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Background: Several electrocardiographic (ECG) algorithms have been developed for predicting accessory pathway (AP) location in Wolff–Parkinson–White syndrome. However, their accuracy may be related to the manifested degree of preexcitation on ECG. Aims: Our goal was to assess the effect of the degree of preexcitation on the accuracy of 4 traditional AP localization algorithms and to compare them with the algorithm specifically designed for ECGs with maximal preexcitation (Pambrun) Methods: The study included 300 patients who underwent successful ablation of an overt atrioventricular AP. Resting and maximally preexcited ECGs obtained during incremental atrial pacing were assessed using 4 traditional AP localization algorithms: Xie, d’Avila, Iturralde, and Taguchi. Maximally preexcited ECGs were additionally assessed with the Pambrun algorithm. We compared the precision of the algorithms to predict accurate or anatomically adjacent AP location. Results: Theoverall accuracy of traditional AP localization algorithms using resting ECG ranged between 26% and 53.7% and improved to a range of 47.3% to 69.7% when adjacent locations were accepted. When used with maximal preexcitation, all algorithms had significantly higher accuracy, with a mean improvement of 14.3 and 15.6 percentage points for precise and adjacent sites, respectively. The Pambrun algorithm for maximally preexcited ECGs had the highest precision for both accurate and adjacent locations of the APs (89.7% and 97%, respectively). Conclusions: Greater preexcitation on ECG improved the accuracy of the traditional AP localization algorithms. The algorithm designed to use maximally preexcited ECGs has the best accuracy. Maximally preexcited ECG recordings should preferably be used in clinical practice to facilitate the ablation procedure.

Background: The CHADS2 and CHA2DS2-VASc scores were shown to predict mortality in patients with atrial fibrillation. However, pathophysiology and treatment outcomes of atrial fibrillation and typical atrial flutter (AFL) differ. Consequently, the prognosis of patients with AFL can also be different. Aims: The aim of the study was to assess CHADS2 and CHA2DS2‑VASc scores as mortality predictors in patients with typical AFL. Methods: Large cohort of consecutive patients with typical AFL who underwent catheter ablation was retrospectively analyzed. The CHADS2 and CHA2DS2‑VASc were calculated using hospital record data. All-cause mortality data was obtained from the registry of national personal identification numbers. The Kaplan–Meier method and multivariable Cox proportional hazard models were applied for survival and hazard ratio analyses, respectively. Results: A total of 469 patients hospitalized for typical AFL ablation were enrolled (mean [SD] age, 63.7 [12.2] years; male sex, 69.1%). Patients were followed from 2 to 12 years resulting in 2974 patient‑years of follow‑up. The Kaplan–Meier survival analysis revealed a negative impact of each component of the CHADS2 and CHA2DS2‑VASc scores on survival with the exception of stroke (not significant) and female sex (related to abetter survival). Consequently, higher scores were predictive of higher all‑cause mortality rates (2.7%–54% at 10 years); the CHA2DS2‑VASc score was equally predictive as the CHADS2 score. Conclusions: In patients referred for typical AFL ablation, the CHADS2 score can be applied for prognostic assessment. A successful AFL ablation procedure should not divert the attention from recognizing and addressing other medical issues that have an impact on long‑term mortality, which remains very high in this population of patients.

We described 2 patients (28-year-old and 69-year-old females) with hypercalcemia (4.47 mmol/L and 4.8 mmol/L), chest painand electrocardiogram with ST-T segment changes mimicking acute coronary syndrome. One patient presented ST segment elevation in right precordial leads V1-V3 max. 4 mm, the second one presented negative T waves in V1-V6 leads. Troponin level was normal in both cases. Additionally, corrected QT apex was shortened in both cases, 250 ms and 206 ms respectively and T wave humps in lateral leads was observed.

Atypical form of tako-tsubo cardiomyopathy (TTC) is associated with regional wall motion abnormalities in basal and/or middle segments or only middle segments with sparing of apical segments or apical and basal segments. We described a case of47-year-old female with atypical form of TTC due to fast atrial fibrillation that converted into ventricular fibrillation in WPW syndrome. The echocardiogram made after direct current cardioversion revealed decreased left ventricular ejection fraction (LVEF 35%) with akinesis of inferior and posterior walls and anterior part of interventricular septum in the middle and the basal segments with hyperkinesis of apical segments. The biochemistry blood samples revealed elevated both troponin T- 0.35 ng/mL and NT-proBNP - 3550 pg/mL plasma level. The ECG showed sinus rhythm 62 bpm, shortened PQ interval 100 ms, widened QRS duration - 115 ms with delta wave, prolonged QT interval - 520 ms, QS in leads: II, III, aVF. NegativeT waves in leads: I, aVL and positive, symmetrical T waves in leads V1-V6. The coronarography revealed normal coronaryarteries. The control echocardiography after 10 days showed normal LVEF 70%, without any wall motion abnormalities. TTC was recognised based on: history of sudden stress situation before, ischaemic ECG changes, positive markers of myocardial injury, transient segmental wall motion abnormalities and normal coronary arteries. The ablation of right postero-septal accessory pathway was successfully performed.

We present a case of broad QRS complex tachycardia and atrioventricular (AV) dissociation that was documented during electrophysiological study to be a supraventricular rather than a ventricular tachycardia. Ablation of AV nodal slow pathway eliminated the arrhythmia confirming the diagnosis of atypical AV nodal reentrant tachycardia.

We here describe a surface 12-lead electrocardiogram (ECG) of a 72-year-old female with a prior history of breast cancer and chemotherapy-induced cardiomyopathy. An echocardiogram revealed left ventricular dysfunction, ejection fraction of 23%, with mild enlarged left ventricle. The 12-lead ECG showed atrial fibrillation with a mean heart rate of about 100 bpm, QRS duration 160 ms, QT interval 400 ms, right bundle branch block (RBBB) and left anterior fascicular block (LAFB). The combination of RBBB features in the precordial leads and LAFB features in the limb leads is known as ''masquerading bundle branch block''. In most cases of RBBB and LAFB, the QRS axis deviation is located between - 80 to -120 degrees. Rarely, when predominant left ventricular forces are present, the QRS axis deviation is near about -90 degrees, turning the pattern into an atypical form. In a situation of RBBB associated with LAFB, the S wave can be absent or very small in lead I. Such a situation is the result of not only purely LAFB but also with left ventricular hypertrophy and/or focal block due to scar (extensive anterior myocardial infarction) or fibrosis (cardiomyopathy). Sometimes, this specific ECG pattern is mistaken for LBBB. RBBB with LAFB may imitate LBBB either in the limb leads (known as 'standard masquerading' - absence of S wave in lead I), or in the precordial leads (called 'precordial masquerading' - absence of S wave in leads V₅ and V₆). Our ECG showed both these types of masquerading bundle branch block - absence of S wave in lead I and in leads V₅ and V₆.

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 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.

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.

We present a case of 8 year-old boy with several episodes of ventricular fibrillation in the course of tachycardia-mediated cardiomyopathy and severe decompensated heart failure. The cardiomyopathy was caused by incessant long-RP tachycardia that was resistant to pharmacotherapy. Despite initial suspition that the arrhythmia was permanent junctional reciprocating tachycardia (PJRT) electrophysiology study revealed atypical atrioventricular nodal reentrant tachycardia. Due to clinical and electrocardiographical presentation mimicking PJRT such arrhythmia merits the name ‘pseudo PJRT’.

A 34-year-old male with dilated cardiomyopathy and advanced heart failure was referred for defibrillator implantation for primary prevention of sudden cardiac death. During implantation despite multiple right ventricular (RV) lead positions (outflow tract, septum, apex) and various defibrillation vector combinations (superior vena cava coil on/off, polarity reversal, tilt change), the maximum energy shock (40 J) from the implanted device was unsuccessful in restoring the sinus rhythm. In a straightforward fashion another regular single coil shocking lead was introduced to the azygos vein using telescoping system for coronary sinus cannulation and coronary vein subselection. The terminal pin of the new shocking coil was inserted into the superior vena cava coil port of the device header; the old superior vena cava coil pin and the redundant RV pacing IS-1 pin of the new lead were caped. This resulted in a successful defibrillation with the energy of 30 J and thus in obtaining the required 10 J safety margin. Azygos vein implantation technique was described and it's merits discussed.

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.

The aim of this study was to evaluate the short term effect of cardiac resynchronisation therapy (CRT) on right ventricular (RV) function assessed by standard echocardiography.Data from 57 patients (54 men, 95%; three women, 5%), aged 66.4 ± 8.7 years with heart failure (HF) was analysed. All patients were in NYHA III-IV functional classes, despite optimal pharmacological treatment according to the current guidelines, had left ventricular ejection fraction ≤ 35% and QRS complex ≥ 120 ms in a standard electrocardiogram. At baseline and three months after CRT implantation the patients' histories were taken, an anthropometrical examination was made, laboratory tests including the level of NT-proBNP and electrocardiogram were performed, and echocardiographic examination was extended by tissue Doppler imaging techniques and complex RV evaluation.Three months after CRT implantation in the whole study group, the average NYHA functional class had decreased from 3.11 ± 0.28 to 2.25 ± 0.68 (p0.001), and the six-minute walk test distance had increased from 298.04 ± 107.42 m to 373.12 ± 127.15 m (p0.001). CRT improved RV systolic function in the whole study group. Tricuspid annular plane systolic excursion had increased from 13.95 ± 2.80 to 15.79 ± 2.33 mm (p0.001), and so likewise had systolic excursion velocity (S'), which rose from 8.84 ± 3.45 to 11.00 ± 3.43 cm/s (p0.001). Tricuspid regurgitation grade decreased from 2.02 ± 0.95 to 1.86 ± 0.91 (p = 0.013). RV systolic pressure decreased from 31.07 ± 20.43 to 27.75 ± 17.35 mm Hg (p0.001). RV fractional area change rose from 31.35 ± 10.30% to 35.40 ± 10.51% (p0.001).This study showed that CRT improved RV systolic function evaluated with parameters assessed in standard echocardiographic examination three months after therapy initiation. The observed improvement was consistent among all applied echocardiographic parameters reflecting RV systolic function.

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.

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.

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.

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 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.

Two cases of frequent ventricular ectopy are described. Case one: a 49 year-old woman with post myocarditis extrasytoles (34 000/24 h). The ectopic focus was located on the tricuspid annulus - directly in the area of largest and sharpest His bundle potential and where direct His bundle capture was observed during all pace mapping attempts. Case two: a 15 year- -old men with idiopathic, very frequent premature ventricular beats from septal aspect of the mitral annulus. The area of earliest activation during the spontaneous ectopy with 12/12 pace map match showed obvious His bundle potential, moreover, the radiofrequency ablation catheter was unstable in that position (inferoseptal from retrograde aortic approach). In both cases treatment with cryoablation was successfully and uneventful. In conclusion, cryoablation instead of radiofrequency current ablation should be used for ventricular ectopy from septal part of the tricuspid or mitral annuli especially in cases of parahisian localisation and/or catheter instability.

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.

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.