Risk Of Angina Research Articles

Relationship between human serum metabolites and angina pectoris: a Mendelian randomization study.

We aimed to explore the causal relationship between human serum metabolites and angina pectoris. This study used two-sample Mendelian randomization (MR) analysis to assess the association between 486 serum metabolites and angina pectoris. The analytical methods employed to reduce study bias included inverse variance weighted, MR-Egger, and weighted median method. A comprehensive sensitivity analysis was performed using the leave-one-out method, while instrumental variable pleiotropy was tested with MR-Pleiotropy RESidual Sum and Outlier. Metabolic pathways of angina-associated metabolites were analysed on the MetaboAnalyst metabolomics analysis tool platform. In this study, 42 serum metabolites were found to be strongly associated with angina pectoris. They mainly belonged to seven groups: amino acids, carbohydrates, cofactors and vitamins, lipids, nucleotides, unknown metabolites, and exogenous substances. Pipecolate posed the highest risk for the development of angina pectoris among the 42 serum metabolites. The main metabolic pathways associated with angina pectoris were glycine, serine, threonine metabolism, primary bile acid biosynthesis, and caffeine metabolism. We identified 25 high-risk and 17 protective human serum metabolites associated with angina pectoris. Their associated major metabolic pathways were also determined. The serum metabolite pipecolate was significantly and positively correlated with the risk of angina pectoris. This finding may serve as a valuable reference for testing serum markers associated with angina pectoris.

Causal association between placental growth factor and coronary heart disease: a Mendelian randomization study.

Placental growth factor (PlGF), an important polypeptide hormone, plays an important regulatory role in various physiological processes. Observational studies have shown that PlGF is associated with the risk of coronary heart disease (CHD). However, the causal association between PlGF and CHD is unclear at present. This study aimed to investigate the causal association between genetically predicted PlGF levels and CHD. Single nucleotide polymorphisms (SNPs) associated with PlGF were selected as instrumental variables (IVs) to evaluate the causal association between genetically predicted circulating PlGF levels and CHD risk by two-sample Mendelian randomization (MR). Inverse variance weighted (IVW) analysis showed that there was a suggestive causal association between genetically predicted PlGF level and the risk of CHD (OR = 0.79, 95% CI: 0.66-0.95, P = 0.011) overall. In addition, PlGF levels had a significant negative causal association with the risk of myocardial infarction (OR = 0.83, 95% CI: 0.72-0.95, P = 0.007). A negative correlation trend was found between PlGF level and the risk of angina pectoris (OR = 0.89, 95% CI: 0.79-1.01, P = 0.067). In addition, PlGF levels had a significant negative association with the risk of unstable angina pectoris (OR = 0.78, 95% CI: 0.64-0.94, P = 0.008). PlGF levels were negatively correlated with CHD events with suggestive significance (OR = 0.89, 95% CI: 0.80-0.99, P = 0.046). Genetically predicted circulating PlGF levels are causally associated with the risk of CHD, especially acute coronary syndrome, and PlGF is a potential therapeutic target for CHD.

Bisphenol A exposure and risk of ischemic heart disease in the Spanish European Prospective Investigation into cancer and nutrition study

BackgroundCardiovascular disease, particularly ischemic heart disease (IHD), is the leading cause of mortality worldwide. Bisphenol A (BPA) is considered an endocrine disruptor and obesogen, present in numerous products of daily use. The aim of this study was to assess the potential association of serum BPA concentrations and the risk of incident IHD in a sub-cohort of the Spanish European Prospective Investigation into Cancer and Nutrition (EPIC). MethodsWe designed a case-cohort study within the EPIC-Spain cohort. The population consisted of 4636 participants from 4 EPIC-Spain centers (946 IHD cases and 3690 sub-cohort participants). BPA exposure was assessed by means of chemical analyses of serum samples collected at recruitment. Follow-up was performed by linking with national and regional databases and reviewing patients’ clinical records. Cox Proportional Hazards Models were used for the statistical analyses. ResultsMedian follow-up time was 16 years and 70% of the participants showed detectable BPA values (>0.2 ng/ml). Geometric mean (GM) values of cases and sub-cohort were 1.22 ng/ml vs 1.19 ng/ml respectively (p = 0.90). Cox regression models showed no significant association of BPA serum levels and IHD, acute myocardial infarction or angina pectoris risk. ConclusionsWe evidenced a similar percentage of detection of BPA among cases and sub-cohort participants from our population, and no clear association with IHD risk was observed. However, further investigation is needed to understand the influence of BPA on IHD risk.

Meta-analysis of C-Reactive Protein and Risk of Angina Pectoris

Associations between elevated C-reactive protein (CRP) levels and the angina pectoris risk have been reported for many years, but the results remain controversial. To address this issue, a meta-analysis was therefore conducted. Eligible studies were identified by searching PubMed, EMBASE, Cochrane library, and web of science up to January 2019. Altogether, 10 prospective cohort studies and 11 case-control studies were included, and they were published from 1997 to 2013 and summed up to 18,316 samples totally. The pooled mean difference of CRP levels was 4.44 (95% confidence interval 2.71 to 6.17) between angina patients and healthy controls. The combined odds ratio of CRP for major adverse cardiac events in angina patients was 1.67 (95% CI 1.23 to 2.26). In conclusion, the meta-analysis indicated that elevated CRP levels were associated with angina pectoris, especially unstable angina pectoris, and were probably a risk factor of major adverse cardiac events.

P1929A randomized controlled trial evaluating outcome impact of cilostazol in patients with coronary artery disease and at a high risk of cardiovascular disease

Abstract Background We and others have previously found that cilostazol has a favorable effect on glucose and lipid homeostasis, endothelial function, anti-atherosclerosis, and vasculo-angiogenesis. However, it is poorly understood that if this compound can provide better clinical outcome. Purpose This study investigated the outcome effect of cilostazol in patients with coronary artery disease (CAD) or at a high risk of cardiovascular (CV) disease. Methods We conducted a randomized, double-blind, placebo controlled trial involving 266 patients to receive cilostazol 200 mg/day (n=134) or dummy placebo (n=132). The primary endpoint was a composite of CV death, non-fatal myocardial infarct, non-fatal stroke, hospitalization for congestive heart failure or unplanned coronary revascularization. Pre-specified secondary endpoints include the composite major coronary event (MCE) and major adverse CV and cerebrovascular event (MACCE) on long-term follow-up. The mean duration of follow-up was 2.9 years. Results Relative to placebo, cilostazol treatment had a borderline effect on risk reduction in the primary endpoint (hazard ratio [HR], 0.67; 95% confidence interval (CI), 0.34–1.33), whereas the beneficial effect in favor of cilostazol was significant in patients with diabetes mellitus or a history of percutaneous coronary intervention (P for interaction, 0.02 and 0.06, respectively). Use of cilostazol, but not placebo, significantly reduced the risk of the MCE (HR, 0.38; 95% CI, 0.17–0.86) and MACCE (HR, 0.47; 95% CI, 0.23–0.96). A significantly lower risk of angina pectoris (HR, 0.38; 95% CI, 0.17–0.86) and unplanned revascularization (HR, 0.13; 95% CI, 0.02–1.09) was also observed in the cilostazol group. After multi-variable adjustment, cilostazol treatment independently predicted a lower risk of the MCE and MACCE. Conclusions Cilostazol treatment significantly reduced the risk of CV events in patients with CAD or at a high risk of CV disease. Acknowledgement/Funding MOST 106-2314-B-006-044, MOHW106-TDU-B-211-113003, MOHW107-TDU-B-211-113003, and MOST107-2314-B-006-076-MY2

Clinical Practice Guidelines for Chronic Cardiovascular Disorders: A Roadmap for the Future

The World Health Organization lists ischemic heart disease and stroke as the top 2 leading causes of death worldwide in 2011, responsible for 7 million and 6.2 million deaths, respectively.1 The concept of risk factors for atherosclerotic cardiovascular disease (CVD) was introduced in 1961, based on epidemiologic observations from the Framingham Heart Study. Hypertension and abnormal blood lipid levels were key risk factors shown to be associated with an increased risk of angina pectoris, myocardial infarction, and sudden cardiac death; later, stroke was identified as an important outcome as well, especially in women and racial/ethnic subgroups. Accordingly, clinicians want to provide their patients with the best possible advice with respect to the management of cardiovascular risk, often implementing evidence-based clinical practice guidelines designed to improve health outcomes.

Risk of Angina Pectoris, Non-fatal Myocardial Infarction and Non-fatal Stroke Among Hypertensives: the CroHort Study

Aim of this study was to investigate association of controlled and uncontrolled hypertension with angina pectoris, non-fatal myocardial infarction and non-fatal cerebrovascular insult on a cohort from Croatian Adult Health Cohort Study (CroHort). Odds for angina pectoris, non-fatal myocardial infarction and non-fatal cerebrovascular insult were calculated for 227 respondents with controlled hypertension and 1,287 respondents with uncontrolled hypertension compared to 1,353 normotensive respondents. The results showed that among men uncontrolled hypertension was significantly associated with risk of non-fatal stroke, while among women no significant associations were recorded. Primary and secondary prevention of hypertension should be public health priority and would contribute to reducing the risk of stroke in Croatian population.

Headache‐type adverse effects of NO donors: vasodilation and beyond

Although nitrate therapy, used in the treatment of cardiovascular disorders, is frequently associated with side-effects, mainly headaches, the summaries of product characteristics of nitrate-containing medicines do not report detailed description of headaches and even do not highlight the possibility of nitrate-induced migraine. Two different types of nitrate-induced headaches have been described: (i) immediate headaches that develop within the first hour of the application, are mild or medium severity without characteristic symptoms for migraine, and ease spontaneously; and (ii) delayed, moderate or severe migraine-type headaches (occurring mainly in subjects with personal or family history of migraine), that develop 3-6 h after the intake of nitrates, with debilitating, long-lasting symptoms including nausea, vomiting, photo- and/or phono-phobia. These two types of headaches are remarkably different, not only in their timing and symptoms, but also in the persons who are at risk. Recent studies provide evidence that the two headache types are caused by different mechanisms: immediate headaches are connected to vasodilation caused by nitric oxide (NO) release, while migraines are triggered by other actions such as the release of calcitonin gene-related peptide or glutamate, or changes in ion channel function mediated by cyclic guanosine monophosphate or S-nitrosylation. Migraines usually need anti-attack medication, such as triptans, but these drugs are contraindicated in most medical conditions that are treated using nitrates. In conclusion, these data recommend the correction of summaries of nitrate product characteristics, and also suggest a need to develop new types of anti-migraine drugs, effective in migraine attacks, that could be used in patients with risk for angina pectoris.

Long-Acting Calcium Antagonists in Patients with Coronary Artery Disease: A Meta-Analysis

Background The use of calcium channel blockers (CCBs) in patients with coronary artery disease remains controversial, with reports of increased risk of myocardial infarction and all-cause mortality. Short-acting CCBs have an unfavorable hemodynamic profile. The role of long-acting CCBs in patients with coronary artery disease is unknown. Methods MEDLINE/CENTRAL/EMBASE database were searched from 1966 to August 2008 for randomized controlled trials of long-acting CCBs in patients with coronary artery disease with follow-up for at least 1 year. We extracted from the studies the baseline characteristics and 6 outcomes: all-cause mortality, cardiovascular mortality, nonfatal myocardial infarction, stroke, angina pectoris, and heart failure. Results Of the 100 randomized controlled trials of CCBs in patients with coronary artery disease, 15 studies evaluating 47,694 patients fulfilled our inclusion criteria. When compared with the comparison group (including placebo), CCBs were not associated with an increased risk of all-cause mortality (relative risk [RR] 0.99; 95% confidence interval [CI], 0.94-1.05), cardiovascular mortality (RR 1.03; 95% CI, 0.95-1.11), nonfatal myocardial infarction (RR 0.96; 95% CI, 0.87-1.06), or heart failure (RR 0.86; 95% CI, 0.71-1.05), and with a 21% reduction in the risk of stroke (95% CI, 0.70-0.89) and 18% reduction in the risk of angina pectoris (95% CI, 0.72-0.94). When compared with placebo, CCBs resulted in a 28% reduction in the risk of heart failure (95% CI, 0.73-0.92). The results were similar for both dihydropyridines and nondihydropyridine CCBs. Conclusions In patients with coronary artery disease, long-acting CCBs (either dihydropyridines or nondihydropyridines), were associated with a reduction in the risk of stroke, angina pectoris, and heart failure, with similar outcomes for other cardiovascular events as the comparison group.

Association between TAFI antigen and Ala147Thr polymorphism of the TAFI gene and the angina pectoris incidence. The PRIME Study (Prospective Epidemiological Study of MI).

Thrombin activatable fibrinolysis inhibitor (TAFI), a recently described inhibitor of fibrinolysis, has been hypothesized as playing a role in atherothrombosis. However, the evidence from retrospective studies, which have evaluated the role of TAFI in vascular risk, is conflicting. In a prospective cohort (the PRIME Study) of nearly 10 000 apparently healthy men recruited in France (Lille, Strasbourg, Toulouse) and Northern Ireland (Belfast), we measured baseline plasma concentration of TAFI antigen among 143 participants (81 from France and 62 from Ireland) who subsequently developed angina pectoris and among 286 age-matched participants who remained free of disease during the 5 years of follow-up. Genotyping of the Ala147Thr polymorphism located in the TAFI gene was performed using an allele specific PCR. In France, mean levels of TAFI were significantly higher at baseline among men who subsequently developed angina pectoris compared with their control subjects (119 versus 107 %; p = 0.02). The risk of future angina pectoris increased with increasing tertiles of TAFI (p = 0.02), such that men in the highest tertile at study entry had a 5-fold higher relative risk than those in the lowest tertile (95% confidence interval, 1.38 to 18.58) after controlling for the conventional cardiovascular risk factors. No such difference was observed in Northern Ireland. In France, Thr/Thr carriers of the Ala147Thr polymorphism were significantly more frequent in cases than in controls (p = 0.01) leading to a relative risk of angina pectoris of 2.7 (95%CI 1.2-5.8). Increase in plasma TAFI antigen levels is a risk factor for angina pectoris in France. Genotyping for the Ala147Thr polymorphism seems to be a reliable tool to assess the risk mediated by TAFI.

Vascular complications in relation to ethnicity in non-insulin-dependent diabetes mellitus.

The purpose of this study was to investigate the effect of ethnicity on the development of diabetic retinopathy and nephropathy as markers for microvascular complications and of angina pectoris as a marker for macrovascular complications. We evaluated data from 1124 patients with non-insulin-dependent diabetes mellitus (NIDDM) of Caucasian, Mongoloid, Asian, Armenian, Northern African and Negroid origin who were referred between January 1993 and December 1994. Logistic regression analyses showed that the occurrence of microvascular complications was significantly associated with duration of NIDDM. In addition, retinopathy was significantly associated with glycated haemoglobin A1c (HbA1c) and nephropathy with triglycerides (P < 0.05 and P < < 0.001 respectively). Northern African origin was associated with retinopathy (P < 0.05) and Asian origin with nephropathy (P < 0.005). Macrovascular complication was associated with age and triglyceride level (P < 0.001 and P < 0.05 respectively). Northern African and Negroid ethnicity exclusively did not show a gradual increase in the risk for angina pectoris with increasing age. Moreover, a negative association between Northern African as well as Negroid ethnicity and macrovascular complication was observed (P = 0.05 and P < 0.05 respectively). In support of these observations, we found a favourable lipid profile in both mentioned groups. In summary, we have shown that, in patients with NIDDM, ethnicity is associated with macrovascular complications and duration of the disease with microvascular complications.

Low vitamin E levels increased the risk for angina pectoris in men

Source Citation Riemersma RA, Wood DA, Macintyre CC, et al. Risk of angina pectoris and plasma concentrations of vitamins A, C, and E and carotene. Lancet. 1991Jan 5;337:1-5.

Risk of angina pectoris and plasma concentrations of vitamins A, C, and E and carotene

The relation between risk of angina pectoris and plasma concentrations of vitamins A, C, and E and carotene was examined in a population case-control study of 110 cases of angina, identified by the Chest Pain Questionnaire, and 394 controls selected from a sample of 6000 men aged 35-54. Plasma concentrations of vitamins C and E and carotene were significantly inversely related to the risk of angina. There was no significant relation with vitamin A. Smoking was a confounding factor. The inverse relation between angina and low plasma carotene disappeared and that with plasma vitamin C was substantially reduced after adjustment for smoking. Vitamin E remained independently and inversely related to the risk of angina after adjustment for age, smoking habit, blood pressure, lipids, and relative weight. The adjusted odds ratio for angina between the lowest and highest quintiles of vitamin E concentrations was 2·68 (95% confidence interval 1·07-6·70; p=0·02). These findings suggest that some populations with a high incidence of coronary heart disease may benefit from eating diets rich in natural antioxidants, particularly vitamin E.

Predictors of clinical course, coronary anatomy and left ventricular function after recovery from acute myocardial infarction.

Patients who survive an acute myocardiac infarction (AMI) have significant coronary disease and are at risk for angina pectoris, recurrent myocardiac infarction and sudden death. This study provides data gathered prospectively for 106 patients surviving myocardial infarction who had coronary arteriography, left ventriculography and 24-hour electrocadiographic recordings before hospital discharge and were followed 30 months. Univariate analysis showed that low ejection fraction, proximal left anterior descending coronary disease and significant disease in all three coronary arteries were associated with a high risk of sudden cardial death. The ECG location or type of infarction was not helpful in predicting mortality, reinfarction or continuing angina. Multivariate analysis of 30 clinical and laboratory variables identified previous myocardial infarction and an ejection fraction less than 40% as the best predictors of mortality; all 13 patients who died were identified by these two variables. Three-vessel coronary artery disease, proximal left coronary disease and complicated late hospital-phase ventricular arrhythmias did not provide additional information about mortality once the information provided by the first two variables was considered. Multivariate analysis identified hypertension, three-vessel coronary disease, postinfarction angina pectoris and previous AMI as significant predictors of recurrent AMI during the 30 month follow-up.