Displaying publications 1 - 20 of 78 in total

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  1. [Possibilities for predicting of cardiac arrhythmias and conductivity disorders in former athletes.]
    Krysiuk OB, Obrezan AG, Zadvorev SF, Yakovlev AA
    Adv Gerontol, 2020;33(1):131-136.
    PMID: 32362096
    In order to analyze the relationship between the athletic qualification and syndrome of cardiac rhythm and conductivity disturbances in former athletes, a retrospective analysis of medical records of 39 male former athletes with cardiovascular complaints (mean age 61,6±11,3 years, mean duration of career in sports 23,9±17,3 years, mean duration of post-athletic period 20,1±9,9 years) was carried out. The patients were screened for cardiac arrhythmias and underwent echocardiography. The overall prevalence of sustained paroxysms of atrial fibrillation was 42%, increasing with the athletic qualification. Ryan grade 4b-5 premature ventricular contractions were found in 14% of patients. 3 parameters were found to be the independent predictors of arrhythmias in former athletes, i. e. athletic qualification, multifocal atherosclerosis (as an anti-risk factor), and age. The coefficient of determinance for the created prognostic model reached 43%. Further prospective studies are needed to validate an algorithm.
    Matched MeSH terms: Arrhythmias, Cardiac/diagnosis
  2. Fulltext Worldwide Survey of COVID-19-Associated Arrhythmias
    Coromilas EJ, Kochav S, Goldenthal I, Biviano A, Garan H, Goldbarg S, et al.
    Circ Arrhythm Electrophysiol, 2021 03;14(3):e009458.
    PMID: 33554620 DOI: 10.1161/CIRCEP.120.009458
    [Figure: see text].
    Matched MeSH terms: Arrhythmias, Cardiac/mortality; Arrhythmias, Cardiac/epidemiology*; Arrhythmias, Cardiac/physiopathology; Arrhythmias, Cardiac/therapy
  3. Fulltext Wellen's syndrome: Challenges in diagnosis
    Agarwal A, Vyas S, Kumar R
    Malays Fam Physician, 2015;10(3):35-7.
    PMID: 27570607
    Wellen's syndrome is a pre-infarction stage of coronary artery disease characterised by predefined clinical and electrocardiographic (ECG) criteria of a subgroup of patients with myocardial ischaemia. Early recognition and appropriate intervention of this syndrome carry significant diagnostic and prognostic value. We report this unusual syndrome in an elderly man who presented with recurrent angina and characteristic ECG changes as T-waves inversion in the precordial leads, especially in V2-V6 during pain-free periods and ECG obtained during episodes of pain demonstrating upright T-waves with possible elevated ST segments from V1-V4. Cardiac enzymes were positive and coronary angiography revealed critical stenosis in the proximal left anterior descending artery. It is important to timely identify this condition and intervene appropriately as these patients may develop extensive myocardial infarction that carries a significant morbidity and mortality.
    Matched MeSH terms: Arrhythmias, Cardiac
  4. Fulltext Ventricular pro-arrhythmic phenotype, arrhythmic substrate, ageing and mitochondrial dysfunction in peroxisome proliferator activated receptor-γ coactivator-1β deficient (Pgc-1β-/-) murine hearts
    Ahmad S, Valli H, Chadda KR, Cranley J, Jeevaratnam K, Huang CL
    Mech Ageing Dev, 2018 Jul;173:92-103.
    PMID: 29763629 DOI: 10.1016/j.mad.2018.05.004
    INTRODUCTION: Ageing and age-related bioenergetic conditions including obesity, diabetes mellitus and heart failure constitute clinical ventricular arrhythmic risk factors.

    MATERIALS AND METHODS: Pro-arrhythmic properties in electrocardiographic and intracellular recordings were compared in young and aged, peroxisome proliferator-activated receptor-γ coactivator-1β knockout (Pgc-1β-/-) and wild type (WT), Langendorff-perfused murine hearts, during regular and programmed stimulation (PES), comparing results by two-way ANOVA.

    RESULTS AND DISCUSSION: Young and aged Pgc-1β-/- showed higher frequencies and durations of arrhythmic episodes through wider PES coupling-interval ranges than WT. Both young and old, regularly-paced, Pgc-1β-/- hearts showed slowed maximum action potential (AP) upstrokes, (dV/dt)max (∼157 vs. 120-130 V s-1), prolonged AP latencies (by ∼20%) and shortened refractory periods (∼58 vs. 51 ms) but similar AP durations (∼50 ms at 90% recovery) compared to WT. However, Pgc-1β-/- genotype and age each influenced extrasystolic AP latencies during PES. Young and aged WT ventricles displayed distinct, but Pgc-1β-/- ventricles displayed similar dependences of AP latency upon (dV/dt)max resembling aged WT. They also independently increased myocardial fibrosis. AP wavelengths combining activation and recovery terms paralleled contrasting arrhythmic incidences in Pgc-1β-/- and WT hearts. Mitochondrial dysfunction thus causes pro-arrhythmic Pgc-1β-/- phenotypes by altering AP conduction through reducing (dV/dt)max and causing age-dependent fibrotic change.

    Matched MeSH terms: Arrhythmias, Cardiac/genetics; Arrhythmias, Cardiac/metabolism*; Arrhythmias, Cardiac/pathology; Arrhythmias, Cardiac/physiopathology
  5. Treatment of thyrotoxicosis with radioactive iodine: a report on 137 cases
    Dharmalingam SK, Taek YS, Mahadev V
    Med J Malaya, 1970 Sep;25(1):3-7.
    PMID: 4249493
    Matched MeSH terms: Arrhythmias, Cardiac/etiology
  6. Fulltext Torsade de pointes and syncopal attacks in a 26-year old woman with congenital complete heart block and prolonged QT interval
    Quek DK, Ong SB
    Singapore Med J, 1990 Apr;31(2):185-8.
    PMID: 2371586
    A 26-year old woman with congenital complete heart block and prolonged QT interval presented for the first time with syncopal attacks associated with torsade de pointes in adulthood. Cardioversion followed by overdrive pacing was needed to finally control the unstable rhythm. During episodes of non-capture, paraoxysms of torsade de pointes leading to ventricular flutter were recorded by a 24-hour ambulatory electrocardiographic monitoring. Beta-blockade and permanent ventricular pacing finally abolished both the syncopal attacks and the torsade phenomena. The prognosis of congenital complete heart block associated with QT prolongation resembles that of the Romano-Ward syndrome. Recognition of this variant would facilitate earlier treatment of this rare but potentially lethal disorder.
    Matched MeSH terms: Arrhythmias, Cardiac/complications*
  7. Fulltext The rationale and design of the Micra Transcatheter Pacing Study: safety and efficacy of a novel miniaturized pacemaker
    Ritter P, Duray GZ, Zhang S, Narasimhan C, Soejima K, Omar R, et al.
    Europace, 2015 May;17(5):807-13.
    PMID: 25855677 DOI: 10.1093/europace/euv026
    Recent advances in miniaturization technologies and battery chemistries have made it possible to develop a pacemaker small enough to implant within the heart while still aiming to provide similar battery longevity to conventional pacemakers. The Micra Transcatheter Pacing System is a miniaturized single-chamber pacemaker system that is delivered via catheter through the femoral vein. The pacemaker is implanted directly inside the right ventricle of the heart, eliminating the need for a device pocket and insertion of a pacing lead, thereby potentially avoiding some of the complications associated with traditional pacing systems.
    Matched MeSH terms: Arrhythmias, Cardiac/diagnosis; Arrhythmias, Cardiac/physiopathology; Arrhythmias, Cardiac/therapy*
  8. Fulltext The RyR2-P2328S mutation downregulates Nav1.5 producing arrhythmic substrate in murine ventricles
    Ning F, Luo L, Ahmad S, Valli H, Jeevaratnam K, Wang T, et al.
    Pflugers Arch., 2016 Apr;468(4):655-65.
    PMID: 26545784 DOI: 10.1007/s00424-015-1750-0
    Catecholaminergic polymorphic ventricular tachycardia (CPVT) predisposes to ventricular arrhythmia due to altered Ca(2+) homeostasis and can arise from ryanodine receptor (RyR2) mutations including RyR2-P2328S. Previous reports established that homozygotic murine RyR2-P2328S (RyR2 (S/S)) hearts show an atrial arrhythmic phenotype associated with reduced action potential (AP) conduction velocity and sodium channel (Nav1.5) expression. We now relate ventricular arrhythmogenicity and slowed AP conduction in RyR2 (S/S) hearts to connexin-43 (Cx43) and Nav1.5 expression and Na(+) current (I Na). Stimulation protocols applying extrasystolic S2 stimulation following 8 Hz S1 pacing at progressively decremented S1S2 intervals confirmed an arrhythmic tendency despite unchanged ventricular effective refractory periods (VERPs) in Langendorff-perfused RyR2 (S/S) hearts. Dynamic pacing imposing S1 stimuli then demonstrated that progressive reductions of basic cycle lengths (BCLs) produced greater reductions in conduction velocity at equivalent BCLs and diastolic intervals in RyR2 (S/S) than WT, but comparable changes in AP durations (APD90) and their alternans. Western blot analyses demonstrated that Cx43 protein expression in whole ventricles was similar, but Nav1.5 expression in both whole tissue and membrane fractions were significantly reduced in RyR2 (S/S) compared to wild-type (WT). Loose patch-clamp studies similarly demonstrated reduced I Na in RyR2 (S/S) ventricles. We thus attribute arrhythmogenesis in RyR2 (S/S) ventricles resulting from arrhythmic substrate produced by reduced conduction velocity to downregulated Nav1.5 reducing I Na, despite normal determinants of repolarization and passive conduction. The measured changes were quantitatively compatible with earlier predictions of linear relationships between conduction velocity and the peak I Na of the AP but nonlinear relationships between peak I Na and maximum Na(+) permeability.
    Matched MeSH terms: Arrhythmias, Cardiac/metabolism*
  9. Fulltext The Perilous PPI: Proton Pump Inhibitor as a Cause of Clinically Significant Hypomagnesaemia
    Tai YT, Tong CV
    J ASEAN Fed Endocr Soc, 2020;35(1):109-113.
    PMID: 33442177 DOI: 10.15605/jafes.035.01.18
    Proton pump inhibitors (PPIs) are the mainstay of therapy for all gastric acid related diseases and are commonly used in current clinical practice. Although widely regarded as safe, PPIs have been associated with a variety of adverse effects, including hypomagnesaemia. The postulated mechanism of PPI-related hypomagnesaemia involves inhibition of intestinal magnesium absorption via transient receptor potential melastin (TRPM) 6 and 7 cation channels. PPIinduced hypomagnesaemia (PPIH) has become a well recognized phenomenon since it was first reported in 2006. Clinical concerns arise from growing number of case reports presenting PPIH as a consequence of long-term PPI use, with more than 30 cases published to date. In this article, we report 2 cases of PPIH associated with the use of pantoprazole. Both patients presented with severe hypomagnesaemia and hypocalcaemia. One of them had associated hypokalemia and cardiac arrhythmia. A casual relation with PPIs postulated and supported by resolution of electrolyte abnormalities after discontinuation of PPIs.
    Matched MeSH terms: Arrhythmias, Cardiac
  10. Techniques for successful early retrieval of the Micra transcatheter pacing system: A worldwide experience
    Afzal MR, Daoud EG, Cunnane R, Mulpuru SK, Koay A, Hussain A, et al.
    Heart Rhythm, 2018 06;15(6):841-846.
    PMID: 29427820 DOI: 10.1016/j.hrthm.2018.02.008
    BACKGROUND: Experience with retrieval of the Micra transcatheter pacing system (TPS) is limited because of its relatively newer technology. Although abandonment of the TPS at end of life is recommended, certain situations such as endovascular infection or device embolization warrant retrieval.

    OBJECTIVE: The purpose of this study was to report the worldwide experience with successful retrieval of the Micra TPS.

    METHODS: A list of all successful retrievals of the currently available leadless pacemakers (LPs) was obtained from the manufacturer of Micra TPS. Pertinent details of retrieval, such as indication, days postimplantation, equipment used, complications, and postretrieval management, were obtained from the database collected by the manufacturer. Other procedural details were obtained directly from the operators at each participating site.

    RESULTS: Data from the manufacturer consisted of 40 successful retrievals of the Micra TPS. Operators for 29 retrievals (73%) provided the consent and procedural details. Of the 29 retrievals, 11 patients underwent retrieval during the initial procedure (immediate retrieval); the other 18 patients underwent retrieval during a separate procedure (delayed retrieval). Median duration before delayed retrieval was 46 days (range 1-95 days). The most common reason for immediate retrieval was elevated pacing threshold after tether removal. The most common reasons for delayed retrieval included elevated pacing threshold at follow-up, endovascular infection, and need for transvenous device. Mean procedure duration was 63.11 ± 56 minutes. All retrievals involved snaring via a Micra TPS delivery catheter or steerable sheath. No serious complications occurred during the reported retrievals.

    CONCLUSION: Early retrieval of the Micra TPS is feasible and safe.

    Matched MeSH terms: Arrhythmias, Cardiac/therapy*
  11. Some disorders of cardiac rhythm and their treatment
    Keele KD
    Malayan Medical Journal, 1937;12:47-9.
    Matched MeSH terms: Arrhythmias, Cardiac
  12. Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis
    Jeevaratnam K, Guzadhur L, Goh YM, Grace AA, Huang CL
    Acta Physiol (Oxf), 2016 Feb;216(2):186-202.
    PMID: 26284956 DOI: 10.1111/apha.12577
    Normal cardiac excitation involves orderly conduction of electrical activation and recovery dependent upon surface membrane, voltage-gated, sodium (Na(+) ) channel α-subunits (Nav 1.5). We summarize experimental studies of physiological and clinical consequences of loss-of-function Na(+) channel mutations. Of these conditions, Brugada syndrome (BrS) and progressive cardiac conduction defect (PCCD) are associated with sudden, often fatal, ventricular tachycardia (VT) or fibrillation. Mouse Scn5a(+/-) hearts replicate important clinical phenotypes modelling these human conditions. The arrhythmic phenotype is associated not only with the primary biophysical change but also with additional, anatomical abnormalities, in turn dependent upon age and sex, each themselves exerting arrhythmic effects. Available evidence suggests a unified binary scheme for the development of arrhythmia in both BrS and PCCD. Previous biophysical studies suggested that Nav 1.5 deficiency produces a background electrophysiological defect compromising conduction, thereby producing an arrhythmic substrate unmasked by flecainide or ajmaline challenge. More recent reports further suggest a progressive decline in conduction velocity and increase in its dispersion particularly in ageing male Nav 1.5 haploinsufficient compared to WT hearts. This appears to involve a selective appearance of slow conduction at the expense of rapidly conducting pathways with changes in their frequency distributions. These changes were related to increased cardiac fibrosis. It is thus the combination of the structural and biophysical changes both accentuating arrhythmic substrate that may produce arrhythmic tendency. This binary scheme explains the combined requirement for separate, biophysical and structural changes, particularly occurring in ageing Nav 1.5 haploinsufficient males in producing clinical arrhythmia.
    Matched MeSH terms: Arrhythmias, Cardiac/genetics*; Arrhythmias, Cardiac/physiopathology*
  13. Fulltext Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes
    Chadda KR, Jeevaratnam K, Lei M, Huang CL
    Pflugers Arch., 2017 06;469(5-6):629-641.
    PMID: 28265756 DOI: 10.1007/s00424-017-1959-1
    Arrhythmias arise from breakdown of orderly action potential (AP) activation, propagation and recovery driven by interactive opening and closing of successive voltage-gated ion channels, in which one or more Na+ current components play critical parts. Early peak, Na+ currents (I Na) reflecting channel activation drive the AP upstroke central to cellular activation and its propagation. Sustained late Na+ currents (I Na-L) include contributions from a component with a delayed inactivation timecourse influencing AP duration (APD) and refractoriness, potentially causing pro-arrhythmic phenotypes. The magnitude of I Na-L can be analysed through overlaps or otherwise in the overall voltage dependences of the steady-state properties and kinetics of activation and inactivation of the Na+ conductance. This was useful in analysing repetitive firing associated with paramyotonia congenita in skeletal muscle. Similarly, genetic cardiac Na+ channel abnormalities increasing I Na-L are implicated in triggering phenomena of automaticity, early and delayed afterdepolarisations and arrhythmic substrate. This review illustrates a wide range of situations that may accentuate I Na-L. These include (1) overlaps between steady-state activation and inactivation increasing window current, (2) kinetic deficiencies in Na+ channel inactivation leading to bursting phenomena associated with repetitive channel openings and (3) non-equilibrium gating processes causing channel re-opening due to more rapid recoveries from inactivation. All these biophysical possibilities were identified in a selection of abnormal human SCN5A genotypes. The latter presented as a broad range of clinical arrhythmic phenotypes, for which effective therapeutic intervention would require specific identification and targeting of the diverse electrophysiological abnormalities underlying their increased I Na-L.
    Matched MeSH terms: Arrhythmias, Cardiac/genetics; Arrhythmias, Cardiac/metabolism*
  14. Severe hypothyroidism presenting with supraventricular tachycardia
    Mak WW, Raja Nurazni RA, Mohamed Badrulnizam LB
    Med J Malaysia, 2018 10;73(5):349-350.
    PMID: 30350825 MyJurnal
    Thyroid disease is common and can have various systemic manifestations including cardiac diseases. Hypothyroidism is commonly associated with sinus bradycardia, low QRS complexes, prolonged QT interval and conduction blocks but rarely may cause arrhythmias. We present a patient who presented with presyncope and supraventricular tachycardia with severe hypothyroidism. Patient responded well to thyroxine replacement with biochemical improvement, the disappearance of arrhythmia after restoration of euthyroidism suggests that hypothyroidism might be the cause of supraventricular tachycardia. The aim of this report is to underline the possible aetiological link between supraventricular tachycardia and hypothyroidism, although supraventricular arrhythmias are ordinary features of hyperthyroidism.
    Matched MeSH terms: Arrhythmias, Cardiac
  15. Fulltext Secular trends of health care resource utilization and costs between Brugada syndrome and congenital long QT syndrome: A territory-wide study
    Lee S, Chung CTS, Radford D, Chou OHI, Lee TTL, Ng ZMW, et al.
    Clin Cardiol, 2023 Oct;46(10):1194-1201.
    PMID: 37489866 DOI: 10.1002/clc.24102
    BACKGROUND: Health care resource utilization (HCRU) and costs are important metrics of health care burden, but they have rarely been explored in the setting of cardiac ion channelopathies.

    HYPOTHESIS: This study tested the hypothesis that attendance-related HCRUs and costs differed between patients with Brugada syndrome (BrS) and congenital long QT syndrome (LQTS).

    METHODS: This was a retrospective cohort study of consecutive BrS and LQTS patients at public hospitals or clinics in Hong Kong, China. HCRUs and costs (in USD) for Accident and Emergency (A&E), inpatient, general outpatient and specialist outpatient attendances were analyzed between 2001 and 2019 at the cohort level. Comparisons were made using incidence rate ratios (IRRs [95% confidence intervals]).

    RESULTS: Over the 19-year period, 516 BrS (median age of initial presentation: 51 [interquartile range: 38-61] years, 92% male) and 134 LQTS (median age of initial presentation: 21 [9-44] years, 32% male) patients were included. Compared to LQTS patients, BrS patients had lower total costs (2 008 126 [2 007 622-2 008 629] vs. 2 343 864 [2 342 828-2 344 900]; IRR: 0.857 [0.855-0.858]), higher costs for A&E attendances (83 113 [83 048-83 177] vs. 70 604 [70 487-70 721]; IRR: 1.177 [1.165-1.189]) and general outpatient services (2,176 [2,166-2,187] vs. 921 [908-935]; IRR: 2.363 [2.187-2.552]), but lower costs for inpatient stay (1 391 624 [1 391 359-1 391 889] vs. 1 713 742 [1 713 166-1 714 319]; IRR: 0.812 [0.810-0.814]) and lower costs for specialist outpatient services (531 213 [531 049-531 376] vs. 558 597 [558268-558926]; IRR: 0.951 [0.947-0.9550]).

    CONCLUSIONS: Overall, BrS patients consume 14% less health care resources compared to LQTS patients in terms of attendance costs. BrS patients require more A&E and general outpatient services, but less inpatient and specialist outpatient services than LQTS patients.

    Matched MeSH terms: Arrhythmias, Cardiac/complications
  16. Response to: Depolarization vs. repolarization: what is the mechanism of ventricular arrhythmogenesis underlying sodium channel haploinsufficiency in mouse hearts?
    Jeevaratnam K, Guzadhur L, Goh YM, Grace AA, Huang CL
    Acta Physiol (Oxf), 2016 12;218(4):236-238.
    PMID: 27272698 DOI: 10.1111/apha.12731
    Matched MeSH terms: Arrhythmias, Cardiac
  17. Fulltext Reduced cardiomyocyte Na+ current in the age-dependent murine Pgc-1β-/- model of ventricular arrhythmia
    Ahmad S, Valli H, Smyth R, Jiang AY, Jeevaratnam K, Matthews HR, et al.
    J Cell Physiol, 2019 Apr;234(4):3921-3932.
    PMID: 30146680 DOI: 10.1002/jcp.27183
    Peroxisome proliferator-activated receptor-γ coactivator-1 deficient (Pgc-1β-/- ) murine hearts model the increased, age-dependent, ventricular arrhythmic risks attributed to clinical conditions associated with mitochondrial energetic dysfunction. These were accompanied by compromised action potential (AP) upstroke rates and impaired conduction velocities potentially producing arrhythmic substrate. We tested a hypothesis implicating compromised Na+ current in these electrophysiological phenotypes by applying loose patch-clamp techniques in intact young and aged, wild-type (WT) and Pgc-1β-/- , ventricular cardiomyocyte preparations for the first time. This allowed conservation of their in vivo extracellular and intracellular conditions. Depolarising steps elicited typical voltage-dependent activating and inactivating inward Na+ currents with peak amplitudes increasing or decreasing with their respective activating or preceding inactivating voltage steps. Two-way analysis of variance associated Pgc-1β-/- genotype with independent reductions in maximum peak ventricular Na+ currents from -36.63 ± 2.14 (n = 20) and -35.43 ± 1.96 (n = 18; young and aged WT, respectively), to -29.06 ± 1.65 (n = 23) and -27.93 ± 1.63 (n = 20; young and aged Pgc-1β-/- , respectively) pA/μm2 (p 
    Matched MeSH terms: Arrhythmias, Cardiac/genetics; Arrhythmias, Cardiac/metabolism*; Arrhythmias, Cardiac/physiopathology
  18. Rate adaptive pacing in an intracardiac pacemaker
    Lloyd M, Reynolds D, Sheldon T, Stromberg K, Hudnall JH, Demmer WM, et al.
    Heart Rhythm, 2017 02;14(2):200-205.
    PMID: 27871854 DOI: 10.1016/j.hrthm.2016.11.016
    BACKGROUND: The Micra transcatheter pacemaker was designed to have similar functionality to conventional transvenous VVIR pacing systems. It provides rate adaptive pacing using a programmable 3-axis accelerometer designed to detect patient activity in the presence of cardiac motion.

    OBJECTIVE: The purpose of this study was to evaluate the system's performance during treadmill tests to maximum exertion in a subset of patients within the Micra Transcatheter Pacing Study.

    METHODS: Patients underwent treadmill testing at 3 or 6 months postimplant with algorithm programming at physician discretion. Normalized sensor rate (SenR) relative to the programmed upper sensor rate was modeled as a function of normalized workload in metabolic equivalents (METS) relative to maximum METS achieved during the test. A normalized METS and SenR were determined at the end of each 1-minute treadmill stage. The proportionality of SenR to workload was evaluated by comparing the slope from this relationship to the prospectively defined tolerance margin (0.65-1.35).

    RESULTS: A total of 69 treadmill tests were attempted by 42 patients at 3 and 6 months postimplant. Thirty tests from 20 patients who completed ≥4 stages with an average slope of 0.86 (90% confidence interval 0.77-0.96) confirmed proportionality to workload. On an individual test basis, 25 of 30 point estimates (83.3%) had a normalized slope within the defined tolerance range (range 0.46-1.08).

    CONCLUSION: Accelerometer-based rate adaptive pacing was proportional to workload, thus confirming rate adaptive pacing commensurate to workload is achievable with an entirely intracardiac pacing system.

    Matched MeSH terms: Arrhythmias, Cardiac/therapy
  19. Pulmonary hypertension and echocardiogram parameters in obstructive sleep apnea
    Wong HT, Chee KH, Chong AW
    Eur Arch Otorhinolaryngol, 2017 Jun;274(6):2601-2606.
    PMID: 28243782 DOI: 10.1007/s00405-017-4491-1
    Obstructive sleep apnea (OSA) is a growing health hazard in the United States and worldwide. OSA is now recognized as a disorder with systemic manifestations and its association with obesity and adverse cardiovascular consequences. There is increasing evidence that OSA may be associated with systemic hypertension and an increased incidence of stroke, heart failure, myocardial infarction, and arrhythmias. Less information is available about the association between OSA and pulmonary hypertension (PH). We therefore conduct this study to look at the prevalence of the pulmonary hypertension in obstructive sleep apnea patient and to identify risk factors leading to pulmonary hypertension among OSA patient. We studied and analyzed all OSA patient confirmed by polysomnograph in the year 2015. Twenty-five patients with OSA were included in this study with prevalence of pulmonary hypertension of 16%. Univariate analysis of various factors revealed a statistically significant association between having the lowest SpO2 of <70% and pulmonary hypertension (p = 0.016). There were no statistically significant associations between age, gender, smoking status, hypertension, body mass index (BMI), or apnea-hypopnea index (AHI) with occurrence of pulmonary hypertension. AHI is not a good predictor for pulmonary hypertension. The real value of using AHI to predict the health risk of OSA is doubtful. We recommend routine echocardiogram among OSA patient. The objective information in the echocardiogram provides evidence for counseling of patient with disease of OSA and hence hopefully can improve compliance of patient to treatment especially usage of CPAP.
    Matched MeSH terms: Arrhythmias, Cardiac
  20. Fulltext Pro-arrhythmic atrial phenotypes in incrementally paced murine Pgc1β-/- hearts: effects of age
    Valli H, Ahmad S, Fraser JA, Jeevaratnam K, Huang CL
    Exp Physiol, 2017 12 01;102(12):1619-1634.
    PMID: 28960529 DOI: 10.1113/EP086589
    NEW FINDINGS: What is the central question of this study? Can we experimentally replicate atrial pro-arrhythmic phenotypes associated with important chronic clinical conditions, including physical inactivity, obesity, diabetes mellitus and metabolic syndrome, compromising mitochondrial function, and clarify their electrophysiological basis? What is the main finding and its importance? Electrocardiographic and intracellular cardiomyocyte recording at progressively incremented pacing rates demonstrated age-dependent atrial arrhythmic phenotypes in Langendorff-perfused murine Pgc1β-/- hearts for the first time. We attributed these to compromised action potential conduction and excitation wavefronts, whilst excluding alterations in recovery properties or temporal electrophysiological instabilities, clarifying these pro-arrhythmic changes in chronic metabolic disease. Atrial arrhythmias, most commonly manifesting as atrial fibrillation, represent a major clinical problem. The incidence of atrial fibrillation increases with both age and conditions associated with energetic dysfunction. Atrial arrhythmic phenotypes were compared in young (12-16 week) and aged (>52 week) wild-type (WT) and peroxisome proliferative activated receptor, gamma, coactivator 1 beta (Ppargc1b)-deficient (Pgc1β-/- ) Langendorff-perfused hearts, previously used to model mitochondrial energetic disorder. Electrophysiological explorations were performed using simultaneous whole-heart ECG and intracellular atrial action potential (AP) recordings. Two stimulation protocols were used: an S1S2 protocol, which imposed extrasystolic stimuli at successively decremented intervals following regular pulse trains; and a regular pacing protocol at successively incremented frequencies. Aged Pgc1β-/- hearts showed greater atrial arrhythmogenicity, presenting as atrial tachycardia and ectopic activity. Maximal rates of AP depolarization (dV/dtmax ) were reduced in Pgc1β-/- hearts. Action potential latencies were increased by the Pgc1β-/- genotype, with an added interactive effect of age. In contrast, AP durations to 90% recovery (APD90 ) were shorter in Pgc1β-/- hearts despite similar atrial effective recovery periods amongst the different groups. These findings accompanied paradoxical decreases in the incidence and duration of alternans in the aged and Pgc1β-/- hearts. Limiting slopes of restitution curves of APD90 against diastolic interval were correspondingly reduced interactively by Pgc1β-/- genotype and age. In contrast, reduced AP wavelengths were associated with Pgc1β-/- genotype, both independently and interacting with age, through the basic cycle lengths explored, with the aged Pgc1β-/- hearts showing the shortest wavelengths. These findings thus implicate AP wavelength in possible mechanisms for the atrial arrhythmic changes reported here.
    Matched MeSH terms: Arrhythmias, Cardiac/genetics; Arrhythmias, Cardiac/metabolism*; Arrhythmias, Cardiac/physiopathology
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