Marked First-degree Atrioventricular Block Research Articles

Marked first-degree AV block may lead to complete AV block development

Abstract Funding Acknowledgements Type of funding sources: None. Background First-degree atrioventricular (AV) block (PR interval >200 ms) is considered a benign condition with rare progression to a higher degree AV block. The site of block is determined with electrophysiological (EP) study and measurement of His-ventricular (HV) interval, with normal values below 55 ms. Prolonged HV interval > 70 ms is predictive of higher-grade AV block development. Marked first-degree AV block with a PR > 300 ms may lead to symptoms such as fatigue, poor exercise tolerance and palpitations. When symptoms are correlated to the conduction delay, permanent pacemaker (PPM) implantation to restore AV synchrony should be considered. In the Framingham heart study, patients with first-degree AV block had a threefold higher risk of PPM implantation. However, there is no data on the HV intervals and the rate of progression of conduction disorder in patients with marked first-degree AV block. Purpose To assess the predictive value of HV interval measurement in patients with marked first-degree AV block for progression to a higher-degree conduction disorder. Methods We prospectively evaluated consecutive patients with symptomatic marked first-degree AV block that underwent a PPM implantation. His electrograms were recorded during the implantation, and HV intervals were measured from the first deflection of the His signal to the earliest onset of ventricular activation on a 12-lead surface ECG. Patients were followed for 6 months with three out-patient visits, during which the PPM was temporarily inhibited to check for intrinsic AV conduction. Results Seventeen patients were evaluated between January 2020 and September 2022. Ten patients (59%) were male, and 7 (41%) were female, with an average age of 61 ± 19 years. All patients had markedly prolonged PR interval (383 ± 47 ms) and narrow QRS complex (100 ± 16 ms). Three patients (17%) had intermittent type 1 second-degree AV block, right bundle branch block was recorded in two (12%) and left anterior fascicular block in four (24%) patients. Except for one patient with a corrected atrial septal defect, there were no echocardiographic signs of structural heart disease with a left ventricular ejection fraction of 61 ± 5%. The HV intervals were on the upper limit of normal values at 54 ± 6ms and no patient had an HV interval above 70 ms. Two patients (12%) developed complete AV block during follow-up: one female, and one male, 28 and 83 years old, respectively, with a PR interval 392 and 363 ms, QRS 104 and 94 ms, and HV 57 and 48 ms. None of the two had any additional conduction blocks at the time of PPM implant. Conclusion In our cohort of patients with symptomatic first-degree AV block (PR>300 ms), two patients (12%) developed complete AV block despite normal HV intervals at the time of implant. Closer monitoring, beyond only EP measurements, of patients with markedly prolonged PR intervals is warranted for the potential progression of conduction disorder.

The effect of hyperkalaemia on cardiac rhythm devices

In patients with pacemakers, hyperkalaemia causes three important abnormalities that usually become manifest when the K level exceeds 7 mEq/L: (i) widening of the paced QRS complex from delayed intraventricular conduction velocity, (ii) Increased atrial and ventricular pacing thresholds that may cause failure to capture. In this respect, the atria are more susceptible to loss of capture than the ventricles, and (iii) Increased latency (usually with ventricular pacing) manifested by a greater delay of the interval from the pacemaker stimulus to the onset of depolarization. First-degree ventricular pacemaker exit block may progress to second-degree Wenckebach (type I) exit block characterized by gradual prolongation of the interval from the pacemaker stimulus to the onset of the paced QRS complex ultimately resulting in an ineffectual stimulus. The disturbance may then progress to 2 : 1, 3 : 1 pacemaker exit block, etc., and eventually to complete exit block with total lack of capture. Ventricular undersensing is uncommonly observed because of frequent antibradycardia pacing. During managed ventricular pacing, hyperkalaemia-induced marked first-degree atrioventricular block may induce a pacemaker syndrome. With implantable cardioverter-defibrillators (ICDs) oversensing of the paced or spontaneous T-wave may occur. The latter may cause inappropriate shocks. A raised impedance from the right ventricular coil to the superior vena cava coil may become an important sign of hyperkalaemia in the asymptomatic or the minimally symptomatic ICD patient.

First successful curative use of digoxin-specific Fab antibody fragments in a life-threatening coconut crab (Birgus latro L.) poisoning

We wish to report the first curative use of digoxin-specific Fab antibody fragments in a coconut crab Birgus latro L. poisoning in New Caledonia. The female patient, aged sixty-three with a previous history of cardiovascular and metabolic dysfunctions, showed marked first-degree atrio-ventricular block and several atrial pauses, and was given 760 mg of digoxin-specific Fab antibody fragments. Shortly after the perfusion her electrocardiogram returned to close to normal with only slight first-degree atrio-ventricular block and no more atrial pauses. Neriifolin LC-MS/MS tests performed on the patient's serum and urine samples confirmed cardenolide poisoning. Another, younger patient, with high neriifolin levels in her serum and urine samples only experienced gastro-intestinal symptoms and was discharged without specific treatment. The consumption of coconut crab in New Caledonia should be avoided even though the first of the two cases reported suggests that digoxin-specific Fab antibody fragments can be effective in the treatment of life-threatening poisoning caused by the ingestion of this crustacean.

Lyme carditis: a reversible cause of complete atrioventricular block

A 54-year-old American woman presented with an episode of syncope. This had occurred against a background of several days of dizziness and palpitations. Her medical history included Bell's palsy, which had been diagnosed three weeks earlier. On examination, she had a resting bradycardia of 31 beats per minute and her electrocardiogram demonstrated third-degree atrioventricular (AV) block. She was referred to cardiology for consideration of permanent pacemaker implantation. Given her facial nerve palsy and AV block, a diagnosis of Lyme borreliosis was suspected. Within 48 hours of initiation of ceftriaxone, she reverted to sinus rhythm, albeit with a marked first-degree AV block. Subsequent serology confirmed the diagnosis. Reversible causes of complete AV block should always be considered and appropriate therapy may avoid the need for permanent pacemaker insertion.

Pseudopacemaker syndrome and marked first-degree atrioventricular block: Case report

Pacemaker syndrome consists of the symptoms and signs present in the single chamber (VVI) pacemaker patient with electrode placed in the right ventricular apex. It is caused by inadequate timing of atrial and ventricular contractions. Pacemaker syndrome without a pacemaker (or pseudopacemaker syndrome) refers to occurrence of symptoms in the presence of marked first-degree atrioventricular (AV) block, when P wave is too close to the preceding QRS complex producing the same haemodynamic disturbance as artificial pacemaker cardiac stimulation with retrograde VA conduction. We present the patient with acute inferior myocardial infarction due to late bare metal stent thrombosis, treated with primary pectutaneous coronary intervention. Hospital course was complicated by complete heart block which was treated with temporary pacing. During the stand-by mode of temporary pacing, sinus rythm with marked first-degree AV block (PQ interval 480 ms) was observed while the patients re-experienced the symptoms that were present prior to pacemaker implantation. Temporary pacing was continued for the next 24 hours when spontaneous shorteninig of PQ interval (250-270 ms) was noticed; since the patient was asymptomatic during the stand-by mode, the pacemaker electrodes were removed and the patient discharged 11 days after admission. Conduction disturbances, such as the varying degrees of AV blocks, are relatively common in acute inferior myocardial infarction. The first degree AV blok is usually asymptomatic and does not require treatment, unless when it is associated with pseudopacemaker syndrome. In that case, temporary pacing provides haemodynamic stability until conduction system recovers.

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.

Persistent left superior vena cava: incidence, significance and clinical correlates

Persistent left superior vena cava (PLSVC) is a remainder of the physical examination was unremarkcommon anomaly of the systemic venous system [1]. able. Multiple ECGs revealed sinus rhythm, with a It results from persistent patency of the left anterior marked first-degree atrioventricular block and left cardinal vein that drains into a dilated coronary sinus. bundle branch block with a heart rate ranging from Its incidence is reported between 0.3 and 0.5% in the 38 to 78 beats per min. Blood chemistries were general population [2]. Approximately 50–70% of within normal limits. She underwent TEE to rule out these patients are at risk of paradoxical embolism an intracardiac source of embolism and atrial septal because of accompanying lesions (atrial septal defect, defect and to define her cardiac anatomy. This unroofed coronary sinus, or direct communication of showed no evidence of cardiac masses, but did the vein to the left atrium). demonstrate a PLSVC draining into the right atrium This case report illustrates the diagnostic role of via a dilated coronary sinus (Fig. 1). Saline contrast echocardiography in the evaluation and diagnosis of injection was negative for intracardiac shunt. There this relatively rare congenital anomaly. was bi-atrial and bi-ventricular enlargement. The A 60-year-old white woman with a recent history estimated left ventricular ejection fraction was 0.45. of dizziness was referred for evaluation. She had a No segmental wall motion abnormalities were noted. history of paroxysmal atrial fibrillation, left ventricuDuring early embryological development, venous lar dysfunction, and a history of a congenital heart return from the head and arms normally drains to the disease with an atrial septal defect repair. Her vital right atrium via the left and right anterior cardinal signs were stable. Cardiac examination revealed a veins. At approximately 8 weeks gestation, the left grade 2/6 holosystolic murmur at the apex radiating brachiocephalic vein develops as a bridge between to the left axilla. There were no gallops or rubs. The the left and right anterior cardinal veins. The portion splitting of the second heart sound was normal. The of the left anterior cardinal vein caudal to the bridging left brachiocephalic vein normally collapses, then degenerates leaving only the right anterior *Corresponding author. Present address: Division of Cardiology, cardinal vein which becomes the superior vena cava. Marshfield Clinic, 1000 Oak Street, WI 54449, USA. Tel.: 11-715-387If the caudal portion of the left anterior cardinal vein 5301; fax: 11-715-389-4555. E-mail address: takt@mfldclin.edu (T. Tak). remains patent, it becomes a PLSVC which drains

Pseudo‐Pacemaker Syndrome Following Inadvertent Fast Pathway Ablation for Atrioventricular Nodal Reentrant Tachycardia

Atrioventricular nodal reentrant tachycardia that is refractory to drug treatment has recently been treated with radiofrequency catheter ablation. In this case report we describe a patient with atrioventricular nodal reentrant tachycardia in whom radiofrequency ablation of slow pathway was attempted, with inadvertent damage to the fast pathway. The patient developed marked first-degree atrioventricular block associated with symptoms mimicking pacemaker syndrome.