patient is suitable for S-ICD implantation S-ICD sensing may remain stable over time. Despite these findings, further studies are needed to support these hypotheses.

New characteristics in ECG induced by ultra-high altitude hypoxia

The partial pressure of oxygen decreases significantly with altitude elevation. Adaptive pathophysiological reactions and non-special electrocardiogram(ECG) changes are common in healthy individuals who are exposed to high altitude environments (greater than2500 m). However, previous literatures reported did not fully reflect the characteristics of the plateau ECG changes. A 27-year-old man living for more than 400 days at an ultra-high altitude (5400 m) presented with a rare but urgent ECG features including a right deviation of the electrical axis, pathological Q-wave, a poor increase of R-wave, and T-wave bidirectional/inversion. The erythrocytosis, pulmonary artery pressure, right heart overload and the reversible dynamic evolution of ECGs were gradually improved after he was rapidly transferred to the a low-altitude hospital. This study may provide a new feature of high-altitude induced ECG changes, indicate the potential mechanismand therapeutic value.

661 TWO CARDIOMYOPATHIES IN ONE HEART: LESSONS FROM CLINICAL CASE

Abstract Case description In November 2020, a 55-years-old female with no significant past medical history, was admitted to our Emergency Department for chest pain after acute stressful event. She had a significant family history of ischemic heart disease, and unclear comatose status of her sister. At admission, she was asymptomatic, blood pressure was 115/80 mmHg, and oxygen saturation was 96%. An electrocardiogram (ECG) showed biphasic T wave in anterolateral leads. Elevated levels of troponin I (hs-TnI of 900 ng/L) and B-type natriuretic peptide (BNP) of 864 pg/mL were detected. Transthoracic echocardiogram (TTE) revealed an ejection fraction (EF) of 30% with apical ballooning of mid and apical segments of the left ventricle (LV) along with a sizable apical thrombus. Aspirin, iv diuretics, iv nitrates and unfractioned heparin were started. After 13 hours, she suffered a sudden transient neurological sign of decreased level of consciousness. Cranial MRI revealed an ischemic lesion in the territory of the apex of basilar artery (thalamic region). After 7 days from stroke, the patients underwent coronary angiography demonstrating unobstructed coronaries. Thus, the diagnosis of takotsubo syndrome was confirmed. During hospitalization, ECG evolution showed T wave inversion in precordial and lateral leads. Hs-TnI declining within normal values. Of note, ventricular arrhythmias burden with polymorphic ventricular contraction (PVC) emerged on continuous ECG-monitoring. Despite resolution of apical balloning and apical thrombosis, there were persistent wall-motion abnormalities in infero-lateral walls and mild LV dysfunction. This was also confirmed by cardiac magnetic resonance (CMR). Further, CMR also showed an intense myocardial edema with elevated LV mass. The patients was discharged on Warfarin, Bisoprolol 2.5 mg/die, Ramipril 5 mg/die, Eplerenone 25 mg/die. A clinical documentation was required to further investigate history of her sister, and neurological sequelae after cardiac arrest at 28s related to ventricular fibrillation emerged. However, no deeply evaluation of underlining heart disease was available. Despite an early favorable follow-up of patient, after six months, she suffered from palpitations and heart failure requiring diuretic therapy. Persistent repolarization abnormalities in infero-lateral leads, and low-voltage in precordial leads were noted. An extensive wall-motion abnormalities and moderate LV dysfunction were detected. Importantly, significant arrhythmic burden with PVC (13%) at 24-hr ECG monitoring was recorded. CMR was requested to further investigate the possibility of underlining coexisting cardiomyopathy. Mild LV dilation, moderate dysfunction (LVEF 39%), wall motion abnormalities and thinning of the inferior wall middle segments were reported. Surprisingly, fibro-fatty replacement in infero-lateral of LV wall was detected, and unexpectedly, right ventricular (RV) fibro-fatty replacement and mild RV dysfunction were also described. Hence, diagnosis of arrhythmogenic cardiomyopathy was made. Since persistent arrhythmic burden despite optimized medical treatment, biventricular involvement, family history of SCD, an implantable cardioverter defibrillator in primary prevention was placed. Furthermore, genetic testing was required and extensive clinical family screening was suggested. Conclusion According to the clinical data collected, takotsubo and arrhytmogenic cardiomyopathy can coexist. A potential link between two myocardial heart disease may be identified in the future, especially among patients presenting takotsubo and long-term unfavorable outcome.

Electrocardiographic evolution in Anderson-Fabry disease patients on and off specific therapy: a potential marker to study the therapeutic cardiac goal

Abstract Background Anderson Fabry disease (AFD) is an X-linked lysosomal storage disorder leading to a deficiency in α-galactosidase A and globotriasylceramide (Gb3) deposition in different organs, including the heart. In AFD patients electrocardiogram (ECG) represents an important tool to detect cardiac involvement. AFD specific therapy (enzyme replacement or chaperon therapy) has shown to modify the natural history of the disease and to decrease Gb3 levels, but so far there are no data on its influence on ECG evolution. Purpose To assess the progression of ECG features in AFD patients on and off specific disease therapy and to evaluate the potential role of ECG in studying the cardiac specific response to therapy. Methods We recruited 170 patients with an established AFD diagnosis, ≥18 years old (64 males 38%, median age 46±15 years) in a multicentre study cohort. We analysed their ECG evolution for a median follow-up of 64±48 months in patients off (group A, N=63) and on (group B, N=107) specific therapy. Results AFD patients off specific disease therapy (group A) had similar age at baseline compared to those on therapy (47±14 vs 44±12 years; p=0,171), however significantly differed for males prevalence [13 (21%) vs 51 (48%); p≤0,001], classic phenotype [36 (57%) vs 82 (77%); p<0,001)] and maximal wall thickness [11±3 vs 13±4 mm; p≤0,0001]. As regards ECG features at baseline, group A showed a lower prevalence of repolarization anomalies [16 (25%) vs 51 (48%), p=0,005], left ventricular hypertrophy [14 (22%) vs 51 (48%), p=0,001], pseudo necrosis [4 (6%) vs 18 (17%) vs, p≤0,060] and short PR [2 (3%) vs 12 (11%), p=0.0845]. During the follow-up ECG progression was observed in 9 patients in group A (14%), characterized by the development of repolarization anomalies (N=5; 8%), incomplete right bundle block (N=4; 6%), shortening of PR interval (N=2; 3%), left ventricular hypertrophy (N=2; 3%), left atrial enlargement (N=2; 3%) and complete right bundle block (N=1; 2%). Differently, in group B an ECG evolution was observed in 31 patients (29%) characterized by the development of repolarization anomalies (N=19; 18%), left atrial enlargement (N=12; 12%), complete right bundle block (N=8; 8%), left anterior fascicular hemiblock (N=4; 4%), left bundle block (N=4, 4%) and left ventricular hypertrophy (N=3; 3%). Among patients off therapy we observed an improvement of ECG in 1 patient characterized by regression of repolarization anomalies, which could be explained with the presence of transient overload anomalies. Conclusion In AFD patients off and on specific disease therapy, ECG evolution was detected in 14% and 29% respectively, consistently with the more advanced cardiac involvement in patients on therapy (higher prevalence of male sex, classic phenotype and higher maximum wall thickness). The fact that one third of the patients showed ECG changes progression despite being on specific disease therapy could be relevant to better defined the therapeutic cardiac goal. Funding Acknowledgement Type of funding sources: None.

From a laboratory to the wearables: a review on history and evolution of electrocardiogram

The development of electrocardiography, one of the top scientific breakthroughs of the 20th century, occurred in the field of cardiology. The history of the ECG began long before its invention, with the advent of the study of electricity in the medical field. The idea of electrophysiology and Waller's initial recording of the ‘electrogram’ encouraged Willem Einthoven to develop new string galvanometers and turn this remarkable physiologic occurrence into a vital clinical recording tool. It has progressed from Einthoven's innovation to wearable technology. In the first part of the 20th century, a number of inventive people achieved a remarkable succession of discoveries and advancements that led to the development of the 12-lead ECG as we know it today. It went further than that. The evolution of science and technology over the years has allowed for continual development in terms of usefulness, ranging from five operators to one operator meant to record the ECG trace, and mobility, ranging from around 300 Kg to roughly around 1 Kg. Electrocardiographs in minimized form now exist thanks to the modern era of digitalization. We will go over the significant processes in the development of the ECG in this article.

Evolution of single-lead ECG for STEMI detection using a deep learning approach

BackgroundWhile ST-Elevation Myocardial Infarction (STEMI) door-to-balloon times are often below 90 min, symptom to door times remain long at 2.5-h, due at least in part to a delay in diagnosis. ObjectivesTo develop and validate a machine learning-guided algorithm which uses a single‑lead electrocardiogram (ECG) for STEMI detection to speed diagnosis. MethodsData was extracted from the Latin America Telemedicine Infarct Network (LATIN), a population-based Acute Myocardial Infarction (AMI) program that provides care to patients in Brazil, Colombia, Mexico, and Argentina through telemedicine. Sample: the first dataset was comprised of 8511 ECGs that were used for various machine learning experiments to test our Deep Learning approach for STEMI diagnosis. The second dataset of 2542 confirmed STEMI diagnosis EKG records, including specific ischemic heart wall information (anterior, inferior, and lateral), was derived from the previous dataset to test the STEMI localization model. Preprocessing: Detection of QRS complexes by wavelet system, segmentation of each EKG record into individual heartbeats with fixed window of 0.4 s to the left and 0.9 s to the right of main. Training & Testing: 90% and 10% of the total dataset, respectively, were used for both models. Classification: two 1-D convolutional neural networks were implemented, two classes were considered for first models (STEMI/Not-STEMI) and three classes for the second model (Anterior/Inferior/Lateral) each corresponding to the heart wall affected. These individual probabilities were aggregated to generate the final label for each model. ResultsThe single‑lead ECG strategy was able to provide an accuracy of 90.5% for STEMI detection with Lead V2, which also yielded the best results overall among individual leads. STEMI Localization model provided promising results for anterior and inferior wall STEMIs but remained suboptimal for Lateral STEMI. ConclusionsAn Artificial Intelligence-enhanced single‑lead ECG is a promising screening tool. This technology provides an autonomous and accurate STEMI diagnostic alternative that can be incorporated into wearable devices, potentially providing patients reliable means to seek treatment early and offers the potential to thereby improve STEMI outcomes in the long run.

Artificial Intelligence-Enabled ECG Algorithm Based on Improved Residual Network for Wearable ECG

Heart disease is the leading cause of death for men and women globally. The residual network (ResNet) evolution of electrocardiogram (ECG) technology has contributed to our understanding of cardiac physiology. We propose an artificial intelligence-enabled ECG algorithm based on an improved ResNet for a wearable ECG. The system hardware consists of a wearable ECG with conductive fabric electrodes, a wireless ECG acquisition module, a mobile terminal App, and a cloud diagnostic platform. The algorithm adopted in this study is based on an improved ResNet for the rapid classification of different types of arrhythmia. First, we visualize ECG data and convert one-dimensional ECG signals into two-dimensional images using Gramian angular fields. Then, we improve the ResNet-50 network model, add multistage shortcut branches to the network, and optimize the residual block. The ReLu activation function is replaced by a scaled exponential linear units (SELUs) activation function to improve the expression ability of the model. Finally, the images are input into the improved ResNet network for classification. The average recognition rate of this classification algorithm against seven types of arrhythmia signals (atrial fibrillation, atrial premature beat, ventricular premature beat, normal beat, ventricular tachycardia, atrial tachycardia, and sinus bradycardia) is 98.3%.

MYOCARDIAL INFARCTION WITH AN INITIALLY NORMAL ELECTROCARDIOGRAM

To analyze the paradox of acute myocardial infarction(AMI) with an initially normal electrocardiogram(ECG), we reviewed the records of 100 patients discharged with 21 final diagnosis of AM1 over a 1-year period. Twentyonepatient were identified whose initial ECG was normal andwho underwent coronary arteriography during the index hospitalization. According to the ECG evolution, three distinctgroups were identified: Group 1 : those who subsequently developedST elevation or Q waves (n = 7), Group 2: those whodeveloped ST depression or T-wave inversion (n = 8), andGroup 3:those whose ECG remained normal (n = 6). Trop-T positive, Peakcreatine kinase (CK), timing of the first ECG change, lifethreateningcomplications, and location of the infarct-relatedcoronary lesion were recorded. Infarct-related coronary lesionswere also classified into those in a major coronary trunkversus those in secondary branches. The incidence of AMI with a normal ECG was 3.7%. There was no difference in thefrequency of coronary artery involvement in the groups studied:left anterior descending (33%), right coronary artery(38%). and circumflex (28%). All ECG changes developedwithin the first 48 h of hospitalization; 17±15 h in Group 1, and24±12 h in Group 2. All six patients who had a persistentlynormal ECG (Group 3) had lesions in branch vessels (p <0.05 when compared with Group 1 plus Group 2). Patientswho developed ST elevation or Q waves (Group 1) alwayshad a major artery trunk involved (p <0.05 when comparedwith Group 2 plus Group 3). Patients in Group 3 had less myocardial damage and fewer complications compared with theother two groups. Myocardial infarction with an initial normalECG is uncommon and may result from involvement of any ofthe three coronary arteries. Electrocardiographic evolutionusually occurs within the first 48 h of hospitalization. Patientswhose ECGs remain normal appear to have culprit lesions incoronary branches, smaller infarctions, and fewer in-hospital complications.

P982 Correlation between electrocardiographic and imaging data in patients with acute myocarditis: a single centre retrospective analysis

Abstract Funding Acknowledgements None Background Acute myocarditis is a clinical and pathological condition defined as an inflammation of the myocardium. Its diagnosis is often challenging and requires multiple information derived from different diagnostic modalities. Purpose The aim of the study is to evaluate the correlation between electrocardiographic and imaging data in patients with acute myocarditis. Methods We made a retrospective analysis of 102 patients admitted to our Centre between January 2012 and April 2019 for suspected acute myocarditis. Diagnosis was confirmed with cardiac magnetic resonance (CMR) by identification of myocardial edema in T2-weighted images and/or typical subepicardial or midwall pattern of late gadolinium enhancement (LGE). Significant coronary artery disease was ruled out with coronary angiography. Electrocardiogram (ECG) was analysed on admission - in order to evaluate the presence of ST segment abnormalities, atrio-ventricular or bundle-branch block and heart rhythm disorders - and at the time of discharge. Every patient underwent echocardiography and CMR: from both these exams we reported the presence of regional wall motion abnormalities and left ventricular ejection fraction (LVEF). Results Mean age of our population was 39 ± 18 years; 92 people (90%) were males. At admission, 85 patients (83%) presented ECG abnormalities; the most frequent was ST-segment elevation (65 cases). Conduction or rhythm disorders were observed in 26 cases (25%). At the time of discharge, 41 out of 85 patients had complete regression of ECG changes. Mean value of LVEF measured with echocardiography was 56.4 ± 7.6%. In patients with normal ECG on admission it was 59.9 ± 3.1%, whereas in patients with abnormal ECG 55.7 ± 7.9% (p = 0.045). Considering CMR, mean LVEF in the population was 58.5 ± 8.6%, varying between 64.0 ± 8.9% in the group with normal ECG and 57.4 ± 10.1% in the group with ECG abnormalities (p = 0.02). Moreover, subjects with altered ECG on admission had a higher prevalence of wall motion abnormalities both in echocardiography (47/85 – 55% vs 3/17 – 18%, p < 0.01) and in CMR (45/85 – 53% vs 3/17 – 18%, p < 0.01). Patients with ECG normalization at discharge had a higher prevalence of ST-segment elevation (88 vs 66%, p = 0.02), while the group with persistent ECG alterations had a higher incidence of AV or bundle-branch block (23 vs 7%, p = 0.048). No statistical difference was noted between these two groups regarding echocardiographic or CMR values. Conclusion In our experience evaluation of ECG at admission in patients with suspected acute myocarditis identifies a subgroup of individuals with lower values of LVEF and a higher prevalence of wall motion abnormalities both in echocardiography and in CMR, while data derived by imaging techniques had no significant predictive value on ECG evolution at the time of discharge.

A New Algorithm to Diagnose Atrial Ectopic Origin from Multi Lead ECG Systems - Insights from 3D Virtual Human Atria and Torso

Rapid atrial arrhythmias such as atrial fibrillation (AF) predispose to ventricular arrhythmias, sudden cardiac death and stroke. Identifying the origin of atrial ectopic activity from the electrocardiogram (ECG) can help to diagnose the early onset of AF in a cost-effective manner. The complex and rapid atrial electrical activity during AF makes it difficult to obtain detailed information on atrial activation using the standard 12-lead ECG alone. Compared to conventional 12-lead ECG, more detailed ECG lead configurations may provide further information about spatio-temporal dynamics of the body surface potential (BSP) during atrial excitation. We apply a recently developed 3D human atrial model to simulate electrical activity during normal sinus rhythm and ectopic pacing. The atrial model is placed into a newly developed torso model which considers the presence of the lungs, liver and spinal cord. A boundary element method is used to compute the BSP resulting from atrial excitation. Elements of the torso mesh corresponding to the locations of the placement of the electrodes in the standard 12-lead and a more detailed 64-lead ECG configuration were selected. The ectopic focal activity was simulated at various origins across all the different regions of the atria. Simulated BSP maps during normal atrial excitation (i.e. sinoatrial node excitation) were compared to those observed experimentally (obtained from the 64-lead ECG system), showing a strong agreement between the evolution in time of the simulated and experimental data in the P-wave morphology of the ECG and dipole evolution. An algorithm to obtain the location of the stimulus from a 64-lead ECG system was developed. The algorithm presented had a success rate of 93%, meaning that it correctly identified the origin of atrial focus in 75/80 simulations, and involved a general approach relevant to any multi-lead ECG system. This represents a significant improvement over previously developed algorithms.

Electrocardiographic Findings in Takotsubo Cardiomyopathy: ECG Evolution and Its Difference from the ECG of Acute Coronary Syndrome

BACKGROUNDElectrocardiogram (ECG) manifestations of takotsubo cardiomyopathy (TC) produce ST-segment elevation or T-wave inversion, mimicking acute coronary syndrome (ACS). We describe the ECG manifestation of TC, including ECG evolution, and its different points from ACS.METHODSWe studied 37 consecutive patients (age 67 ± 15 years, range 23–89, M:F = 12:25) from March 2004 to November 2012 with a diagnosis of TC who were proven to have apical ballooning on echocardiography or left ventricular angiography and normal coronary artery. We analyzed their standard 12-lead ECGs, including rate, PR interval, QRS duration, corrected QT (QTc) interval, ECG evolutions, and arrhythmia events.RESULTSTwo common ECG findings in TC were ST-segment elevation (n = 13, 35%) and T inversion (n = 24, 65%), mostly in the precordial leads. After ST-segment resolution, in a few days (3.5 days), diffuse and often deep T-wave inversion developed. Eight patients (22%) had transient Q-waves lasting a few days in precordial leads. No reciprocal ST-segment depression was noted. T-wave inversion continued for several months. QT prolongation (<440 milliseconds) was observed in 37 patients (97%). There were no significant life-threatening arrhythmias except atrial fibrillation (n = 6, 16%).CONCLUSIONThere are distinct differences between the ECGs of TC and ACS. These differences will help to differentiate TC from ACS.

A brief review: history to understand fundamentals of electrocardiography

The last decade of the 19th century witnessed the rise of a new era in which physicians used technology along with classical history taking and physical examination for the diagnosis of heart disease. The introduction of chest x-rays and the electrocardiograph (electrocardiogram) provided objective information about the structure and function of the heart. In the first half of the 20th century, a number of innovative individuals set in motion a fascinating sequence of discoveries and inventions that led to the 12-lead electrocardiogram, as we know it now. Electrocardiography, nowadays, is an essential part of the initial evaluation for patients presenting with cardiac complaints. As a first line diagnostic tool, health care providers at different levels of training and expertise frequently find it imperative to interpret electrocardiograms. It is likely that an understanding of the electrical basis of electrocardiograms would reduce the likelihood of error. An understanding of the disorders behind electrocardiographic phenomena could reduce the need for memorizing what may seem to be an endless list of patterns. In this article, we will review the important steps in the evolution of electrocardiogram. As is the case in most human endeavors, an understanding of history enables one to deal effectively with the present.

The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction

Acute myocardial infarction (AMI) is a not uncommon diagnosis in the emergency department. During ST-segment elevation AMI (STEMI), the electrocardiogram (ECG) typically follows a progression of abnormality, beginning with hyperacute T waves and culminating with ST-segment elevation; pathologic Q waves can appear early and/or late in the process. Other findings include T-wave inversion and ST-segment depression which can occur before, during, or after the STEMI event. The evolution of ECG through these changes can occur rapidly after coronary artery occlusion. The emergency physician should be aware of the ECG findings that characterize the evolution of an STEMI with a sound understanding of the associated pathophysiology and clinical implication. This review discusses the changing ECG during an AMI. The pathogenesis of these findings is discussed. Finally, the clinical implications at each stage are reviewed.

Electrocardiogram mimics of acute ST-segment elevation myocardial infarction: insights from cardiac magnetic resonance imaging in patients with tako-tsubo (stress) cardiomyopathy

An important subset of patients (∼10%) with chest pain and ST-segment elevation on initial electrocardiogram (ECG) do not have acute coronary occlusion. In our experience, 5% of women presenting with chest pain and ST-segment elevation are proven to have the newly recognized syndrome of tako-tsubo (stress) cardiomyopathy (TC). Patients with TC present with clinical and electrocardiographic features mimicking ST-segment elevation anterior myocardial infarction due to left anterior descending (LAD) occlusion. The initial and subsequent ECG findings in TC are therefore of clinical importance. Thirty-three consecutive patients with TC were identified from within a single institution community-based cardiology practice. All were female aged 32 to 90 years (mean, 68 years) with acute chest pain associated with an emotional or physical stressful event, and akinesia of the mid-distal left ventricle but without significant atherosclerotic coronary artery obstruction. All patients with TC presented with anterior ST-segment elevation most marked in leads V 1 to V 5, maximal in leads V 2 and V 3. Distribution of ST-segment elevation was similar to 44 female control patients with acute (LAD) occlusion. ST-segment elevation magnitude was less in patients with TC (1.4 ± 1.5 mm) than in patients with LAD occlusion (2.4 ± 2.2 mm) ( P < .001) but with considerable overlap. Left ventricular ejection fraction (LVEF) was significantly lower in TC patients (29% ± 9%) than in patients with LAD occlusion (42% ± 13%) ( P < .05). Peak troponin T was significantly lower in patients with TC (0.64 ± 0.86 ng/mL) than in patients with LAD occlusion (3.88 ± 4.9 ng/mL) ( P < .0001). Cardiovascular magnetic resonance imaging detected myocardial necrosis in 1 patient with TC. At follow-up, LVEF returned to normal (> 50%) in all patients with TC. In patients with TC, ECG evolution was characterized by resolution of ST-segment elevation, appearance of T-wave inversion (most marked in precordial leads V 3-V 6 and limb leads aVL, I, and −aVR), QTc interval prolongation (378 ± 60 milliseconds [initial] vs 470 ± 72 milliseconds [follow-up], P < .05), and reappearance of precordial R waves. In conclusion, patients with TC frequently present with anterior ST-segment elevation, which cannot be reliably distinguished from that of acute LAD occlusion. In TC, the combination of minimal troponin release, absent delayed hyperenhancement on cardiac magnetic resonance imaging (in most of patients), and return to normal LVEF is consistent with the presence of significant myocardial stunning. The ECG evolution of progressive T-wave inversion, QTc interval lengthening, and R-wave reappearance could be the electrophysiologic manifestation of an underlying stunned myocardium in this condition.

Myocardial infarction with an initially normal electrocardiogram--angiographic findings.

To analyze the paradox of acute myocardial infarction (AMI) with an initially normal electrocardiogram (ECG), we reviewed the records of 732 patients discharged with a final diagnosis of AMI over a 2-year period. Twenty-one patient were identified whose initial ECG was normal and who underwent coronary arteriography during the index hospitalization. According to the ECG evolution, three distinct groups were identified: Group 1: those who subsequently developed ST elevation or Q waves (n = 7), Group 2: those who developed ST depression or T-wave inversion (n = 8), and Group 3: those whose ECG remained normal ( n = 6). Peak creatine kinase (CK), timing of the first ECG change, life-threatening complications, and location of the infarct-related coronary lesion were recorded. Infarct-related coronary lesions were also classified into those in a major coronary trunk versus those in secondary branches. The incidence of AMI with a normal ECG was 3.7%. There was no difference in the frequency of coronary artery involvement in the groups studied: left anterior descending (33%), right coronary artery (38%), and circumflex (28%). All ECG changes developed within the first 48 h of hospitalization; 17 +/- 15 in Group 1, and 24 +/- 12 h in Group 2. All six patients who had a persistently normal ECG (Group 3) had lesions in branch vessels (p < 0.05 when compared with Group 1 plus Group 2). Patients who developed ST elevation or Q waves (Group 1) always had a major artery trunk involved (p < 0.05 when compared with Group 2 plus Group 3). Patients in Group 3 had less myocardial damage and fewer complications compared with the other two groups. Myocardial infarction with an initial normal ECG is uncommon and may result from involvement of any of the three coronary arteries. Electrocardiographic evolution usually occurs within the first 48 h of hospitalization. Patients whose ECGs remain normal appear to have culprit lesions in coronary branches, smaller infarctions, and fewer in-hospital complications.