Abstract:SummaryThe distribution of atherosclerotic plaque burden in the human coronary arteries is not uniform. Plaques are located mostly in the left anterior descending artery (LAD), then in the right coronary artery (RCA), circumflex branch (LCx) and the left main coronary artery (LM) in a decreasing order of frequency. In the LAD and LCx, plaques tend to cluster within the proximal segment, while in the RCA their distribution is more uniform. Several factors have been involved in this phenomenon, particularly flow… Show more
“…Bearing in mind that a hemodynamic milieu could be involved in the genesis of atherosclerosis, we conclude that the proximal LAD segment susceptibility to atherosclerosis can be attributed to the milking effect of septal perforators. In our opinion, systolic compression of the septal intramural branch segment can lead to disturbed flow in the adjacent LAD segment at the side of the septal origin [ 50 ]. To confirm our findings, further research, including blood flow simulation by computed fluid dynamics analysis and in vitro ultrasound measurements, is warranted to visualize the flow pattern in the LAD segment adjacent to the septal perforator.…”
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).
“…Bearing in mind that a hemodynamic milieu could be involved in the genesis of atherosclerosis, we conclude that the proximal LAD segment susceptibility to atherosclerosis can be attributed to the milking effect of septal perforators. In our opinion, systolic compression of the septal intramural branch segment can lead to disturbed flow in the adjacent LAD segment at the side of the septal origin [ 50 ]. To confirm our findings, further research, including blood flow simulation by computed fluid dynamics analysis and in vitro ultrasound measurements, is warranted to visualize the flow pattern in the LAD segment adjacent to the septal perforator.…”
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).
“…The coronary arteries near the myocardial bridge are easily covered by myocardial fiber bundles, resulting in coronary artery stenosis and myocardial ischemia reaction. Some studies have pointed out that the myocardial bridge may be one of the main causes for the formation of atherosclerotic plaques at the proximal end of the mural coronary artery [ 5 , 6 ]. This indicates that there may be some close relationship between myocardial bridge and coronary atherosclerosis.…”
Objective. To explore the relationship between different degrees of compression and clinical symptoms in patients with the myocardial bridge and the risk factors of proximal atherosclerosis. Methods. The clinical data of 156 patients with the myocardial bridge who underwent selective coronary angiography in our hospital from December 2010 to December 2015 were collected. The patients were divided into Noble grade I group (102 cases) and Noble grades II-III group (54 cases) according to the degree of mural coronary artery systolic stenosis. According to the results of coronary angiography, 156 patients with the myocardial bridge were divided into an atherosclerosis group (the myocardial bridge combined with atherosclerosis at the proximal end of the myocardial bridge of simple wall coronary artery), 91 cases, and a control group (isolated myocardial bridge), 65 cases. The relationship between different degrees of compression and clinical symptoms in patients with the myocardial bridge was observed, and the logistic regression model was used to analyze the risk factors of proximal atherosclerosis in patients with the myocardial bridge. Results. The incidence of atherosclerotic stenosis, angina pectoris, and myocardial infarction in the proximal part of the myocardial bridge in the Noble grades II-III group was higher than that in the Noble grade I group (
P
<
0.05
). The differences in age, hypertension, and Noble classification between the two groups were statistically significant (
P
<
0.05
). The differences of total cholesterol (TC) and C-reactive protein (CRP) between the two groups were statistically significant (
P
<
0.05
). Multivariate analysis showed that age, hypertension, Noble grade, and CRP were all risk factors for proximal atherosclerosis in patients with the myocardial bridge (
P
<
0.05
). Conclusion. The more severe the compression of the myocardial bridge, the greater the risk of cardiovascular events for patients and the higher the incidence of atherosclerotic stenosis in the proximal part of the myocardial bridge. In addition, the occurrence of atherosclerosis in the proximal coronary artery of the myocardial bridge may be affected by age, hypertension, Noble grade, and CRP level.
“…The anterior septal perforator arteries originate from the proximal part of the left anterior descending coronary artery (LAD) and irrigate two-thirds of the upper part of the interventricular septum. They vary in number, with an average of eight branches; the first septal artery is usually the largest and the longest [ 19 , 20 ]. Fig.…”
Background
Cardiovascular magnetic resonance (CMR) late gadolinium enhancement (LGE) is a valuable technique for detecting myocardial disorders and fibrosis. However, we sometimes observe a linear, mid-wall high intensity signal in the basal septum in the short axis view, which often presents diagnostic difficulties in the clinical setting. The purpose of this study was to compare the linear, mid-wall high intensity in the basal septum identified by LGE with the anterior septal perforator arteries identified by coronary computed tomography angiography (CorCTA).
Methods
We retrospectively selected 148 patients who underwent both CorCTA and CMR LGE within 1 year. In the interpretation of LGE, we defined a positive linear high intensity (LHI+) as follows: ① LHI in the basal septum and ② observable for 1.5 cm or more. All other patients were defined as a negative LHI (LHI-). In LHI+ patients, we assessed the correlation between the LHI length and the septal perforator artery length on CorCTA. We also compared the length of the septal perforator artery on CorCTA between LHI+ patients and LHI- patients.
Results
A population of 111 patients were used for further analysis. Among these , there were 55 LHI+ patients and 56 LHI- patients. In LHI+ patients, linear regression analysis revealed that there was a good agreement between LGE LHI and septal perforator arteries by CorCTA in terms of length measurements. The measured length of the anterior septal perforator arteries was significantly shorter in LHI- patients than in LHI+ patients (10 ± 8 mm vs. 21 ± 8 mm; P < 0.05).
Conclusions
The LHI observed in the basal septum on short axis LGE may reflect contrast enhancement of the anterior septal perforator arteries. It is important to interpret this septal LHI against knowledge of anatomic structure, to avoid misinterpretations of LGE and prevent misdiagnosis.
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