Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part I

Cardiac resynchronization therapy (CRT) has added a new dimension to the electrocardiographic evaluation of pacemaker function. During left ventricular (LV) pacing from the posterior or posterolateral coronary vein, a correctly positioned lead V1 registers a tall R wave and there is right axis deviation in the frontal plane with few exceptions. During simultaneous biventricular stimulation from the right ventricular (RV) apex and LV site in the coronary venous system, the QRS complex is often positive (dominant) in lead V1 and the frontal plane QRS axis usually points to the right superior quadrant and occasionally the left superior quadrant. The reported incidence of a dominant R wave in lead V1 during simultaneous biventricular pacing (RV apex) varies from 50% to almost 100% for reasons that are not clear. During simultaneous biventricular pacing from the posterior or posterolateral coronary vein with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). A negative paced QRS complex in lead V1 during simultaneous biventricular pacing with the RV lead at the apex can be caused by incorrect placement of the lead V1 electrode (too high on the chest), lack of LV capture, LV lead displacement, pronounced latency (true exit block), conduction delay around the LV stimulation site, ventricular fusion with the intrinsic QRS complex, coronary venous LV pacing via the middle or anterior cardiac vein, unintended placement of two leads in the RV and severe conduction abnormalities within the LV myocardium. Most of these situations can cause a QS complex in lead V1 which should be interpreted (excluding fusion) as reflecting RV preponderance in the depolarization process. Barring the above causes, a negative complex in lead V1 is unusual and it probably reflects a different activation of a heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation). The latter is basically a diagnosis of exclusion. With a non-dominant R wave in lead V1, programming the V-V interval with LV preceding RV may bring out a diagnostic dominant R wave in lead V1 representing the contribution of LV stimulation to the overall depolarization process. In this situation the emergence of a dominant R wave confirms the diagnosis of prolonged LV latency (exit delay) or an LV intramyocardial conduction abnormality near the LV pacing site but it rules out the various causes of LV lead malfunction or misplacement. (Cardiol J 2011; 18, 5: 476–486

Paradoxical atrial undersensing by a dual chamber pacemaker during atrial fibrillation

This report describes paradoxical atrial undersensing by a dual chamber pacemaker in a patient with paroxysmal atrial fibrillation. Atrial undersensing was present only when the device was programmed to a high sensitivity but sensing normalized when a lower sensitivity was programmed. This unusual response should be differentiated from the recently documented lock-in behavior of pacemakers delivering managed ventricular pacing. (Cardiol J 2012; 19, 2: 207–209

Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part II

The interval from the pacemaker stimulus to the onset of the earliest paced QRS complex (latency) may be prolonged during left ventricular (LV) pacing. Marked latency is more common with LV than right ventricular (RV) pacing because of indirect stimulation through a coronary vein and higher incidence of LV pathology including scars. During simultaneous biventricular (BiV) pacing a prolonged latency interval may give rise to an ECG dominated by the pattern of RV pacing with a left bundle branch block configuration and commonly a QS complex in lead V1. With marked latency programming the V-V interval (LV before RV) often restore the dominant R wave in lead V1 representing the visible contribution of the LV to overall myocardial depolarization. When faced with a negative QRS complex in lead V1 during simultaneous BiV pacing especially in setting of a relatively short PR interval, the most likely diagnosis is ventricular fusion with the intrinsic rhythm. Fusion may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate BiV capture. The diagnosis of fusion depends on temporary reprogramming a very short atrio-ventricular delay or an asynchronous BiV pacing mode. Sequential programming of various interventricular (V-V) delays may bring out a diagnostic dominant QRS complex in lead V1 that was previously negative with simultaneous LV and RV apical pacing even in the absence of an obvious latency problem. The emergence of a dominant R wave by V-V programming strongly indicates that the LV lead captures the LV from the posterior or the posterolateral coronary vein and therefore rules out pacing from the middle or anterior coronary vein. In some cardiac resynchronization systems LV pacing is achieved with the tip electrode of the LV lead as the cathode and the proximal electrode of the bipolar RV as the anode. This arrangement creates a common anode for both RV and LV pacing. RV anodal capture can occur at a high LV output during BiV pacing when it may cause slight ECG changes. During LV only pacing (RV channel turned off) RV anodal pacing may also occur in a more obvious form so that the ECG looks precisely like that during BiV pacing. RV anodal stimulation may complicate threshold testing and ECG interpretation and should not be misinterpreted as pacemaker malfunction. Programming the V-V interval (LV before RV) in the setting of RV anodal stimulation cancels the V-V timing to zero. (Cardiol J 2011; 18, 6: 610–624

Diagnostic challenge of artifactual electrocardiographic tachyarrhythmias

Electrocardiographic artifacts may generate recordings mimicking supraventricular and ventricular tachyarrhythmias. This report describes the diagnostic challenge presented by Holter or loop recordings in two patients, one with pseudo-atrial flutter and the other with pseudo- -polymorphic ventricular tachycardia

Przydatność 12-odprowadzeniowego EKG w monitorowaniu pacjentów z implantowanymi urządzeniami resynchronizującymi. Część I

Terapia resynchronizująca (CRT) wniosła do oceny elektrokardiograficznej funkcji stymulatora nowy wymiar. Podczas stymulacji lewokomorowej poprzez tylną i tylno-boczną żyłę wieńcową, prawidłowo umiejscowione odprowadzenie V1 rejestruje wysoki załamek R oraz skręt osi serca w prawo (poza nielicznymi wyjątkami). Podczas stymulacji obukomorowej z koniuszka prawej komory i lewokomorowej przez żyły wieńcowe wychylenie zespołu QRS jest zazwyczaj dodatnie w oprowadzeniu V1, a oś serca wychyla się w kierunku górnego prawego bądź rzadziej górnego lewego kwadrantu. Występowanie dominującego załamka R w oprowadzeniu V1 podczas stymulacji dwujamowej waha się w przedziale 50–100% przypadków, przyczyny zjawiska nie są jednak do końca jasne. W stymulacji obukomorowej z impulsami otrzymywanymi z tylnej i tylnobocznej żyły wieńcowej oraz elektrody umieszczonej w drodze odpływu prawej komory, stymulowany QRS w odprowadzeniu V1 ma zazwyczaj wychylenie ujemne, a oś serca jest skierowana w stronę dolnego prawego kwadrantu (prawogram). Ujemny zwrot zespołu QRS w odprowadzeniu V1 podczas stymulacji dwujamowej z elektrodą umieszczoną w koniuszku prawej komory może być spowodowany nieprawidłowym, zbyt wysokim umieszczeniem na klatce piersiowej odprowadzenia V1, brakiem stymulacji lewej komory, dyslokacją elektrody stymulującej lewą komorę, opóźnieniem przewodnictwa (blok wyjścia), zaburzeniami przewodzenia w obrębie stymulacji lewej komory, zsumowaniem pobudzeń stymulowanych i własnych zespołów QRS, stymulacją poprzez przednią lub pośrednią żyłę wieńcową, niezamierzonym umieszczeniem obu elektrod w prawej komorze i poważnymi zaburzeniami przewodnictwa w obrębie mięśnia lewej komory. W większości wypadków taka sytuacja prowadzi do powstania zespołu QS w odprowadzeniu V1, co można tłumaczyć przeważającym wpływem prawej komory na proces depolaryzacji. Poza wyżej wymienionymi przyczynami, ujemny zwrot zespołu QRS w odprowadzeniu V1, jako zjawisko rzadkie, może stanowić efekt odmiennej aktywacji heterogennego szlaku przewodzenia (niedokrwienie, blizna, udział układu His–Purkinje). Ostatnie jest rozpoznaniem z wykluczenia. W przypadku niedominującego w odprowadzeniu V1 załamka R, programowanie odstępu V-V z pobudzeniem LV poprzedzającym pobudzenie RV może doprowadzić do powstania dominującego załamka R w odprowadzeniu V1 jako wyrazu dominacji lewej komory w procesie depolaryzacji ogólnej. W takiej sytuacji pojawienie się załamka R potwierdza diagnozę bloku wyjścia LV lub zaburzeń przewodnictwa śródkomorowego w okolicach punktu stymulacji LV z wykluczeniem opcji dyslokacji lub nieprawidłowej funkcji elektrody lewokomorowej

The Spectrum of Acquired Atrioventricular Block in Clinical Practice

ABSTRACT: Type I and type II second-degree AV block characterize block of a single sinus P wave:Type I block describes visible, varying and generally decremental AV conduction and type II block describes apparent all-or-none conduction without visible changes in AV conduction time before and after the blocked impulse. Absence of sinus slowing is an important criterion of type II block because a vagal surge (generally benign) can superficially resemble type II block. The diagnosis of type II block cannot be established if the first postblock P wave is followed by a shortened PR interval or is not discernible. All correctly defined type II blocks are infranodal. A pattern resembling narrow QRS Type II block together with an obvious type I structure in the same recording effectively rules out type II block because the co-existence of both types of narrow-QRS block is rare. Narrow QRS type I block is almost always AV nodal whereas type I block with bundle branch block outside acute myocardial infarction is infranodal in 60-70 % of cases. 2:1 AV block cannot be classified in terms of type I or II blocks and can be nodal or infranodal. Pacing is indicated in symptomatic marked first-degree AV block (>0.30 sec.), but patients with systolic heart failure might benefit more with biventricular pacing. Permanent pacing is almost never needed after inferior myocardial infarction and narrow QRS AV block. It should be considered only if second- or third-degree AV block persist for 14-16 days. Patients with bundle branch block and transient secondand third-degree AV block during anterior myocardial infarction have a high risk of sudden death after hospital discharge usually from ventricular tachyarrhythmias rather than AV block. They should receive an implantable cardioverter- defibrillator rather than a stand-alone pacemaker in the setting of severely depressed systolic left ventricular function. There are many causes of atrioventricular (AV) block but progressive idiopathic fibrosis of the conduction system related to an aging process of the cardiac skeleton is the most common cause of chronic acquired AV block. Barring congenital AV block, Lyme disease is the commonest cause of reversible third-degree AV block in young individuals and it is usually AV nodal. Before implantation of a permanent pacemaker, reversible causes of AV block such as Lyme disease, hypervagotonia, athletic heart, sleep apnea, ischemia, and drug, metabolic, or electrolytic imbalance must be excluded. Table 1 outlines the format used in the 2002 American College of Cardiology/American Heart Association/ North American Society of Pacing and Electrophysiology (ACC/AHA/NASPE) guidelines for pacemaker implantation [1]. The indications for permanent pacing in second- or third- degree AV block unlikely to regress are often straightforward in symptomatic patients but they are more difficult in asymptomatic patients. Some of the ACC/AHA/NASPE guidelines appear somewhat dogmatic. The final responsibility rests with the physician in terms of decisions, and the guidelines only represent a basic framework to start from

Activation of the endogenous coagulation system in patients with atrial flutter: Relationship to echocardiographic markers of thromboembolic risk

Background: Atrial thrombus formation in patients with atrial flutter raises concerns of stroke risk. We investigated patients with isthmus-dependent atrial flutter for coagulation abnormalities before and after cardioversion to sinus rhythm by catheter ablation, and evaluated the relationship of the abnormalities to the echocardiographic risk markers of stroke. Methods and results: Plasma samples were drawn prior to insertion of catheters, immediately after the procedure, and 24 hours afterwards. At baseline, coagulation abnormalities were found in 22 out of 25 patients (88%). von Willebrand factor antigen (vWF-Ag) and factor VIII:C were elevated in 17 patients (68%) and 15 patients (60%), respectively. At baseline, mean plasma levels of vWF-Ag (250.1 &#177; 144.4%) and factor VIII:C (215.0 &#177; 77.1%) were increased. Key markers of thrombin generation, thrombin-antithrombin III complex (TAT; 47.8 &#177; 30.9 &#956;g/L vs 14.5 &#177; 13.8 &#956;g/L; p < 0.05) and prothrombin fragments 1.2 (F1.2; 2.5 &#177; 0.5 nmoL/L vs 1.2 &#177; 1.0 nmoL/L) were significantly elevated in the presence of spontaneous echo contrast. Further, both markers of thrombin generation inversely correlated with left atrial appendage emptying velocity (r = -0.42 and -0.63, p < 0.05). Levels of TAT and F1.2 increased after conversion and ablation. Conclusions: Endothelial-dependent coagulation factors were enhanced in most patients with atrial flutter. Spontaneous echo contrast and decreased atrial contractility were associated with increased thrombin generation. After conversion and ablation, an increase in thrombin generation and fibrinolysis suggest a transient pro-thrombotic state. (Cardiol J 2010; 17, 4: 390-396

Immuno-Electrophysiological Mechanisms of Functional Electrical Connections Between Recipient and Donor Heart in Patients With Orthotopic Heart Transplantation Presenting With Atrial Arrhythmias

[EN] BACKGROUND: The formation of recipient-to donor atrio-atrial connections (AAC) in patients after orthotopic heart transplantation (OHT) is poorly understood. We sought to investigate the mechanisms of atrial tachyarrhythmias after OHT, the role of AACs, and their relationship to the immunologic match. METHODS: In a large series of OHT patients, we performed a retrospective review of 42 patients who underwent catheter ablation for atrial arrhythmias. A realistic 3-dimensional computer model of human atria was used to study AAC conductivity. RESULTS: Patient age was 55 +/- 15 years (71% male). Biatrial anastomosis was present in 24/42 patients (57%). An AAC was found in 9/42 patients (21%, right-sided in 5 patients with biatrial anastomosis, left-sided in 4 patients). The AAC became apparent at the time of the electrophysiology study 10.1 +/- 7.6 years after OHT (range, 0.3-22.2 years). Donor-specific antibodies were present in no patient with AAC but were present in 69% of patients without AAC, P=0.002. In all patients with AAC, a recipient atrial tachycardia propagated via AAC to the donor atrium (4 patients presented with atrial fibrillation). Simulations showed AAC conduction requires an isthmus of >= 2 mm and is cycle length and location dependent. Patients without AAC (n=13) frequently presented with donor atrial arrhythmias, in 77% cavo-tricuspid isthmus flutter was ablated. The procedural success was high, although, 12 patients (29%) required reablation. CONCLUSIONS: AACs are found in 21% of OHT patients with atrial tachyarrhythmias and can manifest very early after OHT. Immune privilege characterized by the absence of donor-specific antibodies may facilitate AAC formation. Propagation across an AAC is width, cycle length, and location dependent. Patients with AAC present with focal atrial tachycardias or atrial fibrillation originating from the recipient atria; patients without most frequently present with cavo-tricuspid isthmus dependent atrial flutter. While multiple arrhythmias frequently require reablation, ablative therapy is highly effective.This study was supported in part by National Institutes of Health grants R21HL138064, and R01HL129136 to Dr Noujaim. This work was partially supported by the Direccion General de Politica Cientifica de la Generalitat Valenciana (PROMETEU2020/043).Herweg, B.; Nellaiyappan, M.; Welter-Frost, AM.; Tran, T.; Mabry, G.; Weston, K.; Tobón, C.... (2021). Immuno-Electrophysiological Mechanisms of Functional Electrical Connections Between Recipient and Donor Heart in Patients With Orthotopic Heart Transplantation Presenting With Atrial Arrhythmias. Circulation Arrhythmia and Electrophysiology. 14(4):412-423. https://doi.org/10.1161/CIRCEP.120.008751S41242314