Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both nature and prognosis of cardiac complications occurring in patients infected by the Human Immunodeficiency Virus-1 (HIV-1) have changed considerably since the introduction of highly acive and anti-retroviral triple therapy ("HART"). Opportunist cardiac infections have thus been displaced and side effects of drugs now occupy the primary aetiological role. Torsades de pointe may be exceptionally triggered by anti-infectious agents such as pentacarinat or trimethoprime-sulfamethoxazole, as are those induced by the association of ketoconazole and terfenadine or cisapride, the dangers of which are well known and the prevention more effective, especially with the association with HIV antiproteases which inhibit the cytochrome P450. The diagnosis of iatrogenic myocardial dysfunction is more difficult, except when it occurs acutely as with phosphonoformate (Foscarnet), or interleukine-2. Progressive cardiomyopathy caused by -interferon and dideoxynucleosides (zidovudine, didanosine and zalcitabine), reversible on withdrawal of the drug responsible in half the cases, should be distinguished from those due to the HIV itself (therapeutic relay) or to another associated cause (alcohol, coronary artery disease). The coronary complications of diseases treated by antiproteases usually occur in smokers whose cholesterol and triglyceride levels are rapidly increased with HAART. In a series of 9 patients (amongst 700 treated with the antiproteases), after the acute phase of myocardial infarction during which the interventional approach is often preferred, the medium-term prognosis is relatively good, on condition that the patients correct the hyperlipidaemia and give up smoking.
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PMID:[Cardiac side effects of anti-HIV agents]. 1097 35

Aspirin protects from cardiovascular events because of its antiaggregant effect. The occurrence of new events in patients who take aspirin has been called clinical aspirin resistance. Many authors believe that aspirin resistance must be detected by biochemical tests, although there is no agreement on which is the best. Nor is there agreement on the term aspirin resistance. Tests used in research laboratories are aggregometry (turbidometric and impedance), tests based on activation-dependent changes in platelet surface, and tests based on activation-dependent release from platelets. Point-of-care tests are PFA-100, IMPACT and VerifyNow, which can detect platelet dysfunction that may be due to aspirin effect, but their use for this purpose is not yet recommended. Aspirin response may be modified by different factors: patient's compliance, dose, smoking, hyperlipidemia, hyperglucemia, acute coronary syndrome, percutaneous revascularization, recent stroke, extracorporeal circulation, heart failure, exercise, circadian rhythm, absorption, concomitant medications, polymorphisms. Patients with aspirin resistance may have an increased risk of cardiovascular events, and possible therapeutic options are to increase the dosage, to replace aspirin with another antiaggregant drug or to add another drug. In conclusion, there are many reasons that explain the variability in individual responsiveness to aspirin. The term resistance is probably not exact in describing this phenomenon.
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PMID:Variability in individual responsiveness to aspirin: clinical implications and treatment. 1822 Jul 26