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  1. Lan BL, Liew YW, Toda M, Kamsani SH
    Chaos, 2020 May;30(5):053137.
    PMID: 32491883 DOI: 10.1063/1.5130524
    Complex dynamical systems can shift abruptly from a stable state to an alternative stable state at a tipping point. Before the critical transition, the system either slows down in its recovery rate or flickers between the basins of attraction of the alternative stable states. Whether the heart critically slows down or flickers before it transitions into and out of paroxysmal atrial fibrillation (PAF) is still an open question. To address this issue, we propose a novel definition of cardiac states based on beat-to-beat (RR) interval fluctuations derived from electrocardiogram data. Our results show the cardiac state flickers before PAF onset and termination. Prior to onset, flickering is due to a "tug-of-war" between the sinus node (the natural pacemaker) and atrial ectopic focus/foci (abnormal pacemakers), or the pacing by the latter interspersed among the pacing by the former. It may also be due to an abnormal autonomic modulation of the sinus node. This abnormal modulation may be the sole cause of flickering prior to termination since atrial ectopic beats are absent. Flickering of the cardiac state could potentially be used as part of an early warning or screening system for PAF and guide the development of new methods to prevent or terminate PAF. The method we have developed to define system states and use them to detect flickering can be adapted to study critical transition in other complex systems.
  2. Roslan A, Kamsani SH, Jauhari Aktifanus AT, Krishnan M, Hakim N, Megat Samsudin WN
    CASE (Phila), 2018 Apr;2(2):63-65.
    PMID: 30062312 DOI: 10.1016/j.case.2017.10.006
  3. Roslan A, Kamsani SH, Nay TW, Tan KL, Hakim N, Tan AM, et al.
    Med J Malaysia, 2018 12;73(6):388-392.
    PMID: 30647209
    OBJECTIVE: Cardiac amyloidosis is under diagnosed and its prevalence is unknown. This is a retrospective, nonrandomised, single centre study of patients with endomyocardial biopsy-proven cardiac amyloidosis focusing on their echocardiographic and electrocardiogram (ECG) presentations. This is the first case series in Malaysia on this subject.

    METHODS: We identified all of our endomyocardial biopsyproven cardiac amyloidosis patients from January 2010 to January 2018 and reviewed their medical records. All patients echocardiographic and ECG findings reviewed and analysed comparing to basic mean population value.

    RESULTS: In total there are 13 biopsy-proven cardiac amyloidosis patients. All of the biopsies shows light chain (AL) amyloid. Majority of the patients (8, 61.5%) is male, and most of our patients (8, 61.5%) is Chinese. All seven patients on whom we performed deformation imaging have apical sparing pattern on longitudinal strain echocardiogram. Mean ejection fraction is 49.3%, (SD=7.9). All patients have concentric left ventricular hypertrophy and right ventricular hypertrophy. Diastolic dysfunction was present in all of our patients with nine out of 13 patients (69.2%) having restrictive filling patterns (E/A ≥2.0 E/e' ≥15). On electrocardiogram, 12 (92%) patients have prolonged PR interval (median 200ms, IQR 76.50ms) and 9 (69.2%) patients have pseudoinfarct pattern.

    CONCLUSION: Echocardiography plays an important role in diagnosing cardiac amyloidosis. The findings of concentric left ventricular hypertrophy with preserved ejection fraction without increased in loading condition should alert the clinician towards its possibility. This is further supported by right ventricular hypertrophy and particularly longitudinal strain imaging showing apical sparing pattern.

  4. Kamsani SH, Middeldorp ME, Chiang G, Stefil M, Evans S, Nguyen MT, et al.
    Heart Rhythm O2, 2024 Jun;5(6):341-350.
    PMID: 38984365 DOI: 10.1016/j.hroo.2024.05.003
    BACKGROUND: Inpatient monitoring is recommended for sotalol initiation.

    OBJECTIVE: The purpose of this study was to assess the safety of outpatient sotalol commencement.

    METHODS: This is a multicenter, retrospective, observational study of patients initiated on sotalol in an outpatient setting. Serial electrocardiogram monitoring at day 3, day 7, 1 month, and subsequently as clinically indicated was performed. Corrected QT (QTc) interval and clinical events were evaluated.

    RESULTS: Between 2008 and 2023, 880 consecutive patients who were commenced on sotalol were evaluated. Indications were atrial fibrillation/flutter in 87.3% (n = 768), ventricular arrhythmias in 9.9% (n = 87), and other arrhythmias in 2.8% (n = 25). The daily dosage at initiation was 131.0 ± 53.2 mg/d. The QTc interval increased from baseline (431 ± 32 ms) to 444 ± 37 ms (day 3) and 440 ± 33 ms (day 7) after sotalol initiation (P < .001). Within the first week, QTc prolongation led to the discontinuation of sotalol in 4 and dose reduction in 1. No ventricular arrhythmia, syncope, or death was observed during the first week. Dose reduction due to asymptomatic bradycardia occurred in 3 and discontinuation due to dyspnea in 3 within the first week. Overall, 1.1% developed QTc prolongation (>500 ms/>25% from baseline); 4 within 3 days, 1 within 1 week, 4 within 60 days, and 1 after >3 years. Discontinuation of sotalol due to other adverse effects occurred in 41 patients within the first month of therapy.

    CONCLUSION: Sotalol initiation in an outpatient setting with protocolized follow-up is safe, with no recorded sotalol-related mortality, ventricular arrhythmias, or syncope. There was a low incidence of significant QTc prolongation necessitating discontinuation within the first month of treatment. Importantly, we observed a small incidence of late QT prolongation, highlighting the need for vigilant outpatient surveillance of individuals on sotalol.

  5. Roslan A, Stanislaus R, Yee Sin T, Aris FA, Ashari A, Shaparudin AA, et al.
    Int J Cardiol Heart Vasc, 2023 Aug;47:101242.
    PMID: 37576081 DOI: 10.1016/j.ijcha.2023.101242
    BACKGROUND: Athletes have changes that can mimic pathological cardiomyopathy.

    METHODS: Echocardiographic study of 50 male, female athletes (MA, FA) and non-athletes (MNA, FNA) age 18 to 30 years. These athletes participate in sports with predominantly endurance component. All participants exhibit no known medical illnesses or symptoms.

    RESULTS: MA have thicker wall (IVSd) than MNA. No MA have IVSd > 1.2 cm and no FA have IVSd > 1.0 cm. Left ventricle internal dimension (LVIDd), left ventricle end diastolic volume index (LVEDVi) is bigger in athletes. None have LVIDd > 5.8 cm. Right ventricle fractional area change (FAC) is lower in athletes. (MA vs MNA, p = 0.013, FA vs FNA, p = 0.025). Athletes have higher septal and lateral e' (Septal e'; MA 13.57 ± 2.66 cm/s vs MNA 11.46 ± 2.93 cm/s, p  1.2 cm and/or LVIDd > 5.8 cm. There is no difference in GLS, RVFWS and GCS but athletes have smaller LArS and LAbS.

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