Meeting News Coverage

Smokers more vulnerable to arterial plaque ruptures

LAS VEGAS — Cigarette smoking is associated with a higher burden of necrotic core in coronary atherosclerotic plaques, which could represent a mechanism for increased CV events in smokers, according to a new report.

Researchers investigated the role of smoking in the pathogenesis of vulnerable coronary plaque, which has been linked to ACS. Uzoma Ibebuogu, MD, from the University of Tennessee, presented the data at the Society for Cardiovascular Angiography and Interventions Scientific Sessions.

Uzoma Ibebuogu, MD

Uzoma Ibebuogu

The study included 160 consecutive patients undergoing cardiac catheterization (mean age, 60 years; 60% men; 31% smokers; 69% admitted for ACS) during a 1-year period. The researchers performed virtual histology IVUS assessment of de novo native coronary artery stenosis. They compared coronary plaque compositions of the culprit lesion between smokers and nonsmokers.

Among all patients, the mean plaque burden was 66%. Fifty-eight percent of plaques were fibrous, 19% of plaques were fibro fatty, 18.3% of plaques had a necrotic core and 5.4% of plaques were composed of dense calcium, according to the data presented.

Compared with nonsmokers, smokers had a higher burden of necrotic core (20.7% vs. 17.2%; P=.04), Ibebuogu and colleagues found.

After controlling for age, sex, lipid profile, BMI and type 2 diabetes, the researchers determined that cigarette smoking was associated with a 4.62% increase in burden of necrotic core (P=.02). In addition, age older than 65 years was a significant predictor of higher necrotic core burden (P=.03), but diabetes was not (19.2% vs. 17.8%; P=.44).

Therefore, the researchers wrote in the abstract, smoking could raise the risk for MI by increasing the necrotic core inside arterial plaques and making less stable. However, further investigation via randomized controlled trials is necessary. – by Erik Swain

For more information:

Ibebuogu U. Abstract B-057. Presented at: the Society for Cardiovascular Angiography and Interventions Scientific Sessions; May 28-31, 2014; Las Vegas.

Disclosure: Ibebuogu reports no relevant financial disclosures.

LAS VEGAS — Cigarette smoking is associated with a higher burden of necrotic core in coronary atherosclerotic plaques, which could represent a mechanism for increased CV events in smokers, according to a new report.

Researchers investigated the role of smoking in the pathogenesis of vulnerable coronary plaque, which has been linked to ACS. Uzoma Ibebuogu, MD, from the University of Tennessee, presented the data at the Society for Cardiovascular Angiography and Interventions Scientific Sessions.

Uzoma Ibebuogu, MD

Uzoma Ibebuogu

The study included 160 consecutive patients undergoing cardiac catheterization (mean age, 60 years; 60% men; 31% smokers; 69% admitted for ACS) during a 1-year period. The researchers performed virtual histology IVUS assessment of de novo native coronary artery stenosis. They compared coronary plaque compositions of the culprit lesion between smokers and nonsmokers.

Among all patients, the mean plaque burden was 66%. Fifty-eight percent of plaques were fibrous, 19% of plaques were fibro fatty, 18.3% of plaques had a necrotic core and 5.4% of plaques were composed of dense calcium, according to the data presented.

Compared with nonsmokers, smokers had a higher burden of necrotic core (20.7% vs. 17.2%; P=.04), Ibebuogu and colleagues found.

After controlling for age, sex, lipid profile, BMI and type 2 diabetes, the researchers determined that cigarette smoking was associated with a 4.62% increase in burden of necrotic core (P=.02). In addition, age older than 65 years was a significant predictor of higher necrotic core burden (P=.03), but diabetes was not (19.2% vs. 17.8%; P=.44).

Therefore, the researchers wrote in the abstract, smoking could raise the risk for MI by increasing the necrotic core inside arterial plaques and making less stable. However, further investigation via randomized controlled trials is necessary. – by Erik Swain

For more information:

Ibebuogu U. Abstract B-057. Presented at: the Society for Cardiovascular Angiography and Interventions Scientific Sessions; May 28-31, 2014; Las Vegas.

Disclosure: Ibebuogu reports no relevant financial disclosures.

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