The Clinical Anatomy of the Coronary Arteries

Loukas, Marios; Sharma, Amit; Blaak, Christa; Sorenson, Edward P.; Mian, Asma

doi:10.1007/s12265-013-9452-5

Cited by 29 publications

(25 citation statements)

References 69 publications

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“…If the observer stands in the nonadjacent sinus and faces the pulmonary trunk then the right coronary artery will originate to the right hand of the observer, from the right hand sinus, or “sinus 1” The left coronary artery will arise to the left hand of the observer, from the left hand sinus, or “sinus 2” (Fig. ; Anderson, ; Loukas et al, ; Loukas et al, a; Loukas et al, in press).…”

Section: Embryology and Anatomymentioning

confidence: 99%

The clinical anatomy of high take‐off coronary arteries

et al. 2015

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A number of criteria are used in the literature to describe high take-off coronary arteries, which can in part, explain the divide in the literature on the pathological significance of this anomaly. This study presents the anatomical variations of high take-off coronary arteries to draw attention to the possible clinical implications they may cause during angiography and other surgical procedures. The English Literature was searched to review high take-off coronary arteries. A high take-off coronary artery arising at least 1 cm in adults or 20% the depth of the sinus in children above the sinutubular junction, is considered of greater clinical relevance and was included in our meta-analysis. High take-off coronaries by other criteria was also included as part of the comprehensive review. Exclusion criteria were reports made in case studies or case reviews. The prevalence of high take-off coronary arteries in our study was 26 of 12,899 (0.202%). High take-off coronary arteries were found to originate up to 5 cm above the sinutubular junction. Right coronary arteries made up 84.46% of high take-off coronary arteries reported in the literature. Three (0.023%) cases that originated more than one centimeter above the sinutubular junction was associated with sudden cardiac death. This is a higher reported association than in studies that used other criteria for classification. It is important for clinicians to recognize the importance of correctly diagnosing high take-off coronary arteries in patients with coexisting cardiac morbidities so that suitable management plans can be developed.

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Section: Embryology and Anatomymentioning

confidence: 99%

The clinical anatomy of high take‐off coronary arteries

et al. 2015

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“…There were no new stenoses, 50% stenoses have progressed, 25% regressed, and 25% unchanged (Table 9). This situation is much better than the one observed in the normal course of coronary atherosclerosis [16]. …”

Section: Resultsmentioning

confidence: 82%

Approach to Reduction of Blood Atherogenicity

Orekhov

Melnichenko

Sobenin

2014

Oxidative Medicine and Cellular Longevity

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We have earlier found that blood sera of patients with coronary heart disease (CHD) increase lipid levels in cells cultured from subendothelial intima of human aorta. We have also revealed that the ability of blood sera to raise intracellular cholesterol; that is, their atherogenicity is caused by at least modified low density lipoprotein (LDL) circulating in the blood of patients and autoantibodies to modified LDL. In the present work we have demonstrated significant impact of nonlipid factor(s) to blood atherogenicity. We have developed an approach to removal of nonlipid atherogenicity factor(s) from blood serum based on the use of immobilized LDL. This approach was used for extracorporeal perfusion of patient's blood through the column with immobilized LDL. Pilot clinical study confirmed the efficacy of this approach for prevention of coronary atherosclerosis progression.

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“…There were no new stenoses, 50% stenoses have progressed, 25% regressed, and 25% remained unchanged. These observations suggest an improved disease progression in comparison to the normal course of coronary atherosclerosis [70]. …”

Section: Revealing a Nonlipid Factor Of Blood Atherogenicitymentioning

confidence: 70%

“…Gnarled structure of the lipoprotein was shown to be the principal cause of LDL(−) association [40]. The secondary structure of apoB in LDL(−) appears to be disturbed [70], with tryptophan residues abnormally exposed to the aqueous environment [41] and lysine residues having an altered ionization state [42]. Lipid moieties of LDL(−) particles also affect their surface tension/fluidity, rendering the particles more-aggregation prone [43].…”

Section: Several Methods Have Been Developed For Isolation and Analysmentioning

confidence: 99%

Circulating Atherogenic Multiple-Modified Low-Density Lipoprotein: Pathophysiology and Clinical Applications

Nikiforov¹,

Zakiev²,

Melnichenko³

et al. 2017

Advances in Lipoprotein Research

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Low-density lipoprotein (LDL) circulating in human bloodstream is the source of lipids that accumulate in arterial intimal cells in atherosclerosis. In-vitro-modified LDL (acetylated, exposed to malondialdehyde, oxidized with transition metal ions, etc.) is atherogenic, that is, it causes accumulation of lipids in cultured cells. We have found that LDL circulating in the atherosclerosis patients' blood is atherogenic, while LDL from healthy donors is not. Atherogenic LDL was found to be desialylated. Moreover, only the desialylated subfraction of human LDL was atherogenic. Desialylated LDL is generally denser, smaller, and more electronegative than native LDL. Consequently, these LDL types are multiply modified, and according to our observations, desialylation is probably the principal and foremost cause of lipoprotein atherogenicity. It was found that desialylated LDL of coronary atherosclerosis patients was also oxidized. Complex formation further increases LDL atherogenicity, with LDL associates, immune complexes with antibodies recognizing modified LDL and complexes with extracellular matrix components being most atherogenic. We hypothesized that a nonlipid factor might be extracted from the blood serum using a column with immobilized LDL. This treatment not only allowed revealing the nonlipid factor of blood atherogenicity but also opened the prospect for reducing atherogenicity in patients.

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The Clinical Anatomy of the Coronary Arteries

Cited by 29 publications

References 69 publications

The clinical anatomy of high take‐off coronary arteries

The clinical anatomy of high take‐off coronary arteries

Approach to Reduction of Blood Atherogenicity

Circulating Atherogenic Multiple-Modified Low-Density Lipoprotein: Pathophysiology and Clinical Applications

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