Elevation In V1 Research Articles

Workup for Suspected Brugada Syndrome: Two Case Reports for the General Practitioner

While a large proportion of ST-segment elevation on EKG is related to myocardial ischemia, the differential diagnosis must include pericarditis, channelopathies, and various genetic conditions. Identifying and working up such abnormalities present a challenge to primary care providers (PCPs). We present two clinical cases of young male patients with ST-segment elevation in anteroseptal leads suspicious for Brugada syndrome and show how to risk stratify and manage them.Our first case presents a 23-year-old male with no past medical history with acute onset substernal chest pain, shortness of breath, and palpitations. Initial workup revealed negative serial troponins and normal B-type natriuretic peptide (BNP). The EKG revealed ST elevation in lead V2. An evaluation for Brugada syndrome was pursued. Upon completion of a procainamide challenge, it was determined that he did not have Brugada syndrome and was shortly discharged.Our second case presents a 33-year-old male with no pertinent cardiac medical history who presented to an outpatient cardiology clinic after discovering an incidental ST elevation in V2 on EKG. His family history was negative for early atherosclerotic cardiovascular events or sudden cardiac death. The patient’s initial workup was negative. Suspicion for Brugada syndrome leads to performing a procainamide challenge, which was significant for ST changes in the anterolateral leads. He was asymptomatic during the challenge and initial presentation, and no further intervention was indicated. He was advised to avoid sodium channel blocking medications and treat any fevers and was sent for genetic testing.These cases illustrate the importance of maintaining an appropriate suspicion for Brugada syndrome in young patients with minimal ischemic risk factors. We discuss a guideline-directed algorithmic workup for PCPs in suspicious individuals. Stratifying patients based on the presence of symptoms, history of tachyarrhythmias, and EKG findings before and after drug challenge allows physicians to guide further management of these patients.

Differentiating typical tako tsubo syndrome from extensive anterior ST-elevation myocardial infarction: look behind the anterior wall

Abstract Funding Acknowledgements Type of funding sources: None. Tako-Tsubo Syndrome (TTS) consists in transient left ventricular dysfunction resembling in its typical form acute anterior ST-elevation myocardial infarction (STEMI). Early non-invasive differential diagnosis, crucial for therapeutic purposes, appears difficult according to available data. Purpose to systematically analyze LV function and ECG changes in patients with acute anterior STEMI and TTS, to identify parameters possibly useful for differential diagnosis. Methods this is a retrospective cohort study, with 2 groups: patients with anterior STEMI and extensive apical involvement at echocardiography (n = 22); patients with TTS (n = 22) and ECG changes diagnostic for anterior STEMI at presentation (n = 22). They underwent a comprehensive clinical and echocardiographic evaluation in acute phase, including 2D speckle tracking longitudinal strain. We created new indexes based on wall motion impairment of inferior and inferior-lateral walls: the Inferior apex ratio (IAR) and inferior-lateral apex ratio (ILAR) (see picture). Results TTS and STEMI patients were similar for age (74.7 ± 9.1 vs 73.4 ± 14.1 y), sex, and main biochemical data except for higher peak troponin I in STEMI (1323 ± 622 vs 377 ± 220 ng/L, p = 0.01). ST segment elevation in V1 (V1e) was significantly less common in TTS (p < 0.001) while increased ratio of ST segment elevation in V4-V6 to V1-V3 (∑Ste V4-V6/∑Ste V1-V3≥1) was more common in TTS (p < 0.001). Among ECG parameters, absence of V1e had the best sensitivity (86%) and specificity (86%) in predicting TTS. LVEF values were similar (means: 45% in both groups) with EDVI greater in TTS (55.5 ±12.3 vs 46.6 ± 11.0 ml/m2, p = 0.02). WMSI was greater in TTS patients (2.2 ± 0.1 vs 1.9 ± 0.1, p < 0.0001), mainly for greater scores of mid segments. Global longitudinal strain was impaired in TTS (-8.1 ± 2.5 %) and in anterior STEMI (-7.9 ± 2.7, p = 0.8). By analyzing the single segments, strain was significantly more compromised in TTS in mid inferior (MI) (-4.3 ± 6.4 vs -9.9 ± 5.5 % in STEMI, p = 0.003) and mid inferior-lateral (MIL) segments (-5.4 ± 5.4 vs -9.6 ± 4.9 %, p = 0.009). Mean IAR was 0.7 ± 0.3 in TTS vs 1.8 ± 0.6 in STEMI, p < 0.0001; mean ILAR was 0.7 ± 0.1 in TTS vs 2.0 ± 0.9 in STEMI, p < 0.0001. ILAR was < I in all TTS patients, and > 1 in all STEMI cases. IAR < 1 showed 90% sensitivity and 95% specificity in predicting TTS. By multivariate linear regression analysis, strain values of MI and MIL segments were significantly associated with TTS (Beta: -0.98 and -0.97 respectively, p < 0.0001), independently from age, sex, and EDVI. IAR and ILAR values were significantly associated with TTS (Beta: -0.81 and -0.76 respectively, p < 0.0001) independently from the same co-variates as above. Conclusions evidence of impaired contractility extending beyond apex to mid inferior and inferior-lateral walls, assed by longitudinal strain or by IAR and ILAR, can help to discriminate TTS from extensive anterior STEMI, more accurately than ECG parameters. Abstract Figure. Examples of ILAR index Abstract Figure. IAR and ILAR distributions

ST-Segment Elevation Mimicking STEMI Due to Hypercalcemia: A Case Report

ST-segment elevation myocardial infarction (STEMI) is an important, life-threatening diagnosis that requires quick diagnosis and treatment, characteristic ECG of which shows ST-segment elevation. Unfortunately, ST-segment elevation is nonspecific, which can be misleading if not careful to be interpreted, as in this case of hypercalcemia seen by us. A 48-year-old male was admitted to our emergency department with recurrent chest pain, nausea and vomiting. Medical history includes hypertension and diabetes. ST-segment elevation in V1 - V4 mimicking STEMI was present on admission. However, immediate coronary angiography revealed nearly normal coronary arteries, his troponin was negative in 6 hours and calcium was 2.95 mmol/L. It was thought that the ECG changes were not indicative of cardiac ischemia but hypercalcemia. He was managed with calcium reduction treatment such as intravenous normal saline and furosemide, with subsequent resolution of ST-segment changes.

Posterior reversible encephalopathy syndrome in spotted fever group of rickettsial infection with brugada syndrome

Rickettsioses are one of the common causes of undifferentiated febrile illness. Patients present commonly with fever, rash, and eschar. Posterior Reversible Encephalopathy Syndrome (PRES) also known as reversible posterior encephalopathy syndrome is a rare condition, in which parts of the brain are affected by swelling as a result of an underlying cause such as infection. However, PRES caused by spotted fever group of rickettsiosis is rarely reported. We are here with reporting such a case. A 55-year-old male was admitted to MVJ Medical College and Research Hospital, Bengaluru, with complaints of fever for 3 days and one episode of Generalized Tonic Clonic Seizures (GTCS) following which he was in altered sensorium. On examination, there was hepatosplenomegaly. Weil-Felix OX19 and OX2 were 1:320. Lumbar puncture was done which showed 15 cells 98% lymphocytes and 2% neutrophils, proteins-119 mg/dl, and sugar- 153 mg/dl. Magnetic resonance imaging of the brain showed bilateral symmetric hyperintensities on T2-weighted imaging in the parietal and occipital lobes. The calcarine and occipital lobes were spared suggestive of posterior reversible encephalopathy syndrome. Electrocardiogram showed ST elevation in V1 and V2 along with T-wave inversion (Brugada sign). Posterior reversible encephalopathy syndrome is usually commonly seen in hypertensive encephalopathy and in infections such as dengue and few cases of scrub typhus. This is one of the rare cases where spotted fever group of rickettsia has caused posterior reversible encephalopathy syndrome and Brugada syndrome.

Clinical presentation and electrocardiographic features of Brugada syndrome in Iraq

Background: Brugada syndrome is a clinical entity composed of twelve leads electrocardiographic changes of coved or saddle shaped ST-segment elevation in V1 and V2 with serious ventricular arrhythmias which may cause sudden cardiac death. Objectives: The objectives of this study is to highlight the clinical presentation and the types of ECG changes of Brugada syndrome cases seen in Iraq and to orient physicians about this fatal condition. Patients and Methods: Patients presented with symptoms of palpitation, dizzy attacks or syncope and diagnosed as Brugada syndrome were included in this case series study. The diagnosis of Brugada syndrome based mainly on the typical coved or saddle shaped or variant ST-Segment elevation in electrocardiographic leads V1, V2. Results: Eighteen patients were included in this case series study. All are males. Age ranged from 15-45 Y. The presenting symptoms were palpitation in 12 patients, syncope in 8, dizzy spells and pre syncope in 14 and chest pain seen in 2. The arrhythmic events were clinically documented in 10. Monomorphic VT seen in 4, VF in 2, atrial fibrillation in 2 and atrial flutter in 2. Induced VF by EP study seen in 2. Type I Brugada ECG pattern was seen in 6 patients, type II in 4 and three of type III. Five showed a variant type of the syndrome. Family history of sudden cardiac death was seen in 8 patients while in 10 it was negative. ICD was implanted in 6 patients. In 12 patients (67%) the diagnosis of Brugada syndrome was missed during the provisional medical contacts. Conclusion: Brugada syndrome is not uncommon in Iraq but needs a high diagnostic suspicion through appreciating the symptomologies and electrocardiographic features of this fatal syndrome to plan management to prevent sudden cardiac death. Key words: Brugada syndrome, Iraq

Kounis syndrome secondary to nimesulide ingestion: a case report

BackgroundKounis syndrome, also known as "allergic myocardial infarction," is a rare co-occurrence of acute coronary syndrome (ACS) in the setting of hypersensitivity reaction to any agent. Non-steroidal anti-inflammatory drugs (NSAIDs) like are often implicated in causing allergic reactions. Here, we present a case of anterior wall myocardial infarction (AWMI) occurred following angioedema secondary to intake of Nimesulide, not described earlier in literature.Case presentationA 45-year-old female developed generalized pruritic, erythematous maculopapular rash, facial puffiness, oral ulcers and hoarseness of voice within few hours following consumption of Nimesulide for fever and body-ache. Due to development of hypotension, electrocardiogram (ECG) was done, which revealed ST elevation in V2–V6, with marked elevation of troponin (TnI) and creatine kinase (CK-MB). He had no chest pain or shortness of breath. Echocardiography showed regional wall motion (RWMA) abnormality in left anterior descending artery (LAD) territory with an ejection fraction of 25%. Coronary angiography showed a complete thrombotic cutoff of LAD, for which Tirofiban infusion was started to decrease thrombus burden. Repeat angiography on next day showed 80% lesion in proximal LAD for which she underwent revascularization with a drug-eluting stent. The patient later showed improvement in cardiac function at 8 months of follow-up.ConclusionsThe occurrence of ACS requiring percutaneous coronary intervention (PCI) in the setting of allergic reactions is rarely reported in the literature. One should be aware of the rare possibility of Kounis syndrome in the setting of hypersensitivity reaction when accompanying features of symptoms suggestive of coronary artery disease co-exists. When indicated, ECG monitoring and cardiac biomarkers in patients with allergic responses help to identify this rare and treatable condition.

FEVER-INDUCED BRUGADA SYNDROME

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Brugada syndrome (BrS) is a rare cause of sudden cardiac death in asymptomatic healthy adults. We present a case of BrS unmasked by fever secondary to COVID-19 infection. CASE PRESENTATION: 38-year-old male with no prior medical history presented with a two-day history of subjective fevers, chills, productive cough, dyspnea, and left-sided pleuritic chest pain. He was noted to be febrile, tachypneic, tachycardic and hypoxic to the low-90s on room air. Bloodwork revealed elevated inflammatory markers with leukocytosis. Imaging and bloodwork were consistent with severe bilateral multifocal pneumonia secondary to COVID-19 infection. EKG on admission showed evidence of sinus tachycardia and type I Brugada pattern in leads V1 and V2 without ischemic changes. He was admitted for treatment of COVID-19 pneumonia with intravenous (IV) Remdesivir, IV steroids, and oxygen supplementation. Despite this, patient continued to be febrile, and interestingly, serial EKGs showed persistent type 1 Brugada pattern, which transformed into type 2 Brugada pattern after day 2 of admission, to persist for the next seven days. Echocardiogram showed normal left ventricular systolic function (ejection fraction 65%) with no significant valvular abnormalities. The Brugada pattern was thought to be induced by the febrile episodes, therefore all fevers were aggressively treated, and patient was closely monitored for any ventricular arrhythmias. Patient was educated on avoiding tricyclic antidepressants and sodium channel blockers as they are contraindicated in BrS. He was discharged home with plans for outpatient electrophysiological study. DISCUSSION: BrS is a clinical entity that can lead to sudden cardiac death and is associated with ECG changes of a 2mm J-point elevation and 1mm ST-segment elevation in two or more of the right precordial leads;type 1 is characterized by coveted-ST elevation in V1 and V2 whereas type 2 involves a saddle-back appearance. Diagnosis is made after excluding all other known causes of ST-segment elevation in right precordial leads, known as phenocopies. Known triggers include fever, intoxication, vagal stimulation, electrolyte imbalances, and various medications. Fever-induced BrS is more common among men in an age group of 30 to 60 years [4], it can precipitate cardiac arrest due to increased arrhythmogenicity of cardiac sodium channels at higher temperatures. Thus, timely and aggressive control of fever is crucial in preventing fatal arrhythmias, with fever-induced BrS leading to cardiac arrest in 18-20% of patients [2,3]. CONCLUSIONS: Clinicians need to be aware of the circumstances that can induce BrS, including fevers and medications, as BrS can be fatal, leading to cardiac arrest in many patients. Early recognition can lead to early intervention, through placement of an implantable pacemaker for documented arrhythmia, to decrease morbidity and mortality. REFERENCE #1: 1. Bayes de Luna A, Brugada J, Baranchuk A, et al. Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report. J Electrocardiol. 2012;45:433-442. [PubMed] [Google Scholar] REFERENCE #2: 2. Amin AS, Meregalli PG, Bardai A, Wilde AA, Tan HL. Fever increases the risk for cardiac arrest in the Brugada syndrome. Ann Intern Med. 2008;149:216-218. [PubMed] [Google Scholar] DISCLOSURES: No relevant relationships by Muhammad Hanif, source=Web Response No relevant relationships by Sudheer Konduru, source=Web Response No relevant relationships by Marino Leonardi, source=Web Response No relevant relationships by SANA MULLA, source=Web Response No relevant relationships by Ruqqiya Mustaqeem, source=Web Response No relevant relationships by Vihitha Thota, source=Web Response

Electrocardiographic findings in true acute left main coronary total occlusion a subanalisys from ATOLMA registry

IntroductionAcute total occlusion of the left main coronary artery (ATOLMA) usually leads to a catastrophic presentation. Prediction of ATOLMA by electrocardiogram (ECG) may contribute to early detection and reperfusion. Limited data have been reported previously. This study aims to identify the admission 12‑leads ECG features that can predict the presence of ATOLMA and in-Hospital mortality in these patients. MethodsThe admission ECGs findings in 24 patients from the previously reported ATOLMA multicenter registry were compared to the ECGs findings in 15 patients with an acute subtotal occlusion of the left main (ASOLMA) and to 15 patients with anterior ST-elevation myocardial infarction of the proximal left anterior descending (LADp-STEMI). ResultsSome ECG features at presentation can predict an ATOLMA: QRS left axis deviation (−61.17 ± 9 degrees); ST-segment elevation in aVL (1.9 ± 0.65 mm); absence of ST-segment elevation in V1 (0.0 ± 0.6 mm); bifascicular block (58%); fragmented QRS (62.5%); prolongation of QTc interval (465 ± 19 ms) and of QRS interval (136 ± 12 mm). The multivariate analysis found that the independent predictors to distinguish ATOLMA from ASOLMA were aVL ST-segment deviation (OR 5.6(95% CI 1.5–21), p = 0.01) and absence of V1 ST-segment elevation (OR 27(95% CI 1.4–52), p = 0.01); and from LADp-STEMI was QRS width (OR 1.1(95% CI 1.02–1.2), p = 0.02). Fragmented QRS was the only independent predictor of in-hospital mortality in ATOLMA (OR 0.125(95% CI 0.01–0.81), p = 0.03). ConclusionsaVL ST-segment elevation, the absence of V1 ST-segment elevation, left axis deviation, the presence of bifascicular block, and prolongation of QRS and QTc interval are predictors of ATOLMA. Fragmented QRS predicts in-hospital mortality in ATOLMA.

The rare presentation of the de Winter's pattern: Case report and literature review

Although not classified as a ST elevated myocardial infarction (STEMI), the patterns known as equivalents also require prompt recognition and treatment. A 50-year-old male with no pertinent history presented to the emergency department for chest pain that radiated to his left shoulder. An electrocardiogram (EKG) revealed findings consistent with the de Winter's pattern, which were greater than 1 mm upsloping ST depressions at the J point in leads V3-V6 (maximally in leads V3–V5), tall, peaked T waves in leads II, III, and V3–V5, ST elevations in lead aVR, and 1 mm ST elevation in V1 and V2. The physical exam, troponins, and other laboratory investigations were unrevealing. Urgent, diagnostic coronary angiography revealed complete occlusion of the proximal left anterior descending (LAD) artery, which was successfully treated with percutaneous coronary intervention (PCI) and two drug-eluting stents. After the stent placement, arterial blood flow was re-established and the ECG normalized. The patient was started on guideline based treatment and discharged home once medically stable. The de Winter's pattern on electrocardiogram indicates a significant coronary artery disease. This pattern requires urgent intervention, typically percutaneous stent placement.

Electrocardiogram (ECG) changes of a patient with severe hyperkalemia

A 55-year-old gentleman with underlying type 2 diabetes mellitus, dyslipidemia, hypertension, and end stage renal disease presented with shortness of breath, vomiting and worsening fatigue for one day after missing his scheduled hemodialysis. Physical examination in revealed tachypnoea with a respiratory rate of 30 breaths per minute, and fine mid inspiratory crepitations at the lung bases. Initial blood investigations in the emergency department revealed severe metabolic acidosis and hyperkalemia with a potassium of 7.6 mmol/L. A 12 lead electrocardiogram was done and several features that suggest hyperkalemia were detected such as a narrow based and symmetrical tall, tented T wave. In V1 the QRS complex is reminiscent of Brugada type 1 which is probably Brugada phenocopy and are often seen in hyperkalemia. There is ST elevation in V2, a single precordial lead. There is no reciprocal ST depression, and a lone ST elevation does not indicate ischemia. This may be caused by hyperkalemia as well. There is a broad QRS of 136ms, widened QRS is characteristic of hyperkalemia. There is a broad P wave and the PR interval is approximately 200ms. Left ventricular hypertrophy is also present. Due to impending respiratory collapse, he was subsequently intubated. His hyperkalemia was treated with intravenous short acting human insulin, dextrose 50%, calcium gluconate, sodium bicarbonate and calcium polystyrene sulfonate. He was subsequently admitted to the intensive care unit (ICU) and had undergone emergency hemodialysis.

C jak COVID-19 — powikłania układu sercowo-naczyniowego u młodego pacjenta

The authors present the case of a 27-year-old patient with cardiovascular complications after undergoing severe acute respiratory syndrome-related coronavirus 2 infection. The first symptoms included muscle aches and somnolence, severe sore throat, and enlargement of submandibular and cervical lymph nodes, followed by dyspnoea and chest pain with body temperature 37.5°C. Because of the medical profession, the patient underwent a routine reverse-transcription polymerase chain reaction test for coronavirus infection, which was positive, before returning to work. In an electrocardiogram, it was observed pathological Q waves in II, III, aVF, V6, and 1 mm of ST elevation in V1–V3. The laboratory tests showed normal levels of cardiac troponin T, creatine kinase MB fraction, and N-terminal pro-B-type natriuretic peptide. Transthoracic echocardiography revealed the hypokinesis of the middle and apical segment of the anterior and lateral wall with preserved left ventricular ejection fraction (LVEF) — 54%. The magnetic resonance imaging (MRI) revealed the normal volume and global left ventricular systolic function (LVEF 52%) with segmental wall motion abnormalities. Subepicardial banded foci of late gadolinium enhancement (LGE), located in the lower right and left ventricular segments of the basal, central and apical segments of the inferior wall suggested inflammatory aetiology of changes found. It may be assumed that the suspected myocarditis was caused by coronavirus disease 2019 (COVID-19) infection. Since LGE was present in the inferior wall, the patient may be considered having a low risk of major cardiac events and heart failure hospitalizations, referring to the ITAMY study. In patients without a history of cardiovascular diseases with COVID-19, cardiac MRI may reveal preserved, mid-range, or reduced LVEF. The patient requires further follow-up. The coronavirus is the most dangerous for the elderly, but it can also affect the hearts of otherwise healthy people, including young adolescents.

Abstract 13718: Automatic Microvolt-level Measurement of ST Level at J-point on 12-lead Electrocardiography Can Distinguish Takotsubo Syndrome and Acute Anterior Myocardial Infarction

Introduction: ST elevation/depression on 12-leads electrocardiography (ECG) at onset was recognized difficult to distinguish Takotsubo syndrome (TTS) and acute anterior myocardial infarction (ant AMI). Diagnostic performance of automatic microvolt-level measurement of the ST levels was not elucidated. Hypothesis: Microvolt-level differences of ST level at J-point on ECG can distinguish TTS and ant AMI in acute phase. Methods: We firstly enrolled consecutive 40 patients of TTS, and among 500 ant AMI patients, one to two random matching was done by their age and gender. Finally, 40+80 patients (74.5±11.2 years, 87 females) were enrolled. ECG at onset of both group was measured by automated system (ECAPs12c: Nihon-Koden). Results: ST level of TTS at J-point in I/II/V4-6 lead was significantly elevated comparing to that of ant AMI. Conversely, Conversely, significant ST depression in aVR and no ST elevation in V1 of TTS was observed in TTS. Logistic regression analysis revealed that ST elevation in I lead and no ST elevation in V1 lead showed high odds ratio and low P value. Conclusions: Automated measurement of microvolt-level difference of ST level at J-point was a powerful tool to distinguish TTS and ant AMI at onset.

Abstract 15591: The Perfect Storm: An Unusual Case of Cardiogenic Shock

A 77-year-old woman with a medical history of constipation and small bowel bacterial overgrowth presented to an outpatient endoscopy center for EGD/colonoscopy. Both procedures went well with no complications, however while in the recovery room, the patient became abruptly hypotensive to the 70s/30s mmHg with nausea and chest pain. She was transferred to our center for further care. In our emergency room she was initially normotensive with a heart rate of 113 in atrial fibrillation, but subsequently decompensated, requiring intubation and pressors. An EKG revealed ST elevations in V1 and AVR with diffuse ST depressions, and thus a CODE STEMI was activated. Coronary angiography revealed no significant coronary disease. At this point we had to step back and reconsider the cause for this patient’s ongoing profound shock. Our differential was broad, and included obstructive shock secondary to pulmonary embolism or tamponade, hypovolemic shock secondary to a GI procedural complication, and anaphylactic shock. Bedside echocardiogram ruled out pericardial effusion and acute valvular disease, revealing a hyperdynamic LV with systolic anterior motion of the mitral valve. Pulmonary arteriogram ruled out pulmonary embolus. Right heart catheterization revealed significantly elevated biventricular filling pressures with a cardiac index of 1.3 L/min/m 2 . Given suspicion for an outflow tract obstruction, she was temporized with an esmolol drip, phenylephrine, and IV fluids. Electrical cardioversion was successful, with immediate rise in her blood pressure despite only a modest improvement in her heart rate. This case demonstrates an unusual presentation of atrial fibrillation resulting in severe hemodynamic compromise. Typically, atrial fibrillation with rates in the 110s, as in our patient, does not cause profound hypotension. This was the principle driver of diagnostic uncertainty. A perfect storm of volume depletion from colonoscopy prep, diastolic dysfunction, dynamic left ventricular outflow tract obstruction due to systolic anterior motion of the mitral valve, and loss of atrial systole resulted in profound cardiogenic shock. This obstructive physiology must be kept in mind in patients with cardiogenic shock who do not improve with usual care.

Differences of ST level at J-point on 12-lead electrocardiography can distinguish takotsubo syndrome and acute anterior myocardial infarction

Abstract Background Qualitative difference of ST elevation/depression on 12-leads electrocardiography (ECG) at onset was reported in patients with Takotsubo syndrome (TTS) and acute anterior myocardial infarction (ant AMI). However, quantitative difference of those was not elucidated. Purpose To investigate differences of ST level at J point on ECG between TTS and ant AMI by automated calculating system. Methods We firstly enrolled consecutive 40 patients of TTS, and among 500 ant AMI patients, one to two random matching was done by their age and gender. Finally, 40+80 patients (74.5±11.2 years, 87 females) were enrolled. ECG at onset of both group was measured by automated system (ECAPs12c: Nihon-Koden). Results ST level of TTS at J-point in I/II/V4–6 lead was significantly elevated comparing to that of ant AMI. Conversely, Conversely, significant ST depression in aVR and no ST elevation in V1 of TTS was observed in TTS. Logistic regression analysis revealed that ST elevation in I lead and no ST elevation in V1 lead showed high odds ratio and low P value. Conclusion Automated measured ST level at J-point was a powerful tool to distinguish TTS and ant AMI at onset. Funding Acknowledgement Type of funding source: None

The de Winter ECG pattern: Distribution and morphology of ST depression.

BackgroundThe reported positive predictive value (PPV) for the “de Winter ECG pattern” to predict an acute left anterior descending artery (LAD) lesion is inconsistent. Besides, the morphology of upsloping or nonupsloping ST depression (STD) may have different significance of severity and prognostication.MethodsWe searched the MEDLINE database using “de Winter” or “junctional ST‐depression with tall symmetrical T‐waves” or “tall T wave” or “STEMI equivalent” as the item up to March 2020. We compared the ECG differences between the different culprit arteries and various morphological STD.ResultsA total of 70 patients with analyzable ECGs were included. In 60 patients (LAD group), the LAD was the culprit artery, while in 10 patients (non‐LAD group), there were other etiologies. Maximal STD in V2 or V3 had a PPV of 89% of all patients and 98% of patients without ST elevation in V2 to detect an acute LAD lesion. The presence of q/Q‐wave or poor R‐wave progression in the precordial leads was significantly more often found in patients with upsloping STD than in patients with nonupsloping STD in the LAD group (84% vs. 27%, p < .01). In 18 patients, the ECG showed a change from upsloping to nonupsloping STD from the leads with maximal STD to the surrounding leads with less STD.ConclusionsThe location of the maximal STD in the precordial leads differs between patients with LAD as the culprit artery and other etiologies of the de Winter ECG pattern. Upsloping STD signifies more severe signs of ischemia than nonupsloping STD.

Ventricular repolarization abnormalities: the electrocardiographic track of cardiac tumoural involvement in an infant with tuberous sclerosis complex. A case report.

BackgroundPrimary cardiac tumours are rare in children. Against this backdrop, Doppler echocardiogram is the main diagnostic procedure, while electrocardiogram (ECG) usually plays a secondary role, by detecting tumoural consequences as cardiac arrhythmias and chambers overload. We describe a case where an electrocardiographic sign was the cornerstone to diagnosis and surveillance of an infant with a cardiac rhabdomyoma.Case summaryA female infant was referred for cardiac evaluation to elucidate an electrocardiographic abnormality, detected during investigation of seizures. She had recently been diagnosed with epilepsy and was under three different anticonvulsants for appropriate control. Cardiovascular symptoms were absent. Skin inspection revealed hypochromic macules. Respiratory and cardiovascular examinations were normal, as well as laboratorial tests and chest radiography. Electrocardiogram (ECG) showed dome-shaped ST-segment elevation in V2 and V3. Transthoracic echocardiogram unveiled a single hyper-echogenic node (0.4 cm2) in the interventricular septum. Cardiac chambers had normal size and function and Doppler analysis was also normal. No specific medication was used to treat the tumour. During follow-up, she remained free of cardiac symptoms. Eighteen months after her first visit to the cardiologist, routine clinical assessment, ECG, and transthoracic Doppler echocardiogram normal results stated the spontaneous and complete involution of the tumoural lesion.DiscussionConvex ST-segment elevation, generally related to myocardial injury, is unusual in paediatric patients. Once it occurs in asymptomatic individuals within this age bracket, exclusion of cardiac tumours is mandatory. However, data regarding the accuracy of such electrocardiographic marker in this clinical setting are still to be defined.

Značaj prehospitalnog prepoznavanja ST elevacije u aVR odvodu u akutnom koronarnom sindromu

Introduction/Objective the acute coronary syndrome is a medical condition that Emergency Medical Service physicians deal with daily. An especially prompt reaction is required when an ST elevation in the aVR lead is discovered, as it signifies a critical coronary lesion. The objective of the article is to present how educated the Emergency Medical Service doctors included in the STEMI network are in recognizing and treating the aVR lead elevation, as an atypical ECG finding. Case report Three patients with chest pain lasting from 30 minutes to 2.5 hours are presented. The ECG recording shows significant ST segment depressions >1mm in 6 or more leads (I, II, III, aVL, aVF, V2-V6) coupled with a 3-4mm ST elevation in the aVR lead and similar or slightly less pronounced ST elevation in V1. The strategy for primary PCI had been initialized for all three patients, who were then, after consultation with interventional cardiologists in UHMC Bezanijska kosa, Clinical Hospital Centre Zvezdara and the Military Medical Academy and having taken the initial dose of dual antiplatelet therapy (except for the third patient), transported to the hospital catheterization labs in these three institutions. Conclusion ST segment depression of 1 mm or more in six or more leads (inferolateral depression) coupled with ST segment elevation in aVR and/or V1 points to the threevessel disease (3VD) or left main coronary artery (LMCA) obstruction. The Emergency Medical Service doctors react adequately and promptly and, pending consultation with interventional cardiologists, the patients arrive directly into the catheterization lab. The final decision about reperfusion therapy is made by cardiologists and cardiac surgeons. Early invasive approach and adequate therapy (PCI/CABG) lower the risk of cardiogenic shock development and death.

Acute myocardial infarction presented with isolated precordial lead elevation in V2

Atrial fibrillation (Af) with acute myocardial infarction (AMI) is a life-threatening disease, and electrocardiogram is indispensable for the initial diagnosis of high-risk patterns in the emergency department. Here we report a case of a 63-year-old male of Af with AMI, presented with isolated elevation of the precordial V2 lead ST-segment, mostly arising from major occlusion of the left main coronary artery and right coronary artery.

The importance of ST elevation in V2–4 ECG leads in athletes

Early repolarization in the anterior ECG leads (ERV2-4) is considered to be a sign of right ventricular (RV) remodeling, but its etiology and importance are unclear. A total of 243 top-level endurance-trained athletes (ETA; 183 men and 60 women, weekly training hours: 15-20) and 120 leisure-time athletes (LTA; 71 men and 49 women, weekly training hours: 5-6) were investigated. The ERV2-4 sign was evaluated concerning type of sport, gender, transthoracic echocardiographic parameters, and ECG changes, which can indicate elevated RV systolic pressure [left atrium enlargement (LAE), right atrium enlargement (RAE), RV conduction defect (RVcd)]. Stroke volume and left ventricular mass were higher in ETAs vs. LTAs in both genders (p < 0.01). Prevalence of the ERV2-4 sign was significantly higher in men than in women [p = 0.000, odds ratio (OR) = 36.4] and in ETAs than in LTAs (p = 0.000). The highest ERV2-4 prevalence appeared in the most highly trained triathlonists and canoe and kayak paddlers (OR = 13.8 and 5.2, respectively). Within the ETA group, the post-exercise LAE, RAE, and RVcd changes developed more frequently in cases with than without ERV2-4 (LAE: men: p < 0.05, females: p < 0.005; RAE: men: p < 0.05, females: p < 0.005; RVcd: N.S.). These post-exercise appearing LAE, RAE, and RVcd are associated with the ERV2-4 sign (OR = 4.0, 3.7, and 3.8, respectively). According to these results, ERV2-4 develops mainly in male ETAs due to long-lasting and repeated endurance training. The ERV2-4 sign indicates RV's adaptation to maintain higher compensatory pulmonary pressure and flow during exercise but its danger regarding malignant arrhythmias is unclear.

Brugada syndrome & AKAP9: Reconciling clinical findings with diagnostic uncertainty

IntroductionBrugada Syndrome typically presents with sudden nocturnal arrhythmias. Diagnosis may be challenging due to variable and transient electrocardiogram patterns and nondiagnostic provocation studies. Genetic testing can establish the etiology, but results may be inconclusive with variants of uncertain significance. CaseA 24-year-old male with family history of sudden cardiac death was found unresponsive due to seizure. He was hemodynamically stable. ECG showed saddle-back ST elevations in V1 and V2. Procainamide challenge was negative. We subsequently performed genetic testing, which demonstrated AKAP9 variant. DiscussionAKAP9 is a scaffolding protein that facilitates phosphorylation of delayed-rectifier potassium channels. The AKAP9 variant alters potassium current causing disordered repolarization and ventricular reentry. It has been previously linked to other channelopathies, but its pathogenicity is fully undetermined. ConclusionGenetic testing is a useful tool to determine the origin of channelopathy, but inconclusive results with variants of uncertain significance should be clinically correlated.