Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report 11 in a group of 21 asymptomatic patients with heterozygous familial hypercholesterolemia (FH) and progressive coronary artery disease to evaluate the role of compensatory mechanism(s), especially coronary collaterals, in providing adequate blood supply to the myocardium, following complete occlusion of one or more major coronary arteries. Diet-colestipol-nicotinic acid treatment decreased their plasma total cholesterol and low density lipoprotein cholesterol (mg/dl, mean +/- SEM) from 442.9 +/- 25.8 and 363.0 +/-24.1, respectively, to 231.2 +/- 11.8 and 185.3 +/- 14.2, respectively, for 6 to 9 years. The initially stenotic lesions of these 11 patients slowly progressed to complete occlusion, while the patients remained free of myocardial ischemia or infarction and exhibited no abnormality on 24-hour ambulatory ECG monitoring, exercise stress, and thallium 201 stress tests. We conclude that coronary occlusion can be retarded in FH patients by strenuous hypocholesterolemic therapy to allow the development of compensatory mechanism including coronary collaterals. Apparently, the angiographically visualizable collaterals combined with subendocardial anastomosis can give adequate myocardial blood supply to this series of FH patients following occlusion of one or more of their major coronary arteries.
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PMID:Protection of myocardium by the compensatory mechanism of coronary collaterals after total occlusion of major coronary arteries shown in patients with familial hypercholesterolemia. 709 Sep 84

Several experimental trials are under way to correct the deficiency of LDL receptor function known as Familial Hypercholesterolemia (FH) that develops devastating atherosclerosis leading to premature fatal coronary occlusion. Recently, a 28-year-old FH homozygous woman has received ex vivo autologous liver transplantation after transduction with retroviral vector expressing functional LDL receptors. The outcome is partially successful but is still controversial because of an argument that the apparent small decrease in the total plasma cholesterol level is not necessarily caused by the correction of the LDL receptor expression. In addition to retrovirus, adenovirus vector and non-viral methods are being employed as potential tools for FH gene therapy.
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PMID:[Perspective of gene therapy in hyperlipoproteinemia]. 785 27

The evaluation of adolescents with chest pain, elevated cardiac enzymes, and abnormal electrocardiograms (ECGs) continues to pose diagnostic and management dilemmas. Myocardial infarction is an uncommon finding in this population and alternative diagnoses must be considered. Our database was retrospectively reviewed for adolescents age 16-18 years without prior cardiac history who underwent cardiac catheterization. Patients who presented with chest pain, elevated cardiac enzymes, normal ejection fraction, and abnormal ECGs were included. Management, diagnostic testing, and final diagnosis were reviewed. Nine adolescents (eight males and one female) without prior cardiac history were identified. The ECG findings in all patients were consistent with myocardial ischemia in a coronary distribution. Thrombotic coronary occlusion was not found in any patient. In adolescents without prior cardiac history of risk factors for myocardial infarction such as Kawasaki disease, familial hypercholesterolemia, or drug use who present with chest pain, multiple diagnoses must be considered even in the presence of focal ischemic ECG changes and elevated cardiac enzymes. Thrombolytic therapy or anticoagulation should be withheld until a definitive diagnosis of myocardial infarction has been made. Magnetic resonance imaging is the most useful tool to differentiate focal myocarditis from myocardial infarction.
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PMID:"Myocardial infarction" in adolescents: do we have the correct diagnosis? 1554 13