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Background: Atrial fibrillation (AF) is the most common clinically-significant arrhythmia in the adult population, and it is a strong independent risk factor for cerebrovascular accidents. Patients with non-valvular AF are five times more likely to suffer a stroke. Despite the clear recommendations for anticoagulant therapy, many clinicians are still reluctant to provide routine oral anticoagulation to patients with AF, despite the potential clinical benefits. Aim: To compare Polish and European populations of patients with AF and the every-day practice of stroke prevention in Poland and in the rest of Europe. Methods: We analysed the baseline data from the two first cohorts of patients enrolled in the GARFIELD-AF registry (an ongo­ing prospective, multicentre, international registry of patients newly diagnosed with AF) in Poland and in the rest of Europe. Results: Polish AF patients are generally younger (median age 67 years in both cohorts vs. 73 in cohort 1 in the rest of Eu­rope and 72 in cohort 2), but they carry a burden of more concomitant diseases. There are some noticeable differences in stroke prevention between Poland and the rest of Europe. The use of vitamin K antagonists (VKAs) is generally higher in other European countries in both cohorts (in Poland 41.7% in cohort 1 and 36.9% in cohort 2 vs. 55.5% in cohort 1 and 41.9% in cohort 2 in the rest of Europe). Meanwhile, it is generally more common in Poland to treat patients with both VKAs and antiplatelets (in cohort 1 20.4% of patients in Poland received vs. 12.0% in the rest of Europe). A total of 5.6% of patients in cohort 1 in Poland receive no antithrombotic treatment (it means: no VKA, oral factor Xa or thrombin inhibitors, antiplate­lets), meanwhile in other countries it amounts to 8.5%. The usage of non-vitamin K oral anticoagulants is growing in Poland similarly to the other European countries. Conclusions: The GARFIELD-AF registry data shows how distant everyday clinical practice is from the guidelines. It shows that still in Poland, as well as in the rest of Europe, too many patients with low stroke risk are treated with anticoagulants, while too frequently patients at high stroke risk are left with no stroke prevention. Although the tendency to use non-vitamin K oral anticoagulants is growing comparably in Poland and in the rest of Europe, the proportion of patients with intermediate and high stroke risk is not growing and more patients at low stroke risk are treated with anticoagulants.

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 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.

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 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.

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.

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.

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.

Acute pulmonary embolism (APE) is a life-threatening disease. Mortality in APE still remains very high in spite of progress in diagnostic tools. Mortality rate is about 30% in patients with unrecognised APE. APE is one of the main causes of in-hospital mortality.To asses management of patients with APE in the Małopolska region.This registry consists of 205 consecutive patients who were hospitalised in 6 cardiology departments between 1 January 2005 and 30 September 2007, with the mean age of 65.1 +/- 15.3 years (124 females and 81 males). Mean hospitalisation duration 14.6 days (1-52 days).During hospitalisation 23 (11.2%) patients died. Complications (death, cardiogenic shock, cardiac arrest, use of catecholamines, respiratory therapy and ventilation) during in-hospital stay were observed in 57 (27.8%) patients. Fifty-three patients were haemodynamically unstable (cardiogenic shock or hypotension). The troponin I or T level was assessed in 147 (71.7%) patients and in 50 (34.0%) was positive. In patients with positive troponin we observed 11 (22.0%) deaths, while in patients with normal troponin T or I level 6 (6.2%) deaths occurred. In patients with normal blood pressure we observed a significant difference in mortality in patients with elevated vs. normal troponin level (14.3 vs. 2.5%, p = 0.02). Thrombolytic therapy was used in 20 (9.8%) patients. In patients treated with thrombolytic therapy 9 (45%) deaths were observed. We divided patients according to the ESC 2008 guidelines risk stratification. The 'non-high risk' group consisted of 152 (74.1%) patients, and mortality was 3.9%. The 'high-risk' group consisted of 53 (26.8%) patients. The 'non-high risk' group was divided into the following subgroups: 1. moderate-high (with 2 risk factors: both RV dysfunction and positive injury markers) mortality - 8.1%; 2. moderate subgroup with one risk factor, mortality - 3.6%; 3. low risk - no risk factors - 0% mortality.1. In our registry mortality rate in patients with APE was 11%. 2. In about 30% of patients APE was under mask of acute coronary syndrome or syncope, 34% of patients had elevated troponin level, and 30% of patients had complication during hospitalisation. 3. In patients treated with thrombolytics mortality rate was 45%. 4. Reperfusion strategy (trombolysis or embolectomy) in the high risk group was used in only 41% of patients. 5. Elevated troponin level in normotensive patient was associated with 4-fold times higher risk of death. 6. New risk stratification according to the ESC guidelines 2008 correctly predicts prognosis in everyday clinical practise.

The postpartum period can unmask LQTS. We described a case of 22-year-old woman with episode of lost of consciousness 6 months after delivery. Holter monitoring showed episodes of QTc prolongation, max. QTc - 618 ms, medium QTc - 538 ms with different morphology types of T wave. Beta-blocker (BB) therapy (metoprolol was initiated) and titrated up to 200 mg daily. The patient was out of symptoms. After 2 years during the second pregnancy she reduced BB to 50 mg/day. In the postpartum period, 3 months after delivery she had syncopal episodes. Holter monitoring showed polymorphic ventricular tachycardia. The cardioverter-defibrillator was implanted.

We present two patients with ventricular fibrillation (VF) during acute myocardial infarction (AMI). First patient had torsade de pointes ventricular tachycardia episodes degenerating into VF 10 days after AMI treated with primary angioplasty. Second patient had multiple episodes of VF during the first day of AMI. He showed ST-segment elevation resembling Brugada pattern. We hypothesise that shape of ST-segment elevation during AMI might be important in assessing risk for VF. We propose that such 'arrhythmogenic' ST elevation might result more from systolic rather than diastolic current of injury during AMI. We discuss genetic predispositions (latent channellopathies) for VF during AMI.

We describe a case of a 56 year old man with myopericarditis complicated with cardiogenic shock within first 3 days, mimicking on admission acute myocardial infarction with ST elevation in inferior ECG leads. Additionally, patient presented hyperthyroidism and totally decompensated diabetes mellitus. He required during the first 3 days intravenous infusion of inotropic agents. Cardiac enzymes levels were elevated. Akinesia in mid-inferior and mid-posterior regions in ECHO was observed. On the 10th day ST segment elevation in I, II, V3-V6 and ST depression in aVR was observed in ECG. After stabilisation patient underwent coronarography which showed normal coronary arteries. The final diagnosis was acute myopericarditis complicated with acute heart failure and cardiogenic shock.

Sudden cardiac death (SCD) is responsible for almost 50% of all cardiac deaths in the U.S. The most common underlying cause of SCD is coronary artery disease, especially acute myocardial infarction (AMI). There are no publications concerning the shape of ST segment elevation in AMI and the risk of ventricular fibrilation (VF) or SCD. We present three cases with AMI and atypical ST segment elevation - 'lambda-wave-like' pattern, complicated with episodes of VF. This ECG pattern resembles the ST segment elevation shape in the type 1C Brugada syndrome. The 'lambda-like' ST segment elevation in AMI may identify patients with increased risk of VF or SCD.

A case of a 61-year-old patient with acute coronary syndrome (ACS) and minimal ECG changes is presented. The patient was admitted to a community hospital, where non-ST-segment elevation ACS was diagnosed. He was given standard pharmacotherapy and was transferred very early to an invasive facility, where coronarography and percutaneous coronary intervention of the large diagonal branch were performed. We stress the importance of non-invasive assessment with ECG and echocardiography, in addition to coronary angiography, for diagnosis and treatment decisions in complex cases.

We present a case of a 78-year-old female who was admitted to the hospital due to clinical and electrographic features of ST-elevation acute myocardial infarction. Coronary angiography revealed normal coronary arteries and severe left ventricular contractility abnormalities, detected initially by echocardiography, which resolved within 20 days from hospital admission. Because of these findings and typical echocardiographic picture, a transient left ventricular apical ballooning syndrome (the tako-tsubo syndrome) was diagnosed.

A case of a 29-year-old male with massive pulmonary embolism is presented. The diagnosis was confirmed by spiral computerised tomography and echocardiography. The patient received streptokinase, but he continued to be in cardiogenic shock without any improvement. Repeated tomography and echocardiography revealed progression of pulmonary embolism. The patient was transferred to a cardiosurgical department where successful embolectomy was performed.

67-year-old woman with thrombocytopenia (treated with prednisolon and azathiopryn) was admitted because of acute myocardial infarction without ST segment elevation (NSTEMI). From the 2nd day we observed increasing QTc interval from 461 ms with normal potassium level. Suddenly on the 6th day of the so far uncomplicated AMI ventricular fibrillation developed and was successfully treated with DC shock, and amiodarone (150 mg i.v.) was administered because of recurrent NSVT. Potassium level was 2.9 mmol/l. Within the next 2 days in the morning hours we observed episodes of recurrent polymorphic ventricular tachycardia (PMVT), always progressing into ventricular fibrillation (VF). The ECG showed QT interval--520 ms, QTc--602 ms. The patient was given an increasing dose of beta-blocker and lidokaine in i.v. infusion. After this regimen PMVT/VF did not recur and QT was normalized. Additionally successful PCI of LAD with 80% stenosis was performed. The paper discusses the problem of PMVT in the settings of AMI.

Right ventricular infarction (RVI) is most commonly associated with inferior wall infarction (20-50% of cases). Clinical presentation of RVI may vary.Assessment of outcome and clinical course of myocardial infarction in patients with inferior wall myocardial infarction with or without RVI. Additionally, risk stratification was attempted in the above-mentioned groups of patients.The analysis involved 181 consecutive patients (pts) with inferior wall myocardial infarction hospitalised between 1 July 2000 and 1 July 2002.Nineteen in-hospital deaths were noted in the study group (mortality 10.5%), reinfarction occurred in 6 (3.3%) pts, ischaemic stroke in 1 (0.6%) patient, and 2 (1.1%) pts had transient ischaemic attack. Cardiogenic shock occurred in 20 (11.0%) pts , ventricular fibrillation in 15 (8.3%) pts, and pulmonary oedema in 9 (4.9%) pts. In the subgroup of 161 pts without cardiogenic shock 8 (4.9%) pts died. Thrombolytic therapy was administered in 96 (53%) subjects. Isolated inferior wall myocardial infarction was diagnosed in 94 (51.9%) of 181 pts and RVI in 65 (35.9%) pts. Mortality rate in the RVI group was significantly higher than in inferior wall myocardial infarction without RVI and was 18.5% vs 2.12% (p=0.0003), respectively (excluding patients with cardiogenic shock: 11.1% vs 1.2%, respectively; p=0.016). In patients with RVI aged above 70 years, the mortality rate was significantly higher than in younger patients (32% vs 10%, p=0.002). In a subgroup with RVI treated with thrombolysis mortality was considerably higher in subjects aged70 years compared to patients below 70 years (38.5% vs 7.7%, p=0.017).RVI is associated with worse prognosis and increased number of in-hospital complications. Older patients aged70 years have definitely poorer prognosis. Thrombolytic therapy in a subgroup of older patients with RVI remains ineffective.

There are many reports evaluating the effects of the amplitude of ST segment elevation in acute myocardial infarction with ST segment elevation (STEMI) on infarction zone and course. There are, however, few publications dealing with the effects of ST segment elevation shape in STEMI patients on their clinical course and prognosis.Assessment of the rate of "tombstoning" of ST segment (TOMB-ST) in STEMI patients and the effects on their clinical outcome.The study involved 207 consecutive patients with STEMI hospitalised in the period 2000-2002 analysed with respect to the in-hospital complication rate.On admission, TOMB-ST was observed in 55 (26.1%) subjects. TOMB-ST was more common in anterior MI (39.8%) than in inferior MI (10.6%). Patients with TOMB-ST compared to non-TOMB-ST ones had a significantly higher mortality rate (38.2% vs 9.9%, p0.001), heart failure (45.6% vs 28.3%, p0.026), ventricular fibrillation (18.1% vs 6.4%, p0.016), and lower left ventricular ejection fraction (40.9% vs 48.6%, p0.001). The sum of amplitudes of ST segment deviations (SigmaST)20 mm was indicative for the subgroup of patients with TOMB-ST and trend towards higher mortality (40% vs 30%, NS). However, in patients without TOMB-ST, SigmaST20 mm identified two subgroups with significantly different mortality rates (20% vs 4%, p=0.001).TOMB-ST was observed in one fourth of patients with STEMI. This abnormality was associated with an increased mortality rate, higher incidence of heart failure and ventricular fibrillation as well as decreased left ventricular ejection fraction. In the population with TOMB-ST, increased mortality was independent of the total amplitude of ST segment displacement; this relation was, however, observed in patients with STEMI without TOMB-ST.

A case of a 59-year-old man with recurrent angina associated with ST-segment elevation in leads II, III, aVF and V4R-V6R, cardiogenic shock and complete atrio-ventricular block, is presented. Coronary angiography was normal. Therapy with calcium channel blockers was effective. Difficulties in the treatment of patients with variant angina are discussed.

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.

We describe a case of a 59-year-old female with paroxysmal atrial fibrillation and arterial hypertension who had syncopal attacks due to polymorphic ventricular tachycardia (PMVT) with a short coupling interval of an initiating beat (280 msec). We excluded structural heart disease. In the resting ECG the QTc interval was 420 msec. During Holter monitoring a slight changes of the ST-T segment in V1 were observed (from positive T wave with ST elevation of 1 mm to flat or negative T wave without ST elevation). Additionally, after PMVT a large U-wave (4 mm of amplitude) with the QTU interval of 600 msec and QTUc interval of 662 msec were observed. The U wave disappeared 9 minutes afterwards. The ajmaline test was positive for the Brugada syndrome. The patient received ICD and sotalol, and during 6-month follow-up she remains asymptomatic.