ST Elevation In V1 Research Articles

Predictive model for left main coronary artery or triple vessel disease in patients with chronic coronary syndromes.

Data about prediction of left main coronary artery disease (LMCAD)/three-vessel disease (TVD) in patients with chronic coronary syndromes (CCS) are lacking. This study aimed to develop a model for predicting patients at risk of LMCAD/TVD. This study used retrospective data from patients with CCS scheduled for invasive coronary angiography (ICA) and who were retrospectively recruited between January 2018 and December 2020. Predictors were obtained and analyzed by using logistic regression analysis, and generated the prediction score. The sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated. The cut-off value and area under the curve (AUC) were analyzed by using the receiver operating characteristic (ROC) curve. We recruited 162 patients with CCS. There were 75 patients in the non-LMCAD/TVD and 87 patients in the LMCAD/TVD groups. After the multivariate analysis, new onset of heart failure (HF) or left ventricular systolic dysfunction (LVSD) and suspected CAD, ST elevation (STE) in aVR, STE in V1 and lateral ST depression (STD) were associated with increased risk of LMCAD/TVD. Based on these 4 predictors, the prediction score was created. The cut-off value of the prediction score by using ROC curve analysis was 3.0. The sensitivity, specificity, PPV, and NPV were 71.26%, 86.67%, 86.11%, and 72.22%, respectively, with an AUC of 0.855. The CCS patients with new onset of HF or LVSD and suspected CAD, STE in aVR, and STE in V1 and lateral STD were associated with increased risk of LMCAD/TVD. The novel prediction score could predict LMCAD/TVD in those patients with acceptable sensitivity, specificity, PPV, and NPV.

WAITING FOR A CONCERT IN SUMMER HEAT: A TRANSIENT ST ELEVATION IN A YOUNG MAN

Abstract A 22–year–old man, without prior cardiological history, was waiting for a concert to start many hours in summer heat. Suddenly he started to feel chest pain, dyspnea, and palpitations. Electrocardiogram (EKG), registered from first aid responders, showed a ST elevation in V1–V3 leads and ventricular repolarization alterations in inferior leads. The patient was brought to Emergency department (ED) where a new EKG resulted normalized, blood test samples showed High Sensitive Troponin T (HsTn) 35 ng/L (at plateau in three seriate measures), serum creatinine 2.0 mg/dL, total Creatine Kinase 646U/L, Ck–MB 10.6 ng/mL, Reactive C Protein (RCP) 1.2 mg/dl. The toxicological evaluation was negative. Transthoracic Echocardiography (TTE) did not show any regional ventricular kinesis alterations nor valvular defects, global systolic function was preserved. A Coronary Computed Tomography (CT) scan showed an intramyocardial bridge on Anterior Descending (DA) Coronary Artery associated to 7 mm pericardial effusion without coronary stenosis. A Cardiac Magnetic Resonance (CMR) with gadolinium was performed, which did not show (in T2 mapping sequences) oedema nor Late Gadolinium Enhancement (LGE). Considering a coexistence of Brugada syndrome pattern at EKG, an Ajmaline testing was performed, which resulted negative. Discussion: Dehydration due to any intake of water after standing many hours in summer heat could have been the trigger for a vasospasm of DA that in this patient has a partially intramyocardial course. This anatomical finding was not known until CT scan was performed. Our diagnostic hypothesis of a vasospasm on DA is supported by EKG alterations and elevation enzymes of myocardionecrosis, in absence of any coronary stenosis. Elevated creatinine values in the absence of other renal concomitant comorbidities were suggestive for acute dehydration too. Differential diagnosis took also into consideration myo–pericarditis, especially for the pericardial effusion finding revealed by CT scan: this diagnosis was not confirmed through CMR but also by the evolution of clinical conditions of our patient. We discharged the patient, asymptomatic with normalized renal function after some intravenous hydration and we prescribed a calcium channel blocker. At a follow up visit, three months after the acute event, our patient was in good clinical condition and denied occurrence of any other similar events.

New ECG Algorithm for the Prediction of Culprit Vessel in Acute Myocardial Infarction Involving Lateral Part of the Ventricle: Ilkay Classification.

Isolated lateral myocardial infarction sometimes does not meet ST-segment elevation myocardial infarction (STEMI) criteria according to contiguous leads. This condition could cause late diagnosis and the need for revascularization therapy. To accurately predict the occlusion of lateral surface of the left ventricle, we defined a new electrocardiogram (ECG) algorithm by using angiographic and electrocardiographic correlations. This was a retrospective, multicenter observational study. The study population consisted of 200 patients with STEMI affecting lateral surface of myocardium, between 2021 and 2022. According to the coronary angiography results, we identified 74 eligible patients for study protocol. The study patients were divided into two groups: isolated DB (14 patients) or circumflex obtuse marginal group (60 patients). ST depression in lead V2 had high positive predictive values for the prediction of obtuse marginal occlusion (positive predictive values (PPV), 100%; negative predictive value (NPV), 90%). ST elevation in V2 in ECG, in conjunction with ST depression in lead III had high positive predictive values for prediction of diagonal branch of LAD. Moreover, the presence of hyperacute T wave (≥10 mm) in lead V2 and ≥2 mm ST depression in lead III had large diagonal branch of LAD (PPV, 98%; NPV, 100%). However, <10 mm T wave in lead V2 and <2 mm ST depression in lead III had small diagonal branch of LAD. We comprehensively classified the lateral STEMI definition through new electrocardiographic scheme as Ilkay classification, whereby we could accurately predict infarct-related artery and its occlusion level in lateral myocardial infarction.

C79 NEGATIVE T WAVES ON ECG: NOT JUST HYPERTROPHIC CARDIOMYOPATHY

Abstract Background Arrhythmogenic cardiomyopathy is still considered a rare and difficult–to–diagnose condition, yet a well–founded clinical–instrumental suspicion and proper diagnostic procedure can unveil this condition early from common instrumental findings. Clinical Case In September, a 34–year–old man presented to our center for the presence on the electrocardiogram of ventricular repolarization changes (negative T waves in D1, inferior site and in all precordial leads with mild ST elevation in V1– V2). He denied family history of cardiological events. In 2018, following a suspected preoperative EKG, he performed an echocardiogram and cardiac magnetic resonance imaging (CMR); these examinations showed mild left ventricular hypertrophy with preserved systolic function. Clinically, the patient reported rare episodes of palpitation presented on ambulatory EKG with the same repolarization changes as mentioned above. In consideration of the clinic–instrumental findings, a diagnostic workup with echocardiogram and CMR was started for suspicion of hypertrophic cardiomyopathy in the first hypothesis. On echocardiogram, an non dilated left ventricle was found with left ventricular ejection fraction, parietal thicknesses, and segmental kinetics within normal limits, in the absence of significant valvulopathy; however, frequent ventricular extrasystoles were reported during the examination. Given the EKG–graphic alterations, although there weren‘t any echocardiographic changes, a CMR was performed, showing extensive irregularity of the epicardial profile of the lateral and infero–lateral mid–apical wall, site of adipose infiltration, in which evidence of intramyocardial late gadolinium enhancement (LGE) was also present; the right ventricle showed extensive microbulging of the mid–basal free wall in the absence of adipose replacement or LGE. In view of the clinical–instrumental pattern, the diagnosis of "left dominant" arrhythmogenic cardiomyopathy with initial involvement of the right ventricle was made. Conclusions EKG–graphic interpretation may in some cases be the only instrumental data underlying clinical suspicion of arrhythmogenic cardiomyopathy, allowing early diagnosis of a condition at high risk of sudden cardiac death.

When not dying breaks the heart!

Introduction: Takotsubo cardiomyopathy (TC) is a reversible cardiac pathology that develops contractility changes in the middle segments of the left ventricle, often precipitated by a stressor event, and which clinically mimics an acute coronary event. It mainly affects postmenopausal women and presents with clinical, electrocardiographic and laboratory characteristics similar to acute coronary syndrome, always constituting a differential diagnosis of this entity. It can be triggered by a physical or emotional stressor. The pathophysiology of TC remains unknown.Case report: We present a clinical case that poses a diagnostic challenge as the clinical presentation did not indicate cardiac comorbidity. 78-year-old woman was referred to the Emergency Department for attempted suicide by drowning in a river. She presented with a depressive mood reactive to recent experiences, social isolation, overvalued thoughts of worthlessness and guilt. She denied complaints of chest pain or dyspnea. Of the complementary diagnostic tests performed on admission, ECG shows sinus rhythm with ST elevation in V2 stand out. Collaboration from the cardiology was requested and it was assumed Takotsubo syndrome as a probable diagnosis. During hospitalization, there was a good clinical evolution, presenting good clinical response and remission of depressive symptoms.Conclusion: TC is a psychosomatic condition that requires a multidisciplinary approach in the treatment of heart and psychiatric disease. Clinicians should suspect TC in patients who report a recent stressful event accompanied by cardiothoracic symptoms. Since many cases are seen primarily by psychiatry, psychiatrists must be familiar with the syndrome, under penalty of delay in diagnosis and treatment.

Lesser Omental Infarction Presenting with ST-Segment Changes on Electrocardiography in A 37-Year Old Male: Coincidence or Causation?

Background: Omental infarction is a rare cause of acute abdominal pain. While the clinical presentation and diagnostic workup of omental infarction have been well-described in the literature, there is currently no published data on the relationship between omental infarction and Electrocardiogram (ECG) changes. Case presentation: A 37-year-old male presented with acute onset of epigastric pain, He had associated ECG changes, including ST elevation in V1 (1 mm), ST depression in leads II, aVF, and V4 so he was diagnosed with omental infarction after exclusion of acute coronary syndrome (ACS) via cardiac catheterization and echocardiography. The patient was managed conservatively with pain control and close observation and was discharged home in stable condition, The ECG changes resolved on follow-up 2 weeks later. Conclusion: Omental infarction should be considered in the differential diagnosis of patients presenting with acute abdominal pain and ECG changes. Further studies are needed to elucidate the pathophysiology of ECG changes in omental infarction and to develop optimal management strategies for these patients.

Abstract 14188: An Unexpected Cause of Anterior ST Segment Elevation After Coronary Intervention

Background: ST elevation (STE) in V1 to V3 is traditionally labeled as anteroseptal infarction due to occlusion of the LAD proximal to the septal branches. An important and uncommon cause for similar ECG findings is an isolated RV myocardial infarction due to occlusion of the proximal RCA and/or its branches. We present a case of anteroseptal ST elevation after jailing of a conus branch during percutaneous coronary intervention (PCI) to the RCA. CASE: 89-year-old female with history of moderate aortic stenosis (AS), hypertension, hypercholesterolemia, and prior stroke presented with progressive dyspnea on exertion and 3 days of chest tightness. Initial echocardiogram showed an EF of 64% and severe AS with peak velocity of 4.27 m/s, mean gradient of 45 mmHg and aortic valve area of 0.43 cm 2 . Coronary angiography showed severe stenosis of the proximal RCA successfully treated with intravascular lithotripsy and drug-eluting stent deployment with jailing of the conus branch. The LAD and LCX had mild nonobstructive disease. Patient developed chest pain after the procedure with new STE in V1 to V3. She was taken for emergent cardiac angiogram due to suspected occlusion of the LAD however this showed unchanged anatomy with patent stent in the RCA and no new severe stenosis or occlusion of the left coronary arteries. There was no flow in the jailed conus branch that was not intervened on due to small vessel size. A repeat echocardiogram showed new mild RV dilatation with unchanged EF and normal LV wall motion. Patient had resolution of the chest pain and STE within 2 hours and was discharged home in stable condition. Conclusion: Occlusion of a conus branch artery with associated isolated RV myocardial infarction is an uncommon cause of STE in anteroseptal leads. High index of suspicion is important to anticipate and manage potential complications like ventricular arrhythmias and RV failure.

Abstract 14888: Arrhythmogenic Right Ventricular Cardiomyopathy-Brugada Syndrome Overlap: A Rare Clinical Entity

Introduction: Arrhythmogenic right ventricular cardiomyopathy (ARVC) and Brugada syndrome (BS) are inherited disorders that predispose individuals to arrhythmic sudden cardiac death. ARVC is a heart muscle disorder of intercellular junctions resulting from mutations of desmosomal (DS) genes, often leading to heart failure, and monomorphic ventricular tachycardia (VT). BS is a channelopathy due to sodium channel mutations, usually presenting as polymorphic VT without cardiomyopathy. Case presentation: A 35-year-old male with history of migraines presented with syncope resulting in a fall. No family history of arrhythmias or sudden cardiac death. Initial EKG showed wide complex monomorphic VT. Repeat EKG (figure 1), revealed coved ST-segment elevations in V1, V2 consistent with Brugada type 1 pattern. Emergent coronary angiography was unremarkable, and echocardiogram showed left ventricular ejection fraction of 55-60%, right ventricle (RV) outflow tract proximal diameter measured 3.5cm and normal RV function. An implantable cardioverter-defibrillator (ICD) was implanted for secondary prevention. Device interrogation on follow-up showed 11 shocks for recurrent episodes of monomorphic VT and patient was started on quinidine maintenance therapy. He remained symptom-free on subsequent visits. Genetic testing was positive for DSC2, DSP, and TMEM43 mutations associated with ARVC, but negative for genes associated with BS. Cardiac MRI results are pending. Discussion: Our patient has overlapping features of ARVC (genotype and monomorphic VT) and BS (EKG with coved ST elevations in V1, V2). Emerging evidence supports the theory that defects in DS proteins may affect the integrity of voltage-gated sodium channels in cardiac intercalated discs, leading to BS like phenotype. Conclusion: ARVC and BS could be related to the same disease spectrum, but further studies are required to understand pathophysiology, to guide treatment decisions.

Differentiating typical Tako‐tsubo syndrome from extensive anterior STEMI: Look behind the anterior wall

Tako-tsubo syndrome (TTS) in its most typical form shares common features with anterior ST-segment elevation myocardial infarction (AMI) during acute presentation. Differential diagnosis between the two conditions is often challenging especially if ST-segment elevation is associated with extensive apical akinesis. We sought to systematically analyze ECG and echocardiographic parameters including LV longitudinal strain and two new indexes: the inferior-apex ratio (IAR) and the inferior-lateral-apex ratio (ILAR), to assess if ventricular involvement may be different in TTS and AMI. A retrospective cohort study was conducted with two groups: patients with TTS (n=22) and patients with extensive anterior STEMI (n=22). Lack of ST elevation in V1 was associated with TTS with sensitivity and specificity of 86%, positive and negative predictive value of 86%. Longitudinal strain in mid inferior and mid inferior-lateral segments were more compromised in TTS: -4.3±6.4% and -5.4±5.4% in TTS versus -10.2±5.5% and -9.9±4.9% in AMI, respectively (p&lt;.01 for all). By multivariate analysis, both longitudinal strain values, inferior-apical ratio (IAR)&lt;1 and inferior-lateral-apical ratio (ILAR)&lt;1 were independently associated with diagnosis of TTS during acute phase. Our results suggest that impaired contractility extending beyond apex to mid inferior and inferior-lateral walls can be easily assessed by IAR and ILAR, and these indexes facilitate non-invasive differentiation of TTS from extensive anterior STEMI.

Combining electrocardiographic criteria for predicting acute total left main coronary artery occlusion.

BackgroundPrediction of left main artery (LM) occlusion may contribute to the administration of early reperfusion. We sought to identify electrocardiographic (ECG) features associated with acute total LM occlusion and explore the relationship between ECG features and collateral circulation.MethodsWe retrospectively studied ECGs in 84 consecutive patients with LM occlusion between January 2001 and April 2022. The ECG findings in these patients were compared with those in 468 consecutive patients with LM subtotal occlusion and non-LM occlusion.ResultsThree main ECG patterns were described according to the characteristics of ST elevation (STE) in LM occlusion: ST-segment elevation myocardial infarction (STEMI), STE in aVR with diffuse ST depression, and STE in both aVR and aVL. These ECG patterns were associated with different collateral filling territories. One-third STEMI in LM occlusion showed STE in the precordial leads including V1, while 2/3 STEMI showed STE in the precordial leads from V2 to V5 without STE in V1. The following ECG characteristics predicted LM occlusion: STE in both aVR and aVL; STE in I, aVL, and V2–V5 without V1; left anterior fascicular block (LAFB); right bundle branch block (RBBB) + LAFB; and prolongation of the QRS interval. The incidences of STE in aVR and STE in aVR and V1 were higher in LM subtotal occlusion than in LM occlusion. The combination of two different STE criteria (STE in aVR and aVL and STE in I, aVL, V2-V5 without V1) predicted LM occlusion with 62% sensitivity and 95% specificity. The combination of the STE criteria and fascicular block criteria (LAFB and LAFB + RBBB) further improved the specificity to 99% but reduced the sensitivity to 39%.ConclusionThe combination of STE criteria predicted LM occlusion with high specificity and moderate sensitivity, and the addition of fascicular block criteria further improved the specificity with some loss of sensitivity.

Riding The Storm: Utilizing VA-ECMO As A Bridge To Recovery In A Patient With Fulminant Necrotizing Eosinophilic Myocarditis

<h3>Background</h3> Fulminant necrotizing eosinophilic myocarditis (FNEM) is a rare form of eosinophilic myocarditis characterized by new onset heart failure often requiring inotropic and mechanical circulatory support (MCS). Early endomyocardial biopsy (EMB) and prompt immunosuppressive therapy can prevent further decompensation and death, especially in patients presenting with cardiogenic shock. <h3>Case presentation</h3> A 52-year-old female with prior history of mild asthma presented with dyspnea and chest tightness. Vital signs were significant for temperature of 100.9 F, pulse of 140 in sinus rhythm and blood pressure of 89/70. Physical exam was remarkable for crackles at the mid-lower lung fields bilaterally. Baseline EKG showed sinus tachycardia, septal Q waves with ST elevation in V1, V2 and diffuse subtle ST-depressions in the other leads (Figure 1A). Troponin T was elevated to 3.25 ng/ml, pro-BNP was 23,424 pg/ml, CRP was 26.2mg/dl and ESR to 116mm/hour . A 2D echo showed severely reduced left ventricular systolic function with left ventricular ejection fraction (LVEF) of 25-29%, normal left ventricular dimensions, and mildly reduced right ventricular systolic function. Emergent coronary angiography demonstrated no significant coronary artery disease. Right heart catheterization showed a pulmonary artery saturation of 55%, fick cardiac index 1.72, systemic vascular resistance (SVR) of 2128 dynes and elevated bi-ventricular filling pressure (mean right atrial pressure; 23, mean pulmonary capillary wedge pressure; 30mmHg). An endomyocardial biopsy was performed which was consistent with necrotizing eosinophilic myocarditis (Figure 1B). The patient was started on pulse dose steroids. During the first 24 hours she continued to be hemodynamically unstable and required two inotropes to maintain adequate end-organ perfusion. She was placed on VA-ECMO simultaneous with an IABP for left ventricular unloading. Eventually, after being on mechanical support for 7 days, her hemodynamic status improved and her biventricular function completely normalized by day 9. Mechanical and inotropic support was successfully weaned. Patient was discharged on day 23 with a goal to continue a long steroid taper for 6 months. <h3>Conclusion</h3> FNEM is an extremely rare and life threatening pathology that often presents with cardiogenic shock. It is eminently treatable if recognized early during its course. Early EMB should be performed to guide decisions for immunosuppressive therapy. We present a case of FNEM with extremis shock successfully managed with early MCS as bridge-to-recovery.

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.

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.

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.

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