Atrioventricular Dissociation Research Articles

Bundle branch reentrant ventricular tachycardia in a patient with Fabry disease

BackgroundBundle branch reentrant ventricular tachycardia is a unique type of VT that employs both bundles and the ventricular septum as integral components of a re-entrant circuit. It is usually observed in dilated cardiomyopathy, and its circuit depends exclusively on the specialized conduction system.Case presentationA 67-year-old man with a history of Fabry disease, and atrial fibrillation ablation, was admitted for a wide QRS tachycardia at 150 bpm, with an LBBB. Pharmacological therapy failed to stop the arrhythmia. Intracardiac recordings confirm the diagnosis. His Bundle recordings are essential, and Atrioventricular (AV) dissociation is typically present. The method used to induce left BBRVT is right ventricle apex stimulation. An electrophysiological study showed an AV dissociation a long HV sequence and a similar QRS morphology between VT and sinus rhythm. An overdrive stopped it. The same arrhythmia reappears and is restored to sinus rhythm by electrical cardioversion. We decided to implant an Implantable Cardiac defibrillator (ICD) with a backup pacing for secondary prevention and to ablate the right bundle branch.ConclusionBBRVT is a rare entity that is underreported. Pharmacological therapy is usually inefficient. An ICD is recommended for secondary prevention and can provide backup pacing, frequently required after catheter ablation to prevent the development of AV block or an excessive prolonged HV interval. Catheter ablation of the bundle branch is the first-line therapy.

Intentional intoxication with monkshood plant leading to atrioventricular dissociation and ventricular ectopy in a 17-year-old female: a case report

BackgroundMonkshood, a toxic plant containing a potent cardio- and neurotoxin called aconitine, can lead to a range of symptoms, including nausea, vomiting, dizziness, seizures, and cardiac arrhythmias. Mortality associated with this intoxication are due to ventricular tachyarrhythmias which are difficult to treat and often refractory in nature.Case presentationWe present a case of a 17-year-old female patient who presented to the emergency department after intentionally ingesting a monkshood plant and developed atrioventricular dissociation and frequent ventricular ectopy. The patient was successfully treated with activated charcoal, supportive care, and cardiac monitoring.ConclusionThis case highlights the importance of early recognition of aconitine poisoning and the need for prompt supportive care, cardiac rhythm monitoring, and preemptive antiarrhythmic treatment planning.

Unusual Manifestation of Atrioventricular Dissociation in A 63 Year-Old Man and Clinical Insights

Unusual Manifestation of Atrioventricular Dissociation in A 63 Year-Old Man and Clinical Insights

Left ventricular remodeling in premature ventricular contraction-induced cardiomyopathy: Effect of coupling intervals and atrioventricular dissociation.

Left ventricular dyssynchrony (LVD) and postextrasystolic potentiation (PESP) associated with premature ventricular contractions (PVCs) may play a role in the development of premature ventricular contraction-induced cardiomyopathy (PVC-CM). Long-coupled (LC) PVCs have a greater LVD than short-coupled (SC) PVCs, whereas SC-PVCs have a stronger PESP than LC-PVCs. The purpose of this study was to compare SC-PVCs and LC-PVCs to evaluate the roles of LVD, PESP, and atrioventricular dissociation (AVD) in the development of PVC-CM. Thirty-six canines underwent pacemaker implantation to induce bigeminal right ventricular apical epicardial PVCs (50% burden) for 12 weeks. Telemetry assessed PVC burden and AVD. Animals were grouped as SC-PVC (coupling interval [CI] 200-220ms), LC-PVC (CI 330 ms), or sham (control). Echocardiographic changes, AVD, and hemodynamics were monitored for 12 weeks. PVC burden was similar between SC-PVC and LC-PVC groups but was statistically higher in the SC-PVC group (50% vs 47.5%; P = .028). After 12 weeks, left ventricular ejection fraction (LVEF) significantly decreased in both SC-PVC and LC-PVC groups (47.1% ± 1.4% and 45.5% ± 2%, respectively) compared to sham group (61% ± 1.6%; P <.001). Overall AVD was similar between SC-PVC and LC-PVC groups, and there was no significant correlation between AVD and reduction in LVEF at 12 weeks (r = 0.09, P = .5; and r = 0.06, P = .8, respectively). Additionally, both SC-PVC and LC-PVC groups experienced substantial declines in max and min dP/dt after 12 weeks compared to baseline. Neither PVC CI nor AVD played an independent role in the development or severity of PVC-CM. LVD and PESP make equal relative contributions to the development of PVC-CM.

P190 TWIDDLER’S SYNDROME IN A 96–YEAR–OLD PATIENT TREATED BY REPOSITIONING THE VENTRICULAR LEAD

Abstract A 96–years–old woman was admitted to our cardiological intensive care unit in December 2022 with atrioventricular dissociation, with a junctional ventricular escape rhythm at a rate of 38 beats per minute, and an atrial rhythm dissociated from the ventricular rhythm, at a rate of 80 beats per minute (Figure 1). The patient had a history of third–degree atrioventricular block, effectively treated with single–chamber pacemaker implantation (Assurity MRI SR, Abbott), operation performed approximately 10 months before access, in February 2022. The patient underwent a chest X–ray, which showed "coiling" of the ventricular catheter in the pacemaker pocket area (left subclavicular), with macroscopic dislocation of the ventricular electrode, which had its distal tip in the right atrium (Figure 2). Therefore, the clinical case was typical of Twiddler‘s syndrome. The patient would therefore have undergone revision surgery. An attempt was made to reposition the original lead, with passive fixation (Isoflex 1948/58, Abbott), by inserting a "straight" stylet, a procedure which was done effectively. The ventricular lead was repositioned in the right ventricular apex. The detected parameters were optimal (sensing 7 mV, ventricular barrier threshold 0.5 mV/0.4 ms, impedance 797 Ohm). The result was considered acceptable. The remainder of the hospital stay was without complications. The patient was discharged on the fifth day in good general condition. Twiddler syndrome is defined as a dislocation of one or more catheters, resulting in the catheters "coiling" in the pocket of the device. It is usually related to the manipulation of the generator by the patient itself. It usually occurs within a year of implantation and is usually more common in females, the elderly, the obese, pediatric patients, or patients with psychiatric disorders. The identification of patients at risk for this pathology, the adequate education of the patient and family regarding the management of the device, the use of catheters with active fixation, as well as the fixation of the generator device to the pectoral muscle, through non–absorbable sutures. In the case described, the patient denied manipulation of the device, which however could not be excluded, given the age of the patient.

Wide complex rhythm in a well neonate: Where are the P waves?

A neonate was seen for an evolving broad QRS complex rhythm initially captured at birth as intermittent escape beats on electrocardiogram. Continuous monitoring recorded features mimicking pre-excitation, but closer analysis revealed a regular broad QRS complex rhythm with isorhythmic atrioventricular dissociation, favouring a ventricular source. Treatment with flecainide and propranolol achieved successful control of the incessant arrhythmia with improvement in cardiac function on echocardiogram.

PO-04-048 LYME CARDITIS PRESENTING AS ACCELERATED JUNCTIONAL RHYTHM IN ADULT PATIENT

Lyme carditis occurs in 1.5%-10% untreated patients infected with Borrelia burgdorferi in United States and usually manifests as varying degrees of atrioventricular (AV) block, myopericarditis, and degenerative valve disease. Several cases of junctional tachycardia have been reported in children with Lyme disease, but there have not been any cases reported in the adult population. Here, we report a case of accelerated junctional tachycardia in a 42-year-old woman with Lyme carditis. To describe a case of a Lyme carditis presenting as accelerated junctional rhythm in a 42-year-old patient. N/A A 42-year-old woman with no significant past medical history presented with complaints of palpitations and lightheadedness. She had a tick bite on her left anterior upper thigh one month prior while working in her yard. The tick was removed after about 3 hours. At that time the patient had no fevers, arthralgias or rashes; however, a month later she developed symptoms of palpitations and lightheadedness. A 12-lead ECG showed accelerated junctional rhythm with AV and VA dissociation and was otherwise normal (Fig 1A). Her primary care physician conducted Lyme serology, which came back positive for both IgG and IgM. A diagnosis of Lyme carditis was made, and the patient was admitted to the hospital for IV antibiotics. Repeat ECG showed sinus with PR prolongation to 252 ms along with episodes of accelerated junctional rhythm (Figure 1B and 1C). She was started on intravenous ceftriaxone with continuous cardiac monitoring. Echocardiogram showed no abnormalities. A peripherally- inserted central catheter line was placed for a 4-week course of ceftriaxone. Her PR interval normalized within 2 weeks of treatment with no junctional rhythm or heart block on serial ECGs and Holter monitors (Figure 1D). Follow-up over the next year showed no recurrence of symptoms or arrhythmias and no other cardiac sequelae. To the best of our knowledge, accelerated junctional rhythm has not been previously reported in the setting of Lyme disease in adult patients. Herein, we report a case of a Lyme carditis presenting as symptomatic accelerated junctional rhythm in a 42-year-old patient, likely caused by inflammation of AV nodal tissue.

Right Ventricular Outflow Tract Stenting is a Safe and Effective Bridge to Definitive Repair in Symptomatic Infants With Tetralogy of Fallot1.

Right ventricular outflow tract (RVOT) stent angioplasty is a palliative procedure for neonates and infants with symptomatic tetralogy of Fallot prior to surgical repair. We review our institutional outcomes of RVOT stenting. Retrospective review of all infants with tetralogy of Fallot under 3 months of age who underwent primary native RVOT stent angioplasty at The Children's Hospital at Westmead, Sydney, Australia between January 2010 and December 2020. Demographics and echocardiographic pulmonary artery dimensions were collected pre-stent angioplasty and prior to surgical repair. Twenty (20) infants underwent primary RVOT stenting. Median age at stent was 14 days (interquartile range [IQR] 7-32) and median weight 2.7 kg (IQR 2.1-3.4). Three patients underwent hybrid per-ventricular procedures. Indication for RVOT stenting was recurrent hyper-cyanotic spells in 12 (60%) and duct-dependent pulmonary blood flow in 8 (40%). Saturations increased from a median of 80% (IQR 75-85) to 91% (IQR 90-95) post procedure (P<0.001). A single major complication occurred: transient complete atrioventricular dissociation requiring isoprenaline infusion for <24 hours. Twelve (12, 60%) required catheter re-intervention prior to definitive repair for further augmentation of pulmonary blood flow. There were two non-cardiac deaths distant from the stent procedure, but prior to surgical repair. Median right and left pulmonary artery Z-scores increased respectively from -2.06 (IQR -2.99 to -0.17) and -1.2 (IQR -2.59 to -0.14) prior to RVOT stent, to -0.74 (IQR [-1.21 to 0.26], P=0.01) and 0.06 (IQR [-1.87 to 1.15], P=0.006) by the time of definitive repair. Eighteen (18) patients achieved definitive repair at a median age of 6.1 months (IQR 4.7-7.3). Palliation with more than one RVOT stent was associated with an increased duration of cardiac bypass (P=0.035) and cross-clamp (P=0.044) time at definitive repair. In symptomatic neonates and infants with tetralogy of Fallot at high-risk of peri-operative complications, RVOT stent angioplasty can safely and effectively augment pulmonary blood flow prior to definitive repair.

Standing genetic variation affects phenotypic heterogeneity in an SCN5A-mutation founder population with excess sudden cardiac death

The Worm Study, ascertained from a multigeneration pedigree segregating a single amino acid deletion in SCN5A (c.4850_4852delTCT, p.(Phe1617del), rs749697698), is characterized by substantial phenotypic heterogeneity and overlap of sudden cardiac death, long-QT syndrome, cardiac conduction disease, Brugada syndrome, and isorhythmic atrioventricular dissociation. Linkage analysis for a synthetic trait derived from these phenotypes identified a single peak (logarithm of the odds [LOD] = 4.52) at the SCN5A/SCN10A/SCN11A locus on chromosome3. This study explored the role of additional genetic variation in the chromosome 3 locus as a source of phenotypic heterogeneity in the Worm Study population. Genotypes underlying the linkage peak (n = 70) were characterized using microarrays. Haplotypes were determined using family-aware phasing and a population-specific reference panel. Variants with minor allele frequencies >0.10 were tested for association with cardiac conduction disease and isorhythmic dissociation using LAMP and logistic regression. Only 1 haplotype carried the p.Phe1617del/rs749697698 deletion, suggesting relatively recent development (∼18 generations); this haplotype contained 5 other missense variants spanning SCN5A/SCN10A/SCN11A. Noncarrier haplotypes (n = 74) ranged in frequency from 0.5% to 5%. Although no variants were associated with cardiac conduction disease, a homozygous missense variant in SCN10A was associated with isorhythmic dissociation after correction for multiple comparisons (odds ratio 11.23; 95% confidence interval 2.76-23.39; P = 1.2 × 10-4). This variant (rs12632942) was previously associated with PR interval. Our data suggest that other variants, alongside a pathogenic mutation, are associated with phenotypic heterogeneity. Single-mutation screening may be insufficient to predict electrical heart disease in patients and family members. In the Worm Study population, segregating a pathogenic SCN5A mutation, compound variation in the SCN5A/SCN10A/SCN11A locus determines arrhythmic outcome.

Rupture of the Left Ventricle in the Atrioventricular Groove After Mitral Valve Replacement: A Case Report

As we grow older, and our population continues to live longer due to advancements in modern medical therapies, we have a growing population of elderly patients. There will inevitably be more patients who present with mitral stenosis secondary to severe mitral annular calcification and a corresponding need for repair due to the nature of increased friable myocardium present within these tissues. Atrioventricular dissociation associated with left ventricular rupture after mitral valve replacement occurs in approximately 1.2% of cases, and of those cases there is up to a 75% mortality rate even when appropriate surgical techniques are performed [1].

Electrocardiographic changes associated with hyperkalaemia in domestic cats

Hyperkalaemia is a life-threatening electrolyte imbalance because it affects cardiac conduction and can lead to fatal arrhythmias if left untreated. The present study describes the occurrence of hyperkalaemia in cats and the electrocardiographic changes associated with this electrolyte imbalance. Hyperkalaemia was identified in 83.33 per cent of the study group subjects. Acute kidney injury and obstructive uropathy were the main clinical conditions associated with it. Electrocardiographic findings in hyperkalaemia in different cats under study included peaked T waves in lead II and the precordial lead CV6LL, atrial standstill and sino-ventricular rhythm, normal sinus rhythm, ventricular tachycardia, first-degree atrio-ventricular block, bradycardia, sinus tachycardia, and atrio-ventricular dissociation. Electrocardiography should always be performed in cases suspected of electrolyte imbalances, particularly hyperkalaemia, so as to identify any fatal arrhythmias and initiate treatment at the earliest.

643 THE HEART WAS MADE TO BE BROKEN: RECURRENT TAKOTSUBO SYNDROME IN AMYOTROPHIC LATERAL SCLEROSIS

Abstract Takotsubo syndrome (TTS) is a rare cardiac disease, characterized by transient regional wall motion abnormalities without evidence of obstructive coronary artery stenoses, mainly triggered by emotion or physical stressors. Reverse Takotsubo syndrome (rTTS), an atypical variant with basal segments involvement, is frequently associated with neurological disorders, including patients with amyotrophic lateral sclerosis (ALS). We reported the case of a 54 years old woman who experienced two consecutive episodes of TTS with different wall motion patterns, complicated by a recurrent episode and arrhythmic events. A Caucasian woman, affected by ALS, was hospitalized in our department due to anemia and recurrent episodes of hematochezia. Following a week of relative clinical stability, the patient experienced acute deterioration with generalized malaise and worsening dyspnea. CT scan excluded pulmonary causes, whereas EKG (ST segment depression in the lower and lateral leads), blood test (increase in high-sensitive cardiac troponins) and TTE (severe impairment of LVEF, with akinesia of basal segments) revealed a cardiac etiology. Coronary angiography and left ventriculography were performed, documenting a wall motion pattern consistent with rTTS. After an initial management in intensive care unit, clinical stability was obtained with a complete recovery of left ventricular systolic function. The patient was discharged but one month later, due to bacterial pneumonia, she was readmitted in our ward and antibiotic therapy was started. Two days later an acute deterioration of clinical status occurred, characterized by dyspnea, altered state of consciousness and marked hypotension. TTE revealed a severe left ventricular systolic dysfunction with apical akinesia and preserved contractility of basal segments, so a diagnosis of typical TTS was made. Three weeks later the clinical scenario became more complicated due to advanced atrioventricular block, with phases of atrioventricular dissociation and ventricular escape-rhythm. Therefore, in light of the increased risk of infectious complications, she underwent implantation of a leadless pacemaker (PMK). This clinical case represents the first report of recurrent episodes of TTS, one of which as rTTS, in a patient affected by ALS. It is worth noting that the first episode of TTS had atypical clinical presentation (dyspnea without chest pain), the EKG showed diffuse ST-segment depression (totally different from classical TTS typical electrocardiographic alterations), and TTE confirmed a different phenotype of segment involvement (unsurprisingly InterTAK Diagnostic Score was low). TTS recurrence is an extremely rare event, even if in this case there were two well defined triggers such as anemia and pneumonia. On the other hand it is reasonable to think that non-use of BBs after the first episode may have contributed to the occurrence of the next event, affecting different segments compared to the previous episode. Furthermore, advanced atrioventricular (AV) block represents a rare complication of TTS, most probably due to catecholamine stress or increased vagal tone, often requiring PMK implantation. In conclusion TTS represents an important frequent cardiac complication in patients affected by ALS, often still underdiagnosed. Therefore clinicians must keep their guard up with TTS, especially in the cases with atypical clinical presentation.

A Peculiar Wide Complex Tachycardia During Flecainide Treatment.

A Peculiar Wide Complex Tachycardia During Flecainide Treatment.

What Is the Mechanism of This Cardiac Rhythm?

An 80-year-old man with syncope was admitted for evaluation. His clinical examination revealed nothing remarkable. He had no history of heart disease, his blood pressure and electrolyte levels were normal, and he was taking no medications known to cause bradyarrhythmia. Overnight telemetry revealed the electrocardiogram displayed below (Fig. 1).The rhythm strip suggests which diagnosis?D) Junctional escape and intermittent capture beatsThe telemetry strip displayed junctional rhythm, sinus capture after every second junctional rhythm, and right bundle branch block (RBBB) of the sinus-captured beat (Fig. 2). This rare phenomenon, wherein a sinus-captured beat occurs after 2 junctional escape beats, is termed escape-reentry-capture trigeminy.1In isorhythmic atrioventricular (AV) dissociation (Answer A), the atria and ventricles beat at the same rate but are dissociated from each other; here, however, the junctional beat with retrograde conduction to the atria rules out dissociation between competing rhythms. The lack of clear P waves preceding the QRS complexes and the absence of progressive PR prolongation makes Mobitz type I AV block (Answer B) unlikely. Premature ventricular contractions in trigeminy (Answer C) are unlikely because the wide complexes with RBBB morphology are preceded by a P wave, and the QRS pattern simulates a “typical” RBBB. The 2 junctional beats followed by P-wave capture makes premature atrial complexes in trigeminy (Answer E) unlikely.Escape-reentry-capture occurs in the presence of sinus nodal dysfunction (sick sinus syndrome) when the sinus impulse rate is slower than the junctional escape rate. The inverted P wave in Figure 2 (arrows) suggests that the first junctional beat was conducted retrograde to the atria, that the next junctional beat was not, and that the subsequent sinus beat was conducted with an RBBB. This aberrancy may be explained by the “long-short” sequence that prolongs the effective refractory period of the right bundle. Consequently, the sinus rate was apparently slow enough to be captured in a trigeminal pattern. Note also that the junctional rhythm did not affect the sinus rate. The patient was given a permanent pacemaker. This case illustrates the escape-reentry-capture phenomenon in a trigeminal pattern caused by sinus nodal dysfunction.Conflict of Interest Disclosure: NoneFunding/Support: None

Repair of atrioventricular disruption after mitral valve replacement utilizing commando procedure principles.

Atrioventricular rupture is a life-threatening complication of mitral valve replacement. We present how incising the intervalvular fibrosa critically improves exposure. The aortic valve sacrifice allows access to a large atrioventricular dissociation defect and reliable repair of the anterolateral aspect of mitral valve annulus.

P319 SOMETHING MORE OF SIMPLE CARDIAC CONDUCTION DISORDERS

Abstract Background Cardiac amyloidosis (CA) is an infiltrative disease caused by extracellular deposition of amyloid fibrils. Possible cardiac manifestations include heart failure with preserved ejection fraction (EF), aortic valve stenosis, microvascular coronary artery disease, atrial fibrillation (AF), ventricular arrhythmias, and cardiac conduction disorders (CCD). We report a case of advanced CCD in a patient first diagnosed with wild–type transthyretin amyloidosis (ATTRwt). Case Report An 88–year–old man went to Emergency Room for chest pain with minimal elevation of troponin I and increase in NTproBNP. The patient reported a recent syncope with ribs fractures. The medical history showed hypertension, paroxysmal AF, carotid atherosclerosis, vascular encephalopathy and prostate cancer. Troponin I monitoring showed plateau values and there were no clinical signs of heart failure. ECG showed regular sinus rhythm with marked first degree atrioventricular block, right bundle branch block and left anterior fascicular block (Fig. 1A). Cardiac telemetry recorded brief phases of atrioventricular dissociation (AVD). Transthoracic echocardiography showed severe left ventricular concentric hypertrophy (LVCH) with granular–sparkling appearance and preserved EF, reduced global longitudinal strain with apical sparing (Fig. 1B), mitral–aortic valve degeneration and dilation of the ascending aorta. Given the advanced CCD with AVD and the recent syncope, the patient underwent a dual–chamber pacemaker implantation. In consideration of the echocardiographic suspicion of CA, following Gillmore’s diagnostic algorithm (GDA), serum electrophoresis and assay of serum free light chains were performed and resulted normal, while 99mTc–DPD bone scintigraphy was positive for significant radiotracer cardiac uptake (Perugini grade 3) (Fig. 1C). Based on this result, we carried out the search for transthyretin gene mutations which resulted negative, and therefore the diagnosis of ATTRwt was made. Discussion Advanced CCD in patients with transthyretin CA are present in about 9.5% of cases at the time of diagnosis, especially in older patients. It is therefore essential, in case of concomitant LVCH, to suspect the presence of CA as the cause of CCD by searching for the disease red flags and following the GDA to non–invasively confirm or exclude the diagnosis of CA. A correct and timely diagnosis of CA makes it possible to treat the disease and its complications, improving the prognosis.

Atypical fetal junctional ectopic tachycardia: a case report and literature review

BackgroundJunctional ectopic tachycardia (JET) is caused by ectopic rhythms, originating in the atrioventricular node, typically with heart rate between 200 and 250 bpm. Herein, we present a case of fetal JET with normal fetal heart rate and a review of nine cases.Case presentationA 32-year-old, gravida 2, para 1, woman in whom fetal JET could not be diagnosed prenatally because the fetal heart rate was within the normal range. The fetus was diagnosed with premature restriction of the foramen ovale, and a cesarean section was performed, owing to the right heart overload that was characterized by fetal ascites and abnormal fetal Doppler velocity. Postnatally, the female neonate was diagnosed with JET on a 12-lead electrocardiogram, which revealed a neonatal heart rate of 158 bpm with narrow QRS and atrioventricular dissociation. After failure to respond to amiodarone therapy, she was treated with flecainide, which controlled the JET rate from 120 to 150 bpm. Fetal tachycardia with ventriculo-atrial (VA) dissociation or 1:1 VA conduction with a shorter VA interval than that of atrioventricular reentrant tachycardia confirmed the diagnosis of fetal JET.ConclusionsJET should be suspected even in the absence of tachycardia in patients with ductus venosus and pulmonary vein retrograde flow or tricuspid and mitral regurgitation without a cardiac anomaly, as tachycardia might sometimes be intermittent in cases of JET.

Takotsubo Syndrome Presenting with Syncope and Third-Degree Atrioventricular Block Requiring Permanent Pacemaker Implantation

Takotsubo syndrome (TS) is an acute but transient heart failure syndrome and it is very uncommon for TS to present with syncope and complete atrioventricular (AV) block. In this report, we discuss a case of TS complicated by a third-degree AV block presented to the emergency department with syncope and requiring permanent pacemaker implantation. A 53-year-old female was admitted to our emergency department with complaints of syncopal episodes and chest pain. Due to ongoing chest pain, electrocardiography (ECG) findings and segmentary wall motion abnormality on the transthoracic echocardiography (TTE), she was immediately transferred to the cardiac catheterization laboratory. Coronary angiogram revealed normal coronary arteries and left ventriculography demonstrated apical ballooning and hypokinesis of the apex. Once the diagnosis of TS was established, the patient was transferred to the coronary intensive care unit (CICU). Initial ECG at CICU demonstrated complete AV block with a heart rate of 35 beats/min. On the third day of hospitalization, repeat TTE showed improved left ventricular functions with an ejection fraction of 50%. During the follow-up period in CICU, complete AV block persisted and the rhythm did not return to normal sinus rhythm after six days of monitorization. An electrophysiological study demonstrated supra-hisian atrioventricular block and atrioventricular dissociation. On the seventh day of hospitalization, TTE demonstrated recovered ventricular functions with an ejection fraction of 65%, and a dual pacemaker was then implanted. Her third-month followup was uneventful and TTE showed normal left ventricular functions but pacemaker interrogation revealed 99% of ventricular pacing. This case report demonstrated that the decision to implant a permanent pacemaker in such patients should be considered on a case-by-case basis, and an electrophysiological study could be valuable on this decision.

Extreme Hypoxia Causing Brady-Arrythmias During Apnea in Elite Breath-Hold Divers.

Introduction: The cardiac electrical conduction system is very sensitive to hypoglycemia and hypoxia, and the consequence may be brady-arrythmias. Weddell seals endure brady-arrythmias during their dives when desaturating to 3.2 kPa and elite breath-hold-divers (BHD), who share metabolic and cardiovascular adaptions including bradycardia with diving mammals, endure similar desaturation during maximum apnea. We hypothesized that hypoxia causes brady-arrythmias during maximum apnea in elite BHD. Hence, this study aimed to define the arterial blood glucose (Glu), peripheral saturation (SAT), heart rhythm (HR), and mean arterial blood pressure (MAP) of elite BHD during maximum apneas.Methods: HR was monitored with Direct-Current-Pads/ECG-lead-II and MAP and Glu from a radial arterial-catheter in nine BHD performing an immersed and head-down maximal static pool apnea after three warm-up apneas. SAT was monitored with a sensor on the neck of the subjects. On a separate day, a 12-lead-ECG-monitored maximum static apnea was repeated dry (n = 6).Results: During pool apnea of maximum duration (385 ± 70 s), SAT decreased from 99.6 ± 0.5 to 58.5 ± 5.5% (∼PaO2 4.8 ± 1.5 kPa, P < 0.001), while Glu increased from 5.8 ± 0.2 to 6.2 ± 0.2 mmol/l (P = 0.009). MAP increased from 103 ± 4 to 155 ± 6 mm Hg (P < 0.005). HR decreased to 46 ± 10 from 86 ± 14 beats/minute (P < 0.001). HR and MAP were unchanged after 3–4 min of apnea. During dry apnea (378 ± 31 s), HR decreased from 55 ± 4 to 40 ± 3 beats/minute (P = 0.031). Atrioventricular dissociation and junctional rhythm were observed both during pool and dry apneas.Conclusion: Our findings contrast with previous studies concluding that Glu decreases during apnea diving. We conclude during maximum apnea in elite BHD that (1) the diving reflex is maximized after 3–4 min, (2) increasing Glu may indicate lactate metabolism in accordance with our previous results, and (3) extreme hypoxia rather than hypoglycemia causes brady-arrythmias in elite BHD similar to diving mammals.

Simple atrioventricular (AV) dissociation or AV dissociation caused by third degree AV block?

The article's abstract is not available.