Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.194 (CAD)
 4,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Excessive unprotected radiation to the heart appears to lead to the development of CAD, even in the absence of significant cardiovascular risk factors. The coexistence of such factors may enhance the probability of CAD. The presence of hypercholesterolemia and concomitant or sequential use of chemotherapeutic agents (especially doxorubicin) could further increase this risk. Therapeutic decisions, as with any other manifestation of CAD, relate to the extent of myocardium at jeopardy and to the overall diffuseness of CAD. Management options possible are PTCA or coronary artery bypass surgery. The latter may be required in left main artery stenosis and complicated ostial lesions. Use of shielding should decrease the associated risk of radiation-induced CAD in future years. However, clinicians should continue to have a high degree of suspicion of CAD in patients treated with thoracic radiation without cardiac shielding.
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PMID:Radiation-induced coronary artery disease. 146 19

Known risk factors for coronary artery disease are very common in the Hopkins Lupus Cohort, in spite of the fact that the average patients age is only 38.3 years. Three or more known risk factors were found in 53% of patients. Risk factors for CAD were common even in patients not on a regimen of prednisone therapy during their cohort follow-up. Hypercholesterolemia increased significantly with greater average prednisone dose. Despite the frequency of risk factors, patients' awareness of the risk of CAD was low, with only 16.9% of patients believing they were at high risk for developing CAD within 5 years. In general, awareness of individual risk factors was lower in black than in white patients with SLE. Preventive practices were most commonly addressed towards hypertension. Preventive practices directed against obesity, hypercholesterolemia, and smoking were underutilized. Whether these known risk factors are sufficient in and of themselves to explain the high frequency of CAD in the cohort (8%) or whether they are "enabling" factors acting upon endothelium damaged by immune-complex disease cannot be addressed by this study. However, both further investigation of these risk factors and attention to lifestyle and pharmacologic approaches to risk factor reduction are indicated by this study.
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PMID:Coronary artery disease risk factors in the Johns Hopkins Lupus Cohort: prevalence, recognition by patients, and preventive practices. 152 5

CAD results from atherosclerosis, a chronic disease process that has its origin in childhood. Children and adolescents can be at higher risk for CAD by virtue of being from families with premature CAD or familial dyslipoproteinemias. The plasma lipid and lipoprotein levels result from a number of complex metabolic processes that are under the control of genetic and environmental (e.g., diet) influences. The normal ranges of plasma lipids and lipoproteins in children are known, and children and adolescents with dyslipoproteinemia are ordinarily defined as those having levels of plasma total, LDL, or triglyceride above the 95th percentile or with a low HDL cholesterol below the 5th percentile. Children of a parent with documented dyslipoproteinemia or with family history of premature CAD may be screened in the fasting state any time after 2 years of age. Following the exclusion of secondary causes of dyslipoproteinemia, the diagnosis of primary dyslipoproteinemia can be made. Lipoprotein patterns are not diagnostic for a given genotype. Efforts to determine further the biochemical defects responsible for a given phenotype have led to the investigation of gene coding for the apolipoproteins, the key enzymes in the lipoproteins pathways (LPL, HDL, and LCAT) and the receptors that process lipoproteins, such as the LDL receptor and the chylomicron remnant receptor. From a practical standpoint, the diagnosis of the kind of dyslipoproteinemia in a child will depend upon the nature and severity of the dyslipoproteinemia, both in the child (or adolescent) and in parents and siblings. Marked increases in plasma total and LDL cholesterol in the child and in at least one of the parents often reflect the presence of familial hypercholesterolemia, an inherited dominant condition due to a defect in the LDL receptor gene. The triglyceride levels are often normal. If the child has a different dyslipoproteinemia pattern from siblings and parents, then the diagnosis of familial combined hyperlipidemia or hyperapobetalipoproteinemia should be considered. Most children with mild or borderline elevations in total and LDL cholesterol will have polygenic hypercholesterolemia. Triglyceride problems in children and adolescents are relatively uncommon, particularly the more severe hypertriglyceridemia such as that found in lipoprotein lipase and apoC-II deficiency, dysbetalipoproteinemia, and type V hyperlipoproteinemia. High levels of Lp(a) lipoprotein, in isolation or in combination with other dyslipoproteinemia, accelerate risk for CAD. Low levels of HDL cholesterol in the absence of other abnormalities suggest the diagnosis of hypoalphalipoproteinemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diagnosis and management of familial dyslipoproteinemia in children and adolescents. 225 50

The interpretation and selection of exercise tests depends on the pretest probability of CAD. Imperfect tests (like exercise tests) provide probability estimates, not definite statements (such as "the patient has CAD" or "the patient does not have CAD"). In patients with a low pretest probability of CAD (asymptomatic persons or men and women with nonanginal chest pain), abnormal exercise test results provide probability estimates that are much too low to conclude that the patient has CAD. In patients with anginal pain and normal exercise tests, the probability of CAD is too high to conclude that the patient has a normal coronary circulation. Exercise tests are not useful for trying to rule out CAD in patients with anginal pain. In patients with an intermediate pretest probability of CAD (men and women with atypical angina and women with typical angina), abnormal exercise tests (particularly the myocardial scintiscan) provide probability estimates that are high enough to justify starting treatment for CAD. Exercise tests are most useful in this group, a conclusion that has been reached by other methods of analysis. The myocardial scintiscan is much more useful than the exercise ECG in women. When CAD is strongly suspected, exercise tests have relatively little diagnostic value but may be useful for prognosis. However, clinical evidence of poor ventricular function may alone suffice to select patients with angina pectoris for coronary arteriography. Conversely, when clinical indicators of congestive heart failure are absent, the prognosis in chronic stable angina is so favorable that any further testing may be unnecessary. Screening asymptomatic persons for CAD is a very low yield practice. Patients who have no cardiac risk factors (hypercholesterolemia, family history of CAD, cigarette smoking, and hypertension) are at especially low risk of a primary cardiac event. Older men with stable typical angina are particularly likely to have left main coronary artery stenosis or three-vessel disease with poor ventricular function. The exercise ECG can identify groups of older men with a relatively high risk of having left main coronary artery stenosis. Physicians should be cautious when applying these recommendations to a primary care practice. The foregoing analysis is based on data obtained from patients who had been selected for coronary arteriography. There are two principal effects of biased selection of study patients: The pretest probability of CAD in clinical subgroups is probably lower than as shown here.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Exercise testing in suspected coronary artery disease. 385 11

The recently completed NHLBI sponsored multicenter double-blind Coronary Heart Disease Prevention Trial has provided the long sought-after proof that hyperlipidemia is a major CAD risk factor and that the incidence of CHD and its complications can be favorable modified by control of hyperlipidemia with appropriate diet-drug therapy. This nationwide study confirms and validates the earlier reports on the feasibility to stabilize or to promote regression of atherosclerotic arterial lesions through hyperlipidemia control. Current investigations suggest that in most instances, simple differentiation of hyperlipidemias into hypercholesterolemia and hypertriglyceridemia (major components of low-density and very low-density lipoprotein) can supply adequate information for clinical practice. In difficult-to-control hyperlipidemias, the application of lipoprotein analysis may provide insight of the underlying genetic-metabolic abnormality for selection of more specific therapeutic modality. Before considering hypolipemic therapy, secondary hyperlipidemias should be excluded. In those cases, treatment should be directed to the primary disease(s) for the solution of the hyperlipemic problem. Life-long dietary modification is the key step to treatment of all types of hyperlipidemias, and especially the primary hyperlipidemias. In this latter group, both the patient and the family should be educated on the principles and the importance of dietary modification to boost compliance. In familial hyperlipidemias, a specifically effective hypolipemic drug, or a combination of drugs with minimal or no long-term toxic and side effects, should be prescribed to augment the therapeutic diet to lower the elevated plasma lipid levels and stabilize them at normal range. Early detection and control of atherosclerosis-prone hyperlipidemias in children and young adults should be vigorously promoted to improve cardiovascular health of the population and to reduce the escalation of health care expenses.
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PMID:When and how to treat hyperlipidemia. 387 80

This article has focused on the appropriate indications for lipid-lowering drugs in adult patients with different lipoprotein disorders, which we have divided into primary hypercholesterolemia, combined hyperlipidemia,and hypertriglyceridemia. The mechanism of action, efficacy, and safety profile of the major drugs have been reviewed, and based on this information, we have presented our views on the appropriate drugs of first choice and appropriate second-choice agents for treatment of adult patients with different dyslipidemias. The rationale for the use of hypolipidemic drugs is strongest in patients with hyperlipidemia who concurrently have evidence for coronary or peripheral vascular disease, in whom the goal of secondary prevention is to retard further progression of atherosclerosis and potentially induce some regression, whereas in selected high-risk patients without evidence of atherosclerosis, the goals of therapy are to prevent the premature development of CAD or, in patients with severe hypertriglyceridemia, prevent the adverse sequelae of hepatomegaly, splenomegaly, and potentially pancreatitis. We have focused on the use of hypolipidemic drugs in adult patients, and the guidelines discussed are not appropriate for use in children with hyperlipidemia, in whom drug therapy should be undertaken selectively and in consultation with a lipid specialist. Many areas of controversy in the use of lipid-lowering drugs remain to be addressed by future studies; these include the use of lipid-lowering drugs in patients with secondary causes of hyperlipidemia (e.g., the nephrotic syndrome), the use of lipid-lowering drugs in women, and recommendations for drug therapy in older patients.
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PMID:Drug treatment of dyslipoproteinemia. 828 33

In addition to traditional risk factors (cigarette smoking, high blood pressure, and elevated cholesterol) psychosocial factors (depression, social isolation, and low socioeconomic status) have an adverse impact on prognosis of patients with CAD. Several studies of psychosocial and behavioral treatments provide encouraging evidence for the clinical efficacy of psychosocial interventions in CAD patients. A new, multicenter clinical trial now underway (see sidebar) will evaluate the impact of psychosocial interventions (compared to usual care) on all-cause mortality and nonfatal MI in post-MI patients with depression or perceived low levels of social support or both.
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PMID:Psychosocial factors and coronary disease. A national multicenter clinical trial (ENRICHD) with a North Carolina focus. 939 58

As we learn more about the origins of coronary artery disease, research has begun to focus on its prevention. The purpose of this study was to determine if exercise stress testing of the offspring of our cardiac rehabilitation patients would be a useful adjunct to their general cardiac risk factor assessment. In addition, we sought to quantitate the number of cardiac risk factors they might have already accumulated. We determined the lifestyle and lipid profiles of 22 young, healthy subjects. Subjects underwent maximal multistage exercise stress tests. Eighty-six percent of subjects had two or more major risk factors for CAD, and 73% had contributory risk factors. Seventy-three percent of subjects also demonstrated hypercholesterolemia. Exercise testing did not induce ischemic changes on electrocardiography of any subject. Our research revealed that these offspring demonstrate an alarming number of coronary artery disease risk factors, even though exercise stress tests were negative.
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PMID:Exercise stress testing and risk factor assessment among offspring of cardiac patients. 948 80

Several cardiovascular risk factors were identified (high LDL-cholesterol, low HDL-cholesterol, homocystein, Lp(a), and many others). Hypercholesterolemia has been shown to be one of the most important cardiovascular risk factors in man. Interventional studies for primary and secondary prevention demonstrate a beneficial effect of cholesterol lowering therapy. However, numerous CAD-patients suffer a second coronary event despite the appropriate lipid-lowering treatment. Furthermore moderate hypercholesterolemia has only poor predictive power indicating an upcoming myocardial infarction. Therefore we need additional research in CAD prevention and in identifying so far unknown or unconsidered CAD risk factors.
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PMID:[Arteriosclerosis and coronary heart disease--strengths and weaknesses in the classical risk factor concept]. 964 96

The evidence of the benefit of lowering cholesterol levels in seniors from epidemiologic studies and RCTs is conflicting. Epidemiologic studies suggest that elevated cholesterol levels in elderly people may be a marker of good health. In some cases, lowering cholesterol in seniors may even prove harmful. Conversely, RCTs of lipid-lowering therapy have shown clear benefits in reducing coronary events in younger and middle-aged adults with or without pre-existing CAD. Both the epidemiologic studies and the RCTs we evaluated have methodologic concerns that make generalization to all seniors difficult. One epidemiologic study, in fact, found that there may be a physiologic decline in cholesterol levels as people age into their 70s and beyond [16]. We still do not appear to have a clear insight into the precise role cholesterol plays in seniors, especially those over the age of 75. In the future, as more data becomes available from RCTs and meta-analyses evaluating seniors in the older age group [15], we hope to have a better understanding of how to treat hypercholesterolaemia in this population. Until further studies are published, treatment plans need to be individualized, and the risks and benefits of treatment on various outcomes must be weighed according to the best evidence we have available.
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PMID:The controversy surrounding cholesterol treatment in older people. 965 42


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