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Background Severe electrocardiographic (ECG) abnormalities in asymptomatic subjects correlate with cardiovascular risk. Hypothesis The role of minor ECG abnormalities is less well‐known. We evaluated the association between a negative T‐wave and mortality, as a possible marker for prognosis. Methods A prospective, population‐based cohort, examined at 50 years, and followed until death. Time to death (event rates) and predictive role of a negative T‐wave (Cox regression) were analyzed. Results Participants (n = 839) with a negative T‐wave (7.3%) had significantly higher blood pressure (BP) (mean systolic 157.9 mmHg vs 136.8 mmHg without negative T‐wave, P =

Hypertrophic cardiomyopathy is one of the main causes of sudden cardiac death in young athletes. Differentiating between this pathological condition and ‘athlete's heart’ can be quite challenging, warranting a thorough clinical and imaging assessment. Clinicians often rely on detraining-induced attenuation of electrocardiographic and echocardiographic findings as a means of distinguishing between pathological and physiological cardiac remodeling. This report describes detraining-related regression of left ventricular hypertrophy in a young soccer player with a diagnosis of hypertrophic cardiomyopathy. It challenges the dogma that regression of electrocardiographic abnormalities and left ventricular hypertrophy is exclusive to physiological remodeling and questions the impact of exercise training in the phenotypic expression and progression of hypertrophic cardiomyopathy. Resumo: A miocardiopatia hipertrófica é uma das principais causas de morte súbita de origem cardíaca em jovens atletas. Distinguir entre esta patologia e o “coração de atleta” pode ser difícil, exigindo uma avaliação clínica e imagiológica exaustiva. Frequentemente recorre-se à atenuação dos achados eletrocardiográficos e ecocardiográficos induzidos pela pausa desportiva como forma de distinguir entre remodelagem fisiológica e patológica. Neste caso clínico descrevemos a regressão da hipertrofia ventricular esquerda induzida pela pausa desportiva num jovem futebolista com o diagnóstico de miocardiopatia hipertrófica. Este caso põe em causa o dogma de que a regressão das alterações eletrocardiográficas e a da hipertrofia ventricular esquerda é exclusiva da remodelação fisiológica e, simultaneamente, levanta dúvidas sobre a influência do treino físico na evolução e expressão fenotípica da miocardiopatia hipertrófica.

One of the rare causes of diffuse T-wave inversion (TWI) in electrocardiogram (ECG) is memory T-waves. This should be considered among the differentials of diffuse TWI in ECG of patients presenting to the emergency department (ED), especially when they have previous episodes of ventricular tachycardia (VT) or pacemaker implantation or Wolff-Parkinson-White syndrome. These TWIs are benign and do not require any treatment. However, it is of paramount importance for the emergency physician to differentiate it from ischemia-related T-wave changes. In the following case series, we report three cases of memory T-waves. Two of the cases had TWI in leads II, III, aVF, and V3 to V6 following reversion of VT. The other patient, with a? VVI (Left ventricle paced, Left ventricle sensed, Inhibition to sensing) pacemaker, had memory T-waves in the ECG taken during normal sinus rhythm. In all the three patients, we considered memory T-waves to be the possible cause of TWI. The electrocardiographic diagnostic criteria for memory T-waves are positive T in lead aVL and positive/isoelectric T in the lead I; and precordial TWI >inferior TWI. These criteria are 92% sensitive and 100% specific. In the following case series, we also provide an algorithmic approach for patients with suspected memory T-waves in their 12-lead ECG when they present to the ED.

Coronavirus disease-2019 (COVID-19) causes severe illness and multi-organ dysfunction. An abnormal electrocardiogram is associated with poor outcome, and QT prolongation during the illness has been linked to pharmacological effects. This study sought to investigate the effects of the COVID-19 illness on the corrected QT interval (QTc).For 293 consecutive patients admitted to our hospital via the emergency department for COVID-19 between 01/03/20 -18/05/20, demographic data, laboratory findings, admission electrocardiograph and clinical observations were compared in those who survived and those who died within 6 weeks. Hospital records were reviewed for prior electrocardiograms for comparison with those recorded on presentation with COVID-19.Patients who died were older than survivors (82 vs 69.8 years, p 0.001), more likely to have cancer (22.3% vs 13.1%, p = 0.034), dementia (25.6% vs 10.7%, p = 0.034) and ischemic heart disease (27.8% vs 10.7%, p 0.001). Deceased patients exhibited higher levels of C-reactive protein (244.6 mg/L vs 146.5 mg/L, p 0.01), troponin (1982.4 ng/L vs 413.4 ng/L, p = 0.017), with a significantly longer QTc interval (461.1 ms vs 449.3 ms, p = 0.007). Pre-COVID electrocardiograms were located for 172 patients; the QTc recorded on presentation with COVID-19 was longer than the prior measurement in both groups, but was more prolonged in the deceased group (448.4 ms vs 472.9 ms, pre-COVID vs COVID, p 0.01). Multivariate Cox-regression analysis revealed age, C-reactive protein and prolonged QTc of 455 ms (males) and 465 ms (females) (p = 0.028, HR 1.49 [1.04-2.13]), as predictors of mortality. QTc prolongation beyond these dichotomy limits was associated with increased mortality risk (p = 0.0027, HR 1.78 [1.2-2.6]).QTc prolongation occurs in COVID-19 illness and is associated with poor outcome.

T-wave inversion in ECG is very frequent and concerning finding as it is often associated with life-threatening conditions. There are numerous conditions mentioned in the literature for transient T-wave inversion such as acute coronary syndrome, cardiac memory T-wave, subarachnoid hemorrhage, electroconvulsive therapy, hyperventilation and indeterminate origin. Hyperventilation is already known as a cause of transient T-wave inversion; however, it is often forgotten in modern clinical settings. A 33-year-old doctor working in the same hospital reported to the emergency department during working hours with a history of acute onset breathing difficulties and atypical chest pain involving the retrosternal region. Arterial blood gas analysis (ABG) findings of respiratory alkalosis with transient T-wave inversion, which normalized soon after normal breathing and reassurance along with normal cardiac workup helped us to reach the correct diagnosis of hyperventilation syndrome.

Precordial lead T‐wave inversion subsequent to early repolarization is thought to be a normal variant in African athletes and that additional testing is unnecessary. With the increasing number of foreign people living in and traveling to Asian countries, it is becoming crucial for Asian physicians to comprehend the abnormal ECG change in African athletes.

OBJECTIVES: This study sought to compare electrocardiogram (ECG) variants in athletic and arrhythmogenic right ventricular cardiomyopathy (ARVC) cohorts matched for the confounders of age, sex, and ethnicity.BACKGROUND: Anterior T-wave inversion (TWIV1-V4) is a common electrocardiographic finding in both athletes and patients with ARVC, and is a frequent conundrum in the setting of pre-participation screening. J-point elevation (JPE) has been proposed as an accurate means of identifying athletes, whereas disease markers, including premature ventricular contractions (PVCs) and low-voltage signals, have been associated with ARVC.METHODS: This study examined 200 subjects with TWI V1-V4, including 100 healthy athletes and 100 ARVC patients matched 1:1 for age, sex, and ethnicity (age: 21 ± 5 years for athletes vs. 22 ± 5 years for ARVC patients; 47% male; 97% Caucasian). The presence of TWI, JPE, PVCs, and left ventricular hypertrophy (LVH) were assessed.RESULTS: JPE was observed in 27% of athletes versus 16% of ARVC patients (p = 0.09). Thus, JPE had poor specificity (27%) and accuracy (60%) in identifying healthy athletes. In contrast, ARVC patients demonstrated a greater prevalence of precordial TWI beyond lead V3 (34% vs. 8%; p < 0.001), inferior TWI (31% vs. 3%; p < 0.001), PVCs (18% vs. 0%; p < 0.001), and lower LVH scores (SV1 + RV5; 19 ± 1 mm vs. 30 ± 1 mm; p < 0.001). These combined factors provided more reliable differentiation between health and disease (specificity 82%, accuracy 81%).CONCLUSIONS: PVCs and low QRS voltages are more prevalent among ARVC patients than athletes, whereas JPE is a relatively poor discriminator of health and disease when the confounders of age, sex, and ethnicity are considered.

Key Clinical Message Electrocardiographic (ECG) changes occurring several hours after the onset of acute cardiogenic pulmonary edema have been seldom described. The proposed explanatory mechanisms are various and not fairly established. In the absence of significant coronary artery disease, these ECG abnormalities could be attributed to mechanisms implicated in coronary microcirculatory dysfunction.

Background Hypertrophic cardiomyopathy is one of the most common causes of sudden cardiac death in young athletes. Performing, comparing, and monitoring serial electrocardiograms over time can help to detect potential cardiovascular diseases and to prevent malignant cardiac events in these populations. Case presentation A young Han Chinese male football player had abnormal electrocardiograms for 8 years without any subjective discomfort. Electrocardiograms revealed that T-wave inversions increased from 1 mm to a maximum of 5 mm on lead I and fluctuated around 5 mm on lead avL. Q-wave duration ranged from 40 ms to 60 ms, its depth increased to a maximum of 8 mm and was much greater than 40% of the R waves in depth in II, III, and avF leads. Echocardiography showed increasingly thickened interventricular septum from 10 mm to 13 mm, enlarged left atrium and ventricle, and reduced left ventricular ejection fraction. Coronary angiography showed no distinct stenosis. Emission computed tomography revealed mild myocardial ischemia of the left ventricular inferior wall. These unusual electrocardiogram manifestations were initially regarded as benign alterations of a highly trained athlete. Upon reviewing the clinical information and the newest criteria for electrocardiographic interpretation in athletes, hypertrophic cardiomyopathy was identified. The misreading of electrocardiograms is not uncommon, thus predisposing such patients to high susceptibility to exercise-induced sudden cardiac death. Conclusions We propose that abnormal electrocardiogram findings reveal the initial expression of underlying cardiac diseases such as hypertrophic cardiomyopathy, preceding the symptoms and signs by many years. Accordingly, early detection and continuous surveillance are important for athletes with such electrocardiogram patterns, and improvement of physicians’ expertise is crucial.

Background: ST segment depression (STD) and T wave inversion (TWI) are typical electrocardiographic (ECG) findings in non-ST elevation myocardial infarction (NSTEMI). In ST elevation myocardial infarction, ST changes represent transmural ischemia. The pathophysiological mechanisms of the ECG changes in NSTEMI are unclear. Purpose: We studied the associations between ECG and the echocardiographic findings in NSTEMI patients. Methods: Twenty patients with acute NSTEMI were recruited during their hospital stay. A comprehensive echocardiography study was performed. The findings were compared with blinded ECG analyses. Results: Nine (45%) patients had STD, and 16 (85%) patients had TWI. In multivariable analysis, STD was independently associated with a lower global early diastolic strain rate (beta=-5.061, p=0.033). TWI was independently associated with lower circumferential strain (beta=0.132, p =0.032). Conclusions: The typical ECG changes in NSTEMI patients were associated with subtle echocardiographic changes. STD was related to changes in diastolic function, and TWI was associated with systolic deterioration. (C) 2017 Elsevier Inc. All rights reserved.

Non-ST-elevation acute coronary syndrome frequently presents with negative T-wave inversion. In acute pulmonary embolism precordial T-wave inversion occurs due to right ventricular strain. We herein report a case of a 48-year-old woman presenting with syncope secondary to massive main pulmonary artery embolism which was initially diagnosed as acute coronary syndrome due to negative anterior T-wave inversion and raised troponin. In addition, her room air saturation was normal and electrocardiogram showed T-wave inversion in inferior wall leads as well. We present this case of massive pulmonary embolism with varied presentation which was initially misdiagnosed as acute coronary syndrome.

Background Both Q waves and T-wave inversion (TWI) in the presenting ECG are associated with a progressed stage of myocardial infarction, possibly with less potential for myocardial salvage with reperfusion therapy. Combining the diagnostic information from the Q- and T-wave analyses could improve the prognostic work-up in ST-elevation myocardial infarction (STEMI) patients. Methods We sought to determine the prognostic impact of Q waves and TWI in the admission ECG on patient outcome in STEMI. We formed four groups according to the presence of Q waves and/or TWI (Q+TWI+; Q-TWI+; Q+TWI-; Q-TWI-). We studied 627 all-comers with STEMI derived from two patient cohorts. Results The patients with Q+TWI+ had the highest and those with Q-TWI- the lowest 30-day and one-year mortality. One-year mortality was similar between Q-TWI+ and Q+TWI-. The survival analysis showed higher early mortality in Q+TWI- but the higher late mortality in Q-TWI+ compensated for the difference at 1 year. The highest peak troponin level was found in the patients with Q+TWI-. Conclusion Q waves and TWI predict adverse outcome, especially if both ECG features are present. Q waves and TWI predict similar one-year mortality. Extending the ECG analysis in STEMI patients to include both Q waves and TWI improves risk stratification.