C-Reactive Protein Levels and Outcomes after Statin Therapy
Statin therapy lowers not only low-density lipoprotein (LDL) cholesterol levels, but also levels of C-reactive protein (CRP), a marker of inflammation. This study examined the independent effects of decreasing LDL cholesterol and CRP levels on subsequent coronary risk in patients with acute coronary...
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| Published in | The New England journal of medicine Vol. 352; no. 1; pp. 20 - 28 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Boston, MA
Massachusetts Medical Society
06.01.2005
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0028-4793 1533-4406 1533-4406 |
| DOI | 10.1056/NEJMoa042378 |
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| Abstract | Statin therapy lowers not only low-density lipoprotein (LDL) cholesterol levels, but also levels of C-reactive protein (CRP), a marker of inflammation. This study examined the independent effects of decreasing LDL cholesterol and CRP levels on subsequent coronary risk in patients with acute coronary syndromes who were receiving pravastatin or atorvastatin. Lowering CRP levels reduced coronary risk irrespective of the extent of LDL cholesterol lowering. Patients with the lowest risk had the lowest levels of both LDL cholesterol and CRP after 30 days of statin therapy.
This study examined the independent effects of decreasing LDL cholesterol and CRP levels on subsequent coronary risk in patients with acute coronary syndromes who were receiving statin therapy.
Statin therapy lowers the risk of cardiovascular events by reducing plasma cholesterol levels, and practice guidelines for patients with known cardiovascular disease emphasize the importance of reaching target goals for low-density lipoprotein (LDL) cholesterol.
1
However, we have shown that statin therapy results in a greater clinical benefit when levels of the inflammatory biomarker C-reactive protein (CRP) are elevated
2
,
3
and that statins lower CRP levels in a manner largely independent of LDL cholesterol levels.
3
–
6
These findings, along with basic laboratory evidence, have led to the hypothesis that, in addition to being potent lipid-lowering agents, statins may also have antiinflammatory . . . |
|---|---|
| AbstractList | Statins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical outcomes is unknown. We evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infarction or death from coronary causes among 3745 patients with acute coronary syndromes. Patients in whom statin therapy resulted in LDL cholesterol levels of less than 70 mg per deciliter (1.8 mmol per liter) had lower event rates than those with higher levels (2.7 vs. 4.0 events per 100 person-years, P=0.008). However, a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels (2.8 vs. 3.9 events per 100 person-years, P=0.006), an effect present at all levels of LDL cholesterol achieved. For patients with post-treatment LDL cholesterol levels of more than 70 mg per deciliter, the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years (P<0.001). Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP, meeting these targets was more important in determining the outcomes than was the specific choice of therapy. Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events (1.9 per 100 person-years). Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol. Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol. Statins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical outcomes is unknown. We evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infarction or death from coronary causes among 3745 patients with acute coronary syndromes. Patients in whom statin therapy resulted in LDL cholesterol levels of less than 70 mg per deciliter (1.8 mmol per liter) had lower event rates than those with higher levels (2.7 vs. 4.0 events per 100 person-years, P=0.008). However, a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels (2.8 vs. 3.9 events per 100 person-years, P=0.006), an effect present at all levels of LDL cholesterol achieved. For patients with post-treatment LDL cholesterol levels of more than 70 mg per deciliter, the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years (P<0.001). Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP, meeting these targets was more important in determining the outcomes than was the specific choice of therapy. Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events (1.9 per 100 person-years). Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol. Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol. Background Statins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical outcomes is unknown. Methods We evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infarction or death from coronary causes among 3745 patients with acute coronary syndromes. Results Patients in whom statin therapy resulted in LDL cholesterol levels of less than 70 mg per deciliter (1.8 mmol per liter) had lower event rates than those with higher levels (2.7 vs. 4.0 events per 100 person-years, P=0.008). However, a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels (2.8 vs. 3.9 events per 100 person-years, P=0.006), an effect present at all levels of LDL cholesterol achieved. For patients with post-treatment LDL cholesterol levels of more than 70 mg per deciliter, the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years (P<0.001). Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP, meeting these targets was more important in determining the outcomes than was the specific choice of therapy. Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events (1.9 per 100 person-years). Conclusions Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol. Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol. Statin therapy lowers not only low-density lipoprotein (LDL) cholesterol levels, but also levels of C-reactive protein (CRP), a marker of inflammation. This study examined the independent effects of decreasing LDL cholesterol and CRP levels on subsequent coronary risk in patients with acute coronary syndromes who were receiving pravastatin or atorvastatin. Lowering CRP levels reduced coronary risk irrespective of the extent of LDL cholesterol lowering. Patients with the lowest risk had the lowest levels of both LDL cholesterol and CRP after 30 days of statin therapy. This study examined the independent effects of decreasing LDL cholesterol and CRP levels on subsequent coronary risk in patients with acute coronary syndromes who were receiving statin therapy. Statin therapy lowers the risk of cardiovascular events by reducing plasma cholesterol levels, and practice guidelines for patients with known cardiovascular disease emphasize the importance of reaching target goals for low-density lipoprotein (LDL) cholesterol. 1 However, we have shown that statin therapy results in a greater clinical benefit when levels of the inflammatory biomarker C-reactive protein (CRP) are elevated 2 , 3 and that statins lower CRP levels in a manner largely independent of LDL cholesterol levels. 3 – 6 These findings, along with basic laboratory evidence, have led to the hypothesis that, in addition to being potent lipid-lowering agents, statins may also have antiinflammatory . . . Statins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical outcomes is unknown.BACKGROUNDStatins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical outcomes is unknown.We evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infarction or death from coronary causes among 3745 patients with acute coronary syndromes.METHODSWe evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infarction or death from coronary causes among 3745 patients with acute coronary syndromes.Patients in whom statin therapy resulted in LDL cholesterol levels of less than 70 mg per deciliter (1.8 mmol per liter) had lower event rates than those with higher levels (2.7 vs. 4.0 events per 100 person-years, P=0.008). However, a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels (2.8 vs. 3.9 events per 100 person-years, P=0.006), an effect present at all levels of LDL cholesterol achieved. For patients with post-treatment LDL cholesterol levels of more than 70 mg per deciliter, the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years (P<0.001). Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP, meeting these targets was more important in determining the outcomes than was the specific choice of therapy. Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events (1.9 per 100 person-years).RESULTSPatients in whom statin therapy resulted in LDL cholesterol levels of less than 70 mg per deciliter (1.8 mmol per liter) had lower event rates than those with higher levels (2.7 vs. 4.0 events per 100 person-years, P=0.008). However, a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels (2.8 vs. 3.9 events per 100 person-years, P=0.006), an effect present at all levels of LDL cholesterol achieved. For patients with post-treatment LDL cholesterol levels of more than 70 mg per deciliter, the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years (P<0.001). Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP, meeting these targets was more important in determining the outcomes than was the specific choice of therapy. Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events (1.9 per 100 person-years).Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol. Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol.CONCLUSIONSPatients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol. Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol. |
| Author | Pfeffer, Marc A Cannon, Christopher P Rifai, Nader Rose, Lynda M Ridker, Paul M Morrow, David McCabe, Carolyn H Braunwald, Eugene |
| Author_xml | – sequence: 1 givenname: Paul M surname: Ridker fullname: Ridker, Paul M – sequence: 2 givenname: Christopher P surname: Cannon fullname: Cannon, Christopher P – sequence: 3 givenname: David surname: Morrow fullname: Morrow, David – sequence: 4 givenname: Nader surname: Rifai fullname: Rifai, Nader – sequence: 5 givenname: Lynda M surname: Rose fullname: Rose, Lynda M – sequence: 6 givenname: Carolyn H surname: McCabe fullname: McCabe, Carolyn H – sequence: 7 givenname: Marc A surname: Pfeffer fullname: Pfeffer, Marc A – sequence: 8 givenname: Eugene surname: Braunwald fullname: Braunwald, Eugene |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16443970$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/15635109$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2005 Massachusetts Medical Society. All rights reserved. 2005 INIST-CNRS Copyright 2005 Massachusetts Medical Society. |
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| Keywords | Medicine Acute phase protein Prognosis Treatment Evolution Statin derivative C reactive protein |
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| Snippet | Statin therapy lowers not only low-density lipoprotein (LDL) cholesterol levels, but also levels of C-reactive protein (CRP), a marker of inflammation. This... Statins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical outcomes is... Background Statins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical... |
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| SubjectTerms | Anticholesteremic Agents - administration & dosage Anticholesteremic Agents - pharmacology Anticholesteremic Agents - therapeutic use Atorvastatin Calcium Biological and medical sciences Biomarkers - blood C-Reactive Protein - drug effects C-Reactive Protein - metabolism Cardiovascular disease Cholesterol Cholesterol, LDL - blood Cholesterol, LDL - drug effects Coronary Disease - blood Coronary Disease - mortality Coronary Disease - prevention & control Female Fluoroquinolones - therapeutic use General aspects Heart attacks Heptanoic Acids - administration & dosage Heptanoic Acids - pharmacology Heptanoic Acids - therapeutic use Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - administration & dosage Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Incidence Male Medical sciences Middle Aged Myocardial Infarction - blood Myocardial Infarction - drug therapy Myocardial Infarction - prevention & control Pravastatin - administration & dosage Pravastatin - pharmacology Pravastatin - therapeutic use Proportional Hazards Models Pyrroles - administration & dosage Pyrroles - pharmacology Pyrroles - therapeutic use Risk Factors Secondary Prevention Statins |
| Title | C-Reactive Protein Levels and Outcomes after Statin Therapy |
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