Correlation of Smoking and Myocardial Infarction Among Sudanese Male Patients Above 40 Years of Age

Elkhader, Bahaaedin A.; Abdulla, Alsafi A.; Omer, Mohammed A. Ali

doi:10.12659/pjr.894068

Cited by 18 publications

(12 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Smoking is considered an important risk factor for the development of CVD like many other chronic diseases [54]. We found an increased risk of CVD with higher DII score in smoking men.…”

Section: Discussionsupporting

confidence: 50%

Positive Association of Dietary Inflammatory Index with Incidence of Cardiovascular Disease: Findings from a Korean Population-Based Prospective Study

et al. 2020

View full text Add to dashboard Cite

Recently, diets with higher inflammatory potentials based on the dietary inflammatory index (DII®) have been shown to be associated with increased cardiovascular disease (CVD) risk in the general population. We aimed to prospectively investigate the association between the DII and CVD risk in the large Korean Genome and Epidemiology Study_Health Examination (KoGES_HEXA) cohort comprised of 162,773 participants (men 55,070; women 107,703). A validated semi-quantitative food frequency questionnaire (SQ-FFQ) was used to calculate the DII score. Statistical analyses were performed by using a multivariable Cox proportional hazard model. During the mean follow-up of 7.4 years, 1111 cases of CVD were diagnosed. Higher DII score was associated with increased risk of CVD in men (hazard ratio [HR]Quintile 5 vs. 1 1.43; 95% CI 1.04–1.96) and in women (HRQuintile 5 vs. 1 1.19; 95% CI 0.85–1.67), although not significant for women. The risk of CVD was significantly higher in physically inactive men (HRQuintile 5 vs. 1 1.80; 95% CI 1.03–3.12), obese men (HRQuintile 5 vs. 1 1.77; 95% CI 1.13–2.76) and men who smoked (HRQuintile 5 vs. 1 1.60; 95% CI 1.10–2.33), respectively. The risk of developing stroke was significantly higher for men (HRQuintile 5 vs. 1 2.06; 95% CI 1.07–3.98; p = 0.003), but not for women. A pro-inflammatory diet, as indicated by higher DII scores, was associated with increased risk of CVD and stroke among men.

show abstract

“…Smoking is considered an important risk factor for the development of CVD like many other chronic diseases [54]. We found an increased risk of CVD with higher DII score in smoking men.…”

Section: Discussionsupporting

confidence: 50%

Positive Association of Dietary Inflammatory Index with Incidence of Cardiovascular Disease: Findings from a Korean Population-Based Prospective Study

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Acute myocardial infarction (AMI) is a severe ischemic disease responsible for cardiac fibrosis, heart failure, and sudden death [ 1 , 2 ]. It has been reported that smoking is a risk factor for the development of myocardial infarction [ 3 ]. Patients with AMI always present severe and persistent pain in the chest, which can be combined with arrhythmia, shock, or heart failure [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy

Zhang¹,

Li²,

Chen³

et al. 2017

Med Sci Monit

View full text Add to dashboard Cite

BackgroundAcute myocardial infarction (AMI) is a severe disease causing heart failure and sudden death. Studies indicate that microRNAs (miRNAs) are involved in the pathophysiology of AMI. In the present study, we carefully explored the effects of miR-122 on myocardial hypoxia injury and its possible underlying mechanism.Material/MethodsmiR-122 expression was analyzed in H9c2 cardiomyocytes after being transfected with miR-122 mimic, ASO-miR-122, or negative control. Cell viability and apoptosis were investigated by CCK-8 assays and flow cytometry analysis, respectively. Cell migration was analyzed using wound-healing assays. Western blotting was performed to analyze the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/AKT and LC3-II/LC3-I.ResultHypoxia exposure significantly inhibited H9c2 cell viability (P<0.01). miR-122 overexpression promoted the hypoxia-induced H9c2 cell proliferation and migration loss (P<0.05), and cell apoptosis was increased (P<0.05). miR-122 knockdown enhanced cell viability and decreased cell apoptosis (P<0.05). Knockdown of miR-122 enhanced PTEN/PI3K/AKT activation and cell autophagy. Overexpression of miR-122 inhibited the PTEN/PI3K/AKT pathway and cell autophagy pathway.ConclusionsThe expression of miR-122 is involved in hypoxia-induced H9c2 cardiomyocyte injury. Knockdown of miR-122 protects H9c2 cells from hypoxia-induced apoptosis and enhances cell viability.

show abstract

“…Cardiovascular diseases (CVDs), such as myocardial infarction (MI), atherosclerosis, vascular dysfunction, arrhythmias, hypertension, stroke and heart failure, lead to increased mortality in humans and the mortality rates are expected to increase to >23.6 million by 2030 ( 1 , 2 ). Interruption of the blood supply to the heart causes injury to cardiomyocytes and leads to MI ( 3 ). Diabetes mellitus (DM), or simply diabetes, is a metabolic disorder in which diabetic patients cannot appropriately regulate their blood glucose levels ( 4 ).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effect of Notch signaling on the development of myocardial infarction complicated by diabetes mellitus

Zhang

et al. 2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

The present study aimed to elucidate the role of Notch signaling in the development of myocardial infarction (MI) concomitant with diabetes in vivo and in vitro and evaluated the therapeutic effect of the Notch signaling in vitro. Streptozotocin-induced diabetic rats were subjected to 25 min of ischemia and 2 h of reperfusion. Cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB) isoenzyme levels were detected. Infarct size was measured by 2,3,5-triphenyltetrazolium chloride staining. Myocardial apoptosis and fibrosis were examined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and Masson Trichrome staining, respectively. The mRNA and protein levels of Notch signaling components, including Notch1, Notch4, Delta-like 1, Jagged1, Mastermind-like protein 1 and p300, were quantified by reverse transcription-quantitative polymerase chain reaction and western blotting analyses, respectively. H9c2 cells were treated with/without 33 mM high glucose (HG) and/or subjected to hypoxia in the presence/absence of Jagged1. Cell viability and apoptosis were determined by MTT assay and Annexin V-fluorescein isothiocyanate/propidium iodide assay. Levels of the Notch signaling pathway members were examined. The present findings revealed that diabetes elevated CK-MB and cTnT, increased infarct size, induced myocardial apoptosis and inhibited the Notch signaling pathway in vivo after ischemia/reperfusion. Ischemia/reperfusion augmented the severity of MI in diabetic rats. Furthermore, HG reduced cell viability and induced cell apoptosis in H9c2 cells after hypoxia exposure, which was inhibited by Jagged1. We also found that HG inhibited Notch signaling in H9c2 cells after hypoxia, whereas Jagged1 exerted its cardioprotective effect on hypoxic injury (in HG environments or not) by activating the Notch signaling pathway. In conclusion, these findings suggest that diabetes promoted the progression of MI in vivo and in vitro via the inhibition of the Notch signaling pathway. Jagged1 may protect against MI in in vitro models by activating Notch signaling.

show abstract

Correlation of Smoking and Myocardial Infarction Among Sudanese Male Patients Above 40 Years of Age

Cited by 18 publications

References 11 publications

Positive Association of Dietary Inflammatory Index with Incidence of Cardiovascular Disease: Findings from a Korean Population-Based Prospective Study

Positive Association of Dietary Inflammatory Index with Incidence of Cardiovascular Disease: Findings from a Korean Population-Based Prospective Study

Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy

Cardioprotective effect of Notch signaling on the development of myocardial infarction complicated by diabetes mellitus

Contact Info

Product

Resources

About