Displaying publications 121 - 140 of 560 in total

Abstract:
Sort:
  1. Sazlina SG, Sooryanarayana R, Ho BK, Omar MA, Krishnapillai AD, Mohd Tohit N, et al.
    PLoS One, 2020;15(10):e0240826.
    PMID: 33085718 DOI: 10.1371/journal.pone.0240826
    Study on cardiovascular disease (CVD) risk factors and their prevalence among the older people in Malaysia is limited. We aimed to determine the prevalence and factors associated with CVD risk factors using the non-laboratory Framingham Generalized 10-Year CVD risk score among older people in Malaysia. This was a population-based cross-sectional study using data of 3,375 participants aged ≥60 years from the National Health and Morbidity Survey 2015. Sociodemographic, health factors and clinical assessments (anthropometry and blood pressure) were included. Complex survey analysis was used to obtain prevalence with 95% confidence intervals (CI). We applied ordinal regression to determine the factors associated with CVD risk. The prevalence for the high 10-year CVD risk was 72.1%. Body mass index was higher among those aged 60-69 years in men (25.4kg/m2, 95%CI 25.1-25.8) and women (26.7kg/m2, 95%CI 26.3-27.1) than the other age groups. The factors associated with moderate and high 10-year CVD risk were Malay ethnicity (Odds Ratio(OR) 0.76, 95%CI 0.63-0.92, p = 0.004), unmarried status (OR 1.55, 95%CI 1.22-1.97, p<0.001) and physically inactive (OR 0.72, 95%CI 0.55-0.95, p = 0.020). There is a need for future study to evaluate preventive strategies to improve the health of older people in order to promote healthy ageing.
    Matched MeSH terms: Cardiovascular Diseases/epidemiology*; Cardiovascular Diseases/physiopathology*
  2. Daud A, Sedek SSHAB, Shahadan SZ
    Enferm Clin, 2019 09;29 Suppl 2:96-100.
    PMID: 31248730 DOI: 10.1016/j.enfcli.2019.04.015
    OBJECTIVE: This study aims to assess the association between the walking time spent and high sensitivity C-reactive protein (hs-CRP) level to determine the risk for cardiovascular disease (CVD) among obese women.

    METHODS: Cross-sectional study was conducted in Kuantan, Pahang. The purposive sampling method was chosen. 76 obese women aged 18 years old and above were included in the study. Data were collected by using the set of the self-reported questionnaire consisted of socio-demographic and the walking time for the past 7 days. The sample blood test was taken to check for hs-CRP level.

    RESULTS: Walking time spent in minutes was found to be significantly inverse associated with the hs-CRP level (p=0.040) among obese women.

    CONCLUSION: The increase in walking time spent can help reduce the hs-CRP level, therefore reduce the risk for CVD.

    Matched MeSH terms: Cardiovascular Diseases/etiology; Cardiovascular Diseases/epidemiology
  3. Leong SL, Chaiyakunapruk N, Tassaneeyakul W, Arunmanakul P, Nathisuwan S, Lee SWH
    Int J Cardiol, 2019 04 01;280:190-197.
    PMID: 30594345 DOI: 10.1016/j.ijcard.2018.12.049
    BACKGROUND: Exploration on genetic roles in antineoplastic-related cardiovascular toxicity has increased with the advancement of genotyping technology. However, knowledge on the extent of genetic determinants in affecting the susceptibility to the cardiovascular toxicities of antineoplastic is limited. This study aims to identify potential single nucleotide polymorphism (SNP) in predicting non-anthracycline antineoplastic-related cardiovascular toxicity.

    METHODS: We systematically searched for original research in PubMed, Cochrane Central Register of Controlled Studies, CINAHL Plus, EMBASE and HuGE Navigator from database inception until January 2018. Studies on association between polymorphism and antineoplastic-induced cardiovascular toxicity in patients treated for cancer of all antineoplastic agents were included except for anthracycline. Case reports, conference abstracts, reviews and non-patient studies were excluded. Data extracted by two independent reviewers were combined with random-effects model and reported according to PRISMA and MOOSE guidelines.

    RESULTS: The 35 studies included examined a total of 219 SNPs in 80 genes, 11 antineoplastic and 5 types of cardiovascular toxicities. Meta-analyses showed that human epidermal growth factor receptor 2 (HER2) rs1136201, a risk variants (pooled OR: 2.43; 1.17-5.06, p = 0.018) is a potential predictors for trastuzumab-related cardiotoxicity. Gene dose effect analysis showed number of variant allele may contribute to the risk too.

    CONCLUSIONS: This review found that HER2 rs1136201 can have the potential in predicting trastuzumab-related heart failure. As such, further studies are needed to confirm the validity of these results as well as determine the economic aspect of using SNPs prior to its implementation as a clinical practice.

    Matched MeSH terms: Cardiovascular Diseases/chemically induced*; Cardiovascular Diseases/genetics*
  4. Gan R, Rosoman NP, Henshaw DJE, Noble EP, Georgius P, Sommerfeld N
    Med Hypotheses, 2020 Nov;144:110024.
    PMID: 32758871 DOI: 10.1016/j.mehy.2020.110024
    SARS-CoV-2, the agent of COVID-19, shares a lineage with SARS-CoV-1, and a common fatal pulmonary profile but with striking differences in presentation, clinical course, and response to treatment. In contrast to SARS-CoV-1 (SARS), COVID-19 has presented as an often bi-phasic, multi-organ pathology, with a proclivity for severe disease in the elderly and those with hypertension, diabetes and cardiovascular disease. Whilst death is usually related to respiratory collapse, autopsy reveals multi-organ pathology. Chronic pulmonary disease is underrepresented in the group with severe COVID-19. A commonality of aberrant renin angiotensin system (RAS) is suggested in the at-risk group. The identification of angiotensin-converting-enzyme 2 (ACE2) as the receptor allowing viral entry to cells precipitated our interest in the role of ACE2 in COVID-19 pathogenesis. We propose that COVID-19 is a viral multisystem disease, with dominant vascular pathology, mediated by global reduction in ACE2 function, pronounced in disease conditions with RAS bias toward angiotensin-converting-enzyme (ACE) over ACE2. It is further complicated by organ specific pathology related to loss of ACE2 expressing cells particularly affecting the endothelium, alveolus, glomerulus and cardiac microvasculature. The possible upregulation in ACE2 receptor expression may predispose individuals with aberrant RAS status to higher viral load on infection and relatively more cell loss. Relative ACE2 deficiency leads to enhanced and protracted tissue, and vessel exposure to angiotensin II, characterised by vasoconstriction, enhanced thrombosis, cell proliferation and recruitment, increased tissue permeability, and cytokine production (including IL-6) resulting in inflammation. Additionally, there is a profound loss of the "protective" angiotensin (1-7), a vasodilator with anti-inflammatory, anti-thrombotic, antiproliferative, antifibrotic, anti-arrhythmic, and antioxidant activity. Our model predicts global vascular insult related to direct endothelial cell damage, vasoconstriction and thrombosis with a disease specific cytokine profile related to angiotensin II rather than "cytokine storm". Our proposed mechanism of lung injury provides an explanation for early hypoxia without reduction in lung compliance and suggests a need for revision of treatment protocols to address vasoconstriction, thromboprophylaxis, and to minimize additional small airways and alveolar trauma via ventilation choice. Our model predicts long term sequelae of scarring/fibrosis in vessels, lungs, renal and cardiac tissue with protracted illness in at-risk individuals. It is hoped that our model stimulates review of current diagnostic and therapeutic intervention protocols, particularly with respect to early anticoagulation, vasodilatation and revision of ventilatory support choices.
    Matched MeSH terms: Cardiovascular Diseases/complications; Cardiovascular Diseases/physiopathology
  5. Thomas S, Borges F, Bhandari M, De Beer J, Urrútia Cuchí G, Adili A, et al.
    J Bone Joint Surg Am, 2020 May 20;102(10):880-888.
    PMID: 32118652 DOI: 10.2106/JBJS.18.01305
    BACKGROUND: Myocardial injury after noncardiac surgery (MINS) is common and of prognostic importance. Little is known about MINS in orthopaedic surgery. The diagnostic criterion for MINS was a level of ≥0.03 ng/mL on a non-high-sensitivity troponin T (TnT) assay due to myocardial ischemia.

    METHODS: We undertook an international, prospective study of 15,103 patients ≥45 years of age who had inpatient noncardiac surgery; 3,092 underwent orthopaedic surgery. Non-high-sensitivity TnT assays were performed on postoperative days 0, 1, 2, and 3. Among orthopaedic patients, we determined (1) the prognostic relevance of the MINS diagnostic criteria, (2) the 30-day mortality rate for those with and without MINS, and (3) the probable proportion of MINS cases that would go undetected without troponin monitoring because of a lack of an ischemic symptom.

    RESULTS: Three hundred and sixty-seven orthopaedic patients (11.9%) had MINS. MINS was associated independently with 30-day mortality including among those who had had orthopaedic surgery. Orthopaedic patients without and with MINS had a 30-day mortality rate of 1.0% and 9.8%, respectively (odds ratio [OR], 11.28; 95% confidence interval [CI], 6.72 to 18.92). The 30-day mortality rate was increased for patients with MINS who had an ischemic feature (i.e., symptoms, or evidence of ischemia on electrocardiography or imaging) (OR, 18.25; 95% CI, 10.06 to 33.10) and for those who did not have an ischemic feature (OR, 7.35; 95% CI, 3.37 to 16.01). The proportion of orthopaedic patients with MINS who were asymptomatic and in whom the myocardial injury would have probably gone undetected without TnT monitoring was 81.3% (95% CI, 76.3% to 85.4%).

    CONCLUSIONS: One in 8 orthopaedic patients in our study had MINS, and MINS was associated with a higher mortality rate regardless of symptoms. Troponin levels should be measured after surgery in at-risk patients because most MINS cases (>80%) are asymptomatic and would go undetected without routine measurements.

    LEVEL OF EVIDENCE: Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence.

    Matched MeSH terms: Cardiovascular Diseases/mortality; Cardiovascular Diseases/epidemiology*
  6. Ahmad Zamri L, Appannah G, Zahari Sham SY, Mansor F, Ambak R, Mohd Nor NS, et al.
    J Obes, 2020;2020:3198326.
    PMID: 32399286 DOI: 10.1155/2020/3198326
    Objectives: To examine the association of weight loss magnitude with changes in cardiometabolic risk markers in overweight and obese women from low socioeconomic areas engaged in a lifestyle intervention.

    Methods: Analyses were performed on 243 women (mean body mass index 31.27 ± 4.14 kg/m2) who completed a 12-month lifestyle intervention in low socioeconomic communities in Klang Valley, Malaysia. Analysis of covariance (ANCOVA) was used to compare changes of cardiometabolic risk factors across weight change categories (2% gain, ±2% maintain, >2 to <5% loss, and 5 to 20% loss) within intervention and control group.

    Results: A graded association for changes in waist circumference, fasting insulin, and total cholesterol (p=0.002, for all variables) across the weight change categories were observed within the intervention group at six months postintervention. Participants who lost 5 to 20% of weight had the greatest improvements in those risk markers (-5.67 cm CI: -7.98 to -3.36, -4.27 μU/mL CI: -7.35, -1.19, and -0.59 mmol/L CI: -.99, -0.19, respectively) compared to those who did not. Those who lost >2% to <5% weight reduced more waist circumference (-4.24 cm CI: -5.44 to -3.04) and fasting insulin (-0.36 μU/mL CI: -1.95 to 1.24) than those who maintained or gained weight. No significant association was detected in changes of risk markers across the weight change categories within the control group except for waist circumference and adiponectin.

    Conclusion: Weight loss of >2 to <5% obtained through lifestyle intervention may represent a reasonable initial weight loss target for women in the low socioeconomic community as it led to improvements in selected risk markers, particularly of diabetes risk.

    Matched MeSH terms: Cardiovascular Diseases/etiology; Cardiovascular Diseases/prevention & control*
  7. Syafruddin SE, Mohtar MA, Wan Mohamad Nazarie WF, Low TY
    Biomolecules, 2020 09 28;10(10).
    PMID: 32998281 DOI: 10.3390/biom10101378
    The Krüppel-like factors (KLFs) family of proteins control several key biological processes that include proliferation, differentiation, metabolism, apoptosis and inflammation. Dysregulation of KLF functions have been shown to disrupt cellular homeostasis and contribute to disease development. KLF6 is a relevant example; a range of functional and expression assays suggested that the dysregulation of KLF6 contributes to the onset of cancer, inflammation-associated diseases as well as cardiovascular diseases. KLF6 expression is either suppressed or elevated depending on the disease, and this is largely due to alternative splicing events producing KLF6 isoforms with specialised functions. Hence, the aim of this review is to discuss the known aspects of KLF6 biology that covers the gene and protein architecture, gene regulation, post-translational modifications and functions of KLF6 in health and diseases. We put special emphasis on the equivocal roles of its full-length and spliced variants. We also deliberate on the therapeutic strategies of KLF6 and its associated signalling pathways. Finally, we provide compelling basic and clinical questions to enhance the knowledge and research on elucidating the roles of KLF6 in physiological and pathophysiological processes.
    Matched MeSH terms: Cardiovascular Diseases/metabolism; Cardiovascular Diseases/physiopathology*
  8. Saffian SM, Duffull SB, Wright D
    Clin. Pharmacol. Ther., 2017 Aug;102(2):297-304.
    PMID: 28160278 DOI: 10.1002/cpt.649
    There is preliminary evidence to suggest that some published warfarin dosing algorithms produce biased maintenance dose predictions in patients who require higher than average doses. We conducted a meta-analysis of warfarin dosing algorithms to determine if there exists a systematic under- or overprediction of dose requirements for patients requiring ≥7 mg/day across published algorithms. Medline and Embase databases were searched up to September 2015. We quantified the proportion of over- and underpredicted doses in patients whose observed maintenance dose was ≥7 mg/day. The meta-analysis included 47 evaluations of 22 different warfarin dosing algorithms from 16 studies. The meta-analysis included data from 1,492 patients who required warfarin doses of ≥7 mg/day. All 22 algorithms were found to underpredict warfarin dosing requirements in patients who required ≥7 mg/day by an average of 2.3 mg/day with a pooled estimate of underpredicted doses of 92.3% (95% confidence interval 90.3-94.1, I(2) = 24%).
    Matched MeSH terms: Cardiovascular Diseases/diagnosis; Cardiovascular Diseases/drug therapy*
  9. Nishimura A, Sunggip C, Oda S, Numaga-Tomita T, Tsuda M, Nishida M
    Pharmacol Ther, 2017 Dec;180:113-128.
    PMID: 28648830 DOI: 10.1016/j.pharmthera.2017.06.010
    Purinergic signaling, mediated mainly by G protein-coupled P2Y receptors (P2YRs), is now attracting attention as a new therapeutic target for preventing or treating cardiovascular diseases. Observations using mice with genetically modified P2YRs and/or treated with a pharmacological P2YR inhibitor have helped us understand the physiological and pathological significance of P2YRs in the cardiovascular system. P2YR-mediated biological functions are predominantly activated by mononucleotides released from non-adrenergic, non-cholinergic nerve endings or non-secretory tissues in response to physical stress or cell injury, though recent studies have suggested the occurrence of ligand-independent P2YR function through receptor-receptor interactions (oligomerization) in several biological processes. In this review, we introduce the functions of P2YRs and possible dimerization with G protein-coupled receptors (GPCRs) in the cardiovascular system. We focus especially on the crosstalk between uridine nucleotide-responsive P2Y6R and angiotensin (Ang) II type1 receptor (AT1R) signaling, and introduce our recent finding that the P2Y6R antagonist MRS2578 interrupts heterodimerization between P2Y6R and AT1R, thereby reducing the risk of AT1R-stimulated hypertension in mice. These results strongly suggest that targeting P2Y6R oligomerization could be an effective new strategy to reduce the risk of cardiovascular diseases.
    Matched MeSH terms: Cardiovascular Diseases/drug therapy*; Cardiovascular Diseases/metabolism
  10. Jeyamalar R, Wan Azman WA, Nawawi H, Choo GH, Ng WK, Rosli MA, et al.
    Med J Malaysia, 2018 06;73(3):154-162.
    PMID: 29962499 MyJurnal
    Cardiovascular disease (CVD) has been the main cause of mortality and an important cause of morbidity in Malaysia for several years. To reduce global cardiovascular (CV) risk in the population, primary preventive strategies need to be implemented. Hypercholesterolaemia is one of the major risk factors for CVD. This paper is an expert review on the management of hypercholesterolemia focusing on high and very high risk individuals. In low and Intermediate risk individuals, therapeutic lifestyle changes (TLC) and a healthy lifestyle alone may suffice. In high and very high risk individuals, drug therapy in conjunction with TLC are necessary to achieve the target LDL-C levels which have been shown to slow down progression and sometimes even result in regression of atherosclerotic plaques. Statins are first-line drugs because they have been shown in numerous randomized controlled trials to be effective in reducing CV events and to be safe. In some high risk individuals, despite maximally tolerated statin therapy, target Low Density Lipoprotein Cholesterol (LDL-C) levels are not achieved. These include those with familial hypercholesterolaemia and statin intolerance. This paper discusses non-statin therapies, such as ezetimibe and the newer Proprotein convertase subtilisin/kexin type 9 Inhibitors (PCSK9-i).
    Matched MeSH terms: Cardiovascular Diseases/etiology; Cardiovascular Diseases/prevention & control*
  11. Cheong AT, Khoo EM, Tong SF, Liew SM
    PLoS One, 2016;11(7):e0159438.
    PMID: 27415432 DOI: 10.1371/journal.pone.0159438
    BACKGROUND: More than half of the general population does not attend screening for cardiovascular diseases (CVD) hence they are unaware of their risks. The objective of this study was to explore the views and experiences of the public in deciding to undergo health checks for CVD prevention.

    METHODS: This was a qualitative study utilising the constructivist grounded theory approach. A total of 31 individuals aged 30 years and above from the community were sampled purposively. Eight interviews and six focus groups were involved, using a semi-structured topic guide.

    RESULTS: A conceptual framework was developed to explain the public's decision-making process on health check participation for CVD prevention. The intention to participate in health checks was influenced by the interplay between perceived relevance and the individual's readiness to face the outcome of health checks. Health checks were deemed relevant if people perceived themselves to be at risk of CVD and there was an advantage in knowing their cardiovascular status. People were ready to face the outcome of health checks if they wanted to know the results and were prepared to deal with the subsequent management. The decision to participate in health checks was also influenced by external factors such as the views of significant others, and the accessibility and availability of resources including time and finances.

    CONCLUSIONS: The intention to screen for CVD is motivated by two internal factors: the perceived relevance of the disease and readiness to face screening outcomes. Strategies targeting the internal decision-making process may prove to be key in improving the uptake of screening.

    Matched MeSH terms: Cardiovascular Diseases/prevention & control*; Cardiovascular Diseases/psychology
  12. Thomas B, Matsushita K, Abate KH, Al-Aly Z, Ärnlöv J, Asayama K, et al.
    J Am Soc Nephrol, 2017 Jul;28(7):2167-2179.
    PMID: 28408440 DOI: 10.1681/ASN.2016050562
    The burden of premature death and health loss from ESRD is well described. Less is known regarding the burden of cardiovascular disease attributable to reduced GFR. We estimated the prevalence of reduced GFR categories 3, 4, and 5 (not on RRT) for 188 countries at six time points from 1990 to 2013. Relative risks of cardiovascular outcomes by three categories of reduced GFR were calculated by pooled random effects meta-analysis. Results are presented as deaths for outcomes of cardiovascular disease and ESRD and as disability-adjusted life years for outcomes of cardiovascular disease, GFR categories 3, 4, and 5, and ESRD. In 2013, reduced GFR was associated with 4% of deaths worldwide, or 2.2 million deaths (95% uncertainty interval [95% UI], 2.0 to 2.4 million). More than half of these attributable deaths were cardiovascular deaths (1.2 million; 95% UI, 1.1 to 1.4 million), whereas 0.96 million (95% UI, 0.81 to 1.0 million) were ESRD-related deaths. Compared with metabolic risk factors, reduced GFR ranked below high systolic BP, high body mass index, and high fasting plasma glucose, and similarly with high total cholesterol as a risk factor for disability-adjusted life years in both developed and developing world regions. In conclusion, by 2013, cardiovascular deaths attributed to reduced GFR outnumbered ESRD deaths throughout the world. Studies are needed to evaluate the benefit of early detection of CKD and treatment to decrease these deaths.
    Matched MeSH terms: Cardiovascular Diseases/etiology*; Cardiovascular Diseases/epidemiology*
  13. Perak AM, Lancki N, Kuang A, Labarthe DR, Allen NB, Shah SH, et al.
    JAMA, 2021 02 16;325(7):658-668.
    PMID: 33591345 DOI: 10.1001/jama.2021.0247
    Importance: Pregnancy may be a key window to optimize cardiovascular health (CVH) for the mother and influence lifelong CVH for her child.

    Objective: To examine associations between maternal gestational CVH and offspring CVH.

    Design, Setting, and Participants: This cohort study used data from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study (examinations: July 2000-April 2006) and HAPO Follow-Up Study (examinations: February 2013-December 2016). The analyses included 2302 mother-child dyads, comprising 48% of HAPO Follow-Up Study participants, in an ancillary CVH study. Participants were from 9 field centers across the United States, Barbados, United Kingdom, China, Thailand, and Canada.

    Exposures: Maternal gestational CVH at a target of 28 weeks' gestation, based on 5 metrics: body mass index, blood pressure, total cholesterol level, glucose level, and smoking. Each metric was categorized as ideal, intermediate, or poor using pregnancy guidelines. Total CVH was categorized as follows: all ideal metrics, 1 or more intermediate (but 0 poor) metrics, 1 poor metric, or 2 or more poor metrics.

    Main Outcomes and Measures: Offspring CVH at ages 10 to 14 years, based on 4 metrics: body mass index, blood pressure, total cholesterol level, and glucose level. Total CVH was categorized as for mothers.

    Results: Among 2302 dyads, the mean (SD) ages were 29.6 (2.7) years for pregnant mothers and 11.3 (1.1) years for children. During pregnancy, the mean (SD) maternal CVH score was 8.6 (1.4) out of 10. Among pregnant mothers, the prevalence of all ideal metrics was 32.8% (95% CI, 30.6%-35.1%), 31.7% (95% CI, 29.4%-34.0%) for 1 or more intermediate metrics, 29.5% (95% CI, 27.2%-31.7%) for 1 poor metric, and 6.0% (95% CI, 3.8%-8.3%) for 2 or more poor metrics. Among children of mothers with all ideal metrics, the prevalence of all ideal metrics was 42.2% (95% CI, 38.4%-46.2%), 36.7% (95% CI, 32.9%-40.7%) for 1 or more intermediate metrics, 18.4% (95% CI, 14.6%-22.4%) for 1 poor metric, and 2.6% (95% CI, 0%-6.6%) for 2 or more poor metrics. Among children of mothers with 2 or more poor metrics, the prevalence of all ideal metrics was 30.7% (95% CI, 22.0%-40.4%), 28.3% (95% CI, 19.7%-38.1%) for 1 or more intermediate metrics, 30.7% (95% CI, 22.0%-40.4%) for 1 poor metric, and 10.2% (95% CI, 1.6%-20.0%) for 2 or more poor metrics. The adjusted relative risks associated with 1 or more intermediate, 1 poor, and 2 or more poor (vs all ideal) metrics, respectively, in mothers during pregnancy were 1.17 (95% CI, 0.96-1.42), 1.66 (95% CI, 1.39-1.99), and 2.02 (95% CI, 1.55-2.64) for offspring to have 1 poor (vs all ideal) metrics, and the relative risks were 2.15 (95% CI, 1.23-3.75), 3.32 (95% CI,1.96-5.62), and 7.82 (95% CI, 4.12-14.85) for offspring to have 2 or more poor (vs all ideal) metrics. Additional adjustment for categorical birth factors (eg, preeclampsia) did not fully explain these significant associations (eg, relative risk for association between 2 or more poor metrics among mothers during pregnancy and 2 or more poor metrics among offspring after adjustment for an extended set of birth factors, 6.23 [95% CI, 3.03-12.82]).

    Conclusions and Relevance: In this multinational cohort, better maternal CVH at 28 weeks' gestation was significantly associated with better offspring CVH at ages 10 to 14 years.

    Matched MeSH terms: Cardiovascular Diseases/epidemiology; Cardiovascular Diseases/prevention & control
  14. Thangiah N, Su TT, Chinna K, Jalaludin MY, Mohamed MNA, Majid HA
    Sci Rep, 2021 09 27;11(1):19135.
    PMID: 34580328 DOI: 10.1038/s41598-021-98127-0
    The study aims to create a composite risk index of CVD among adolescents and examine the influence of demographic, socioeconomic and lifestyle-related risk factors on the composite risk index of biological CVD risk factors among adolescents in Malaysia. A Malaysian adolescent cohort of 1320 adolescents were assessed at 13, 15 and 17 years. Seven biological CVD risk factors with moderate correlation were identified, standardized and averaged to form a composite CVD risk index. Generalised estimating equation using longitudinal linear regression was used to examine the effects of changes in adolescent lifestyle-related risk factors on the composite CVD risk index over time. From the ages 13 to 17 years, physical fitness (β = - 0.001, 90% CI = - 0.003, 0.00002) and BMI (β = 0.051, 95% CI = 0.042, 0.060) were significant predictors of attaining high scores of CVD risk. Female (β = 0.118, 95% CI = 0.040, 0.197), Chinese (β = 0.122, 95% CI = 0.006, 0.239), Indians (β = - 0.114, 95% CI = - 0.216, - 0.012) and adolescents from rural schools (β = 0.066, 95% CI = - 0.005, 0.136) were also found to be considerably significant. A more robust and gender-specific intervention programme focusing on healthy lifestyle (including achieving ideal BMI and improving physical fitness) need to be implemented among school-going adolescents.
    Matched MeSH terms: Cardiovascular Diseases/epidemiology*; Cardiovascular Diseases/prevention & control
  15. Mente A, Dehghan M, Rangarajan S, McQueen M, Dagenais G, Wielgosz A, et al.
    Lancet Diabetes Endocrinol, 2017 10;5(10):774-787.
    PMID: 28864143 DOI: 10.1016/S2213-8587(17)30283-8
    BACKGROUND: The relation between dietary nutrients and cardiovascular disease risk markers in many regions worldwide is unknown. In this study, we investigated the effect of dietary nutrients on blood lipids and blood pressure, two of the most important risk factors for cardiovascular disease, in low-income, middle-income, and high-income countries.

    METHODS: We studied 125 287 participants from 18 countries in North America, South America, Europe, Africa, and Asia in the Prospective Urban Rural Epidemiology (PURE) study. Habitual food intake was measured with validated food frequency questionnaires. We assessed the associations between nutrients (total fats, saturated fatty acids, monounsaturated fatty acids, polyunsaturated fatty acids, carbohydrates, protein, and dietary cholesterol) and cardiovascular disease risk markers using multilevel modelling. The effect of isocaloric replacement of saturated fatty acids with other fats and carbohydrates was determined overall and by levels of intakes by use of nutrient density models. We did simulation modelling in which we assumed that the effects of saturated fatty acids on cardiovascular disease events was solely related to their association through an individual risk marker, and then compared these simulated risk marker-based estimates with directly observed associations of saturated fatty acids with cardiovascular disease events.

    FINDINGS: Participants were enrolled into the study from Jan 1, 2003, to March 31, 2013. Intake of total fat and each type of fat was associated with higher concentrations of total cholesterol and LDL cholesterol, but also with higher HDL cholesterol and apolipoprotein A1 (ApoA1), and lower triglycerides, ratio of total cholesterol to HDL cholesterol, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein B (ApoB) to ApoA1 (all ptrend<0·0001). Higher carbohydrate intake was associated with lower total cholesterol, LDL cholesterol, and ApoB, but also with lower HDL cholesterol and ApoA1, and higher triglycerides, ratio of total cholesterol to HDL cholesterol, ratio of triglycerides to HDL cholesterol, and ApoB-to-ApoA1 ratio (all ptrend<0·0001, apart from ApoB [ptrend=0·0014]). Higher intakes of total fat, saturated fatty acids, and carbohydrates were associated with higher blood pressure, whereas higher protein intake was associated with lower blood pressure. Replacement of saturated fatty acids with carbohydrates was associated with the most adverse effects on lipids, whereas replacement of saturated fatty acids with unsaturated fats improved some risk markers (LDL cholesterol and blood pressure), but seemed to worsen others (HDL cholesterol and triglycerides). The observed associations between saturated fatty acids and cardiovascular disease events were approximated by the simulated associations mediated through the effects on the ApoB-to-ApoA1 ratio, but not with other lipid markers including LDL cholesterol.

    INTERPRETATION: Our data are at odds with current recommendations to reduce total fat and saturated fats. Reducing saturated fatty acid intake and replacing it with carbohydrate has an adverse effect on blood lipids. Substituting saturated fatty acids with unsaturated fats might improve some risk markers, but might worsen others. Simulations suggest that ApoB-to-ApoA1 ratio probably provides the best overall indication of the effect of saturated fatty acids on cardiovascular disease risk among the markers tested. Focusing on a single lipid marker such as LDL cholesterol alone does not capture the net clinical effects of nutrients on cardiovascular risk.

    FUNDING: Full funding sources listed at the end of the paper (see Acknowledgments).

    Matched MeSH terms: Cardiovascular Diseases/blood; Cardiovascular Diseases/epidemiology*
  16. Ooi BK, Goh BH, Yap WH
    Int J Mol Sci, 2017 Nov 05;18(11).
    PMID: 29113088 DOI: 10.3390/ijms18112336
    Oxidative stress is an important risk factor contributing to the pathogenesis of cardiovascular diseases. Oxidative stress that results from excessive reactive oxygen species (ROS) production accounts for impaired endothelial function, a process which promotes atherosclerotic lesion or fatty streaks formation (foam cells). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor involved in cellular redox homeostasis. Upon exposure to oxidative stress, Nrf2 is dissociated from its inhibitor Keap-1 and translocated into the nucleus, where it results in the transcriptional activation of cell defense genes. Nrf2 has been demonstrated to be involved in the protection against foam cells formation by regulating the expression of antioxidant proteins (HO-1, Prxs, and GPx1), ATP-binding cassette (ABC) efflux transporters (ABCA1 and ABCG1) and scavenger receptors (scavenger receptor class B (CD36), scavenger receptor class A (SR-A) and lectin-type oxidized LDL receptor (LOX-1)). However, Nrf2 has also been reported to exhibit pro-atherogenic effects. A better understanding on the mechanism of Nrf2 in oxidative stress-induced cardiac injury, as well as the regulation of cholesterol uptake and efflux, are required before it can serve as a novel therapeutic target for cardiovascular diseases prevention and treatment.
    Matched MeSH terms: Cardiovascular Diseases/metabolism*; Cardiovascular Diseases/pathology
  17. Perak AM, Marino BS, de Ferranti SD
    Pediatrics, 2018 Apr;141(4).
    PMID: 29588338 DOI: 10.1542/peds.2017-2075
    Matched MeSH terms: Cardiovascular Diseases/epidemiology; Cardiovascular Diseases/prevention & control*
  18. Ibrahim N', Fairus S, Zulfarina MS, Naina Mohamed I
    Nutrients, 2020 Feb 05;12(2).
    PMID: 32033387 DOI: 10.3390/nu12020414
    INTRODUCTION: Cardiovascular disease (CVD) is the leading cause of death worldwide. Squalene (SQ), an intermediate for the cholesterol biosynthesis, has been proposed to act similarly to statins via inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase in the liver.

    PURPOSE: This paper explores the effects of SQ in CVD.

    METHODS: A systematic review of the literature was performed to identify relevant studies about SQ and CVD. A comprehensive search in Medline and Scopus for relevant studies published between the years 1946 and 2019 was performed. The main inclusion criteria were that the study was published in English; that the study reported association or effect of SQ and CVD; and that CVD should be related to lifestyle variables, aging, or experimentally induced conditions.

    RESULTS: The literature searches identified 5562 potentially relevant articles, whereby 21 studies met the inclusion criteria. There were three human studies and 18 animal experimental studies included in this paper. Only one human study reported positive outcome of SQ in CVD. The remaining two studies reported inconsistent and/or no effect. For animal studies, 15 studies reported positive effect while the remaining reported negative and/or no effect of SQ on various related parameters.

    CONCLUSIONS: This evidence-based review emphasizes the potential of SQ being used for cardiovascular-related diseases. The effect of SQ, especially of plant-based warrants further exploration. Controlled human observational studies should be performed to provide comprehensive evidence.

    Matched MeSH terms: Cardiovascular Diseases/etiology; Cardiovascular Diseases/prevention & control*
  19. Ramli AS, Daher AM, Nor-Ashikin MN, Mat-Nasir N, Ng KK, Miskan M, et al.
    Biomed Res Int, 2013;2013:760963.
    PMID: 24175300 DOI: 10.1155/2013/760963
    Metabolic syndrome (MetS) is a steering force for the cardiovascular diseases epidemic in Asia. This study aimed to compare the prevalence of MetS in Malaysian adults using NCEP-ATP III, IDF, and JIS definitions, identify the demographic factors associated with MetS, and determine the level of agreement between these definitions. The analytic sample consisted of 8,836 adults aged ≥30 years recruited at baseline in 2007-2011 from the Cardiovascular Risk Prevention Study (CRisPS), an ongoing, prospective cohort study involving 18 urban and 22 rural communities in Malaysia. JIS definition gave the highest overall prevalence (43.4%) compared to NCEP-ATP III (26.5%) and IDF (37.4%), P < 0.001. Indians had significantly higher age-adjusted prevalence compared to other ethnic groups across all MetS definitions (30.1% by NCEP-ATP III, 50.8% by IDF, and 56.5% by JIS). The likelihood of having MetS amongst the rural and urban populations was similar across all definitions. A high level of agreement between the IDF and JIS was observed (Kappa index = 0.867), while there was a lower level of agreement between the IDF and NCEP-ATP III (Kappa index = 0.580). JIS definition identified more Malaysian adults with MetS and therefore should be recommended as the preferred diagnostic criterion.
    Matched MeSH terms: Cardiovascular Diseases/metabolism; Cardiovascular Diseases/epidemiology; Cardiovascular Diseases/pathology; Cardiovascular Diseases/physiopathology
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links