Search

Background: Associations between dietary fats and mortality are unclear., Methods: We evaluated the relationship between quartiles of total fat, mono-unsaturated (MUFA), polyunsaturated (PUFA) and saturated fatty acid (SFA) consumption, and all-cause, coronary heart disease (CHD), stroke, and type 2 diabetes (T2D)-associated mortality in 24,144 participants from the National Health and Nutrition Examination Surveys (NHANES) 1999-2010. We added our results to a meta-analysis based on searches until November 2018., Results: In fully adjusted Cox-proportional hazard models in our prospective study, there was an inverse association between total fat (HR: 0.90, 95% confidence interval 0.82, 0.99, Q4 vs Q1) and PUFA (0.81, 0.78-0.84) consumption and all-cause mortality, whereas SFA were associated with the increased mortality (1.08, 1.04-1.11). In the meta-analysis of 29 prospective cohorts (n = 1,164,029) we found a significant inverse association between total fat (0.89, 0.82-0.97), MUFA (0.94, 0.89-0.99) and PUFA (0.89, 0.84-0.94) consumption and all-cause mortality. No association was observed between total fat and CVD (0.93, 0.80-1.08) or CHD mortality (1.03 0.99-1.09). A significant association between SFA intake and CHD mortality (1.10, 1.01-1.21) was observed. Neither MUFA nor PUFA were associated with CVD or CHD mortality. Inverse associations were observed between MUFA (0.80, 0.67-0.96) and PUFA (0.84, 0.80-0.90) intakes and stroke mortality., Conclusions: We showed differential associations of total fat, MUFA and PUFA with all-cause mortality, but not CVD or CHD mortalities. SFA was associated with higher all-cause mortality in NHANES and with CHD mortality in our meta-analysis. The type of fat intake appears to be associated with important health outcomes., (Copyright © 2020 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

The associations of egg consumption with total, coronary heart disease (CHD), and stroke mortality are poorly understood. We prospectively evaluated the link between total, CHD, and stroke mortality with egg consumption using a randomly selected sample of U.S. adults. Next we validated these results within a meta-analysis and systematic review of all available prospective results. We assessed the mean of cardiometabolic risk factors across the intake of eggs. We made the analysis based on data from the National Health and Nutrition Examination Surveys (NHANES; 1999-2010). In NHANES, vital status through December 31, 2011, was ascertained. Cox proportional hazard regression models were used to relate baseline egg consumption with all-cause and cause-specific mortality. PubMed, Scopus, Web of Science, and Google Scholar databases were also searched (up to December 2017). The DerSimonian-Laird method and generic inverse variance methods were used for quantitative data synthesis. Overall, 23,524 participants from NHANES were included (mean age of 47.7 years; 48.7% were men). Across increasing the intake of eggs, adjusted mean levels of cardiometabolic risk factors worsened. Adjusted logistic regression showed that participants in the highest category of egg intake had a greater risk of diabetes (T2DM; 30%) and hypertension (HTN; 48%). With regard to total and CHD mortality, multivariable Cox regression in a fully adjusted model showed no link in males and females. In males, egg intake had a reverse (66%) association with stroke mortality, while this link was not significant among females. The results of pooling data from published prospective studies also showed no link between CHD and total mortality with egg consumption, whereas we observed a reverse (28%) association between egg intake and stroke mortality. These findings were robust after sensitivity analysis. According to our findings, egg intake had no association with CHD and total mortality, whereas was associated with lower risk of mortality from stroke. Egg consumption was associated with T2DM, HTN, C-reactive protein, and markers of glucose/insulin homeostasis. If confirmed in clinical trials (causation), this information may have applications for population-wide health measures. Key teaching points No link between total and CHD mortality with eggs intake in males and females. In males, egg intake had a reverse association with stroke mortality, while this link was not significant among females. The results of pooling data from published prospective studies also showed no link between CHD and total mortality with egg consumption, whereas we observed a reverse association between egg intake and stroke mortality.

Background: The health outcomes associated with extremely low or high plasma concentrations of high-density lipoprotein cholesterol (HDL-C) are not well documented mainly because of the small numbers of participants with such values included in the clinical trials., Objective: We prospectively investigated the association between extremely low and high HDL-C with: 1) the risk of overall, coronary heart disease (CHD), cerebrovascular and cancer mortality, and, 2) their link with inflammatory factors., Methods: Analysis was based on subjects ≥18 years old from the National Health and Nutrition Examination Surveys (NHANES). We categorized HDL-C levels as follows: [low HDL-C group ≤30 (extremely low), 30-40 (low), and ≥40 (reference)] [high HDL-C group = 40-80 (reference), 80-100 (high) and ≥100 mg/dl (extremely high). Cox proportional hazard regression models and analysis of covariance accounted for survey design, masked variance and sample weights., Results: After adjustment for age, race and sex, we found that the very low HDL-C category (<30 mg/dl) had a greater risk of total mortality (risk ratio [RR]: 3.00, 95%CI: 2.20-4.09). RR for CHD and stroke mortality was 2.00 and 2.53, respectively; there was no link between cancer and level of HDL-C (p = 0.235). The association between total mortality, CHD and stroke with the level of HDL-C attenuated but remained significant even after adjustment for demographics, dietary, cardiovascular risk factors and treatment for dyslipidemia (all p < 0.001). After adjustments, subjects with extremely high HDL-C levels had a higher risk of mortalities (all p < 0.001). Mexican-American ethnicity, subjects in the low level of HDL-C (30-40 mg/dl) category had higher risk of mortalities than those with a very low level (all p < 0.001). Concentration of C-reactive protein, fibrinogen and white blood count significantly decreased as the level of the HDL-C increased; these findings were robust after adjustment for demographics, dietary, cardiovascular risk factors and treatment for dyslipidemia (all p < 0.001); further subjects with extremely high HDL-C levels have a greater levels of inflammatory factors (all p < 0.001)., Conclusions: Both extremely low and high HDL-C levels were associated with greater risk of mortalities (total, CHD and stroke) and higher level of inflammatory factors, while there was no link between level of HDL-C and risk of cancer. Moreover, we found evidence of an HDL-C paradox in Mexican-American ethnicity participants., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Aims: Relatively little is known about the health outcomes associated with very low plasma concentrations of high-density lipoprotein cholesterol (HDL-C) mainly because of the small numbers of individuals with such extreme values included in clinical trials. We, therefore, investigated the association between low and very low HDL-C concentration at baseline and incident all-cause-mortality, death from malignant disease (i.e. cancer), and with fatal or non-fatal incident coronary heart disease (CHD) in individuals from the Reasons for Geographical And Racial Differences in Stroke (REGARDS) study., Methods and Results: Analysis was based on 21 751 participants from the REGARDS study who were free of CHD, other cardiovascular disease, and cancer at baseline and were categorized by baseline HDL-C into <30 mg/dL (very low), 30-<40 mg/dL (low), and ≥40 mg/dL (reference). A series of incremental Cox proportional hazards models were employed to assess the association between the HDL-C categories and outcomes. Statistical analysis was performed using both complete case methods and multiple imputations with chained equations. After adjustment for age, race, and sex, the hazard ratios (HRs) comparing the lowest and highest HDL-C categories were 1.48 [95% confidence interval (CI) 1.28-1.73] for all-cause mortality, 1.35 (95% CI 1.03-1.77) for cancer-specific mortality and 1.39 (95% CI 0.99-1.96) for incident CHD. These associations became non-significant in models adjusting for demographics, cardiovascular risk factors, and treatment for dyslipidaemia. We found evidence for an HDL paradox, whereby low HDL (30-<40 mg/dL) was associated with reduced risk of incident CHD in black participants in a fully adjusted complete case model (HR 0.63; 95% CI 0.46-0.88) and after multiple imputation analyses (HR 0.76; 95% CI 0.58-0.98). HDL-C (<30 mg/dL) was significantly associated with poorer outcomes in women for all outcomes, especially with respect to cancer mortality (HR 2.31; 95% CI 1.28-4.16) in a fully adjusted complete case model, replicated using multiple imputation (HR 1.81; 95% CI 1.03-3.20)., Conclusion: Low HDL-C was associated with reduced risk of incident CHD in black participants suggesting a potential HDL paradox for incident CHD. Very low HDL-C in women was significantly associated with cancer mortality in a fully adjusted complete case model.

Purpose of Review: Type 2 diabetes mellitus (T2DM) is associated with increased coronary heart disease (CHD) morbidity and mortality. These patients are also more prone to heart failure, arrhythmias and sudden cardiac death. Furthermore, coronary interventions performed in such high-risk patients have worse outcomes. In this narrative review, we discuss the role of diabetic dyslipidaemia on the risk of CHD in patients with T2DM. The effects of hypolipidaemic, antihypertensive and antidiabetic drugs on lipid and glucose metabolism in T2DM are also considered., Recent Findings: Among CHD risk factors, diabetic dyslipidaemia characterized by moderately elevated low-density lipoprotein (LDL) cholesterol, increased triglycerides and small, dense LDL particles as well as decreased high-density lipoprotein cholesterol levels may contribute to the increased CHD risk associated with T2DM. Hypolipidaemic, antihypertensive and antidiabetic drugs can affect lipid and glucose parameters thus potentially influencing CHD risk. Such drugs may improve not only the quantity, but also the quality of LDL as well as postprandial lipaemia., Summary: Current data highlight the importance of treating diabetic dyslipidaemia in order to minimize CHD risk. Both fasting and postprandial lipids are influenced by drugs in patients with T2DM; physicians should take this into consideration in clinical decision making.

Purpose of Review: This narrative review discusses the associations between metabolic and inflammatory diseases, as well as radiotherapy and chemotherapy with coronary heart disease (CHD) and related risk factors, to support (or not) their potential role as CHD equivalents., Recent Findings: Although not regarded as CHD equivalents, several metabolic and inflammatory disorders are associated with an increased risk of CHD morbidity and/or mortality. These conditions include metabolic syndrome, impaired glucose metabolism, nonalcoholic fatty liver disease, obstructive sleep apnoea syndrome, erectile dysfunction, periodontitis, inflammatory bowel diseases, systemic vasculitis and HIV infection, as well as chemotherapy and radiotherapy., Summary: More research should be carried out to identify which conditions can be added to the list of CHD equivalents.

Coronary heart disease (CHD) is the leading cause of death in the developed world in both men and women. Elevated low-density lipoprotein cholesterol (LDL-C) levels are strong and independent vascular risk factors in both genders. Statins effectively decrease LDL-C levels, reduce vascular morbidity and mortality and are an essential component of CHD preventive strategies. However, women are less likely to be prescribed statins than men in both primary and secondary prevention settings. It was argued that there is no conclusive evidence showing that statins are beneficial for the prevention of vascular disease in women, particularly in those without established CHD. This review summarizes the evidence regarding the effects of statins in the prevention of CHD in women. Accumulating data suggest that statins are equally effective in both men and women. The lack of significant effects in some studies appears to be primarily due to the under-representation of women and the ensuing lack of statistical power. Current guidelines for the prevention of vascular disease also recommend a similar management of dyslipidemia in both men and women. Therefore, statin treatment should be implemented with the same criteria and with the same goals in both genders.

Background: Apolipoprotein (apo) E polymorphism has been associated with coronary heart disease (CHD) and obesity. We aimed to determine whether apoE polymorphism is related to CHD in patients with different body mass index (BMI)., Patients and Methods: A total of 359 CHD men and 248 healthy controls with BMI <27 kg/m2 were genotyped for the apoE polymorphism. The CHD patients were divided into: normoweight (BMI: 24 +/- 1 kg/m2, n=98), overweight (BMI: 27 +/- 1 kg/m2, n=189) and obese (BMI: 32 +/- 2 kg/m2, n=72) groups., Results: There was a significant difference in apoE genotype frequency between normoweight CHD patients and healthy controls (epsilon2epsilon2 + epsilon2epsilon3: 6% vs. 15%, p=0.029; epsilon3epsilon3: 83% vs. 70%, p=0.045, respectively). The apo epsilon3epsilon4 + epsilon4epsilon4 frequency was higher in obese compared with normoweight CHD patients (p=0.043). The severity of CHD was similar in all patients with CHD., Conclusion: Normoweight CHD patients, despite having a lower BMI and more favorable lipid profile, did not display any significant difference in CHD severity. This could be partially attributed to the lower frequency of the epsilon2 cardio-protective allele in normoweight CHD patients compared with normoweight healthy individuals.

Omega-3 fatty acids (FAs) are divided into long-chain fatty acids (eicosapentaenoic acid and docosahexaenoic acid ), which are found in fatty fish, and intermediate-chain FAs (alpha-linolenic acid), which are found in vegetable oils. Omega-3 FAs favorably modulate a variety of vascular risk factors and also exert antiarrhythmic effects. Epidemiologic data suggest that increased consumption of marine omega-3 FAs is associated with reduced coronary heart disease (CHD) mortality. Randomized controlled studies also show that supplementation with EPA and DHA reduces CHD risk, primarily in the secondary prevention setting. Data are more limited on the efficacy of marine omega-3 FAs for the primary prevention of CHD and on the role of alpha-linolenic acid. Increased intake of EPA and DHA represents a valuable tool for vascular disease prevention and should be recommended in all patients with CHD.

South Asians originate from the Indian sub-continent (India, Pakistan, Bangladesh, Sri Lanka and Nepal) and represent one fifth of the world's population. Several studies suggested that South Asians have an increased risk of developing coronary heart disease (CHD) when compared with European populations. We review the role of traditional and emerging risk factors in the increased CHD risk in South Asians. The high prevalence of insulin resistance and type 2 diabetes mellitus in South Asians may be a major cause for their elevated vascular risk. However, other established and emerging risk factors are also overrepresented in South Asians. Large-scale prospective studies could determine the relative contribution of established and emerging vascular risk factors in South Asians. There is an urgent need for trials in South Asians that will evaluate clinical outcomes following treatment of these risk factors.

Background: Preliminary data suggest that apolipoprotein J (ApoJ) may play a role in the development and progression of atherosclerosis. Leptin, an adipose tissue hormone, exerts important cardiovascular effects. The association between serum ApoJ and leptin concentrations was assessed in patients with established or suspected coronary heart disease (CHD)., Patients and Methods: Serum ApoJ and leptin concentrations were evaluated in 67 CHD patients undergoing coronary angiography [54 individuals with significant (> or =50%) coronary artery stenosis and 13 patients without significant coronary artery stenosis on angiography]., Results: Serum ApoJ concentrations in patients with significant coronary artery stenosis were significantly higher than in those without (303.9+/-118.6 vs. 121.2+/-37.5 microg/mL, respectively; p<0.001). The reverse pattern was observed for serum leptin levels (8.6+/-5.5 vs. 20.6+/-17.1 ng/ml, respectively; p=0.016). There was a significant negative correlation between ApoJ and leptin levels (r=-0.353; p=0.003)., Conclusion: ApoJ and leptin may be markers for CHD.

Background: Reducing low-density lipoprotein cholesterol (LDL-C) levels to National Cholesterol Expert Panel (NCEP) goal is recommended. However, sex-specific effects may influence benefit., Methods and Results: In this post hoc analysis of the GREek Atorvastatin and Coronary heart disease (CHD) Evaluation [GREACE] study we investigated the extent in vascular event reduction by statin treatment according to sex. From a total of 1600 patients with stable CHD, 624/176 and 632/168 were men/women on atorvastatin or on usual care, respectively. During 3-year follow-up, comparison of atorvastatin treatment with usual care demonstrated a relative risk reduction (RRR) of the primary end point (all vascular events) of 54% in women (hazard ratio [HR] 0.46, 95% confidence interval [CI] 0.24-0.87, p=0.003) and of 50% in men (HR 0.50, 95% CI 0.32-0.70, p<0.001). The fall in LDL-C levels played the key role in end point reduction in both sexes. However, in men there was an additional benefit related to the atorvastatin-induced increase in high density lipoprotein cholesterol (HDL-C) and estimated glomerular filtration rate (eGFR), while in women end points were related to a substantial triglycerides (TG) reduction., Conclusions: Treatment with atorvastatin to the NCEP LDL-C goal compared with 'usual care' significantly reduced CHD morbidity and mortality in both men and women. Both men and women benefited from statin treatment possibly with different mechanisms making a contribution over and above LDL-C reduction.

Retrospective studies show that statin use prevents congestive heart failure and decreases mortality in patients with congestive heart failure; however, only one prospective study is available. In the Controlled Rosuvastatin Multinational Trial in Heart Failure study, rosuvastatin (10 mg/d) was compared with placebo in patients with advanced coronary heart disease-related congestive heart failure. There was no significant difference between rosuvastatin and placebo except for hospitalization rates. Statins must be given to all patients with coronary heart disease as early as possible because they may not work in patients with advanced congestive heart failure.

The purpose of this study was to investigate the relationship between alcohol consumption and the prevalence of the metabolic syndrome (MetS), type 2 diabetes mellitus (DM), coronary heart disease (CHD), stroke, peripheral arterial disease (PAD), and overall cardiovascular disease (CVD) in a Mediterranean cohort. It consisted of a cross-sectional analysis of a representative sample of Greek adults (n = 4,153) classified as never, occasional, mild, moderate, or heavy drinkers. Cases with overt CHD, stroke, or PAD were recorded. In our population, 17% were never, 23% occasional, 27% mild, 24% moderate, and 9% heavy drinkers. Moderate alcohol consumption was associated with a lower trend for the prevalence of the MetS (P = .0001), DM (P < .0001), CHD (P = .0002), PAD (P = .005), and overall CVD (P = .001) but not stroke compared with no alcohol use. Heavy drinking was associated with an increase in the prevalence of all of these disease states. Wine consumption was associated with a slightly better effect than beer or spirits consumption on the prevalence of total CVD, and beer consumption was associated with a better effect than spirits consumption. Alcohol intake was positively related with body weight, high-density lipoprotein cholesterol levels, and hypertension. Moderate alcohol consumption is associated with a lower prevalence of the MetS, DM, PAD, CHD, and overall CVD but not stroke compared with no alcohol use in a Mediterranean population. Heavy drinking was associated with an increase in the prevalence of all of these disease states. Advice on alcohol consumption should probably mainly aim at reducing heavy drinking.

High triacylglycerol (TAG) levels may predict vascular risk. The effect of a statin-induced reduction in TAG levels, irrespective of HDL-C increase, on clinical outcome has not yet been addressed by an endpoint study in patients with coronary heart disease (CHD). The GREACE study compared usual with structured care aimed at achieving LDL-C = 100 mg/dL (2.6 mmol/L) by dose titration with atorvastatin. All patients had CHD and were followed for 3 years. This post hoc analysis of GREACE examines the effect of statins on TAG levels and their relation with cardiovascular disease (CVD) events in all patients and in the subgroup of patients with metabolic syndrome (MetS). Baseline TAG levels >150 mg/dL (1.7 mmol/L) were predictive of subsequent CVD events [cardiac mortality, non-fatal myocardial infarction (MI), unstable angina (UA), revascularisation, congestive heart failure (CHF), and stroke] only in statin untreated patients. Stepwise regression analysis showed that with every 20% statin-related TAG reduction there was a decrease in CVD risk by 12% (HR 0.88, 95% CI 0.75-0.95, P = 0.007) in the structured care group vs. the usual care group, by 8% (HR 0.92, 95% CI 0.81-0.97, P = 0.02) in all statin treated patients vs. the untreated ones and by 15% (HR 0.85, 95% CI 0.65-0.94, P = 0.005) in those with MetS treated with a statin vs. those untreated. Using the same analysis but only taking into consideration vascular events (cardiac mortality, non-fatal MI, UA, revascularisation, and stroke) there was a 18% (HR = 0.82, 95% CI 0.57-0.96, P = 0.03) decrease in risk in the MetS (+) patients treated with a statin vs. those not on a statin, and a decrease in risk by 16% (HR = 0.84, 95% CI 0.53-1.07, P = 0.08), when only hard vascular endpoints (cardiac mortality, non-fatal MI, and stroke) were considered. TAG levels are predictive of subsequent CVD events in statin untreated CHD patients. Statin (mainly atorvastatin)-induced decrease in TAG levels was related to a significant reduction in subsequent CVD events. This benefit was more pronounced in CHD MetS (+) patients.

Background and Aims: Statins are an essential component of the therapeutic approach of patients with atherosclerotic disease. Statin use is also associated with improved peri-operative and long-term outcomes in these patients. We aimed to define the role of statin treatment in patients undergoing percutaneous revascularization procedures., Literature Search Method: We searched Medline for studies assessing the effect of statin treatment on percutaneous interventions., Literature Search Results: Early statin treatment is associated with improved outcomes in patients undergoing percutaneous coronary intervention procedures. Current evidence implies that statin treatment may also play a beneficial role in the management of patients undergoing percutaneous renal artery revascularization and endovascular abdominal aortic aneurysm repair, carotid angioplasty/stenting and endovascular peripheral arterial interventions., Conclusions: Preliminary data suggest that statins exert multiple beneficial actions in patients undergoing percutaneous interventions. Future randomized trials are expected to further evaluate the beneficial effects of statins in these procedures.

Objective: We aimed to define the role of treatment using statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) in the management of patients with carotid artery disease., Literature Search Methods: We searched PubMed for studies evaluating the effect of statins on carotid IMT and the occurrence of cerebrovascular events., Literature Search Results: Current evidence indicates that routine statin therapy reduces carotid intima-media thickness progression and stroke risk. Additionally, statin treatment significantly reduces perioperative as well as long-term morbidity and mortality in patients undergoing carotid surgery or endovascular interventions. It would also be expected that statins would reduce coronary events in this high-risk population., Conclusions: Statins should be considered as an essential component of the therapeutic approach of patients with carotid artery stenosis.

Background: Metabolic syndrome (MetS) is associated with increased risk for both vascular and chronic kidney disease. Whether statins ameliorate these risks is not established., Methods: This post hoc analysis of the GREek Atorvastatin and Coronary heart disease (CHD). Evaluation (GREACE) examines the effect of statins on estimated glomerular filtration rate (e-GFR) and serum uric acid (SUA) levels and their relation to vascular events in CHD patients with MetS. MetS patients were divided into two groups: Group A (n = 365) received lifestyle advice, target-driven treatment with statins (mainly atorvastatin) and treatment for hypertension and elevated glucose. Group B (n = 347) received the same except for statins. Patients without MetS were divided into those who received treatment similar to Group A and Group B [Groups C (n = 504) and D (n = 384), respectively]. All patients were followed for 3 years., Results: A total of 12.1% of patients in Group A experienced a vascular event vs 28% in Group B; risk ratio (RR) 0.43, 95% confidence interval (CI) 0.20-0.64, P < 0.0001, while in those without MetS (Group C vs Group D), the respective RR was 0.59, 95% CI 0.41-0.79, P < 0.0001. In Group A, e-GFR increased by 13.7% and SUA levels fell by 8.9%, while in Group B e-GFR was reduced by 5.8% and SUA increased by 4.3% (P < 0.005). Stepwise regression analysis showed that these changes were independently related to vascular events., Conclusion: Among CHD patients, those with MetS benefited more from statin treatment than those without MetS. This benefit could be partially attributed to favourable changes in e-GFR and SUA levels probably induced by statin treatment.

Background: Postprandial hyperlipidaemia may be a predictor of vascular risk., Design: We evaluated postprandial lipaemia after an oral fat tolerance test (OFTT) in men (n=41) and women (n=21) with metabolic syndrome (MetS)., Methods: Triglyceride (TG) levels were measured before and 2, 4, 6 and 8 h after the fat load., Results: Men showed a greater plasma TG response 8 h after the fat load (284+/-117 versus 224+/-126 mg/dl, P=0.029). Only fasting TG levels significantly predicted the TG area under the curve (AUC) and incremental AUC., Conclusions: Men had a more pronounced postprandial hypertriglyceridaemia and seem to have delayed TG clearance.

Apolipoprotein (apo) E polymorphism has been associated with coronary heart disease (CHD) although its relation to the age of CHD onset is still not defined. The age of onset of established CHD was obtained from 502 Greek men and compared to 103 healthy men. The age grouping was based on the age of CHD onset (earlier < or =44 years, n = 73, intermediate 45-64 years, n = 321, and later > or =65 years, n = 108). Apo E genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and the lipid profile was assessed. No differences in genotype and allele frequencies were found within the CHD groups. The apo epsilon3/4 genotype and the apo epsilon4 allele were less frequent in the earlier-onset group than in healthy men (11.0 % vs 22.3%, Pearson Chi-Square p = 0.028 and 6.8% vs 13.6%, Pearson Chi-Square p = 0.023, respectively). The lipid profile was similar in all genotypes of all groups except for high-density lipoprotein cholesterol levels, which were higher in epsilon2 carriers compared to non-epsilon2 carriers (in mg/dL [+/-SD]; 44 [9] vs 39 [10], in mmol/L [+/-SD]; 1.1 [0.2] vs 1.0 [0.3] p = 0.005). There is an association between apo E genotype and early onset of CHD in Greek men. In the earlier CHD onset group, the apo epsilon3/4 genotype was less frequent compared to healthy men. This supports that the apo epsilon3/4 genotype is associated with decreased risk of premature CHD. Because the results of similar studies are not consistent, it may be that the relationship between apo E genotype and CHD is related to ethnicity rather than a universal phenomenon.

Declaration of Interest: The GREACE study was conducted independently; no Company or Institution has supported it financially. Some of the authors have attended conferences and participated in other trials sponsored by various pharmaceutical companies. We assessed the possible 'synergy' of statins and aspirin (ASA) in reducing vascular events in patients with coronary heart disease, in a post hoc analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. All patients (n = 1600) were divided into four groups according to long-term treatment: Group A (n = 787; statin + ASA), B (n = 93; statin - no ASA), C (n = 599; no statin - on ASA) and D (n = 121; no statin - no ASA). From all patients 692 were either on a statin or ASA monotherapy (Groups B + C). Relative risk reductions (RRRs) in 'all events' (primary endpoint) between groups were assessed. During the 3-year follow-up there were 292 cardiovascular events; 92 (12% of patients) in Group A, 14 (15%) in group B, 144 in Group C (24%) and 42 events in Group D (35%). The total number of events in Group B + C was 158 (23%). The RRRs in the primary endpoint were: Group A versus B 24% (P = 0.1912), A versus C 51% (P < 0.0001), A versus B + C 49% (P < 0.0001) and A versus D 71% (P < 0.0001). The RRRs in Group B versus C was 36% (P = 0.0431) and B versus D 57% (P = 0.0012), while in C versus D 33% (P = 0.0084). Our findings show that statins and ASA have an additive effect in reducing cardiovascular events. Aggressive statin use in the absence of ASA also substantially reduced cardiovascular events. Treatment with ASA in the absence of statin use reduced clinical events in comparison to patients not treated with either drug.

Background: Although available guidelines suggest reducing low-density lipoprotein cholesterol (LDL-C) to below 100 mg/dL (2.6 mmol/L), the importance of target-oriented therapy remains controversial. To assess whether achieving guideline-based targets is of benefit, the relationship between clinical outcomes and lipid levels (baseline and on-study) was evaluated in the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. This study demonstrated significant reductions in morbidity and mortality associated with active dose titration of atorvastatin and structured management of dyslipidaemia., Methods and Results: Intention-to-treat analysis (Cox proportional hazards model) was used to assess the relationship between lipid values and coronary events. Higher levels of LDL-C at baseline were associated with a greater risk of subsequent events among patients randomized to usual care. Reducing the LDL-C and the non-high density lipoprotein cholesterol (non-HDL-C) level to the National Cholesterol Educational Program (NCEP) Adult Treatment Panel (ATP) III goals required greater doses of atorvastatin for the higher baseline quartile of LDL-C. During the study there was a greater reduction in the risk of coronary heart disease (CHD) events in atorvastatin-treated patients who were in the highest quartile of LDL-C at baseline, after achieving the LDL-C treatment goal, in comparison to the usual care patients in the highest baseline LDL-C quartile., Conclusions: Achieving the NCEP ATP III LDL-C and non-HDL-C goals by titrating up the dose of atorvastatin was associated with a significant reduction in vascular events in patients with CHD. The greatest benefit was seen in those patients with the highest baseline LDL-C levels.

Objective: To investigate the relationship between changes in high density lipoprotein cholesterol(HDL-C) levels after statin treatment and the risk for coronary heart disease (CHD)-related events in the secondary CHD prevention GREek Atorvastatin and Coronary heart disease Evaluation (GREACE) Study. These findings suggested that dose titration with atorvastatin (10-80 mg/day, mean 24 mg/day)achieves the National Cholesterol Educational Program treatment goals and significantly reduces morbidity and mortality, in comparison to usual care., Methods: Analysis of variance was used to assess the effect of atorvastatin on HDL-C over time (up to 48 months) in 1600 CHD patients. The time-dependent multivariate Cox predictive model,involving backward stepwise logistic regression,was used to evaluate the relation between coronary events and HDL-C changes., Results: The mean increase in HDL-C levels during the study was 7%. All doses of atorvastatin significantly increased HDL-C levels. Increases were greater in men (7.8 vs 6.1%; p = 0.02), in combined hyperlipidaemia (7.9 vs 6.4% for hypercholesterolaemia; p = 0.04), and in the lower baseline HDL-C quartile (9.2 vs 5.3%, 1st vs 4th quartile; p = 0.001). After adjustment for 24 predictors of coronary events, multivariate analysis revealed a Hazards Ratio of 0.85 (95% confidence interval 0.76-0.94; p = 0.002) for every 4 mg/dL(0.1 mmol/L) increase in HDL-C., Conclusions: There was a significant beneficial effect on HDL-C levels across the dose range of atorvastatin. Clinical outcomes in the structured care arm of GREACE were determined in part by the extent of atorvastatin-induced HDL-C increase. This effect was independent from benefit induced by low density lipoprotein cholesterol (LDL-C)reduction, suggesting that the CHD risk reduction associated with a rise in a low HDL-C at baseline remains significant under aggressive (-46%) LDL-C lowering conditions. However, the relationship between HDL-C and vascular risk may be weaker when LDL-C levels are aggressively lowered.

Background: Little is known about the effect of dyslipidemia on serum uric acid (SUA) levels, and less is known about the effect of statin treatment on them. The GREek Atorvastatin and Coronary-heart-disease Evaluation study suggested that a mean atorvastatin dose of 24 mg/d achieves the National Cholesterol Educational Program treatment goals and significantly reduces morbidity and mortality in patients with coronary heart disease (CHD) in comparison to the usual care. Here, we report the time course of SUA levels in usual-care patients undertreated for their dyslipidemia (12% were administered statins) in comparison to structured-care patients treated with atorvastatin in the vast majority (98%)., Methods: Mean on-study SUA levels (up to 48 months) were compared with those at baseline by using analyses of variance to assess differences over time within and between treatment groups. Cox multivariate analysis was used to investigate whether changes in SUA levels during the study were clinically relevant., Results: All patients had normal renal function at baseline; serum creatinine (SCr) levels less than 1.3 mg/dL (<115 micromol/L) and moderately elevated SUA levels (mean, 7.1 +/- 0.9 [SD] mg/dL [425 +/- 52 micromol/L]; upper normal limit, 7.0 mg/dL [415 micromol/L]). Usual-care patients (n = 800) showed an increase in SUA levels by 3.3% ( P < 0.0001). Structured-care patients (n = 800) had an 8.2% reduction in SUA levels ( P < 0.0001). In all patients not administered diuretics (n = 1,407), SUA level changes showed a positive correlation with changes in SCr levels ( r = 0.82; P < 0.0001) and an inverse correlation with estimated glomerular filtration rate ( r = -0.77; P < 0.0001). After adjustment for 19 predictors of all CHD-related events, Cox multivariate analysis involving backward stepwise logistic regression showed a hazard ratio (HR) of 0.89 (95% confidence interval [CI], 0.78 to 0.96; P = 0.03) with every 0.5-mg (30-micromol/L) reduction in SUA level, an HR of 0.76 (95% CI, 0.62 to 0.89; P = 0.001) with every 1-mg (60-micromol/L) reduction, an HR of 1.14 (95% CI, 1.03 to 1.27; P = 0.02) with every 0.5-mg increase, and an HR of 1.29 (95% CI, 1.17 to 1.43; P = 0.001) with every 1-mg increase in SUA levels., Conclusion: Data suggest that SUA level is an independent predictor of CHD recurrent events. Atorvastatin treatment significantly reduces SUA levels in patients with CHD, thus offsetting an additional factor associated with CHD risk.

Activated platelets play a role in the pathogenesis of coronary heart disease (CHD). Following activation, platelets change shape, aggregate, and release several bioactive substances. The aim of this review is to identify if there is a simple and cost-effective method that indicates platelet activation and predicts the risk of CHD and vascular events. The rationale for identifying high-risk patients is to reduce their risk of vascular events by administering appropriate and effective antiplatelet treatment, like aspirin, clopidogrel, or combination regimens. Many laboratory tests estimating platelet activity have been described. Some are relatively simple, such as spontaneous or agonist-induced platelet aggregation. Other tests include measuring the mean platelet volume (MPV) or plasma soluble P-selectin levels. Some more complex tests include flow cytometry to determine platelet GP IIb/IIIa receptors, platelet surface P-selectin, platelet-monocyte aggregates, and microparticles. Only few prospective studies assessed the predictive value of platelet activation in healthy individuals. Although the MPV seems an 'easy' method, there are insufficient data supporting its ability to predict the risk of a vascular event in healthy adults. Platelet aggregation, in whole blood or in platelet-rich plasma was not consistently predictive of vascular risk. Soluble P-selectin measurement is a promising method but it needs further evaluation. Flow cytometry methods are costly, time-consuming, and need specialized equipment. Thus, they are unlikely to be useful in estimating the risk in large numbers of patients. There is as yet no ideal test for the detection of platelet activation. Each currently available test has merits and disadvantages. Simple methods such as the MPV and the determination of platelet release products need further evaluation.

The GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) Study compared two standards (structured vs. usual care) of lipid lowering treatment in 1600 patients with coronary heart disease (CHD). Structured care aimed at achieving (with atorvastatin 10-80 mg) the low-density lipoprotein cholesterol (LDL-C) (2.6 mmol/l; 100 mg/dl) goal described in the NCEP ATP II and III guidelines for patients with CHD. Structured care was associated with a significant reduction in overall mortality and coronary events compared to usual care. In the present brief report we interpret the results of GREACE using the United Kingdom (UK) and European Atherosclerosis Society (EAS) treatment goal for LDL-C in secondary CHD prevention (3.0 mmol/l; 115 mg/dl. The mean dose of atorvastatin decreased from 24 mg to 22 mg/day. More patients achieved the UK and EAS LDL-C target (95.6 vs. 95%) in the structured care arm of the trial; 90% of the patients achieved this target with 10 or 20 mg atorvastatin. These findings may have cost implications, especially if the LDL-C target for high-risk patients will fall below those described above.

Epidemiological studies have established that low levels of high-density lipoprotein cholesterol (HDL-C) are associated with an increased risk of coronary heart disease (CHD). Recent studies have demonstrated that low HDL-C levels, and high triglycerides and total cholesterol levels are independent predictors of CHD, and that the combination of these lipid abnormalities increases the risk of coronary events. In lipid-modifying intervention studies, agents that raise HDL-C levels have been shown to reduce the incidence of major coronary events. The VA-HIT study consisted of patients with low-density lipoprotein cholesterol (LDL-C) levels similar to those recommended by several guidelines but with low levels of HDL-C. This trial demonstrated that raising HDL-C levels with gemfibrozil reduced the risk of CHD-related events. While the mechanisms by which HDL-C exerts its anti-atherogenic effects have yet to be fully elucidated, its role in the reverse transport of cholesterol and the beneficial effects on endothelial function are plausible explanations for these actions. Although LDL-C reduction is the primary goal in the treatment of dyslipidaemia, current guidelines recognise low HDL-C levels as a major risk factor for CHD. Indeed, the NCEP ATP III guidelines suggest that the treatment of isolated low HDL-C levels in CHD patients or individuals with CHD risk equivalents should be considered. The differing abilities of statins to raise HDL-C levels may be an important factor when making treatment decisions. New lipid-modifying drugs with beneficial effects on both HDL-C and LDL-C levels would be desirable additions to the currently available therapeutic options.

In the last several years there has been a large debate whether patients with type 2 diabetes (T2DM) should be treated as those with high or very high cardiovascular risk, and whether T2DM should be considered as equivalent to coronary heart disease (CHD). It all started in the 2001 in National Cholesterol Education Program - Adult Treatment Panel III recommendations, and the knowledge has changed on this issue at least several times. But the main problem is that due to these inconsistencies and different approaches to the cardiovascular risk of T2DM patients, we have more and more patients with T2DM not effectively treated, and diabetologists mostly focus on glucose (glucocentric approach), often forgetting about the overall cardiovascular risk of those patients. In this review we discuss the above-mentioned topic, try to give some practical suggestions, and raise the issue of whether we should start a discussion on treating all patients with T2DM as those at very high cardiovascular risk, or to at least to try to unify the definition and find such variables/risk factors which are easy to measure to help physicians to treat those patients optimally. We have obviously discussed these issues in the context of new European Society of Cardiology (ESC)/European Association for the Study of Diabetes (EASD) Guidelines 2019. [ABSTRACT FROM AUTHOR]

The no-reflow (NR) phenomenon represents an acute reduction in coronary blood flow without coronary vessel obstruction, coronary vessel dissection, spasm, or thrombosis. No reflow is an important complication among patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). The complete blood count (CBC) is one of the most frequently ordered laboratory tests in clinical practice. Various studies have evaluated the performance of CBC parameters to predict disease severity and mortality risk. Automated cell counters are routinely available in many clinical laboratories and can be used to determine red blood cell distrubiton width (RDW), platetecrit, platelet count, and and some ratios like the neutrophil-lymphocyte ratio and RDW-platelet ratio. These hematological markers have been reported to be independent predictors of impaired angiographic reperfusion and long-term mortality among patients with STEMI undergoing pPCI. In this context, we reviewed the role of admission CBC parameters for the prediction of NR in patients with STEMI undergoing pPCI. [ABSTRACT FROM AUTHOR]

The ear lobe crease (ELC) has been defined as a deep wrinkle that extends backwards from the tragus to the auricle. It has been proposed that ELC is a predictor of coronary artery disease (CAD). In this review, we consider the possible association between ELC and CAD. Our aim is to systematically address all the relevant evidence in this field. There are many studies that support an association between ELC and CAD. However, other studies did not find such an association. A recent meta-analysis supports the hypothesis that ELC could be a marker of CAD. However, several limitations raise doubts as to whether we should accept this link. [ABSTRACT FROM AUTHOR]

Abstract: Takotsubo cardiomyopathy is defined as acute chest pain during stressful incidents which is associated with ST-segment abnormalities and/or increased serum troponin levels. There is also regressive systolic dysfunction which is usually localized in the apical and medial left ventricles but there are no significant coronary artery lesions. The ventricular asynergy is also described in the right ventricle but is less common. Almost all the patients are women. The onset of this disease is typically triggered by an acute emotional or stress event or by an accumulation of trivial and repetitive stresses. The etiology of this syndrome remains unclear. Myocardial ischemia and reperfusion due to microvascular spasm, aborted myocardial infarction and related no-reflow phenomenon have been proposed as inducers of Takotsubo cardiomyopathy. The temporal relationship between the stressful event and the triggering of the clinical syndrome as well as the report of elevated catecholamine plasma levels during the acute phase suggest a possible involvement of the sympathetic nervous system. A smaller left ventricular size and hormonal disturbances in women may also play a role. [Copyright &y& Elsevier]

In vitro studies attribute antiatherogenic and insulin-like properties to zinc (Zn). However, only a few conflicting clinical data exist concerning the relationship between Zn and coronary artery disease (CAD) as well as glycemic indices. We studied 72 patients without prior history of myocardial infarction or revascularization procedures, who underwent coronary angiography for evaluation of chest pain. Coronary artery disease severity was estimated using 3 angiographic scores. Zn in serum and 24-hour urine, as well as serum Zn/24-hour urine Zn ratio were determined. Serum Zn was not associated with CAD prevalence and severity. However, urinary Zn loss was significantly higher among patients with CAD and showed a positive association with CAD severity. Serum Zn/24-hour urine Zn ratio was inversely associated with CAD, as well as with diabetes mellitus prevalence, fasting glucose, and glycated hemoglobin levels. Low serum Zn/24-hour urine Zn ratio is associated with angiographically severe atherosclerosis and impaired glucose homeostasis. [ABSTRACT FROM AUTHOR]

Introduction: Elevated serum leptin levels are associated with cardiovascular events. We investigated the role of serum leptin in patients undergoing carotid endarterectomy (CEA). Methods: A total of 74 patients (55 men; 38 symptomatic and 36 asymptomatic; mean age 66.9 ± 8.2 years) undergoing CEA for >70% carotid artery stenosis were enrolled. Results: Serum leptin levels were lower in symptomatic compared with asymptomatic patients (7.1 ± 1.3 vs 14.4 ± 4.7 ng/dL; P < .001). Interleukin-6 (IL-6) levels were higher in symptomatic compared with asymptomatic patients (4.3 ± 1.7 vs 3.3 ± 1.1 pg/dL; P = .017). Symptomatic patients had more intense macrophage accumulation (0.7% ± 0.1% vs 0.3% ± 0.1%; P < .001). Serum leptin and serum IL-6 levels were independently associated with the presence of symptoms in multivariate analysis. Conclusion: Serum leptin levels were decreased in symptomatic carotid artery disease. This finding requires further investigation in larger studies. [ABSTRACT FROM AUTHOR]

It has been proposed that apolipoprotein J (apo J) and paraoxonase-1 (PON1) correlate with the extent and severity of ischemic heart disease (IHD). This article compares apo J and PON1 serum concentrations, PON1 activity, and the apo J/PONI ratio in 138 IHD patients (64 statins users and 74 statin nonusers) referred for angiography and possible percutaneous coronary intervention. The effect of statin treatment on apo J and PON1 concentrations, PONI activity, and the degree of coronary artery stenosis were evaluated. In both groups, apo J levels were increased, whereas PON 1 concentration and activity decreased. IHD patients on statins had significantly lower apo J concentration and higher PON1 concentration and activity. Patients on statins had less coronary artery stenosis. High apo J levels, low PON1 levels, low PON 1 activity, and a high apo J/PON 1 ratio were associated with IHD. Statin treatment reverses these changes, probably by multiple beneficial actions. [ABSTRACT FROM AUTHOR]

Medline was searched for studies investigating the perioperative and long-term results that derive from statin use in patients with abdominal aortic aneurysm and the clinical and experimental evidence dealing with aneurysm expansion. Data suggest that statins improve the perioperative and long-term outcomes of aneurysm operations and may also reduce expansion rates. International guidelines recommend the use of statins in these patients because abdominal aortic aneurysms are considered as a coronary heart disease equivalent. These guidelines do not appear to have been widely implemented. Preliminary results suggest that statins might play a role in the management of abdominal aortic aneurysms. Verification of these results in large-scale trials may hold implications for a more comprehensive approach of patients with abdominal aortic aneurysms as well as population-wide aneurysm screening programs. Irrespective of the role of statins on aneurysm expansion rates, it is important to ensure that all abdominal aortic aneurysm patients receive statin therapy to improve perioperative and long-term morbidity and mortality. [ABSTRACT FROM AUTHOR]