The Clinical Efficacy Assessment Subcommittee of the American College of Physicians–American Society of Internal Medicine acknowledges the scientific validity of this product as a background paper and as a review that captures the levels of evidence in the management of patients with chronic stable angina as of November 17, 2002





The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or a full revision is needed This process gives priority to areas in which major changes in text, and particularly recommendations, are merited on the basis of new understanding or evidence Minor changes in verbiage and references are discouraged

The ACC/AHA/American College of Physicians–American Society of Internal Medicine (ACP-ASIM) Guidelines for the Management of Patients With Chronic Stable Angina, which were published in June 1999, have now been updated The full-text guideline incorporating the updated material is available on the Internet (wwwaccorg or wwwamericanheartorg) in both a track-changes version showing the changes in the 1999 guideline in strike-out (deleted text) and highlighting …

https://cdr.lib.unc.edu/downloads/bz60cz34d

ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Chronic Stable Angina)

High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study

Obesity has become a major worldwide health problem. In every single country in the world, the incidence of obesity is rising continuously and therefore, the associated morbidity, mortality and both medical and economical costs are expected to increase as well. The majority of these complications are related to co-morbid conditions that include coronary artery disease, hypertension, type 2 diabetes mellitus, respiratory disorders and dyslipidemia. Obesity increases cardiovascular risk through risk factors such as increased fasting plasma triglycerides, high LDL cholesterol, low HDL cholesterol, elevated blood glucose and insulin levels and high blood pressure. Novel lipid dependent, metabolic risk factors associated to obesity are the presence of the small dense LDL phenotype, postprandial hyperlipidemia with accumulation of atherogenic remnants and hepatic overproduction of apoB containing lipoproteins. All these lipid abnormalities are typical features of the metabolic syndrome and may be associated to a pro-inflammatory gradient which in part may originate in the adipose tissue itself and directly affect the endothelium. An important link between obesity, the metabolic syndrome and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis and from adipose tissue resistant to the antilipolytic effects of insulin. The current review will focus on these aspects of lipid metabolism in obesity and potential interventions to treat the obesity related dyslipidemia.

/pdf/dyslipidemia-in-obesity-mechanisms-and-potential-targets-vfumw8bf6u.pdf

Dyslipidemia in Obesity: Mechanisms and Potential Targets

Objective The present paper reviews the evidence that depression is a risk factor for the development and progression of coronary artery disease (CAD). Methods MEDLINE searches and reviews of bibliographies were used to identify relevant articles. Articles were clustered by theme: depression as a risk factor, biobehavioral mechanisms, and treatment outcome studies. Results Depression confers a relative risk between 1.5 and 2.0 for the onset of CAD in healthy individuals, whereas depression in patients with existing CAD confers a relative risk between 1.5 and 2.5 for cardiac morbidity and mortality. A number of plausible biobehavioral mechanisms linking depression and CAD have been identified, including treatment adherence, lifestyle factors, traditional risk factors, alterations in autonomic nervous system (ANS) and hypothalamic pituitary adrenal (HPA) axis functioning, platelet activation, and inflammation. Conclusion There is substantial evidence for a relationship between depression and adverse clinical outcomes. However, despite the availability of effective therapies for depression, there is a paucity of data to support the efficacy of these interventions to improve clinical outcomes for depressed CAD patients. Randomized clinical trials are needed to further evaluate the value of treating depression in CAD patients to improve survival and reduce morbidity.

Depression as a risk factor for coronary artery disease: evidence, mechanisms, and treatment.

Risk factors for type 2 diabetes and cardiovascular disease (CVD) often cluster, including obesity (particularly central), insulin resistance, hyperglycemia, dyslipoproteinemia, and hypertension. These conditions can also occur in isolation, and they are exaggerated by physical inactivity and smoking. Since each of these factors increases risk of CVD, the concept of global cardiometabolic risk (CMR) (Fig. 1) is of value (1). Lipoprotein abnormalities, including elevated triglycerides, low HDL cholesterol, and increased numbers of small dense LDL particles, are common findings in patients with CMR. Clinical entities with increased CMR include type 2 diabetes, familial combined hyperlipidemia, familial hypoalphalipoproteinemia, and polycystic ovary syndrome (2). These disorders often share the CMR characteristics of central obesity, insulin resistance, dyslipoproteinemia, and hypertension.

There are stringent lipid treatment goals for patients with type 2 diabetes or CVD; however, guidelines for treatment of dyslipoproteinemia in high-risk subjects without diabetes or CVD are less intense and are based primarily on LDL cholesterol concentrations, with non-HDL concentrations a secondary consideration in some subjects. Numerous trials have demonstrated that therapies (primarily statins) directed at LDL cholesterol lowering clearly reduce risk of CVD events in patients with diabetes and in those without diabetes but with other CVD risk factors; yet, a number of questions remain. Even with adequate LDL cholesterol lowering, many patients on statin therapy have significant residual CVD risk. It is unclear whether lipoprotein parameters other than LDL or non-HDL cholesterol provide clinically significant additional prognostic information regarding CVD risk, yield more information about the effectiveness of therapy, or indicate more appropriate treatment targets. Many patients with CMR or diabetes have relatively normal levels of LDL cholesterol but increased numbers of small dense LDL particles and other atherogenic lipoproteins. Some have advocated that assessment of other lipoprotein parameters might be more helpful than assessment limited to LDL or non-HDL …

https://care.diabetesjournals.org/content/diacare/31/4/811.full.pdf

Lipoprotein management in patients with cardiometabolic risk: consensus statement from the American Diabetes Association and the American College of Cardiology Foundation.

It has been recognized over the past years that women form a distinct subpopulation within patients with coronary heart disease. This phenomenon should be acknowledged in the management and in the assessment of coronary heart disease. Over the past years remarkable progress has been made concerning our knowledge of cardiovascular risk factors related to gender. For instance, diabetes, high density lipoproteins and triglycerides levels have been found to have a greater impact on coronary heart disease risk in women compared to men. On the other hand, evidence showing that lipoprotein (a) is a cardiovascular risk factor seems to be stronger in men than in women. For optimal treatment and prevention of coronary heart disease it is necessary to acknowledge that it is not self-evident that women and men show similar responses to risk factors or to treatment. This review article addresses the role of cardiovascular risk factors focusing on the differential impact they might have on men and women.

Risk factors for coronary heart disease: implications of gender.

—The effect of untreated total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) as cardiovascular risk factors in both primary and secondary prevention has been extensively ...

Apolipoprotein Concentrations During Treatment and Recurrent Coronary Artery Disease Events

Abnormal postprandial apolipoprotein B-48 and triglyceride responses in normolipidemic women with greater than 70% stenotic coronary artery disease: a case-control study

The association between plasma apolipoprotein (apo) B concentrations and angiographically determined coronary artery disease (CAD) was investigated in women in a cross-sectional study. Stenosis of >60% in 1 or more coronary arteries was classified as CAD+. CAD- was defined as a maximum stenosis of 10% in any coronary artery. Fasting plasma concentrations of apoB, apoA-I, cholesterol (chol), low density lipoprotein cholesterol (LDL-chol), high density lipoprotein cholesterol (HDL-chol), and triglycerides (TGs) were determined. Information on nonlipid risk factors was obtained from questionnaires. CAD+ women (n=160) were older than CAD- women (n=129), 64.0+/-7.8 vs 57.8+/-11.1 years, respectively. CAD+ compared with CAD- women had higher frequencies of diabetes (14.7% vs 5.8%, P=0.05), hypertension (53% vs 37%, P=0.018), and ever-smoking (48% vs 35%, P<0.001). CAD+ women had higher plasma concentrations of apoB (1.48+/-0.32 vs 1.25+/-0.34 g/L, P<0.001), chol (7.01+/-1.19 vs 6.38+/-1.22 mmol/L, P=0.001), LDL-chol (4.74+/-1.09 vs 4.13+/-1.13 mmol/L, P<0.001), and TGs (1.98+/-0.84 vs 1.71+/-0.93 mmol/L, P=0.007) and lower levels of HDL-chol (1.28+/-0.28 vs 1.37+/-1.38 mmol/L, P=0.028). After correction for nonlipid risk factors, apoB, chol, LDL-chol, HDL-chol, and TG were independently related to CAD. In the lowest quartiles of chol, LDL-chol, and TG, CAD+ women had higher apoB concentrations than CAD- women. In contrast, chol, LDL-chol, TG, or HDL-chol levels were not different in any quartile of apoB. ApoB showed the most significant relation with the number of stenotic vessels, and apoB was associated with CAD in the normolipidemic subgroup. In conclusion, apoB was superior to chol, LDL-chol, HDL-chol, TG, and apoA-I in discriminating between CAD+ and CAD-.

Apolipoprotein B and Coronary Artery Disease in Women A Cross-sectional Study in Women Undergoing Their First Coronary Angiography

The aim of the study was to characterize postprandial high-density lipoprotein (HDL) cholesterol metabolism in postmenopausal women and to evaluate the effect of replacement therapy with 17β-estradiol. Sixteen healthy normolipidemic (plasma cholesterol, 5.39 ± 0.68 mmol/L; plasma triglycerides [TGs], 1.24 ± 0.55 mmol/L) postmenopausal women received an oral vitamin A fat tolerance test (50 g fat with 60,000 IU vitamin A/m2 body surface area). Venous blood samples were taken before the test, at hourly intervals up to 8 hours, and 24 hours after ingestion of the fat load for determination of HDL cholesterol, HDL TG, and HDL apolipoprotein (apo) A-I concentrations. TG and vitamin A concentrations were also measured. A subgroup of six women were treated with 2 mg micronized 17β-estradiol orally each day for 6 weeks, after which the oral vitamin A fat tolerance test was repeated. A reduction in plasma HDL cholesterol concentrations was observed 3 to 8 hours after ingestion of the fat load, and the minimal postprandial HDL cholesterol concentration was, on average, 31.7% (P = .04) lower than the fasting HDL cholesterol concentration. HDL cholesterol had returned to the initial value 24 hours after the fat load. The decrease in postprandial HDL cholesterol concentrations was attenuated by treatment with 17β-estradiol. The area under the curve (AUC) for the postprandial reduction in HDL cholesterol improved substantially by 66% during 17β-estradiol (−2.4 ± 2.6 mmol · h · L−1 before 17β-estradiol and −1.1 ± 1.2 mmol · h · L−1 during 17β-estradiol, P = .038). In conclusion, HDL cholesterol concentrations decreased by 32% in the postprandial state in normolipidemic postmenopausal women, indicating that HDL cholesterol must be measured in the fasting state. Replacement therapy with 17β-estradiol reduced the postprandial decrease in HDL cholesterol by 66%. This effect of 17β-estradiol can be beneficial in reducing the risk of coronary artery disease.

H. Tineke Westerveld

Papers

Risk factors for coronary heart disease: implications of gender.

Apolipoprotein Concentrations During Treatment and Recurrent Coronary Artery Disease Events

Abnormal postprandial apolipoprotein B-48 and triglyceride responses in normolipidemic women with greater than 70% stenotic coronary artery disease: a case-control study

Apolipoprotein B and Coronary Artery Disease in Women A Cross-sectional Study in Women Undergoing Their First Coronary Angiography

Postprandial reduction in high-density lipoprotein cholesterol concentrations in postmenopausal women: Improvement by 17β-estradiol☆