Journal articles: 'Premature coronary atherosclerosis'

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Turek, Łukasz, Anna Polewczyk, Marianna Janion, and Marcin Sadowski. "Coronary artery fistula and premature coronary atherosclerosis." Cardiology Journal 26, no. 3 (June 27, 2019): 296–97. http://dx.doi.org/10.5603/cj.2019.0059.

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Kaplan, Mehmet, Ozge Ozcan Abacýoglu, Fethi Yavuz, Gizem Ilgýn Kaplan, Betül Düzen, Nurbanu Bursa, and Ferhat Zorlu. "Intraocular pressure predicts premature coronary atherosclerosis." Revista da Associação Médica Brasileira 66, no. 12 (December 2020): 1707–11. http://dx.doi.org/10.1590/1806-9282.66.12.1707.

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SUMMARY OBJECTIVE: The aim of this study was to investigate the association between intraocular pressure (IOP) and premature atherosclerotic coronary artery disease (PACAD) by comparing central corneal thicknesses (CCTs) measurements. METHODS: One hundred-eighty-six subjects were enrolled in this cross-sectional study, 100 in the PACAD group and 86 in the control group. All participants underwent a physical examination and routine biochemical tests. Ophthalmological examinations, including IOP and CCTs measurements, were performed for each subject. Additionally, pulse wave velocity measurements were obtained and recorded. RESULTS: Participants with PACAD showed significantly higher IOP values than those without atherosclerosis (p = 0.001), and there was no statistically significant difference between the groups in terms of CCT (p = 0.343). Also, pulse wave velocity (PWV) values were statistically significantly higher in the PACAD group (p = 0.001). High IOP was not significantly associated with metabolic syndrome parameters (p > 0.05). CONCLUSIONS: A relationship was found between PACAD and IOP, but CCTs were not associated with PACAD. The IOP measurement is affected by CCT; therefore, CCT is used to correct IOP values. To our knowledge, this is the first study to report a positive relationship between PACAD and IOP based on CCTs measurements.

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van den Handel Vestergaard, Majken, Ann Bovin, and Erik Lerkevang Grove. "Coronary Atherosclerosis and Aortic Valve Disease as Long-Term Sequelae of Radiation Therapy in Childhood." Case Reports in Cardiology 2021 (November 30, 2021): 1–2. http://dx.doi.org/10.1155/2021/9324573.

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Coronary atherosclerosis and valvular heart disease are rare, but potentially severe sequelae following mediastinal radiation therapy. We present a case of premature ischemic heart disease and severe aortic stenosis in a 40-year-old woman following radiation therapy in childhood. We stress the awareness of prior mediastinal radiation therapy as an important risk factor for premature coronary atherosclerosis and valvular heart disease, particularly in younger patients without classical risk factors for coronary artery disease.

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Culebras, C., M. Irurita, J. Irurita, J. Fuentes, L. Lopez, C. Deniz, M. Martinez Saavedra, R. Chirino, and V. Nievo. "W01.15 Interleukin inflammatory phenotypes in premature coronary atherosclerosis." Atherosclerosis Supplements 5, no. 1 (April 2004): 4. http://dx.doi.org/10.1016/s1567-5688(04)90015-9.

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CULEBRAS, C. "W01.15 Interleukin inflammatory phenotypes in premature coronary atherosclerosis." Atherosclerosis 5, no. 1 (April 2004): 4. http://dx.doi.org/10.1016/s0021-9150(04)90015-9.

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Asanuma, Yu, Annette Oeser, Ayumi K. Shintani, Elizabeth Turner, Nancy Olsen, Sergio Fazio, MacRae F. Linton, Paolo Raggi, and C. Michael Stein. "Premature Coronary-Artery Atherosclerosis in Systemic Lupus Erythematosus." New England Journal of Medicine 349, no. 25 (December 18, 2003): 2407–15. http://dx.doi.org/10.1056/nejmoa035611.

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Rho, Young Hee, Cecilia P. Chung, Annette Oeser, Joseph Solus, Yu Asanuma, Tuulikki Sokka, Theodore Pincus, et al. "Inflammatory mediators and premature coronary atherosclerosis in rheumatoid arthritis." Arthritis & Rheumatism 61, no. 11 (November 15, 2009): 1580–85. http://dx.doi.org/10.1002/art.25009.

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Welson, GeorgeM, and AhmedA Reda. "Premature coronary atherosclerosis and its relation to familial hypercholesterolemia." Menoufia Medical Journal 35, no. 2 (2022): 331. http://dx.doi.org/10.4103/mmj.mmj_182_21.

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Farhat, Nada, Nathalie Thorin-Trescases, Guillaume Voghel, Louis Villeneuve, Maya Mamarbachi, Louis P. Perrault, Michel Carrier, and Eric Thorin. "Stress-induced senescence predominates in endothelial cells isolated from atherosclerotic chronic smokers." Canadian Journal of Physiology and Pharmacology 86, no. 11 (November 2008): 761–69. http://dx.doi.org/10.1139/y08-082.

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Age-associated telomere shortening leads to replicative senescence of human endothelial cells (EC). Risk factors for cardiovascular disease (CVD) accelerate ageing, while there is a concomitant rise in oxidative stress known to promote stress-induced senescence (SIS) in vitro. Of all risk factors for CVD, smoking is most associated with the development of inflammation and accelerated atherosclerosis due to a prooxidant–antioxidant imbalance. We tested the hypothesis that SIS predominates in EC isolated from chronic smokers with premature atherosclerosis undergoing coronary artery bypass graft surgery (CABG). We isolated and cultured EC from segments of internal mammary arteries from smoker, former smoker, and nonsmoker coronary patients. Senescence of EC was induced by serial passage and quantified by the measurement of telomere length and senescence-associated β-galactosidase activity. Compared with nonsmokers, smoker patients were 10 years younger at the time of CABG, evidence of premature atherosclerosis. Cellular senescence was independent of telomere length and directly related to oxidative damage. EC exhibited higher expression levels of markers of oxidative stress (lipid peroxydation level and caveolin-1 mRNA), inflammation (angiopoietin-like 2 mRNA), hypoxia (vascular endothelial growth factor (VEGF)-A mRNA), and cell damage (p53 mRNA). In conclusion, a high oxidative stress environment in EC isolated from atherosclerotic chronic smokers predisposes to SIS rather than replicative senescence.

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Juneja, Manish, Pankaj Raut, Milind Lohkare, and Harshawardhan Dhanraj Ramteke. "Systemic Lupus Erythematosus and Atherosclerosis." Vidarbha Journal of Internal Medicine 32 (August 10, 2022): 129–31. http://dx.doi.org/10.25259/vjim_20_2022.

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Disorders likely ‘inflammatory’ in nature are known to be linked to accelerated atherosclerotic processes that increase the chances of cardiovascular disease. Systemic lupus erythematosus (SLE) is a well-known autoimmune disease for its ability to affect any organ and cause morbidity. One such major cause of morbidity and mortality in SLE is premature coronary heart disease. Inflammation is considered to be the main pathogenesis of atherosclerosis and an important risk factor for vascular disease. Many clinical trials and studies of epidemiological and pathogenesis-related factors revealed that there is a common link between the pathogenesis of autoimmune diseases such as SLE, causing inflammatory responses similar to those seen in atherosclerosis. In the following review article, we will describe how SLE, inflammation and its traditional risk factors, promotes atherosclerosis.

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Gholoobi, Arash, and Hoorak Poorzand. "Single coronary artery anomaly: Report of an extremely rare variation." Asian Cardiovascular and Thoracic Annals 25, no. 6 (December 17, 2015): 459–62. http://dx.doi.org/10.1177/0218492315622101.

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A 43-year-old man presented with unstable angina. Coronary angiography revealed a single coronary artery originating from the left sinus of Valsalva, giving rise to a left main stem trifurcating to the left anterior descending artery, left circumflex artery, and an anomalous right coronary artery. The anomalous right coronary artery had a retroaortic course and significant proximal tubular stenosis which was stented. The coronary anomaly and abnormal course was confirmed by transesophageal echocardiography. The patient was symptom-free at one-year follow-up. This anomaly does not predispose to accelerated atherosclerosis, and the premature atherosclerosis in our patient was probably due an unhealthy lifestyle.

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Mattu, Amal, Joyce Petrini, Sharon Swencki, Chirag Chaudhari, and William J. Brady. "Premature atherosclerosis and acute coronary syndrome in systemic lupus erythematosus." American Journal of Emergency Medicine 23, no. 5 (September 2005): 696–703. http://dx.doi.org/10.1016/j.ajem.2004.12.012.

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Zylbeari, Lutfi, Sihana Ahmeti Lika, Nasir Behxheti, Mirlind Behxheti, Zamira Bexheti, Jetmire Jakupi-Alimani, Hanife Ahmeti, Ferizate Dika Haxhirexha, Ledia Kaci, and Kastriot Haxhirexha. "Homocysteine and Risk of Premature Coronary Heart Disease." Albanian Journal of Trauma and Emergency Surgery 2, no. 1 (January 20, 2018): 41–51. http://dx.doi.org/10.32391/ajtes.v2i1.156.

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Background: Homocystinuria is a rare autosomal recessive disease complicated by early and aggressive occlusive arterial disease. This may be related to the grossly increased homocysteine concentrations seen in this disease. More recently, milder hyperhomocysteinemia has been proposed as an independent risk factor for coronary artery disease. Cardiovascular disease (CVD) is among the diseases with multiple contributing factors, hence making it difficult to pinpoint a particular factor alone. The main factor that is of relevance to this study is homocysteine. Coronary artery disease is the narrowing or blockage of the arteries and vessels that supply oxygen and nutrients to the heart (1, 2). CVD is the major cause of morbidity and mortality worldwide. Obesity, HTA, Diabetes mellitus, hypercholesterolemia, and smoking have been recognized as major risk factors for CVD. Aim: Aim of this paper is to examine concentrations of Hcyt and lipid profiles in patients with CVD and positive personal history for CVD, comparing them with the control group composed of healthy individuals. Our study aimed to verify the role of Homocysteine as a new independent risk factor on the onset of early atherosclerosis and atheromatous processes in coronary arteries in patients with CVD. Materials and methods: The results obtained represent the average value earned once every three months in the 3 year period. 5ccm serum with a few heparin spots was sent to the Clinical Laboratory of the University Clinic of Skopje. Results: The results obtained from patients with CVD and control groups are presented in the following text, where a statistically significant difference was observed for p <0.0001 between the parameters obtained by patients with CVD compared to the control group. Concentrations of homocysteine and lipids in patients with CVD compared to the control group showed statistically significant difference with p<0.0001, expected results, and verified in many other multicentric studies. These facts show that raised Hcyt has more impact on the onset of CVD. When Hcy levels are in the blood, the activity of the cystathionine-synthetase enzyme is raised. It is believed that this enzyme plays a vital role in the metabolism of Hcyt. In recent years a lot of studies have been made on the effect of hyperhomocysteinemia and its impact on the onset of coronary and all have verified that hyperhomocysteinemia is a significant parameter for the onset of early atherosclerosis of coronary and CVD(6,7,8). Conclusions: In the above-mentioned cases, it is recommended substitutive therapy with folic acid, pyridoxine, vitamin B12, vitamin E and other antioxidants which are found that have an effect on the prevention of premature atherosclerosis in patients with CVD and raised Hcyt: acute myocardial infarction, CARB, angina pectoris. PTCA, Stenting, and prevention of stroke.

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Xie, Jianchang, Jie Qi, Hengyi Mao, Ningfu Wang, Xianhua Ye, Liang Zhou, Guoxin Tong, Jianmin Yang, Hao Pan, and Jinyu Huang. "Coronary plaque tissue characterization in patients with premature coronary artery disease." International Journal of Cardiovascular Imaging 36, no. 6 (February 20, 2020): 1003–11. http://dx.doi.org/10.1007/s10554-020-01794-9.

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Abstract Premature coronary artery disease (CAD) studies rarely involve coronary plaque characterization. We characterize coronary plaque tissue by radiofrequency intravascular ultrasound (IVUS) in patients with premature CAD. From July 2015 to December 2017, 220 patients from the Department of Cardiology, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine with first occurrence of angina or myocardial infarction within 3 months were enrolled. Patients with premature CAD (n = 47, males aged < 55 years, and females aged < 65 years) or later CAD (n = 155) were retrospectively compared for cardiovascular risk factors, laboratory examination findings, coronary angiography data, gray-scale IVUS, and iMap-IVUS. The mean age was 53.53 ± 7.24 vs. 70.48 ± 8.74 years (p < 0.001). The groups were similar for traditional coronary risk factors except homocysteine (18.60 ± 5.15 vs. 17.08 ± 4.27 µmol/L, p = 0.043). After matching for baseline characteristics, LDL cholesterol (LDL-C) was higher for premature CAD than later CAD (2.50 ± 0.96 vs. 2.17 ± 0.80 mmol/L, p = 0.019). Before the matching procedure, the premature CAD group had shorter target lesion length [18.50 (12.60–32.00) vs. 27.90 (18.70–37.40) mm, p = 0.002], less plaque volume [175.59 (96.60–240.50) vs. 214.73 (139.74–330.00) mm3, p = 0.013] than the later CAD group. After the matching procedure, the premature CAD group appeared to be less plaque burden (72.69 ± 9.99 vs. 74.85 ± 9.80%, p = 0.005), and positive remodeling (1.03 ± 0.12 vs. 0.94 ± 0.18, p = 0.034), and lower high risk feature incidence (p = 0.006) than the later CAD group. At the plaque’s minimum lumen, premature CAD had more fibrotic (p < 0.001), less necrotic (p = 0.001) and less calcified areas (p = 0.012). Coronary plaque tissue was more fibrotic with less necrotic and calcified components in premature than in later CAD, and the range and degree of atherosclerosis were significantly lower.

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Wang, Jinjie, Kunxiang He, Chun Yang, Xiao Lin, Xin Zhang, Yuhui Wang, George Liu, and Xunde Xian. "Dietary Cholesterol Is Highly Associated with Severity of Hyperlipidemia and Atherosclerotic Lesions in Heterozygous LDLR-Deficient Hamsters." International Journal of Molecular Sciences 20, no. 14 (July 18, 2019): 3515. http://dx.doi.org/10.3390/ijms20143515.

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Objective: Familial hypercholesterolemia (FH) is a dominant inherited disease caused mainly by low-density lipoprotein receptor (LDLR) gene mutations. To different extents, both heterozygous and homozygous FH patients develop premature coronary heart disease (CHD). However, most of the experimental animal models with LDLR deficiency could not fully recapitulate FH because they develop hyperlipidemia and atherosclerosis only in homozygous, but not in heterozygous, form. In the current study, we investigated the responsiveness of the LDLR+/− hamster to dietary cholesterol and whether plasma cholesterol levels were positively associated with the severity of atherosclerosis. Approach and Methods: wild type WT and LDLR+/− hamsters were fed a high fat diet with different cholesterol contents (HCHF) for 12 or 16 weeks. Plasma lipids, (apo)lipoproteins, and atherosclerosis in both the aorta and coronary arteries were analyzed. After a HCHF diet challenge, the levels of total cholesterol (TC) in WT and LDLR+/− hamsters were significantly elevated, but the latter showed a more pronounced lipoprotein profile, with higher cholesterol levels that were positively correlated with dietary cholesterol contents. The LDLR+/− hamsters also showed accelerated atherosclerotic lesions in the aorta and coronary arteries, whereas only mild aortic lesions were observed in WT hamsters. Conclusions: Our findings demonstrate that, unlike other rodent animals, the levels of plasma cholesterol in hamsters can be significantly modulated by the intervention of dietary cholesterol, which were closely associated with severity of atherosclerosis in LDLR+/− hamsters, suggesting that the LDLR+/− hamster is an ideal animal model for FH and has great potential in the study of FH and atherosclerosis-related CHD.

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Andriastuti, Murti, Sudigdo Sastroasmoro, and Agus Firmansyah. "Risk factors of coronary heart disease in children and young adults with parental history of premature coronary heart disease." Paediatrica Indonesiana 43, no. 2 (October 10, 2016): 51. http://dx.doi.org/10.14238/pi43.2.2003.51-8.

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Background Morbidity and mortality of coronary heart disease(CHD) are recently increasing. This is related to changes in lifestyle,such as lack of activity and high consumption of fatty diet. Themain cause of CHD is atherosclerosis. The development of ath-erosclerosis takes a long time, is asymptomatic, and might beginin childhood. The important risk factors that have roles in increas-ing the likelihood of atherosclerosis are family history of prematureCHD, hypertension, hyperlipidemia, obesity, smoking and irregu-lar activity.Objective The aim of this study was to find out the prevalence ofCHD risk factors in children and young adults who had parentalhistory of premature CHD.Methods This was a descriptive cross sectional study conductedon offspring of premature CHD patients who were admitted in theintensive cardiology care unit (ICCU) of Cipto MangunkusumoHospital between January 1999 to December 2001 and of prema-ture CHD patients who visited the Cardiology Clinic of the Depart-ment of Internal Medicine, Cipto Mangunkusumo Hospital duringMarch and April 2002. Subjects were aged 12 to 25 year-old.Results Among the subjects, 40% had hyperlipidemia, 8% hadhypertension, 11% were obese, 21% were active smokers, 41%were passive smokers, and 73% had irregular activity. Ninety-sevenpercents subjects had more than 1 risk factors.Conclusions The prevalence of hyperlipidemia, hypertension,obesity, passive smoker, active smoker and irregular activity inchildren and young adults with parental history of premature CHDin this study were higher than those in the normal population.Most had more than 1 risk factor, increasing the likelihood of CHD.A screening test should be performed on children with parentalhistory of premature CHD so that early preventive measures mightbe done to minimize the risk factors

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Moon, Yoon Gi, Yong Joo Kim, Doo Soo Jeon, Dong Heon Kang, Man Young Lee, Ki Bae Seung, Chang Sung Chae, et al. "A Case of Premature Coronary Atherosclerosis Associated with Systemic Lupus Erythematosus." Korean Circulation Journal 25, no. 3 (1995): 691. http://dx.doi.org/10.4070/kcj.1995.25.3.691.

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Jaeger, Beate Roxane, Theoharis Tsobanelis, Frank Bengel, Markus Schwaiger, and Dietrich Seidel. "Long-term prevention of premature coronary atherosclerosis in homozygous familial hypercholesterolemia." Journal of Pediatrics 141, no. 1 (July 2002): 125–28. http://dx.doi.org/10.1067/mpd.2002.124384.

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Shirish, S. Borkar, S. Ganesh Kamath, Sagar C. V. Sunil, Bedjirgi Chidanand, and Kashyap Nitin. "Triple Vessel Coronary Artery Bypass Grafting in a 14-year-old Child with Familial Hypercholesterolemia-A Rare Case Report." Open Journal of Cardiovascular Surgery 2 (January 2009): OJCS.S3713. http://dx.doi.org/10.4137/ojcs.s3713.

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Familial hypercholesterolemia is a genetic disorder caused by a mutation in the low density lipoprotein (LDL) receptor gene. The homozygous type of the disease is rare and causes tendon xanthomas and coronary artery disease during the early years of life. Premature coronary artery occlusive disease in familial homozygous hypercholesterolemia might necessitate coronary bypass surgery in children and young adults We present the case of a 14-year-old boy with familial hypercholesterolemia and coronary artery disease. He underwent triple-vessel coronary artery bypass grafting with bilateral pedicled internal mammary artery and saphenous vein grafting without adverse events. Pediatric patients with familial hypercholesterolemia may present with premature coronary atherosclerosis requiring coronary artery bypass grafting. In situ internal mammary artery grafts should be the graft of choice. To the best of our knowledge, he is one of the youngest such patients reported in the English-language literature who underwent coronary artery bypass surgery.

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Liu, T., N. Shi, S. Zhang, G. J. Silverman, X.-W. Duan, S. Zhang, and H. Niu. "Systemic lupus erythematosus aggravates atherosclerosis by promoting IgG deposition and inflammatory cell imbalance." Lupus 29, no. 3 (February 19, 2020): 273–82. http://dx.doi.org/10.1177/0961203320904779.

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Background Systemic lupus erythematosus (SLE) patients experience a premature and more severe presentation of coronary artery disease. The underlying mechanisms of accelerated coronary artery disease in SLE patients remain to be elucidated. Methods By using atherosclerosis combining a SLE murine model, we proved that the onset of SLE aggravates atherosclerosis. Although the onset of SLE reduced blood lipids slightly, immune deviation contributed to aggravated atherosclerosis in lupus mice. Lupus atheroma were characterized by inflammatory cell infiltration, such as gathered dendritic cells, macrophages, and IgG deposition. Results Decreased lymphocytes and magnified dendritic cells in the spleen were also observed in lupus mice. Hydroxychloroquine prevented atherosclerosis progression mainly by reversing immune status abnormality caused by SLE. Serum interferon alfa levels were not changed in lupus mice. Conclusion These findings strongly suggested that anti-inflammatory therapies and hydroxychloroquine provide a new possible strategy for treating SLE patients with atherosclerosis.

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YIU, KAI-HANG, SILUN WANG, MO-YIN MOK, GAIK CHENG OOI, PEK-LAN KHONG, CHU-PAK LAU, WING-HON LAI, et al. "Role of Circulating Endothelial Progenitor Cells in Patients with Rheumatoid Arthritis with Coronary Calcification." Journal of Rheumatology 37, no. 3 (January 15, 2010): 529–35. http://dx.doi.org/10.3899/jrheum.090782.

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Objective.Patients with rheumatoid arthritis (RA) are prone to premature atherosclerosis. We hypothesize that depletion of circulating endothelial progenitor cells (EPC) related to RA can contribute to the development of atherosclerosis.Methods.We studied coronary calcifications by multidetector computed tomography and their relationship with different subtypes of circulating EPC in 70 patients with RA and 35 age- and sex-matched controls (mean age 54.1 ± 10.2 yrs, 87% were women). The presence of coronary atherosclerosis was defined as an Agatston score ≥ 10. Four subpopulations of EPC were determined by flow cytometry on the basis of surface expression of CD34, CD133, and KDR antigen: CD34+, CD34/KDR+, CD133+, and CD133/KDR+ EPC, respectively.Results.Among those with RA, 15 patients (21%) had coronary atherosclerosis. The mean Agatston score was higher (61.8 ± 201.7 vs 0.14 ± 0.69; p = 0.01) and coronary atherosclerosis was more prevalent (21.4% vs 0%; p < 0.01) in patients with RA compared to controls. RA patients with coronary atherosclerosis were older (66.2 ± 6.9 vs 51.5 ± 16.2 yrs; p < 0.01), had higher prevalence of hypertension (46.7% vs 14.5%; p = 0.01), and had lower CD133/KDR+ (0.45% ± 0.28% vs 0.89% ± 0.81%; p < 0.01) and CD133+ EPC levels (0.74% ± 0.39% vs 1.22% ± 0.83%; p < 0.01), but similar CD34/KDR+ and CD34+ EPC levels (all p > 0.05) compared to those without. Multiple logistic regression revealed that older age (OR 1.25, 95% CI 1.10–1.41, p < 0.01) and lower CD133/KDR+ EPC (OR 0.07, 95% CI 0.00–0.97, p < 0.01) were independent predictors for coronary atherosclerosis in patients with RA.Conclusion.Our results demonstrated that RA patients with coronary atherosclerosis have significantly lower levels of CD133/KDR+ and CD133+ EPC than those without. In addition to older age, lower levels of circulating CD133/KDR+ EPC also predicted occurrence of coronary atherosclerosis in RA patients.

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Haidari, Mehran, Ebrahim Javadi, Arashmidos Sanati, Mehrdad Hajilooi, and Jafar Ghanbili. "Association of Increased Ferritin with Premature Coronary Stenosis in Men." Clinical Chemistry 47, no. 9 (September 1, 2001): 1666–72. http://dx.doi.org/10.1093/clinchem/47.9.1666.

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Abstract Background: Body iron status has been implicated in atherosclerotic cardiovascular disease. The main hypothesis is that high iron status is associated with increased oxidation of LDL. We investigated the potential role of ferritin as an additional risk factor promoting atherosclerosis among a young population with coronary artery disease (CAD). Methods: Four hundred consecutive patients (218 males, 182 females) referred for diagnostic coronary angiography were examined, and risk factors for CAD, lipids, C-reactive protein (CRP), and ferritin concentrations were recorded for all participants. Results: Ferritin was higher in the male patients with CAD (121 μg/L; range, 56–258 μg/L) than in the men without significant CAD (73 μg/L; range, 32–138 μg/L; P <0.002). Multiple logistic regression analysis, after adjustment for the established coronary risk factors, showed ferritin as an independent discriminating risk factor for CAD (P <0.01). Men in the highest quartile of ferritin had an odds ratio (OR) of 1.62 [95% confidence interval (95% CI), 1.12–2.42; P <0.01] compared with men in the lowest quartile of ferritin. The association between ferritin and CAD was more pronounced in male patients ≤50 years (OR = 2.65; 95% CI, 1.35–5.51; P <0.003). Ferritin was significantly higher in diabetic male patients in comparison with nondiabetic male patients [168 μg/L (range, 74–406 μg/L) vs 106 μg/L (range, 44–221 μg/L), respectively; P <0.002]. No association was observed between ferritin and CAD among the female patients. Conclusion: Our data suggest that increased ferritin might be an independent predictor of premature CAD in male Iranian patients.

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Januszek, Rafał, Magdalena Jędrychowska, Piotr Jankowski, Dariusz Dudek, and Stanisław Bartuś. "Delayed Diagnosis of Non-ST Segment Elevation Myocardial Infarction in a Young Patient with Multivessel Disease and Familial Hypercholesterolemia Complicated by Cardiogenic Shock Finally Treated with Intra-Aortic Balloon Pump as a Bridge to Extra Corporeal Membrane Oxygenation." Case Reports in Cardiology 2019 (January 17, 2019): 1–4. http://dx.doi.org/10.1155/2019/9470131.

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Delayed diagnosis of coronary artery disease in young patients after cardiac arrest of unknown origin could increase the risk of death in further diagnostic and therapeutic process. Familial history of premature coronary atherosclerosis and hypercholesterolemia could help in proper diagnosis and treatment. We present a case of a 29-year-old female admitted to the catheterization laboratory with cardiogenic shock and multivessel coronary artery disease treated successfully with multivessel percutaneous coronary intervention and intra-aortic balloon counterpulsation as a bridge to extracorporeal membrane oxygenation.

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Lai, Edward Chia-Cheng, Ya-Chun Huang, Tzu-Chi Liao, and Meng-Yu Weng. "Premature coronary artery disease in patients with immune-mediated inflammatory disease: a population-based study." RMD Open 8, no. 1 (January 2022): e001993. http://dx.doi.org/10.1136/rmdopen-2021-001993.

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BackgroundThe associations between premature atherosclerosis and immune-mediated inflammatory diseases (IMIDs) are not fully investigated. To determine whether IMIDs are associated with premature atherosclerosis, we examined the risk of incident coronary artery disease (CAD) in men less than 45 years old and women less than 50 years old with various forms of IMIDs compared with general population.MethodsA population-based cohort was established and included patients with IMID, who were followed until the development of CAD, withdrawal from the insurance system, death, or 31 December 2016, whichever point came first. Patients with IMID included rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), primary Sjogren’s syndrome (SjS), idiopathic inflammatory myositis, systemic sclerosis (SSc), Behcet’s disease (BD), and systemic vasculitis (SV). The comparison group was 1 000 000 beneficiaries sampled at random from the whole population as matched control participants. The Kaplan-Meier method was used to compare the cumulative incidences of CAD in patients with and without IMID.ResultsAmong 58 862 patients with IMID, 2139 (3.6%) developed CAD and 346 (1.3%) developed premature CAD. Relative to the comparison cohorts, the adjusted HRs for premature CAD were 1.43 (95% CI 1.09 to 1.86) for primary SjS, 2.85 (95% CI 2.63 to 3.43) for SLE, 3.18 (95% CI 1.99 to 5.09) for SSc and 2.27 (95% CI 1.01 to 5.07) for SV.ConclusionsPrimary Sjogren’s syndrome, SLE, SSc and SV are associated with an increased risk of premature CAD. Our ﬁndings will support essential efforts to improve awareness of IMID impacting young adults.

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van Loo, Karen M. J., Tim Dejaegere, Martine van Zweeden, Jessica E. van Schijndel, Cisca Wijmenga, Mieke D. Trip, and Gerard J. M. Martens. "Male-Specific Association between a γ-Secretase Polymorphism and Premature Coronary Atherosclerosis." PLoS ONE 3, no. 11 (November 6, 2008): e3662. http://dx.doi.org/10.1371/journal.pone.0003662.

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Othman, Khaled Mohamed Said, and Naglaa Youssef Assaf. "Early detection of premature subclinical coronary atherosclerosis in systemic lupus erythematosus patients." Egyptian Heart Journal 65, no. 4 (December 2013): 281–88. http://dx.doi.org/10.1016/j.ehj.2012.12.003.

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Heshmat, Tarek S., Noha M. Khalil, Huda Abd Elhamid, Safa Labib, and Mamdoh Mahfouz. "Assessment of premature coronary atherosclerosis in patients with systemic lupus erythematosus disease." Egyptian Rheumatologist 37, no. 4 (October 2015): S43—S47. http://dx.doi.org/10.1016/j.ejr.2015.04.001.

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Taraboanta, Catalin, Evelyn Wu, Scott Lear, Stefanie DiPalma, John Hill, G. B. John Mancini, and Jiri Frohlich. "Subclinical atherosclerosis in subjects with family history of premature coronary artery disease." American Heart Journal 155, no. 6 (June 2008): 1020–26. http://dx.doi.org/10.1016/j.ahj.2007.11.046.

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Milic, Gordana, Jasna Gacic, Ana Mladenovic-Markovic, Ivan Soldatovic, Dragan Matic, Srdjan Popovic, Zeljko Markovic, and Svetozar Damjanovic. "Carotid intima-media thickness, 25-OH vitamin D, homocysteine and subclinical coronary artery atherosclerosis in patients with type 1 diabetes mellitus." Archives of Biological Sciences 71, no. 4 (2019): 655–63. http://dx.doi.org/10.2298/abs190706048m.

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Individuals with type 1 diabetes have an increased risk of premature atherosclerosis. The aim of this study was to evaluate the possible predictive significance of elevated plasma total homocysteine (tHcy), lower serum 25-hydroxy vitamin D (25(OH)D) concentrations and increased carotid intima-media thickness (CIMT) for the development of coronary atherosclerosis in patients with type 1 diabetes mellitus (T1D) and no previous history of ischemic heart disease. The study included 73 patients previously diagnosed with T1D. The patients were divided into groups with and without non-obstructive moderate coronary artery stenosis. Coronary artery stenosis was examined using coronary multidetector computed tomographic angiography (MDCTA); CIMT was measured by B-mode ultrasound. The patients with moderate stenosis had significantly higher HbA1c (p<0.001), elevated tHcy (p<0.001), increased CIMTmax. (p<0.001) but lower 25(OH)D (p<0.001) in comparison to patients without detectable coronary atherosclerosis. Homocysteine (AUCHcy=0.955; p<0.001), vitamin D (AUCvit D=0.792; p<0.001) and CIMT max (AUCCIMT=0.743; p<0.001) (AUC or area under the curve) appear to be adequate markers for detecting stenosis of coronary arteries using receiver operating characteristic (ROC) curve analysis. Multivariate logistic regression analysis showed that serum homocysteine was the only significant predictor of moderate coronary artery stenosis. Our study implies that tHcy can be used as a reliable predictor of coronary artery atherosclerosis in patients with T1D. 25(OH)D and CIMT can also be used, but with lower diagnostic accuracy.

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Suresh Kumar, Gayatri, Mohammad F. Mathbout, Ibrahim Fahsah, and Shahab Ghafghazi. "Case of homozygous familial hypercholesterolaemia with premature coronary artery disease." BMJ Case Reports 14, no. 5 (May 2021): e242114. http://dx.doi.org/10.1136/bcr-2021-242114.

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Familial hypercholesterolaemia is a genetic disorder secondary to mutation of one or more of the genes critical for low-density lipoprotein cholesterol (LDL-C) metabolism; these mutation(s) cause highly elevated serum LDL-C, significantly increasing the risk of early cardiovascular events and mortality. Homozygous familial hypercholesterolaemia (HoFH) is rare and often leads to accelerated coronary atherosclerosis presenting within the first two decades of life. We report a case of a 14-year-old boy who presented after surviving a ventricular fibrillation cardiac arrest. His highly elevated LDL-C level prompted further workup and led to a diagnosis of HoFH. The treatment included medical therapy and coronary artery bypass grafting. The patient also required referral for lipid apheresis to meet goal LDL-C level, and an automated implantable cardioverter defibrillator for secondary prevention of sudden cardiac death. HoFH, if left untreated, can have devastating consequences Therefore, timely diagnosis initiating appropriate therapy is important.

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Chait, Robert, Rajesh Ramineni, and Erin A. Fender. "Precocious virulent coronary atherosclerosis in the very young." Cardiology in the Young 22, no. 2 (August 31, 2011): 184–87. http://dx.doi.org/10.1017/s1047951111001156.

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AbstractBackgroundThe incidence of Myocardial Infarction (MI) in patients under the age of 30 has been rarely addressed. Moreover, it is not understood why these patients develop symptomatic Coronary Artery Disease (CAD) at such an early age. Traditional risk factor assessment has not been successful in identifying these patients before they present with MI.MethodsRetrospective, single cohort, observational study of 14,704 cardiac catheterizations performed in a community hospital between January 2006–January 2010 identified 12 cases age <30 with MI secondary to a fixed atherosclerotic lesion requiring angioplasty and stenting. The angiograms and charts were reviewed to assess the incidence and frequency of traditional risk factors such as smoking, dyslipidemia and diabetes and family history.ResultsAll the patients had single vessel disease. Many of the patients were noted to have traditional CAD risk factors. 2 patients had an intervention and then months later sustained another acute MI secondary to a new culprit lesion despite aggressive risk factor modification.ConclusionEvaluating patients for premature CAD by screening for traditional risk factors has not effectively identified at risk patients prior to presentation with MI. There is a role for studies evaluating new and novel risk factors and imaging modalities so that these patients can be identified prior to experiencing MI.

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Pogosova, N. V., Y. M. Yufereva, N. P. Kachanova, V. A. Metelskaya, I. Y. Koltunov, V. P. Voronina, A. P. Mazaev, A. A. Arutyunov, and V. A. Vygodin. "Prediction of Subclinical Coronary Atherosclerosis in Patients with High and Very High Cardiovascular Risk." Kardiologiia 60, no. 2 (March 5, 2020): 75–82. http://dx.doi.org/10.18087/cardio.2020.2.n964.

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Objective To develop a diagnostic rule for detection of patients (pts) with high probability of subclinical atherosclerosis among those with high or very high cardiovascular (CV) risk.Materials and Methods This cross-sectional study enrolled 52 pts (32 men [62 %]), aged 40 to 65 years [mean age 54.6±8.0]) with high or very high CV risk (5–9 and ≥10 % by The Systematic Coronary Risk Estimation Scale [SCORE], respectively). All participants underwent cardiac computed tomography (CT) angiography and calcium scoring. Traditional risk factors (RFs) (family history of premature CVD, smoking, overweight / obesity and abdominal obesity, hypertension, type 2 diabetes mellitus, lipids parameters (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides) and lipids-related markers (apolipoprotein A1, apolipoprotein B, ApoB / ApoA1 ratio), biomarkers of inflammation (high-sensitivity C-reactive protein [hs CRP], fibrinogen), indicator carbohydrate metabolism (glucose), ankle-brachial index, stress-test, carotid plaques according to ultrasound were evaluated in all pts. Psychological RFs were evaluated using Hospital Anxiety and Depression Scale and DS-14 for type D personality.Results All pts were divided into 2 groups according to the CT angiography results: pts in the main group (n=21) had any non-obstructive lesions or calcium score >0, pts in the control group (n=31) had intact coronary arteries. The groups did not differ in age or gender. 26 multiple linear logistic models for any subclinical atherosclerosis were developed based on obtained diagnostic features. Taking into account R-square = 0.344 (p=0.0008), the best fitting model was follows: subclinical coronary atherosclerosis= –1.576 + 0.234 x SCORE ≥5 % + 0.541 x hs CRP >2 g / l +0.015 x heart rate (bpm) +0.311 family history of premature CVD. The developed algorithm had sensitivity of 63 % and specificity of 80 %.Conclusion The created diagnostic model diagnostic model suggests the presence of subclinical coronary atherosclerosis in patients with high / very high CV risk with a high degree of probability. This easy-to-use method can be used in routine clinical practice to improve risk stratification and management choices in high-risk pts.

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Djeric, Mirjana. "New aspects of normolipidemic dyslipoproteinemias." Medical review 57, no. 11-12 (2004): 605–9. http://dx.doi.org/10.2298/mpns0412605d.

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Introduction Normolipidemic dislipoproteinemias include various disorders of different lipoproteins, of their subfractions or some apolipoproteins, of primary or secondary origin, which are widespread among general population and, like hyperlipoproteinemias, they are associated with the risk for premature atherosclerosis. Decreased level of HDL cholesterol It is a primary, familial hypoalphalipoproteinemia, which is commonly associated with obesity, diet rich in carbohydrates, decreased physical activity and excessive use of coffee and some drugs. Hyperapobetalipoproteinemia It is characterized by increase of apo B-100 in LDL particles, most probably as a consequence of increased hepatic synthesis. Apolipoprotein E isoforms ApoE4 isoform is associated with elevated LDL-cholesterol concentration due to rapid IDL to LDL conversion. Electrophoretic disorders The most important is the latent type IV (pre-beta) or IVb (pre-beta1) with decreased VLDL clearance. Prolonged postprandial lipemia It is common in obesity, NIDDM and coronary heart disease, as an independent risk factor for premature atherosclerosis. Increased oxidative modification of the LDL and HDL particles Oxidatively modified LDL may have a key role in the pathogenesis of atherosclerosis and oxidative modification of HDL reduces its transport capacity and its inhibition of LDL oxidation. Increased level of Lp(a) Lp(a) is an independent risk factor for premature atherosclerosis, primarily in young and middle-aged men, in persons with elevated global cardiovascular risk factor profile, decreased HDL-cholesterol, and hypertension. The risk is smaller in persons taking hypocholesterolemic drugs. Also, it is elevated in NIDDM, hypothyroidism and kidney disease.

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Ates, Ahmet Hakan, Hikmet Yorgun, Ugur Canpolat, Muhammed Dural, Yusuf Ziya Sener, Metin Oksul, Sevilay Karahan, and Kudret Aytemir. "Subclinical Coronary Atherosclerosis in Patients Undergoing Catheter Ablation for Idiopathic Premature Ventricular Complexes." European Journal of Therapeutics 26, no. 3 (September 23, 2020): 245–50. http://dx.doi.org/10.5152/eurjther.2020.20058.

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Martini, S., G. Mazzetto, L. Previato, I. Cortella, G. Maraglino, G. Frigo, P. Zucchetta, et al. "Premature coronary and extracoronary atherosclerosis in familial hypercholesterolemia caused by padua-1 mutation." Atherosclerosis Supplements 2, no. 2 (May 2001): 64. http://dx.doi.org/10.1016/s1567-5688(01)80121-5.

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Nanni, Samuele, Giovanni Melandri, Roeland Hanemaaijer, Vittorio Cervi, Luciana Tomasi, Annalisa Altimari, Natascha Van Lent, Pierluigi Tricoci, Letizia Bacchi, and Angelo Branzi. "Matrix metalloproteinases in premature coronary atherosclerosis: influence of inhibitors, inflammation, and genetic polymorphisms." Translational Research 149, no. 3 (March 2007): 137–44. http://dx.doi.org/10.1016/j.trsl.2006.09.001.

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Fabbi, Patrizia, Giorgio Ghigliotti, Claudio Brunelli, Manrico Balbi, Paolo Spallarossa, Pierfranco Rossettin, Antonio Barsotti, Patrizio Odetti, and Silvano Garibaldi. "Intense lipid peroxidation in premature clinical coronary atherosclerosis is associated with metabolic abnormalities." Journal of Laboratory and Clinical Medicine 143, no. 2 (February 2004): 99–105. http://dx.doi.org/10.1016/j.lab.2003.10.009.

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Shohet, Ralph V., Azam Anwar, John M. Johnston, and Jonathan C. Cohen. "Plasma platelet-activating factor acetylhydrolase activity is not associated with premature coronary atherosclerosis." American Journal of Cardiology 83, no. 1 (January 1999): 109–11. http://dx.doi.org/10.1016/s0002-9149(98)00791-7.

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Wysocka, Anna, Marek Cybulski, Andrzej P.Wysokiński, Henryk Berbeć, Janusz Stążka, and Tomasz Zapolski. "Paraoxonase 1 Activity, Polymorphism and Atherosclerosis Risk Factors in Patients Undergoing Coronary Artery Surgery." Journal of Clinical Medicine 8, no. 4 (March 30, 2019): 441. http://dx.doi.org/10.3390/jcm8040441.

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Background: Paraoxonase1 (PON1), an enzyme connected to high density lipoproteins (HDL) particles, plays an important role in protecting arteries against atherosclerosis. The serum activity and concentration of PON1 depends on several genetic polymorphisms as well as environmental factors. Materials and methods: Investigated population consisted of 71 patients aged 43–76 years with confirmed coronary heart disease (CHD). Established risk factors of CHD such as hypertension, elevated total cholesterol and LDL cholesterol (LDL-C), low HDL cholesterol (HDL-C), diabetes mellitus, obesity, smoking and premature CHD in family history were assessed. PON1 genotype for –108C/T promotor region was determined by polymerase chain reaction-restriction fragments length polymorphism (PCR–RFLP) method. Paraoxonase activity towards paraoxon and arylesterase activity towards phenyl acetate were measured spectrophotometrically. Results: Significant correlations between diabetes mellitus and paraoxonase activity (R = –0.264, p = 0.026) and between the premature coronary heart disease in family history and PON1 activity (R = –0.293, p = 0.013) were found. In multivariate analysis, PON1 paraoxonase activity was independently of confounding factors associated with diabetes (OR = 0.985; p = 0.024) and premature CHD in family history (OR = 0.983; p = 0.027). PON1 activity towards aryl acetate positively correlated with HDL-C level (R = 0.255, p = 0.032). In patients treated with statins, PON1 paraoxonase activity was significantly (p = 0.033) higher than in patients without treatment. Conclusions: In diabetic patients with CHD, paraoxonase activity is lower than in normoglycemic patients despite similar lipid profiles. Diabetes and positive family history in patients with overt CHD are associated with the serum PON1 activity, which might be an additional factor helpful in evaluating cardiovascular risk in this group of patients.

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Santiago-Hernandez, Aranzazu, Paula J. Martinez, Marta Agudiez, Angeles Heredero, Laura Gonzalez-Calero, Alma Yuste-Montalvo, Vanesa Esteban, Gonzalo Aldamiz-Echevarria, Marta Martin-Lorenzo, and Gloria Alvarez-Llamas. "Metabolic Alterations Identified in Urine, Plasma and Aortic Smooth Muscle Cells Reflect Cardiovascular Risk in Patients with Programmed Coronary Artery Bypass Grafting." Antioxidants 10, no. 9 (August 27, 2021): 1369. http://dx.doi.org/10.3390/antiox10091369.

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Atherosclerosis is the predominant pathology associated to premature deaths due to cardiovascular disease. However, early intervention based on a personalized diagnosis of cardiovascular risk is very limited. We have previously identified metabolic alterations during atherosclerosis development in a rabbit model and in subjects suffering from an acute coronary syndrome. Here we aim to identify specific metabolic signatures which may set the basis for novel tools aiding cardiovascular risk diagnosis in clinical practice. In a cohort of subjects with programmed coronary artery bypass grafting (CABG), we have performed liquid chromatography and targeted mass spectrometry analysis in urine and plasma. The role of vascular smooth muscle cells from human aorta (HA-VSMCs) was also investigated by analyzing the intra and extracellular metabolites in response to a pro-atherosclerotic stimulus. Statistically significant variation was considered if p value < 0.05 (Mann-Whitney test). Urinary trimethylamine N-oxide (TMAO), arabitol and spermidine showed higher levels in the CVrisk group compared with a control group; while glutamine and pantothenate showed lower levels. The same trend was found for plasma TMAO and glutamine. Plasma choline, acetylcholine and valine were also decreased in CVrisk group, while pyruvate was found increased. In the secretome of HA-VSMCs, TMAO, pantothenate, glycerophosphocholine, glutathion, spermidine and acetylcholine increased after pro-atherosclerotic stimulus, while secreted glutamine decreased. At intracellular level, TMAO, pantothenate and glycerophosphocholine increased with stimulation. Observed metabolic deregulations pointed to an inflammatory response together with a deregulation of oxidative stress counteraction.

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Reilly, Muredach P., Megan L. Wolfe, Jennifer Dykhouse, Karthik Reddy, Russell A. Localio, and Daniel J. Rader. "Intercellular Adhesion Molecule 1 (ICAM-1) Gene Variant Is Associated with Coronary Artery Calcification Independent of Soluble ICAM-1 Levels." Journal of Investigative Medicine 52, no. 8 (December 1, 2004): 515–22. http://dx.doi.org/10.1136/jim-52-08-23.

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BackgroundAlthough circulating levels of soluble intercellular adhesion molecule 1 (sICAM-1) predict cardiovascular events, no studies have examined intercellular adhesion molecule 1 (ICAM-1) gene variants, plasma sICAM-1 levels, and atherosclerosis in the same sample.MethodsWe examined the association of the ICAM-1 K469E gene variant and plasma sICAM-1 with coronary artery calcification (CAC) in 632 asymptomatic subjects, recruited on the basis of a family history of premature cardiovascular disease.ResultsIn age-adjusted ordinal regression, sICAM-1 levels were associated with CAC (odds ratio [OR] [95% confidence interval (CI)] 1.30 [1.04-1.6] per 100 ng/dL sICAM-1; p = .02), but this association was lost after adjusting for traditional risk factors (OR [95% CI] 0.9 [0.69-1.16]). In men, but not women (interaction p = .018), the ICAM-1 K469E GG genotype predicted lower CAC after adjusting for traditional risk factors (OR [95% CI] 0.33 [0.17-0.61]; p = .001) and further controlling for plasma sICAM-1 (OR [95% CI] 0.27 [0.14-0.52]; p < .001).ConclusionsIn a study sample specifically selected for the characteristic of a family history of premature coronary heart disease, ICAM K469E GG was associated with lower CAC scores in men but not women even after controlling for plasma levels of sICAM-1. These studies suggest that ICAM-1 variants may modulate atherosclerosis in humans and provide support for the concept that inflammatory gene polymorphisms may influence atherosclerosis independent of plasma levels of their gene products.

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Kryczka, Karolina E., Mariusz Kruk, Marcin Demkow, and Barbara Lubiszewska. "Fibrinogen and a Triad of Thrombosis, Inflammation, and the Renin-Angiotensin System in Premature Coronary Artery Disease in Women: A New Insight into Sex-Related Differences in the Pathogenesis of the Disease." Biomolecules 11, no. 7 (July 15, 2021): 1036. http://dx.doi.org/10.3390/biom11071036.

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Coronary artery disease (CAD) is the leading cause of morbidity and mortality in women worldwide. Its social impact in the case of premature CAD is particularly devastating. Many differences in the presentation of the disease in women as compared to men, including atypical symptoms, microvascular involvement, and differences in pathology of plaque formation or progression, make CAD diagnosis in women a challenge. The contribution of different risk factors, such as smoking, diabetes, hyperlipidemia, or obesity, may vary between women and men. Certain pathological pathways may have different sex-related magnitudes on CAD formation and progression. In spite of the already known differences, we lack sufficiently powered studies, both clinical and experimental, that assess the multipathogenic differences in CAD formation and progression related to sex in different age periods. A growing quantity of data that are presented in this article suggest that thrombosis with fibrinogen is of more concern in the case of premature CAD in women than are other coagulation factors, such as factors VII and VIII, tissue-type plasminogen activator, and plasminogen inhibitor-1. The rise in fibrinogen levels in inflammation is mainly affected by interleukin-6 (IL-6). The renin–angiotensin (RA) system affects the inflammatory process by increasing the IL-6 level. Unlike in men, in young women, the hypertensive arm of the RA system is naturally downregulated by estrogens. At the same time, estrogens promote the fibrinolytic path of the RA system. In young women, the promoted fibrinolytic process upregulates IL-6 release from leukocytes via fibrin degradation products. Moreover, fibrinogen, whose higher levels are observed in women, increases IL-6 synthesis and exacerbates inflammation, contributing to CAD. Therefore, the synergistic interplay between thrombosis, inflammation, and the RA system appears to have a more significant influence on the underlying CAD atherosclerotic plaque formation in young women than in men. This issue is further discussed in this review. Fibrinogen is the biomolecule that is central to these three pathways. In this review, fibrinogen is shown as the biomolecule that possesses a different impact on CAD formation, progression, and destabilization in women to that observed in men, being more pathogenic in women at the early stages of the disease than in men. Fibrinogen is a three-chain glycoprotein involved in thrombosis. Although the role of thrombosis is of great magnitude in acute coronary events, fibrinogen also induces atherosclerosis formation by accumulating in the arterial wall and enabling low-density lipoprotein cholesterol aggregation. Its level rises during inflammation and is associated with most cardiovascular risk factors, particularly smoking and diabetes. It was noted that fibrinogen levels were higher in women than in men as well as in the case of premature CAD in women. The causes of this phenomenon are not well understood. The higher fibrinogen levels were found to be associated with a greater extent of coronary atherosclerosis in women with CAD but not in men. Moreover, the lysability of a fibrin clot, which is dependent on fibrinogen properties, was reduced in women with subclinical CAD compared to men at the same stage of the disease, as well as in comparison to women without coronary artery atherosclerosis. These findings suggest that the magnitude of the pathological pathways contributing to premature CAD differs in women and men, and they are discussed in this review. While many gaps in both experimental and clinical studies on sex-related differences in premature CAD exist, further studies on pathological pathways are needed.

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Ayu Ikeningrum, Dyah, Djanggan Sargowo, Novi Kurnianingsih, and Anna Fuji Rahimah. "Type 1 Diabetes Mellitus and Premature Coronary Artery Disease." Heart Science Journal 03, no. 03 (July 1, 2022): 4–9. http://dx.doi.org/10.21776/ub.hsj.2022.003.03.2.

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Cardiovascular disease, which affects more than half of all diabetics, is the leading cause of morbidity and mortality in patients with type 1 and type 2 Diabetes Mellitus (DM). Around 55% of diabetes patients are thought to have it, in comparison to 2-4% of the general population. A significant risk factor for the development of Coronary Artery Disease (CAD) exists in people with Type 1 Diabetes Mellitus (T1DM). However, it is worth noting that the present Models of risk prediction for T1DM have a variety of flaws. CAD risk is expected to double or quadruple over the next two to four decades, and diabetes mellitus is the third most significant risk factor for the etiology of illness. As a result, diabetes increases the chance of developing Acute Coronary Syndromes (ACS), whose incidence surpasses 20% after seven years, compared to a rate of 3.5 percent in non-diabetics – a rate comparable to individuals who have already experienced an Acute Myocardial Infarction (AMI). Additionally, it is crucial to identify any well-defined specific risk factors for T1DM as well as any extra subclinical atherosclerosis that may influence these patients at an advanced stage of disease progression. T1DM patients have more severe lesions, a lower left ventricle (LV) ejection fraction, a higher risk of cardiac events, and a higher rate of silent ischemia when compared to non-diabetics. They continue to have impaired microcirculation and endothelial function, both of which contribute to tissue perfusion problems.

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Paiker, J. E., F. J. Raal, and M. von Arb. "Auto-antibodies against oxidized LDL as a marker of coronary artery disease in patients with familial hypercholesterolaemia." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 37, no. 2 (March 1, 2000): 174–78. http://dx.doi.org/10.1258/0004563001899177.

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Auto-antibodies to oxidized low-density lipoprotein (ox-LDL) are thought to play a pivotal role in the pathogenesis of atherosclerosis. This study investigates the value of auto-antibodies to ox-LDL as a predictive marker of atherosclerosis in patients with both homozygous and heterozygous familial hypercholesterolaemia (FH), who are known to suffer from severe premature atherosclerosis. The influences of well-established risk factors for atherosclerosis such as age, LDL-cholesterol levels and smoking on the results were also determined. Auto-antibody titres to ox-LDL and fasting lipid profiles were measured in 26 homozygous FH patients, 20 heterozygous FH patients without documented coronary artery disease (CAD), 24 heterozygotes with overt CAD and 10 healthy normocholesterolaemic controls. Carotid intima-media thickness, used as an in vivo assessment of atherosclerosis, was also measured in the homozygous FH patients. Ox-LDL titres did not differ between the groups. There was also no association between ox-LDL titres and the LDL-cholesterol level ( P=0·14), presence or absence of CAD ( P=0·69), age ( P=0·50), carotid intima-media thickness ( P=0·51) or smoking ( P=1·0). In conclusion, antibody titres against ox-LDL cannot be used as a predictive marker of the presence or severity of atherosclerosis in patients with FH.

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Cozen, Aaron E., Hideaki Moriwaki, Michal Kremen, Mary Beth DeYoung, Helén L. Dichek, Katherine I. Slezicki, Stephen G. Young, Murielle Véniant, and David A. Dichek. "Macrophage-Targeted Overexpression of Urokinase Causes Accelerated Atherosclerosis, Coronary Artery Occlusions, and Premature Death." Circulation 109, no. 17 (May 4, 2004): 2129–35. http://dx.doi.org/10.1161/01.cir.0000127369.24127.03.

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Horinek, A., R. Ceska, J. Sobra, and M. Vrablik. "Familial defective apolipoprotein B-100 homozygote with premature coronary atherosclerosis. A case report 1." Journal of Internal Medicine 246, no. 2 (August 1999): 235–36. http://dx.doi.org/10.1046/j.1365-2796.1999.00518.x.

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Ibrahim, Rehab Rashad, Khalid Tammam, Salwa Mohammed Ghoneim, Salwa Mohammed Ghoneim, El Sayed Mohammed Farag, and Alaa Elsayed Salama. "Non-Traditional Predictors for Occurrence and Severity of Premature Atherosclerosis in Acute Coronary Syndrome." Egyptian Journal of Hospital Medicine 88, no. 1 (June 9, 2022): 2948–54. http://dx.doi.org/10.21608/ejhm.2022.243001.

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Chakraborty, Rajkumar, Manphool Singhal, Vignesh Pandiarajan, Avinash Sharma, Rakesh K. Pilania, and Surjit Singh. "Coronary arterial abnormalities detected in children over 10 years following initial Kawasaki disease using cardiac computed tomography." Cardiology in the Young 31, no. 6 (January 28, 2021): 998–1002. http://dx.doi.org/10.1017/s1047951121000020.

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AbstractObjective:To evaluate whether Kawasaki disease predisposes to premature atherosclerosis and to assess status of coronary artery abnormalities at least 10 years after diagnosis.Material and methods:A prospective study was carried out on 21 patients who were diagnosed with Kawasaki disease at least 10 years back and are on regular follow-up. The study was conducted on 128 Slice Dual Source computed tomography scanner with electrocardiography-triggered radiation optimised protocols for assessment of coronary artery abnormalities and calcifications.Results:Study cohort had 21 subjects – 15 males and 6 females (age range: 11–23 years; mean: 15.76 + 3.72 years). Mean age at time of diagnosis was 3.21 + 2.48 years. Mean time interval from diagnosis of Kawasaki disease to computed tomography coronary angiography was 12.59 + 2.89 years. Four children had evidence of coronary artery abnormalities on transthoracic echocardiography at time of diagnosis. Of these, two had persistent abnormalities on computed tomography coronary angiography. One subject (4.76%) had coronary calcification that was localised to abnormal coronary artery segment. Four coronary artery abnormalities (one saccular; three fusiform aneurysms) were noted in two subjects.Conclusion:Prevalence of coronary artery calcification is low and, if present, is localised to abnormal segments. This calcification is likely dystrophic rather than atherosclerotic. It appears that coronary artery abnormalities can persist for several years after acute episode of Kawasaki disease. Periodic follow-up by computed tomography coronary angiography is now a feasible non-invasive imaging modality for long term surveillance of patients with Kawasaki disease who had coronary artery abnormalities at time of diagnosis.

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Andreenko, E. Yu, I. S. Yavelov, М. М. Loukianov, A. N. Vernohaeva, O. M. Drapkina, and S. A. Boytsov. "Ischemic Heart Disease in Subjects of Young Age: Current State of the Problem. Features of Etiology, Clinical Manifestation and Prognosis." Kardiologiia 58, no. 11 (November 24, 2018): 24–34. http://dx.doi.org/10.18087/cardio.2018.11.10195.

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In addition to conventional risk factors in young patients with ischemic heart disease (IHD) numerous other risk factors including genetics play an important role in its causation. Molecular genetic testing is recommended for the detection of monogenic diseases with a high risk of developing IHD, such as familial hypercholesterolemia. In majority ofyoung patients, the first manifestation of IHD is an acute coronary syndrome. Young patients with IHD more often have normal coronary arteries or single-vessel coronary disease, and in up to 20% of them cause of myocardial ischemia is not related to atherosclerosis. In general, young patients with IHD have better prognosis. However, there are sex differences in IHD outcomes the prognosis of patients with premature IHD and reason for this is still unclear.

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Gursul, Erdal, Serdar Bayata, Ercan Aksit, and Basak Ugurlu. "Development of ST Elevation Myocardial Infarction and Atrial Fibrillation after an Electrical Injury." Case Reports in Emergency Medicine 2015 (2015): 1–3. http://dx.doi.org/10.1155/2015/953102.

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Electrical energy is a type of energy that is commonly used in daily life. Ventricular premature beats, ventricular tachycardia, ventricular fibrillation, atrial tachycardia, atrial fibrillation, bundle branch blocks, and AV block are arrhythmic complications that are encountered in case of electric shocks. Myocardial infarction is one of the rarely seen complications of electric shocks yet it has fatal outcomes. Coronary arteries were detected to be normal in most of the patients who had myocardial infarction following an electric shock. So, etiology of myocardial infarction is thought to be unrelated to coronary atherosclerosis in these cases. Coronary artery vasospasm is thought to be the primary etiological cause. In our case report, we presented a patient who developed ST elevation MI with atrial fibrillation after an electric shock.

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Journal articles on the topic 'Premature coronary atherosclerosis'

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