Displaying publications 1 - 20 of 24 in total

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  1. 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: Myocardial Infarction/physiopathology*
  2. Ng WH, Ahmad Z
    Med J Malaysia, 1978 Dec;33(2):128-32.
    PMID: 755162
    Matched MeSH terms: Myocardial Infarction/physiopathology*
  3. Selvarajah S, Fong AY, Selvaraj G, Haniff J, Uiterwaal CS, Bots ML
    PLoS One, 2012;7(7):e40249.
    PMID: 22815733 DOI: 10.1371/journal.pone.0040249
    Risk stratification in ST-elevation myocardial infarction (STEMI) is important, such that the most resource intensive strategy is used to achieve the greatest clinical benefit. This is essential in developing countries with wide variation in health care facilities, scarce resources and increasing burden of cardiovascular diseases. This study sought to validate the Thrombolysis In Myocardial Infarction (TIMI) risk score for STEMI in a multi-ethnic developing country.
    Matched MeSH terms: Myocardial Infarction/physiopathology*
  4. Selvarajah S, Fong AY, Selvaraj G, Haniff J, Hairi NN, Bulgiba A, et al.
    Am J Cardiol, 2013 May 1;111(9):1270-6.
    PMID: 23415636 DOI: 10.1016/j.amjcard.2013.01.271
    Developing countries face challenges in providing the best reperfusion strategy for patients with ST-segment elevation myocardial infarction because of limited resources. This causes wide variation in the provision of cardiac care. The aim of this study was to assess the impact of variation in cardiac care provision and reperfusion strategies on patient outcomes in Malaysia. Data from a prospective national registry of acute coronary syndromes were used. Thirty-day all-cause mortality in 4,562 patients with ST-segment elevation myocardial infarctions was assessed by (1) cardiac care provision (specialist vs nonspecialist centers), and (2) primary reperfusion therapy (thrombolysis or primary percutaneous coronary intervention [P-PCI]). All patients were risk adjusted by Thrombolysis In Myocardial Infarction (TIMI) risk score. Thrombolytic therapy was administered to 75% of patients with ST-segment elevation myocardial infarctions (12% prehospital and 63% in-hospital fibrinolytics), 7.6% underwent P-PCI, and the remainder received conservative management. In-hospital acute reperfusion therapy was administered to 68% and 73% of patients at specialist and nonspecialist cardiac care facilities, respectively. Timely reperfusion was low, at 24% versus 31%, respectively, for in-hospital fibrinolysis and 28% for P-PCI. Specialist centers had statistically significantly higher use of evidence-based treatments. The adjusted 30-day mortality rates for in-hospital fibrinolytics and P-PCI were 7% (95% confidence interval 5% to 9%) and 7% (95% confidence interval 3% to 11%), respectively (p = 0.75). In conclusion, variation in cardiac care provision and reperfusion strategy did not adversely affect patient outcomes. However, to further improve cardiac care, increased use of evidence-based resources, improvement in the quality of P-PCI care, and reduction in door-to-reperfusion times should be achieved.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  5. Foo CY, Bonsu KO, Nallamothu BK, Reid CM, Dhippayom T, Reidpath DD, et al.
    Heart, 2018 08;104(16):1362-1369.
    PMID: 29437704 DOI: 10.1136/heartjnl-2017-312517
    OBJECTIVE: This study aims to determine the relationship between door-to-balloon delay in primary percutaneous coronary intervention and ST-elevation myocardial infarction (MI) outcomes and examine for potential effect modifiers.

    METHODS: We conducted a systematic review and meta-analysis of prospective observational studies that have investigated the relationship of door-to-balloon delay and clinical outcomes. The main outcomes include mortality and heart failure.

    RESULTS: 32 studies involving 299 320 patients contained adequate data for quantitative reporting. Patients with ST-elevation MI who experienced longer (>90 min) door-to-balloon delay had a higher risk of short-term mortality (pooled OR 1.52, 95% CI 1.40 to 1.65) and medium-term to long-term mortality (pooled OR 1.53, 95% CI 1.13 to 2.06). A non-linear time-risk relation was observed (P=0.004 for non-linearity). The association between longer door-to-balloon delay and short-term mortality differed between those presented early and late after symptom onset (Cochran's Q 3.88, P value 0.049) with a stronger relationship among those with shorter prehospital delays.

    CONCLUSION: Longer door-to-balloon delay in primary percutaneous coronary intervention for ST-elevation MI is related to higher risk of adverse outcomes. Prehospital delays modified this effect. The non-linearity of the time-risk relation might explain the lack of population effect despite an improved door-to-balloon time in the USA.

    CLINICAL TRIAL REGISTRATION: PROSPERO (CRD42015026069).

    Matched MeSH terms: ST Elevation Myocardial Infarction/physiopathology
  6. Chin SP, Poey AC, Wong CY, Chang SK, Teh W, Mohr TJ, et al.
    Cytotherapy, 2010;12(1):31-7.
    PMID: 19878080 DOI: 10.3109/14653240903313966
    Bone marrow (BM) mesenchymal stromal cells (MSC) represent a novel therapy for severe heart failure with extensive myocardial scarring, especially when performed concurrently with conventional revascularization. However, stem cells are difficult to transport in culture media without risk of contamination, infection and reduced viability. We tested the feasibility and safety of off-site MSC culture and expansion with freeze-controlled cryopreservation and subsequent rapid thawing of cells immediately prior to implantation to treat severe dilated ischemic cardiomyopathy.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  7. Leong CN, Lim E, Andriyana A, Al Abed A, Lovell NH, Hayward C, et al.
    PMID: 27043925 DOI: 10.1002/cnm.2794
    Infarct extension, a process involving progressive extension of the infarct zone (IZ) into the normally perfused border zone (BZ), leads to continuous degradation of the myocardial function and adverse remodelling. Despite carrying a high risk of mortality, detailed understanding of the mechanisms leading to BZ hypoxia and infarct extension remains unexplored. In the present study, we developed a 3D truncated ellipsoidal left ventricular model incorporating realistic electromechanical properties and fibre orientation to examine the mechanical interaction among the remote, infarct and BZs in the presence of varying infarct transmural extent (TME). Localized highly abnormal systolic fibre stress was observed at the BZ, owing to the simultaneous presence of moderately increased stiffness and fibre strain at this region, caused by the mechanical tethering effect imposed by the overstretched IZ. Our simulations also demonstrated the greatest tethering effect and stress in BZ regions with fibre direction tangential to the BZ-remote zone boundary. This can be explained by the lower stiffness in the cross-fibre direction, which gave rise to a greater stretching of the IZ in this direction. The average fibre strain of the IZ, as well as the maximum stress in the sub-endocardial layer, increased steeply from 10% to 50% infarct TME, and slower thereafter. Based on our stress-strain loop analysis, we found impairment in the myocardial energy efficiency and elevated energy expenditure with increasing infarct TME, which we believe to place the BZ at further risk of hypoxia. Copyright © 2016 John Wiley & Sons, Ltd.
    Matched MeSH terms: Myocardial Infarction/physiopathology*
  8. Khalil MI, Tanvir EM, Afroz R, Sulaiman SA, Gan SH
    Biomed Res Int, 2015;2015:286051.
    PMID: 26064893 DOI: 10.1155/2015/286051
    The present study was designed to investigate the cardioprotective effects of Malaysian Tualang honey against isoproterenol- (ISO-) induced myocardial infarction (MI) in rats by investigating changes in the levels of cardiac marker enzymes, cardiac troponin I (cTnI), triglycerides (TG), total cholesterol (TC), lipid peroxidation (LPO) products, and antioxidant defense system combined with histopathological examination. Male albino Wistar rats (n = 40) were pretreated orally with Tualang honey (3 g/kg/day) for 45 days. Subcutaneous injection of ISO (85 mg/kg in saline) for two consecutive days caused a significant increase in serum cardiac marker enzymes (creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate transaminase (AST)), cTnI, serum TC, and TG levels. In addition, ISO-induced myocardial injury was confirmed by a significant increase in heart lipid peroxidation (LPO) products (TBARS) and a significant decrease in antioxidant enzymes (SOD, GPx, GRx, and GST). Pretreatment of ischemic rats with Tualang honey conferred significant protective effects on all of the investigated biochemical parameters. The biochemical findings were further confirmed by histopathological examination in both Tualang-honey-pretreated and ISO-treated hearts. The present study demonstrates that Tualang honey confers cardioprotective effects on ISO-induced oxidative stress by contributing to endogenous antioxidant enzyme activity via inhibition of lipid peroxidation.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  9. Hishamuddin HM, Azmi NN, Jackson N
    Singapore Med J, 1993 Aug;34(4):316-8.
    PMID: 8266202
    Thrombolytic therapy is a well-established therapy in acute myocardial infarction (AMI), reducing mortality and infarct size. This study is a retrospective analysis of survival and complications after the use of streptokinase at Hospital Universiti Sains Malaysia. Streptokinase was first used here in March 1990. Between then and February 1992, 126 patients were admitted to the Coronary Care Unit. Thirty-two patients who fulfilled our criteria for thrombolytic treatment were given an hour intravenous infusion of 1.5 MU streptokinase, and started on aspirin. A control group of 64 patients selected from before March 1990, and matched for age, sex and site of infarct, was given standard therapy. The survival at 4 weeks post-AMI was 91% in the streptokinase therapy group and 91% in both groups (p > 0.05). The complications encountered were reperfusion arrhythmias (2 patients), hypotension(1), maculopapular rash(1) and gum bleeding(1). None of these complications were statistically increased when compared to the control group and none resulted in the death of a patient. We conclude that streptokinase therapy can be given safely in a rural Malaysian setting. Our survival and complication rates are comparable with other published series.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  10. Kannan P, Raman S, Ramani VS, Jeyamalar R
    Aust N Z J Obstet Gynaecol, 1993 Nov;33(4):424-6.
    PMID: 8179560
    Matched MeSH terms: Myocardial Infarction/physiopathology
  11. Musa S, Xin LZ, Govindasamy V, Fuen FW, Kasim NH
    Expert Opin Biol Ther, 2014 Jan;14(1):63-73.
    PMID: 24191782 DOI: 10.1517/14712598.2014.858694
    Acute myocardial infarction is the primary cause of heart disease-related death in the world. Reperfusion therapy is currently the backbone of treatment for acute myocardial infarction albeit with many limitations. With the emergence of stem cells as potential therapeutic agents, attempts in using them to enhance cardiac function have increased exponentially. However, it has its own disadvantages, and we postulate that the primary drawback is choosing the right cell type and solving this may significantly contribute to ambitious goal of using stem cells in the regeneration medicine.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  12. Liew CK, Leong WS
    Med J Malaysia, 2012 Feb;67(1):108-10.
    PMID: 22582559 MyJurnal
    Coronary arteries vasospasm (CAS) is commonly seen in invasive cardiology laboratory during diagnostic catheterization or coronary intervention. Though the incidence of Printzmetal angina is uncommon, coronary vasospasm resulting in acute myocardial infarct is rare, especially if there is no significant atherosclerotic plaque within the coronary vasculature.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  13. Chan BT, Yeoh HK, Liew YM, Dokos S, Al Abed A, Chee KH, et al.
    Coron Artery Dis, 2018 06;29(4):316-324.
    PMID: 29261521 DOI: 10.1097/MCA.0000000000000596
    OBJECTIVE: This study investigated the intraventricular flow dynamics in ischaemic heart disease patients.

    PATIENTS AND METHODS: Fourteen patients with normal ejection fraction and 16 patients with reduced ejection fraction were compared with 20 healthy individuals. Phase-contrast MRI was used to assess intraventricular flow variables and speckle-tracking echocardiography to assess myocardial strain and left ventricular (LV) dyssynchrony. Infarct size was acquired using delayed-enhancement MRI.

    RESULTS: The results obtained showed no significant differences in intraventricular flow variables between the healthy group and the patients with normal ejection fraction group, whereas considerable reductions in kinetic energy (KE) fluctuation index, E' (P<0.001) and vortex KE (P=0.003) were found in the patients with reduced ejection fraction group. In multivariate analysis, only vortex KE and infarct size were significantly related to LV ejection fraction (P<0.001); furthermore, vortex KE was correlated negatively with energy dissipation, energy dissipation index (r=-0.44, P=0.021).

    CONCLUSION: This study highlights that flow energetic indices have limited applicability as early predictors of LV progressive dysfunction, whereas vortex KE could be an alternative to LV performance.

    Matched MeSH terms: ST Elevation Myocardial Infarction/physiopathology*
  14. 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: Myocardial Infarction/physiopathology*
  15. Quek DK, Ong SB, Lim LY
    Med J Malaysia, 1989 Mar;44(1):14-22.
    PMID: 2626108
    Circadian variations have been observed in the onset of acute coronary syndromes including acute myocardial infarction. We studied 422 acute myocardial infarction patients who presented to the coronary care unit of General Hospital Kuala Lumpur. Of the 318 (75.4%) patients whose data was complete, a circadian rhythm with bimodal peak was demonstrated. The second quarter of the day i.e. 6.00 a.m. to 12 noon was shown to have a significantly increased frequency of onset of acute myocardial infarction (p less than 0.05). Time delay in presenting to the hospital was also determined. This showed that 56.8% of acute myocardial infarction patients presented early, within four hours of the onset of symptoms. By six hours, more than 71% had sought hospital care. This early presentation to the hospital may offer a realistic opportunity for optimal thrombolytic therapy should this treatment modality be offered as routine to infarct patients.
    Matched MeSH terms: Myocardial Infarction/physiopathology*
  16. Wickramatilake CM, Mohideen MR, Pathirana C
    Indian Heart J, 2017 02 12;69(2):291.
    PMID: 28460787 DOI: 10.1016/j.ihj.2017.02.002
    Matched MeSH terms: ST Elevation Myocardial Infarction/physiopathology
  17. Jasmin R, Ng CT, Sockalingam S, Yahya F, Cheah TE, Sadiq MA
    Lupus, 2013 Dec;22(14):1518-22.
    PMID: 24004952 DOI: 10.1177/0961203313503913
    We report a 13-year-old girl diagnosed with systemic lupus erythematosus (SLE) who presented with left-sided chest pain, with ECG changes and elevation troponins that were suggestive of an acute inferior wall myocardial infarction (MI). Her multi-slice computed tomography coronary angiogram and standard angiogram were normal. The cardiac magnetic resonance imaging revealed an area of infarcted myocardium that was in the right coronary artery territory. We believe her MI was most likely secondary to coronary vasospasm. MI is rare and coronary vasospasm is an uncommon cause of MI in children and adolescents with SLE.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  18. Gupta ED, Sakthiswary R
    Asian Cardiovasc Thorac Ann, 2014 May;22(4):397-401.
    PMID: 24771726 DOI: 10.1177/0218492313484917
    The objectives of this study were to determine the incidence of a myocardial infarction "false alarm" and evaluate the efficacy of the initial electrocardiogram and cardiac enzymes in diagnosing myocardial infarction in Malaysia.
    Matched MeSH terms: Myocardial Infarction/physiopathology
  19. Soo CS
    Singapore Med J, 1995 Apr;36(2):216, 236-7.
    PMID: 7676272
    Matched MeSH terms: Myocardial Infarction/physiopathology
  20. Tan JH, Ng ZQ, Vendargon S
    BMJ Case Rep, 2018 Apr 17;2018.
    PMID: 29666108 DOI: 10.1136/bcr-2018-225271
    Matched MeSH terms: Non-ST Elevated Myocardial Infarction/physiopathology
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