Single Premature Beats Research Articles

The Importance of Cardiac Magnetic Resonance in the Assessment Risk of Cardiac Arrhythmias in Patients with Arterial Hypertension.

Objectives: Arterial hypertension (AH) is one of the major risk factors for cardiovascular diseases. An association between untreated AH and arrhythmia is observed. Cardiac magnetic resonance (CMR) assesses myocardial fibrosis by detecting foci of late gadolinium enhancement (LGE). Clinical significance of LGE at the right ventricular insertion point (RVIP) is not fully established. This study aimed to assess the relationship between the presence of LGE at the RVIP determined by CMR and the incidence of arrhythmia in a group suffering from arterial hypertension. Methods: The study group consisted of 81 patients with AH (37 men and 44 women, age: 56.7 ± 7.1 years). All subjects underwent CMR and 24 h Holter ECG monitoring. Two subgroups were distinguished in the study group based on the criterion of the presence of LGE at the RVIP in CMR. The RVIP+ subgroup consisted of patients with LGE at the RVIP, while the RVIP- group consisted of patients without LGE at the RVIP. Results: The RVIP+ subgroup was characterized by higher maximum and minimum heart rates in 24 h Holter ECG recordings compared to the RVIP- subgroup (p < 0.05). The RVIP+ subgroup had a statistically significantly higher number of single premature supraventricular beats, supraventricular tachycardias, and single premature ventricular beats than the RVIP- subgroup (p < 0.05). Regression analysis documented that a longer duration of AH (counted from diagnosis) as well as the occurrence of LGE at the RVIP (assessed by CMR) are independent risk factors for arrhythmia (p < 0.05). Conclusions: Due to the possibility of detecting LGE at the RVIP, CMR may be a useful diagnostic method in estimating the risk of arrhythmias in the group of patients with AH.

THE IMPORTANCE OF CARDIAC MAGNETIC RESONANCE IMAGING IN THE ASSESSMENT OF THE RISK OF CARDIAC ARRHYTHMIAS IN PATIENTS WITH ARTERIAL HYPERTENSION

Objective: Arterial hypertension leads to organ changes, including left ventricular hypertrophy. The increased mass of left ventricle increases the risk of cardiac arrhythmias, which enhances the risk of sudden cardiac death. Cardiac magnetic resonance imaging (CMRI) can identify the presence of myocardial fibrosis by assessing late gadolinium enhancement (LGE). The aim of the study was to assess the relationship between the presence of late gadolinium enhancement at the right ventricular insertion point (RVIP) determined by CMRI and the occurrence of cardiac arrhythmias in patients with arterial hypertension. Design and method: 30 patients with essential hypertension were qualified for the study, 18 men and 12 women, the average age of the subjects was 55.5 ± 12.4 years. All subjects underwent cardiac magnetic resonance imaging and 24-hour Holter ECG monitoring. Based on the presence of LGE at the right ventricular insertion point, assessed by CMRI, the subjects were divided into two subgroups. The first subgroup consisted of subjects with LGE at the right ventricular insertion point (RVIP + subgroup), while the second subgroup consisted of subjects without LGE at the right ventricular insertion point (RVIP - subgroup). Results: Subjects with LGE at the right ventricular insertion point were characterized by higher maximum and minimum heart rates in 24-hour Holter ECG recordings compared to subjects without LGE at the right ventricular insertion point (p &lt; 0.05). In subjects with LGE at the right ventricular insertion point, Holter ECG evaluation revealed a statistically significantly higher number of single premature supraventricular beats, single premature ventricular beats and supraventricular tachycardias compared to subjects without LGE at the right ventricular insertion point (p &lt; 0.05). The regression analysis performed showed that a longer time from the diagnosis of hypertension and the occurrence of LGE at the right ventricular insertion point assessed using CMRI are independent risk factors for cardiac arrhythmias (p &lt; 0.05). Conclusions: Cardiac magnetic resonance imaging by identifying of late gadolinium enhancement at the right ventricular insertion point may be a useful diagnostic method in assessing the risk of cardiac arrhythmias in a group of patients with arterial hypertension.

Non-invasive electrocardiographic ventricular mapping based on the equivalent double layer model: different workflows, same accuracy

Abstract Funding Acknowledgements Type of funding sources: None. Background and aim Electrocardiographic imaging (ECGI) is capable of performing activation maps with a single premature beat. The endo-epicardial ECGI system based on the equivalent double layer model (EDL), is a portable system that uses a patient-specific heart torso geometry obtained from a CT-scan or cardiac magnetic resonance (CMR), and a conventional 12-lead ECG. The simplicity of the system allows for its use either as a pre-procedural or intra-procedural tool. The aim of this study was to assess the accuracy of the system in centres using different workflows. Methods We studied consecutive patients referred for ablation of ventricular arrhythmias that had an ECGI performed with the endo-epicardial system based on the EDL model to guide mapping and catheter ablation, at four centres. Three centres performed the ECGI pre-procedurally, two with the use of a bedside portable ECG recorder and one on ambulatory basis with a 12-lead Holter recorder, and ablation was performed either manually or with remote magnetic navigation (RMN). The fourth centre performed the ECGI intra-procedurally, recording the ECG directly from the electrophysiology digital multichannel system, and the ablation was performed manually with the use of intracardiac echo (ICE) in all cases. VAs were localised using a segmental model, which included 22 left ventricular segments (classical 17-segment model, plus the aortic cusps and the papillary muscles), and 12 segments on the right ventricle including 4 on the right ventricular outflow tract (RVOT): Anterior, lateral, right septum and left septum. A perfect match (PM) was defined as a predicted location within the same anatomic segment, whereas a near match (NM) was defined as a predicted location within the same segment or a contiguous one. We studied the three different workflows. Results Sixty-three arrhythmias were studied in 58 patients. The ECGI was performed pre-procedurally with a bedside ECG recorder in 26 cases, pre-procedurally with a Holter recorder in 27 cases and intra-procedurally in 10 cases. The results according to each group are presented in the Table. The accuracy of the ECGI was not different between groups. The system correctly identified the SOO of the VAs in the same or a contiguous segment when compared to the invasive mapping in all patients, regardless of the approach used. The percentage of PM was also not significantly different. The group with ICE guidance had lower fluoroscopy and mapping times, but the success and recurrence rates were similar. Conclusions The results of this multicentre experience show that this ECGI system, using a conventional 12 -lead ECG is simple and accurate across different clinical workflows, and presents a useful and versatile tool to facilitate planning the ablation strategy as well as intra-procedural guidance for mapping and ablation of patients with VAs.

ЭМПАГЛИФЛОЗИН В ЛЕЧЕНИИ ПАЦИЕНТОВ С ХРОНИЧЕСКОЙ СЕРДЕЧНОЙ НЕДОСТАТОЧНОСТЬЮ, ЕГО ВЛИЯНИЕ НА ЖЕЛУДОЧКОВЫЕ НАРУШЕНИЯ РИТМА

The study aims to assess empagliflozin affecting ventricular dysrhythmia and late potential of ventricles in patients with chronic heart failure with low etiology ejection fraction. The study included 35 male patients (61.7 ± 11.2 years old) who received standard therapy, followed by 10 mg empagliflozin in 6 months. The examination included echocardioscopy, 12-leads electrocardiography, signal-averaged electrocardiography, and daily electrocardiography monitoring. 10 mg empagliflozin added to the standard therapy provided for a statistically significant decrease in the number of single premature heart beats by 67.7 % (p = 0.001), in the episodes of unstable ventricular tachycardia by 74.5 % (p = 0.001), in the frequency of late ventricular potential by 31 % (Chisquare = 5.51; р = 0.019), and for a statistically insignificant trend to ejection fraction increase (p &gt; 0.05).

Abstract 14991: Local Prolongation of Repolarization Prevents Post Myocardial Infarction Ventricular Tachycardia

Introduction: Reentry is the predominant mechanism underlying ventricular arrhythmias in chronic myocardial infarction patients. Reentry can be prevented by prolonging effective refractory period, thereby blocking reexcitation of recently activated tissue. This is currently achieved with systemically administered class III antiarrhythmic drugs. These therapies are limited by their risk of provoking ventricular arrhythmias by off-target effects. Hypothesis: Local prolongation of repolarization in healthy myocardium adjacent to the exit site attenuates reentry and postinfarction arrhythmias. Method and results: We used a pig model and generated myocardial infarction by balloon occlusion of the left anterior descending coronary artery and performed epicardial mapping 6 weeks later during Langendorff-perfusion. Programmed stimulation induced reentry leading to ventricular premature beats and sustained ventricular tachycardia (VT). Local injection of Sotalol adjacent to the infarcted myocardium prolonged repolarization and prevented VT after programmed stimulation. To translate these experimental findings to the patient situation we used a virtual heart based on data from a patient suffering from postmyocardial infarction VTs. The patient underwent pre-ablation cardiac late gadolinium enhanced- magnetic resonance imaging followed by geometrical reconstruction of the left ventricle and computational electrophysiological modelling of VT induction. We used a rapid pacing protocol to induce VT and determined the site where the activation front exited the infarct zone and reactivated the adjacent normal myocardium. Next, we prolonged repolarization of the normal myocardium adjacent to the exit site with 50 ms and performed rapid pacing to induce VT. This only resulted in a single premature ventricular beat after which sinus rhythm restored. Conclusion: Our experimental and in silico findings show the potential of local prolongation of repolarization a novel potentially genetic anti-arrhythmic therapy in post-infarction patients.

A rare case of complex ventricular arrhythmia and heart failure in a 15.5-year-old athlete

A 15.5-year-old boy, an athlete, reported to his general practitioner due to episodes of chest pain during exercise, weakness and a feeling of irregular heartbeat that had been occurring for a month. He reported episodes of fainting in the past. Physical examination revealed arrhythmia and the patient was referred for a cardiological consultation, and then admitted to a reference cardiology department for extended cardiac diagnosis. Approximately 66,000/day (49.8%) of premature ventricular beats were recorded in 24-hour Holter electrocardiogram, including episodes of non-sustained ventricular tachycardia. Echocardiography revealed left ventricular systolic dysfunction with a decrease in its ejection fraction to 51.5%. Magnetic resonance imaging of the heart was performed, which showed foci of late post-contrast enhancement, located subepicardialy in the side wall of the left ventricle, corresponding to post-inflammatory changes in the myocardium. Left and right ventricular ejection fraction on magnetic resonance imaging were 48% and 46%, respectively. Pharmacological treatment included a beta-blocker (metoprolol), propafenone and an angiotensin converting enzyme inhibitor (enalapril). During the treatment, ventricular arrhythmia subsided almost completely, a gradual improvement in left ventricular systolic function was observed, and the patient was relieved of pain. The boy was discharged home with a recommendation to continue pharmacological treatment, lead a sparing lifestyle, and postpone practicing sports. At present, the boy’s general condition is good, he does not report any complaints, takes medications regularly, and does sports only for recreation. A follow-up Holter showed only single premature ventricular beats, while echocardiography showed an improved left ventricular systolic function (ejection fraction 63%), which is a good prognostic indicator.

Premature Beats Rejection Strategy on Paroxysmal Atrial Fibrillation Detection.

Paroxysmal atrial fibrillation (PAF) may related to the risk of thromboembolism and is the most common cardiac risk factor of cryptogenic stroke (CS). Due to its paroxysmal characteristics, it is usually diagnosed by continuous long-term ECG. Patients with paroxysmal atrial fibrillation usually have premature beats at the same time which is easy to be confused with the rhythm of atrial fibrillation. Therefore, in this article, we designed a screening algorithm for single premature beat, multi premature beats, bigeminy and trigeminy premature beats, according to their rhythm characteristics to reduce false detection caused by premature beats during the PAF detection process. The proposed elimination method was verified on ECG segments with different types of premature beats, and tested on long-term ECG data of PAF patients. ECG segments of different kinds of premature beats were selected from MIT Atrial Fibrillation database (MIT-AFDB), MIT-BIH Arrhythmia database (MIT-AR) and wearable ECG data from the China Physiological Signal Challenge 2021 (CPSC 2021). The proposed method can effectively eliminate single premature beat segments with 99.5% accuracy, and it also can eliminate more than 95% of ECG segments with other types of premature beats. We designed PAF-score as a new index to evaluate the accuracy of detection, and we also calculate the misjudged and missed segments to comprehensively evaluate the PAF detection algorithm. The proposed method get a PAF-score of 0.912 on MIT-AFDB. The proposed method also has the potential to implant low computing power wearable devices for real-time analysis.

Eliminating the trigger for polymorphic ventricular tachycardia

A 60-year-old female patient was referred to our hospital because of recurrent syncope. The resting 12-lead ECG showed sinus rhythm with left bundle branch block and a high burden of monomorphic single premature ventricular beats (PVCs). Imaging studies confirmed a structurally normal heart and ischaemic heart disease was ruled out by coronary angiography. Telemetry revealed repeated episodes of polymorphic ventricular tachycardia (VT) triggered by monomorphic PVCs causing syncope. Therefore, an ICD was implanted and the patient was discharged on bisoprolol 10 mg/day. A few weeks later, she was referred to our hospital owing to repeated ICD shocks triggered by monomorphic PVCs with long-short sequences. Radio­frequency catheter ablation targeting the monomorphic PVC causing polymorphic VT was performed. With an almost perfect pace map within the distal coronary sinus, ablation in this region did not abolish the PVC. Therefore, we antegradely mapped the LV via transseptal access. Endocardial mapping at the anterior mitral anulus using the reverse S-curve technique revealed the earliest bipolar activation in close proximity to the ablated region within the coronary sinus. Ablation at this site abolished the clinical PVC. ECG monitoring at 3, 6 and 12 months did not reveal any PVC, and no ICD discharges have occurred since ablation.

Ranolazine effectively suppresses atrial fibrillation in the setting of heart failure.

There is a critical need for safer and more effective pharmacological management of atrial fibrillation (AF) in the setting of heart failure (HF). This study investigates the electrophysiological, antiarrhythmic, and proarrhythmic effects of a clinically relevant concentration of ranolazine (5 μmol/L) in coronary-perfused right atrial and left ventricular preparations isolated from the hearts of HF dogs. HF was induced by ventricular tachypacing (2-6 weeks at 200-240 beats per minute; n=17). Transmembrane action potentials were recorded using standard microelectrode techniques. In atria, ranolazine slightly prolonged action potential duration but significantly depressed sodium channel current-dependent parameters causing a reduction of maximum rate of rise of the action potential upstroke, a prolongation of the effective refractory period secondary to the development of postrepolarization refractoriness, and an increase in diastolic threshold of excitation and atrial conduction time. Ranolazine did not significantly alter these parameters or promote arrhythmias in the ventricles. Ranolazine produced greater inhibition of peak sodium channel current in atrial cells isolated from HF versus normal dogs. A single premature beat reproducibly induced self-terminating AF in 10 of 17 atria. Ranolazine (5 μmol/L) suppressed induction of AF in 7 of 10 (70%) atria. In the remaining 3 atria, ranolazine reduced frequency and duration of AF. Our results demonstrate more potent suppression of AF by ranolazine in the setting of HF than previously demonstrated in nonfailing hearts and absence of ventricular proarrhythmia. The data suggest that ranolazine may be of benefit as an alternative to amiodarone and dofetilide in the management of AF in patients with HF.

The Value of a Rate Change in Determining the Tachycardia Mechanism: What is the Mechanism?

A 28-year-old male patient with a 3-year history of re-current tachycardia was referred for electrophysiologic eval-uation and catheter ablation. The patient had no other co-morbidities. Propafenone was discontinued 7 days beforeadmission.Electrophysiologic study: normal baseline intervals dur-ing sinus rhythm (PA = 20, AH = 68, HV = 50 ms). Anarrow QRS tachycardia was repeatedly induced by a singleatrial premature beat following a pacing drive of 400 ms, orfollowing 2 premature beats delivered during sinus rhythm.In contrast, a wide QRS tachycardia was always inducedby 2 right ventricular premature beats delivered during sinusrhythm.Thisleftbundlebranchblock(LBBB)-liketachycar-dia with a cycle length of 330–340 ms would spontaneouslychange into a slower, narrow QRS tachycardia with a cyclelengthof370msafterstabilizationoftheRRinterval(Fig.1).Transitionfromwidetonarrowtachycardiawassudden.Thecycle length of the first RR interval after disappearance oftheLBBBpatternwas310msbutincreasedthereafter.Whatwas the mechanism of change in cycle length?

Atrial Premature Beats During Decrementally Conducting Antidromic Tachycardia

Advancement of ventricular activation by an atrial premature beat (APB) given during His bundle refractoriness followed by resetting of an antidromic tachycardia (AT) in patients with decrementally conducting accessory pathway (DAP) is a helpful maneuver to prove pathway existence and participation in the circuit. We aim to assess in a large cohort the role of APB during AT in patients with a DAP. Thirty-three patients with a DAP having 34 AT were included in the study: 29 patients had an atriofascicular pathway, 1 had a long atrioventricular DAP, and 4 had a short atrioventricular fiber. APBs were delivered initially from the lateral right atrium, scanning diastole with a 10-ms decrement until AT termination or refractoriness. We observed 4 patterns of response after APB during AT: advancement of activation (29 cases), delay (2), advancement followed by delay (3), and termination (7). Eight patients required an earlier APB to advance or delay ventricular activation. These 8 patients had a shorter AT cycle length (median of 273 versus 315 ms; P=0.003) and had a shorter resetting zone (median coupling interval of 30 versus 50 ms; P=0.01). APB delivered during AT in patients with a DAP advanced and/or delayed ventricular activation in all patients. In 1 of 5 of cases the AT was terminated by a single APB. In approximately a quarter of the patients an earlier coupled APB was needed to reset AT. The high RA was an adequate stimulation site in all right-sided DAP.

Abstract 19252: Onset Scenarios of Paroxysmal Atrial Fibrillation in Patients with Ischemic Stroke

The characterization of onset scenarios of paroxysmal atrial fibrillation (pAF) has recently gained prominence to determine various underlying arrhythmogenic trigger mechanisms. It is hypothesized that there might be specific onset scenarios of pAF in patients with ischemic stroke, however, onset scenarios of pAF have not yet been systematically analysed in a broad patient population without pacemaker indication and especially those patients after ischemic stroke. Methods and Results: From a total of 20.546 consecutive ambulatory 24-hour-Holter-ECG-recordings, 668 episodes of pAF (lasting &gt; 1 minute) were identified in 343 patients without previous stroke (155 females; 71±10years) and 35 pAF episodes in 20 patients after ischemic stroke (8 females; 67±15 years). The dominant portion of episodes of pAF was preceded by atrial ectopy [single atrial premature beats (APB), blocked APB, multiple APB, short atrial runs, short-long-short sequences] or heart rate alterations [bradycardia, tachycardia, sudden rate drop, ventricular premature beats (VPB)]. Almost one third of all pAF episodes were not preceded by either ectopy or heart rate alterations (i.e. sudden-onset pAF). There were no significant differences between patients with or without stroke regarding the distribution of pAF-onset patterns. Mean RR-interval during sinus-rhythm tended to be higher in patients after ischemic stroke (866±184ms vs 845±190ms; p=0.1) Conclusion: There are no significant differences regarding specific onset-scenarios of pAF patients after ischemic stroke and in patients without stroke. Interestingly, patients with stroke tended to have lower heart rates during sinus rhythm.

Ranolazine Causes Atrial-Selective Electrophysiological Effects and Suppresses the Induction of Atrial Fibrillation in a Canine Model of Heart Failure

Background Heart failure (HF) and atrial fibrillation (AF) frequently coexist. There is a critical need for safer and more effective pharmacologic treatment of AF in the setting of HF. The atrial-selective electrophysiologic (EP) effects as well as anti-AF efficacy of ranolazine (RAN) have been demonstrated in healthy canine atria. In the current study, we investigated the EP and anti-AF effects of a clinically relevant concentration of RAN (5 μM) in coronary-perfused right atrial (RA) and left ventricular (LV) preparations isolated from the hearts of HF dogs. Methods HF was induced by ventricular tachypacing (2–6 weeks at 200–240 bpm; n=17 dogs). Transmembrane action potentials were recorded using standard microelectrode techniques. Results A single premature beat reproducibly induced AF in 10/17 atria lasting up to 20 minutes. RAN (5 μM) suppressed induction of AF in 7/10 atria. In the remaining 3 atria, ranolazine slowed AF frequency and reduced the duration. In RA, RAN caused little change in action potential duration (APD 70 : from 105 ± 12 to 114 ± 15 ms, P = NS) but significantly prolonged effective refractory period ([ERP] from 127 ± 21 to 176 ± 25 ms, P max ) decreased (229 ± 55 vs 189 ± 50 V/s), diastolic threshold of excitation (DTE) increased (0.24 ± 0.05 vs 0.42 ± 0.16 mA), and P-wave duration (atrial conduction time) prolonged in response to 5 μM RAN (31.6 ± 7.6 vs 36.5 ± 6.5 ms, P 90 , ERP, DTE, V max , and QRS duration (n = 5–6). Conclusions Our results demonstrate the effect of a relatively low concentration of RAN to suppress induction of AF much more effectively (70%) in an HF model of AF than previously described in vagal models of AF. In both models, depression of peak sodium channel current-dependent parameters is atrial selective. In view of the clinical safety of RAN (MERLIN-TIMI 36), our results suggest a need for studies specifically designed to evaluate the clinical utility of RAN for rhythm control of AF in patients with HF.

Is Pitx2 Growing Up?

In this issue of Circulation: Cardiovascular Genetics , Kirchhof et al1 present an interesting study on the expression of the developmental transcription factor Pitx2c in adult heart and its potential role in atrial fibrillation (AF). AF is the most common sustained cardiac arrhythmia, with a prevalence that increases with age and affects 1% to 2% of the general population.2 Despite recent advances in AF research, underlying pathophysiologic mechanisms are not fully understood. In general, initiation and perpetuation of AF needs a trigger for its onset and a vulnerable substrate for its maintenance.3 Focal ectopic activity can act as a trigger to initiate AF on the basis of a single- or multiple-circuit reentry.4 Especially, cardiomyocyte sleeves around the pulmonary veins have been shown as an origin of focal activity.5 Underlying mechanisms are early and delayed after depolarizations as a result of disturbances in depolarizing inward (Na+ or Ca2+) or repolarizing outward (K+) currents.6 Article see p 123 Once initiated, AF itself induces structural and electric remodeling, which stabilizes reentry and AF maintenance.6 Structural remodeling due to signaling through angiotensin, profibrotic cytokines like transforming growth factor-β, or microRNAs leads to upregulation of extracellular matrix proteins (eg, collagen) and downregulation of matrix-degrading enzymes (eg, matrix metalloproteinase), resulting in progressive atrial fibrosis. Electric remodeling is caused by expressional changes in ion channel subunits. AF induces calcium overload and increases activity of protein phosphatases, leading to downregulation of depolarizing L-type calcium channels and upregulation of repolarizing potassium channels. Measurable substrate of these changes in atrial electric properties is the shortening of action potential duration (APD), leading to shortening of refractory period and enabling reentry mechanisms. In most cases, therefore, AF is self-terminating (paroxysmal) in the beginning, developing to more sustained forms (persistent and permanent) over …

12 Both opening and closing of gap junctions may result in protection against the acute ischaemia-induced severe ventricular arrhythmias in anaesthetised dogs

The objective was to examine whether opening or closing of gap junctions (GJ) modify the acute ischaemia-induced ventricular arrhythmias. In chloralose-urethane anaesthetised dogs myocardial ischaemia was induced by a 60...

ECG variations in patients pre- and post-local anaesthesia and analgesia

To determine the incidence of ECG abnormalities in a healthy adults undergoing a surgical extraction of third molar teeth pre-and post-operatively and to study the effect of local anaesthetics, surgical stress and analgesics on cardiac rhythm. One hundred and ninety-eight healthy adult patients taking part in a clinical trial of analgesics were randomly selected for this study. All patients required the removal of at least one impacted mandibular wisdom tooth under local anaesthetic. An ECG was taken at a screening visit and repeated post-operatively 30 minutes after analgesia was given. The effects of analgesia were also monitored to ascertain whether any changes were related to pain experience or the analgesic itself. ECG abnormalities were detected in 44 patients at the screening visit. Of these patients, 20 showed rsR complex patterns, seven showed non-specific ST elevation, six patients had an abnormal P wave axis, three patients presented with single atrial premature beats and three patients showed a short PR interval. Other minor abnormalities were occasionally seen. The results recorded were of minimal clinical significance and the numbers are in line with previous research. Post-operative abnormalities were seen in 60 patients. Nineteen patients showed rsR complex patterns, sinus arrhythmias were seen in 11 individuals, seven patients showed non-specific ST elevation and six patients had an abnormal P-wave axis. Other minor abnormalities were occasionally seen. Although the results were not statistically significant, some of the patients did show clinically relevant abnormalities which necessitated referral to a cardiologist. These included: marked ST elevation; marked ST depression and one case of Right Bundle Branch Block (RBBB).

Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle

A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB.

Point:Counterpoint: Respiratory sinus arrhythmia is due to a central mechanism vs. respiratory sinus arrhythmia is due to the baroreflex mechanism

Blood pressure and heart periods fluctuate at respiratory frequencies in healthy humans. Some researchers ([8][1], [23][2]) explain this as a cause-and-effect relation: blood pressure changes trigger baroreflex-mediated R-R interval changes. Here I make the case that respiratory sinus arrhythmia is

EFFECT OF BENAZEPRIL ON HEART RATE TURBULENCE IN PATIENTS WITH DILATED CARDIOMYOPATHY

1. Heart rate (HR) turbulence describes short-term sinus rhythmic fluctuation after a single premature ventricular beat. Turbulence onset (TO) and turbulence slope (TS) are two essential parameters in HR turbulence. Turbulence onset and TS have been used to evaluate cardiac autonomic nerve function. 2. In the present study, we measured the HR turbulence in dilated cardiomyopathy (DCM) and determined the possible role of benazepril, an angiotensin-converting enzyme inhibitor (ACEI), on these parameters. There were three groups: control, DCM and DCM treated with benazepril. The control group consisted of normal subjects with PVB, but no structural heart disease. Ambulatory electrocardiogram, blood pressure and echocardiography were analysed. 3. There was an increase in TO and a decrease in TS in DCM patients. Benazepril treatment (10 mg/day, p.o.) reduced those changes. There were no significant differences in blood pressure and left ventricular ejection fraction (LVEF) between DCM patients and DCM patients treated with benazepril. 4. Linear regression analysis showed that TO was negatively correlated with LVEF, whereas TS was positively correlated with LVEF, in the DCM group. After benazepril treatment, the correlations between TO and TS and LVEF disappeared. 5. It is concluded that the TO and TS of HR turbulence are altered in patients with DCM. These alterations indicate a dysfunction of the autonomic control of cardiac electrophysiology in DCM patients. Although TO and TS are correlated with LVEF in DCM patients, the effect of benazepril in improving HR turbulence parameters is not a result of its action on heart function, which suggests a new beneficial effect of ACEI in the treatment of DCM patients.

Radiofrequency catheter ablation in frequently single premature ventricular beats

目的 探讨射频消融术对频发单形室性早搏的疗效.方法对频发性室性早搏患者19例采取激动标测及起搏标测相结合,以起搏时与室性早搏QRS波形态完全相同点为消融靶点行射频消融治疗.结果18例即刻成功,1例无效,无并发症.术后2周24 h动态心电图检测,随诊6个月至2年,17例无复发或早搏无增多,1例出现另一形态室性早搏.结论射频消融治疗频发单形室性流出道室性早搏安全、有效。