Coronary Artery Disease Equivalent Research Articles

Myocardial Bridging Increases the Risk of Adverse Cardiovascular Events in Patients without Coronary Atherosclerosis.

Background: Myocardial bridging (MB) is a congenital coronary anomaly and an important cause of chest pain. The long-term effects of MB on cardiovascular events remain elusive. Methods: We used the National Health Insurance Research Database of Taiwan to conduct an analysis. All patients who had undergone coronary angiography were considered for inclusion. The primary endpoint was a composite of nonfatal myocardial infarction, nonfatal ischemic stroke, and cardiovascular death. Results: We identified 10,749 patients from 2008 to 2018 and matched them with an equal number of controls by propensity-score matching. The mean follow-up period was 5.78 years. In patients without coronary artery disease, MB increased the risk of the composite endpoint (hazard ratio [HR]: 1.57, 95% confidence interval [CI]: 1.44-1.72, p < 0.001), which was driven by increased risks of nonfatal myocardial infarction and cardiovascular death. In patients with significant coronary artery disease, MB did not increase the risk of major adverse cardiovascular events. MB was identical to insignificant coronary artery disease from the viewpoint of clinical outcomes. Conclusions: The presence of MB significantly increases cardiovascular risks in patients with normal coronary vessels. Atherosclerotic coronary artery disease mitigates the effect of MB on cardiovascular outcomes. MB can be considered an insignificant coronary artery disease equivalent.

Myocardial repolarization is affected in patients with diabetic retinopathy

Background/Aim: Diabetes Mellitus (DM), considered the equivalent of coronary artery disease, is one cause of ventricular repolarization (VR) dispersion. Retinopathy is one of the vascular consequences of diabetes. The association between myocardial repolarization dispersion and diabetic retinopathy is not fully elucidated. We aimed to evaluate ventricular repolarization using Tp-e interval and corrected (c) Tp-e/QT ratio in DM patients with and without retinopathy. Methods: A total of 124 diabetic subjects were included in this retrospective cohort study. All medical data were obtained from the electronic database of our university hospital. The subjects were divided into the no diabetic retinopathy (NDR) group (n=45), and the diabetic retinopathy (DR) group (n=79), which were compared in terms of demographic features, clinic and laboratory findings, and electrocardiographic findings such as QT, QTc, Tp-e, Tp-e/QT, Tp-e/QTc. Results: The groups were similar in terms of demographic features (P>0.05). Both Tp-e interval and Tp-e/QTc were significantly prolonged in the DR group compared to the NDR group. There were significant correlations between Tp-e, Tp-e/QTc, DM duration, and age. In multivariate logistic regression analysis, Tp-e (OR=6.01, %95 CI=4.17-7.52, P=0.012), Tp-e/QTc (OR=1.215, 95% CI=0.874-1.612, P=0.029), and DM duration (OR=1.422, 95% CI= 1.146–1.712, P<0.001) were independent predictors of DR. Conclusion: We showed that DM patients with retinopathy may also have an increased risk for sudden cardiac death due to ventricular arrhythmogenesis.

Coronary artery disease: New Insights into revascularization treatment of diabetic patients.

Diabetes mellitus is an independent cardiovascular risk factor, considered an equivalent of coronary artery disease in terms of prognosis. A history of acute coronary syndrome is a strong predictor of another coronary episode, and cardiovascular complications are the leading cause of mortality in diabetic patients. Many patients with coronary artery disease suffer from concomitant diabetes or pre-diabetes. There are 3 strategies of coronary artery disease treatment: conservative management, coronary artery bypass graft (CABG) and percutaneous coronary intervention (PCI). Since drug-eluting stents (DES) were developed, PCI has become one of the most widespread interventional cardiology procedures performed in Europe and worldwide. Among all coronary risk factors, diabetes mellitus remains the most important predictor of unfavorable outcomes of revascularization therapy. This paper reviews the current evidence regarding revascularization in diabetic patients, with particular emphasis on PCI. A systematic analysis of clinical trials of CABG and PCI, especially with DES, was conducted.

Prognostic Assessment of Diabetics Using Myocardial Perfusion Imaging: Diabetes Mellitus is Still a Coronary Artery Disease Equivalent.

Background:Even though diabetes mellitus (DM) has been considered a “Coronary Artery Disease (CAD) equivalent”, that is still controversial, especially in a contemporary population subject to optimized treatment.Objective:We aimed to assess the cardiovascular risk of diabetics by myocardial perfusion scintigraphy (MPS).Methods:Consecutive patients who underwent MPS from 2008 to 2012 were studied. Perfusion scores were calculated, and abnormal MPS was defined as a summed stress score >3. Patients were followed for 3±1 years for all-cause death, which was compared between patients with DM (without known CAD) and patients with known CAD but without DM.Results:Among 3409 patients, 471 (13.8%) were diabetics without known CAD (DM group) and 638 (18.7%) had CAD without diabetes (CAD group). Annualized death rates were not significantly different between DM or CAD patients (0.9 vs 1.5%, p=0.09). With normal MPS, death rates were 0.7% for DM and 0.6% for CAD (p=0.8). With abnormal MPS, death rates increased similarly in the DM and CAD groups.Conclusions:In diabetic patients without known CAD, the rate of death was not significantly different from patients with prior CAD and without DM. Abnormal MPS increased risk similarly in diabetic patients and in those with CAD. These findings suggest that DM may still be considered a high-risk condition, comparable to known CAD, and effectively stratified by MPS.

Exploring cardiovascular disease risk evaluation in patients with inflammatory joint diseases

ObjectivesCardiovascular disease (CVD) risk calculators developed for the general population have been shown to inaccurately predict CVD events in patients with inflammatory joint disease (IJD). European guidelines for CVD prevention recognize the presence of carotid plaques (CP) as a very high CVD risk factor, equivalent of coronary artery disease. Patients with IJD have a high prevalence of CP. We evaluated if CP resulted in reclassification of patients with IJD into a more appropriate CVD risk class and recommended lipid lowering treatment. MethodsCVD risk evaluation was performed in patients with IJD using SCORE and ACC/AHA risk calculators to predict CVD events. ResultsOf the 335 IJD patients evaluated (including rheumatoid arthritis n=201, ankylosing spondylitis n=85 and psoriatic arthritis n=49), 183 and 159 IJD patients had a calculated CVD risk by SCORE and ACC/AHA <5%, indicating no need of lipid lowering treatment (LLT). However, of patients with low to moderate risk calculated by SCORE and ACC/AHA, 67 (36.6%) and 48 (30.2%) had CP and should according to guidelines receive intensive LLT. For patients with high risk, in the LLT considered group, 54.9% and 58.1% were reclassified to correct treatment when adding information on the presence of CP. Our results reveal a considerable reclassification into correct CVD risk category when adding CP in female patients. ConclusionThe high frequency of asymptomatic atherosclerosis in patients with IJD has a notable impact on CVD risk stratification. Identification of CP will reclassify patients into recommended CVD preventive treatment group, which may be clinically important.

Effect of Financial Incentives to Physicians, Patients, or Both on Lipid Levels: A Randomized Clinical Trial.

Financial incentives to physicians or patients are increasingly used, but their effectiveness is not well established. To determine whether physician financial incentives, patient incentives, or shared physician and patient incentives are more effective than control in reducing levels of low-density lipoprotein cholesterol (LDL-C) among patients with high cardiovascular risk. Four-group, multicenter, cluster randomized clinical trial with a 12-month intervention conducted from 2011 to 2014 in 3 primary care practices in the northeastern United States. Three hundred forty eligible primary care physicians (PCPs) were enrolled from a pool of 421. Of 25,627 potentially eligible patients of those PCPs, 1503 enrolled. Patients aged 18 to 80 years were eligible if they had a 10-year Framingham Risk Score (FRS) of 20% or greater, had coronary artery disease equivalents with LDL-C levels of 120 mg/dL or greater, or had an FRS of 10% to 20% with LDL-C levels of 140 mg/dL or greater. Investigators were blinded to study group, but participants were not. Primary care physicians were randomly assigned to control, physician incentives, patient incentives, or shared physician-patient incentives. Physicians in the physician incentives group were eligible to receive up to $1024 per enrolled patient meeting LDL-C goals. Patients in the patient incentives group were eligible for the same amount, distributed through daily lotteries tied to medication adherence. Physicians and patients in the shared incentives group shared these incentives. Physicians and patients in the control group received no incentives tied to outcomes, but all patient participants received up to $355 each for trial participation. Change in LDL-C level at 12 months. Patients in the shared physician-patient incentives group achieved a mean reduction in LDL-C of 33.6 mg/dL (95% CI, 30.1-37.1; baseline, 160.1 mg/dL; 12 months, 126.4 mg/dL); those in physician incentives achieved a mean reduction of 27.9 mg/dL (95% CI, 24.9-31.0; baseline, 159.9 mg/dL; 12 months, 132.0 mg/dL); those in patient incentives achieved a mean reduction of 25.1 mg/dL (95% CI, 21.6-28.5; baseline, 160.6 mg/dL; 12 months, 135.5 mg/dL); and those in the control group achieved a mean reduction of 25.1 mg/dL (95% CI, 21.7-28.5; baseline, 161.5 mg/dL; 12 months, 136.4 mg/dL; P < .001 for comparison of all 4 groups). Only patients in the shared physician-patient incentives group achieved reductions in LDL-C levels statistically different from those in the control group (8.5 mg/dL; 95% CI, 3.8-13.3; P = .002). In primary care practices, shared financial incentives for physicians and patients, but not incentives to physicians or patients alone, resulted in a statistically significant difference in reduction of LDL-C levels at 12 months. This reduction was modest, however, and further information is needed to understand whether this approach represents good value. clinicaltrials.gov Identifier: NCT01346189.

The role of C-reactive protein genetic variability in the onset of carotid artery disease and renal function impairment in patients with diabetes mellitus type 2

The role of diabetes mellitus (DM) in cardiovascular disease is well established and currently is considered as an equivalent of coronary artery disease. Studies have also reported that DM is associated with the prevalence of occlusive carotid artery disease (AD) [ [1] Kuebler T.W. Bendick P.J. Fineberg S.E. et al. Diabetes mellitus and cerebrovascular disease: prevalence of carotid artery occlusive disease and associated risk factors in 482 adult diabetic patients. Diabetes Care. 1983; 6: 274-278 Crossref PubMed Scopus (21) Google Scholar ] as well as the grade carotid artery stenosis [ [2] Göksan B. Erkol G. Bozluolcay M. Ince B. Diabetes as a determinant of high-grade carotid artery stenosis: evaluation of 1,058 cases by Doppler sonography. J Stroke Cerebrovasc Dis. 2001; 10: 252-256 Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar ]. In addition, DM is related to impaired renal function via several mechanisms [ [3] Vallon V. Thomson S.C. Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney. Annu Rev Physiol. 2012; 74: 351-375 Crossref PubMed Scopus (237) Google Scholar ]. During the last years novel data have arisen for the role of genetics in the initiation and progression of carotid AD [ 4 Pessi T. Eklund C. Huhtala H. et al. CRP and FCGR2A genes have an epistatic effect on carotid artery intima-media thickness: the Cardiovascular Risk in Young Finns Study. Int J Immunogenet. 2009; 36: 39-45 Crossref PubMed Scopus (6) Google Scholar , 5 Jylhävä J. Eklund C. Pessi T. et al. Genetics of C-reactive protein and complement factor H have an epistatic effect on carotid artery compliance: the Cardiovascular Risk in Young Finns Study. Clin Exp Immunol. 2009; 155: 53-58 Crossref PubMed Scopus (16) Google Scholar , 6 Bleil M.E. Ferrell R.E. Sutton-Tyrrell K. Muldoon M.F. Manuck S.B. Apolipoprotein E polymorphism and preclinical carotid artery disease in untreated hypertensive men. Eur J Cardiovasc Prev Rehabil. 2006; 13: 98-100 Crossref PubMed Scopus (4) Google Scholar , 7 Losito A. Selvi A. Jeffery S. Afzal A.R. Parente B. Cao P.G. Angiotensin-converting enzyme gene I/D polymorphism and carotid artery disease in renovascular hypertension. Am J Hypertens. 2000; 13: 128-133 Crossref PubMed Scopus (16) Google Scholar , 8 Diamantopoulos E.J. Andreadis E. Kakou M. et al. Atherosclerosis of carotid arteries and the ace insertion/deletion polymorphism in subjects with diabetes mellitus type 2. Int Angiol. 2002; 21: 63-69 PubMed Google Scholar ] as well as for impaired renal function [ 9 Hung A.M. Ikizler T.A. Griffin M.R. et al. CRP polymorphisms and chronic kidney disease in the third national health and nutrition examination survey. BMC Med Genet. 2011; 12: 65 Crossref PubMed Scopus (11) Google Scholar , 10 Cooper Worobey C. Fisher N.D. Cox D. Forman J.P. Curhan G.C. Genetic polymorphisms and the risk of accelerated renal function decline in women. PLoS One. 2009; 4: e4787 Crossref PubMed Scopus (12) Google Scholar ]. However, scarce data exist regarding genetic polymorphisms in patients with diabetes mellitus and their role in carotid artery disease and renal function. Thus, in the present study we examined the potential role of a single nucleotide polymorphism (SNP) on C-reactive protein (CRP) gene in the onset of carotid AD and impaired renal function in patients with diabetes mellitus type 2.

Should diabetes still be considered a coronary artery disease equivalent?

Diabetes is well established as a cardiovascular risk factor and is currently regarded as a coronary artery disease equivalent. However, some recent data have contradicted the concept. We review the currently available data and usefulness or otherwise of this concept. While the concept of coronary artery disease equivalence has served to highlight the importance of diabetes as a risk factor, it has a number of problems. We propose that it would be more useful to consider diabetes as a myocardial infarction risk equivalent. This is not only more precise and in line with the literature but also conveys better the message that patients with diabetes and one or more previous myocardial infarction(s) are at even higher risk.

Prediabetes, becoming the equivalent of coronary artery disease

Prediabetes refers to a state where blood glucose levels are higher than normal, but not high enough to meet the diagnostic criteria for diabetes mellitus. Similar to the worldwide trend, data derived from large studies has shown an increasing trend in the prevalence of prediabetes in Turkey. According to the Centers for Disease Control and Prevention data, 79 million individuals in the United States have prediabetes. This implies a large population worldwide is at risk of developing diabetes in the near future. In addition to its strong association with the development of diabetes, prediabetes itself represents an increased risk of developing cardiovascular disease and its complications. This review will focus on definition, detection, association with cardiovascular disease and treatment of prediabetes.

Prediabetes, becoming the equivalent of coronary artery disease

Prediabetes, becoming the equivalent of coronary artery disease

Type 2 DM is not coronary artery disease equivalent

Type 2 DM is not coronary artery disease equivalent

Peripheral arterial disease--what do we need to know?

Peripheral artery disease (PAD) results from progressive narrowing of arteries secondary to atherosclerosis and is defined as an Ankle Brachial Index of <0.9. PAD is highly prevalent and is an increasing burden on both the economy and the patient, especially given the rapid shift in demographics in the United States. Despite its prevalence and association with cardiovascular disease, PAD is still underdiagnosed and undertreated. This may, in part, be related to lack of recognition from the physician's side or paucity of evidence from clinical trials. It has been shown that medical therapy approved for cardiovascular disease is effective in the treatment of PAD and decreases cardiovascular events. Various revascularization strategies are also available for improving symptoms and quality of life in these patients, yet they are underutilized. In an attempt to increase its recognition, PAD has been considered a coronary artery disease equivalent. This article reviews the diagnosis and management of PAD. © 2011 Wiley Periodicals, Inc. The authors have no funding, financial relationships, or conflicts of interest to disclose.

Treatment options for hypertension in high-risk patients

Patients are considered to be at high risk of cardiovascular events if they have diabetes, chronic kidney disease, stroke, established coronary artery disease, or a coronary artery disease equivalent. Blood pressure-lowering therapy has been shown to reduce cardiovascular events in these patients significantly. Identification of high-risk patients by global risk evaluation is recommended for every hypertensive patient. Treatment of hypertension in high-risk patients with an angiotensin-converting enzyme inhibitor or an angiotensin receptor antagonist, with or without addition of a dihydropyridine calcium channel antagonist, is a reasonable approach based on current clinical trials.

GGT levels in type II diabetic patients with acute coronary syndrome (does diabetes have any effect on GGT levels in acute coronary syndrome?)

Elevated gamma-glutamyltransferase (GGT) level is independently correlated with conditions associated with increased atherosclerosis, such as obesity, elevated serum cholesterol, high blood pressure and myocardial infarction. It is demonstrated that serum GGT activity is an independent risk factor for myocardial infarction and cardiac death in patients with coronary artery disease. Diabetes is also a well-known cardiovascular risk factor and an equivalent of coronary artery disease. Although the relationship between GGT and coronary artery disease has been reported, there are limited data exploring the changes of GGT in acute coronary syndromes, especially in patients with diabetes. So, this study aimed to determine changes in GGT level in diabetic and non-diabetic acute coronary syndromes. This trial was carried out at Kosuyolu Cardiovascular Training and Research Hospital and Van Yuksek Ihtisas Hospital, Turkey. A total of 219 patients (177 men and 42 women) presenting with acute coronary syndrome) and 51 control subjects between September 2007 and September 2008 were included in the study. Serum γ-glutamyltransferase and serum lipoprotein levels were determined. The resuls indicated that serum GGT levels were higher in acute coronary syndrome patients compared with control. In subgroup analyses, there was no difference between diabetic and non-diabetic subgroups. There was also weak correlation between GGT and blood glucose levels. There was no correlation between GGT and serum lipoprotein levels. In conclusion, serum GGT levels were higher in acute coronary syndrome patients. In subgroup analyses, There was no difference between diabetic and non diabetic subgroup.

Effect of Ezetimibe/Atorvastatin Combination on Oxidized Low Density Lipoprotein Cholesterol in Patients With Coronary Artery Disease or Coronary Artery Disease Equivalent

Ezetimibe is effective in providing additional low-density lipoprotein (LDL) cholesterol lowering when coadministered with statins, but its effect beyond LDL cholesterol lowering is unknown. Oxidized LDL (ox-LDL) is a better predictor of adverse cardiovascular events than standard lipid parameters. The objective of this study was to investigate the effect of ezetimibe on ox-LDL. A total of 100 patients with coronary artery disease or coronary artery disease equivalent were randomized to atorvastatin 40 mg/day and ezetimibe 10 mg/day or to atorvastatin 40 mg/day and placebo. LDL cholesterol, LDL cholesterol subfractions, and ox-LDL were measured at baseline and after 8 weeks of therapy. The ezetimibe group had a larger reduction in total LDL cholesterol compared to placebo. This was due mainly to a larger reduction in large buoyant LDL (24% vs 10%, p = 0.008). Ox-LDL level did not change in the placebo group (50 +/- 13 vs 51 +/- 13 U/L), while it decreased in the ezetimibe group, from 51 +/- 13 to 46 +/- 10 U/L (p = 0.01 vs baseline and p = 0.02 vs final level in placebo). The change in ox-LDL correlated significantly with those in total LDL and in large buoyant LDL (r = 0.6 and r = 0.5, respectively, p <0.01 for both), but not with that of small dense LDL, high-density lipoprotein, or very low density lipoprotein. In conclusion, this study demonstrates that ezetimibe decreases ox-LDL cholesterol through reductions in total LDL cholesterol and in large buoyant LDL cholesterol.

Diastolic stress echocardiography detects coronary artery disease in patients with asymptomatic type II diabetes

Diabetes mellitus is considered as an equivalent of coronary artery disease (CAD). Aim of the study was to investigate whether in asymptomatic patients with type II diabetes, diastolic stress echocardiography may represent an alternative tool for the detection of CAD. The study population consisted of 105 patients with diabetes mellitus (age 61+/-9 years, 26% female, duration of diabetes 37+/-14 months). We performed an exercise stress test, followed by an echo-study and a single-positron emission tomography. Coronary angiography was performed within 1 month. Coronary angiography revealed a coronary artery stenosis of at least 70% in 72 patients (69%, CAD group), while the remaining formed the non-CAD group. Exercise induced an increase of both E/E' lateral and septal ratios as well as their average in the CAD group and on the contrary a decrease of these ratios in the non-CAD group. Receiver operating curve analysis for discrimination between patients with and without obstructive CAD showed an optimal cut-off value of -0.0708 for the exercise-induced change of E/E' average (area under curve 0.892, P<0.001). Sensitivities of scintigraphy and of diastolic stress echocardiography for detection of CAD were 75.0 and 93.1%, respectively; specificity was 78.8% for both methods. In asymptomatic patients, sensitivities of scintigraphy and diastolic stress echocardiography were 76.9 and 92.3%; specificity of both was 80%. In patients with type II diabetes, diastolic stress echocardiography, by means of E/E' ratio exercise-induced changes, can be used for the diagnosis and severity of CAD and for the detection of occult myocardial ischemia.

Evidence for a lower target blood pressure for people with heart disease

The review assesses the evidence for the benefit of lower blood pressure (BP) targets in hypertension management. The current consensus target for the treatment of hypertension is a BP of below 140/90 mmHg for all patients, and a BP of below 130/80 mmHg for those with diabetes or chronic kidney disease. Recently added to the list of conditions warranting the lower BP target are coronary artery disease and coronary artery disease equivalents (stroke, carotid disease, aortic aneurysm, and peripheral vascular disease), as well as those individuals with a Framingham Risk Score of at least 10%. One theoretical issue with lower BP targets may be the existence of a J-shaped curve of BP versus cardiovascular event rate, implying a greater risk, especially of myocardial ischemia, of lowering diastolic BP, which is also the filling pressure of the coronary arteries, below the lower limit of coronary autoregulation. The evidence that this is not a compelling concern is provided by animal studies, clinical trials with both surrogate and hard endpoints, and epidemiologic data. There is at present no proof that more aggressive treatment is harmful and much indirect evidence that it may be beneficial, although the clinical trials that specifically address this question are still in progress.