Paroxysmal Atrioventricular Block Research Articles

Paroxysmal atrioventricular block precipitated by an atrial premature beat. What is the mechanism?

A 65 year-old woman presented with two epi-sodes of syncope. She developed paroxysmal atrio-ventricular (AV) block when an ECG was being re-corded (Fig. 1). She developed at least one othersimilar episode. Then, she developed complete AVblock with a stable escape ventricular rhythm ofabout 30 bpm during which an atrial premature beatwas conducted (Fig. 2). Isoproterenol was admi-nistered which increased the ventricular rate to47 bpm. The patient remained stable and laterreceived a permanent dual chamber pacemaker.Lee et al. [1] reported 68 cases of bradycardia-dependent AV block (30 cases [group I] were fromthe investigators’ two institutions and 38 caseswere added from the literature [group II]) [2–5].Paroxysmal AV block (PAVB) was defined as theabrupt occurrence of pause-dependent (phase 4) AVblock in a patient with apparently normal 1:1 AVconduction between the episodes of PAVB [1]. Mostpatients present with syncope or near-syncope.There were 19 of 68 patients (28%) with a normalECG as in our patient (Fig. 1). Thus, a normal ECGdoes not rule out PAVB. This form of AV block canbe precipitated by atrial or ventricular prematurebeats, His bundle extrasystoles, sinus slowing ei-ther spontaneous or induced by carotid sinus mas-sage and rarely after supraventricular tachycardiaby overdrive suppression upon termination. In

Diagnostic Usefulness of an Implantable Loop Recorder in a Patient with Repetitive Syncope due to Paroxysmal Complete Atrioventricular Block

Diagnostic Usefulness of an Implantable Loop Recorder in a Patient with Repetitive Syncope due to Paroxysmal Complete Atrioventricular Block

Bloc auriculoventriculaire complet transitoire chez un africain : la drépanocytose comme cause

This case report shows a rare cardiac complication of sickle cell anemia in a young African patient which was an acute paroxysmal atrio-ventricular block. Acute paroxysmal atrioventricular block is a rare complication of polymerization of hemoglobin S during sickle cell disease. Hence, sickle cell anemia should be considered as a cause of auriculoventricular block in black African patients. Cardiac complications of sickle cell anemia are presented in this article.

Reverse Wenckebach “pseudo-supernormal” conduction or paroxysmal atrioventricular block

Paroxysmal atrioventricular-block is a poorly-recognized cause of atrioventricular conduction abnormality leading to syncope and can be fatal. Here we report a case of paroxysmal atrioventricular-block presenting as syncope treated effectively with pacemaker implantation and review the current literature on prevalence, known mechanisms and treatment for it. Importantly we provide the diagnostically important differentiating points between vagally mediated block and paroxysmal atrioventricular-block as well as the highlight the vastly varying prognosis between the two.

Pacemaker “Dysfunction” Treated by Radiofrequency Ablation

A 68-year-old female with a history of paroxysmal atrial fibrillation and complete atrioventricular (AV) block was referred for palpitations and suspicion of pacemaker dysfunction (model Philos II DR-T, Biotronik, Berlin, Germany). Baseline electrocardiogram (ECG) showed a dual-chamber pacemaker with an inappropriate behavior (Fig. 1, Panel A). Pacemaker programmed parameters were as follows: pacing mode DDD-R; basic rate 60 beats per minute (bpm); upper rate 130 bpm; dynamic paced AV delay 180/140 ms; dynamic sensed AV delay 135/95 ms; AV safety window 100 ms; atrial sensitivity 0.5 mV (bipolar); ventricular sensitivity 2.5 mV (bipolar); atrial and ventricular pulse amplitude and width 3.6 V and 0.40 ms, respectively (both unipolar). Pacemaker testing showed the following results: battery impedance 0.3 k ; sensed P wave 3 mV, sensed R wave 25 mV; atrial and ventricular pacing thresholds 0.6 and 0.4 V, respectively; atrial and ventricular lead impedances 442 and 560 , respectively (stable). Testing of the atrial pacing threshold in AAI mode at 70 bpm allowed the diagnosis to be made (Fig. 1, Panel B). What is the mechanism of the pacemaker “dysfunction”? How can it be solved?

Near Elimination of Ventricular Pacing in SafeR Mode Compared to DDD Modes: A Randomized Study of 422 Patients

SafeR performance versus DDD/automatic mode conversion (DDD/AMC) and DDD with a 250-ms atrioventricular (AV) delay (DDD/LD) modes was assessed toward ventricular pacing (Vp) reduction. After a 1-month run-in phase, recipients of dual-chamber pacemakers without persistent AV block and persistent atrial fibrillation (AF) were randomly assigned to SafeR, DDD/AMC, or DDD/LD in a 1:1:1 design. The main endpoint was the percentage of Vp (%Vp) at 2 months and 1 year after randomization, ascertained from device memories. Secondary endpoints include %Vp at 1 year according to pacing indication and 1-year AF incidence based on automatic mode switch device stored episodes. Among 422 randomized patients (73.2±10.6 years, 50% men, sinus node dysfunction 47.4%, paroxysmal AV block 30.3%, bradycardia-tachycardia syndrome 21.8%), 141 were assigned to SafeR versus 146 to DDD/AMC and 135 to DDD/LD modes. Mean %Vp at 2 months was 3.4±12.6% in SafeR versus 33.6±34.7% and 14.0±26.0% in DDD/AMC and DDD/LD modes, respectively (P<0.0001 for both). At 1 year, mean %Vp in SafeR was 4.5±15.3% versus 37.9±34.4% and 16.7±28.0% in DDD/AMC and DDD/LD modes, respectively (P<0.0001 for both). The proportion of patients in whom Vp was completely eliminated was significantly higher in SafeR (69%) versus DDD/AMC (15%) and DDD/LD (45%) modes (P<0.0001 for both), regardless of pacing indication. The absolute risk of developing permanent AF or of remaining in AF for >30% of the time was 5.4% lower in SafeR than in the DDD pacing group (ns). In this selected patient population, SafeR markedly suppressed unnecessary Vp compared with DDD modes.

Treating Cardiac Arrhythmias Detected With an Implantable Cardiac Monitor in Patients After an Acute Myocardial Infarction

Using an implantable cardiac monitor (ICM) in patients with acute myocardial infarction (MI) allows continuous electrocardiogram monitoring and provides a much more detailed picture of the incidence of brady- and tachyarrhythmias than conventional follow-up. The CARISMA study was the first to use the ICM in post-MI patients with moderate to severe left ventricular systolic dysfunction. Atrial fibrillation (AF) events lasting longer than 30s were associated with an almost threefold increase in the risk of major cardiac events. This confirms the current definition of clinically significant AF episodes, as patients with episodes of shorter duration were not at increased risk. The association of AF to progressive heart failure, reinfarction, and cardiovascular death underlines the need for an intensive follow-up of post-MI patients with new-onset AF in order to reveal underlying causes of AF such as progressive left ventricular dysfunction or myocardial ischemia. Asymptomatic, especially nightly, bradycardia episodes including high-degree 2°-3° atrioventricular (AV) block, sinus bradycardia, and sinus arrest were frequently documented by ICM in the CARISMA study. Ten percent of patients experienced high-degree 2°-3° AV block, of which the main part was nightly and asymptomatic, and 50% of all cardiovascular deaths occurred in this group, most from severe heart failure. Therefore, in post-MI patients with paroxysmal high-degree AV block, pacemaker implantation should be done, and in the case of left ventricular dysfunction (LVEF ≤ 35%), an implantable cardioverter defibrillator/cardiac resynchronization therapy defibrillator (ICD/CRT-D) may be indicated. Nonsustained ventricular tachycardia (VT) is very frequent in post-MI patients, and in the CARISMA study, high-risk patients with nonsustained VT were implanted with an ICD. Furthermore, in 10% of the patients, the ICM recorded nonsustained VT episodes of ≥ 16 beats per minute, resulting in a twofold increase in the risk for cardiac death. Thus, patients with nonsustained VT should undergo careful investigation, and we recommend a repeat echocardiography and electrophysiological stimulation in these patients. Patients with sustained VT or VF should receive an ICD.

Syncope triggered by a premature ventricular complex: A case of atrial fibrillation and paroxysmal atrioventricular block

An 85-year-old man with a history of hypertension presented to the hospital with 3 syncopal episodes. The admission electrocardiogram showed the presence of atrial fibrillation, a right bundle branch block (RBBB), and left anterior fascicular block (LAFB) (Figure 1A). The patient experienced 2 syncopal events in the hospital with ventricular asystole documented on telemetry monitoring (Figure 1B). Both events were initiated by a premature ventricular complex likely arising from the left posterior fascicle (*).

Cardiac tamponade and paroxysmal third-degree atrioventricular block revealing a primary cardiac non-Hodgkin large B-cell lymphoma of the right ventricle: a case report

IntroductionPrimary cardiac lymphoma is rare.Case PresentationWe report the case of a 64-year-old non-immunodeficient Caucasian man, with cardiac tamponade and paroxysmal third-degree atrioventricular block. Echocardiography revealed the presence of a large pericardial effusion with signs of tamponade and a right ventricular mass was suspected. Scanner investigations clarified the sites, extension and anatomic details of myocardial and pericardial infiltration. Surgical resection was performed due to the rapid impairment of his cardiac function. Analysis of the pericardial fluid and histology confirmed the diagnosis of non-Hodgkin large B-cell lymphoma. He was treated with chemotherapy.ConclusionThe prognosis remains poor for this type of tumor due to delays in diagnosis and the importance of the site of disease.

Dorsal spinal cord injury as a cause of recurrent asystole requiring permanent cardiac pacing

Numerous unusual causes of atrioventricular block (AVB) with cardiac pacemaker implantation have been documented including cough, deglutition, or other vagally mediated mechanism. In spinal cord lesions, only high cervical spinal cord lesion has been reported as a cause of severe bradycardia. We report a case with not cervical but dorsal vertebral trauma and persistent paroxysmal AVB requiring cardiac pacemaker implantation.

Is There Any Room for Adenosine Test in Syncope of Unknown Origin

SUMMARY Some patients with unexplained syncope develop different degrees of paroxysmal AV block with bolus infusion of 18-mg of adenosine. This finding had a low positive predictive value in recent trials, although its use was not standardized. Objective To present the experience in our institution in follow up of patients with a first episode of unexplained malignant syncope of uncertain etiology (SUE), to whom were systematically carried out an adenosine test. Material and Methods There were included, in a prospective and consecutive way, patients who presented unexplained syncope with severe trauma, none of them had a previous history of syncope, without suspected vasovagal etiology, without organic cardiopathy, with normal neurological and cardiological studies (including sensitized tilt test), to those who underwent an adenosine test. The test was carried out at the end of the electrophysiological study. It was infused in bolus of 18-mg of adenosine through the femoral vein under continuous ECG monitoring; positive test was defined by the development of complete AV block with pauses longer than 6 seconds. Background

Syncope Due to Idiopathic Paroxysmal Atrioventricular Block: Long-Term Follow-Up of a Distinct Form of Atrioventricular Block

We present data on patients with syncope due to paroxysmal atrioventricular (AV) block unexplainable in terms of currently known mechanisms. Paroxysmal AV block is known to be due to intrinsic AV conduction disease or to heightened vagal tone. We evaluated 18 patients presenting with unexplained syncope who had: 1) normal baseline standard electrocardiogram (ECG); 2) absence of structural heart disease; and 3) documentation, by means of prolonged ECG monitoring at the time of syncopal relapse, of paroxysmal third-degree AV block with abrupt onset and absence of other rhythm disturbances before or during the block. The study group consisted of 9 men and 9 women, mean age 55 ± 19 years, who had recurrent unexplained syncope for 8 ± 7 years and were subsequently followed up for as long as 14 years (4 ± 4 years on average). The patients had no structural heart disease, standard ECG was normal, and electrophysiological study was negative. In all patients, prolonged ECG monitoring documented paroxysmal complete AV block with 1 or multiple consecutive pauses (mean longest pause: 9 ± 7 s at the time of syncope); AV block occurred without P-P cycle lengthening or PR interval prolongation. During the observation time, no patient had permanent AV block; on permanent cardiac pacing, no patient had further syncopal recurrences. Common clinical and electrophysiological features define a distinct form of syncope due to idiopathic paroxysmal AV block characterized by a long history of recurrent syncope, absence of progression to persistent forms of AV block, and efficacy of cardiac pacing therapy.

Síncope y bloqueo de rama. Rendimiento del uso escalonado del estudio electrofisiológico y de la monitorización electrocardiográfica prolongada

Introduction and objectives The objective of this study was to determine the diagnostic yield of a stepped protocol involving an electrophysiologic study (EPS) and implantable loop recorders (ILR) in patients with syncope and bundle branch block (BBB). Methods Eighty-five consecutive patients referred for syncope and BBB after initial non-diagnostic assessment underwent EPS including a pharmacological challenge with procainamide. Those patients without indication for defibrillator implantation received ILRs. Follow-up continued until diagnosis or end of battery life. Results The EPS was diagnostic in 36 patients (42%). The most frequent diagnoses were paroxysmal atrioventricular block (AVB) (n = 27), followed by ventricular tachycardia (VT) (n = 6). All patients with VT had structural heart disease; left BBB was more prevalent in this group. Thirty-eight patients received ILRs and diagnosis was achieved in 13 (34%) of them; paroxysmal AVB (n = 10) was the most frequent diagnosis. Median follow-up to diagnosis of paroxysmal AVB was 97 days (interquartile range 60-117 days). Paroxysmal AVB was more frequent in patients with right BBB and prolonged PR interval and/or axis deviation. We found no occurrence of VT or arrhythmic death during follow-up. Conclusions The most common etiology of syncope in patients with BBB was paroxysmal AVB, followed by VT. The stepped use of EPS and ILR in negative patients enables us to safely achieve a high diagnostic yield, given that VT is usually diagnosed during EPS. Full English text available from: www.revespcardiol.org

Syncope and Bundle Branch Block. Diagnostic Yield of a Stepped Use of Electrophysiology Study and Implantable Loop Recorders

Introduction and objectives The objective of this study was to determine the diagnostic yield of a stepped protocol involving an electrophysiologic study (EPS) and implantable loop recorders (ILR) in patients with syncope and bundle branch block (BBB). Methods Eighty-five consecutive patients referred for syncope and BBB after initial non-diagnostic assessment underwent EPS including a pharmacological challenge with procainamide. Those patients without indication for defibrillator implantation received ILRs. Follow-up continued until diagnosis or end of battery life. Results The EPS was diagnostic in 36 patients (42%). The most frequent diagnoses were paroxysmal atrioventricular block (AVB) (n = 27), followed by ventricular tachycardia (VT) (n = 6). All patients with VT had structural heart disease; left BBB was more prevalent in this group. Thirty-eight patients received ILRs and diagnosis was achieved in 13 (34%) of them; paroxysmal AVB (n = 10) was the most frequent diagnosis. Median follow-up to diagnosis of paroxysmal AVB was 97 days (interquartile range 60-117 days). Paroxysmal AVB was more frequent in patients with right BBB and prolonged PR interval and/or axis deviation. We found no occurrence of VT or arrhythmic death during follow-up. Conclusions The most common etiology of syncope in patients with BBB was paroxysmal AVB, followed by VT. The stepped use of EPS and ILR in negative patients enables us to safely achieve a high diagnostic yield, given that VT is usually diagnosed during EPS.

Blocking out the real diagnosis

In March, 2010, a 65-year-old woman presented to our clinic with refractory epileptic seizures that had started 4 years earlier. Carbamazepine made these episodes worse, and she was put on levetiracetam 2·0 g per day. In the week before presentation, seizures recurred daily. She also had a history of hypertension treated with ramipril 5 mg per day. The seizures lasted up to 30 s, and they began with a feeling of fear and epigastric discomfort that was often followed by impairment of consciousness, a facial expression of fear, lip automatisms, and left upward eye-deviation, but without pallor. Subsequently, she felt mentally confused for a few minutes. No precipitating factor was identifi ed, and she also experienced events during sleep that woke her. During her seizures she never fell or had diaphoresis, visual changes, or incontinence. Neurological examination, electroencephalogram (EEG), 12-lead electrocardiogram (ECG), echo cardiogram, brain MRI, and blood tests were normal. Although the key clinical features pointed to epilepsy, in our opinion two factors argued against this diagnosis. The fi rst was the drug-resistance, because prognosis of new-onset seizures in elderly patients is good, especially if seizures are not symptomatic. The second factor was the normal EEG, because the yield of epileptiform EEGs is high if the recording is made during a period of increased seizure frequency. Video-EEG/ECG monitoring was used to capture one of our patient’s seizures while she was awake and sitting in bed with her eyes open. ECG recording revealed an abrupt asystole that spontaneously resolved after 16 s with reappearance of normal sinus rhythm. The EEG showed the characteristic “slow-fl at-slow” pattern of syncope, which started 7 s after the asystole onset and lasted 17 s. The aura of fear coincided with the EEG slowing, and loss of consciousness with the fl at EEG. During a 12-lead ECG recording, another spontaneous paroxysmal asystole was stopped by temporary trans-cutaneous pacing stimulation, which also prevented the electroclinical features. During continuous cardiac monitoring, occasional episodes of sudden change from normal 1:1 atrio-ventricular conduction to complete heart block were recorded and treated by temporary pacing in the right ventricle until normal sinus rhythm was restored (fi gure). Further investigations identifi ed no cardiac disease. A diagnosis of paroxysmal atrioventricular block (PAVB) was made, and a dual-chamber pacemaker device was implanted. At her last outpatient visit, in December, 2010, she had remained seizure-free. PAVB is a poorly-recognised condition that consists of the abrupt occurrence of repetitive block of the atrial impulse, with a relatively long (>2 s) ventricular asystole, leading to potential sudden cardiac death. Patients reported with PAVB usually have unambiguous syncopes, but unlike our patient, most of them have concomitant cardiac disease or defi nite triggering factors. In our patient, the key clinical features, the spontaneous occurrence of episodes even at night, and the lack of evidence for atrioventricular conduction disease between episodes, were less likely to raise suspicion of cardiac syncope and thus more prone to misdiagnosis. Detailed history-taking and careful examination led us to the appropriate diagnosis of PAVB. In exceptional cases, asystole can be the consequence of focal epileptic seizures and a likely cause of sudden unexplained death in epilepsy. However, unlike PAVB, epileptic asystole always occurs several seconds after the EEG seizure activity. Our patient reinforces the diffi culty that exists in diagnosing seizure and syncope, and emphasises the need to consider cardiac causes in patients with drugresistant epilepsy.

A case with paroxysmal AV block and cardiac arrest during about 3 minutes

A case with paroxysmal AV block and cardiac arrest during about 3 minutes

Paroxysmal atrioventricular block: Are phase 3 and phase 4 block mechanisms or misnomers?

Paroxysmal atrioventricular block (PAVB), defined as the sudden and unexpected repetitive block of the atrial impulse on its way to the ventricles, is an important etiology of syncope primarily caused by the delayed emergence of an adequate escape rhythm.1 The majority of cases of PAVB develop in conjunction with increased rate of the atrial input to the atrioventricular (AV) conduction system, that is, TD-PAVB.2,3 On the other hand, there are published examples in which PAVB was initiated by a supraventricular pause.1,4–6 These cases have been labeled as either “bradycardia- dependent PAVB” or “phase 4 PAVB.” However, as demonstrated below, they are more accurately described as “pause-dependent PAVB” (PD-PAVB). In an unpublished series of 42 cases seen by one of us (NE-S), tachycardia-dependent PAVB (TD-PAVB) occurred in 37 patients (88%), while PD-PAVB occurred in the remaining five patients (12%). In many of these patients, the presenting symptoms were presyncope or syncope, depending on the duration of ventricular asystole. Yet in a few patients the early emergence of a stable escape rhythm prevented the development of significant symptoms. Although PAVB is a serious arrhythmia, its association with sudden cardiac death in some cases is difficult to ascertain. In a study of 22 patients with syncope, an implantable loop recorder revealed episodes of PAVB in association with syncope in 17 patients.7 None of these patients suffered injury attributable to syncopal relapse, and a majority of patients eventually received a permanent pacemaker. However, in some patients, syncope associated with PAVB can result in serious injury.

Paroxysmal atrioventricular block

Paroxysmal atrioventricular block (AVB) is a poorly defined clinical entity characterized by abrupt and unexpected change from 1:1 atrioventricular conduction to complete heart block, leading to syncope and potential sudden cardiac death. Although a dangerous condition because of unreliable escape mechanism, proper diagnosis of paroxysmal AVB is often missed and overlooked because of its unfamiliarity, unpredictability, and in some cases, no clear evidence of atrioventricular conduction disease during normal 1:1 conduction.

Late Onset Paroxysmal AV Block after Transplantation

We report the case of a 19-year-old female who developed recurrent dizziness and syncope 2 years after cardiac transplant. During a pre-syncopal episode, a loop monitor revealed paroxysmal atrio-ventricular block (PAVB). The placement of a permanent transvenous pacemaker led to the resolution of her symptoms. In this report, we discuss the causes of PAVB, review the literature on PAVB in heart transplant patients, examine the electrophysiology of PAVB, and consider additional causes of PAVB in pediatric transplant patients.

Paroxysmal Mobitz type-I atrioventricular block Luciani–Wenckebach conduction, acute myocardial infarction and severe three vessels coronary artery disease

Paroxysmal atrioventricular block has been reported in patients without acute coronary syndrome and without significant coronary artery stenosis, in patients with acute coronary syndrome and without significant coronary artery stenosis, in patients without acute coronary syndrome and with significant coronary artery stenosis and in patients with acute coronary syndrome and significant coronary artery stenosis. Conflicting roles for alternating periods of second degree atrioventricular block (also known as Mobitz I or Luciani–Wenckebach periodicity) have been reported. Both hypotheses have been reported, that paroxysmal Wenckebach periods are compatible with a benign prognosis and that paroxysmal Wenckebach periods are associated with hemodynamic deterioration. We present a case of paroxysmal Mobitz Type-I atrioventricular block Luciani–Wenckebach conduction in a 75-year-old Italian man with acute myocardial infarction and severe three vessels coronary artery disease.