Effect of atorvastatin on hemorheologic-hemostatic parameters and serum fibrinogen levels in hyperlipidemic patients

Dujovne, Carlos A.; Harris, William S.; Altman, Raúl; Overhiser, R W; Black, Donald M.

doi:10.1016/s0002-9149(99)00745-6

Cited by 75 publications

(43 citation statements)

References 21 publications

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“…A modest increase in Lp(a) concentrations was found in patients with increased cholesterol receiving simvastatin (78 ), and a 36% increase in plasma Lp(a) concentrations was reported in patients receiving atorvastatin (79 ). Use of pravastatin did not influence Lp(a) values (80 ), whereas fluvastatin was found to significantly reduce Lp(a) concentrations (81 ).…”

Section: Modulation Of Plasma Lp(a) Concentrationsmentioning

confidence: 99%

Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: Recent Advances and Future Directions

et al. 2003

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It has been estimated that ϳ37% of the US population judged to be at high risk for developing coronary artery disease (CAD), based on the National Cholesterol Education Program guidelines, have increased plasma lipoprotein(a) [Lp(a)], whereas Lp(a) is increased in only 14% of those judged to be at low risk. Therefore, the importance of establishing a better understanding of the relative contribution of Lp(a) to the risk burden for CAD and other forms of vascular disease, as well as the underlying mechanisms, is clearly evident. However, the structural complexity and size heterogeneity of Lp(a) have hindered the development of immunoassays to accurately measure Lp(a) concentrations in plasma. The large intermethod variation in Lp(a) values has made it difficult to compare data from different clinical studies and to achieve a uniform interpretation of clinical data. A workshop was recently convened by the National Heart, Lung, and Blood Institute (NHLBI) to evaluate our current understanding of Lp(a) as a risk factor for atherosclerotic disorders; to determine how future studies could be designed to more clearly define the extent to which, and mechanisms by which, Lp(a) participates in these processes; and to present the results of the NHLBI-supported program for the evaluation and standardization of Lp(a) immunoassays. This report includes the most recent data presented by the workshop participants and the resulting practical and research recommendations.

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Section: Modulation Of Plasma Lp(a) Concentrationsmentioning

confidence: 99%

Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: Recent Advances and Future Directions

et al. 2003

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“…Endothelial dysfunction is also characterized by elevated levels of the vasoconstrictive substance endothelin-1, 13 and statins have also been shown to inhibit the expression of endothelin-1 in vascular endothelial cells. 14 In addition, statins have demonstrated the ability to inhibit platelet aggregation 15,16 and monocyte adhesion to the endothelial surface 17,18 and to possess antioxidant 19 and antiinflammatory activity, particularly the reduction in C-reactive protein levels. 20,21 Although some of these nonlipid effects may be operative even before substantial lipid benefits accrue, others may not be truly independent of lipid reduction.…”

Section: See P 2280mentioning

confidence: 99%

There Is No Evidence for an Increase in Acute Coronary Syndromes After Short-Term Abrupt Discontinuation of Statins in Stable Cardiac Patients

McGowan

2004

Circulation

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Background-For a variety of reasons, many patients abruptly discontinue statin therapy. The present analysis was conducted to determine whether the risk of cardiovascular outcomes increases after withdrawal of statin therapy in a stable cardiac population. Methods and Results-In the Treating to New Target (TNT) study, 2 doses of atorvastatin (10 and 80 mg once daily) are being used in a double-blind parallel-group design. Of the 18 468 patients screened for study participation, 16 619 entered a dietary lead-in/drug-washout period, and of these, 15 432 eligible participants began treatment with atorvastatin 10 mg/d on an open-label basis. Of the subjects who entered the dietary lead-in/drug-washout period, 57% were receiving prior statin therapy. During the 6-week drug-washout period, there were 24 primary events (defined as coronary heart disease death, nonfatal myocardial infarction, resuscitated cardiac arrest, and fatal or nonfatal stroke); throughout the subsequent 8-week open-label period, there were 31 primary events. This equated to monthly Kaplan-Meier event rates of 0.20% during washout and 0.26% in the open-label phase. Event rates were therefore similar during the 2 phases. Conclusions-The present analysis demonstrates that short-term discontinuation of statin therapy in stable cardiac patients apparently does not lead to a clinically important increased risk of acute coronary syndromes.

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“…54 Lipid lowering after dietary, fibrate, or statin treatment has been shown to significantly reduce factor VII coagulation activity and mass. 54,[63][64][65] Recently, statin-induced reduction of prothrombin activation has also been associated with inhibition of factor V activation, as well as an increase in factor Va inactivation (Figure 3). 66 Thus, statin action on factors V and VII results in a synergistic effect in reducing thrombin generation.…”

Section: Statin-mediated Modulation Of Thrombogenesismentioning

confidence: 99%

Statin Therapy in Acute Coronary Syndromes

Sposito

Chapman

2002

ATVB

142

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Abstract-Randomized trials have established that statin treatment reduces coronary events in primary prevention and in patients with stable coronary artery disease. In unstable coronary artery disease, however, the pathophysiological background is distinct, and the potential benefits of statin therapy have not been evaluated until recently. Data from animal models and clinical studies indicate that statin treatment can influence a spectrum of molecular and cellular mechanisms that are intimately related to the pathogenesis of acute coronary syndromes; these include the reduction of circulating levels of atherogenic lipoproteins (very low density lipoprotein, very low density lipoprotein remnants, intermediate density lipoprotein, and low density lipoprotein) and thus of arterial lipid deposition and the attenuation of inflammation, modulation of thrombogenesis and thrombolysis, improvement of endothelial dysfunction, and reduction of ischemia/reperfusion injury. Indeed, findings from prospective and observational studies have demonstrated that statin treatment significantly improves clinical outcome after acute coronary syndromes. Therefore, early initiation of statin therapy after an acute coronary event not only enhances adherence to treatment but also preempts the occurrence of new events. In this review, we discuss recent important developments in our knowledge of the clinical evidence of the beneficial effects of early statin therapy in acute coronary syndromes and the biological mechanisms that underlie them. arge clinical trials have demonstrated that statin treatment reduces the risk of coronary events and total mortality in patients with stable coronary artery disease (CAD). After an acute coronary event, an enhanced incidence of new events occurs over a prolonged period of time, and as a consequence, there is a higher mortality. In fact, compared with patients with stable disease, patients after an acute coronary event have a 2-to 6-fold higher incidence of recurrent events. 1 Recently, the early introduction of statin treatment during the acute phase of a coronary event has been highlighted as a possible therapeutic approach for improving the outcome in patients with unstable disease. However, distinct clinical, biochemical, and histological features have indicated that these 2 clinically distinct forms of CAD, ie, unstable and stable forms, are derived from distinct pathophysiological backgrounds. Indeed, several clinical investigations have been undertaken to clarify the mechanisms by which lipid-lowering treatment can minimize the risk of recurrence after an initial coronary event.By competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is a key enzyme of cholesterol biosynthesis, statins reduce cellular cholesterol content, notably in liver cells (Figure 1). Indeed, hepatocytes respond to sterol depletion by activating nuclear sterol regulatory element-binding protein-2, which upregulates the transcription of key genes implicated in cholesterol metabolism, incl...

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Effect of atorvastatin on hemorheologic-hemostatic parameters and serum fibrinogen levels in hyperlipidemic patients

Cited by 75 publications

References 21 publications

Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: Recent Advances and Future Directions

Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: Recent Advances and Future Directions

There Is No Evidence for an Increase in Acute Coronary Syndromes After Short-Term Abrupt Discontinuation of Statins in Stable Cardiac Patients

Statin Therapy in Acute Coronary Syndromes

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