2001

DOI: 10.1161/hc3801.097475

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AHA/ACC Guidelines for Preventing Heart Attack and Death in Patients With Atherosclerotic Cardiovascular Disease: 2001 Update

Sidney C. Smith

¹

,

Steven N. Blair

²

,

Robert O. Bonow

³

et al.

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How Might Depression Lead To Cardiac Events?1

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Cited by 520 publications

(166 citation statements)

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“…In the case presented, the patient was nonadherent to the cardiovascular medications that he was prescribed following CABG surgery. Because depression is associated with medication nonadherence and because preventive medications decrease morbidity and mortality in patients with cardiovascular disease, [34][35][36] it is possible that depression and its associated medication nonadherence contributed to this patient's MI. Medication nonadherence may also be a marker of other unhealthy behaviors that increase risk of cardiac events in depressed patients.…”

Section: How Might Depression Lead To Cardiac Events?mentioning

confidence: 99%

Depression and Cardiovascular Disease

2006

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Major depressive disorder is a risk factor for the development of incident coronary heart disease events in healthy patients and for adverse cardiovascular outcomes in patients with established heart disease. Depression is present in 1 of 5 outpatients with coronary heart disease and in 1 of 3 outpatients with congestive heart failure, yet the majority of cases are not recognized or appropriately treated. It is not known whether treating depression improves cardiovascular outcomes, but antidepressant treatment with selective serotonin reuptake inhibitors is generally safe, alleviates depression, and improves quality of life. This article evaluates the importance of major depression in patients with cardiovascular disease, and provides practical guidance for identifying and treating this disorder. CASE PRESENTATIONA 58-year-old man with a history of coronary heart disease (CHD), type 2 diabetes mellitus, hypertension, smoking, and alcohol dependence presented for routine medical care. He had initially sought medical attention for exertional angina 5 years previously, at which time he underwent exercise treadmill testing with thallium that was positive for reversible perfusion defects in the anterior, septal, and inferior walls. Subsequent coronary angiography revealed diffuse heavy calcifications in the left anterior descending artery with a moderate lesion prior to the first diagonal. Several major septal perforators had significant lesions at their origins. In the dominant right coronary artery, there were diffuse calcifications but no significant lesions. The left circumflex and large ramus intermedius were free of discrete lesions. Left ventricular function was normal.The patient underwent single-vessel (left internal mammary artery to left anterior descending artery) coronary artery bypass grafting (CABG) surgery. He was prescribed atenolol 100 mg/ d, lisinopril 40 mg/d, lovastatin 80 mg/d, aspirin 325 mg/d, metformin 850 mg 3 times a day, and glipizide 10 mg 2 times a day. Despite being nonadherent to his prescribed medications, he remained stable for 5 years, but then one day, while doing household chores, he suddenly developed chest pressure, shortness of breath, and diaphoresis that lasted 12 hours. On admission to the hospital his troponin I was elevated and peaked at 0.7 ng/mL (normal, <0.05 ng/mL), consistent with a myocardial infarction (MI). His electrocardiogram had not changed.

“…In the case presented, the patient was nonadherent to the cardiovascular medications that he was prescribed following CABG surgery. Because depression is associated with medication nonadherence and because preventive medications decrease morbidity and mortality in patients with cardiovascular disease, [34][35][36] it is possible that depression and its associated medication nonadherence contributed to this patient's MI. Medication nonadherence may also be a marker of other unhealthy behaviors that increase risk of cardiac events in depressed patients.…”

Section: How Might Depression Lead To Cardiac Events?mentioning

confidence: 99%

Depression and Cardiovascular Disease

2006

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Major depressive disorder is a risk factor for the development of incident coronary heart disease events in healthy patients and for adverse cardiovascular outcomes in patients with established heart disease. Depression is present in 1 of 5 outpatients with coronary heart disease and in 1 of 3 outpatients with congestive heart failure, yet the majority of cases are not recognized or appropriately treated. It is not known whether treating depression improves cardiovascular outcomes, but antidepressant treatment with selective serotonin reuptake inhibitors is generally safe, alleviates depression, and improves quality of life. This article evaluates the importance of major depression in patients with cardiovascular disease, and provides practical guidance for identifying and treating this disorder. CASE PRESENTATIONA 58-year-old man with a history of coronary heart disease (CHD), type 2 diabetes mellitus, hypertension, smoking, and alcohol dependence presented for routine medical care. He had initially sought medical attention for exertional angina 5 years previously, at which time he underwent exercise treadmill testing with thallium that was positive for reversible perfusion defects in the anterior, septal, and inferior walls. Subsequent coronary angiography revealed diffuse heavy calcifications in the left anterior descending artery with a moderate lesion prior to the first diagonal. Several major septal perforators had significant lesions at their origins. In the dominant right coronary artery, there were diffuse calcifications but no significant lesions. The left circumflex and large ramus intermedius were free of discrete lesions. Left ventricular function was normal.The patient underwent single-vessel (left internal mammary artery to left anterior descending artery) coronary artery bypass grafting (CABG) surgery. He was prescribed atenolol 100 mg/ d, lisinopril 40 mg/d, lovastatin 80 mg/d, aspirin 325 mg/d, metformin 850 mg 3 times a day, and glipizide 10 mg 2 times a day. Despite being nonadherent to his prescribed medications, he remained stable for 5 years, but then one day, while doing household chores, he suddenly developed chest pressure, shortness of breath, and diaphoresis that lasted 12 hours. On admission to the hospital his troponin I was elevated and peaked at 0.7 ng/mL (normal, <0.05 ng/mL), consistent with a myocardial infarction (MI). His electrocardiogram had not changed.

“…1,2 The American Heart Association and American College of Cardiology guidelines for secondary prevention in coronary artery disease (CAD) have identified obesity as a major modifiable cardiovascular disease (CVD) risk factor. 3 The health risk associated with central obesity has been reported to be greater than general obesity as measured by body mass index (BMI). 4,5 However, genetic factors may modify this association 6 and the appropriate indices of risk may therefore differ in different ethnic groups, for example, Asians and Caucasians, in whom great differences in susceptibility to abdominal obesity and its co-morbidities such as diabetes mellitus and hypertension have been documented.…”

Section: Introductionmentioning

confidence: 99%

Appropriate cutoff values of anthropometric variables to predict cardiovascular outcomes: 7.6 years follow-up in an Iranian population

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et al. 2009

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Objective: To determine cutoff points of anthropometric variables for predicting incident cardiovascular disease (CVD) in Iranian adults. Design: It is a population-based longitudinal study. Subjects: A total of 1614 men and 2006 women, aged X40 years, free of CVD at baseline were included in the study. Measurements: Body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR) and cardiovascular risks were assessed. Incident CVD was ascertained over a median of 7.6 years follow-up. The adjusted hazard ratios (HRs) for CVD were calculated for 1 s.d. change in all obesity variables using Cox proportional hazards regression analysis. Receiver operator characteristic (ROC) curve analysis was used as the method of defining the points of the maximum sum of sensitivity and specificity (MAXss) of each variable as a predictor of CVD. Results: We found 333 CVD events during follow-up. The risk-factor-adjusted HRs were significant for all anthropometric variables in males and WHR in females and were 1.19, 1.24, 1.21 and 1.24 for BMI, WC, WHR and WHtR in males and 1.27 for WHR in females, respectively (all Po0.05). ROC analysis showed the highest area under curve (AUC) for WHR, WHtR and WC, followed by BMI in males and both genders agedp60 years. In females, WHR and WHtR had the highest AUC, followed by WC and BMI. Among those 460 years old, all the anthropometric variables showed same CVD predicting power. The cutoff values (MAXss) for CVD prediction in males and females were BMIs 26.95 and 29.19 kg m À2 ,WCs 94.5 and 94.5 cm, WHRs 0.95 and 0.90, and WHtR 0.55 and 0.62, respectively. Conclusion: There was no difference between central obesity variables in predicting CVD in males, whereas in females WHR and WHtR were more appropriate. The cutoff values of anthropometric variables were higher in the Iranian than in other Asian populations.

“…In patients with myocardial infarction, angiotensin‐converting enzyme inhibitors were proven to prevent left ventricular remodeling and improve outcomes 16. However, the persistent use of angiotensin‐converting enzyme inhibitors in patients receiving angiotensin‐converting enzyme inhibitors after myocardial infarction at 2 years is only 50% 17.…”

mentioning

confidence: 99%

Persistence and Discontinuation of Oral Anticoagulant: Remaining Issues Not Addressed by Phase III Clinical Trials

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2016

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