Apolipoprotein CIII and Triglycerides in the Necrotic Core Contribute to Plaque Vulnerability in Patients with Stable Coronary Disease - European Medical Journal

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Apolipoprotein CIII and Triglycerides in the Necrotic Core Contribute to Plaque Vulnerability in Patients with Stable Coronary Disease

1 Mins
Cardiology
Authors:
*Takayuki Ohwada, Kenichi Watanabe, Takayuki Sakamoto, Kazuaki Amami, Yasuchika Takeishi

Fukushima Red Cross Hospital, Fukushima City, Japan
*Correspondence to [email protected]

Disclosure:

The authors have declared no conflicts of interest.

Citation:
EMJ Cardiol. ;5[1]:42-43. Abstract Review No. AR5.
Keywords:
Atherosclerosis, stable coronary disease, plaque vulnerability, coronary plaque progression, apolipoprotein CIII (Apo CIII), triglyceride (TG)

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

Apolipoprotein CIII (Apo CIII) not only regulates triglyceride (TG) metabolism1 but also contributes to atherosclerotic formation and cardiovascular disease.2,3 However, it is unclear whether Apo CIII and TG affect vascular composition in humans and whether they are associated with plaque vulnerability. This study aimed to elucidate the relationship between plaque composition, determined using virtual histology-intravascular ultrasound (VH-IVUS), and Apo CIII and TG levels in 115 consecutive patients with stable coronary disease. We categorised patients, according to median Apo CIII level (8.5 mg/dL), into low Apo CIII (LAC group [≤8.5 mg/dL; n=59]), and high Apo CIII (HAC group [≥8.5 mg/dL; n=56]) groups and compared VH-IVUS findings between the two groups. Plaque vulnerability was estimated by measuring high-sensitivity C-reactive protein (hsCRP) levels in all patients, and the independent factor associated with plaque vulnerability was identified using lipids, including TG, low-density lipoprotein cholesterol, high density lipoprotein cholesterol, Apo CIII, apolipoprotein B, and apolipoprotein A-I.

Lesion length, plaque volume, and percentage necrotic core volume (assessed by VH-IVUS) were significantly greater in the HAC group than the LAC group. The hsCRP level was also significantly higher in the HAC group than the LAC group (1,861.464±420.424 ng/mL and 1,468.140±512.799 ng/mL, respectively; p=0.0104). Interestingly, the percentage necrotic core volume correlated with levels of Apo CIII (r=0.246; p=0.0079) and TG (r=0.289; p=0.0019). Moreover, Apo CIII levels strongly correlated with TG levels (r=0.731; p<0.0001).

We defined patients with hsCRP levels above the 3rd quartile level (1,245 ng/mL) as being susceptible to a coronary event (postsurgical cardiac event). Multiple logistic regression analyses revealed that TG was the only independent risk factor for a postsurgical cardiac event (odds ratio: 1.008; 95% confidence interval: 1.0010–1.0151; p=0.025). Our results suggest that Apo CIII and TG expand the necrotic core, contributing to the progression of plaque vulnerability in humans. Furthermore, compared with other lipids, TG, including the Apo CIII-TG system, are the most influential independent factors for latent vulnerability of a stable plaque.

References
Gaudet D et al. Targeting APOC3 in the familial chylomicronemia syndrome. N Engl J Med. 2014;371(23):2200-6. Luo M, Peng D. The emerging role of apolipoprotein C-III: Beyond effects on triglyceride metabolism. Lipids Health Dis. 2016;15(1):184. Gaudet D et al. Antisense inhibition of apolipoprotein C-III in patients with hypertriglyceridemia. N Engl J Med. 2015;373(5):438-47.

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