Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study included 30 IHD patients with primary hypercholesterolemia (22 males and 8 females). 18 and 12 patients have received a single daily dose of fluvastatin 20 and 40 mg, respectively, in the evening for 12 weeks. The drug effect was assessed by changes in the clinical status, lipid spectrum, transport-metabolic and absorption-secretory functions of the liver. IHD patients with hypercholesterolemia were found to have dysfunction of the hepatobiliary system. Fluvastatin treatment reduced the level of total cholesterol (Ch), LDLP Ch, triglycerides. HDLP Ch levels remained unchanged. Atherogenic lipoproteins aggregation diminished. Positive changes occurred in hepatic metabolism: bilirubin concentrations lowered, serum albumin went up, absorption-secretory function of hepatocytes normalized, hepatic mono-oxidase system activated. Fluvastatin-related hepatic damage was not reported in the course of 12-month follow-up.
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PMID:[The effect of fluvastatin (Lescol) treatment on the clinical status and function of the liver in patients with ischemic heart disease]. 917 80

Previous investigations revealed that hypolipidaemic treatment of patients with IHD in the Czech Republic is inadequate. Patients after revascularization operations are discharged from cardiosurgical departments without suitable medication and moreover the values of the lipid spectrum are affected by the surgical intervention. The objective of the investigation was to evaluate the indication of hypolipidaemic treatment during hospitalization or later during check-up examinations by attending physicians. The authors evaluated retrospectively 100 patients after revascularization operations of the heart discharged without hypolipidaemic treatment and 40 patients treated with fluvastatin because of the lipid values before surgery. Using questionnaires it was revealed that in the group without pharmacological intervention in 36% patients the lipid levels were checked and hypolipidaemic treatment was started in 14% of the patients. In the patients with pharmacological treatment 100% adherence to treatment and improvement of the lipid spectrum was found similarly as in comparable trials. Fluvastatin treatment was well tolerated. In the authors view hypolipidaemic treatment after revascularization should be started before discharge from hospital with regard to preoperative results of the lipid spectrum.
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PMID:[Tactics of hypolipidemic therapy after myocardial revascularization]. 982 91

We examined the effect of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on the production of hydroxyl radical (*OH) generation via nitric oxide synthase (NOS) activation by an in vivo microdialysis technique. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rats and tissue was perfused with Ringer's solution through the microdialysis probe at a rate of 1 microl/min. Sodium salicylate in Ringer's solution (0.5 nmol/microl/min) was infused directly through a microdialysis probe to detect the generation of *OH. Induction of [K(+)](o) (70 mM) or tyramine (1 mM), significantly increased the formation of *OH trapped as 2,3-dihydroxybenzoic acid (DHBA). The application of N(G)-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, significantly decreased the K(+) depolarization-induced *OH formation, but the effect of tyramine significantly increased the level of 2,3-DHBA. When fluvastatin (100 microM), an inhibitor of low-density lipoprotein (LDL) oxidation, was administered to L-NAME-pretreated animals, both KCl and tyramine failed to increase the level of 2,3-DHBA formation. The effect of fluvastatin may be unrelated to K(+) depolarization-induced *OH generation. To examine the effect of fluvastatin on ischemic/reperfused rat myocardium, the heart was subjected to myocardial ischemia for 15 min by occlusion of the left anterior descending coronary artery (LAD). When the heart was reperfused, a marked elevation of the level of 2,3-DHBA was observed. However, in the presence of fluvastatin (100 microM), the elevation of 2,3-DHBA was not observed in ischemia/reperfused rat heart. Fluvastatin, orally at a dose of 3 mg/kg/day for 4 weeks, significantly blunted the rise of serum creatine phosphokinase and improved the electrocardiogram 2 h after coronary occlusion. These results suggest that fluvastatin is associated with a cardioprotective effect due to the suppression of noradrenaline-induced *OH generation by inhibiting LDL oxidation in the heart.
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PMID:Effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on nitric oxide-induced hydroxyl radical generation in the rat heart. 1133 4

There are conflicting data with regard to the effect of statins, including fluvastatin, on plasma fibrinogen levels. We undertook the present study to examine the influence of fluvastatin (40 mg/day) on plasma fibrinogen levels in hypercholesterolemic non-smoker patients with normal triglyceride levels (< 2.25 mmol/l) (n = 65). Fluvastatin administration was followed by a significant decrease of plasma fibrinogen levels by 8% (from 3.6 g/l to 3.33 g/l median value, p < 0.02). No correlation was found between the change in lipids and that in fibrinogen levels. Furthermore, there was no correlation between plasma fibrinogen levels and the change in fibrinogen concentration after fluvastatin administration. These results are in contrast with previously published data. However, the majority of the previous studies included patients with ischemic heart disease, unlike our study population. Furthermore, in some of these studies, which Included relatively small numbers of patients, there was a trend towards a decrease in plasma fibrinogen concentration after fluvastatin administration. We conclude that fluvastatin can significantly decrease plasma fibrinogen levels. However, more studies using fluvastatin and other drugs of this class are necessary to clarify this issue.
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PMID:The effect of fluvastatin on plasma fibrinogen levels. 1209 25

The use of statin agents in patients with acute coronary syndromes (ACSs) remains an area of intense clinical interest. Statin therapy has an established secondary preventive benefit in patients with coronary artery disease, and its extension to ACS seems logical. A number of observational studies have shown an association between initiation of statin therapy early in ACS and improved clinical outcome. Additionally, 4 randomized controlled trials have examined the use of statin therapy for ACS: the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study, the Pravastatin Turkish Trial, the Fluvastatin on Risk Diminishing After Acute Myocardial Infarction (FLORIDA) study, and the Lipid-Coronary Artery Disease (L-CAD) study. Three of these trials showed a benefit with early initiation of statin therapy, whereas 1 trial demonstrated neither benefit nor harm. All the available trials lacked the power and design to sufficiently evaluate whether early initiation of statin therapy reduces mortality and reinfarction in patients with ACS. Four ongoing trials have been designed and sufficiently powered to determine whether statin therapy reduces the risk of death and reinfarction when initiated early in ACS treatment. A body of evidence suggests that the pleiotropic actions of statin agents might modulate benefit in ACS. This article summarizes the available data and provides a rationale for early initiation of statin therapy for patients with ACS.
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PMID:Statin lipid-lowering therapy for acute myocardial infarction and unstable angina: efficacy and mechanism of benefit. 1263 May 93

In high-risk patients, long-term statin therapy prevents cardiovascular events. Short-term clinical benefit of statin therapy has been recently evaluated by randomized clinical trials in the setting of vascular surgery, coronary bypass surgery and percutaneous coronary interventions. According to the trial scheme, statin therapy was started either few weeks or few hours before the intervention. In the field of vascular surgery, the clinical benefit of preprocedure statin administration has been supported by DECREASE III trial. Fluvastatin significantly decreased the incidence of periprocedural myocardial ischemia as defined by ECG changes or troponin elevation. However, this study has methodological flaws, including primary endpoint modification during the trial and the lack of clinical relevance of this endpoint. The administration of statins before a coronary bypass could reduce the occurrence of postoperative atrial fibrillation, according to 4 randomized trials. This finding is discordant with the result of a recent meta-analysis of long-term published and unpublished long-term trials that showed no significant beneficial effects of statins on atrial fibrillation. Several trials have evaluated the usefulness of statin pretreatment before PCI. Most of them have found that statin pretreatment prevents periprocedural myocardial infarctions or major cardiac events. However, most of these events were isolated enzymatic elevations. Moreover, myocardial infarction definition was at odds with the recommendations in some of these trials. A recent meta-analysis of these trials has found that statin pretreatment leads to a 44% reduction in the incidence of major cardiac events at 30 days. The magnitude of this decrease is not consistent with the results of previous long-term trials evaluating statins after acute coronary syndromes. Current evidence does not strongly support short-term clinical benefit of pre-procedural statin administration.
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PMID:[Short-term clinical effects of periprocedural statin therapy]. 2288 40

Background: The superior cervical ganglion (SCG) of the autonomic nervous system plays an important role in different cardiovascular diseases. In this study, we investigated the effects of ischemia and fluvastatin treatment on the ion channel characteristics of SCG neurons in a rabbit myocardial ischemia (MI) model. Methods: MI was induced by abdominal subcutaneous injections of isoproterenol (ISO). The properties of the delayed rectifier potassium channel current (IK ), sodium channel current (INa ), and action potential (APs) on isolated SCG neurons in the control, MI-7d, MI-14d, fluvastatin-7d (fluvastatin pretreated 14 days and treated 7 days after ISO-induced MI), and fluvastatin-14d (fluvastatin pretreated 14 days and treated 14 days after ISO-induced MI) groups were studied. In addition, the RNA expressions of KCNQ3 and SCN9A in the SCG tissue were determined by performing real-time PCR. Intracellular calcium concentration was monitored using laser scanning confocal microscopy. Results: Compared with the control group, the current amplitude of IK and INa were increased in the MI-7d and MI-14d groups. KCNQ3 RNA (corresponding to channel proteins of IK ) expression and SCN9A RNA (corresponding to channel proteins of INa ) expression were also increased in MI groups. Activation and inactivation curves for INa in the two MI groups shifted negatively compared with the control group. These changes were reversed by fluvastatin treatment. Intracellular calcium concentration in SCG neurons was not altered significantly by MI or fluvastatin treatment. By contrast, increased AP amplitude and shortened APD90 were observed in the MI-7d and MI-14d groups. These changes were reversed in the fluvastatin-treated MI group. Conclusion: Fluvastatin treatment partly reversed the characteristics of SCG neurons in MI. The ion channel of SCG neurons could be one of the potential targets of fluvastatin in treating coronary heart diseases.
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PMID:Modulation of Ion Channels in the Superior Cervical Ganglion Neurons by Myocardial Ischemia and Fluvastatin Treatment. 3024 10