Ischemic Heart Disease In Population Research Articles

Assessment of Knowledge of Symptoms of Ischemic Heart Disease in Population Visiting a Tertiary Care Hospital in Pakistan

IntroductionCardiovascular diseases are an important cause of mortality in Pakistan. Developing nations like Pakistan with poor literacy rates and the majority of the population living in rural areas seem to be insufficient in their knowledge of symptoms. A study indicated that about half of the cardiac deaths occur within one hour of onset of symptoms, thus it is necessary to have adequate knowledge of symptoms to identify the sufferer and to pursue medical services as early as possible. The aim of our study was to assess the knowledge of ischemic heart disease (IHD) symptoms in the population and to investigate the relationship of age, gender, socio-economic status, education, and occupation with knowledge.Materials and MethodsThis was a descriptive cross-sectional study carried out in the Holy Family Hospital, Rawalpindi, Pakistan over a period of four months from May 2018 to August 2018. The study population comprised of people visiting the hospital. Individuals aged 18 and above were included while medical professionals were excluded. An interviewer-assisted semi-structured questionnaire was used as the data collection tool. After taking consent, 225 participants were asked about their demographic profile and to enlist as many symptoms of IHD as possible. Reference was made to the seven typical symptoms of IHD as recognized by the World Health Organization (WHO). Statistical Package for Social Sciences (SPSS), v23.0 (IBM SPSS Statistics, Armonk, NY) was used for the analysis. Independent samples t-test and one-way ANOVA test were applied; p ≤ 0.05 was considered significant. ResultsOut of the seven symptoms endorsed by WHO, chest pain was most frequently identified (42%), followed by pain in the arm (23%), diaphoresis (19%), weakness and fainting (16%), dyspnea (15%), paleness (8%), and sickness and vomiting (5%). Mean score, out of seven symptoms, was 1.28 ± 1.19. Among the total participants, 34% could not enlist any symptom. Participants with higher education, skilled workers, and those having relatives who suffered from IHD showed significantly higher knowledge about IHD symptoms.ConclusionsThe study showed a paucity of knowledge about IHD symptoms among the participants. Hence it provides grounds for future awareness campaigns to educate the masses.

Análisis de epistasia de polimorfismos de genes metabólicos asociados a cardiopatía isquémica en Yucatán

ObjectiveEpistasis is a type of genetic interaction that could explain much of the phenotypic variability of complex diseases. In this work, the effect of epistasis of metabolic genes and cardiovascular risk on the susceptibility to the development of ischemic heart disease in Yucatan was determined. MethodsCase-control study in 79 Yucatecan patients with ischemic heart disease and 101 healthy controls matched by age and origin with cases. The polymorphisms -108CT, Q192R, L55M (paraoxonase 1; PON1), C677T, A1298C (methylenetetrahydrofolate reductase; MTHFR), and the presence/absence of the glutathione S-transferase T1 (GSTT1) gene were genotyped. Epistasis analysis was performed using the multifactorial dimensional reduction method. The best risk prediction model was selected based on precision (%), statistical significance (P<0.05), and cross-validation consistency. ResultsWe found an independent association of the null genotype GSTT1*0/0 (OR=3.39, CI: 1.29-8.87, P=0.017) and the null allele (OR=1.86, CI: 1.19-2.91, P=0.007) with ischemic heart disease. The GSTT1*0 deletion and the 677TT genotype (MTHFR) were identified as being at a high cardiovascular risk, whereas the GSTT1*1 wild type genotype and the CC677 variant were at low risk. The gene-environment interaction identified the GSTT1 gene, C677T polymorphism (MTHFR), and hypertension as the factors that best explain ischemic heart disease in the study population. ConclusionsThe interaction of the MTHFR, GSTT1 and hypertension may constitute a predictive model of risk for early onset ischemic heart disease in the population of Yucatan.

The cognitive biological function, difference in etiology and generality of pathogenesis of metabolic pandemics. The metabolism regulation in carnivorous and herbivorous animals under effect of environment factors.

In phylogenesis, carnivorous animals initially and later herbivorous animals formed separate transfer of exogenous fatty acids in blood, predominantly palmitic acid and later - endogenous oleic acid pool, synthesized in hepatocytes from glucose. In vivo, exogenous fatty acids transfer α-lipoproteins to all cells and chylomicrons to hepatocytes. The endogenous oleic fatty acid, synthesized in hepatocytes is transferred to all cells by β-lipoproteins and to insulin-dependent lipoproteins of very low density. The limitation of cognitive biological function in herbivorous animals underlies the process of transferring of surplus amount of exogenous palmitic acid and alcohol cholesterol by β-lipoproteins becoming a non-physiological one. The bio-availability is affected concerning cells of exogenous polyene fatty acids that transfer in blood α-lipoproteins in carnivorous animals and at the first stage in herbivorous animals. The formation of palmitic non-ligand very low density lipoproteins-β-proteins is affected and their collection and partial utilization in intima generates lipoidosis. In summary, all this becomes a cause of formation of atherosclerosis and atheromatosis. The limitations in phylogenesis of cognitive biological function are considered as an etiological factor of metabolic pandemics. The etiological factors are specific for every one of metabolic pandemics and pathogenesis of all pandemics is developed following common algorithm. It is likely that metabolic pandemics (atherosclerosis and atheromatosis, metabolic essential arterial hypertension, metabolic syndrome, syndrome of insulin resistance, obesity and non-alcoholic fatty disease of liver)are quite not identical to nosologic forms of diseases if considered according etiological factors, pathogenesis and pathology rate in population. The exclusion of all inherent forms of disorder of metabolism of fatty acids and their transfer in β-lipoproteins demonstrates that problem of atherosclerosis, atheromatosis, coronarosclerosis and ischemic heart disease mainly turns out to be a case of eaten one's fill , a result of environment factors impact, disorder of biological function of trophology, biological reaction of exotrophy (external nutrition) and biological function of homeostasis. The prevention of atherosclerosis, atheromatosis and ischemic heart disease in population will be effective only under condition of obligatory individual support of actioning cognitive biological function by more complete biological function of intelligence. The active prevention of metabolic pandemics by force of personal development of cognitive biological function, intelligence function, provides no application of pharmaceuticals. The disorder of cognitive biological function is needed to be improved, incorrect positioning of Homo Sapiens species as omnivorous in animal world; Homo Sapiens is a herbivorous one.

Low ambient oxygen prevents atherosclerosis.

Large population studies have shown that living at higher altitudes, which lowers ambient oxygen exposure, is associated with reduced cardiovascular disease mortality. However, hypoxia has also been reported to promote atherosclerosis by worsening lipid metabolism and inflammation. We sought to address these disparate reports by reducing the ambient oxygen exposure of ApoE-/- mice. We observed that long-term adaptation to 10% O2 (equivalent to oxygen content at ∼5000 m), compared to 21% O2 (room air at sea level), resulted in a marked decrease in aortic atherosclerosis in ApoE-/- mice. This effect was associated with increased expression of the anti-inflammatory cytokine interleukin-10 (IL-10), known to be anti-atherogenic and regulated by hypoxia-inducible transcription factor-1α (HIF-1α). Supporting these observations, ApoE-/- mice that were deficient in IL-10 (IL10-/- ApoE-/- double knockout) failed to show reduced atherosclerosis in 10% oxygen. Our study reveals a specific mechanism that can help explain the decreased prevalence of ischemic heart disease in populations living at high altitudes and identifies ambient oxygen exposure as a potential factor that could be modulated to alter pathogenesis. Key messages: Chronic low ambient oxygen exposure decreases atherosclerosis in mice. Anti-inflammatory cytokine IL-10 levels are increased by low ambient O2. This is consistent with the established role of HIF-1α in IL10 transactivation. Absence of IL-10 results in the loss of the anti-atherosclerosis effect of low O2. This mechanism may contribute to decreased atherosclerosis at high altitudes.

Low ambient oxygen prevents atherosclerosis (HUM1P.254)

Abstract Large epidemiolgic studies show that living at high altitude, which decreases oxygen exposure, is associated with reduced cardiovascular and cancer mortality. However, some experimental data show that acute hypoxia exposure can increase atherosclerosis by worsening inflammation and blood lipid profiles. We sought to address these disparate observations by chronically controlling the oxygen exposure of ApoE-/- mice and examining its effect on atherosclerosis. Herein, we report that reducing oxygen exposure by 50% caused a marked decrease in aortic atherosclerosis, associated with the inhibition of pro-inflammatory cytokines in circulation and increased anti-inflammatory IL10 levels in aortic tissue. We further show that the expression of IL10, well established to prevent atherosclerosis, was induced by low oxygen in a hypoxia inducible factor-1α (HIF1 α) dependent manner. We propose that this anti-inflammatory mechanism may contribute to the lower incidence of ischemic heart disease in populations living at high altitudes and suggest a potential therapeutic pathway for disease prevention.

Active Breathing Coordinator reduces radiation dose to the heart and preserves local control in patients with left breast cancer: Report of a prospective trial

PurposeIncidental radiation dose to the heart and lung during breast radiation therapy (RT) has been associated with an increased risk of cardiopulmonary morbidity. We conducted a prospective trial to determine if RT with the Active Breathing Coordinator (ABC) can reduce the mean heart dose (MHD) by ≥20% and dose to the lung. Methods and materialsPatients with stages 0-III left breast cancer (LBC) were enrolled and underwent simulation with both free breathing (FB) and ABC for comparison of dosimetry. ABC was used during the patient’s RT course if the MHD was reduced by ≥5%. The median prescription dose was 50.4Gy plus a boost in 77 patients (90%). The primary endpoint was the magnitude of MHD reduction when comparing ABC to FB. Secondary endpoints included dose reduction to the heart and lung, procedural success rate, and adverse events. ResultsA total of 112 patients with LBC were enrolled from 2002 to 2011 and 86 eligible patients underwent both FB and ABC simulation. Ultimately, 81 patients received RT using ABC, corresponding to 72% procedural success. The primary endpoint was achieved as use of ABC reduced MHD by 20% or greater in 88% of patients (P < .0001). The median values for absolute and relative reduction in MHD were 1.7Gy and 62%, respectively. RT with ABC provided a statistically significant dose reduction to the left lung. After a median follow up of 81months, 8-year estimates of locoregional relapse, disease-free, and overall survival were 7%, 90%, and 96%, respectively. ConclusionsABC was well tolerated and significantly reduced MHD while preserving local control. Use of the ABC device during RT should be considered to reduce the risk of ischemic heart disease in populations at risk.

Utility of self-reported diagnosis and electrocardiogram Q-waves for estimating myocardial infarction prevalence: an international comparison study

ObjectiveSelf-report of physician diagnosis and ECG ‘Q’ waves are common survey measures of prior myocardial infarction (MI) prevalence. We sought to assess relative prevalence of self-reported prior MI and ECG...

Body mass index and mortality from ischaemic heart disease in a lean population: 10 year prospective study of 220 000 adult men

Increased body mass index (BMI) is known to be related to ischaemic heart disease (IHD) in populations where many are overweight (BMI>or=25 kg/m2) or obese (BMI>or=30). Substantial uncertainty remains, however, about the relationship between BMI and IHD in populations with lower BMI levels. We examined the data from a population-based, prospective cohort study of 222,000 Chinese men aged 40-79. Relative and absolute risks of death from IHD by baseline BMI were calculated, standardized for age, smoking, and other potential confounding factors. The mean baseline BMI was 21.7 kg/m2, and 1942 IHD deaths were recorded during 10 years of follow-up (6.5% of all such deaths). Among men without prior vascular diseases at baseline, there was a J-shaped association between BMI and IHD mortality. Above 20 kg/m2 there was a positive association of BMI with risk, with each 2 kg/m2 higher in usual BMI associated with 12% (95% CI 6-19%, 2P=0.0001) higher IHD mortality. Below this BMI range, however, the association appeared to be reversed, with risk ratios of 1.00, 1.09, and 1.15, respectively, for men with BMI 20-21.9, 18-19.9, and <18 kg/m2. The excess IHD risk observed at low BMI levels persisted after restricting analysis to never smokers or excluding the first 3 years of follow-up, and became about twice as great after allowing for blood pressure. Lower BMI is associated with lower IHD risk among people in the so-called normal range of BMI values (20-25 kg/m2), but below that range the association may well be reversed.

Adverse effects of fish oil

To the Editor .— Fisher et al 1 in their article on n-3 fatty acids and cellular aspects of atherogenesis suggest that urgent trials of n-3 fatty acid supplementation are needed to assess their effects on atherosclerotic disease. While epidemiological studies 2,3 have documented a reduced incidence of ischemic heart disease in populations with a high intake of n-3 fatty acids, there is also an unexplained increased incidence of stroke. 2,3 Apart from a high incidence of unpleasant side effects in patients taking fish oil supplements, clinical 4 and laboratory studies 5 have shown evidence of raised blood pressure in groups taking omega-3 fatty acid supplementation. In addition, recent epidemiological evidence has shown an increased incidence and prevalence of hypertensive related diseases 3 in the same type of population in whom there is a low incidence of ischemic heart disease. While the theoretical benefits of n-3 fatty acid supplementation are

Adverse Effects of Fish Oil

To the Editor .— Fisher et al 1 in their article on n-3 fatty acids and cellular aspects of atherogenesis suggest that urgent trials of n-3 fatty acid supplementation are needed to assess their effects on atherosclerotic disease. While epidemiological studies 2,3 have documented a reduced incidence of ischemic heart disease in populations with a high intake of n-3 fatty acids, there is also an unexplained increased incidence of stroke. 2,3 Apart from a high incidence of unpleasant side effects in patients taking fish oil supplements, clinical 4 and laboratory studies 5 have shown evidence of raised blood pressure in groups taking omega-3 fatty acid supplementation. In addition, recent epidemiological evidence has shown an increased incidence and prevalence of hypertensive related diseases 3 in the same type of population in whom there is a low incidence of ischemic heart disease. While the theoretical benefits of n-3 fatty acid supplementation are

Cod liver oil inhibits neutrophil and monocyte chemotaxis in healthy males

Epidemiological evidence suggests a reduced rate of chronic inflammatory diseases and ischaemic heart disease in populations with a high consumption of fish. This has been ascribed to the high content in sea food of polyunsaturated fatty acids (PUFAs), belonging to the n - 3 family. We have studied neutrophil and monocyte chemotaxis in 12 healthy males before and after 6 weeks supplementation with cod liver oil, corresponding to 5.3 g n - 3 PUFAs daily. Neutrophil and monocyte chemotaxis were investigated using the under agarose technique with N-formyl-methionyl-leucyl-phenylalanine ( N-FMLP) and autologous serum as chemoattractants. Neutrophil chemotaxis towards both chemoattractants and monocyte chemotaxis towards N-FMLP were significantly reduced after supplementation with cod liver oil.