Association study of NAFLD with pericoronary adipose tissue and pericardial adipose tissue: Diagnosis of stable CAD patients with NAFLD based on radiomic features.

BACKGROUND AND AIM: Nonalcoholic fatty liver disease (NAFLD) is prone to complicated cardiovascular disease, and we aimed to identify patients with NAFLD who are prone to developing stable coronary artery disease (CAD). METHODS AND RESULTS: We retrospectively recruited adults who underwent coronary computed tomography angiography (CTA). A total of 127 NAFLD patients and 127 non-NAFLD patients were included in this study. Clinical features and imaging parameters were analysed, mainly including pericardial adipose tissue (PAT), pericoronary adipose tissue (PCAT), and radiomic features of 6792 PCATs. The inflammatory associations of NAFLD patients with PAT and PCAT were analysed. Clinical features (model 1), CTA parameters (model 2), the radscore (model 3), and a composite model (model 4) were constructed to identify patients with NAFLD with stable CAD. The presence of NAFLD resulted in a greater inflammatory involvement in all three coronary arteries (all P < 0.01) and was associated with increased PAT volume (r = 0.178**, P < 0.05). In the presence of NAFLD, the mean CT value of the PAT was significantly correlated with the fat attenuation index (FAI) in all three vessels and had the strongest correlation with the RCA FAI (r = 0.55, p < 0.001). A total of 9 radiomic features were screened by LASSO regression to calculate radiomic scores. In the model comparison, model 4 had the best performance of all models (AUC 0.914 [0.863-0.965]) and the highest overall diagnostic value of the model (sensitivity: 0.814, specificity: 0.941). CONCLUSIONS: NAFLD correlates with PAT volume and PCAT inflammation. Furthermore, combining clinical features, CTA parameters, and radiomic scores can improve the efficiency of early diagnosis of stable CAD in patients with NAFLD.

KLRD1, FOSL2 and LILRB3 as potential biomarkers for plaques progression in acute myocardial infarction and stable coronary artery disease.

BACKGROUND: Myocardial infarction (MI) contributes to high mortality and morbidity and can also accelerate atherosclerosis, thus inducing recurrent event due to status changing of coronary artery walls or plaques. The research aimed to investigate the differentially expressed genes (DEGs), which may be potential therapeutic targets for plaques progression in stable coronary artery disease (CAD) and ST-elevated MI (STEMI). METHODS: Two human datasets (GSE56885 and GSE59867) were analyzed by GEO2R and enrichment analysis was applied through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. To explore the seed genes, the protein-protein interaction (PPI) network was constructed and seed genes, as well as top30 ranking neighbours were screened out. To validate these findings, one human dataset GSE120521 was analyzed. Linear regression analysis and ROC curve were also performed to determine which seed genes above mentioned could be independent factors for plaques progression. Mice MI model and ELISA of seed genes were applied and ROC curve was also performed for in vivo validation. RESULTS: 169 DEGs and 573 DEGs were screened out in GSE56885 and GSE59867, respectively. Utilizing GO and KEGG analysis, these DEGs mainly enriched in immune system response and cytokines interaction. PPI network analysis was carried out and 19 seed genes were screened out. To validate these findings, GSE120521 was analyzed and three genes were demonstrated to be targets for plaques progression and stable CAD progression, including KLRD1, FOSL2 and LILRB3. KLRD1 and LILRB3 were demonstrated to be high-expressed at 1d after MI compared to SHAM group and FOSL2 expression was low-expressed at 1d and 1w. To investigate the diagnostic abilities of seed genes, ROC analysis was applied and the AUCs of KLRD1, FOSL2 and LILRB3, were 0.771, 0.938 and 0.972, respectively. CONCLUSION: This study provided the screened seed genes, KLRD1, FOSL2 and LILRB3, as credible molecular biomarkers for plaques status changing in CAD progression and MI recurrence. Other seed genes, such as FOS, SOCS3 and MCL1, may also be potential targets for treatment due to their special clinical value in cardiovascular diseases.

Long-term prognostic utility of low-density lipoprotein (LDL) triglyceride in real-world patients with coronary artery disease and diabetes or prediabetes.

BACKGROUND: Recent guidelines highlighted the association between atherosclerosis and triglyceride-enriched lipoproteins in patients with impaired glucose metabolism. However, evidence from prospective studies for long-term prognostic utility of low-density lipoprotein triglyceride (LDL-TG) in real-world patients with prediabetes (Pre-DM) or diabetes mellitus (DM) and coronary artery disease (CAD) is currently not available. The aim of the present study was to evaluate the impact of LDL-TG on major adverse cardiovascular events (MACEs) in patients with stable CAD under different glucose metabolism status. METHODS: A total of 4381 patients with CAD were consecutively enrolled and plasma LDL-TG level was measured by an automated homogeneous assay. They were categorized according to both status of glucose metabolism [DM, Pre-DM, normal glycaemia regulation (NGR)] and tertiles of LDL-TG. All subjects were followed up for the occurrence of MACEs. RESULTS: During a median of 5.1 (interquartile range 3.9 to 5.9) years' follow-up, 507 (11.6%) MACEs occurred. Cubic spline models showed a significant association between LDL-TG and MACEs in DM and Pre-DM but not in NGR. When the combined effect of elevated LDL-TG and glucose disorders was considered for risk stratification, the medium tertile of LDL-TG plus DM, and the highest tertile of LDL-TG plus Pre-DM or plus DM subgroups were associated with significantly higher risk of MACEs after adjustment of confounders including triglyceride [hazard ratios (95% confidence intervals): 1.843 (1.149-2.955), 1.828 (1.165-2.867), 2.212 (1.396-3.507), all p < 0.05]. Moreover, adding LDL-TG into the original model increased the C-statistic from 0.687 to 0.704 (∆C-statistic = 0.016, p = 0.028) and from 0.734 to 0.749 (∆C-statistic = 0.014, p = 0.002) in Pre-DM and DM, respectively. CONCLUSIONS: In this longitudinal cohort study on real-world practice, higher LDL-TG was associated with worse outcomes among Pre-DM and DM patients with stable CAD.

Development, optimization and validation of an absolute specific assay for active myeloperoxidase (MPO) and its application in a clinical context: role of MPO specific activity in coronary artery disease.

Background Myeloperoxidase (MPO) is an enzyme with a recognized prognostic role in coronary artery disease (CAD), which is also emerging as a promising biomarker for cardiac risk stratification. However, the lack of a consensus method for its quantification has hindered its implementation in clinical practice. The aim of our work was to optimize an absolute sensitive assay for active MPO without external standards, to validate the method in the clinical context of CAD patients, and to estimate the enzyme specific activity. Methods In order to determine the MPO concentration using fluorescence readings, this ELISA assay exploits the activity of the enzyme recognized by specific antibodies. The assay was validated in a small cohort of patients that included: healthy subjects (n=60); patients with acute myocardial infarction (AMI, n=25); patients with stable CAD (SCAD, n=25) and a concomitant chronic obstructive pulmonary disease (COPD). Then, total MPO concentration and specific activity (activity/total MPO) were determined. Results The assay showed an intra- and inter-assay coefficient of variation of 5.8% and 10.4%, respectively, with a limit of detection (LoD) of 0.074 µU. Both AMI and SCAD patients had higher active and total MPO than controls (p<0.0001 and p<0.01, respectively). The specific activity of MPO was higher in SCAD patients compared to both controls and AMI (p<0.0001). Conclusions The study presents a robust and sensitive method for assaying MPO activity in biological fluids with low variability. Moreover, the determination of the specific activity could provide novel insight into the role of MPO in cardiovascular diseases (CVDs).

[Upper gastrointestinal bleeding in patients with stable coronary artery disease (registry of antithrombotic therapy "REGATТA" results)].

INTRODUCTION: Upper gastrointestinal (UGI) bleeding is a common complication of antiplatelet therapy. Data from real clinical practice that characterize the range of risk factors for UGI bleeding, prophylactic proton pump inhibitors (PPIs) therapy, bleeding frequency and their long-term effects in patients with stable coronary artery disease (CAD) are limited. AIM: To identify predictors of UGI bleeding in patients with stable CAD, to assess the role of PPI in the prevention of bleeding and the long-term prognosis of patients after bleeding. MATERIALS AND METHODS: 934 patients with stable CAD (median age 61 [5368] years, 78.6% men) were included in the single institution prospective REGistry of Long-term AnTithrombotic TherApy (REGATTA). Atherosclerosis of peripheral arteries (APA) and abdominal aortic aneurysm (AAA) screening was performed by doctor decision, as well as esophagogastroduodenoscopy. 76% of patients received dual antiplatelet therapy for 612 months after elective PCI. PPIs were prescribed in 28.3% of cases. RESULTS: The median follow-up was 2.5 [1.15.1] years. The frequency of overt UGI bleeding was 1.9 per 100 patients per year. Anamnesis of peptic ulcer disease (OR 4.7; 95% CI 1.911.8;p=0.001), erosion of the upper gastrointestinal tract (OR 6.7; 2.716.6;p=0.00004 ), as well as concomitant diseases associated with a decrease in blood supply to the mucosa, such as heart failure HF (OR 6.1; 2.316.0;p=0.0002), AAA (OR 9.3; 2.534.2;p=0.0008) and APA (OR 2.3; 0.985.5;p=0.05) turned out to be independent predictors of UGI bleeding. The frequency of AAA among those who underwent UGI bleeding was 19.6% (in patients without bleeding 1.4%;p0.001). 90.2% of patients with UGI bleeding received PPI; the frequency of UGI bleeding in patients receiving pantoprazole and omeprazole did not differ significantly. After UGI bleeding, rebleeding rate was 7.8%, thrombotic events (TE) rate 31.4%, mortality rate 17.7% for 30 days, 19.4% for 1 year and 35.3% for the entire observation period. The predictors of deaths were AAA (OR 92.5; 7.7107.9;p0.0001), APA (OR 4.2; 1.0317.2;p=0.045) and HF (OR 34.5; 8.5140.6;p0.0001). The worst prognosis was expected for patients who underwent UGI bleeding and thrombotic events: 2/3 of these patients died. CONCLUSION: In a prospective analysis of patients with stable CAD, we identified UGI bleeding was a significant risk factor for late thromboembolism and death, compared with patients without bleeding. Predictors of UGI bleeding and poor prognosis are factors that indicate atherothrombotic burden abdominal aortic aneurysm, peripheral atherosclerosis and HF. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04347200.

Low expression of PRMT5 in peripheral blood may serve as a potential independent risk factor in assessments of the risk of stable CAD and AMI.

BACKGROUND: Protein arginine methyltransferases (PRMTs) can catalyse the methylation of arginine and participate in many important cellular reaction processes. The purpose of this research is to determine whether the expression levels of the PRMT5 gene in peripheral blood can be used as a biomarker for predicting the risk of Acute Myocardial Infarction (AMI). METHODS: In this research, peripheral blood was collected from 91 patients with AMI and 87 patients with stable coronary artery disease (CAD). Real-time fluorescent quantitative PCR was performed to measure the expression levels of the PRMT5 gene at the mRNA level, and a western blot analysis was performed to measure the expression levels of the PRMT5 gene at the protein level. RESULTS: The results indicate that at both the RNA and protein levels, the expression levels of the PRMT5 gene in peripheral blood from patients with AMI are significantly lower than those in peripheral blood from patients with stable CAD (Z = - 4.813, P = 0.000). The low expression of the PRMT5 gene is relevant to the Gensini score of the coronary artery (rs = - 0.205, P = 0.015) but is irrelevant to the serum level of blood lipids, level of cardiac troponin (rs = - 0.125, P = 0.413) and time intervals of occurrence (rs = - 0.146, P = 0.211). Patients who have a low PRMT5 expression in the peripheral blood are 5.472 times more likely to suffer from AMI than other patients. CONCLUSION: Compared to stable CAD patients, AMI patients have a lower expression of the PRMT5 gene in their peripheral blood. Patients who have low PRMT5 gene expression in the peripheral blood are more likely to suffer from AMI than those with stable CAD. A low expression of the PRMT5 gene serves as an independent risk factor for the occurrence of AMI.

Examining the Pre- and Post-percutaneous Coronary Intervention Blood Pressure Variability Using Ambulatory Blood Pressure Monitoring in Patients With Stable and Unstable Coronary Artery Disease.

Introduction The World Health Organization has drawn attention to the fact that coronary artery disease (CAD) is our modern "epidemic." Nowadays, sudden death during sleep has become prevalent due to a lack of oxygen supply to the heart. CAD causes more deaths and disabilities and incurs greater economic costs than any other illness in the developed world. The prevalence of cardiovascular disorders and heart disease is on the rise in India. Hypertension is one of the leading risk factors for all cardiovascular diseases. This study aims to compare blood pressure variability before and after percutaneous coronary intervention (PCI), using ambulatory blood pressure monitoring (ABPM) in patients with stable and unstable CAD. Materials and methods This prospective observational study was conducted among 52 patients with stable and unstable CAD, admitted to the medicine department, who required PCI at a tertiary care hospital. Before and after PCI, the same antihypertensive drugs were orally administered. ABPM was performed before PCI and one day after PCI. ABPM was conducted every 30 minutes during the day and every 60 minutes during the night over a 24-hour period using a mobil-o-graph (IEM, Germany). The results of the observed parameters were analyzed using the HMS Client-Server 4.0 system (Informer Technologies, Inc., Los Angeles, USA). The collected data were analyzed using SPSS Statistics version 21.0 software (IBM Corp. Released 2012. IBM SPSS Statistics for Windows, Version 21.0. Armonk, NY: IBM Corp.). Results Out of 52 patients, 28 (53.8%) had stable CAD and 24 (46.2%) had unstable CAD. The mean age of patients with stable and unstable CAD was 56.64±9.44 and 57.04±12.36 years, respectively. The majority of patients with stable (67.9%) and unstable CAD (62.5%) were males. Various other variables were considered, such as lipid profile, blood sugar, cardiac troponin-I, and medical history, including hypertension and type 2 diabetes mellitus. Among stable CAD patients, a comparison between pre- and post-PCI systolic blood pressure (SBP) did not show a significant difference in all SBP measurements (p>0.05). However, the mean diurnal index was significantly lower following PCI compared to before PCI (p=0.019). Among unstable CAD patients, a comparison between pre- and post-PCI SBP showed a significant change in peak daytime, average daytime, and diurnal index (p<0.05). For all other SBP measurements, the difference between pre- and post-PCI measurements was not statistically significant (p>0.05). In patients with stable CAD, a statistically significant change in diastolic blood pressure (DBP) following PCI was observed for peak daytime, peak nighttime, and average nighttime values. In contrast, for patients with unstable CAD, a statistically significant change in DBP following PCI was observed for peak daytime, peak nighttime, and minimum daytime values (p<0.05). Statistically, post-PCI, there was no significant difference between the two groups for SBP and DBP measurements (p>0.05). Additionally, there was no significant difference between the two groups pre- and post-PCI in the pattern of dipping. Conclusion A comparison of the ABPM before and after PCI showed that, within 48 hours post-PCI, the ambulatory blood pressure indicators did not differ statistically from those before PCI.

Utility of Fractional Flow Reserve Computed Tomography Angiography in Patients With Stable Coronary Artery Disease.

Coronary computed tomography angiography is a modality with high negative predictive value for evaluation of coronary artery disease (CAD). However, its diagnostic accuracy for obstructive CAD is limited by multiple factors. Fractional flow reserve (FFR) computed tomography (FFRCT) is an emerging analysis tool for identifying flow-limiting disease; nonetheless, the prognostic value of FFRCT is not well established. This meta-analysis aims to evaluate the association of FFRCT with clinical outcomes in patients with stable CAD. A literature search was conducted for studies reporting the association between FFRCT measurements and all-cause mortality, major adverse cardiovascular events (MACEs), acute myocardial infarction (AMI), and any need for coronary revascularization. Obstructive disease was defined as a FFR value ≤0.80; nonobstructive disease was defined as an FFR value >0.80. Ten studies were identified to meet the inclusion criteria; mean follow-up was 17 months (range, 3 to 56 months). There was no difference in risk of all-cause mortality between patients with obstructive and those with nonobstructive CAD on FFRCT. However, obstructive lesions were associated with increased risk of MACE, AMI, and any need for revascularization. FFRCT is a useful adjunctive modality for further risk stratification of patients with stable CAD. Obstructive lesions identified by FFRCT are associated with increased risk of MACE, AMI, and any need for revascularization.

Effects of percutaneous coronary intervention on dyspnea in stable coronary artery disease.

BACKGROUND: Dyspnea is a frequent symptom in patients with stable coronary artery disease (CAD) and is recognized as a possible angina equivalent. OBJECTIVES: This study was to assess the impact of percutaneous coronary intervention (PCI) on dyspnea, quality of life, and angina pectoris in patients with stable CAD. METHODS: The prospective, multi-center PLA-pCi-EBO-pilot trial included 144 patients with symptomatic stable CAD and successful PCI. The prespecified endpoints angina pectoris (Seattle Angina Questionnaire-SAQ) and dyspnea (NYHA scale) were assessed 6 months after PCI. Predictors for symptomatic improvement were assessed with uni- and multivariable logistic regression analyses. RESULTS: Patients with concomitant dyspnea had worse SAQ physical limitation scores at baseline (49.5 ± 21.0 vs 58.9 ± 22.0, p = 0.013) but showed no difference for angina frequency or quality of life. Overall, symptomatic burden of angina pectoris and dyspnea was alleviated by PCI. However, patients with concomitant dyspnea had markedly worse scores for physical limitation (78.9 ± 25.0 vs 94.3 ± 10.6, p < 0.001), angina frequency (77.9 ± 22.8 vs 91.1 ± 12.4, p < 0.001), and quality of life (69.4 ± 24.1 vs 82.5 ± 14.4, p < 0.001) after PCI. The prevalence of dyspnea (NYHA class ≥ 2) declined from 73% before PCI to 54%. Of 95 initially dyspneic patients, 57 (60%) improved at least one NYHA class 6 months after PCI. In a multivariable logistic regression analysis, "atypical angina pectoris" was associated with improved NYHA class, whereas "diabetes mellitus" had a negative association. CONCLUSION: PCI effectively reduced dyspnea, which is a frequent and demanding symptom in patients with CAD. The German Clinical Trials Register registration number is DRKS0001752 ( www.drks.de ).

Triglyceride glucose and haemoglobin glycation index for predicting outcomes in diabetes patients with new-onset, stable coronary artery disease: a nested case-control study.

AIM: Previous studies have shown that both triglyceride glucose (TyG) and haemoglobin glycation indexes (HGI) are predictors of cardiovascular risk. However, the prognostic value of TyG index and HGI in patients with type 2 diabetes mellitus (T2DM) and stable coronary artery disease (CAD) is not determined. METHODS: We conducted a nested case-control study among 1282 T2DM patients with stable CAD. Patients were followed up for 3846 person-years. A total of 160 patients with events (12.5%) were identified and matched individually on age, gender, previous use of lipid lowering agents and duration of follow-up with 640 controls. RESULTS: In Kaplan-Meier analysis, the upper tertiles of TyG index and HGI had a significant lower event-free survival (p = .002; p = .036, respectively). Of the note, both TyG index and HGI were associated with increased risk of MACCEs after adjusting for confounding risk factors [adjusted HR (95% CI): 1.693 (1.238-2.316); 1.215 (1.046-1.411), respectively]. Moreover, adding TyG index to the Cox model increased the C-statistic to 0.638 (95%CI: 0.595-0.683, p = .002) while the C-statistic was not statistically improved when HGI was included (p = .240). CONCLUSIONS: Both TyG index and HGI could predict cardiovascular outcomes in T2DM patients with new-onset, stable CAD while TyG index might be better. Key messages Both TyG and HGI are predictors of cardiovascular risk. The prognostic value of TyG index and HGI in T2DM patients with stable coronary artery disease is not determined. Our study firstly indicates that TyG index might have better prognostic value than HGI in T2DM patients with new-onset, stable CAD.

Management standards for stable coronary artery disease in India.

Coronary artery disease (CAD) is one of the important causes of cardiovascular morbidity and mortality globally, giving rise to more than 7 million deaths annually. An increasing burden of CAD in India is a major cause of concern with angina being the leading manifestation. Stable coronary artery disease (SCAD) is characterised by episodes of transient central chest pain (angina pectoris), often triggered by exercise, emotion or other forms of stress, generally triggered by a reversible mismatch between myocardial oxygen demand and supply resulting in myocardial ischemia or hypoxia. A stabilised, frequently asymptomatic phase following an acute coronary syndrome (ACS) is also classified as SCAD. This definition of SCAD also encompasses vasospastic and microvascular angina under the common umbrella.

Severe multivessel coronary artery disease and high-sensitive troponin T.

INTRODUCTION: A key problem in stable coronary artery disease (CAD) is non-invasive identification of patients with severe multivessel CAD. Determination of biomarkers that have pro-inflammatory properties (C-reactive protein - hsCRP) and indicate heart muscle ischemia (high-sensitive troponin T - hsTnT) can contribute to the improvement of stratification in this regard. THE AIM OF THE STUDY: The aim of the study was to identify factors associated with the presence of multivessel CAD in clinically stable men. MATERIAL AND METHODS: The study included 92 symptomatic men (mean age 64.05 ± 9.42 years) with preserved left ventricular function, scheduled for elective coronary angiography. Patients were divided and analyzed in two groups: with multivessel coronary artery disease (2-3-vessel disease, n = 46) vs. without multivessel coronary artery disease (n = 46). RESULTS: Patients with multivessel CAD had significantly higher levels of hsTnT (0.01 vs. 0.007, p = 0.0021) and fasting glucose (6.0 vs. 5.45, p = 0.0112). Based on the drawn ROC curves, the cut-off points were determined for hsTnT ≥ 0.0085 ng/ml and fasting plasma glucose ≥ 5.85 mmol/l. From multivariate analysis only hsTnT in concentration higher than the cut-off point enhanced the risk of multivessel CAD (OR 4.286, 95% CI: 1.79-10.263, p = 0.001). CONCLUSIONS: In men with stable CAD, preserved systolic left ventricular function and non-high cardiovascular risk determined from the initial concentration of hsCRP, elevated level of hsTnT was independently associated with the risk of multivessel coronary artery disease.

Geographical variations in the prevalence and management of cardiovascular risk factors in outpatients with CAD: Data from the contemporary CLARIFY registry.

AIM: To determine the current prevalence and control of major cardiovascular risk factors in stable CAD outpatients worldwide. METHODS: We analysed variations in cardiovascular risk factors in stable CAD outpatients from CLARIFY, a 5-year observational longitudinal cohort study, in seven geographical zones (Western/Central Europe; Canada/South Africa/Australia/UK; Eastern Europe; Central/South America; Middle East; East Asia; and India). RESULTS: Patient presentation (N=32,954, mean age 64.2 years, 78% male) varied between zones, as did prevalence of risk factors (all p < 0.0001). Obesity ranged from 20% (East Asia) to 42% (Middle East), raised blood pressure from 28% (Central/South America and East Asia) to 48% (Eastern Europe), raised LDL cholesterol from 24% (Canada/South Africa/Australia/UK) to 65% (Eastern Europe), elevated heart rate (≥70 bpm) from 38% (Western/Central Europe) to 78% (India), diabetes from 17% (Eastern Europe) to 60% (Middle East), and smoking from 6% (Central/South America) to 19% (Eastern Europe). Aspirin and lipid-lowering drugs were widely used everywhere (≥84% and ≥88%, respectively). Rates of risk factor control varied geographically (all p < 0.0001). Rate of controlled blood pressure in hypertension varied from 47% (Eastern Europe) to 66% (Central/South America), glucose control in diabetes from 23% (India) to 51% (Western/Central Europe and East Asia), controlled LDL cholesterol and dyslipidaemia from 32% (Eastern Europe) to 75% (Canada/South Africa/Australia/UK), heart rate <70 bpm from 22% (India) to 62% (Western/Central Europe), and heart rate ≤60 bpm in angina patients from 2% (India) to 29% (Canada/South Africa/Australia/UK and Central/South America). CONCLUSION: Prevalence and control of major cardiovascular risk factors in stable CAD vary markedly worldwide. Many stable CAD outpatients are being treated suboptimally.

Inadequate heart rate control despite widespread use of beta-blockers in outpatients with stable CAD: findings from the international prospective CLARIFY registry.

BACKGROUND: To use CLARIFY, a prospective registry of patients with stable CAD (45 countries), to explore heart rate (HR) control and beta-blocker use. METHODS: We analyzed the CLARIFY population according to beta-blocker use via descriptive statistics with Pearson's χ(2) test for comparisons, as well as a multivariable stepwise model. RESULTS: Data on beta-blocker use was available for 32,914 patients, in whom HR was 68 ± 11 bpm; patients with angina, previous myocardial infarction, and heart failure had HRs of 69 ± 12, 68 ± 11, and 70 ± 12 bpm, respectively. 75% of these patients were receiving beta-blockers. Bisoprolol (34%), metoprolol tartrate (16%) or succinate (13%), atenolol (15%), and carvedilol (12%) were mostly used; mean dosages were 49%, 76%, 35%, 53%, and 45% of maximum doses, respectively. Patients aged <65 years were more likely to receive beta-blockers than patients ≥ 75 years (P<0.0001). Gender had no effect. Subjects with HR ≤ 60 bpm were more likely to be on beta-blockers than patients with HR ≥ 70 bpm (P<0.0001). Patients with angina, previous myocardial infarction, heart failure, and hypertension were more frequently receiving beta-blockers (all P<0.0001), and those with PAD and asthma/COPD less frequently (both P<0.0001). Beta-blocker use varied according to geographical region (from 87% to 67%). CONCLUSIONS: Three-quarters of patients with stable CAD receive beta-blockers. Even so, HR is insufficiently controlled in many patients, despite recent guidelines for the management of CAD. There is still much room for improvement in HR control in the management of stable CAD.

Percutaneous coronary intervention versus medical therapy in stable coronary artery disease: the unresolved conundrum.

One of the major dilemmas facing physicians is what diagnostic and therapeutic approaches should be recommended to those stable coronary artery disease patients whose symptoms are adequately controlled on medical therapy. This study sought to assess the evidence-based data relating to whether: 1) all patients with significant coronary lesions (i.e., ischemia-producing) should undergo percutaneous coronary intervention (PCI); 2) the best therapeutic approach is optimal medical therapy; or 3) PCI should be performed, but only in certain subsets of patients. We reviewed all recent meta-analyses of prospective randomized trials that compared the outcomes of medical therapy and PCI in stable, symptomatically controlled, coronary artery disease patients. To provide greater insights to the clinician, we then analyzed, in depth, 3 comprehensive and widely quoted randomized trials. Review of recently published (2012) meta-analyses, and the detailed analyses of 3 widely quoted individual studies, indicate no difference exists between PCI and medical therapy in nonfatal MI or in all-cause or cardiovascular mortality. Thus, clinical equipoise exists: in other words, there is no evidence-based justification for adopting 1 therapeutic strategy over the other. Therefore, it is not inappropriate, until additional evidence emerges, for the responsible, experienced physician to weigh several sources of information in formulating a recommendation to the patient, even though definitive evidence-based data are not as yet available. Such sources may include assessment of the individual patient's clinical presentation, assessment of the severity of ischemia, and the patient's precise coronary anatomy. Critical for more-reliable decision making will be future development of accurate measures of the individual patient's risk of MI and/or death, whether by biomarker, imaging, or ischemia assessments.