Leads V1 V3 Research Articles

P163 THE ELECTROCARDIOGRAPHIC CHANGES ASSOCIATED WITH HYPOTHERMIA: THE OSBORN WAVE

Abstract A 93–year–old patient came to our observation for general malaise, sensory obnubilation, aphasia and dysphagia. He had arterial hypertension in drug treatment. At the first medical contact, the body temperature was 28 °C. The ECG showed a non–evaluable atrial activity (likely atrial paralysis) with the presence of a junctional rhythm at the frequency of 37 bpm. Blood pressure was around 100/60 mmHg with preserved cardiovascular compensation, in the presence of a moderately depressed cardiac function. Furthermore, the presence of a positive deflection in the terminal part of the QRS complex with elevation of the point J, in the precordial lateral leads V4–V6, and a terminal slowing of the QRS complex in the inferior leads, the so–called ‘wave of Osborn’, were also observed Figure 1. Given the reduction of the sensory, the patient was subjected to brain CT scan with finding of a thin hyperdense layer around the right and left hemispheric convexity suggestive for subdural haematoma. After adequate warming and supportive therapy, a progressive increase in heart rate was observed with restoration of the sinus rhythm and disappearance of the Osborn wave, Figure 2. The Osborn wave is the most specific electrocardiographic sign of hypothermia. It consists of an electrocardiographic deflection which is manifested as a late delta wave or as a small r ’wave following the QRS. It is the manifestation on the surface ECG of the electric gradient between a more prominent spike and dome action potential of epicardial cells than that of endocardial cells, an effect that is believed to be linked to a slowing down of the kinetics of activation of K þ channels Ito compared to calcium channels, associated with low temperature. This wave is not specific for hypothermia but can also occur in other clinical conditions such as subarachnoid haemorrhage, myocardial ischaemia, acidosis, in the presence of hypercalcemia, early repolarization and even in normal subjects. Its amplitude also tends to increase in conjunction with the reduction in body temperature. The bradyarrhythmias and conduction disorders associated with hypothermia cease spontaneously with an increase in body temperature, so the use of beta stimulating drugs and the insertion of transvenous pacemakers, the latter for the mechanical irritation effect on the endocardium, should be considered with caution due to the high risk of inducing ventricular tachyarrhythmias and ventricular fibrillation.

Right ventricular myocarditis and rapid fibrosis induced by pazopanib.

A 56-year-old woman with metastatic chondrosarcoma visited our emergency department because of chest discomfort. Treatment with oral pazopanib, a multi-targeted tyrosine kinase inhibitor that targets angiogenesis growth factor receptors, fibroblast growth factor receptors, platelet-derived growth factor receptors, and vascular endothelial growth factor receptors, was initiated 26 days previously. Electrocardiography showed new-onset significant ST elevation in the precordial leads V1–V3 and pathologic Q-waves in leads III and aVF (Panel A). The cardiac and inflammatory biomarker levels were elevated as follows: creatine kinase (CK), 705 (reference range, 32–135 IU/L); CK-myocardial band (MB) fraction, 12.5 (reference range, 0–5 ng/mL); troponin-T, 402 (reference range, 0–14 pg/mL); NT-proBNP, 11 230 (reference range, 0–287 pg/mL); and C-reactive protein, 77.3 (reference range, 0–8 mg/L). Echocardiography showed newly developed akinesia with thinning in the septum and throughout the right ventricle with markedly reduced biventricular systolic dysfunction compared with echocardiography performed 1 month ago (Panel B and Supplementary data online, Video). Luminal narrowing or thrombosis in the coronary arteries was not observed on emergency coronary angiography (Panel C). Cardiac magnetic resonance imaging performed on the second day of hospitalization showed diffuse late gadolinium enhancement in the right ventricular wall and the right side of the septum (Panel D). The nails of both hands showed hyperpigmentation and onycholysis induced by taking pazopanib (Panel E). Despite the discontinuation of pazopanib and heart failure management, she developed fatal ventricular tachycardia and cardiogenic shock (Panel F). Imaging findings show pazopanib-induced right ventricular myocarditis with subsequent rapid wall thinning and fibrosis.

Early Changes in Acute Myocardial Infarction in Pigs: Achieving Early Detection with Wearable Devices

We examined the changes in variables that could be recorded on wearable devices during the early stages of acute myocardial infarction (AMI) in an animal model. Early diagnosis of AMI is important for prognosis; however, delayed diagnosis is common because of patient hesitation and lack of timely evaluations. Wearable devices are becoming increasingly sophisticated in the ability to track indicators. In this study, we retrospectively reviewed the changes in four variables during AMI in a pig model to assess their ability to help predict AMI onset. AMI was created in 33 pigs by 90-min balloon occlusion of the left anterior descending artery. Blood pressure, EKG, and lactate and cardiac troponin I levels were recorded during the occlusion period. Blood pressure declined significantly within 15 min after balloon inflation (mean arterial pressure, from 61 ± 8 to 50 ± 8 mmHg) and remained at this low level. Within 5 min of balloon inflation, the EKG showed ST-elevation in precordial leads V1-V3. Blood lactate levels increased gradually after occlusion and peaked at 60 min (from 1.48 to 2.53 mmol/L). The continuous transdermal troponin sensor demonstrated a gradual increase in troponin levels over time. Our data suggest that significant changes in key indicators (blood pressure, EKG leads V1-V3, and lactate and troponin levels) occurred at the onset of AMI. Monitoring of these variables could be used to develop an algorithm and alert patients early at the onset of AMI with the help of a wearable device.

Lung cancer presenting with acute myocardial infarction and pulmonary embolism within 1 month

Acute myocardial infarction and pulmonary embolism can have life-threatening consequences such as congestive heart and respiratory failure, respectively. Cancer patients are at great risk of both acute myocardial infarction and pulmonary embolism complications because the malignancy sparks the patient’s blood hypercoagulable state. Nevertheless, the literature currently offers only a few reports on acute myocardial infarction associated with pulmonary embolism, and two of them occurred in the same cancer patient. Here, we present a case of a 60-year-old woman who had been diagnosed with lung cancer. She was admitted to the emergency department twice. She was diagnosed with acute myocardial infarction at her first admission, when she experienced sudden-onset chest pain. Electrocardiography showed ST-segment elevation in leads V1–V3 with inverted T wave and pathological Q wave, suggesting an acute myocardial infarction. Coronary angiography revealed a thrombus in the left anterior descending coronary artery, and thrombus aspiration was performed. After 1 month, she had an attack of pulmonary embolism with syncope upon the second admission. A computed tomographic pulmonary angiography showed branches of right and left pulmonary embolism. Anticoagulation and antiplatelet measures were taken. In this article, we discuss the relationship between cancer and thrombosis with a special focus on the conservative management strategy regarding anticoagulant and antiplatelet therapy in our case.

1102 ARRYTHMOGENIC CARDIOMYOPATHY: LESSONS FROM A LARGE FAMILY

Abstract Background Arrhythmogenic cardiomyopathy is a genetically-inherited cardiomyopathy. PKP2 mutations are the most common cause of the disease, associated with conventional ARVC phenotype. Case presentation We presented a 14 years old sportswoman admitted to our emergency department for cardiac arrest-related to ventricular fibrillation. The patient was asymptomatic leading up to cardiac arrest. At admission, she met the diagnosis of AC with bi-ventricular involvement (T negative waves in V1-V6 and inferior leads; severe biventricular dysfunction with fibrofatty replacement involving both ventricles). Family history revealed that her cousin, a 15 years competitive athlete, received a recent diagnosis of ARVC, wherein pathogenetic variant p.Tyr857_Lys859 in heterozygosity in the PKP2 gene was found. As expected, the index case presented the same mutations in PKP2 gene, and no other mutations were found. Implanted cardioverter defibrillator (ICD) and strength follow-up, including heart failure management, was performed. Cascade screening of family members allowed us to identify 19 mutations carriers. Of these, 5 patients were identified to have disease expression. The first to be studied was her 9 years old sister, who involved in high level of sport activities. She presented abnormal ECG with negative T waves in V2-V4, significance burden of premature ventricular complex (PVC >500/24 h) with mild right ventricle dilatation. Of others family members, four patients presented early signs of myocardial disease and significant arrhythmias burden. Except for one patient, all these members were involved in amateur sport activities. Two members had signs of left ventricle (LV) involvement (inverted T waves in leads V4–V6 and inferior leads, LV wall motion abnormalities and late enhancement), whereas one patient (P3) showed a fulfilled ARVD. Three patients presented significant PVC on 24-hour ambulatory ECG monitoring (PVC >500/24 h) (P2, P3 and P5). The arrhythmic burden was more pronounced in two young patients having a sports activity (P2 and P3). This trend was also confirmed at exercise testing. Except for one patient, these findings appear to be related to sport activity, even if this is no high-intensity activity. Among other carriers of pathogenic mutation, three patients showed ECG abnormalities in infero-lateral leads and significance PVC at 24-hour ECG monitoring in absence of other findings related-cardiomyopathy. All family members carried PKP2 mutation were restricted in sports activities, and, in patients presented early disease and arrhythmogenic burden, treatment with beta-blockers was started. Conclusion In this family presenting PKP2 mutation, heterogenicity of disease expression and a close relationship with sport activity was found. This large family case encourages future ACM studies to better understand disease expression and their relationship with sports activity across the entire ACM phenotypic spectrum and ages. Also, this case underscores the importance of early familiar screening, including children involved high-level of sports activity.

The R-S difference index: A new electrocardiographic method for differentiating idiopathic premature ventricular contractions originating from the left and right ventricular outflow tracts presenting a left bundle branch block pattern.

Introduction: Differentiating idiopathic premature ventricular contractions (PVCs) originating from the right and left ventricular outflow tracts with a left bundle branch block (LBBB) morphology is relevant to catheter ablation planning and important for lowering the risk of complications. This study established a novel electrocardiographic (ECG) criterion to discriminate PVCs originating from the septum of the right ventricular outflow tract (s-RVOT) and those originating from the aortic sinus cusp of the left ventricular outflow tract (LVOT-ASC). Methods: A total of 259 patients with idiopathic PVCs originating from ventricular outflow tract with a LBBB pattern who underwent successful catheter ablation were retrospectively included. Among them, the PVCs originated from the s-RVOT in 183 patients and from the LVOT-ASC in 76 patients. The surface ECGs of the PVCs and sinus beats were analyzed using an electronic caliper. The R-S difference index in the precordial leads was calculated as V2R + V3R + V4R − V1S. Results: PVCs originating from both the s-RVOT and LVOT-ASC displayed an inferior axis (dominant R waves in leads II, III, and aVF). Compared with the s-RVOT group, the R-wave amplitudes on leads II, III, and aVF were significantly larger in the LVOT-ASC group (p < 0.001, p < 0.003, and p < 0.001, respectively). Compared to the LVOT-ASC group, the s-RVOT group showed smaller R-wave amplitudes on leads V1–V6 (p = 0.021, p < 0.001, p < 0.001, p < 0.001, p < 0.001, and p < 0.001, respectively) and larger S-wave amplitudes on leads V1–V3 (p < 0.001, p < 0.001, and p < 0.001, respectively). Lead V3 was the most common transitional lead in both groups. Analysis of the receiver operating characteristic curve showed that the R-wave amplitude on lead V3 had the largest area under the curve (AUC) of 0.856 followed by the R-wave amplitudes on leads V4 (0.834) and V2 (0.806). The AUC of the R-S difference index was 0.867. An R-S difference index greater than 20.9 predicted an LVOT-ASC origin with 73.7% sensitivity and 86.3% specificity. This index is superior to previous criteria in differentiating PVCs with LBBB morphology and inferior axis originating from s-RVOT vs. LVOT-ASC. Conclusions: The R-S difference index in precordial leads is a useful new ECG criterion for distinguishing LVOT-PVCs from RVOT-PVCs with LBBB morphology.

Clinical manifestations of cardiovascular disease in children as a sequela of coronavirus disease (COVID-19) (a clinical case)

The aim of the work: to provide medical practitioners with a clinical case of cardiovascular affection with ST-segment elevation in a child as a result of coronavirus disease (COVID-19). Materials and methods. Here is a clinical case of our own observation of the clinical course of post-COVID cardiovascular system involvement with ST-segment elevation in the child who was treated at the City Children’s Hospital No. 5 of Zaporizhzhia City Council. Results. The patient with severe post-COVID cardiovascular implication, COVID in anamnesis confirmed by COVID-19 IgG positivity with negative IgM and PCR test results. The following laboratory findings were also detected when the child was admitted to the hospital: Troponin I was 136 ƞg /ml (referent value – less than 0.32 ƞg/ml), Lactate Dehydrogenase – 4199 U/l (referent value – 110–295), Creatine Phosphokinase-MB – 25.4 U/l (referent value – 0–24), CRP was increased to 6.2 mg/l, D-dimer – to 3221.12 ng/mL (referent value – less than 500 ng/mL). ECG showed QS-waves in leads V3–V6, I, 2.0–2.5 mm ST-segment elevation in leads V4–V6, and Р-mitrale. The clinical course was characterized by cardiogenic shock development. During intensive care, there was moderate positive clinical and laboratory dynamics. Peculiarities of post-COVID myocarditis in children were characterized based on the comparative analysis of this clinical case and results of relevant clinical studies, world recommendations and guidelines. Conclusions. Peculiarity of the case is severe post-COVID syndrome after almost asymptomatic COVID-19. Physicians should be aware after coronavirus disease while providing a close follow-up for six months. Myocardial ischemia is among casuistic post-COVID manifestations in children. The basic treatment is a complex therapy of heart failure, anticoagulant and antiplatelet therapy, as well as corticosteroids administration, which is pathogenetically justified and leads to regression of major clinical and laboratory symptoms.

Prevalence of Physiological Electrocardiographic Findings in a Brazilian Cohort of Young Football Players: B-Pro Foot ECG Pilot Study

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Hospital de Clínicas de Porto Alegre Research and Event Incentive Fund (FIPE-HCPA) Introduction The 12-lead electrocardiogram (ECG-12) is a useful tool in the assessment of athletes, and it may present findings compatible with physiological adaptations to regular exercise. ECG-12 findings in Brazilian soccer players are unknown. Purpose To describe the prevalence of physiological ECG-12 findings in young Brazilian soccer players based on the "2017 International Criteria for Electrocardiographic Interpretation in Athletes". Methods Continuous variables were displayed as mean and standard deviation or median and interquartile range, while prevalence’s with 95% confidence intervals, and stratified by race. Intra-group differences were estimated by linear models or binomial and multinomial logistic regressions. Type I error was set to set a at 0.05. An additional margin of 0.025 was considered at the discretion of the statistician conditioned to the quality of the model. All analysis were running in Stata version 16.0.0. Results 2,581 athletes from 27 clubs (mainly first division), aged 15-35 years (median: 18 years) were evaluated. 1,268 (49.1%) were Caucasians, 796 (30.8%) Mixed-race (MR) and 517 (20.1%) Afro-Brazilians (AB). In this sample from across the country, we identified the following findings and its respective prevalence: sinus bradycardia (50%), ectopic atrial rhythm (1.4%), junctional rhythm (0.3%), incomplete right bundle branch block (23.7%), first-degree atrioventricular (AV) block (3.0%), Mobitz type I AV block (0.1%), and increase QRS voltage for left or right ventricular hypertrophy (35.2% and 17.3%, respectively). The mean PR interval was 153.9±28.7 ms, corrected QT interval 399.2±28.0 ms, and QRS duration 96.0±14.0 ms. ST elevation followed by T-wave inversion in leads V1–V4 was identified in 11/517 (2.1%) of AB athletes. Early repolarization was present in 828 athletes (32.1%), being more prevalent in AB when compared to MR and Caucasians (P = 0.003). Likewise, AB had a greater PR interval in comparison to MR and Caucasians (P &amp;lt;0.001 and P = 0.007, respectively). On the other hand, Caucasians had a significant longer QRS duration compared to AB. For all remaining variables there was no difference among races. Conclusions To the best of our knowledge, this is the first large study to describe the prevalence of physiological electrocardiographic finding in young Brazilian soccer players, according to "2017 International Criteria for Electrocardiographic Interpretation in Athletes". Future studies comparing the frequency of these findings with the prevalence observed in other cohorts are welcome.

Exploring the Correlation Between Fibrosis Biomarkers and Clinical Disease Severity in PLN p.Arg14del Patients.

Background: Pathogenic variants in phospholamban (PLN, like p. Arg14del), are found in patients diagnosed with arrhythmogenic (ACM) and dilated cardiomyopathy (DCM). Fibrosis formation in the heart is one of the hallmarks in PLN p.Arg14del carriers. During collagen synthesis and breakdown, propeptides are released into the circulation, such as procollagen type I carboxy-terminal propeptide (PICP) and C-terminal telopeptide collagen type I (ICTP).Aim: To investigate if PICP/ICTP levels in blood are correlative biomarkers for clinical disease severity and outcome in PLN p.Arg14del variant carriers.Methods: Serum and EDTA blood samples were collected from 72 PLN p.Arg14del carriers (age 50.5 years, 63% female) diagnosed with ACM (n = 12), DCM (n = 14), and preclinical variant carriers (n = 46). PICP levels were measured with an enzyme-linked immune sorbent assay and ICTP with a radio immuno-assay. Increased PICP/ICTP ratios suggest a higher collagen deposition. Clinical data including electrocardiographic, and imaging results were adjudicated from medical records.Results: No correlation between PICP/ICTP ratios and late gadolinium enhancement (LGE) was found. Moderate correlations were found between the PICP/ICTP ratio and end-diastolic/systolic volume (both rs = 0.40, n = 23, p = 0.06). PICP/ICTP ratio was significantly higher in patients with T wave inversion (TWI), especially in leads V4–V6, II, III, and aVF (p < 0.022) and in patients with premature ventricular contractions (PVCs) during an exercise tolerance test (p = 0.007).Conclusion: High PICP/ICTP ratios correlated with clinical parameters, such as TWI and PVCs. Given the limited size and heterogeneity of the patient group, additional studies are required to substantiate the incremental prognostic value of these fibrosis biomarkers in PLN p.Arg14del patients.

179 ICD or not ICD? A difficult choice for a young patient presenting with palpitations in emergency department

Abstract A fit-and-well 52-year-old worker, with negative familiar story, was admitted to Emergency Department (ED) with haemodynamically unstable but well bore broad complex tachycardia of 180 b.p.m. (Figure 1). Twenty years before the patient had heart-surgery to repair atrial septal venous sinus defect with patch. The defect determined anomalous pulmonary venous return in right atrium with left to right shunt and moderate pulmonary hypertension. The surgery, 20 years before, was complicated by a single event of supraventricular tachycardia pharmacology resolved. Next follow-up was normal although at transthoracic echocardiography severe right ventricular (RV) dilation was reported. In the ED the patient had palpitation but not chest pain or dyspnoea. General clinical examination was normal but he was hypertensive (170/137 mmHg) and with heart rate of 180 b.p.m. Valsalva manoeuver was performed and adenosine (6 mg–12 mg–12 mg) was administered without benefit. Eventually, the patient was cardioverted to sinus rhythm with a single 100 J shock. His baseline ECG (Figure 2) showed sinus rhythm, normal axis, as well as right bundle branch block and T-wave inversion in leads V1–V4 and a waves with a small spike upward in lead V1 which represent characteristic epsilon waves. Successively patient was admitted to Cardiology Department where transthoracic echocardiography showed severe RV dilation and moderate hypokinesia with a tricuspid annular plane excursion of 15 mm, TAV 9.6 cm/s, fractional area change of 29%. The right atrium was moderate dilated (volume 70 ml, indexed volume 35.53 ml/m2). Left chambers were normal. No shunts were observed. An electrophysiology study with isoprenaline infusion was performed but no arrhythmias were induced. Cardiac magnetic resonance imaging (MRI) was normal save for global RV dilatation, increased RV end diastolic volume (156 ml/m2), and global RV systolic dysfunction (reduction of RV ejection fraction 31%). Arrhythmogenic cardiomyopathy was excluded as patient’s background suggested RV dilation was due the overload caused by the history of left–right shunt. Blood tests and personal history negative initially exclude myocarditis and cardiac MRI confirmed the absence of oedema. An accurate ECG analysis excluded Brugada syndrome. Following discussion between electrophysiologists, clinical cardiologists, and the patient who first need to be informed, trans-venous ICD was implanted. 179 Figure 1ECG in ED. Figure 2 Baseline ECG. Figure 3 Cardiac MRI.

Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia).

BackgroundOcclusion myocardial infarctions (OMIs) of the posterolateral walls are commonly missed by ST‐segment–elevation myocardial infarction (STEMI) criteria, with >50% of patients with circumflex occlusion not receiving emergent reperfusion and experiencing increased mortality. ST‐segment depression maximal in leads V1–V4 (STDmaxV1–4) has been suggested as an indicator of posterior OMI.Methods and ResultsWe retrospectively reviewed a high‐risk population with acute coronary syndrome. OMI was defined from prior studies as a culprit lesion with TIMI (Thrombolysis in Myocardial Infarction) 0 to 2 flow or TIMI 3 flow plus peak troponin T >1.0 ng/mL or troponin I >10 ng/mL. STEMI was defined by the Fourth Universal Definition of Myocardial Infarction. ECGs were interpreted blinded to outcomes. Among 808 patients, there were 265 OMIs, 108 (41%) meeting STEMI criteria. A total of 118 (15%) patients had “suspected ischemic” STDmaxV1–4, of whom 106 (90%) had an acute culprit lesion, 99 (84%) had OMI, and 95 (81%) underwent percutaneous coronary intervention. Suspected ischemic STDmaxV1–4 had 97% specificity and 37% sensitivity for OMI. Of the 99 OMIs detected by STDmaxV1–4, 34% had <1 mm ST‐segment depression, and only 47 (47%) had accompanying STEMI criteria, of which 17 (36%) were identified a median 1.00 hour earlier by STDmaxV1–4 than STEMI criteria. Despite similar infarct size, TIMI flow, and coronary interventions, patients with STEMI(−) OMI and STDmaxV1–4 were less likely than STEMI(+) patients to undergo catheterization within 90 minutes (46% versus 68%; P=0.028).ConclusionsAmong patients with high‐risk acute coronary syndrome, the specificity of ischemic STDmaxV1–4 was 97% for OMI and 96% for OMI requiring emergent percutaneous coronary intervention. STEMI criteria missed half of OMIs detected by STDmaxV1–4. Ischemic STDmaxV1–V4 in acute coronary syndrome should be considered OMI until proven otherwise.

Machine learning-derived electrocardiographic algorithm for the detection of cardiac amyloidosis

BackgroundDiagnosis of cardiac amyloidosis (CA) requires advanced imaging techniques. Typical surface ECG patterns have been described, but their diagnostic abilities are limited.ObjectiveThe aim was to perform a thorough electrophysiological characterisation...

Isolated ST-Elevation Myocardial Infarction Involving Leads I and aVL: Angiographic and Electrocardiographic Correlations from a Tertiary Care Center.

Background Determining the infarct-related artery in STEMI during a coronary angiogram can be challenging due to the affliction of multiple vessels. Isolated STEMI involving only EKG leads I and aVL is infrequent. Localization of infarct-related artery based on EKG findings has not been previously done in this subset. Methods All consecutive de novo acute coronary syndrome (ACS) patients admitted to coronary care unit with ST elevations involving only leads I and aVL were screened for enrollment. Patients with ST elevation in any additional lead and those who refused a coronary angiogram were excluded. Subsequently, a coronary angiogram was done as part of primary PCI or a pharmacoinvasive approach to identify the infract-related artery (IRA). IRA was defined by characteristics of lesion, flow of blood through stenosis, and presence of intracoronary thrombus. Coronary angiogram was interpreted by two independent observers blinded to the EKG findings. ST changes in inferior and precordial leads were analyzed to find ECG predictors of the culprit artery. Results A total of 54 eligible patients of ACS were included in the study. The first major diagonal (D1) was the most frequent IRA in 35.2% followed by left circumflex-obtuse marginal (LCX-OM11) in 29.6%, left anterior descending (LAD) in 20.4%, and ramus intermedius (RI) in 14.8%. Out of total patients with ST depression in lead V2, the LCX-OM11 group was IRA in 50% cases while the RI, D1, and LAD groups accounted for 31.8%, 13.6%, and 4.5%, respectively (p < 0.001). Similarly, LCX-OM1 was the most frequent IRA subjects with ST depressions in leads V1 and V3 (44.4%; p = 0.010 and 46.2%; p = 0.003, resp.). On the contrary, in patients with ST depression in lead III, LAD and D1 were the most frequent IRA as compared to LCX-OM1 and RI though statistical significance was not attained (p = 0.857 for lead III). ST-segment depression in lead V2 had a positive predictive value of 60% and a negative predictive value of 100% for LCX-OM1 as IRA. Similarly, ST-segment depression in lead V2 had a positive predictive value of 20% and a negative predictive value of 100% for the RI group. Conclusions In patients presenting with isolated ST elevation in leads I and aVL, the most frequent IRA on angiogram was first diagonal. ST depressions in EKG leads V1–V3 were the most common predictor of LCX–OM1 while those in inferior leads indicated LAD-D1 as the IRA.

The precordial R-prime wave: a novel discriminator between cardiac sarcoidosis and arrhythmogenic right ventricular cardiomyopathy in patients presenting with ventricular tachycardia

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): The department of cardiology from Leiden University Medical Center receives unrestricted grants from Edwards Lifesciences, Biotronik, Medtronik, Boston Scientific and BioSense Webster. MS was supported by the Research Fellowship of the European Society of Cardiology 2017/2018. Background Cardiac sarcoidosis (CS) with right ventricular (RV) involvement may mimic ARVC. Histopathological differences may result in disease specific RV activation patterns, detectable on the 12-lead electrocardiogram (ECG). Scar in ARVC progresses from epicardium to endocardium and may lead to delayed activation of areas with reduced voltages, translating into terminal activation delay and occasionally an (epsilon) wave with small amplitude on the ECG. On the contrary, patchy transmural RV scar in CS may lead to conduction block, and therefore late activated areas with preserved voltages, reflected as preserved R’-waves in the right precordial leads. Purpose To determine whether the terminal activation patterns in precordial leads V1-V3 distinguish CS with RV involvement from ARVC. Methods This is a multicenter retrospective study including patients with either 1) CS with RV involvement or 2) gene-positive ARVC referred for VT ablation. A non-ventricular paced 12-lead surface ECG prior to ablation was obtained (25mm/s and 10mm/mV). For detailed analysis, Leiden ECG Analysis and Decomposition Software (LEADS) was used. After detection of QRST complexes in the spatial velocity signal, LEADS generates a representative and low-noise averaged beat. Then, measurements per lead were performed using the measurement tool in Adobe Pro DC. Based on the hypothesis that conduction block in CS will lead to late activated areas with preserved voltages, we measured the surface area (SA) of the R’-wave in V1-V3. An R’-wave was defined as any positive deflection from baseline after an S-wave. Results 13 CS patients with RV involvement (54 ± 8years, 62% male) and 23 ARVC patients (37 ± 15years, 78% male) were included. A R’-wave in V1-V3 was present in all CS patients, compared to 11 (48%) of ARVC patients (p = 0.002). The maximum R’-wave SA in lead V1-V3 was 3.55 (IQR:2.18-5.81) mm2 in CS vs. 0.00 (IQR:0.00-0.43) mm2 in ARVC (p &amp;lt; 0.001; Figure A). By ROC-analysis, the maximum R’-wave SA in lead V1-V3 was an excellent discriminator (area under the curve 0.980 [95%CI: 0.945-1.000]). A cutoff of ≥1.65mm2 had a sensitivity of 85% and specificity of 96% for diagnosing CS. An algorithm was created including the presence of an R’-wave in V1-V3 and the SA of this R’-wave (Figure B). This was validated in a second cohort (18 CS and 40 ARVC) with 72% sensitivity and 88% specificity. Conclusion Transmural RV scars in CS may cause localized conduction block, leading to late activated areas with preserved voltages, reflected as large R’-wave on the 12-lead surface ECG. An easily applicable algorithm including the surface area of the largest R’-wave in lead V1-V3 ≥1.65mm2 distinguishes CS from ARVC with good sensitivity and specificity. The QRS terminal activation in precordial leads V1-V2 may reflect disease specific scar patterns (for examples: Figure C). Abstract Figure

Extended Precordial T Wave Inversions Are Associated with Right Ventricular Enlargement and Poor Prognosis in Pulmonary Hypertension.

In pulmonary hypertension (PH), T wave inversions (TWI) are typically observed in precordial leads V1–V3 but can also extend further to the left-sided leads. To date, the cause and prognostic significance of this extension have not yet been assessed. Therefore, we aimed to assess the relationship between heart morphology and precordial TWI range, and the role of TWI in monitoring treatment efficacy and predicting survival. We retrospectively analyzed patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) treated in a reference pulmonary hypertension center. Patients were enrolled if they had a cardiac magnetic resonance (cMR) and 12-lead surface ECG performed at the time of assessment. They were followed from October 2008 until March 2021. We enrolled 77 patients with PAH and 56 patients with inoperable CTEPH. They were followed for a mean of 51 ± 33.5 months, and during this time 47 patients died (35.3%). Precordial TWI in V1–V6 were present in 42 (31.6%) patients, while no precordial TWI were observed only in 9 (6.8%) patients. The precordial TWI range correlated with markers of PH severity, including right ventricle to left ventricle volume (R = 0.76, p < 0.0001). The presence of TWI in consecutive leads from V1 to at least V5 predicted severe RV dilatation ( ≥ 2.3) with a sensitivity of 88.9% and specificity of 84.1% (AUC of 0.90, 95% CI = 0.83–0.94, p < 0.0001). Presence of TWI from V1 to at least V5 was also a predictor of mortality in Kaplan–Meier estimation (p = 0.02). Presence of TWI from V1 to at least V5 had a specificity of 64.3%, sensitivity of 58.1%, negative predictive value of 75%, and positive predictive value of 45.5% as a mortality predictor. In patients showing a reduction in TWI range of at least one lead after treatment compared with patients without this reduction, we observed a significant improvement in RV-EDV and . We concluded that the extension of TWI to left-sided precordial leads reflects significant pathological alterations in heart geometry represented by an increase in RV/LV volume and predicts poor survival in patients with PAH and CTEPH. Additionally, we found that analysis of precordial TWI range can be used to monitor the effectiveness of hemodynamic response to treatment of pulmonary hypertension.

Impact of Prone Position on 12-Lead Electrocardiogram in Healthy Adults: A Comparison Study with Standard Electrocardiogram.

Background The standard electrocardiogram (ECG) is commonly performed in the supine posture. It may be difficult to report ECG in a supine posture for those who are unable to adopt the supine posture because of certain circumstances such as acute respiratory distress syndrome—patients who are placed in a prone position for long periods to improve oxygenation. Few data are available on the impact of the prone position on the ECG recording with electrodes on the posterior chest. Examining and analyzing the type and extent of changes observed in the prone ECG in healthy adults have become vitally valuable. Methods A cross-sectional observational study enrolled forty healthy adults (24 males and 16 females) aged between 18 and 40 years. The ECG was performed in two different body positions, supine and prone. Influence of prone position on the heart rate, mean QRS axis, amplitude, morphology, duration, mean T wave axis and polarity, mean P wave axis, PR, and mean QTc duration was evaluated. Results The mean heart rate was higher in the prone position (73.2 ± 12.4 bpm) compared with the supine position (69.5 ± 11.5 bpm, p = 0.03). The QRS duration decreased considerably from supine (92.8 ± 12.6 ms) to prone (84.9 ± 11.9 ms, p < 0.001). The mean QRS axis moved to the left in the prone posture (40.5° ± 32°) relative to the supine (49° ± 28°, p=0.015). The QRS amplitude in the precordial leads was significantly decreased from supine (7.42 ± 3.1 mV) to prone (3.68 ± 1.7 mV, p < 0.001). In addition, changes in the QRS morphology in leads V1–V3 with the appearance of new Q waves were noted. A notable variation in the mean corrected QT (QTc) period with decrease in duration in prone posture ECG (385 ± 64.8) relative to supine (406 ± 18.8, p=0.05). Conclusions Prone position ECG resulted in significant changes in healthy adults that should be aware of this as this can affect diagnosis and management strategies. Further studies are needed to investigate the impact of prone position on ECG recording in patients with cardiovascular diseases.

Acute chest pain with ST-segment elevation in lead V1–V3: when you hear hoofbeats, also look for zebras

ST-segment elevation (STE) in the anterior precordial leads is the hallmark of anterior myocardial infarction. In rare cases, this ECG pattern may be due to isolated infarction of the right ventricle since leads V1-V3 directly overlie the right ventricular free wall. Herein, we aimed to provide clues to recognize and understand this diagnostic pitfall through a series of 4 patients presenting with STE in the anterior leads.

Early electrocardiographic indices for predicting chronic doxorubicin-induced cardiotoxicity

BackgroundDealing with chemotherapy-related cardiac dysfunction (CTRCD) remains a significant problem complicated by the difficulty in early detection of cardiotoxicity. Electrocardiogram (ECG) is expected to be the most realistic methodology due to lower cost-performance and non-invasiveness. We investigated the long-term visual fluctuations in the ECG waveforms in patients with chronic doxorubicin (DOX)-induced cardiotoxicity to identify ECG indices for the early detection of cardiotoxicity. MethodsWe conducted a retrospective case series study by reviewing the medical records of 470 consecutive patients with malignant lymphoma who were treated with DOX at our institute between January 2010 and December 2017. Of them, 23 (4.9%) patients developed left ventricular dysfunction and were diagnosed with CTRCD using echocardiography. We assessed the ECG indices on 12-lead ECG recordings before and after treatment in 15 patients; eight patients were excluded due to conduction disturbances or atrial fibrillation. ResultsCTRCD was detected at a median of 475 (interquartile range, IQR: 341–1333) days after initiating chemotherapy. The evaluation of ECG indices preceding CTRCD development was performed 93 (IQR: 52–232) days before the detection of CTRCD. In the stage of CTRCD, the most significant ECG change was T-wave flattening in leads V3–V6 (12 patients, 80%). Additionally, QTa prolongation was observed in leads I and aVL (n = 10, 66%), leads II, III, and aVF (n = 9, 60%), and leads V3–V6 (n = 10, 73%). These ECG changes were not observed before the treatment but were detected mildly in the pre-CTRCD stage, which subsequently worsened in the CTRCD stage. ConclusionsThis study indicated that T-wave changes and QTa prolongation may be useful as an early indicator before the onset of CTRCD in patients with DOX-induced cardiotoxicity.

Brugada Syndrome – Report of Familial Occurrence Diagnosed in the Emergency Department

Abstract Introduction: Brugada syndrome represents the clinical manifestation of a rare disease with genetic etiology. The syndrome is characterized by ventricular dysrhythmias associated with syncope or sudden cardiac death in the lack of any structural cardiac disease. The diagnosis of Brugada syndrome is established if a type 1 electrocardiographic (ECG) pattern of ST-segment and QRS morphology is present, in association with certain clinical manifestations and/or familial history. Case presentation: A 31-year-old male patient, without any medical history, presented in the emergency department (ED) of a clinical center. His only complaints consisted in palpitations, chest discomfort, and emotional stress related to the recent death of his wife. Earlier on the same day, his wife, a 25-year-old female was brought via emergency medical services (EMS) to the ED after presenting ventricular fibrillation. The female patient presented a long term history of chest pain and one year prior to this episode she presented idiopathic ventricular fibrillation, for which she had undergone implantation of an automated cardioverter defibrillator. As the couple were cousins, the EMS specialist suspected the presence of a familial cardiac disorder. The electrocardiogram of the male patient revealed a coved-type ST-segment elevation of 4 mm in leads V1–V3 compatible with type 1 Brugada syndrome. Conclusion: In case of Brugada syndrome, a genetic disorder associated with increased risk of SCD, the patient's first-degree relatives should be investigated as well, in order to identify the presence of the syndrome and to prevent SCD. As the sole established effective therapeutic measure for patients diagnosed with Brugada syndrome, ICD implantation should be considered in order to decrease the risk of syncope and SCD. This case is particular because a rare disease with familial etiology was identified in both husband and wife, who were cousins.

Brugada syndrome in a young patient with type 1 myotonic dystrophy requiring an implantable cardioverter defibrillator for primary prevention: a case report.

Background Cardiac electrical disturbances represent the most frequent cardiac manifestations of myotonic dystrophy Type 1 (MD1). Limited data suggest that the prevalence of Brugada syndrome in MD1 may be increased compared to the general population.Case summary We report a case of a 22-year-old asymptomatic man with repolarization abnormalities in leads V1–V3 suggestive of Type III Brugada pattern. The patient had a family history of MD and incidents of sudden death in relatives. Drug-induced Brugada Type 1 syndrome was revealed after procainamide challenge. A ventricular stimulation study was positive since a polymorphic ventricular tachycardia was induced after two extrastimuli. The patient underwent implantation of a single chamber cardiac defibrillator (ICD). Eight months after the procedure he suffered an appropriate ICD shock due to rapid polymorphic ventricular tachycardia.Discussion Brugada syndrome is linked with MD1. Potential life-threatening arrhythmias may develop in the adult life of MD1 patients. Electrocardiographic surveillance and tailored invasive treatment with ICDs can prevent sudden cardiac death in this setting.