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Because of its powerful genetics, the adult zebrafish has been increasingly used for studying cardiovascular diseases. Considering its heart rate of ~100 beats per minute at ambient temperature, which is very close to human, we assessed the use of this vertebrate animal for modeling heart rhythm disorders such as sinus arrest (SA) and sick sinus syndrome (SSS). We firstly optimized a protocol to measure electrocardiogram in adult zebrafish. We determined the location of the probes, implemented an open-chest microsurgery procedure, measured the effects of temperature, and determined appropriate anesthesia dose and time. We then proposed an PP interval of more than 1.5 seconds as an arbitrary criterion to define an SA episode in an adult fish at ambient temperature, based on comparison between the current definition of an SA episode in humans and our studies of candidate SA episodes in aged wild-type fish and Tg(SCN5A-D1275N) fish (a fish model for inherited SSS). With this criterion, a subpopulation of about 5% wild-type fish can be considered to have SA episodes, and this percentage significantly increases to about 25% in 3-year-old fish. In response to atropine, this subpopulation has both common SSS phenotypic traits that are shared with the Tg(SCN5A-D1275N) model, such as bradycardia; and unique SSS phenotypic traits, such as increased QRS/P ratio and chronotropic incompetence. In summary, this study defined baseline SA and SSS in adult zebrafish and underscored use of the zebrafish as an alternative model to study aging-associated SSS.

Background Leadless pacemaker has been acknowledged as a promising pacing strategy to prevent pocket and lead-related complications. Although rare, cardiac perforation remains a major safety concern for implantation of Micra transcatheter pacing system (TPS). Case presentation A 83-year-old female with low body mass index (18.9 kg m −2 ) on dual anti-platelet therapy, was indicated for Micra TPS implantation due to sinus arrest and paroxysmal atrial flutter. The patient developed mild pericardial effusion during the procedure since the delivery catheter was accidentally placed into the coronary sinus for several times. Cardiac perforation with moderate pericardial effusion and pericardial tamponade was detected 2 h post-procedure. The patient was treated with immediately pericardiocentesis and recovered without further invasive therapy. Conclusion Pericardial effusion caused by accidently placing a delivery catheter into the coronary sinus is rare but should be carefully considered in Micra TPS implantation, especially for those with periprocedural anti-platelet therapy.

Objective: The treatment of syncope depends largely on its possible etiology. Therefore, identifying the cause of syncope is very important in treatment planning. Herein, we report an etiology of syncope caused by pulmonary hypertension (PH) associated with canine filariasis, followed by syncope due to bradyarrhythmia 1 year later. Materials and Methods: An 8-year-old male English Cocker Spaniel was referred to our hospital for a second opinion regarding syncope that the dog had started experiencing approximately 2 months prior. Based on the examination findings, we diagnosed that the fainting was due to heartworm disease and associated PH. After increasing the dose of pimobendan (0.50 mg/kg, q12h), the syncope subsided. However, syncope recurred on the 215th day of the first episode. Results: The findings that differed from those during the initial examination were that car¬diac arrest was observed for approximately 5 sec during auscultation, along with sinus arrest. Therefore, to further investigate for syncope, a Holter electrocardiograph was obtained for 3 days. Consequently, sinus arrest was identified as the etiology of the recurrent syncope, and the patient was diagnosed with sick sinus syndrome, Rubenstein classification type II. Following cilostazol (10 mg/kg, q12h) administration, the syncope subsided. Conclusion: This case reports syncope in a dog, which typically occurs due to different etiologies. When a dog has PH, it may be important to think about the possibility of arrhythmias caused by a bigger right heart.

Background Ambulatory electrocardiographic (ECG) monitoring is the standard to screen for high-risk arrhythmias. We evaluated the clinical utility of a novel, leadless electrode, single-patient-use ECG monitor that stores up to 14 days of a continuous recording to measure the burden and timing of potentially high-risk arrhythmias. Methods We examined data from 122,815 long term continuous ambulatory monitors (iRhythm ZIO® Service, San Francisco) prescribed from 2011 to 2013 and categorized potentially high-risk arrhythmias into two types: (1) ventricular arrhythmias including non-sustained and sustained ventricular tachycardia and (2) bradyarrhythmias including sinus pauses >3 s, atrial fibrillation pauses >5 s, and high-grade heart block (Mobitz Type II or third-degree heart block). Results Of 122,815 ZIO® recordings, median wear time was 9.9 (IQR 6.8–13.8) days and median analyzable time was 9.1 (IQR 6.4–13.1) days. There were 22,443 (18.3 %) with at least one episode of non-sustained ventricular tachycardia (NSVT), 238 (0.2 %) with sustained VT, 1766 (1.4 %) with a sinus pause >3 s (SP), 520 (0.4 %) with a pause during atrial fibrillation >5 s (AFP), and 1486 (1.2 %) with high-grade heart block (HGHB). Median time to first arrhythmia was 74 h (IQR 26–149 h) for NSVT, 22 h (IQR 5–73 h) for sustained VT, 22 h (IQR 7–64 h) for SP, 31 h (IQR 11–82 h) for AFP, and 40 h (SD 10–118 h) for HGHB. Conclusions A significant percentage of potentially high-risk arrhythmias are not identified within 48-h of ambulatory ECG monitoring. Longer-term continuous ambulatory ECG monitoring provides incremental detection of these potentially clinically relevant arrhythmic events.

We present a case of sinus arrest and junctional escape rhythm from sinus node artery (SNA) thrombus in a 55-year-old man after revascularisation of right coronary and proximal circumflex arteries for infero-posterior wall ST-segement elevation myocardial infarction (STEMI). Sinus arrest from occlusion of the SNA is uncommon. The ensuing bradycardia may have haemodynamic consequences requiring temporary pacing but is almost always self-limited.

Background Patients with kidney disease may have concurrent hypertension and infection. Dihydropyridine calcium-channel blockers (CCB) are the most popular class of antihypertensive drugs used in clinical settings and can be metabolized by cytochrome P450 isoenzyme 3A4 (CYP3A4). Voriconazole is a commonly used antifungal treatment and a CYP3A4-inhibitor. Insufficient attention to drug interactions from the concomitant use of CCB and voriconazole may result in serious adverse reactions. Case presentation Here, we report a patient with acute kidney injury on stable anti-neutrophil cytoplasm antibody associated vasculitis who developed hyperkalemia resulting in sinus arrest with junctional escape rhythm attributed to drug interactions of CCB with voriconazole. This is a very rarely reported case and may be an under-recognized complication. After continuous renal replacement therapy and changing the anti-hypertensive drugs, symptoms, and laboratory abnormalities of the patient fully recovered. Conclusions This case warns us of severe consequences of drug interactions. Co-prescription of CYP3A4-inhibitors with calcium-channel blockers increases the risk of hypotension and acute kidney injury, which may further induce hyperkalemia and arrhythmia.

Pyrethroids are common household insecticides. Even though they are less toxic to humans, reports of accidental and suicidal poisoning are not uncommon. Cardiotoxicity due to pyrethroid poisoning is rare. We report a case of cardiac conduction disturbance due to a pyrethroid, prallethrin. A 28-year-old female presented after a suicidal consumption of prallethrin. Her clinical and laboratory parameters were normal during the first 24 h of hospital stay. On the second hospital day, she developed metabolic acidosis and sinus arrest with escape junctional rhythm. Despite correction of metabolic acidosis, the sinus arrest persisted for 3 days. She reverted back to sinus rhythm with bradycardia after this period and was discharged on the seventh hospital day. Her follow-up was uneventful. Pyrethroid poisoning can affect the gastrointestinal, respiratory, and nervous system. Most serious effects of the toxin in humans are seizures and coma. Mechanism of pyrethroid neurotoxicity is believed to be due to its ability to modify sodium, chloride, and calcium channels of the neurons. Our case raises the possibility that cardiac arrhythmia due to pyrethroid poisoning can occur due to its effect on sodium channels in the heart.

Purpose: Previous studies have shown that the underlying pathophysiologic mechanism in children with breath holding may be generalised autonomic dysregulation. Thus, we performed cardiac rhythm and heart rate variability analyses using 24-hour Holter monitoring to evaluate the cardiac effects of autonomic dysregulation in children with breath-holding spells. Methods: We performed cardiac rhythm and heart rate analyses using 24-hour Holter monitors to evaluate the cardiac effects of autonomic dysregulation in children during a breath-holding spell. Our study group consisted of 68 children with breath-holding spells – 56 cyanotic type and 12 pallid type – and 39 healthy controls. Results: Clinical and heart rate variability results were compared between each spell type – cyanotic or pallid – and the control group; significant differences (p<0.05) in standard deviation of all NN intervals, mean of the standard deviations of all NN intervals for all 5-minute segments, percentage of differences between adjacent RR intervals >50 ms, and square root of the mean of the sum of squares of the differences between adjacent NN intervals values were found between the pallid and cyanotic groups. Conclusions: Holter monitoring for 24 hours and heart rate variability parameters, particularly in children with pallid spells, are crucial for evaluation of cardiac rhythm changes.

Syncope is defined as a transient, self-limiting loss of consciousness and postural tone due to transient global cerebral hypoperfusion. After syncope the following questions have to be answered: was it a syncopal episode, has the etiological diagnosis been determined, are there data suggestive of a high risk of cardiovascular events or death and what are the therapeutic options? Therefore, a standardized diagnostic work-up is necessary. This diagnostic work-up with differential diagnostic considerations is given for three clinical cases: a 52-year-old man experienced syncope while driving a car and on the morning of the same day syncope had previously occurred while in a standing position. The initial cardiological and neurological evaluation revealed no pathological findings but after implantation of a loop recorder a further syncope with a sinus arrest of 17 s occurred 1 year later. The patient received a single chamber pacemaker. The second case is a 79-year-old female with Parkinson's disease for many years and a primary autonomic dysfunction leading to dizziness and syncope due to pronounced blood pressure fluctuations with hypertensive and hypotensive phases. The last patient is a 22-year-old female with postural orthostatic tachycardia syndrome and recurrent syncope. The diagnostic evaluation and treatment proved to be difficult.