Key result
A growing body of evidence suggests that C-reactive protein (CRP) may be as crucial as cholesterol in assessing heart attack risk, though its exact causal role remains unclear.
Why the study?
Does the presence of inflammation trigger rising CRP levels that lead to heart disease, or is inflammation a byproduct of the disease?
Understanding whether inflammation is a cause or byproduct of cardiovascular disease could significantly impact early diagnosis and treatment.
CARDIOVASCULAR DISEASEA growing body of evidence suggests that a molecular marker for inflammation known as C-reactive protein (CRP) may be as crucial as cholesterol deposition and clogged arteries in assessing risk of heart attack. That discovery, the result of considerable work over the past decade, has spawned more questions, starting with the most fundamental one: Does the presence of inflammation trigger rising CRP levels that lead to heart disease, or is inflammation a byproduct of the disease? The answer could greatly affect the standard of care for the disease, from early diagnosis through treatment.
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Gary Taubes (2002) conducted an editorial in Cardiovascular disease. C-reactive protein (CRP) was evaluated. A growing body of evidence suggests that C-reactive protein (CRP) may be as crucial as cholesterol in assessing heart attack risk, though its exact causal role remains unclear.
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