Culprit Plaques


MEDICINE IS NOT AN EXACT SCIENCE

RAMON F. ABARQUEZ, JR., MD, EFACC, FASCC, FPCP, FPCC, CSPSH Academician Project, National Academy of Science and Technology Professor Emeritus, College of Medicine, UP Manila

Dr. Ramon F. Abarquez, Jr. has been one of the most prolific consultant writers of H&L and its sister publication, Vital Signs. Highly esteemed in the medical community, he is the founding president of Philippine Society of Hypertension and a past president of the Philippine College of Physicians

For comments, ramonfabarquezjr@yahoo.com.ph


Intra-coronary plaque growth extraluminal expansion to some extent could preserve epicardial coronary lumen diameter. ‘Silent’ ischemic episodes may precede first acute coronary syndrome (ACS) among non-culprit lesion with/without plaque rupture fibroatheroma, coronary microcirculation recovery, fractional flow reserve negative (FFR-) ischemia.

CTA calcium score, HbA1c, nonalcoholic fatty liver disease (NAFLD), smoking and metabolic syndrome (MeTs) are relevant scenario pre-ACS.

ACS pathophysiology

Do most acute coronary events arise from ruptures of mildly stenotic plaques? Multiple studies had measured the degree of angiographic luminal narrowing in culprit plaques months to years before myocardial infarction. However, angiographic studies within three months before and immediately after ACS with thrombus aspiration or fibrinolytic therapy, or postmortem pathological data have all shown that ACS culprit plaques have severely stenotic CAD due to sudden rapid lesion progression based on serial angiogram.

The possible mechanisms for such rapid plaque progression include recurrent plaque rupture and healing, intra-plaque neovascularization, hemorrhage with deposition of erythrocyte-derived free cholesterol. leading to larger plaque volume and necrotic core size with greater positive vessel remodeling compared with plaques, which remain asymptomatic during several years follow-up, although these large atheromatous vulnerable plaques may angiographically seem mild.

Vulnerable plaques are more prone to rapid plaque progression and more likely to become clinically evident. Therefore, in addition to characterizing plaque morphology, inflammatory activity, and severity, detection of the rate of plaque progression might identify vulnerable plaques with an increased potential for adverse outcomes. (Ahmadi, Circ Res. 2015 Jun 19;117(1):99-104)

Plaque progression parameters

Progression of stable coronary artery disease (CAD) towards acute coronary syndrome (ACS) is a dynamic and heterogeneous process such as distorted lipid metabolism, vascular inflammation, endothelial dysfunction, increased thrombogenicity and ischemia during which patients with CAD are at high short-term risk of developing an ACS. (Oemrawsingh, BMJ Open. 2016 Dec 23;6(12):e012929)

Culprit lesions were categorized into 141 ruptured plaque (RPs), 131 intact fibrous cap (IFCs), and 46 massive thrombosis (MTs). IFC group exhibited a smaller remodeling index and less frequently attenuated plaques on IVUS. Three hundred and seven patients (96.5 percent) with median follow-up of 576 days and adverse cardiac events were observed in 93 patients (30.3 percent).

Kaplan-Meier analysis demonstrated a significantly lower event rate in IFC group and IFC and multivessel disease were independent predictors of adverse events. Culprit lesions with IFC showed smaller remodeling indices by IVUS, and were associated with better long-term prognosis compared with those with plaque rupture [Yonetsu, Int J Cardiol. 2016 Jan 15;203:766-74]

Majority of fibroatheromatous lesion FAs (73.6 percent) were located within 40 mm of the ostium, and the vessel area and plaque burden progressively decreased from proximal to distal FA location (both p < 0.001). In a multivariate logistic regression model, large vessel area, plaque burden, proximal location, right coronary artery location, and lack of calcium were associated with FA plaque rupture. The present study suggests that among these variables, vessel area may be the strongest predictor of plaque rupture among nonleft main coronary arteries. [Zheng, JACC Cardiovasc Imaging. 2015 Oct;8(10):1180-7]

Patients with upstream rupture more frequently presented with ST-segment elevation myocardial infarction and with TIMI flow grade. Longitudinal lesion asymmetry can affect regional distribution of hemodynamic stress, was associated with the location of rupture and with clinical STEMI presentation. [Lee, JACC Cardiovasc Imaging. 2016 Sep 21. pii: S1936-878X(16)30563-0]

Patients with pre-procedural TIMI 0 to 1 had a greater lipid arc (P=0.037), a longer lipid length (P=0.021), and a greater lipid index (P=0.007) based on optical coherence tomography and a larger external elastic membrane cross-sectional area (P=0.030) and plaque plus media cross-sectional area (P=0.030) based on intravascular ultrasound, compared with patients with pre-procedural TIMI 2 to 3.

Thus, ST-segment-elevation myocardial infarction patients with reduced TIMI flow grade at baseline have greater lipid burden, larger vessel sizes, and larger plaque areas. [Higuma, Circ Cardiovasc Interv. 2016 Sep;9(9) . pii: e003913]

September 2017 Health and Lifestyle

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