Relationship between left main trifurcation angulation,  calcium score, and the onset of plaque formation

Czaja-Ziółkowska, Monika; Głowacki, Jan; Krysiński, Mateusz

doi:10.33963/kp.a2022.0161

Cited by 4 publications

(4 citation statements)

References 27 publications

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“…In the RCA, there was a predilection for narrowing between the infundibular and acute marginal branches and specifically around the origin of the right ventricular branch [ 44 ]. According to the Cardiovascular Medicine Database of Saitama Sekishinkai Hospital, of 3,268 patients with chronic kidney disease who underwent percutaneous coronary intervention, coronary lesions were observed in LAD in 56% of patients, compared to 28% and 22% in the RCA and LCx, respectively [ 45 ].…”

Section: The Distribution Of Atherosclerotic Plaques In Invasive Coro...mentioning

confidence: 99%

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The site-specific distribution of atheromatous plaques in the coronary arteries

Wasilewski,

Czaja-Ziółkowska,

Gąsior

2023

pwki

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The etiology of atherosclerosis is still unknown, but there are several hypotheses trying to explain this complex disease. Most consider atherosclerosis as a cholesterol storage disease. However, hypercholesterolemia is not a cause but a risk factor. Besides, like other well-known systemic risk factors, it does not explain the uneven distribution of atheromatous plaques in the vasculature. Atherosclerotic lesions develop mainly at vulnerable “risk points” of the arterial wall such as curvatures and near side branches, and predominantly in the left anterior descending (LAD), while the left circumflex (LCx) artery is relatively spared. Furthermore, atheromatous plaques are present mainly in the proximal segments in the LAD and LCx, in contrast to the right coronary artery (RCA), where plaques are more evenly distributed. The hemodynamic theory explains to some extent the distribution of atherosclerotic lesions and considers atherosclerosis as a reactive biological response of endothelial cells to wall shear stress. In this review, we discuss the interplay of concentration of low-density lipoproteins at the luminal surface and local hemodynamic forces (disturbed flow) that reduce wall shear stress in the process of plaque formation. Moreover, we present the distribution of atheromatous plaques in the coronary arteries in autopsy studies and imaging methods such as cardiac computed tomography angiography and invasive coronary angiography.

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Section: The Distribution Of Atherosclerotic Plaques In Invasive Coro...mentioning

confidence: 99%

“…Database of Saitama Sekishinkai Hospital, of 3,268 patients with chronic kidney disease who underwent percutaneous coronary intervention, coronary lesions were observed in LAD in 56% of patients, compared to 28% and 22% in the RCA and LCx, respectively [45].…”

Section: A B Cmentioning

confidence: 99%

The site-specific distribution of atheromatous plaques in the coronary arteries

Wasilewski,

Czaja-Ziółkowska,

Gąsior

2023

pwki

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“…Nevertheless, given the current CACS and age, it is possible to estimate the age at which the CACS was converted from zero to positive [ 31 ], which is related to the concept of arterial “age” and will be discussed in the next section.…”

Section: Does Cacs Progression Mean Plaque Progression or Plaque Stab...mentioning

confidence: 99%

An update on the coronary calcium score: a review for clinicians

Czaja-Ziółkowska¹,

Wasilewski²,

Gąsior³

et al. 2022

pwki

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The clinical manifestation of coronary artery atherosclerosis is coronary artery disease (CAD) with symptoms ranging from exertional chest pain due to reduction of coronary flow reserve to acute coronary syndrome due to rupture of usually a nonobstructive plaque with abrupt coronary blood flow reduction. CAD is the leading cause of morbidity and mortality worldwide. Therefore, identifying asymptomatic people at risk of CAD is pivotal to guide decision-making for primary prevention. Coronary artery calcium (CAC) is a hallmark of coronary artery atherosclerosis. It can be detected using cardiac computed tomography and quantified by the Agatston method. CAC examination is a cheap, fast and low radiation dose test, without injecting a contrast agent. It provides prognostic information over other traditional cardiovascular risk markers and established scoring systems, especially for low-risk subgroups such as women and younger adults, and indicates the appropriate moment to implement primary prevention, including acetylsalicylic acid and statins. In this review, we discuss the methods of CAC evaluation, the meaning of a zero CAC score (CACS), its conversion to CACS > 0 and the impact of this fact on cardiovascular risk, the effect of statins and proprotein convertase subtilisin/ kexin type 9 inhibitor on CAC progression, interpretation of CACS results, and CACS prognostic value in both asymptomatic and symptomatic patients.

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“…During the last 20 years, considerable progress in the treatment of coronary bifurcation lesions has been achieved [1][2][3][4]. Nowadays there is much broader knowledge considering the treatment technique of coronary bifurcation stenoses which results in better clinical outcomes [5][6][7][8]. The one-stent technique with proximal optimization is fundamental in our current philosophy of coronary bifurcation intervention [4].…”

Section: Introductionmentioning

confidence: 99%

Side branch predilatation during percutaneous coronary bifurcation intervention: Long-term mortality analysis

Vassilev,

Mileva,

Panayotov

et al. 2024

Pol Heart J

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Background: Side branch predilatation (SBPD) during coronary bifurcation interventions is a technique that is not recommended by the latest guidelines. However, the data about the clinical outcomes after SBPD are surprisingly few. Aims:The current study aimed to explore the association between SBPD and mortality in long-term follow-up.Methods: All patients with coronary bifurcation stenoses revascularized with percutaneous coronary intervention were included in a prospective registry. Patients with stable angina and a bifurcation lesion with ≥50% diameter stenosis were included in the current analysis. Patients were assigned to two groups -those with SBPD(+) and those without SBPD(-). Propensity score matching was performed to equalize the risk factors and severity of coronary artery disease between the groups. A Kaplan-Meier analysis with a log-rank test for between-group differences was also performed.Results: From January 2013 to June 2021, 813 patients were included in the final study population. The mean age was 67 (10) years. After propensity score matching, 648 patients remained for analysis -324 in each group. At a median follow-up of 57 months patients in the SBPD(+) group had a higher all-cause mortality (n = 107 (33%) vs. n = 98 [30.2%]; P = 0.045) and cardiovascular mortality (n = 82 [25.3%] vs. n = 70 [21.6%]; P = 0.03) when compared with SBPD(-) patients. SBPD was independently associated with all-cause and cardiovascular mortality. Conclusion:SBPD treatment of coronary bifurcation stenoses is associated with worse patient survival in the follow-up of up to 8 years. SBPD treatment gives better angiographic results, but this did not translate into better clinical outcomes.

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Relationship between left main trifurcation angulation, calcium score, and the onset of plaque formation

Cited by 4 publications

References 27 publications

The site-specific distribution of atheromatous plaques in the coronary arteries

The site-specific distribution of atheromatous plaques in the coronary arteries

An update on the coronary calcium score: a review for clinicians

Side branch predilatation during percutaneous coronary bifurcation intervention: Long-term mortality analysis

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