Predominant location of coronary artery atherosclerosis in the left anterior descending artery. The impact of septal perforators and the myocardial bridging effect

Abstract

IntroductionCoronary artery atherosclerosis presents characteristic patterns of plaque distribution despite systemic exposure to risk factors. We hypothesized that local hemodynamic forces induced by the systolic compression of intramuscular septal perforators could be involved in atherosclerotic processes in the left anterior descending artery (LAD) adjacent to the septal perforators’ origin. Therefore we studied the spatial distribution of atherosclerosis in coronary arteries, especially in relation to the septal perforators’ origin.Material and methods64-slice computed tomography angiography was performed in 309 consecutive patients (92 male and 217 female) with a mean age of 59.9 years. Spatial plaque distribution in the LAD was analyzed in relation to the septal perforators’ origin. Additionally, plaque distribution throughout the coronary artery tree is discussed.ResultsThe coronary calcium score (CCS) was positive in 164 patients (53.1%). In subjects with a CCS > 0, calcifications were more frequent in the LAD (n = 150, 91.5%) compared with the right coronary artery (RCA) (n = 94, 57.3%), circumflex branch (CX) (n = 76, 46.3%) or the left main stem (n = 42, 25.6%) (p < 0.001). Total CCS was higher in the LAD at 46.1 (IQR: 104.2) and RCA at 34.1 (IQR: 90.7) than in the CX at 16.8 (IQR: 61.3) (p = 0.007). In patients with calcifications restricted to a single vessel (n = 54), the most frequently affected artery was the LAD (n = 42, 77.8%). In patients with lesions limited to the LAD, the plaque was located mostly (n = 37, 88.1%) adjacent to the septal perforators’ origin.ConclusionsWe demonstrated that coronary calcifications are most frequently located in the LAD in proximity to the septal branch origin. A possible explanation for this phenomenon could be the dynamic compression of the tunneled septal branches, which may result in disturbed blood flow in the adjacent LAD segment (milking effect).

Acute coronary syndromes and atherosclerotic plaque burden distribution in coronary arteries among patients with valvular heart disease (BIA-WAD registry)

“…LAD is more often affected by atherosclerotic changes and calcifications than RCA and Cx [12]. Similar data are presented in studies evaluating coronary artery calcium score, confirming the predominance of atherosclerosis in LAD, followed by the RCA, Cx and LM [13]. In a retrospective analysis of over 13 000 coronarographies, an isolated change in RCA was found in 6.5% of cases, while a similar lesion was present over five times more frequently in the left artery (34.7%) [14][15][16][17].…”

The relationships between the myocardial bridge and ramus interventricularis paraconalis characteristics in lamb and sheep

“…One of the congenital anomalies is known as the myocardial bridge (MB) that the myocardial fibres cover over a segment of the subepicardial coronary arteries or their branches. The clinically most important location of the MB in humans is on the left anterior intraventricular branch of the arteria coronaria sinistra (corresponding to the ramus interventricularis paraconalis in domestic animals) (Ishii et al., 2014; Möhlenkamp et al., 2002; Teofilovski‐Parapid et al., 2017; Wasilewski et al., 2015). The MB may cause the haemodynamic changes in this branch depending on the characteristics of the bridges (Alegria et al., 2005).…”

“…These haemodynamic changes influence the arterial geometries such as the wall thickness of the arteries or vice versa (Maksuti et al., 2017; Spanos et al., 2016; Watanabe et al., 2016). Researchers almost reach a consensus that the atherosclerotic changes are developed in the pre‐B level (Alegria et al., 2005; Wasilewski et al., 2015; Zeina et al., 2007); however, the clinical consequences of the MB have changed with a wide spectrum from being asymptomatic to the sudden death (Rozenberg, & Nepomnyashchikh, 2004). In the animals compared with humans, the coronary arterial diseases and the clinical consequences of the MB have not been fully investigated (Scansen, 2017).…”

Coronary Embolism and Myocardial Infarction: A Scoping Study

“…These reports did not provide enough data to draw conclusions about how CE presents on ECG versus MI-CAD. Vessel distribution, determined angiographically, followed a similar pattern to MI-CAD [ 21 ]. However, micro-emboli and advancement of CE into small caliber vessels may lead to infarction in territories of angiographically normal vessels, contributing to underdiagnosis [ 22 , 23 ].…”