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Conduction system pacing (CSP) has emerged as a more physiological alternative to right ventricular pacing and is also being used in selected cases for cardiac resynchronization therapy. His bundle pacing was first introduced over two decades ago and its use has risen over the last five years with the advent of tools which have facilitated implantation. Left bundle branch area pacing is more recent but its adoption is growing fast due to a wider target area and excellent electrical parameters. Nevertheless, as with any intervention, proper technique is a prerequisite for safe and effective delivery of therapy. This document aims to standardize the procedure and to provide a framework for physicians who wish to start CSP implantation, or who wish to improve their technique.

Conduction system pacing (CSP) has emerged as a more physiological alternative to right ventricular pacing and is also being used in selected cases for cardiac resynchronization therapy. His bundle pacing was first introduced over two decades ago and its use has risen over the last years with the advent of tools which have facilitated implantation. Left bundle branch area pacing is more recent but its adoption is growing fast due to a wider target area and excellent electrical parameters. Nevertheless, as with any intervention, proper technique is a prerequisite for safe and effective delivery of therapy. This document aims to standardize the procedure and to provide a framework for physicians who wish to start CSP implantation, or who wish to improve their technique. A synopsis is provided in this print edition of EP-Europace. The full document may be consulted online, and a ‘Key Messages’ App can be downloaded from the EHRA website.

BACKGROUND Cardiac resynchronization therapy (CRT) using bi-ventricular pacing (BVP) is effective in patients with heart failure, left bundle branch block (LBBB), and reduced left ventricular function. Left bundle branch area pacing (LBBAP) has been reported as an alternative option for CRT. OBJECTIVE The purpose of this study was to assess the feasibility and outcomes of LBBAP in patients who failed conventional BVP because of coronary venous (CV) lead complications or who were nonresponders to BVP. METHODS At 16 international centers, LBBAP was attempted in patients with conventional CRT indication who failed BVP because of CV lead complications or lack of therapeutic response to BVP. Heart failure hospitalization (HFH) and death, echocardiographic outcomes, procedural data, pacing parameters, and lead complications including CV lead failure are reported. RESULTS LBBAP was successfully performed in 200 patients (CV lead failures 156; nonresponders 44) (age 68 +/- 11 years; female 35%; LBBB 55%; right ventricular pacing 23%; ischemic cardiomyopathy 28%; nonischemic cardiomyopathy 63%; left ventricular ejection fraction [LVEF]

Cardiac resynchronization therapy (CRT) using biventricular pacing has limited efficacy in patients with heart failure (HF) and right bundle branch block (RBBB). Left bundle branch area pacing (LBBAP) is a novel physiologic pacing option. OBJECTIVE The aim of the study was to assess the feasibility and outcomes of LBBAP in HF patients with RBBB and reduced left ventricular systolic function, and indication for CRT or ventricular pacing. METHODS LBBAP was attempted in patients with left ventricular ejection fraction (LVEF) = 5% increase in ejection fraction) to LBBAP were assessed. RESULTS LBBAP was attempted in 121 patients and successful in 107 (88%). Patient characteristics included age 74 +/- 12 years, female 25%, ischemic cardiomyopathy 49%, and ejection fraction 35% +/- 9%. QRS axis at baseline was normal in 24%, left axis 63%, right axis 13%. LBBAP threshold and R-wave amplitudes were 0.8 +/- 0.3 V@ 0.5 ms and 10 +/- 9 mV at implant and remained stable during mean follow-up of 13 +/- 8 months. LBBAP resulted in narrowing of QRS duration (156 +/- 20 ms to 150 +/- 24 ms (P = .01) with R-wave peak times in V-6 of 85 +/- 16 ms. LVEF improved from 35% +/- 9% to 43% +/- 12% (P,.01). Clinical and echocardiographic response was observed in 60% and 61% of patients, respectively. Female sex and reduction in QRS duration with LBBAP were predictive of echocardiographic response and super-response. CONCLUSION LBBAP is a feasible alternative to deliver CRT or physiologic ventricular pacing in patients with RBBB, HF, and LV dysfunction.

AimsThe field of conduction system pacing (CSP) is evolving, and our aim was to obtain a contemporary picture of European CSP practice.Methods and resultsA survey was devised by a European CSP Expert Group and sent electronically to cardiologists utilizing CSP. A total of 284 physicians were invited to contribute of which 171 physicians (60.2%; 85% electrophysiologists) responded. Most (77%) had experience with both His-bundle pacing (HBP) and left bundle branch area pacing (LBBAP). Pacing indications ranked highest for CSP were atrioventricular block (irrespective of left ventricular ejection fraction) and when coronary sinus lead implantation failed. For patients with left bundle branch block (LBBB) and heart failure (HF), conventional biventricular pacing remained first-line treatment. For most indications, operators preferred LBBAP over HBP as a first-line approach. When HBP was attempted as an initial approach, reasons reported for transitioning to utilizing LBBAP were: (i) high threshold (reported as >2 V at 1 ms), (ii) failure to reverse bundle branch block, or (iii) > 30 min attempting to implant at His-bundle sites. Backup right ventricular lead use for HBP was low (median 20%) and predominated in pace-and-ablate scenarios. Twelve-lead electrocardiogram assessment was deemed highly important during follow-up. This, coupled with limitations from current capture management algorithms, limits remote monitoring for CSP patients.ConclusionsThis survey provides a snapshot of CSP implementation in Europe. Currently, CSP is predominantly used for bradycardia indications. For HF patients with LBBB, most operators reserve CSP for biventricular implant failures. Left bundle branch area pacing ostensibly has practical advantages over HBP and is therefore preferred by many operators. Practical limitations remain, and large randomized clinical trial data are currently lacking.

Nonselective His-bundle pacing (nsHBp), nonselective left bundle branch pacing (nsLBBp), and left ventricular septal myocardial pacing (LVSP) are recognized as physiological pacing techniques.The purpose of this study was to compare differences in ventricular depolarization between these techniques using ultra-high-frequency electrocardiography (UHF-ECG).In patients with bradycardia, nsHBp, nsLBBp (confirmed concomitant left bundle branch [LBB] and myocardial capture), and LVSP (pacing in left ventricular [LV] septal position without proven LBB capture) were performed. Timings of ventricular activations in precordial leads were displayed using UHF-ECG, and electrical dyssynchrony (e-DYS) was calculated as the difference between the first and last activation. Duration of local depolarization (Vd) was determined as width of the UHF-QRS complex at 50% of its amplitude.In 68 patients, data were collected during nsLBBp (35), LVSP (96), and nsHBp (55). nsLBBp resulted in larger e-DYS than did LVSP and nsHBp [- 24 ms (-28;-19) vs -12 ms (-16;-9) vs 10 ms (7;14), respectively; P.001]. nsLBBp produced similar values of Vd in leads Vnslbbp preserves physiological LV depolarization but increases interventricular electrical dyssynchrony. LV lateral wall depolarization during LVSP is prolonged, but interventricular synchrony is preserved.

The aim of this study was to assess the feasibility and outcomes of left bundle branch area pacing (LBBAP) in patients eligible for cardiac resynchronization therapy (CRT) in an international, multicenter, collaborative study.CRT using biventricular pacing is effective in patients with heart failure and left bundle branch block (LBBB). LBBAP has been reported as an alternative option for CRT.LBBAP was attempted in patients with left ventricular ejection fraction (LVEF) 50% and indications for CRT or pacing. Procedural outcomes, left bundle branch capture, New York Heart Association functional class, heart failure hospitalization, echocardiographic data, and lead complications were recorded. Clinical (no heart failure hospitalization and improvement in New York Heart Association functional class) and echocardiographic responses (≥5% improvement in LVEF) were assessed.LBBAP was attempted in 325 patients, and CRT was successfully achieved in 277 (85%) (mean age 71 ± 12 years, 35% women, ischemic cardiomyopathy in 44%). QRS configuration at baseline was LBBB in 39% and non-LBBB in 46%. Procedure and fluoroscopy duration were 105 ± 54 and 19 ± 15 min, respectively. LBBAP threshold and R-wave amplitudes were 0.6 ± 0.3 V at 0.5 ms and 10.6 ± 6 mV at implantation and remained stable during mean follow-up of 6 ± 5 months. LBBAP resulted in significant QRS narrowing from 152 ± 32 to 137 ± 22 ms (p 0.01). LVEF improved from 33 ± 10% to 44 ± 11% (p 0.01). Clinical and echocardiographic responses were observed in 72% and 73% of patients, respectively. Baseline LBBB (odds ratio: 3.96; 95% confidence interval: 1.64 to 9.26; p 0.01) and left ventricular end-diastolic diameter (odds ratio: 0.62; 95% confidence interval: 0.49 to 0.79; p 0.01) were independent predictors of echocardiographic response.LBBAP is feasible and safe and provides an alternative option for CRT. LBBAP provides remarkably low and stable pacing thresholds and was associated with improved clinical and echocardiographic outcomes.

A variant of the ether-à-go-go related channel (hERG), p.Arg148Trp (R148W) was found at heterozygous state in two infants who died from sudden infant death syndrome (SIDS), one with documented prolonged QTc and Torsade de Pointes (TdP), and in an adult woman with QTc500 ms, atrioventricular block and TdP. This variant was previously reported in cases of severe ventricular arrhythmia but very rarely in control subjects. Its classification as mutation or polymorphism awaited electrophysiological characterization.The properties of this N-terminal, proximal domain, hERG variant were explored in Xenopus oocytes injected with the same amount of RNA encoding for either hERG/WT or hERG/R148W or their equimolar mixture. The human ventricular cell (TNNP) model was used to test the effects of changes in hERG current.R148W alone produced a current similar to the WT (369 ± 76 nA (mean ± SEM), n=13 versus 342 ± 55 nA in WT, n=13), while the co-expression of 1/2 WT+1/2 R148W lowered the current by 29% versus WT (243 ± 35 nA, n=13, p0.05). The voltage dependencies of steady-state activation and inactivation were not changed in the variant alone or in co-expression with the WT. The time constants of fast recovery from inactivation and of fast and slow deactivation analyzed between -120 and +20 mV were not changed. The voltage-dependent distribution of the current amplitudes among fast-, slow- and non-deactivating fractions was unaltered. A 6.6% increase in APD90 from 323.5 ms to 345 ms was observed using the human cardiac ventricular myocyte model.Such a decrease in hERG current as evidenced here when co-expressing the hERG/R148W variant with the WT may have predisposed to the observed long QT syndrome and associated TdP. Therefore, the heterozygous carriers of hERG/R148W may be at risk of cardiac sudden death.

A 76-year old woman with a history of stage 3 arterial hypertension, paroxysmal atrial fibrillation, hypercholesterolemia and type 2 diabetes mellitus. Ventricular tachycardia was the first clinical manifestation of the disease. Echocardiography revealed hypertrophic cardiomyopathy with a high intraventricular gradient of 47 mmHg and midventricular obstruction at the level of the papillary muscles (the lumen of the left ventricle was 1-2 mm during systole). No ventricular aneurysm was found but the ventricle was elongated and dilated in the periapical part where systolic function was decreased but synchronized in time. Coronary angiograms showed no narrowing of coronary arteries. A single-chamber cardioverter-defibrillator (ICD, implantable cardioverter-defibrillator) was implanted to prevent sudden cardiac death. Modified-release metoprolol and amiodarone were administered in antiarrhythmic therapy. This case represents a rare kind of hypertrophic cardiomyopathy in an elderly woman which is characterized by midventricular obstruction.

This editorial refers to ‘Transvenous phrenic nerve stimulation for the treatment of central sleep apnoea in heart failure’, by P. Ponikowski et al. , doi:10.1093/eurheartj/ehr298 The prevalence of central sleep apnoea (CSA) is 100-fold greater in chronic heart failure (HF) due to impaired systolic function than in the general population.1 It afflicts principally elderly male patients who have atrial fibrillation, implanted pacemakers, low arterial PCO2 when awake, or high diuretic requirements.1 Its presence identifies HF patients with higher night- and day-time sympathetic nervous system activity,2 at increased of risk of malignant ventricular arrhythmias,3 whose survival is foreshortened.4 The primary abnormality in CSA is neither the upper airway collapse of obstructive sleep apnoea (OSA), which can be treated quite effectively with continuous positive airway pressure (CPAP), nor a paucity of ventilation, but rather the compromise of mechanisms that normally stabilize breathing due to the confluence of pulmonary congestion, circulatory delay, altered cerebrovascular blood flow, and enhanced central sensitivity to CO2, all predisposing to hyperventilation.4 Although the reality is more complex, to simplify, in HF the cyclical oscillations between hyperpnoea and apnoea, known commonly as Cheyne–Stokes respiration, are initiated by the hyperpnoea, which can be stimulated by spontaneous arousal from sleep, or by pulmonary congestion. During sleep, the latter is exacerbated both by fluid shifts from the periphery to the cardiopulmonary reservoir,5 and by pre-existing pulmonary–cardiac–chemoreceptor circulatory delay. Thus, when increases in pulmonary capillary and venous pressures stimulate pulmonary irritant receptors, triggering a bout of hyperpnoea, the already low PaCO2 is driven below the patient's apnoeic threshold. Central drive to the muscles of breathing pauses until the rising PaCO2 and falling PaO2 are sensed, eventually, by chemoreceptors, which then initiate a new cycle of hyperpnoea, hypocapnia, and apnoea. CSA is …

There is a paucity of data concerning the use of QRS morphology patterns for identifying pacing sites during left ventricle (LV)-only epicardial pacing in patients with a biventricular device. The objective of this study was to identify QRS patterns during LV-only pacing, and to establish their relationship with LV lead position. In addition, to validate the diagnostic performance of such electrocardiogram (ECG) patterns for predicting posterolateral versus anterior and apical versus nonapical LV pacing site.The study retrospectively analyzed data from 376 cardiac resynchronization therapy device patients. Data analyzed included ECGs registered during LV-only VVI pacing, fluoroscopic projections, and lateral chest roentgenograms that documented postimplantation LV lead position. Phase one of the study involved categorization of the ECG patterns of the first 66 study cases. Phase two of the study examined the association between ECG pattern and different LV lead positions.As the LV epicardial pacing site became more anteroapical, the LV-only paced QRS complexes in the precordial leads became more negative. Three ECG patterns were identified (posterolateral, intermediate, and anteroapical), and their distribution was found to be associated with LV lead position (P0.001). The posterolateral ECG pattern was mostly observed in cases where the LV lead was in the posterolateral area (diagnostic accuracy of 89.1% for predicting a nonapical LV lead position). The anteroapical ECG pattern was associated with LV leads in anteroapical segments (specificity of 98.5%, accuracy of 89.1% for predicting an anteroapical pacing site).Posterolateral and anteroapical ECG patterns are highly predictive of LV lead position.

Assessment of left ventricular (LV) capture is of paramount importance in patients with biventricular (BiV) pacing. Our goal was to identify electrocardiographic features that differentiate between BiV and right ventricular (RV)-only pacing in patients with nonapical RV leads.The study enrolled 300 consecutive patients with BiV devices and nonapical RV leads, and obtained from them 558 electrocardiograms with either BiV pacing (n = 300) or RV-only pacing (n = 258). RV pacing served as a surrogate for loss of LV capture. Electrocardiograms from the first 150 patients were used to identify BiV-specific features, and to construct an algorithm to differentiate between BiV and RV-only pacing. Electrocardiograms from the second 150 patients were used to validate the algorithm.The following electrocardiographic features typical of BiV pacing were identified: QS in lead V6 (specificity = 98.7%, sensitivity = 54.7%), dominant R in lead V1 (specificity = 100%, sensitivity = 23.3%), q in lead V6 (specificity = 96%, sensitivity = 22.7%), and a QRS160 ms (specificity = 100%, sensitivity = 66.0%). The algorithm based on those features was found to have an overall diagnostic accuracy of 95.0%, a specificity of 96.0%, and a sensitivity of 93.5%.The study identified QRS features that were very specific for BiV pacing in patients with nonapical RV leads. Sequential arrangement of those features resulted in an algorithm that was very accurate for differentiating between BiV pacing and loss of LV capture.

The treatment of bipolar disorders is based on the concomitant use of the mood stabilizers and antipsychotics. In the first case carbamazepine is frequently used, in the second case second-generation (atypical) neuroleptics like quetiapine. This drug combination in a significant number of cases prevent recurrence of mania and depression, normalizes mood and emotion and improves lifestyle. However, this treatment is related to increased interactions and risk of the side effects. Even greater risks involve mixed drug intoxications with these groups of drugs. In this paper we present acute poisoning with carbamazepine and quetiapine complicated cardiotoxic effects in the form of arrhythmias and conduction disorders of the heart. This symptoms disappeared spontaneously after resolution of the poisoning.

The aim of the study was to assess the influence of cardiac resynchronization therapy(CRT) on a series of humoral parameters crucial for the pathophysiology of chronic heart failure such as aldosterone or the inflammatory markers. Thirty eight consecutive patients (aged 66.3 +/- 9.6 years, 31 men - 82% ) with chronic heart failure (57.9% with ischaemic background and 42.1% of non-ischaemic etiology) in stable for at least 3 months, NYHA class III - IV despite optimized pharmacotherapy, with left ventricular ejection fraction (LVEF)or = 35% and wide QRS complex (or = 120 ms) had the blood serum tested for the concentrations of interleukin-6 (IL-6), interleukin-18 (IL-18), C-reactive protein (CRP) and aldosterone before and 12-16 weeks after CRT introduction. In the study group aldosterone concentrations were significantly reduced. Among the inflammatory markers the level of IL-6 decreased, IL-18 concentrations showed a falling trend (445.1 +/- 225.7 pg/ml vs 418.4 +/- 229.6 pg/ml, p = 0.052), whereas no change of CRP serum contain was noted. It was showed that cardiac resynchronization therapy had an impact on systemic inflammation and hormonal status in patients with chronic heart failure during short-term observation.

Left ventricular (LV)-only pacing has a significant effect on delay in depolarization of parts of the ventricles that are likely oversensed in the right atrial channel. The study aimed to assess the impact of ventricular activation sequence on QRS oversensing and far-field endless-loop pacemaker tachycardia (ELT) in patients who received cardiac resynchronization therapy (CRT) devices.The study examined 102 patients with CRT devices. Oversensing artifacts in the atrial channel were inspected on intracardiac electrograms, and their timing with respect to the beginning of QRS was determined during DDD-right ventricular (RV), DDD-LV, DDD-biventricular (BiV), and AAI pacing modes. The occurrence of ELT during DDD-LV pacing with a postventricular atrial refractory period (PVARP) of 250 ms was also assessed.The timing of oversensing artifacts (in relation to the beginning of surface QRS) was dependent on ventricular activation sequence, occurring promptly following intrinsic activation via the right bundle branch (47.1 ± 26.4 ms), later during RV pacing (108.7 ± 22.5 ms) or BiV pacing (109.4 ± 23.1 ms), and significantly later, corresponding to the final part of the QRS, during LV pacing (209.6 ± 40.0 ms, range: 140-340 ms, P0.001). Oversensing was significantly more frequent during LV than during RV pacing (35.3% vs 22.5%, P0.001). Far-field ELT was observed in six patients.Oversensing artifacts in the atrial channel are likely caused by depolarization of the basal part of the right ventricle. The novel mechanism of QRS oversensing outside PVARP, caused by a reversed ventricular activation sequence during LV-only pacing, may be important in some CRT patients.

Sleep-related breathing disorders are common in patients with chronic heart failure (CHF) and contribute to exacerbation of CHF. The effects of biventricular stimulation (CRT) seem to exceed the improvement of mechanical heart performance and are likely to affect other aspects of CHF pathophysiology. The aim of the study was to assess the influence of CRT on subjective and objective sleep features.Twenty seven consecutive patients (aged 67.7 +/- 8.7 years, 23 men - 85%) with chronic heart failure (62.9% with ischaemic background and 37.1% of non-ischaemic etiology) in stable for at least 3 months NYHA class III - IV despite optimized pharmacotherapy, with left ventricular end-diastolic diameter (LVEDd)55 mm, left ventricular ejection fraction (LVEF)or = 35% and wide QRS complex (or = 120 ms) were appraised before and 12-16 weeks after CRT introduction clinically (including 6-minute walk test--6-MWT), echocardiographically and in polisomnography. The apnea-hypopnea index (AHI) and apnea indexes (AI) of central, obstructive and mixed types were calculated. The sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI), daytime sleepiness with the Epworth Sleepiness Scale (ESS).LVEF increased, 6-MWT distance rose. Left ventricular diameters and left ventricular end-systolic volume decreased. PQSI and ESS fell (9.3 +/- 4.2 vs 6.2 +/- 3.2, p0.001 and 8.4 +/- 4.1 vs 7.0 +/- 3.4, p0.001, respectively). AHI, obstructive AL and mixed AL did not alter but significant reduction of central AL was noted (9.6 +/- 13.0 vs 3.7 +/- 6.2, p = 0.023).CRT decreases central sleep apnea and improves quality of sleep and daytime sleepiness in patients with CHF.

Two cases of inappropriate sinus tachycardia refractory to combined pharmacotherapy (beta-blocker, ivabradine) are described. Both were female patients (28 and 45 years-old) and underwent sinus node modification/ablation using non-contact mapping (EnSite Array). Since ablation had to be performed in both cases very close to the phrenic nerve (captured during 10V pacing at ablation spots) its function was monitored during ablation with constant phrenic nerve pacing from the superior vena cava. One case was successful after single and straightforward ablation session, the other case despite several attempts and initially good result had recurrences; first recurrence two days after cryoablation, and second three weeks after radiofrequency ablation with irrigated tip catheter.

The current report describes a manifestation of linking phenomenon in DDD pacemaker recipients: impairment of atrioventricular (AV) conduction and ensuing unnecessary right ventricular (RV) pacing.Three patients with second-degree AV block and sudden impairment of native AV conduction following pacemaker implantation are presented. Loss of native AV conduction was considered functional and related to repetitive retrograde invasion of ventricular depolarization to the AV junction that was "linked" to ventricular pacing triggered by nonconducted P-waves.This case series demonstrates that linking phenomenon should be considered in analysis of pacemaker behavior, and that retrograde concealment can be responsible for unnecessary RV pacing.

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.

Solid evidence shows that cardiac resynchronization therapy (CRT) improves prognosis, physical capacity and quality of life in selected groups of patients with chronic heart failure (CHF). Nonetheless, marked percentage of patients seem not to benefit from CRT.Sixty consecutive patients (aged 66.3 +/- 8.7 years, 57 men - 95%, 3 women - 5%) with CHF (71.7% with ischaemic and 28,3% with non-ischaemic origin) of stable foror = 3 months NYHA III or IV class despite optimized pharmacotherapy, with left ventricle end-diastolic diameter (LVEDd)or = 55 mm, left ventricular ejection fraction (EF)or = 35% and QRS130 ms were evaluated before and 3 months after CRT implementation (biventricular stimulation BiV) echocardiographically and clinically.EF increased (21.7% vs 26,6%, p0,0001), 6-minute walk distance (6-MWT) rose (298.0 m vs 373.1 m, p0,0001), left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) decreased (244.3 ml vs 226,4 ml, p=0.0002; 192.8 ml vs 168,7 ml, p0,0001 respectively). Mean NYHA class dropped from 3.1 to 2.2 (p0.0001). Absolute increase in EF ofor = 4%,or = 5%,or = 6% was observed in 63.2%, 52.6%, and 35.7% respectively; relative increase ofor = 25% presented 21.1%,or = 10% reduction of LVESV--59.7%,or = 15% reduction of LVESV--43.8%, decrease in NYHA class--78.3%,or = 10% reduction of 6-MWT--66.7%, no death and no hospitalization due to heart failure--78.3%.Response to CRT rate differs markedly according to the applied definition.

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 electrocardiograms of a 70-year-old man with a history of inferior wall myocardial infarction. Since the infarction he had frequent episodes of ventricular tachycardia that was on many occasions misdiagnosed as either supraventricular tachycardia or atrial flutter. We contribute the mistakes to the presence of relatively narrow QRS complexes and QRS alternans that imitated fusion beats. The QRS morphology similar to that seen in idiopathic ventricular tachycardia suggested participation of the Purkinje fibers of the posterior fascicle in the reentrant circuit. The arrhythmia was ablated with single radiofrequency current application in the mid-paraseptal area of the left ventricle.

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.

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.

The prognostic value of chronic inflammation markers in patients after myocardial infarction (MI) in the era of interventional treatment, statin and aspirin use is still unclear.The study was carried out on 107 patients with a first MI who were followed up for 18 months. The end points were cardiac death, reinfarction or unstable angina pectoris. At 10 days and at 10 weeks we measured C-reactive protein (CRP), fibrinogen, soluble intercellular adhesion molecule 1 (sICAM-1), erythrocyte sedimentation rate (ESR), white blood cell count (WBC) and Chlamydia preumoniae antibodies.During the follow-up period there were 22 events. The patients were divided into two subgroups: those with recurrent episodes and those without coronary events. Patients with recurrent episodes had significantly higher values of CRP (7.07 vs. 3.77 mg/l, p = 0.02), ESR at 1 h (24.3 vs. 13.3 mm; p = 0.01) and sICAM-1 (287.9 vs. 260.9 ng/ml, p = 0.04) at 10 weeks following infarction. Statistical analysis showed that sICAM-1270 ng/ml, CRP1.83 mg/l and ESR at 1 h14 mm measured at 10 weeks were independent risk factors for recurrent cardiovascular events. In patients with coronary events between the 10th day and 10th week there was no decrease in inflammatory indices (WBC, ESR) and a tendency towards increasing sICAM-1.Increased inflammatory markers (CRP, ESR, sICAM-1) at 10 weeks after MI are independent risk factors for recurrent cardiovascular events. Measuring CRP, ESR and sICAM-1 at this time point is useful in long-term prognosis after MI. Changes in inflammatory indices (ESR, WBC, sICAM-1) measured at 10 days and 10 weeks following infarction show a different pattern in patients with and without recurrent cardiovascular events. (Cardiol J 2007; 14: 50-58).

We report a case of an otherwise healthy 63-year-old male with incessant, highly symptomatic ventricular arrhythmia that displayed over 60,000 premature ventricular contractions and 499 runs of non-sustained ventricular tachycardia (VT) during 24 hours of ECG monitoring. The ventricular ectopy had a QRS morphology of the left bundle branch block (LBBB), however, with a superior axis. Structural heart disease was absent and the history was negative. Therefore the arrhythmia was considered to be atypical idiopathic repetitive monomorphic VT. Radiofrequency catheter ablation in an inferior region of the tricuspid ring at a site with good pacemap was successful. We conclude that idiopathic repetitive monomorphic VT may originate from uncommon locations and that QRS morphology (superior axis, LBBB, notching in inferior leads, transition at V4, durationor = 160 ms) can help diagnose inferior free wall tricuspid location.

We describe a case of an otherwise healthy 50-year-old man with frequent attacks of heart palpitations. During electrophysiological study two episodes of atrial fibrillation (AF) were induced. In both cases AF was preceded by a few seconds of atrioventricular nodal reentrant tachycardia (AVNRT). Ablation of atrioventricular node slow pathway successfully eliminated both tachyarrhythmias during 6 months follow-up. Since during AVNRT a few short coupled atrial ectopic beats appeared, we hypothesized that AVNRT did not trigger AF directly but by inducing ectopic beats form a pulmonary vein or an atrial focus that became a direct trigger of AF.

Postmyocardial infarction left ventricular remodeling is modified by inflammatory processes and structural changes in the myocardium. Chlamydia pneumoniae (Chp) causes chronic myocyte infection, affects apoptosis and TNF-alpha production, and may induce cross reactivity with alpha myosin. This is the way in which this intracellular pathogen may modulate remodeling on the cellular and organ level.The study was conducted in 101 patients with a first myocardial infarction in whom we evaluated the serological features of Chp infection using the ELISA method and echocardiographic left ventricular volume at 10 days and 10 weeks after the infarction.Patients with chronic Chp infection had a tendency toward higher end-diastolic volume at 10 weeks after the infarction (123 +/- 32.9 ml vs. 134 +/- 34.7 ml, p = 0.09). In order to better define this relationship we used ROC analysis and measured levels of antibodies: IgG = 117 EIU and IgA = 15.6 EIU by which we divided the patients into two subgroups. Those with IgGor = 117 EIU and IgAor = 15.6 EIU belong to the subgroup with chronic and active Chp infection. These patients had larger left ventricular end-diastolic volumes (155.8 vs. 123.1 ml, p = 0.0005) and end-systolic volumes (77.4 vs. 59.5 ml, p = 0.006) at 10 weeks after the infarction. Both subgroups were similar with respect to age, gender, history of arterial hypertension, systolic and diastolic blood pressure values, infarct site, reperfusion, infarct size, left ventricular ejection fraction and left ventricular contractility index. Type of reperfusion therapy and pharmacological treatment at 10 days and at 10 weeks did not differ, either.Chronic Chlamydia pneumonie infection modifies the course of left ventricular remodeling.

Inflammatory markers have been reported to be elevated in hypertension.We compared levels of inflammatory markers between hypertensives (HT) with target organ damage (TOD) but without associated clinical conditions (ACC), n=55, HT with ACC, n=42, HT without TOD/ACC, n=22 and normotensive controls, n=41.Serum levels of CRP, fibrinogen, TNF-alpha and anti-HSP60 antibodies were measured. Hypertensive complications were assessed on the basis of clinical history and the following investigations: M-mode echocardiography (left ventricular hypertrophy), Doppler: mitral and pulmonary vein flow and isovolumetric relaxation time (diastolic dysfunction), vascular ultrasound (common carotid artery intima-media thickness--IMT), pulse wave velocity (carotid-femoral arterial stiffness) and creatinine concentration (renal function).HT with TOD had higher concentrations of CRP than controls (1.71 vs 0.76 mg/l, p0.0001); higher fibrinogen and TNF-a vs controls and also vs HT without TOD/ACC (2.80 vs 2.53 vs 2.49 g/l, p0.0001) and (2.49 vs 2.00 vs 1.83 pg/ml, p=0.04), respectively. HT without TOD/ACC did not differ from the control group in inflammatory marker concentrations. HT with ACC did not differ from HT with TOD in inflammatory marker concentrations. There were no differences in anti-HSP60 antibody concentrations between all groups. In multiple regression analysis only IMT was influenced by inflammatory markers: fibrinogen (beta=0.2, p=0.02) and TNF-alpha, (beta=0.17, p=0.05).We conclude that inflammatory markers are elevated in HT with TOD and are not elevated in uncomplicated HT without TOD.

Two cases of hypertrophic cardiomyopathy with massive hypertrophy and high defibrillation threshold (DFT) are described. A 14-year-old boy, whose single risk factor for sudden death was extreme hypertrophy with maximum interventricular septum (IVS) thickness of 43 mm, survived an episode of ventricular fibrillation. During ICD implantation DFT testing showed energy requirements30 J and the procedure was aborted. Amiodarone and verapamil treatment was discontinued and treatment with oral sotalol was instituted. After a period of amiodarone washout the procedure was repeated and DFT of 24 J was encountered. An 18-year-old female with massive hypertrophy (IVS thickness=35 mm) and other risk factors for sudden death underwent ICD implantation for primary prevention. During the procedure DFT=20 J and ICD with 30 J maximal output was implanted. An increase in DFT to more than 20 J was encountered during pre-discharge test. Lack of 10 J safety margin warranted ICD system revision and upgrade; during the second procedure DFT was 24 J and ICD with 35 J maximal output was implanted. In summary, in both cases ICDs with 35 J maximal output were successfully implanted.

Beta-blockers are routinely used in all forms of ischaemic heart disease except variant angina. Recently, III generation beta-blockers were introduced into practice. New beta-blockers often have ancillary properties like vaso-dilating or antioxidant properties. Also slow-release formulas of old beta-blockers are now available. Several studies show that these new agents are more efficient when compared with old beta-blockers. Moreover, adverse effects of new beta-blockers are often less severe than in the case of older agents. Especially the influence on bronchi, peripheral arteries and lipid and glucose metabolism is less pronounced. The frequency of beta-blockers use is too low in Poland as well as in other European countries, despite overwhelming evidence that these agents improve prognosis. The results of Cracovian Program for Secondary Prevention of Ischaemic Heart Disease showed that the proportions of patients after myocardial infarction or myocardial revascularization prescribed beta-blockers are too low. One of the reasons is probably the doctors' concern about side effects of beta-blockers. Widespread use of new beta-blockers in everyday clinical practice may increase beta-blocker use in general and in this way improve prognosis of ischaemic heart disease patients in Europe.