Evidence map›Paper›PMID 18647585›Full record

ArticleCurrent treatment options in cardiovascular medicine2008

Therapeutic options for premature coronary artery disease.

Ameen F Person, Cam Patterson

Abstract read
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Article in Current treatment options in cardiovascular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Ameen F PersonDivision of Cardiology and Carolina Cardiovascular Biology Center, The University of North Carolina at Chapel Hill, 8200 Medical Biomolecular Research Building, Chapel Hill, NC 27599, USA.
Cam Patterson

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cardiovascular disease is commonly recognized as a disease of the elderly, young patients are also at risk for coronary atherosclerosis, which has a devastating impact on their more active lifestyle. In identifying patients at risk for a cardiovascular event, global risk models often fail to assess family history, an important risk factor in patients with premature coronary artery disease (P-CAD). P-CAD refers to the accelerated development of coronary atherosclerosis before age 55 in men and 65 in women, which may be the result of acquired or primary causes. Acquired P-CAD is associated with an underlying medical condition or influencing factor, such as systemic lupus erythematosus or cocaine use, that directly contributes to the rapid progression of coronary atherosclerosis. It is important to evaluate young patients for acquired P-CAD because in many instances treatment may be tailored to the underlying medical condition. Most cases of P-CAD, however, are the result of primary causes involving more complex interactions among genetic, metabolic, and environmental risk factors. Patients with primary P-CAD usually have a family history of coronary disease, suggesting a strong genetic component. With the use of genome-wide association analysis, several chromosome loci have been identified as being linked to the development of coronary atherosclerosis and risk factors. The chromosome 9p21.3 locus, which is the most replicated to date, has provided some insight into the pathologic mechanism of coronary disease. The confirmation and replication of these associations through further study will lead to earlier detection of P-CAD in at-risk patients and a better understanding of the underlying pathologic mechanisms, thereby influencing the development of preventive therapies.

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.