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Electrocardiographic (ECG) abnormalities in the setting of acute pulmonary embolism (PE) are being increasingly characterized and mounting evidence suggests that ECG plays a valuable role in prognostication for PE. We review the historical 21‐point ECG prognostic score for the severity of PE and examine the updated evidence surrounding the utility of ECG abnormalities in prognostication for severity of acute PE. We performed a literature search of MEDLINE, EMBASE, and PubMed up to February 2015. Article titles and abstracts were screened, and articles were included if they were observational studies that used a surface 12‐lead ECG as the instrument for measurement, a diagnosis of PE was confirmed by imaging, arteriography or autopsy, and analysis of prognostic outcomes was performed. Thirty‐six articles met our inclusion criteria. We review the prognostic value of ECG abnormalities included in the 21‐point ECG score, including new evidence that has arisen since the time of its publication. We also discuss the potential prognostic value of several ECG abnormalities with newly identified prognostic value in the setting of acute PE.

We report a case of 82‐year‐old female with total masquerading bundle branch block. We discuss the problems with ECG analysis.

To establish an appropriate treatment strategy and determine if ablation is indicated for patients with narrow QRS complex supraventricular tachycardia (SVT), analysis of a standard 12-lead electrocardiogram (ECG) is required, which can differentiate between the 2 most common mechanisms underlying SVT: atrioventricular nodal reentry tachycardia (AVNRT) and orthodromic atrioventricular reentry tachycardia (OAVRT). Recently, new, highly accurate electrocardiographic criteria for the differential diagnosis of SVT in adults were proposed; however, those criteria have not yet been validated in a pediatric population. All ECGs were recorded during invasive electrophysiology study of pediatric patients (n = 212; age: 13.2 ± 3.5, range: 1–18; girls: 48%). We assessed the diagnostic value of the 2 new and 7 standard criteria for differentiating AVNRT from OAVRT in a pediatric population. Two of the standard criteria were found significantly more often in ECGs from the OAVRT group than from the AVNRT group (retrograde P waves [63% vs 11%, P

A 46-year-old male was admitted to our emergency department due to a narrow QRS tachycardia of 230 bpm with impeding hemodynamic collapse. His only remarkable medical history was mild hypertension. Adenosine administration was ineffective in stopping the tachycardia, and sinus rhythm was restored using an electrical cardioversion. A few weeks later, during an electrophysiology study an identical tachycardia was immediately induced during the introduction of diagnostic catheters into the right atrium (Fig. 1, upper panel). A rate-related right bundle branch block aberration was present for most of the time. Atrial activation was simultaneous with ventricular activation, ruling out atrioventricular reentrant tachycardia (AVRT), and suggesting atrioventricular nodal reentrant tachycardia (AVNRT) (Fig. 1, lower panel). To confirm the absence of atrial tachycardia, ventricular entrainment pacing using a cycle length shorter by 30 milliseconds than the tachycardia cycle length was performed. The atrial rate accelerated to the pacing rate (Fig. 2), and when ventricular (V) pacing was ceased, the activation sequence was the last entrained atrium (A) followed by the ventricle (V) (i.e., a V-A-V response). Such a response is considered to rule out atrial tachycardia and these findings were repeatable. Therefore, by exclusion of all other possible causes a diagnosis of AVNRT could have been considered irrefutable. However, long VA interval during entrainment and the atrial activation sequence with atrial depolarization later on His catheter than on high right atrial catheter (Fig. 1, lower panel) were not compatible with slow-fast AVNRT, either. Moreover, multiple attempts to stop the tachycardia with fast ventricular and atrial burst pacing failed. This prompted a more detailed assessment of the atrial activation sequence and an analysis of entrainment from the right atrium. Those analyses both led to an unquestionable diagnosis of a macroreentrant right atrial tachycardia with a reentrant circuit identical to that observed in a typical clockwise atrial flutter, albeit slower, which resulted in a rate below the arbitrary thresh

BACKGROUND: Electrocardiography (ECG) is still one of the first tests performed at admission, mostly in patients (pts) with chest pain or dyspnea. The aim of this study was to assess the correlation between electrocardiographic abnormalities and cardiac biomarkers as well as echocardiographic parameter in patients with acute pulmonary embolism. METHODS: We performed a retrospective analysis of 614 pts. (F/M 334/280; mean age of 67.9 ± 16.6 years) with confirmed acute pulmonary embolism (APE) who were enrolled to the ZATPOL‐2 Registry between 2012 and 2014. RESULTS: Elevated cardiac biomarkers were observed in 358 pts (74.4%). In this group the presence of atrial fibrillation (p = .008), right axis deviation (p = .004), S(1)Q(3)T(3) sign (p

T-wave inversion (TWI) is a common ECG finding in patients with acute pulmonary embolism (APE).To determine the prevalence of TWI in patients with APE and to describe their relationship to outcomes.Retrospective study of 437 patients with APE. TWI patterns were described in two distributions: inferior (II, III, aVF) and precordial (V1-V6).TWI was observed in 258 (59%) patients. The mortality rate was significantly higher in the group with TWI in the inferior AND precordial leads compared to the group without TWI (OR: 2.74; p = 0.024) and the group with TWI in the inferior OR precordial leads (OR: 2.43; p = 0.035). As compared those with TWI in5 leads, patients with TWI in ≥5 leads experienced significantly higher rates of death (17.1% vs. 6.6%, OR: 2.92; p = 0.002) and complications.TWI and the quantitative assessment thereof can be useful to risk stratify patients with APE.

Acute cerebro-vascular disorders (ACVD) such as subarachnoid haemorrhage (SAH) increase sympathetic activity and a-adrenergic stimulation. Pathologic a-adrenergic stimulation can provoke several electrocardiogram (ECG) changes including ST-segment depression, wide, broad T-waves, U-waves merging into the T-waves, and QTc prolongation. Previous reports have shown that J-waves can appear in patients with ACVD and a brain injury [1–3]. J-wave is a deflection occurring at the J-point described by Osborn and called ‘the injury current’ in experimental models of hypothermia in dogs [4]. In addition to hypothermic patients, the J-wave can be observed in hypercalcaemia and arrythmogenic disorders such as in patients with idiopathic ventricular fibrillation (VF) who usually depict the so-called ‘Haissaguerre pattern’ [5, 6]. We previously reported the case of patient with SAH and a prominent J-wave associated with VF [7]. The aim of this presentation is to report an unusual ECG presentation in a patient with SAH. We present the case of a 36-year-old man with recent SAH. He was admitted to the ER because of persistent and ‘in-crescendo’ headache. ECG on admission showed sinus rhythm at 60 bpm, PQ interval of 180 ms, QTc of 480 ms

We report a case of 22 years old woman with long QT syndrome type with the first cardiac incidents in the post partum period. We discuss the actual treatment recommendation in the long QT syndrome with special attention on indications for implantation of defibrillator‑cardioverter. JRCD 2014; 1 (6): 15–20

Cardiogenic shock (CS) is a predictor of poor prognosis in patients with acute pulmonary embolism (APE).The aim of this study was to compare electrocardiography (ECG) parameters in patients with APE presenting with or without CS.A 12-lead ECG was recorded on admission at a paper speed of 25 mm/s and 10 mm/mV amplification. All ECGs were examined by a single cardiologist who was blinded to all other clinical data. All ECG measurements were made manually.Electrocardiographic data from 500 patients with APE were analyzed, including 92 patients with CS. The following ECG parameters were associated with CS: S1Q3T3 sign, (odds ratio [OR]: 2.85, P.001), qR or QR morphology of QRS in lead V1, (OR: 3.63, P.001), right bundle branch block (RBBB) (OR: 2.46, P=.004), QRS fragmentation in lead V1 (OR: 2.94, P=.002), low QRS voltage (OR: 3.21, P.001), negative T waves in leads V2 to V4 (OR: 1.81, P=.011), ST-segment depression in leads V4 to V6 (OR: 3.28, P.001), ST-segment elevation in lead III (OR: 4.2, P.001), ST-segment elevation in lead V1 (OR: 6.78, P.01), and ST-segment elevation in lead aVR (OR: 4.35, P.01). The multivariate analysis showed that low QRS voltage, RBBB, and ST-segment elevation in lead V1 remained statistically significant predictors of CS.In patients with APE, low QRS voltage, RBBB, and ST-segment elevation in lead V1 were associated with CS.

Background European recommendations on the management of acute pulmonary embolism (APE) divide patients into 3 risk categories: high, intermediate, and low. Mortality has previously been estimated at 3% to 15% in the intermediate group. The aim of this study was to use a new metric "ischemic electrocardiographic (ECG) patterns" to more precisely estimate the risk (complications or death) of APE patients identified as "intermediate risk" by current European Society of Cardiology (ESC) criteria. Methods The study group consisted of 500 consecutive patients (290 females), with a mean age 66.3 ± 15.2 years, and 245 (72.8%) patients were initially classified as intermediate risk. Four ischemic ECG patterns were studied: (i) ST-segment ischemic pattern (STIP), (ii) global ischemic pattern (GIP), (iii) negative T wave pattern, and (iv) control group consisting of patients with no ischemic changes. Results Predictors of death in univariate analysis included elevated troponin concentration (odds ratio [OR], 6.8; 95% confidence interval [CI], 1.28-169; P = 0.02]) and ischemic ECG patterns: STIP (OR, 6.3; 95% CI, 1.6-46.0; P = 0.007). Patients with right ventricular dysfunction (RVD) who were STIP (+) experienced significantly higher mortality rate compared to RVD patients who were STIP(−) (11.4% vs 1.6%; OR, 7.26; 95% CI, 1.82-52.8; P = 0.004). In patients with STIP (+) as compared to STIP (−), rate of death (OR, 6.35; P = 0.007) and rate of complications (OR, 4.19; P = 0.002) were significantly higher. Neither presence of negative T-waves nor GIP pattern was associated with a worse prognosis. Conclusions In patients with APE, an ischemic ECG pattern on hospital admission, when identified in addition to classic risk markers, is an independent risk factor for worse in-hospital outcomes.

We present the case of a 72-year-old man who was admitted because of acute ST-segment elevation myocardial infarction and presented with second-degree atrioventricular block with 4:2 conduction. We propose 3 alternative explanations for such an unusual conduction pattern: (1) supernormal conduction, (2) 2-level block with 4:1 conduction ratio in the upper level and 3:2 conduction ratio in the lower level, and (3) presence of 2 populations of Purkinje cells in the remaining, critically injured fascicle, one with the phase-3 block and the other with slow diastolic depolarization, leading, during a pause after the first nonconducted P, to phase-4 block.

We describe 5 cases of a rare and often lethal arrhythmia: short-coupled variant of torsade de pointes. In the light of quitecharacteristic electrocardiograms and clinical picture of this arrhythmia, we consider the name ‘short-coupled variant torsade de pointes’ as more appropriate than, the more commonly applied term for such cases — ‘idiopathic ventricular fibrillation’. We suggest that in patients with unexplained syncope, normal echocardiogram, normal QT interval and frequent premature ventricular contraction with short coupling this arrhythmogenic entity should be suspected. We stress that these premature beats are often misclassified as supraventricular since the two major factors (slow initial depolarisation of the working myocardium and structural abnormalities of the left ventricle) responsible for typical morphological features of ventricular beats are lacking.

We present the cases of two patients with hypothermia, with a detailed description of electrocardiographic changes associated with hypothermia. In both cases, J wave was initially misdiagnosed as left bundle branch block (LBBB). We discuss the differentiation of J wave from LBBB.

547-5271/$ -see front matter © 2013 Heart Rhythm Society. All rights reserved isolated with 3 freezes per vein. At the very end of the procedure, however, during the assessment of PV isolation, the tip electrode disengaged from the lasso catheter (Lexx, Biotronik, Berlin, Germany; reprocessed) and “dropped” from the antrum deep into the right superior PV. Apparently, this tiny metal object (7 F in diameter and 2 mm long, Figure 1, inset) moved against the flow of blood and reached a small PV, in which it became wedged. Attempts to reach this venous branch with a catheter or guidewire were un

We described a case of 30 year-old woman with episodes of syncope primarily diagnosed as epilepsy, and finally recognised as long QT syndrome. Based on QTc prolongation > 600 ms in series of electrocardiograms and Holter monitoring the patient was implanted with cardioverter-defibrillator (ICD). During follow-up many appropriate ICD shocks due to ventricular fibrillation occurred.

We present electrocardiograms of a 37 year-old male with frequent extrasystoles and second-degree atrioventricular block. Electrophysiological study confirmed the initial diagnosis of manifest and concealed His bundle ectopy as the cause of his brady- and tachyarrhythmia.

A case of a 33 year-old female with continuous murmur was admitted to the hospital for diagnostic purposes. TEE was inconclusive. Coronary angiography revealed an aneurysm of left anterior descending with the fistula to the right ventricle. The patient underwent implantation of inset of left internal mammary artery graft and ligation of fistula during open heart surgery.

We described a case of a 59-year-old woman without clinical significance. Abnormal resting electrocardiogram (ECG) was the cause of the cardiology consultation. The patient complained of the poor exercise tolerance for a year. The resting ECG showed: sinus rhythm 58/min, left axis deviation (QRS axis: 79(o)), PQ interval: 108 ms, P wave axis: 77(o), QRS duration: 106 ms, QT/QTc interval: 452/450 ms. QS morphology in leads: II, III, aVF and V(5)-V(6) with QRS (QS) fragmentation. The Q wave in lead V(4) with its duration of 20 ms, and amplitude of 2 mm. The poor progression of R wave in leads V2 and V(3). Positive, symmetric T waves in leads: II, III, aVF and V(5)-V(5). Negative T wave in leads I and aVL. Increased S wave amplitude in leads: V(2) - 33 mm, V(3) - 29 mm. Positive QRS direction in lead aVR. What should be taken into consideration in differential diagnosis? 1) previous infero-lateral myocardial infarction; 2) myocardial hypertrophy; 3) possibility of preexcitation. Based on echocardiography hypertrophic cardiomyopathy was recognised with marked septum hypertrophy to 28 mm and with normal thickness of posterior wall (9 mm). The magnetic resonance of the heart confirmed the echocardiography findings.

Epsilon waves (EW) in right precordial leads are reliable diagnostic electrocardiographic criteria of arrhythmogenic right ventricular dysplasia-cardiomyopathy (ARVD/C). The definition of EW remains difficult because within the QRS complex are inscribed notches or deflections called fragmentation of the QRS complex (f-QRS). The f-QRS at the beginning, on the top, and at the end of QRS complex (termed "pre-, top-, and postsilons") was proposed as typical extended definition of EW. We described a 59-year-old female with ARVD with severe left ventricular involvement, ejection fraction - 23%. The standard 12-lead ECG showed QRS fragmentation in 7 leads. It can be a marker of ARVD with severe left ventricular disease. EW may be enhanced visually to 50-75% by following placing: the left arm should be placed on the xyphoid process and the right arm lead on the manubrium sternum, with the left leg in the location of V4 or V5 this is called the Fontaine bipolar precordial lead (F-ECG). Detection of right precordial f-QRS can be improved using higher right precordial leads (similar as in Brugada syndrome). The case we described reminds that EW could be enhancing by F-ECG leads and f-QRS by using higher right precodial leads.

We described ECG of a 22-year-old healthy man, professional basketball player, who has been training since he was 14. Physical examination was normal. In ECG the following abnormalities of repolarisation were observed: biphasic, positive/negative T waves in leads V3-V6. This changes normalised during deep breathing test. The echocardiogram revealed normal size of the heart's chambers, left ventricular walls hypertrophy - septum and posterior wall: 14 mm, normal mitral inflow - E/A = 1.1, normal ejection fraction (68%). The exercise test (ExT, 20 METS) was without symptoms. During ExT normalisation of repolarisation abnormalities was observed. From 6(th) minute of the recovery phase the repolarisation abnormalities were observed again. In unselected population of young athletes abnormal ECG is observed in 4.8-11.8% of athletes. Negative T waves in precordial leads are observed 2.3% of the young athletes and in 2.7% young, professional athletes. The repolarisation abnormalities described in our patient belong to electrocardiographic spectrum of the early repolarisation pattern mainly seen in black, young athletes.

A case of a 44-year-old-man with chronic thromboembolic pulmonary hypertension (PH) and C-protein deficiency, with a history of previous acute pulmonary embolism is presented. The ECG showed negative T waves in leads: II, III, aVF and V(1)-V(6). The follow-up echocardiography revealed severe PH with the right ventricular systolic pressure (RVSP) - 95-100 mm Hg, markedly enlarged right ventricular end-diastolic diameter (RVEDD), and decreased left ventricular end-diastolic diameter (LVEDD). The patient was in NYHA III/IV class. He was referred for pulmonary thromboendarterectomy. Three months after thromboendarterectomy echocardiography showed marked reduction of RVEDD, increased LVEDD, RVSP - 50-55 mm Hg. The 3 months follow-up ECG showed normalisation to positive T waves. The patient was in NYHA class I and he stayed on the anticoagulation therapy.

Background: Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J‐wave pattern was suggested to be a marker of a disorder associated with life‐threatening arrhythmias. Results: We report the case of a patient with vasospastic angina and J‐wave pattern in inferior and lateral leads associated with polymorphic ventricular tachycardia which was effectively treated only with quinidine—vasodilating drugs were not able to prevent the arrhythmia although they were effective in preventing ischemic events. Conclusion: The J‐wave pattern in inferolateral leads may be a sign of electrical vulnerability to lethal ventricular arrhythmia in patients suffering from vasospastic angina—quinidine can effectively prevent such arrhythmias in these patients.

Early repolarisation syndrome (ERS) appears in 2-7% of general population, mainly seen in young men, athletes and blacks. Recent publications change the benign character of ERS. It was suggested that ERS can be associated with sudden cardiac death, idiopathic ventricular fibrillation. This article described history and evolution of ERS.

Patients with inferior wall ST segment elevation myocardial infarction (STEMI) are considered to be at lower risk than patients with anterior wall STEMI. Nonetheless, 30-40% of all acute inferior wall MI cases have a poor prognosis.To assess the frequency of ST segment changes (elevation or depression) in lead aVR in inferior STEMI patients, and to determine the clinical course and short-term prognosis of such patients.The study retrospectively analysed the records of 320 consecutive patients with inferior wall STEMI (206 males, 114 females, mean age 65.6 ± 11.1 years). Patients were divided into three groups based on treatment: group A, primary percutaneous coronary intervention (134 patients); group B, fibrinolytic therapy (96 patients); and group C, conservative treatment (no reperfusion therapy) (90 patients). The mean time from onset of pain to the first ECG for all patients was 6.1 h. The total number of in-hospital deaths was 29 (9.0%), comprising 11 (8.2%) in group A, seven (7.3%) in group B, and 11 (12.2%) in group C (NS). The mean maximum creatine phosphokinase was 2,021 ± 1,837 U/L in group A, 1,734 ± 1,581 U/L in group B, and 1,217 ± 981 U/L in group C (p = 0.01). The mean left ventricular ejection fraction was 50.2% ± 9.0%, 54.9 ± 8.6%, and 51.3% ± 9.7% for groups A, B and C, respectively (NS).ST segment changes in lead aVR were observed in 135 (42.2%) patients, comprising elevation in 47 (14.7%) patients and depression in 88 (27.5%) patients. The in-hospital mortality rates for patients with ST segment elevation, ST segment depression, and no ST segment changes were 27.7%, 16.5%, and 1.0%, respectively (p 〈 0.001). For group A, the in-hospital mortality rate was higher in patients with ST segment elevation than in patients with no ST segment changes (15.4% vs 1.2%, p 〈 0.001). For group B, the in-hospital mortality rates were 33.3%, 12.9%, and 0%, in patients with ST segment elevation, ST segment depression, and no ST changes, respectively (p = 0.006). For group C, the in-hospital mortality rate was higher in patients with ST segment elevation (32%) than in patients with ST segment depression (12.5%) and patients with no ST segment changes (2%, p = 0.006). Logistic regression analysis found that female gender, diabetes, hypertension, lower ejection fraction, and cardiogenic shock on admission were independent predictors of ST segment elevation.ST segment changes in lead aVR occurred in approximately half of inferior wall STEMI patients. The presence of such ST segment changes was associated with a poorer prognosis during the hospital stay, and the changes were not associated with the type of reperfusion treatment.

We present a case of a 45 year-old woman with epilepsy diagnosed 24 years earlier. Epilepsy was confirmed by EEG and many seizures episodes were treated with different combination of anticonvulsive drugs. A 24-h Holter ECG monitoring revealed an episode of asystole lasting 82 s. The pacemaker was implanted and antiepileptic therapy with valproic acid chrono (1800 mg/d.) was continued. We review in this article present data on arrhythmic epilepsy.

A case of a 19 year-old female with the Niemann-Pick disease and transient left ventricular dysfunction following epileptic seizures is presented. Electrocardiographic features and differentid diagnosis of this condition are presented.

We report a case of 59-year-old man with subarachnoid haemorrhage (SAH) complicated by ventricular fibrillation (VF). Continuous electrocardiogram monitoring revealed that J-waves appeared immediately before the VF. The present report is the first to describe a J-wave-associated VF as another possible mechanism of sudden cardiac death in patients with SAH.

A 35-year-old female, mother of 4 children was admitted to the hospital for coronary angiography before scheduled surgical correction of severe mitral insufficiency. During angiography anomalous ostium of left main artery from pulmonary trunk was found. The patient underwent mitral ring correction, implantation of LIMA-LAD graft and ligation of left coronary artery during open heart surgery.

The electrocardiogram (ECG) is characterised by little sensitivity and specificity in the diagnostic evaluation of acute pulmonary embolism (APE).To assess the significance of ECG changes in predicting myocardial injury and prognosis in patients with APE.The study group consisted of 225 patients (137 women and 88 men), mean age: 66.0 ± 15.2 years, in whom the diagnosis of APE was made, mostly based on computed tomography (n = 206, 92%).We observed 26 in-hospital deaths (mortality rate: 11.5%) and complications occurred in 58 (25.7%) patients. Elevated levels of troponin were observed in 103 (46%) patients. Logistic regression analysis showed that in-hospital mortality was associated with: coronary chest pain (0.06-0.53, OR 0.18), systolic blood pressure below 100 mm Hg (2.3-13.64, OR 5.61), heart rate above 100 bpm (1.17-15.11, OR 4.21), the S1Q3T3 sign (1.31-6.99, OR 3.02), QR in V(1) (1.60-12.32, OR 4.45), ST-segment depression in V(4)-V(6) (0.99-5.40, OR 2.31), ST-segment elevation in III (0.99-6.96, OR 2.64), ST-segment elevation in V(1) (1.74-9.49, OR 4.07); borderline (1.51-16.07, OR 4.93), moderate (1.42-17.74, OR 5.01) and severe troponin elevation (2.88-36.38, OR 10.24). In patients with cTnT(+), compared to patients with normal troponin levels, the following ECG changes were significantly more common: the S1Q3T3 sign (43 vs 21%, p = 0.003), negative T waves in V(2)-V(4) (57 vs 27%, p = 0.0001), ST-segment depression in V(4)-V(6) (40 vs 14%, p = 0.001), ST-segment elevation in III (22 vs 7%, p = 0.0006), V(1) and V(2) (43 vs 10%, p = 0.0001) and QR in V(1) (16 vs 5%, p = 0.007).ECG parameters are useful in predicting myocardial injury and assessing prognosis in patients with APE.

Electrocardiogram (ECG) in patients with acute pulmonary embolism (APE) presents many abnormalities. There are no data concerning prognostic significance of ST-elevation (STE) in lead aVR in patients with APE.To assess the prevalence of STE in aVR in patients with APE and its correlation with clinical course as well as other ECG parameters recorded at admission.The retrospective analysis of 293 patients with APE diagnosed according to the ESC guidelines (182 females, 111 males, mean age 65.4 ± 15.5 years).The STE in lead aVR was observed in 133 (45.3%) patients. In comparison with patients without STE, patients with STE in lead aVR (STaVR[+]) had significantly more often systolic blood pressure 〈 90 mm Hg on admission (27% vs 10%, p 〈 0.001) and positive troponin level (64.8% vs 27.9%, p 〈 0.001). Thrombolytic therapy (14.3% vs 5.6%, p = 0.009) and catecholamines (29.3% vs 7.5%, p 〈 0.001) were more frequently used in patients with STaVR(+). The overall mortality (16.5% vs 6.9%, p = 0.009) and complication rates during hospitalisation (38.3% vs 12.5%, p 〈 0.001) were significantly higher in patients with STaVR(+). The STaVR(+) was significantly more frequent in patients with negative T-waves in inferior leads (59.4% vs 39.4%, p 〈 0.001), STE in lead III (24% vs 5.6%, p 〈 0.001), STE in lead V1 (46.6% vs 7.5%, p 〈 0.001), ST depression in lead V(4)-V(6) (48.9% vs 7.5%, p 〈 0.001), right bundle branch block (15.8% vs 8.1%, p = 0.04), QR sign in lead V1 (18% vs 6.2%, p 〈 0.001) and SI-QIII-TIII (46.6% vs 21.2%, p 〈 0.001).The presence of STE in lead aVR in patients with APE is associated with poor prognosis. The presence of STE in lead aVR could be an easily obtainable and noninvasive ECG parameter, helpful in risk stratification of patients with APE.

We assessed the specificity of wide QRS complex tachycardia (WCT) differentiating algorithms in patients with preexistent left bundle branch block (LBBB) and heart failure.Three hundred fourteen patients with resynchronization devices were retrospectively screened. electrocardiograms with supraventricular LBBB rhythm were used as a surrogate for supraventricular tachycardia QRS morphology. The Pava lead II criterion, ventricular activation velocity ratio (Vi/Vt) ratio in V(2), Vereckei aVR, Brugada, Griffith, and Bayesian algorithms were investigated.The WCT algorithms had a lower specificity (33%-69%) in patients with LBBB than in general WCT populations. The Pava lead II criterion and Brugada algorithm had higher specificity than other algorithms (P.05). Several of the single criteria (absence of an RS complex in V(1) through V(6), initial R wave in aVR, Vi/Vt1 in V(2)) had specificities of 92% to 99%.In patients with heart failure and LBBB, an electrocardiographic diagnosis of ventricular tachycardia should be based on selected, specific criteria rather than on WCT algorithms.

We describe 2 patients with arrhythmogenic right ventricular cardiomyopathy (ARVD): 58 year-old female and 48 year-old man. Both patients presented with echocardiographic features typical for ARVD and impaired systolic left ventricular function. Both patients had symptoms resembling acute coronary syndrome and received cardioverter-defibrillator due to recurrent sustained ventricular tachycardia.

Some de- and re-polarization patterns can reflect an increased risk of ventricular tachyarrhythmias. We studied whether some electrocardiographic (ECG) patterns are able to predict the development of ventricular fibrillation (VF) during acute myocardial infarction (MI).We compared the patterns of ST-T segment of 78 patients who developed VF during acute MI (patient with VF) vs 170 comparable patients with acute MI but with no VF complications.Of the VF group, 47 developed out-of-hospital VF and 31 developed VF after their admission to the hospital. A steep downsloping ST segment toward a negative T wave with or without a short, flat, or rising portion at the initial portion was observed in 69.2% of the 78 patients: 61.3% in patients with pre-VF and 74.5% in patients with post-VF, vs 9.4% of patients who did not develop VF (P.0001). In 90.6% of the latter, a typical upward-concave or convex "ischemic" pattern of the ST segment was observed. Thus, the characteristic ST-T patterns were highly associated with VF with a specificity greater than 90%.A steep downsloping ST segment may characterize the ECGs of patients who develop VF during acute MI.

The clinical picture of acute pulmonary embolism (APE) is often uncharacteristic and may mimic acute coronary syndrome (ACS) or lung diseases, leading to misdiagnosis. In 50% of patients, APE is accompanied by chest pain and in 30-50% of the patients markers of myocardial injury are elevated.To perform a retrospective assessment of how often clinical manifestations and investigations (ECG findings and elevated markers of myocardial injury) in patients with APE may be suggestive of ACS.We included 292 consecutive patients (109 men and 183 women) from 17 to 89 years of age (mean age 65.4 ± 15.5 years) with APE diagnosed according the ESC guidelines.Among the 292 patients included in the study 33 patients died during hospitalisation (mortality rate 11.3%) and 73 (25.0%) patients developed complications. A total of 75 (25.7%) patients were classified as high risk according to the ESC risk stratification, 163 (55.8%) as intermediate risk and 54 (18.5%) as low risk. Chest pain on and/or before admission was reported by 128 (43.8%) patients, including 73 (57.0%) patients with chest pain of coronary origin, 52 (40.6%) patients with chest pain of pleural origin and 3 patients with pain of undeterminable origin based on the available documentation. A total of 56 (19.2%) patients had a history of ischaemic heart disease and 5 (1.7%) had a history of myocardial infarction. A total of 8 (2.7%) patients were admitted with the initial diagnosis of ACS. The high-risk group consisted of 15 (20.6%) patients with a typical retrosternal chest pain and 60 (27.3%) patients without the typical anginal pain. Elevated troponin was observed in 103 (35.3%) patients. The ECG changes suggestive of myocardial ischaemia (inverted T waves, ST-segment depression or elevation) were observed in 208 (71.2%) patients. The following findings were significantly more common in high-risk versus non-high-risk patients: ST-segment depression in V4-V6 (42.6% vs 23.9%, p = 0.02), ST-segment elevation in V1 (46.7% vs 20.0%, p = 0.0002) and aVR (70.7% vs 40.1%, p = 0.0007).One third of patients with APE may present with all the manifestations (pain, elevated troponin and ECG changes) suggestive of ACS. The ECG changes suggestive of myocardial ischaemia are observed in 70% of the patients with ST-segment depression in V4-V6 and ST-segment elevation in V1 and aVR being significantly more common in high-risk vs non-high-risk patients.

Wellens syndrome is characterised by negative or biphasic T waves in V2-V4 leads and critical stenosis of proximal part of the left descending coronary artery. These ECG changes without atherosclerotic changes in coronary angiography, i.e. coronary artery spasm are called pseudo-Wellens syndrome. We describe a patient with acute coronary syndrome and pseudo-Wellens syndrome as a cause of vasospastic angina. These ECG abnormalities need differentiation with acute pulmonary embolism.

Background : To assess the influence of electrocardiographic (ECG) pattern on prognosis and complications of patients hospitalized with acute pulmonary embolism (APE). Methods : We performed a retrospective analysis of 292 patients who had confirmed APE. There were 183 females and 109 males, the age range was 17 to 89 years, and the mean age was 65.4 ± 15.5 years. Results : In our study group, there were 33 deaths (mortality rate, 11.3%), and 73 (25%) patients developed complications during hospitalization. Based on European Society of Cardiology risk stratification, we classified 75 (25.7%) patients as high risk, 163 (55.8%) patients as intermediate risk, and 54 (18.5%) patients as low risk. A comparison between patients with complicated APE and those with no complications during hospitalization indicated that the following ECG parameters were more common in patients who had complications: atrial fibrillation, S1Q3T3 sign, negative T waves in leads V2–V4, ST segment depression in leads V4–V6, ST segment elevation in leads III, V1 and aVR, qR in lead V1, complete right bundle branch block (RBBB), greater number of leads with negative T waves, and greater sum of the amplitude of negative T waves. In multivariate analysis, the sum of negative T waves (OR 0.88; p = 0.22), number of leads with negative T waves (OR 1.46; p = 0.001), RBBB (OR 2.87; p = 0.02) and ST segment elevation in leads V1 (OR 3.99; p = 0.00017) and aVR (OR 2.49; p = 0.011) were independent predictors of complications during hospitalization. In turn, in multivariate analysis, only the sum of negative T waves (OR 0.81; p = 0.0098), number of leads with negative T waves [OR 1.68; p = 0.00068] and ST segment elevation in lead V1 (OR 4.47; p = 0.0003) were independent predictors of death during hospitalization. Conclusions : In our population of APE patients, the sum of negative T waves, the number of leads with negative T waves and the ST segment elevation in lead V1 were independent predictors of death during hospitalization. In turn, the sum of negative T waves, the number of leads with negative T waves, and RBBB and ST segment elevation in leads V1 and aVR were independent predictors of complications during hospitalization. We conclude that ECG analysis may be a useful noninvasive method for risk stratification of patients with APE. ( Cardiol J 2011; 18, 6: 648–653 )

We present the case of a 25 year-old man referred for an electrophysiological study due to suspected pre-excitation as the cause of two recent syncopal episodes. The admission electrocardiogram (ECG) showed a borderline PR interval of 120 ms and apparently small delta waves visible in leads V2-V4. Intracardiac recordings showed a short HV interval of 18 ms that was stable despite decremental atrioventricular conduction. A fasciculoventricular accessory pathway was diagnosed. Administration of ajmaline normalized ECG and HV interval. We discuss electrocardiographical features of this rare bypass tract.

We describe a case of an 85-year-old woman admitted to hospital because of syncope with palpitations. The patient had mistakenly taken sotalol 120 mg/d together with carvedilol 6.25 mg/d. On hospital admission, ECG showed sinus bradycardia 52 bpm with marked QT prolongation: QTc presented variability from beat to beat (840 ms - 640 ms - 820 ms - 640 ms, respectively) with associated macro-alternans of T wave. T wave alternans was observed within the ascending portion of negative T wave. Beside it a J wave was seen.