Displaying publications 1 - 20 of 26 in total

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  1. Alwi M, Choo KK, Radzi NA, Samion H, Pau KK, Hew CC
    J. Thorac. Cardiovasc. Surg., 2011 Jun;141(6):1355-61.
    PMID: 21227471 DOI: 10.1016/j.jtcvs.2010.08.085
    Objectives: Our objective was to determine the feasibility and early to medium-term outcome of stenting the patent ductus arteriosus at the time of radiofrequency valvotomy in the subgroup of patients with pulmonary atresia with intact ventricular septum and intermediate right ventricle.
    Background: Stenting of the patent ductus arteriosus and radiofrequency valvotomy have been proposed as the initial intervention for patients with intermediate right ventricle inasmuch as the sustainability for biventricular circulation or 1½-ventricle repair is unclear in the early period.
    Methods: Between January 2001 and April 2009, of 143 patients with pulmonary atresia and intact ventricular septum, 37 who had bipartite right ventricle underwent radiofrequency valvotomy and stenting of the patent ductus arteriosus as the initial procedure. The mean tricuspid valve z-score was -3.8 ± 2.2 and the mean tricuspid valve/mitral valve ratio was 0.62 ± 0.16.
    Results: Median age was 10 days (3-65 days) and median weight 3.1 kg (2.4-4.9 kg). There was no procedural mortality. Acute stent thrombosis developed in 1 patient and necessitated emergency systemic-pulmonary shunt. There were 2 early in-hospital deaths owing to low cardiac output syndrome. One late death occurred owing to right ventricular failure after the operation. Survival after the initial procedure was 94% at 6 months and 91% at 5 years. At a median follow-up of 4 years (6 months to 8 years), 17 (48%) attained biventricular circulation with or without other interventions and 9 (26%) achieved 1½-ventricle repair. The freedom from reintervention was 80%, 68%, 58%, and 40% at 1, 2, 3, and 4 years, respectively.
    Conclusions: Concomitant stenting of the patent ductus arteriosus at the time of radiofrequency valvotomy in patients with pulmonary atresia with intact ventricular septum and intermediate right ventricle is feasible and safe with encouraging medium-term outcome.
    Matched MeSH terms: Heart Ventricles/physiopathology
  2. 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: Heart Ventricles/physiopathology
  3. Edling CE, Fazmin IT, Chadda KR, Ahmad S, Valli H, Grace AA, et al.
    Biosci Rep, 2019 04 30;39(4).
    PMID: 30914453 DOI: 10.1042/BSR20190127
    Mice deficient in mitochondrial promoter peroxisome proliferator activated receptor-γ co-activator-1β (Pgc-1β-/- ) is a valuable model for metabolic diseases and has been found to present with several pathologies including ventricular arrhythmia. In the present study, our aim was to shed light on the molecular mechanisms behind the observed arrhythmic substrate by studying how the expression of selected genes critical for cardiac function differs in wild-type (WT) compared with Pgc-1β knockout mice and young compared with aged mice. We found that a clear majority of genes are down-regulated in the Pgc-1β-/- ventricular tissue compared with the WT. Although most individual genes are not significantly differentially expressed, a pattern is apparent when the genes are grouped according to their functional properties. Genes encoding proteins relating to ATPase activity, potassium ion channels relating to repolarisation and resting membrane potential, and genes encoding proteins in the cAMP pathway are found to be significantly down-regulated in the Pgc-1β deficient mice. On the contrary, the pacemaker channel genes Hcn3 and Hcn4 are up-regulated in subsets of the Pgc-1β deficient tissue. Furthermore, we found that with age, especially in the Pgc-1β-/- genotype, most genes are up-regulated including genes relating to the resting membrane potential, calcium homeostasis, the cAMP pathway, and most of the tested adrenoceptors. In conclusion, we here demonstrate how a complex pattern of many modest changes at gene level may explain major functional differences of the action potential related to ageing and mitochondrial dysfunction.
    Matched MeSH terms: Heart Ventricles/physiopathology
  4. Chinitz L, Ritter P, Khelae SK, Iacopino S, Garweg C, Grazia-Bongiorni M, et al.
    Heart Rhythm, 2018 09;15(9):1363-1371.
    PMID: 29758405 DOI: 10.1016/j.hrthm.2018.05.004
    BACKGROUND: Micra is a leadless pacemaker that is implanted in the right ventricle and provides rate response via a 3-axis accelerometer (ACC). Custom software was developed to detect atrial contraction using the ACC enabling atrioventricular (AV) synchronous pacing.

    OBJECTIVE: The purpose of this study was to sense atrial contractions from the Micra ACC signal and provide AV synchronous pacing.

    METHODS: The Micra Accelerometer Sensor Sub-Study (MASS) and MASS2 early feasibility studies showed intracardiac accelerations related to atrial contraction can be measured via ACC in the Micra leadless pacemaker. The Micra Atrial TRacking Using A Ventricular AccELerometer (MARVEL) study was a prospective multicenter study designed to characterize the closed-loop performance of an AV synchronous algorithm downloaded into previously implanted Micra devices. Atrioventricular synchrony (AVS) was measured during 30 minutes of rest and during VVI pacing. AVS was defined as a P wave visible on surface ECG followed by a ventricular event <300 ms.

    RESULTS: A total of 64 patients completed the MARVEL study procedure at 12 centers in 9 countries. Patients were implanted with a Micra for a median of 6.0 months (range 0-41.4). High-degree AV block was present in 33 patients, whereas 31 had predominantly intrinsic conduction during the study. Average AVS during AV algorithm pacing was 87.0% (95% confidence interval 81.8%-90.9%), 80.0% in high-degree block patients and 94.4% in patients with intrinsic conduction. AVS was significantly greater (P

    Matched MeSH terms: Heart Ventricles/physiopathology*
  5. Adeyemi O, Alvarez-Laviada A, Schultz F, Ibrahim E, Trauner M, Williamson C, et al.
    PLoS One, 2017;12(9):e0183167.
    PMID: 28934223 DOI: 10.1371/journal.pone.0183167
    BACKGROUND: Increased maternal serum bile acid concentrations in intrahepatic cholestasis of pregnancy (ICP) are associated with fetal cardiac arrhythmias. Ursodeoxycholic acid (UDCA) has been shown to demonstrate anti-arrhythmic properties via preventing ICP-associated cardiac conduction slowing and development of reentrant arrhythmias, although the cellular mechanism is still being elucidated.

    METHODS: High-resolution fluorescent optical mapping of electrical activity and electrocardiogram measurements were used to characterize effects of UDCA on one-day-old neonatal and adult female Langendorff-perfused rat hearts. ICP was modelled by perfusion of taurocholic acid (TC, 400μM). Whole-cell calcium currents were recorded from neonatal rat and human fetal cardiomyocytes.

    RESULTS: TC significantly prolonged the PR interval by 11.0±3.5% (P<0.05) and slowed ventricular conduction velocity (CV) by 38.9±5.1% (P<0.05) exclusively in neonatal and not in maternal hearts. A similar CV decline was observed with the selective T-type calcium current (ICa,T) blocker mibefradil 1μM (23.0±6.2%, P<0.05), but not with the L-type calcium current (ICa,L) blocker nifedipine 1μM (6.9±6.6%, NS). The sodium channel blocker lidocaine (30μM) reduced CV by 60.4±4.5% (P<0.05). UDCA co-treatment was protective against CV slowing induced by TC and mibefradil, but not against lidocaine. UDCA prevented the TC-induced reduction in the ICa,T density in both isolated human fetal (-10.2±1.5 versus -5.5±0.9 pA/pF, P<0.05) and neonatal rat ventricular myocytes (-22.3±1.1 versus -9.6±0.8 pA/pF, P<0.0001), whereas UDCA had limited efficacy on the ICa,L.

    CONCLUSION: Our findings demonstrate that ICa,T plays a significant role in ICP-associated fetal cardiac conduction slowing and arrhythmogenesis, and is an important component of the fetus-specific anti-arrhythmic activity of UDCA.

    Matched MeSH terms: Heart Ventricles/physiopathology*
  6. Crossley GH, Biffi M, Johnson B, Lin A, Gras D, Hussin A, et al.
    Heart Rhythm, 2015 Apr;12(4):751-8.
    PMID: 25533587 DOI: 10.1016/j.hrthm.2014.12.019
    The Medtronic Attain Performa quadripolar leads provide 16 pacing vectors with steroid on every electrode. This includes a short bipolar configuration between the middle 2 electrodes.
    Matched MeSH terms: Heart Ventricles/physiopathology
  7. Yee R, Gadler F, Hussin A, Bin Omar R, Khaykin Y, Verma A, et al.
    Heart Rhythm, 2014 Jul;11(7):1150-5.
    PMID: 24801899 DOI: 10.1016/j.hrthm.2014.04.020
    Left ventricular (LV) lead implantation for cardiac resynchronization therapy (CRT) is associated with lead dislodgement rates ranging from 3% to 10%, and some implant approaches to prevent dislodgement may contribute to suboptimal CRT response. We report our early human experience with an LV lead with a side helix for active fixation to the coronary vein wall.
    Matched MeSH terms: Heart Ventricles/physiopathology
  8. Chan BT, Lim E, Chee KH, Abu Osman NA
    Comput Biol Med, 2013 May;43(4):377-85.
    PMID: 23428371 DOI: 10.1016/j.compbiomed.2013.01.013
    The heart is a sophisticated functional organ that plays a crucial role in the blood circulatory system. Hemodynamics within the heart chamber can be indicative of exert cardiac health. Due to the limitations of current cardiac imaging modalities, computational fluid dynamics (CFD) have been widely used for the purposes of cardiac function assessment and heart disease diagnosis, as they provide detailed insights into the cardiac flow field. An understanding of ventricular hemodynamics and pathological severities can be gained through studies that employ the CFD method. In this research the hemodynamics of two common myocardial diseases, dilated cardiomyopathy (DCM) and myocardial infarction (MI) were investigated, during both the filling phase and the whole cardiac cycle, through a prescribed geometry and fluid structure interaction (FSI) approach. The results of the research indicated that early stage disease identification and the improvement of cardiac assisting devices and therapeutic procedures can be facilitated through the use of the CFD method.
    Matched MeSH terms: Heart Ventricles/physiopathology
  9. Garweg C, Khelae SK, Steinwender C, Chan JYS, Ritter P, Johansen JB, et al.
    Heart Rhythm, 2020 12;17(12):2037-2045.
    PMID: 32717315 DOI: 10.1016/j.hrthm.2020.07.024
    BACKGROUND: The MARVEL (Micra Atrial TRacking Using a Ventricular AccELerometer) 2 study assessed the efficacy of atrioventricular (AV) synchronous pacing with a Micra leadless pacemaker. Average atrioventricular synchrony (AVS) was 89.2%. Previously, low amplitude of the Micra-sensed atrial signal (A4) was observed to be a factor of low AVS.

    OBJECTIVE: The purpose of this study was to identify predictors of A4 amplitude and high AVS.

    METHODS: We analyzed 64 patients enrolled in MARVEL 2 who had visible P waves on electrocardiogram for assessing A4 amplitude and 40 patients with third-degree AV block for assessing AVS at rest. High AVS was defined as >90% correct atrial-triggered ventricular pacing. The association between clinical factors and echocardiographic parameters with A4 amplitude was investigated using a multivariable model with lasso variable selection. Variables associated with A4 amplitude together with premature ventricular contraction burden, sinus rate, and sinus rate variability (standard deviation of successive differences of P-P intervals [SDSD]) were assessed for association with AVS.

    RESULTS: In univariate analysis, low A4 amplitude was inversely related to atrial function assessed by E/A ratio and e'/a' ratio, and was directly related to atrial contraction excursion (ACE) and atrial strain (Ɛa) on echocardiography (all P ≤.05). The multivariable lasso regression model found coronary artery bypass graft history, E/A ratio, ACE, and Ɛa were associated with low A4 amplitude. E/A ratio and SDSD were multivariable predictors of high AVS, with >90% probability if E/A <0.94 and SDSD <5 bpm.

    CONCLUSION: Clinical parameters and echocardiographic markers of atrial function are associated with A4 signal amplitude. High AVS can be predicted by E/A ratio <0.94 and low sinus rate variability at rest.

    Matched MeSH terms: Heart Ventricles/physiopathology*
  10. Aslannif R, Suraya K, Koh HB, Tey YS, Tan KL, Tham CH, et al.
    Med J Malaysia, 2019 12;74(6):521-526.
    PMID: 31929479
    INTRODUCTION: Apical Hypertrophic Cardiomyopathy (Apical HCM) is an uncommon variant of hypertrophic cardiomyopathy, but it is relatively more common in Asian countries. This is a retrospective, non-randomised, single centre study of patients with Apical HCM focusing on their diastolic dysfunction grading, echocardiographic parameters and electrocardiograms (ECG).

    METHODS: All Apical HCM patients coming for clinic visits at the Institut Jantung Negara from September 2017 to September 2018 were included. We assessed their echocardiography images, grade their diastolic function and reviewed their ECG on presentation.

    RESULTS: Fifty patient were included, 82% (n=41) were males and 18% (n=9) females. The diastolic function grading of 37 (74%) patients were able to be determined using the updated 2016 American Society of Echocardiography (ASE) diastolic guidelines. Fifty percent (n=25) had the typical ace-ofspades shape left ventricle (LV) appearance in diastole and 12% (n=6) had apical pouch. All patients had T inversion in the anterior leads of their ECG, and only 52% (n=26) fulfilled the ECG left ventricular hypertrophy (LVH) criteria. Majority of our patients presented with symptoms of chest pain (52%, n=26) and dyspnoea (42%, n=21).

    CONCLUSION: The updated 2016 ASE guideline makes it easier to evaluate LV diastolic function in most patients with Apical HCM. It also helps in elucidating the aetiology of dyspnoea, based on left atrial pressure. Clinicians should have a high index of suspicion for Apical HCM when faced with deep T inversion on ECG, in addition to a thick LV apex with an aceof- spades appearance during diastole.

    Matched MeSH terms: Heart Ventricles/physiopathology*
  11. Ahmad S, Valli H, Edling CE, Grace AA, Jeevaratnam K, Huang CL
    Pflugers Arch., 2017 Dec;469(12):1579-1590.
    PMID: 28821956 DOI: 10.1007/s00424-017-2054-3
    A range of chronic clinical conditions accompany cardiomyocyte energetic dysfunction and constitute independent risk factors for cardiac arrhythmia. We investigated pro-arrhythmic and arrhythmic phenotypes in energetically deficient C57BL mice with genetic ablation of the mitochondrial promoter peroxisome proliferator-activated receptor-γ coactivator-1β (Pgc-1β), a known model of ventricular arrhythmia. Pro-arrhythmic and cellular action potential (AP) characteristics were compared in intact Langendorff-perfused hearts from young (12-16 week) and aged (> 52 week), wild-type (WT) and Pgc-1β -/- mice. Simultaneous electrocardiographic and intracellular microelectrode recordings were made through successive trains of 100 regular stimuli at progressively incremented heart rates. Aged Pgc-1β -/- hearts displayed an increased incidence of arrhythmia compared to other groups. Young and aged Pgc-1β -/- hearts showed higher incidences of alternans in both AP activation (maximum AP upshoot velocity (dV/dt)max and latency), recovery (action potential duration (APD90) and resting membrane potential (RMP) characteristics compared to WT hearts. This was particularly apparent at lower pacing frequencies. These findings accompanied reduced (dV/dt)max and increased AP latency values in the Pgc-1β -/- hearts. APs observed prior to termination of the protocol showed lower (dV/dt)max and longer AP latencies, but indistinguishable APD90 and RMPs in arrhythmic compared to those in non-arrhythmic hearts. APD restitution analysis showed that Pgc-1β -/- and WT hearts showed similar limiting gradients. However, Pgc-1β -/- hearts had shortened plateau AP wavelengths, particularly in aged Pgc-1β -/- hearts. Pgc-1β -/- hearts therefore show pro-arrhythmic instabilities attributable to altered AP conduction and activation rather than recovery characteristics.
    Matched MeSH terms: Heart Ventricles/physiopathology
  12. Chan BT, Abu Osman NA, Lim E, Chee KH, Abdul Aziz YF, Abed AA, et al.
    PLoS One, 2013;8(6):e67097.
    PMID: 23825628 DOI: 10.1371/journal.pone.0067097
    Dilated cardiomyopathy (DCM) is the most common myocardial disease. It not only leads to systolic dysfunction but also diastolic deficiency. We sought to investigate the effect of idiopathic and ischemic DCM on the intraventricular fluid dynamics and myocardial wall mechanics using a 2D axisymmetrical fluid structure interaction model. In addition, we also studied the individual effect of parameters related to DCM, i.e. peak E-wave velocity, end systolic volume, wall compliance and sphericity index on several important fluid dynamics and myocardial wall mechanics variables during ventricular filling. Intraventricular fluid dynamics and myocardial wall deformation are significantly impaired under DCM conditions, being demonstrated by low vortex intensity, low flow propagation velocity, low intraventricular pressure difference (IVPD) and strain rates, and high-end diastolic pressure and wall stress. Our sensitivity analysis results showed that flow propagation velocity substantially decreases with an increase in wall stiffness, and is relatively independent of preload at low-peak E-wave velocity. Early IVPD is mainly affected by the rate of change of the early filling velocity and end systolic volume which changes the ventriculo:annular ratio. Regional strain rate, on the other hand, is significantly correlated with regional stiffness, and therefore forms a useful indicator for myocardial regional ischemia. The sensitivity analysis results enhance our understanding of the mechanisms leading to clinically observable changes in patients with DCM.
    Matched MeSH terms: Heart Ventricles/physiopathology*
  13. Steinwender C, Khelae SK, Garweg C, Chan JYS, Ritter P, Johansen JB, et al.
    JACC Clin Electrophysiol, 2020 01;6(1):94-106.
    PMID: 31709982 DOI: 10.1016/j.jacep.2019.10.017
    OBJECTIVES: This study reports on the performance of a leadless ventricular pacemaker with automated, enhanced accelerometer-based algorithms that provide atrioventricular (AV) synchronous pacing.

    BACKGROUND: Despite many advantages, leadless pacemakers are currently only capable of single-chamber ventricular pacing.

    METHODS: The prospective MARVEL 2 (Micra Atrial tRacking using a Ventricular accELerometer 2) study assessed the performance of an automated, enhanced accelerometer-based algorithm downloaded to the Micra leadless pacemaker for up to 5 h in patients with AV block. The primary efficacy objective was to demonstrate the superiority of the algorithm to provide AV synchronous (VDD) pacing versus VVI-50 pacing in patients with sinus rhythm and complete AV block. The primary safety objective was to demonstrate that the algorithm did not result in pauses or heart rates of >100 beats/min.

    RESULTS: Overall, 75 patients from 12 centers were enrolled; an accelerometer-based algorithm was downloaded to their leadless pacemakers. Among the 40 patients with sinus rhythm and complete AV block included in the primary efficacy objective analysis, the proportion of patients with ≥70% AV synchrony at rest was significantly greater with VDD pacing than with VVI pacing (95% vs. 0%; p 

    Matched MeSH terms: Heart Ventricles/physiopathology*
  14. Chan BT, Yeoh HK, Liew YM, Aziz YFA, Sridhar GS, Hamilton-Craig C, et al.
    Med Biol Eng Comput, 2017 Oct;55(10):1883-1893.
    PMID: 28321684 DOI: 10.1007/s11517-017-1639-5
    This study aims to investigate the measurement of left ventricular flow propagation velocity, V p, using phase contrast magnetic resonance imaging and to assess the discrepancies resulting from inflow jet direction and individual left ventricular size. Three V p measuring techniques, namely non-adaptive (NA), adaptive positions (AP) and adaptive vectors (AV) method, were suggested and compared. We performed the comparison on nine healthy volunteers and nine post-infarct patients at four measurement positions, respectively, at one-third, one-half, two-thirds and the conventional 4 cm distances from the mitral valve leaflet into the left ventricle. We found that the V p measurement was affected by both the inflow jet direction and measurement positions. Both NA and AP methods overestimated V p, especially in dilated left ventricles, while the AV method showed the strongest correlation with the isovolumic relaxation myocardial strain rate (r = 0.53, p 
    Matched MeSH terms: Heart Ventricles/physiopathology*
  15. Piccini JP, Stromberg K, Jackson KP, Kowal RC, Duray GZ, El-Chami MF, et al.
    Europace, 2019 Nov 01;21(11):1686-1693.
    PMID: 31681964 DOI: 10.1093/europace/euz230
    AIMS: Patient selection is a key component of securing optimal patient outcomes with leadless pacing. We sought to describe and compare patient characteristics and outcomes of Micra patients with and without a primary pacing indication associated with atrial fibrillation (AF) in the Micra IDE trial.

    METHODS AND RESULTS: The primary outcome (risk of cardiac failure, pacemaker syndrome, or syncope related to the Micra system or procedure) was compared between successfully implanted patients from the Micra IDE trial with a primary pacing indication associated with AF or history of AF (AF group) and those without (non-AF group). Among 720 patients successfully implanted with Micra, 228 (31.7%) were in the non-AF group. Reasons for selecting VVI pacing in non-AF patients included an expectation for infrequent pacing (66.2%) and advanced age (27.2%). More patients in the non-AF group had a condition that precluded the use of a transvenous pacemaker (9.6% vs. 4.7%, P = 0.013). Atrial fibrillation patients programmed to VVI received significantly more ventricular pacing compared to non-AF patients (median 67.8% vs. 12.6%; P 

    Matched MeSH terms: Heart Ventricles/physiopathology*
  16. Leong CN, Dokos S, Andriyana A, Liew YM, Chan BT, Abdul Aziz YF, et al.
    Int J Numer Method Biomed Eng, 2020 01;36(1):e3291.
    PMID: 31799767 DOI: 10.1002/cnm.3291
    Myocardial infarct extension, a process involving the enlargement of infarct and border zone, leads to progressive degeneration of left ventricular (LV) function and eventually gives rise to heart failure. Despite carrying a high risk, the causation of infarct extension is still a subject of much speculation. In this study, patient-specific LV models were developed to investigate the correlation between infarct extension and impaired regional mechanics. Subsequently, sensitivity analysis was performed to examine the causal factors responsible for the impaired regional mechanics observed in regions surrounding the infarct and border zone. From our simulations, fibre strain, fibre stress and fibre stress-strain loop (FSSL) were the key biomechanical variables affected in these regions. Among these variables, only FSSL was correlated with infarct extension, as reflected in its work density dissipation (WDD) index value, with high WDD indices recorded at regions with infarct extension. Impaired FSSL is caused by inadequate contraction force generation during the isovolumic contraction and ejection phases. Our further analysis revealed that the inadequacy in contraction force generation is not necessarily due to impaired myocardial intrinsic contractility, but at least in part, due to inadequate muscle fibre stretch at end-diastole, which depresses the ability of myocardium to generate adequate contraction force in the subsequent systole (according to the Frank-Starling law). Moreover, an excessively stiff infarct may cause its neighbouring myocardium to be understretched at end-diastole, subsequently depressing the systolic contractile force of the neighbouring myocardium, which was found to be correlated with infarct extension.
    Matched MeSH terms: Heart Ventricles/physiopathology
  17. Khor KH, Campbell FE, Owen H, Shiels IA, Mills PC
    Vet J, 2015 Feb;203(2):161-8.
    PMID: 25573453 DOI: 10.1016/j.tvjl.2014.11.018
    The histological features of feline hypertrophic cardiomyopathy (HCM) have been well documented, but there are no reports describing the histological features in mild pre-clinical disease, since cats are rarely screened for the disease in the early stages before clinical signs are apparent. Histological changes at the early stage of the disease in pre-clinical cats could contribute to an improved understanding of disease aetiology or progression. The aim of this study was to evaluate the histological features of HCM in the left ventricular (LV) myocardium of cats diagnosed with pre-clinical HCM. Clinically healthy cats with normal (n = 11) and pre-clinical HCM (n = 6) were identified on the basis of echocardiography; LV free wall dimensions (LVFWd) and/or interventricular septal wall (IVSd) dimensions during diastole of 6-7 mm were defined as HCM, while equivalent dimensions <5.5 mm were defined as normal. LV myocardial sections were assessed and collagen content and inflammatory cell infiltrates were quantified objectively. Multifocal areas of inflammatory cell infiltration, predominantly lymphocytes, were observed frequently in the left myocardium of cats with pre-clinical HCM. Tissue from cats with pre-clinical HCM also had a higher number of neutrophils and a greater collagen content than the myocardium of normal cats. The myocardium variably demonstrated other features characteristic of HCM, including arteriolar mural hypertrophy and interstitial fibrosis and, to a lesser extent, myocardial fibre disarray and cardiomyocyte hypertrophy. These results suggest that an inflammatory process could contribute to increased collagen content and the myocardial fibrosis known to be associated with HCM.
    Matched MeSH terms: Heart Ventricles/physiopathology*
  18. Ota N, Sivalingam S, Pau KK, Hew CC, Dillon J, Latiff HA, et al.
    PMID: 29310554 DOI: 10.1177/2150135117743225
    OBJECTIVE: We introduced primary arterial switch operation for the patient with transposition of great arteries and intact ventricular septum (TGA-IVS) who had more than 3.5 mm of posterior left ventricle (LV) wall thickness.

    METHODS: Between January 2013 and June 2015, a total of 116 patients underwent arterial switch operation. Of the 116 patients, 26 with TGA-IVS underwent primary arterial switch operation at more than 30 days of age.

    RESULTS: The age and body weight (mean ± SD) at the operation were 120.4 ± 93.8 days and 4.1 ±1.0 kg, respectively. There was no hospital mortality. The thickness of posterior LV wall (preoperation vs postoperation; mm) was 4.04 ± 0.71 versus 5.90 ± 1.3; P < .0001; interval: 11.8 ± 6.5 days. The left atrial pressure (mm Hg; postoperative day 0 vs 3) was 20.0 ± 3.2 versus 10.0 ± 2.0; P < .0001; and the maximum blood lactate level (mmol/dL) was 4.7 ± 1.4 versus 1.4 ± 0.3; P < .0001, which showed significant improvement in the postoperative course. All cases had delayed sternal closure. The patients who belonged to the thin LV posterior wall group (<4 mm [preoperative echo]: n = 13) had significantly longer ventilation time (days; 10.6 ± 4.8 vs 4.8 ± 1.7, P = .0039), and the intensive care unit stay (days) was 14 ± 9.2 versus 7.5 ± 3.5; P = .025, compared with thick LV wall group (≥4.0 mm: n = 13).

    CONCLUSIONS: The children older than 30 days with TGA-IVS can benefit from primary arterial switch operation with acceptable results under our indication. However, we need further investigation for LV function.

    Matched MeSH terms: Heart Ventricles/physiopathology
  19. Hassaballah AI, Hassan MA, Mardi AN, Hamdi M
    PLoS One, 2013;8(12):e82703.
    PMID: 24367544 DOI: 10.1371/journal.pone.0082703
    The determination of the myocardium's tissue properties is important in constructing functional finite element (FE) models of the human heart. To obtain accurate properties especially for functional modeling of a heart, tissue properties have to be determined in vivo. At present, there are only few in vivo methods that can be applied to characterize the internal myocardium tissue mechanics. This work introduced and evaluated an FE inverse method to determine the myocardial tissue compressibility. Specifically, it combined an inverse FE method with the experimentally-measured left ventricular (LV) internal cavity pressure and volume versus time curves. Results indicated that the FE inverse method showed good correlation between LV repolarization and the variations in the myocardium tissue bulk modulus K (K = 1/compressibility), as well as provided an ability to describe in vivo human myocardium material behavior. The myocardium bulk modulus can be effectively used as a diagnostic tool of the heart ejection fraction. The model developed is proved to be robust and efficient. It offers a new perspective and means to the study of living-myocardium tissue properties, as it shows the variation of the bulk modulus throughout the cardiac cycle.
    Matched MeSH terms: Heart Ventricles/physiopathology*
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