Evidence map›Paper›PMID 12473160›Full record

ArticleCardiovascular diabetology2002

Silent coronary artery disease in type 2 diabetes mellitus: the role of Lipoprotein(a), homocysteine and apo(a) polymorphism.

Carmine Gazzaruso, Adriana Garzaniti, Stefano Giordanetti, Colomba Falcone, Pietro Fratino

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Article in Cardiovascular diabetology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

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12citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

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4 · The record

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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

5 authors.

Carmine GazzarusoInternal Medicine Unit, IRCCS Maugeri Foundation Hospital, Pavia, Italy. cgazzaruso@fsm.it
Adriana Garzaniti
Stefano Giordanetti
Colomba Falcone
Pietro Fratino

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is little data on the relationship between novel cardiovascular risk factors and silent coronary artery disease (CAD) in diabetic patients. We investigated whether Lipoprotein(a), homocysteine and apolipoprotein(a) polymorphism are associated with angiographically assessed asymptomatic coronary artery disease (CAD) in diabetic patients.

methods1,971 type 2 diabetic patients without clinical signs of cardiovascular diseases and with a negative history of CAD were consecutively evaluated. Among them, 179 patients showed electrocardiographic abnormalities suggestive of ischemia or previous asymptomatic myocardial infarction. These 179 patients were subjected to a non-invasive test for CAD (ECG stress testing and/or scintigraphy). Among patients with a highly positive stress testing (n = 19) or a positive scintigraphy (n = 74), 75 showed an angiographically documented CAD (CAD group). Seventy-five patients without CAD (NO CAD group) were matched by age, sex and duration of diabetes to CAD patients. In NO CAD patients an exercise ECG test, a 48-hour ambulatory ECG and a stress echocardiogram were negative for CAD.

resultsLipoprotein(a) levels (22.0 +/- 18.9 versus 16.0 +/- 19.4 mg/dl; p < 0.05), homocysteine levels (13.6 +/- 6.6 versus 11.4 +/- 4.9 mmol/l; p < 0.05) and the percentage of subjects with at least one small apolipoprotein(a) isoform (70.7% versus 29.3%; p < 0.0001) were higher in CAD than NO CAD group. Logistic regression analysis showed that apolipoprotein(a) polymorphism (OR:8.65; 95%CI:3.05-24.55), microalbuminuria (OR:6.16; 95%CI:2.21-17.18), smoking (OR:2.53; 95%CI:1.05-6.08), HDL (OR:3.16; 95%CI:1.28-7.81), homocysteine (OR:2.25; 95%CI:1.14-4.43) and Lipoprotein(a) (OR:2.62; 95%CI:1.01-6.79) were independent predictors of asymptomatic CAD.

conclusionsThe present investigation shows an independent association of Lipoprotein(a), homocysteine and apo(a) polymorphism with silent CAD. Other studies are needed to establish whether these parameters are suitable for CAD screening in diabetic patients.

Identifiers

PMID12473160
PMCPMC149426

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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.