Independent Risk Factor For Atherosclerosis Research Articles

Crystal arthritides - gout and calcium pyrophosphate arthritis : Part2: clinical features, diagnosis and differential diagnostics.

Gout develops in four stages beginning with an asymptomatic increase in blood levels of uric acid. An acute gout attack is an expression of an underlying inflammatory process, which in the course of time is self-limiting. Without therapy monosodium urate crystals remain in the synovial fluid and synovial membrane and trigger more acute attacks. In the course of the disease monosodium urate crystals form deposits (tophi) leading in severe forms to irreversible joint deformities with loss of functionality. In 20% of cases gout leads to involvement of the kidneys. Overproduction of uric acid can cause nephrolithiasis. These stones can be composed of uric acid or calcium phosphate. Another form of kidney disease caused by gout is uric acid nephropathy. This is aform of abacterial chronic inflammatory response with deposition of sodium urate crystals in the medullary interstitium. Acute obstructive nephropathy is relatively rare and characterized by renal failure due to uric acid precipitation in the tubules because of rapid cell lysis that occurs, for example, with chemotherapy. There is acausal interdependence between the occurrence of hyperuricemia and hypertension. Uric acid activates the renin-angiotensin-aldosterone (RAA) system and inhibits nitric oxide (NO) with the possible consequence of arise in systemic vascular resistance or arteriolar vasculopathy; however, uric acid is also an apparently independent risk factor for atherosclerosis. In contrast to young patients, the diagnosis of an acute gout attack in the elderly can be achallenge for the physician. Polyarticular manifestations and obscure symptoms can make it difficult to differentiate it from rheumatoid arthritis and calcium pyrophosphate deposition disease (CPPD). Aspiration of synovial fluid with visualization of urate crystals using compensated polarized light microscopy is the gold standard for diagnosis of acute gout. Moreover, analysis of synovial fluid enables a distinction from septic arthritis by Gram staining and bacterial culture. Soft tissue ultrasonography is useful to detect affected synovial tissue and monosodium urate crystals within the synovial fluid. Involvement of bone occurs relatively late in the disease so that x‑ray images are not useful in the early stages but might be helpful in differential diagnostics. Dual energy computed tomography (CT) and magnetic resonance imaging (MRI) can be used for certain indications.

Involvement of histone methylation in macrophage apoptosis and unstable plaque formation in methionine-induced hyperhomocysteinemic ApoE−/− mice

AimsHyperhomocysteinemia (Hhcy) is an independent risk factor of atherosclerosis and promotes unstable plaque formation. Epigenetic mechanisms play an important role in the pathogenesis of atherosclerosis induced by Hhcy. However, the exact mechanism is still undefined. Lesional apoptotic cells and necrotic core formation contribute greatly to the progression of plaque. The present study sought to determine whether modification of histone methylation is involved in macrophage apoptosis and unstable plaque formation in the condition of Hhcy. Materials and methodsThe unstable plaque formation, lesional apoptotic cells and status of histone methylation were monitored in the aortas of Hhcy ApoE−/− mice induced by a high-methionine (HM) diet for 20weeks. Involvement of histone methylation in macrophage apoptosis and foam cell formation were assessed in macrophage Raw 264.7 cells after being challenged with homocysteine alone or in combination with the histone methylation inhibitor BIX 01294. Key findingsThe unstable plaque formation and lesion apoptotic cells are increased in ApoE−/− mice supplemented with high-methionine (HM), accompanied with a decreased expression of histone H3 lysine 9 dimethylation. Hhcy increases the apoptosis of macrophages and inhibits the histone H3 lysine 9 dimethylation, as well as the expression of histone methyltransferase G9a in vitro. Inhibition of histone methylation by BIX01294 enhances macrophage apoptosis and foam cell formation in vitro. SignificanceOur data suggest that Hhcy promotes the progression of atherosclerosis via macrophage apoptosis. Histone methylation might be involved in macrophage apoptosis and unstable plaque formation in methionine induced hyperhomocysteinemic ApoE−/− mice.

Soluble Urokinase Plasminogen Activator Receptor and the Risk of Coronary Artery Disease in Young Chinese Patients.

Background Soluble urokinase plasminogen activator receptor (suPAR) is a novel marker of chronic inflammation and is considered to be a risk factor for coronary artery disease (CAD) in Caucasians. This study investigated the role of suPAR in young Chinese patients with CAD. Methods The study involved a total of 196 consecutive young (age ≤ 55 years) patients with angiographically proven CAD and 188 age-matched non-CAD individuals as controls. Traditional risk factors were evaluated using conventional assays, and levels of suPAR were measured by sandwich enzyme-linked immunosorbent assays. Results Levels of suPAR were significantly correlated with age (r = 0.20, P = 0.04), smoking (r = 0.33, P = 0.008), body mass index (r = 0.21, P = 0.03), and high-sensitivity C-reactive protein (hs-CRP; r = 0.31, P = 0.01). Multivariate logistic regression analysis showed that male sex (odds ratio (OR) = 3.12; 95% confidence interval (CI) = 1.18–8.25, P = 0.02), smoking (OR = 3.41, 95% CI = 1.55–7.50, P = 0.002), triglyceride (OR = 1.89, 95% CI = 1.10–3.25, P = 0.02), high-sensitivity C-reactive protein (OR = 1.24, 95% CI = 1.02–0.03, P = 0.03), and suPAR (OR = 1.37, 95% CI = 1.09–1.72, P = 0.007) were independently associated with CAD risk in young patients. Conclusions SuPAR is a novel independent risk factor for CAD in young Chinese patients. Further studies evaluating the effect of anti-inflammatory treatment on the suPAR levels and the risk of CAD are needed.

Predictive Value of Nutritional Risk Index in Prevalence of Coronary Artery Disease in Chinese Middle-Aged and Older Male Patients

Objective: Cardiovascular disease and malnutrition may be interrelated, and malnutrition may directly contribute to a fatal outcome. We aimed to evaluate the predictive role of Nutritional Risk Index (NRI) in prevalence of Coronary Artery Disease (CAD) in Chinese middle-aged and elderly male patients. Methods: Levels of serum albumin, prealbumin and hemoglobin were determined at hospital admission in 197 enrolled patients. The body mass index (BMI) was calculated as weight in kilograms divided by height (meters²). The NRI formula as follows: NRI= (1.519 × serum albumin, g/dL) + (41.7 × present weight (kg)/ideal body weight (kg)). Results: There were high levels of albumin and NRI in CAD cases as compared to controls. The percentages of malnutrition in all patients, CAD patients and control cases were 37.56%, 33.96% and 52.63%, respectively. The patients with malnutrition had lower prevalence of coronary artery disease as compared to the patients with better nutrition (69.64% vs. 86.14%). NRI value was closely related to prevalence of CAD, and was an independent risk factor for CAD. The area under the curve of NRI was 0.65, and the Youden index of NRI was 0.33. The sensitivity and specificity of NRI for predicting prevalence of CAD were 89.18% and 43.56%, respectively. The optimal diagnosis criterion of NRI for CAD was higher than 45.29. Conclusion: Malnutrition as assessed by NRI is associated with prevalence of CAD, and is a more reliable and independent indicator of prevalence of CAD in Chinese middle-aged and elderly male patients.

Simvastatin inhibits homocysteine-induced CRP generation via interfering with the ROS-p38/ERK1/2 signal pathway in rat vascular smooth muscle cells

Inflammation plays a pivotal role throughout the formation and progression of atherosclerosis. As the most representative inflammatory marker, C-reactive protein (CRP) directly participates in the initiation and development of atherosclerosis. The elevated homocysteine (Hcy) level in plasma is an independent risk factor for atherosclerosis. We previously reported that Hcy produces a pro-inflammatory effect by stimulating CRP expression in vascular smooth muscle cells (VSMCs). The present study observed the effect of simvastatin on Hcy-induced CRP expression in VSMCs and the molecular mechanisms. The in vitro experiments revealed that pretreatment of VSMCs with simvastatin decreased Hcy-induced mRNA and protein expression of CRP in a concentration-dependent fashion. The in vivo results showed that simvastatin not only inhibited CRP expression in the vessel walls in mRNA and protein levels, but also reduced the circulating CRP level in hyperhomocysteinemic rats. Further experiments displayed that simvastatin reduced Hcy-induced reactive oxygen species (ROS) generation, ameliorated Hcy-activated phosphorylations of ERK1/2 and p38, and antagonized Hcy-downregulated peroxisome proliferator-activated receptor gamma expression in VSMCs. These data demonstrate that simvastatin is able to inhibit Hcy-induced CRP generation in VSMCs so to relieve the vascular inflammatory response via interfering with the ROS-MAPK signal pathway. The present results provide new evidence for understanding of the potential anti-inflammatory and anti-atherosclerotic effects of simvastatin. As the high level of Hcy in plasma is related to atherosclerosis formation and mediates cardiovascular risk, our findings emphasize the importance and necessity of therapy with statins for hyperhomocysteinemia in atherosclerosis.

Is periodontitis an independent risk factor for subclinical atherosclerosis?

ObjectivesThe aim of this study was to assess the interrelationship between periodontitis and atherosclerosis by comparing the ultrasound and clinical markers of atherosclerosis in systemically healthy patients with and without periodontitis and whether periodontitis can be an independent risk factor for atherosclerosis. Materials and methodsTotal 40 subjects, of same socioeconomic status, belonging to age group of 35–65 years, were recruited and divided into two groups - Group I (Chronic Generalised Periodontitis without any systemic disease: CP-SH), Group II (Normal healthy patients without periodontitis and any systemic disease - SH). Clinical measurements and ultrasound examinations were carried out. Qualitative variables were analyzed using Chi square test and qualitative variables using Unpaired Student t test. Statistical significance was accepted for p≤0.05. ResultsCarotid ultrasound revealed right and left intima media thickness (IMT) of 0.626±0.016mm and 0.715±0.037mm respectively in cases versus 0.495±0.009mm and 0.518±0.009mm respectively in controls, with the difference being statistically significant. In cases, mean diastolic blood pressure (DBP) was 83.45±4.07mmHg versus 79.25±3.63mmHg in controls, with the difference being statistically significant. ConclusionIn this study, we found statistically significant differences in carotid IMT and DBP values between cases and controls. These findings suggest independent role of periodontal disease in subclinical atherosclerosis.

Total serum bilirubin is an independent risk factor for coronary artery disease in men compared to women

Objective An elevated total serum bilirubin level has been demonstrated to be protective against cardiovascular disease with the majority of evidence limited to males. We assessed the hypothesis that total bilirubin is an independent risk factor for the presence of coronary artery disease (CAD) in men compared to women in high-risk patients.Methods and results Analysis was performed on 563 men and 249 women presenting for coronary angiography at our institution between October 2009 and March 2014. CAD was defined by 50% stenosis or more in the left anterior descending artery, left circumflex artery or right coronary artery. CAD was present in 78% of men and 55% of women. In males, patients with CAD had lower median total serum bilirubin levels compared to patients without CAD (12 vs 13 μmol/L, P= 0.002). There was no difference seen in the female population (10 vs 10 μmol/L, P= 0.344). On multivariate logistic regression, total serum bilirubin was an independent risk factor of CAD in the males (OR 0.96; 95% CI 0.93-0.99; P= 0.018) but not in females (OR 1.00; 95% CI 0.93-1.08; P= 0.908).Conclusion Total serum bilirubin is an independent risk factor for angiographically defined CAD in men and not in women. Serum bilirubin is readily available and inexpensive and may be a biomarker in addition to recognised cardiovascular risk factors.

IL-34 is associated with the presence and severity of renal dysfunction and coronary artery disease in patients with heart failure.

Pro-inflammatory mediators are identified in patients with heart failure (HF), some of which may be used as biomarkers with diagnostic or prognostic value. As an additional ligand of Colony Stimulating Factor-1 Receptor (CSF-1R), interleukin-34 (IL-34) has been identified as a pro-inflammatory cytokine participating in chronic heart failure (CHF). However, the potential impact of IL-34 in CHF complications remains unknown. In order to determine the clinical significance of serum IL-34 in CHF patients, especially those with kidney dysfunction and coronary artery disease (CAD) comorbid conditions, serum IL-34 was measured in 510 consecutive patients with CHF in a cross-sectional study. The present study demonstrated that higher serum IL-34 levels were associated with poorer renal function and more severe anemia in patients with CHF. After adjusting for age, gender, conventional risk factors, and other significant covariates, IL-34 positively correlated with the presence and severity of renal dysfunction (as measured by eGFR and cystatin C) on multivariable linear and logistic regression analysis. IL-34 was also demonstrated to be an independent risk factor for CAD among HF patients. In conclusion, elevated serum IL-34 levels were demonstrated to be independently associated with renal insufficiency and CAD in patients with CHF, regardless of the systolic function.

Abstract 12796: Plaque Surface Irregularity and Calcification Length Within Carotid Plaque Predict Secondary Events in Patients With Coronary Artery Disease

Introduction: Although comprehensive risk factor modification is recommended, a uniform management strategy does not necessarily prevent secondary events in patients with coronary artery disease (CAD). Therefore, identification of high-risk patients who may benefit from more intensive interventions may improve prognosis. Carotid ultrasound can reliably identify systemic atherosclerosis, and carotid plaque and intima-media thickness (IMT) are known independent risk factors for CAD. However, it is unclear whether findings on carotid ultrasound can improve prediction of secondary CAD events. Methods: The study population comprised 146 consecutive patients with CAD (mean age, 66 ± 9 years; 126 with angina pectoris, 20 with myocardial infarction). IMT, plaque score, plaque area, plaque surface irregularity, and calcification length (calculated by summing the calcified lesions within each plaque accompanied by acoustic shadow) were measured at baseline. Patients were followed for 10 years to ascertain secondary CAD events. Results: Of 146 patients, secondary CAD events occurred in 63 after a median follow-up of 10 years. In univariate analysis, calcification length (P < 0.05) and plaque surface irregularity (P < 0.01) were associated with secondary CAD events, whereas IMT, plaque score, and plaque area were not. Multiple regression analysis demonstrated that calcification length (odds ratio, 1.06; P < 0.05) and plaque surface irregularity (odds ratio, 3.85; P < 0.01) remained independently associated with secondary CAD events after adjustment for age, sex, diabetes mellitus, dyslipidemia, hypertension, chronic kidney disease, and smoking. Moreover, when patients were divided into 4 groups according to calcification length and presence or absence of plaque surface irregularity, the group with longer calcification and plaque surface irregularity had greater risk of secondary CAD events (relative risk, 3.82; P < 0.05). Conclusions: These findings suggest that the combination of calcification length and plaque surface irregularity has additional value beyond traditional risk classification. Intensive intervention for these high-risk patients may avoid or delay progression of atherosclerosis towards secondary CAD events.

Nicotine Accelerates Atherosclerosis in Apolipoprotein E-Deficient Mice by Activating α7 Nicotinic Acetylcholine Receptor on Mast Cells.

Cigarette smoking is an independent risk factor for atherosclerosis. Nicotine, the addictive component of cigarettes, induces mast cell (MC) release and contributes to atherogenesis. The purpose of this study was to determine whether nicotine accelerates atherosclerosis through MC-mediated mechanisms and whether MC stabilizer prevents this pathological process. Nicotine administration increased the size of atherosclerotic lesions in apolipoprotein E-deficient (Apoe-/-) mice fed a fat-enriched diet. This was accompanied by enhanced intraplaque macrophage content and lipid deposition but reduced collagen and smooth muscle cell contents. MC deficiency in Apoe-/- mice (Apoe-/-KitW-sh/W-sh) diminished nicotine-induced atherosclerosis. Nicotine activated bone marrow-derived MCs in vitro, which was inhibited by a MC stabilizer disodium cromoglycate or a nonselective nicotinic acetylcholine receptor blocker mecamylamine. Further investigation revealed that α7 nicotinic acetylcholine receptor was a target for nicotine activation in MCs. Nicotine did not change atherosclerotic lesion size of Apoe-/-KitW-sh/W-sh mice reconstituted with MCs from Apoe-/-α7nAChR-/- animals. Activation of α7 nicotinic acetylcholine receptor on MCs is a mechanism by which nicotine enhances atherosclerosis.

Plaque surface irregularity and calcification length within carotid plaque predict secondary events in patients with coronary artery disease

Background and aimsAlthough comprehensive risk factor modification is recommended, a uniform management strategy does not necessarily prevent secondary events in patients with coronary artery disease (CAD). Therefore, identification of high-risk patients who may benefit from more intensive interventions may improve prognosis. Carotid ultrasound can reliably identify systemic atherosclerosis, and carotid plaque and intima-media thickness (IMT) are known independent risk factors for CAD. However, it is unclear whether findings on carotid ultrasound can improve prediction of secondary CAD events. MethodsThe study population comprised 146 consecutive patients with CAD (mean age, 66 ± 9 years; 126 with angina pectoris, 20 with acute myocardial infarction). IMT, plaque score, plaque area, plaque surface irregularity, and calcification length (calculated by summing the calcified lesions within each plaque accompanied by acoustic shadow) were measured at baseline. Patients were followed for 10 years to ascertain secondary CAD events defined as hard major adverse cardiovascular events (MACE; cardiac death and acute myocardial infarction) and as total MACE (hard MACE and angina pectoris with coronary revascularization). ResultsMultiple regression analysis demonstrated that calcification length (p < 0.05) and plaque surface irregularity (p < 0.01) remained independently associated with total MACE after adjustment for age, sex, diabetes mellitus, dyslipidemia, hypertension, chronic kidney disease, smoking, and multivessel CAD. ConclusionsThese findings suggest that the combination of calcification length and plaque surface irregularity has additional value beyond traditional risk classification. Intensive intervention for these high-risk patients may avoid or delay progression of atherosclerosis towards secondary CAD events.

IL-23 plasma level is strongly associated with CMV status and reactivation of CMV in renal transplant recipients.

BackgroundCytomegalovirus seropositivity is an independent risk factor for atherosclerosis in patients with ESRD. Donor CMV seropositivity is associated with higher graft loss. Dendritic cells, macrophages and Th17 lymphocytes are defined as producers of IL-23. IL-23 is thought to be involved in the promotion of Th17 cell polarization. Latent CMV-induced Th17 might be involved in the pathogenesis of CMV infection in patients with ESRD. We aimed to evaluate associations of Th17-dependent cytokines with ESRD, CMV status and post-transplant outcome in kidney transplantation.ResultsIL-21 plasma levels were similar in patients and healthy controls (p = 0.47), whereas IL-9 (p = 0.02) and IL-23 (p < 0.0001) levels were significantly higher in ESRD patients. CMV-seronegative (p = 0.002) and –seropositive (p < 0.001) patients had significantly higher IL-23 plasma levels than controls. CMV-seropositive patients showed excessively higher IL-23 (p < 0.001) plasma levels than CMV-seronegative patients. Patients with post-transplant CMV reactivation had higher IL-23 plasma levels than patients without CMV reactivation (p = 0.025).ConclusionsOur results indicate that latent CMV induces IL-23. IL-23 might be an inflammatory mediator of latent CMV infection in patients with ESRD and predisposes patients for post-transplant CMV reactivation.

Urinary Sodium and Potassium Excretion and Carotid Atherosclerosis in Chinese Men and Women.

Limited studies have examined the association between sodium (Na) and potassium (K) levels and the risk of atherosclerosis. This study examined whether higher Na and Na/K levels and low K levels were independent risk factors for atherosclerosis. This community-based cross-sectional study included 3290 subjects (1067 men and 2223 women) 40 to 75 years of age in Guangzhou, China, between 2011 and 2013. Urinary excretion of Na and K were measured from the first morning void, and creatinine-adjusted values were used. The intima-media thickness (IMT) of the carotid common artery and the carotid bifurcation was measured with high-resolution B-mode ultrasonography. Dietary K and Na intake and other covariates were obtained by face-to-face interviews. A significant positive association was seen between urinary Na excretion and carotid atherosclerosis after adjustment for age, sex, and other lifestyle covariates. The odds ratios (OR) and 95% confidence interval (CI) of the highest (vs. lowest) quartile of urinary Na were 1.32 (1.04–1.66) for carotid plaques, 1.48 (1.18–1.87) for increased common carotid artery IMT, and 1.55 (1.23–1.96) for increased carotid bifurcation IMT (all p-trend < 0.01). A similar positive association was observed between urinary Na/K levels and carotid plaque and increased IMT, and between dietary Na intake and increased bifurcation IMT. Regarding potassium data, we only found a significantly lower presence of carotid plaque (OR 0.72, 95% CI 0.57–0.91) for quartile 2 (vs. 1) of urinary K. Our findings suggest that higher levels of urinary excretion Na and Na/K are significantly associated with greater presence of carotid atherosclerosis in Chinese adults.

Intermittent hypoxia induces murine macrophage foam cell formation by IKK-β-dependent NF-κB pathway activation

Obstructive sleep apnea (OSA) is a common sleep disorder characterized by intermittent hypoxia (IH). Clinical studies have previously shown that OSA is an independent risk factor for atherosclerosis. Atherogenicity in OSA patients has been assumed to be associated with the NF-κB pathways. Although foam cells are considered to be a hallmark of atherosclerosis, how IH as in OSA affects their development has not been fully understood. Therefore, we hypothesized that IH induces macrophage foam cell formation through NF-κB pathway activation. To test this hypothesis, peritoneal macrophages collected from myeloid-restricted IKK-β-deleted mice were incubated with native LDL and exposed to either IH or normoxia. After exposure, NF-κB pathway activity and intracellular cholesterol were measured. In control macrophages, IH significantly increased NF-κB pathway activity by 93% compared with normoxia (P < 0.05). However, such response to IH was diminished by IKK-β deletion (increased by +31% compared with normoxia; P = 0.64), suggesting that IKK-β is critical for IH-induced NF-κB pathway activation. Likewise, in control macrophages, total cholesterol was increased in IH compared with normoxia (65.7 ± 3.8 μg/mg cellular protein and 53.2 ± 1.2, respectively; P < 0.05). However, this IH-induced foam cell formation was disappeared when IKK-β was deleted (52.2 ± 1.2 μg/mg cellular protein for IH and 46.3 ± 1.7 for normoxia; P = 0.55). This IH-mediated effect still existed in macrophages without LDL receptor. Taken together, our findings show that IH activates the IKK-β-dependent NF-κB pathway and that this, in turn, induces foam cell formation in murine macrophages.

Ischemic stroke in a young adult with extremely elevated lipoprotein(a): A case report and review of literature

Lipoprotein(a) [Lp(a)] is an apolipoprotein(a) molecule bound to 1 apolipoprotein B-100. Elevated levels of Lp(a) are thought to be an independent risk factor for atherosclerosis and to promote thrombosis through incompletely understood mechanisms. We report a 34-year-old man with an ischemic stroke in the setting of an extremely high Lp(a) level—212 mg/dL. He developed severe carotid artery stenosis over a 6-year period and had thrombus formation post-carotid endarterectomy. To our knowledge, this case is unique because the Lp(a) is the highest reported level in a patient without renal disease. Moreover, this is the first reported case of the youngest individual with a stroke presumably related to development of carotid plaque over a 6-year period. The thrombotic complication after endarterectomy may have been related to the prothrombotic properties of Lp(a). Of note, the Lp(a) level did not respond to atorvastatin but did decrease 15% after aspirin 325 mg was added although his Lp(a) levels were variable, and it is not clear that this was cause and effect. This case highlights the need to better understand the relation between Lp(a) and vascular disease and the need to screen family members for elevated Lp(a). We also review treatment options to lower Lp(a) and ongoing clinical trials of newer lipid-lowering drugs that can also lower Lp(a).

Clinical Characteristics of Young Type 2 Diabetes Patients with Atherosclerosis.

ObjectiveThe prevalence of type 2 diabetes is increasing rapidly in the young population. The clinical characteristics and risk factors for young type 2 diabetes patients with atherosclerosis are not fully explicated. The aim of the present study was to investigate various clinical and biochemical characteristics of young type 2 diabetic patients with atherosclerosis.Design and MethodsThis was a cross-sectional study. The study involved 2199 hospitalized patients with type 2 diabetes. The young patients were classified into the atherosclerotic group or the non-atherosclerotic group, and we also enrolled an older group with peripheral atherosclerosis disease and an age of at least 45 years. Comparisons were made between the different groups to investigate the cardiovascular and metabolic risk profiles of young type 2 diabetes patients with atherosclerosis. We also used logistic regression models to assess the atherosclerosis risk factors for young patients.ResultsCompared to older type 2 diabetes patients with atherosclerosis, young patients with atherosclerosis had more deleterious profiles of weight and hyperlipidemia. Only age and diabetes duration were found to be significant independent risk factors for atherosclerosis in young patients. The ratio of the presence of atherosclerosis in the lower extremity arteries alone was significantly higher in young patients than older patients (26.4% vs. 14.0%, P = 0.000).ConclusionYoung type 2 diabetes patients with atherosclerosis have more adverse cardiovascular risk profiles and inadequate control of these risk factors. Lower extremity examination is of high importance in young patients.

Circulating miRNA in patients with non-alcoholic fatty liver disease and coronary artery disease

BackgroundNon-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and coronary artery disease (CAD) is the cardiac manifestation of metabolic syndrome. NAFLD is strongly linked to CAD...

Oxidative stress markers in coronary artery disease patients with diabetes mellitus

Coronary artery disease (CAD) is the major cause of morbidity and mortality. Diabetes is one of the powerful and independent risk factor for CAD. Hyperglycemia and hypercholesterolemia initiate the oxidative stress and complications like atherosclerosis which induces poor prognosis in diabetic CAD patients. The aim of the present study was to assess oxidative stress by comparing the levels of malondialdehyde and comet tail length in diabetic CAD patients, non-diabetic CAD patients and healthy controls. The study included 400 subjects of which 200 were healthy controls, 100 were diabetic CAD patients, and 100 were non-diabetic CAD patients. Fasting and postprandial glucose levels, glycosylated hemoglobin, serum lipid levels, malondialdehyde, and DNA damage were estimated in all subjects by using commercially available kits and standard protocols. FBS (185.60 ± 6.0 mg/dL), PPG (250 ± 7.06 mg/dL), HbA1c (10.65 ± 2.01 %), TC (280.72 ± 5.25 mg/dL), TG (195.11 ± 5.99 mg/dL), LDL (163.28 ± 5.68 mg/dL), MDA (9.74 ± 2.33 n moles/mL), and comet tail length (21.60 ± 5.69 μm) were significantly high in diabetic CAD patients (p < 0.05) compared to non-diabetic CAD patients and controls. Fasting and postprandial blood sugar levels significantly correlated with oxidative stress markers like MDA (r = 0.553, r = 0.557, p < 0.01) and comet tail length (r = 0.489, r = 0.626, p < 0.01) in diabetic CAD patients compared to non-diabetic CAD patients. Our study showed that diabetic CAD patients with increased levels of oxidative stress markers (MDA and DNA damage) might have the poor prognosis than non-diabetic CAD patients.

Revisit lipoprotein(a): An independent risk factor for coronary artery disease severity in Indian population and its correlation with Gensini score

AimsLipoprotein(a) [Lp(a)] levels have shown wide ethnic variations. Further studies are needed, as there are sparse data in Indian population on mean Lp(a) levels and its link with clinical variables and severity of coronary artery disease (CAD). MethodsIn present study total 516 patients of suspected CAD undergoing coronary angiography were included after applying inclusion and exclusion criteria on the target population. Serum Lp(a) estimation was performed by immunoturbidimetric method. ResultsAmong patients with normal coronaries, 67.3% patients had lipoprotein(a) levels <25 and 32.7% patients had lipoprotein(a) levels ≥25. In patients where 1 vessel was involved, 66.7% patients had lipoprotein(a) levels <25 and 33.3% patients had lipoprotein(a) levels ≥25. In patients where 2 vessels were involved 56% patients had lipoprotein(a) levels <25 and 44% patients had lipoprotein(a) levels ≥25. In patients where 3 vessels were involved 27.6% patients had lipoprotein(a) levels <25 and 72.6% patients had lipoprotein(a) levels ≥25. These results were significant and the p-value <0.001. The Gensini score was 29, when patients had lipoprotein(a) levels <25, while the Gensini score was 61, when patients had lipoprotein(a) levels ≥25 (p-value <0.001). Mean number of diseased vessels, when lipoprotein(a) levels were <25 was 1, while the mean number of vessels were 3 when the lipoprotein(a) levels were ≥25 (p-value of <0.001). ConclusionLipoprotein(a) was found to be an important independent risk factor for CAD in Indian population and raised Lp(a) levels were also associated with increasing severity of the coronary vessel disease and multivessel CAD.

Effect of Serum Homocysteine on Coronary Artery Disease in Younger and Older Ischaemic Heart Disease Patients

Background: Hyperhomocysteinemia is known as an independent risk factor of atherosclerosis. But the probable role of Hyperhomocysteinemia in Premature Coronary Artery Disease (CAD) is not well studied. The aim of this study was to assess the role of serum homocysteine on angiographically documented CAD in younger and older ischaemic heart disease (IHD) patients.Methods: Total 120 patients with IHD admitted in the Department of Cardiology, Dhaka Medical College Hospital for CAG were selected by purposive sampling method and divided into two groups. 60 patients in Group-I, d” 40 years of age (Younger); 60 patients in Group-II, &gt;40 years of age (Older). Homocysteine was measured in all patients and other demographical and clinical data were collected. Homocysteine level was correlated with the presence and severity of CAD.Results: Smoking, positive family history of IHD, dyslipidaemia and hyper homocysteinemia were important risk factors in younger IHD patients. Whereas, hypertension, diabetes mellitus and dyslipidaemia were important cardiovascular risk factors in older age group. Obesity was not an important risk factors as evidenced by mean BMI. Serum homocysteine was not well related to presence of CAD or extent of CAD in older IHD patients. However in younger patients hyperhomocysteinemia was related to both presence and severity of CAD.Conclusion: In younger IHD patients hyperhomocysteinemia is an important cardiovascular risk factor. But in older patients it loses its significance. So serum homocysteine level should be screened routinely in younger IHD patients.Cardiovasc. j. 2016; 8(2): 138-142