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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.

(Fig. 1). Echocardiographyexcluded structural heart disease. A stress-test didnot induce ischemia or arrhythmias. An electro-physiology study did not induce arrhythmias. Animplantable cardioverter-defibrillator (ICD) wasimplanted due to syncope and spontaneous type1 Brugada ECG pattern. Three weeks later, thepatient presented an electrical storm (6 appropriateICD therapies –5 ATP for VT and 1 shock for VF).Onemonthlater,anepisodeofVFwassuccessfullytreated by the ICD. Quinidine therapy at 600 mgdaily was started. No arrhythmia recurrences wereobserved in a follow-up period of 6 months.

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 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.

A case of a 27-year-old pregnant female (first trimester) is described. The patient was hospitalised due to pregnancy complications and immobilised for 3 weeks. At the end of this period patient's clinical condition rapidly deteriorated and she developed shock, followed by cardiac arrest. Echocardiography was consistent with acute pulmonary embolism and the patient received streptokinase. This treatment was complicated by a massive bleeding due to the rupture of the uterus. She underwent hysterectomy and recovered thereafter.

Five patients with amiodarone-induced QT prolongation and torsade de pointes are described. Hypokalemia was present in three patients, marked bradycardia - in two, and T-wave alternans - also in two patients. Patients with negative T waves in precordial leads were at higher risk of ventricular fibrillation than the patients with positive T waves. Beta-blocker, lidocaine and, in two patients, tosylate bretylate were effective. All patients survived to hospital discharge, however, one patient died four months later.

Clinical value of electrocardiographic features of torsade de pointes (TdP) has not yet been well established.To compare the mode of onset and ECG characteristics of slow (s-TdP) and fast (f-TdP) episodes of TdP.54 episodes of TdP recorded in 6 patients (5 females, one male, mean age 64.4 years) with acquired long QT syndrome were analysed. Baseline rate of TdP (V-V), ventricular rate variability (VRV), coupling interval (CI) at the onset of TdP, prematurity index (PI) and the first cycle length (FCL) were compared between 31 s-TdP (200 beats/min) and 23 f-TdP (or =220) episodes of TdP.Episodes of f-TdP were preceded by a significantly faster basal rhythm than s-TdP (R-R interval: 922 ms vs 1062 ms, p=0.03). QT interval was almost identical in both groups (517 ms vs 515 ms, NS, respectively). No significant differences were noted in the CI of the initiating beat (488 ms vs 472 ms, NS) nor in the PI (0.53 vs 0.47, NS). TdP was most frequently spontaneously terminated by a gradual slowing of the tachycardia rate; 58% of s-TdP and 39% of f-TdP episodes stopped in this way. An acceleration of ventricular rate before termination of TdP was noted in 32% of s-TdP and in 26% of f-TdP episodes. Episodes of f-TdP were longer than s-TdP episodes (mean of 19.7 vs 6.7 ventricular complexes per one episode, p=0.0003). There were significant differences in the VRV parameter (p=0.0005) and FCL (p=0.004) between both types of TdP. Faster TdP were characterised by lower ventricular rate variability (VRV - 19.5 msec) than s-TdP (VRV - 39.4 msec). Of 54 episodes of TdP, 9 (16.6%) degenerated into VF and required DC shock. Of 31 s-TdP episodes, one (3.2%) degenerated into VF compared with 8 (34.7%) episodes of f-TdP (p0.04).Episodes of fast TdP were characterised by a longer duration, shorter first cycle of the arrhythmia and lower ventricular rate variability than episodes of slow TdP. Fast episodes of TdP were preceded by faster baseline rhythm before TdP. Faster TdP more frequently degenerated into VF than slower episodes.

We present a case of a 65-year-old female admitted to the hospital due to severe intracranial hemorrhagia complicated by recurrences of polymorphic ventricular tachycardia of torsade de pointes type. ECG showed a marked prolongation of QT interval and giant U waves. The potassium level was 2.9 mmol/l and magnesium level - 0.6 mmol/l. Intravenous lidocaine and magnesium caused a complete supression of arrhythmia. Unfortunately, the patient died three days later due to cerebral damage and respiratory failure.

A case of 78 year-old woman with primary hypothyroidism and atrial fibrillation treated with sotalol, complicated with cardiac arrest due to ventricular fibrillation (VF) and torsade de pointes (TdP) is presented. The QT interval was prolonged to 660 msec. Episodes of polymorphic ventricular tachycardia and VF recurred. Lidocaine, tosylate bretylate and betabloker successfully eliminated VF but short-lasting episodes of TdP were still present. Increased doses of hormonal substitution with thyroid hormones successfully eliminated malignant ventricular arrhythmias and normalised QT interval to 430 msec.

We have prepared the following response to the letter submitted by Drs Vereckei and Miller.1 1. Our study compared the ability of five electrocardiographic methods to differentiate ventricular tachycardia (VT) from other broad QRS tachycardias. We used the methodologies described in the original five publications, and a uniform definition of VT/non-VT (SVT). We made it clear that the VT group comprised patients that had only VT.2 2. In the original papers describing the Brugada and Griffith's algorithms and the lead II criterion, pre-excited tachycardias were not grouped with VTs. In those studies, a diagnosis of VT was only deemed correct when …

A 68-year-old female was admitted after syncope. Her ECG showed a sinus rhythm of 54 bpm with deep, negative T-waves in leads I, II, III, aVF, and V2–V6 with a prolonged QT interval (QTcV4 of 610 ms and QTcIII of 503 ms; Figure 1, upper trace). Bedside echocardiography revealed the presence of prominent left ventricular (LV) hypertrophy (diastolic interventricular septum thickness of 25 mm, diastolic posterior wall thickness of 11 mm, and apical thickness of 16 mm) and an LV ejection fraction of 60%. The patient did not take any medications that could impact the QT interval, and no electrolyte disturbances were observed. Therefore, a diagnosis of hypertrophic cardiomyopathy and long-QT syndrome was made. Continuous ECG monitoring revealed ventricular ectopic beats with episodes of non-sustained ventricular

Background: Changes in U-wave amplitude after premature ventricular contractions (PVC) are known as prognostic markers in the long QT syndrome dependent on bradycardia. The purpose of the study was to find correlation between postextrasystolic ST-U segment changes and a history of sustained ventricular tachycardia or ventricular fibrillation (VT/VF). Methods: The ST-U segment configurations were taken from the 24-hour ambulatory ECG. The comparison of the morphology of these segments was performed between sinus beats preceding PVC's and first postextrasystolic beats. Population: Two groups of patients were evaluated: 1) 32 patients with VT/VF history (VT/VF group), and 2) 36 patients with potentially malignant arrhythmia (structural heart disease with frequent PVCs and/or nonsustained VT-nsVT) tnon-VT/VF group). Results: We found T-wave changes in 8 patients (25%) from the VT/VF group and in 12 patients (33.3%) from the nonVT/VF group (P = NS) and U-wave changes in 13 patients (40.6%) and 3 patients (8.3%), respectively (P < 0.05). Other ECG indexes related to PVC's were also considered: RR interval, coupling interval (Cl), prematurity index (Pl), and postextrasystolic pause (PP). The analysis of these ECG indices revealed, when compared with patients without T-U-wave changes, that the occurrence of U-wave changes was significantly related to longer RR interval of the sinus rhythm preceding PVC: 1025 ± 211 vs 918 ± 200 ms (P < 0.05). The prematurity index was lowest in patients with U-wave changes: 0.54 ± 0.12 vs 0.65 ± 0.16 (P < 0.01) while postextrasystolic pauses leading to the postextrasystolic U-wave changes were significantly longer: 1383 ± 223 vs 1130 ± 247 ms (P < 0.001). Cl did not differentiate patients: 556 ± 108 vs 584 ± 117 ms (P = NS). Conclusions: Postextrasystolic changes in ST-U segment configuration are dependent on bradycardia, low prematurity index of the PVC, and the lengthening of the postextrasystolic pause. U-wave changes more frequently appeared in patients with malignant arrhythmias. Follow-up study is needed to assess if they might be predictive for the occurrence or reoccurrence of arrhythmic episodes. A.N.E. 2002;7(1):17–21