Acute Coronary and Acute Aortic Syndromes

Gulhane, Avanti; Litt, Harold

doi:10.1016/j.rcl.2018.08.004

Cited by 4 publications

(2 citation statements)

References 49 publications

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“…Typically, the left main coronary artery (LMCA) arises from the left sinus of Valsalva (LSV) and courses 2-4 mm though the aortic wall, running at about 90° from the aortic ostium. It travels posterior to the pulmonary trunk, and then in the left atrioventricular groove, leftward, posterior and superior as it courses to its bifurcation or trifurcation into the left anterior descending, circumflex coronary arteries and ramus intermedius respectively (13)(14)(15). The RCA typically arises from the right sinus of Valsalva (RSV), courses anteriorly and to the right between the right atrial appendage and the PA and then descends vertically in the right atrioventricular sulcus.…”

Section: Relevant Anatomymentioning

confidence: 99%

Extrinsic compression of coronary and pulmonary vasculature

Batra¹,

Saboo²,

Kandathil³

et al. 2021

Cardiovasc Diagn Ther

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Coronary artery disease from atherosclerosis induced stenosis remains the leading cause of acute coronary syndrome (ACS) and death worldwide, however extrinsic compression of coronary arteries from adjacent anatomical and pathological structures is an infrequent but important diagnosis to be aware of, especially given the nonspecific symptoms of chest pain that mimic angina in patients with pulmonary hypertension (PHT) and congenital heart disease. Non-invasive CT angiography is an invaluable diagnostic tool for detection of coronary artery compression, pulmonary artery dilatation and pulmonary vascular compression. Although established guidelines are not available for management of left main coronary artery (LMCA) compression syndrome, percutaneous coronary intervention and stent implantation remain a feasible option for the treatment, specifically for patients with a high surgical risk. Treatment of pulmonary vein or artery compression is more varied and determined by etiology. This review article is focused on detailed discussion of extrinsic compression of coronary arteries, mainly the LMCA and brief discussion on pulmonary vasculature compression by surrounding anatomical and pathological entities, with focus on pathophysiology, clinical features, complications and role of imaging in its diagnosis and management.

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Section: Relevant Anatomymentioning

confidence: 99%

Extrinsic compression of coronary and pulmonary vasculature

Batra¹,

Saboo²,

Kandathil³

et al. 2021

Cardiovasc Diagn Ther

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“…Around half of Americans experience myocardial infarction each year. Moreover, the clinical cardiology tends to concentrate on the administration of healing or healed infarcts [8]. Hence, much advance has been accomplished by pharmacological treatments to counteract or restrict left ventricle remodelling which can prevent advancement to fully dilated heart failure [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Detailed structural assessment of healthy interventricular septum in the presence of remodeling infarct in the free wall – A finite element model

Ṋemavhola¹

2019

Heliyon

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Purpose Computational modelling may improve the fundamental understanding of various mechanisms of diseases more particularly related to clinical challenges. In this study the effect of remodeling infarct presence in the left ventricle on the interventricular septal wall is studied using the finite element methods. Methods In this study, two rat heart (one model with healthy myocardium and one model with remodeling free wall and healthy septal wall) with magnetic resonance imaging data was gathered to reconstruct three-dimensional (3D) rat heart models. 3D data points from Segment® were imported into SolidEdge® for creation of 3D rat heart models. Abaqus® was used for finite element modeling. Results The strain in the healthy interventricular septum of the infarcted left ventricle wall increased when compared to the healthy interventricular septum in the healthy left ventricle. Similarly, the average stress in the healthy left ventricle was observed to have increased on the healthy the interventricular septum where the free wall is subjected to remodeling infarct. When comparing the infarcted models to the healthy model, it was found that the average strain had greatly increased by up to 50.0 %. Conclusions The remodeling infarct in the left ventricle has an impact on the healthy interventricular septal wall. Even though the interventricular septal wall was modelled as healthy, it was observed that it has undergone considerable changes in stresses and strains in circumferential and longitudinal direction. The observed changes in myocardial stresses and strains may result in poor global functioning of the heart.

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