Radosław Kiedrowicz

Effect of cardiac resynchronisation therapy on coronary blood flow in patients with non-ischaemic dilated cardiomyopathy

BACKGROUND Cardiac resynchronisation therapy (CRT) has beneficial effects on cardiac function, exercise tolerance, symptoms, and prognosis. Coronary blood flow impairment has been observed in patients with non-ischaemic dilated cardiomyopathy (DCM) despite angiographically normal coronary arteries. No data are available on coronary blood flow and coronary flow reserve (CFR) measured by intracoronary Doppler in different coronary arteries in patients with DCM and left bundle branch block (LBBB) before and during treatment with CRT. AIM Thus, the major aim of our study was to assess the effect of CRT on coronary blood flow in patients with non-ischaemic DCM and to compare coronary blood flow and CFR measured in the 3 major coronary arteries (left anterior descending [LAD], left circumflex [LCX], and right coronary artery [RCA]). METHODS Twenty one patients with DCM and LBBB (mean left ventricular ejection fraction 26 ± 7%, 5 females, mean age 57.8 ± 8.1 years) were studied. Average peak velocity, diastolic/systolic velocity ratio and CFR were measured using intracoronary Doppler before and 6-9 months after implantation of CRT-D or CRT-P. RESULTS In patients with a clinical improvement (71.4%), CFR increased in LAD. CFR measured in LCX and RCA did not improve either in the overall study group or in patients with a clinical improvement. The observed increase in CFR in LAD correlated only with reduction of QRS duration. CONCLUSIONS In non-ischaemic DCM, CFR is reduced only in LAD. A significant improvement of CFR in LAD after CRT correlates with reduction of QRS duration.

Multiple cardiovascular complications in a patient with missed small apical myocardial infarction caused by a coronary artery thrombus of uncertain origin

An 82 year-old hypertensive male with no concomitant diseases was admitted because of missed myocardial infarction (MI), 3 days after chest pain onset. On admission, the patient was pain free with stable haemodynamics and normal physical examination. The ECG (Fig. 1) showed atrial fibrillation (AF) and ischaemic changes with its resolution at follow-up. During coronarography (Fig. 2), the presence of a thrombus in the apical part of the left anterior descending (LAD) artery, atherosclerotic plaques with lack of culprit lesion clearly connected to the thrombus, and insignificant myocardial bridging (MB) were demonstrated. The patient was followed conservatively. Troponin and CK-MB elevation with decreasing consecutive values was observed. Transthoracic echocardiography (TTE) delineated left atrial (LA) enlargement, akinesia limited to the left ventricular apex with preserved global ejection fraction of 60% as well as a recent, partially movable, apical left ventricular mural thrombus (LVMT) (Fig. 3A). Warfarin therapy was introduced. On day 2, he developed acute ischaemic stroke (AIS). Carotid artery disease was excluded. On day 6, a systolic murmur demonstrated by echocardiography as an apical ventricular septal rupture (VSR) with left-to-right shunt and a thrombus partially occluding the defect which was smaller and less movable was diagnosed (Fig. 3B). The cardiothoracic surgeon recommended delaying surgical treatment. The patient’s haemodynamic status worsened gradually with signs of exclusive right ventricular failure. An intra-aortic balloon pump was not used due to lack of patient co-operation. On day 18, the family requested that he be discharged home where he finally died. It is most likely that atherosclerotic plaque was involved in the thrombus formation and coronary occlusion, although an AF related embolism is quite possible. These hypotheses could not be verified because there was no culprit lesion and no LA thrombus confirmation. Less probably, MB could have given rise to coronary thrombosis with subsequent MI. Finally, tako-tsubo cardiomyopathy, coronary vasospasm or MB can be a primary cause of apical akinesia, blood stagnation, LVMT development and secondary coronary embolism. LVMT and VSR are strongly associated with extensive anterior MI. In this case it was small and limited to the apex, but proximal LAD occlusion with downstream thrombus migration is possible. Moreover, we speculate that ST elevation in inferior leads might be related to dominant LAD and that ST depression in precordial leads might be a reciprocal change. A coincidence of LVMT and VSR has rarely been documented. Moreover, we observed the partial occlusion of the defect by the thrombus which might delay its recognition and slow the natural evolution. The most probable explanation for AIS is embolisation related to recent LVMT or AF.

The Value of Ablation Parameter Indices for Predicting Mature Atrial Scar Formation in Humans: An In Vivo Assessment using Cardiac Magnetic Resonance Imaging: CHUBB et al.

The VisiTag module (CARTO3) provides an objective assessment of radiofrequency (RF) ablation parameters. This study aimed to determine the predictive value and optimal VisiTag threshold settings for prediction of gaps in mature atrial scar, as assessed non‐invasively using cardiac magnetic resonance (CMR) imaging.

The effect of atrial pacing site on electrophysiological properties of the atrioventricular junction and induction of atrioventricular nodal reentry in patients with typical atrioventricular nodal reentrant tachycardia

BACKGROUND Clinical studies in humans have shown the site of atrial stimulation to influence atrioventricular (AV) conduction times and refractory periods, the demonstration of dual AV nodal (AVN) pathways, and induction of AVN reentry. These studies often found conflicting results. Moreover, among enrolled patients a minority of them were found to have AVN reentrant tachycardia (AVNRT). AIM The purpose of this study was to investigate the effect of right and left atrial pacing on the electrophysiological properties of the AV junction in the typical AVNRT population. METHODS Ninety-two consecutive patients with typical AVNRT were included. Atrial pacing was performed from the high right atrium (HRA) and the left atrium via the proximal coronary sinus (CS). RESULTS Stimulation from either the HRA or the CS could result in dual AVN physiology and AVNRT. No site-dependent differences in the ease of induction of dual AVN pathways with variability of initiation from either site were found. However, AVNRT was easier to induce from the HRA. With CS pacing the leftward but not the rightward AVN approaches were the entry point to the AV node because of significantly shorter AH conduction times compared to HRA pacing. Conduction over the leftward AVN extensions could initiate the tachycardia with significantly shorter critical AH interval compared to conduction over the rightward AVN extensions; however, the AH interval during AVNRT and its cycle length were not significantly different. CONCLUSIONS Rightward and leftward AVN extensions are regular features of the AV node. Their different electrophysiological properties lead to variation in the demonstration of discontinuous AVN conduction and AVNRT during right and left atrial pacing. Despite the observation that the left AVN extensions could compose the entry point to the reentrant circuit, there is no evidence that they constitute the critical component of sustained typical AVNRT.

Ocena przebiegu klinicznego i czynników wpływających na historię naturalną typowego częstoskurczu węzłowego nawrotnego

Introduction. Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common regular tachyarrhythmia; however, its clinical presentation has not been investigated in detail. The aim of the study was to assess the clinical presentation and identify the potential factors significantly affecting the natural history of AVNRT in patients undergoing RF ablation. Material and methods. Ninety-two consecutive patients with invasive diagnosis of typical AVNRT who underwent RF ablation were included. All patients were actively screened for the presence of structural heart disease (SHD). The retrospective, arrhythmia focused interviews regarding its clinical history, affecting factors and treatment were conducted. The medical records and tachycardia ECG tracings data were included, if available. Results. Seventy-five percent of patients had evidence of the arrhythmia exacerbation. No relationship between the coronary (66%) or brain (33%) hypoperfusion symptoms and clinical factors was found. Time to the tachycardia diagnosis was significantly longer in women (13 ± 11 vs 7 ± 8 years, p = 0.006). Pharmacological AVNRT management was not consistent with the ESC guidelines. The arrhythmia symptoms were occurring later if SHD was present (44 ± 13 vs 30 ± 5 years, p = 0.001). The longer AVNRT cycle length (CL), modified by the age when symptoms appeared and the presence of impaired myocardial contractility, the longer time to the arrhythmia diagnosis and exacerbation. Mitral valve prolapse (MVP) was more common in female patients compared with the general population and was found to be the factor delaying AVNRT diagnosis. Conclusions. In the majority of patients AVNRT exacerbation takes place. The coronary and brain hypoperfusion symptoms that patients often experience are nonspecific. There is a significant delay in the arrhythmia diagnosis, especially in women. SHD, AVNRT CL and MVP were identified as factors that significantly modify the arrhythmia clinical presentation.

Cryoballoon ablation of paroxysmal atrial fibrillation and underlying atrial tachycardia and ectopy arising from a common trigger focus limited to a right inferior pulmonary vein

A 69-year-old woman (case 1) and a 36-year-old man (case 2) without comorbidities, normal pulmonary veins (PV) anatomy and atrial, mitral, PV dimensions were referred for cryoballoon ablation of paroxysmal atrial fibrillation (AF). Although atrial tachycardia (AT) and a frequent atrial ectopy (AE) had never been documented, ongoing AT or AE mimicking sinus rhythm (SR) were noticed at admission. An electrophysiological study, in a drug free state, with catheters placed into the coronary sinus, in the right atrium (RA) and His bundle was performed. The positive P wave in lead V1, superimposed on the negative T wave and the negative P wave in lead aVL in case 1 (Figs. 1A, B), and similarities in the P wave morphology during AE and SR and negative P waves in lead aVL in case 2 (Figs. 2A–C), suggested PV AT/AE. Activation mapping with a circular catheter within each PV was performed. Right inferior PV (RIPV) depolarisation preceded the onset of the ectopic P wave by 60 ms (Fig. 1A) and 50 ms (Fig. 2B), respectively. During cryoapplication with a 28 mm cryoballoon catheter (Fig. 3), SR was restored (Figs. 1B, 2C). We did not notice PV electrical activity within other PVs during AT/AE and SR. Although a single culprit PV was found, isolation of the remaining PVs was performed. Post-ablation, there was a bidirectional block within all PVs and no AT/AF was induced. No recurrences of any atrial arrhythmias were seen during the 18 month drug free post ablation follow-up. Focal AT/AE is a rare arrhythmia mainly arising from the RA (83%). The most frequent foci within the left atrium (LA) are superior PV ostia. Their origin from RIPV and coexisting AF with a trigger limited to the same PV, while it is commonly associated with multiple triggers from multiple veins (94%), is uncommon. Although AT and AF may be initiated by PV triggers, it is unclear whether in the presented cases there were two independent arrhythmogenic foci within one PV or a single AT/AE focus that resulted in a long-term AF. Many authors have suggested that PV AT and PV AF represent distinct entities. PV foci initiating AF have been identified to be located deep within the PV, in contrast to a more ostial location for AT. PV AT patients have a discrete, in contrast to diffuse, process involving PVs and the LA seen in AF. In PV AT patients without a history of AF following a focal ablation, AF episodes have not been documented during long-term follow-up. A single documented episode of a PV AT/AE indicates that the supposed previous episodes were short lasting and self-terminating, or just initiated AF.

NOninvasive Monitoring for Early Detection of Atrial Fibrillation: rationale and Design of the NOMED-AF study

1Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Poland 2Silesian Park of Medical Technology Cardio-Med Silesia, Zabrze, Poland 31st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland 4Department of Preventive Medicine and Education, Medical University of Gdansk, Gdansk, Poland 5Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Krakow, Poland 6Department of Cardiology, Pomeranian Medical University, Szczecin, Poland 7Comarch Healthcare SA, Krakow, Poland 8Comarch SA, Krakow, Poland 9Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, United Kingdom