Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipid-lowering therapy with statins reduces the risk of cardiovascular events in patients with coronary artery disease. Recent in vitro and in vivo studies demonstrated a low-density lipoprotein-independent action of this class of drugs, which appears to modulate endothelial function, inflammation, and thrombosis. Randomized studies showed a beneficial effect of short-term statin pretreatment in reducing periprocedural cardiac marker release in patients undergoing percutaneous coronary intervention (PCI). In particular, the ARMYDA (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) investigators--initially in stable angina patients, then in patients with acute coronary syndrome, and then in patients already on chronic statin therapy--demonstrated an improvement in 30-day major adverse cardiac event rates, which were driven by a reduced rate of periprocedural myocardial infarction. Moreover, statin therapy at the time of PCI significantly decreased the incidence of contrast-induced nephropathy. These observations support high-dose statin pretreatment in all patients who are candidates for PCI.
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PMID:Statins and their role in pre-percutaneous coronary intervention. 2044 May 82

After the advent of Statins in 1960's, they are being extensively used as Antiathrogenic drug for Primary Hyperlipidemia, Angina, Ischemic Heart Disease (Medical or Post Surgical), Atherosclerosis, Diabetes mellitus and Hypertension. Rarely, these drugs have been observed to cause hypocholesterolemia. We present a case of forty years old male who was started on Atorvastatin after his angioplasty following anterior myocardial infarction. Six weeks after the start of antilipid drug patient developed symptoms of phobias, nightmares, insomnia, forgetfulness, body aches, muscle cramps, cognitive, sexual and psychomotor disturbances. On investigation he was found to have hypocholesterolemia. Atorvastatin was stopped and dietary restrictrictions were lifted. Over five month patients symptoms resolved as the serum cholesterol levels became normal. Because of similarities of symptoms of hypocholesterolemia secondary to antilipid therapy and the disease itself, hypocholesterolemia was overlooked initially by physicians. Patients on antilipids must be evaluated for any fall in serum cholerterol if they develop unusual symptoms and patients on long-term antilipids must have regularly lipid profile checked.
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PMID:Hypocholesterolemia secondary to atrovastatin therapy. 2233 62

Congenital anomalies of coronary arteries, albeit rare, may be significant contributors to angina pectoris, hemodynamic abnormalities, and sudden cardiac death. A 47-year-old man referred to us with atypical chest pain. Electrocardiography demonstrated no significant ischemic changes, but cardiac troponin I test was positive. The patient underwent coronary angiography, which revealed a single coronary artery from the left Valsalva sinus. In addition, the left anterior descending (LAD) and the left circumflex (LCx) arteries were in normal position with significant stenosis in the mid-portion of the LAD and the distal portion of the LCx. A large branch originated from the distal portion of the LCx and tapered toward the proximal portion as the right coronary artery (RCA). This is a rare coronary anomaly that has no ischemic result. Coronary lesions were the cause of the patient's angina pectoris. Angioplasty and stenting of the LAD and LCx was done, and medical therapy (Clopidogrel, Aspirin, Atorvastatin, and Metoprolol) was continued. The patient was asymptomatic at 8 months' follow-up.
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PMID:Single coronary artery with anomalous origin of the right coronary artery from the distal portion of left circumflex artery: a very rare case. 2439 67

Inflammation can be activated as a defensive response by the attack of acute coronary syndrome (ACS) for ischemic tissue injury. The aim of the present study was to investigate the impact of ACS-activated inflammation on adipokine imbalance and the effects of statins on the crosstalk between inflammation and adipokine imbalance during ACS. In this study, 586 subjects were categorized into: (1) control group; (2) SA (stable angina) group; and (3) ACS group. Circulating levels of hs-CRP, adiponectin and resistin were measured by ELISA. Furthermore, forty C57BL/6 mice were randomized into: sham, AMI, low-statin (atorvastatin, 2 mg/kg/day) and high-statin (atorvastatin, 20 mg/kg/day) group. After 3 weeks, AMI models were established by surgical coronary artery ligation. Circulating levels and adipose expressions of adiponectin and resistin were assessed in animals. Besides, we investigate the effects of atorvastatin on ox-LDL-induced adipokine imbalance in vitro. As a result, we found that ACS patients had higher hs-CRP and resistin levels and lower adiponectin levels. Our correlation analysis demonstrated hs-CRP concentrations were positively correlated with resistin but negatively with adiponectin levels in humans. Our animal findings indicated higher circulating hs-CRP and resistin levels and lower adiponectin levels in AMI mice. Atorvastatin pre-treatment dose-dependently decreased hs-CRP and resistin levels but increased adiponectin levels in mice. The consistent findings were observed about the adipose expressions of resistin and adiponectin in mice. In study in vitro, ox-LDL increased cellular resistin expressions and otherwise for adiponectin expressions, which dose-dependently reversed by the addition of atorvastatin. Therefore, our study indicates that the ACS attack activates inflammation leading to adipokine imbalance that can be ameliorated by anti-inflammation of atorvastatin.
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PMID:Inflammation Activation Contributes to Adipokine Imbalance in Patients with Acute Coronary Syndrome. 2698 75


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