Previous History Of Coronary Artery Disease Research Articles

Subclinical hypothyroidism represents an additional risk factor for coronary artery calcification, especially in subjects with intermediate and high cardiovascular risk scores.

Several studies have suggested an association between subclinical hypothyroidism (SCH) and increased cardiovascular risk. The aim of this study was to evaluate the presence of coronary artery disease (CAD) in asymptomatic patients with SCH by measuring the coronary artery calcium score (CACS). A total of 222 asymptomatic subjects (103 SCH and 119 euthyroid (EU)), who were between the ages of 35 and 65 years and had no previous history of CAD, were enrolled for this cross-sectional analysis. The criteria for SCH included a confirmed normal serum free thyroxine and high TSH levels. Lipid profile, Framingham risk score (FRS) and CACS analyses were performed for all subjects. The SCH and EU groups were comparable with respect to age, gender, BMI and frequency of diabetes, systemic arterial hypertension, hypercholesterolaemia and smoking. There was no difference in the median CACS between the SCH and EU groups. However, in the subgroup of subjects with intermediate/high FRS (AR10y ≥10%), CACS was higher in the SCH subjects compared with EU subjects (EU vs SCH, 0.0 (57.0) vs 23.0 (161.5); P=0.045). Multivariate analysis revealed that the risk for CACS >100 was independently associated with male gender, age >55 years, and the presence of simultaneous SCH and AR10y ≥10% (OR=87.5 (CI=2.1-3500); P=0.001). Serum TSH was positively correlated with CACS, especially in intermediate/high FRS subjects (rs=0.301, P=0.045). It was demonstrated that SCH represents an additional risk factor for CAD, notably in intermediate and high FRS subjects.

Relation of Angiographic Thrombus Burden With Electrocardiographic Grade III Ischemia in Patients With ST-Segment Elevation Myocardial Infarction

We aimed to investigate the association between electrocardiographic (ECG) grade III ischemia and angiographic thrombus burden in patients with acute ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (pPCI). The study population consisted of 307 patients with STEMI. Baseline ECGs of the patients were analyzed for grade III ischemia; angiographic thrombus burden was assessed by thrombolysis in myocardial infarction thrombus classification. A total of 108 (35%) patients had low thrombus burden whereas 199 (65%) patients had high thrombus burden. Grade III ischemia was more prevalent in patients with high thrombus burden (25.1% vs 11.1%, P = .004). Only grade III ischemia (odds ratio: 2.59, 95% confidence interval 1.24-5.39, P = .011) and history of coronary artery disease (CAD) were found to be the independent predictors of high thrombus burden. Grade III ischemia on ECG and previous history of CAD were independent predictors of coronary thrombus burden in patients with STEMI who underwent pPCI.

Prevalence and Risk Factors of Peripheral Artery Disease in Elderly Chronic Ischemic Stroke Patients: A Study of a Single Geriatric Hospital

Results: Of the 96 patients, 55 (57.3%) had PAD (ABI<0.9) of which 6 patients (6.3%) had severe PAD (ABI<0.5) and 22 patients (22.9%) had bilateral PAD. PAD was more frequently observed in patients with diabetes (65% vs. 15%, p=0.001), hypercholesterolemia (65% vs. 15%, p<0.001), previous history of coronary artery disease (CAD) (25% vs. 5%, p=0.01) and recurrent ischemic stroke (36% vs. 12%, p=0.01). The means of the total cholesterol and blood urea nitrogen were higher in patients with PAD. From the results of the binary logistic regression analysis, presence of diabetes (odds ratio [OR], 4.740; p=0.026), hypercholesterolemia (OR, 18.991; p<0.001), previous history of CAD (OR, 7.579; p=0.038) and lower Korean version of Modified Barthel Index (OR, 0.971; p=0.009) were independent risk factors for PAD. Conclusion: PAD is frequently observed in elderly patients with chronic ischemic stroke. Measuring ABI to diagnose PAD and controlling risk factors may be beneficial in these patients seen at geriatric hospitals and centers.

Prognostic value of Morise clinical score, calcium score and computed tomography coronary angiography in patients with suspected or known coronary artery disease

Our aim was to determine the prognostic value of computed tomography coronary angiography (CTCA), coronary artery calcium scoring (CACS) and Morise clinical score in patients with known or suspected coronary artery disease (CAD). A total of 722 patients (480 men; 62.7±10.9 years) who were referred for further cardiac evaluation underwent CACS and contrast-enhanced CTCA to evaluate the presence and severity of CAD. Of these, 511 (71%) patients were without previous history of CAD. Patients were stratified according to the Morise clinical score (low, intermediate, high), to CACS (0-10, 11-100, 101-400, 401-1,000, >1,000) and to CTCA (absence of CAD, nonsignificant CAD, obstructive CAD). Patients were followed up for the occurrence of major events: cardiac death, nonfatal myocardial infarction, unstable angina and revascularisation. Significant CAD (>50% luminal narrowing) was detected in 260 (36%) patients; nonsignificant CAD (<50% luminal narrowing) in 250 (35%) and absence of CAD in 212 (29%). During a mean follow-up of 20±4 months, 116 events (21 hard) occurred. In patients with normal coronary arteries on CTCA, the major event rate was 0% vs. 1.7% in patients with nonsignificant CAD and 7.3% in patients with significant CAD (p<0.0001). Three hard events (14%) occurred in patients with CACS≤100 and two (9.5%) in patients with intermediate Morise score; one revascularisation was observed in a patient with low Morise score. At multivariate analysis, diabetes, obstructive CAD and CACS >1,000 were significant predictors of events (p<0.05). An excellent prognosis was noted in patients with a normal CTCA (0% event rate). CACS ≤100 and low-intermediate Morise score did not exclude the possibility of events at follow-up.

Independent and incremental value of stress echocardiography over clinical and stress electrocardiographic parameters for the prediction of hard cardiac events in new-onset suspected angina with no history of coronary artery disease

Recent data have shown that exercise electrocardiogram (ECG) has no incremental prognostic value over clinical and rest ECG parameters in chest pain patients without a history of coronary artery disease (CAD). The incremental prognostic value of stress echocardiography (SE) in this population is unknown. Accordingly, 547 consecutive patients (68 ± 4.9 years) with chest pain but no previous history of CAD, referred for SE (exercise and dobutamine), were identified. Patients were followed up for death and acute myocardial infarction (AMI). At a median follow-up period of 28 months, there were a total of 35 hard cardiac events (5 deaths and 30 non-fatal AMI). Among the prognostic clinical, resting/stress ECG, and SE data, univariate predictors were the Framingham risk score (P = 0.025), diabetes (P = 0.06), hypercholesterolaemia (P = 0.06), stress ECG ischaemia (P = 0.044), stress heart rate (P = 0.019), and SE-determined ischaemic burden (stress-rest wall thickening score index; P < 0.001). In a multivariate model, ischaemic burden was the only independent predictor of events (P < 0.001). SE also showed incremental prognostic value over and above clinical (Framingham's risk score) and stress ECG changes in a global χ(2) model. This was true also for patients undergoing only exercise SE (n = 347). SE provides both independent and incremental prognostic value for the prediction of hard cardiac events in chest pain patients without a previous history of CAD-over and above clinical, ECG, and stress ECG data.

Serum folate and homocysteine and the incidence of acute coronary events: the Kuopio Ischaemic Heart Disease Risk Factor Study

Several, but not all, prospective studies have shown that low folate intakes, low circulating folate concentrations, or high plasma total homocysteine (tHcy) concentrations are associated with an increased risk of coronary artery disease (CAD). We examined the relations of both serum folate and serum tHcy concentrations with acute coronary events in middle-aged men from eastern Finland who had no CAD at baseline. In a population-based prospective cohort study, 1027 men aged 46-64 y were examined in 1991-1993 as part of the Kuopio Ischaemic Heart Disease Risk Factor Study. During an average follow-up of 7.7 y (7900 person-years of follow-up), 114 acute coronary events were observed in 61 men who had no previous history of CAD (n = 810). In a Cox model, compared with men whose serum folate concentrations were in the lowest tertile, those whose concentrations were in the highest tertile had a risk factor-adjusted relative risk of acute coronary events of 0.35 (95% CI: 0.17, 0.73; P = 0.005). Serum tHcy concentrations were not significantly associated with the risk of acute coronary events (for the highest tertile compared with the lowest, adjusted relative risk = 1.03; 95% CI: 0.57, 1.87; P = 0.932). The results of this prospective cohort study do not support the hypothesis that a high circulating tHcy concentration is a risk factor for acute coronary events in a male population free of prior heart disease. However, they do suggest that moderate-to-high serum folate concentrations are associated with a greatly reduced incidence of acute coronary events.

Pharmacoeconomics of lipid-lowering agents for primary and secondary prevention of coronary artery disease.

Cardiovascular disease is the leading cause of death and the leading source of healthcare expenditure in the US and most other industrialised countries. Cholesterol lowering by pharmacological means prevents atherosclerotic plaque progression and has been shown to reduce both fatal and nonfatal coronary events in patients with or without coronary artery disease (CAD). Because of their excellent efficacy and safety profiles, the introduction of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors (also known an 'statins') in 1987 raised hopes for demonstrating the survival benefit of cholesterol reduction. In the past decade, several large-scale placebo-controlled trials with statin therapy have revisited the relationship between cholesterol reduction, cardiovascular disease and mortality. The West of Scotland Coronary Prevention Study (WOSCOPS) [pravastatin] and the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) [lovastatin] have shown significant cardiovascular disease reduction in primary prevention trials of patients with elevated and normal cholesterol levels, respectively. The Scandinavian Simvastatin Survival Study (4S), the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study and the Cholesterol and Recurrent Events (CARE) trial [pravastatin] have shown significant cardiovascular disease reduction in patients with a previous history of CAD with high, moderate and normal cholesterol levels, respectively. Three of these studies (4S, WOSCOPS and LIPID) have shown significant reduction in all-cause mortality, while all the statin secondary prevention trials (4S, CARE and LIPID) have demonstrated significant reduction in cerebrovascular disease/ Earlier cholesterol reduction cost-effectiveness studies with nonstatin treatments (bile acid resins, fibrates, niacin and diet) suggested that only patients at extremely high risk could be treated with lipid therapy in a cost-effective manner. More recently, rigorous outcomes evidence demonstrates that statins, particularly for simvastatin for secondary prevention and lovastatin for primary prevention, have a broadly favourable cost-effectiveness profile. Based on US medical price levels and the available clinical trial data on statins, it would be cost effective [e.g. cost less than $US50,000/year of life saved] to intervene with statin therapy in any patient with an annual CAD risk exceeding 1%. This includes all patients with pre-existing CAD or diabetes mellitus, and many more primary prevention patients than are currently contemplated by the US National Cholesterol Education Panel treatment guidelines. Achieving such a goal will require enormous changes in patient education, clinical perspective, healthcare practice and healthcare finances. But any proven opportunity for saving the lives of 25% of those dying from cardiovascular disease each year deserves to be considered with the utmost seriousness and urgency.

Acute coronary syndromes: unstable angina and non-Q-wave myocardial infarction.

Ischemic heart disease includes a wide spectrum of conditions, ranging from silent ischemia and exertion-induced angina, through unstable angina, to acute MI. Unstable angina occupies the center of this spectrum, causing disability and risk greater than that of chronic stable angina but less than that of acute MI1 (Fig 1⇓). Although non–Q-wave MI for many years was considered prognostically similar to unstable angina, recent longitudinal studies indicate that it is similar to Q-wave infarction2 3 (Fig 2⇓). Figure 1. Cumulative 6-month mortality from ischemic heart disease. Diagnosis on admission to hospital (n=21 761; 1985 to 1992). From Duke Cardiovascular Database. Reproduced with permission from Reference 1. Figure 2. Top, Cumulative 1-year combined death or MI among patients with Q-wave and non–Q-wave MI treated with fibrinolysis. Reproduced with permission from Reference 2. Bottom, Risk of subsequent cardiac events in stable convalescing patients after first non–Q-wave and Q-wave MI. Reproduced with permission from Reference 3. The concept of unstable angina has emerged from observations of frequent symptoms preceding acute MI, followed by prospective documentation that unstable symptoms frequently culminated in acute MI. The syndrome was rapidly accepted as a well-defined clinical entity as specific clinical manifestations, pathophysiological mechanisms, laboratory findings, and treatment became better characterized. Unstable angina is currently one of the leading causes of hospital admission for CAD, and non–Q-wave MI accounts for >30% of admissions for acute MI.1 4 Yet, the diagnosis of unstable angina remains clinical, based on symptom recognition. The physician caring for patients with unstable angina is in a privileged position of recognizing rapidly evolving CAD and being able to intervene to prevent irreversible left ventricular damage and progression of CAD. Unstable angina is classically described as a heterogeneous disease, referring to a wide spectrum of clinical manifestations from stable angina to MI, of disease …