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Grand Summary and Conclusions
Published in Mark C Houston, The Truth About Heart Disease, 2023
Coronary heart disease is caused by a reduction in the blood supply due to obstruction by a plaque in one or more of the coronary arteries to the heart muscle (myocardium), which results in decreased delivery of fresh blood, oxygen, and nutrients. Less commonly, vasospasm may cause CHD. The plaque is made up of fatty material, oxidized cholesterol and fats, inflammatory cells, white blood cells, immune cells, smooth muscle cells, and other substances. The top five CHD risk factors (hypertension, diabetes mellitus, dyslipidemia (abnormal cholesterol), obesity, and smoking) must be redefined based on new information, and the top 25 CHD risk factors need to be assessed as well. There are actually over 400 risk factors for CHD. There are an infinite number of insults to the coronary artery to cause CHD but only three finite responses: inflammation, oxidative stress, and vascular immune dysfunction. Seventy-five percent of myocardial infarctions are caused by unstable plaque rupture and a blood clot (thrombus) in a coronary artery without previous angina symptoms.
Case 24
Published in Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta, Clinical Cases, 2021
Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta
A coronary angiogram is a central investigation for coronary heart disease. It is both diagnostic and potentially therapeutic. It helps with the diagnostic process by ascertaining whether or not coronary vasospasm or any form of local arterial dissection is present. It also localises lesions of tight coronary artery stenosis. It is performed by a trained cardiologist via arterial puncture of the radial (or femoral artery), and radio-opaque contrast demonstrates the findings.
What determines health?
Published in Jim Connelly, Chris Worth, Making Sense of Public Health Medicine, 2018
Three risk factors, in particular, have been identified as major causes of coronary heart disease: cigarette smoking, high blood pressure and high blood cholesterol. Each of these risk factors is, in theory, modifiable by changing behaviour. Reducing or, preferably, quitting smoking, eating less dietary salt and eating less saturated fats and more monosaturated fats would reduce risks from smoking, high blood pressure and raised blood cholesterol, respectively.
Myristicin regulates proliferation and apoptosis in oxidized low-density lipoprotein-stimulated human vascular smooth muscle cells and human umbilical vein endothelial cells by regulating the PI3K/Akt/NF-κB signalling pathway
Published in Pharmaceutical Biology, 2022
Liang Luo, Huiying Liang, Luoying Liu
Coronary heart disease refers to heart disease caused by atherosclerosis (AS) of the coronary arteries, narrowing or occluding the vascular lumen, leading to myocardial ischaemia, hypoxia or necrosis. AS, the main cause of coronary heart and peripheral vascular disease, has been identified as a chronic inflammatory disease (Libby et al. 2019). AS is characterized by arterial intimal lesions, accumulation of complex carbohydrates, fibrous tissue hyperplasia and calcification, as well as arterial wall thickening and hardening (Feig et al. 2012; Gistera and Hansson 2017). Furthermore, previous reports have demonstrated that the accumulation of human vascular smooth muscle cells (hVSMCs) and dysfunction of human umbilical vein endothelial cells (HUVECs) are associated with the pathogenesis of AS. For example, Tao et al. (2019) revealed that long non-coding RNA (lncRNA) cancer susceptibility 11 improves AS by downregulating IL-9 and regulating VSMC apoptosis and proliferation. A study by Soltani et al. (2016) demonstrated that curcumin protects against ionizing radiation-induced AS by suppressing the adhesion of HUVECs to monocytes. Furthermore, oxidized low-density lipoprotein (ox-LDL) is considered to be the main marker of AS, and the accumulation of ox-LDL may lead to chronic inflammation, further accelerating the development of AS (Bian et al. 2020; Yang et al. 2020). However, the mechanism of ox-LDL in regulating the proliferation and apoptosis of hVSMCs and HUVECs requires further exploration.
The changing landscape of cardiac rehabilitation; from early mobilisation and reduced mortality to chronic multi-morbidity management
Published in Disability and Rehabilitation, 2021
With the combined prominence of increasing survival rates from coronary heart disease occurring in the twenty first century [55], there has been a corresponding increase in the incidence and prevalence of subsequent heart failure [51,52,56]. This evidence also demonstrates the onset of symptomatic disease diagnosis at an older age. The common co-morbidities prevalent among coronary heart disease patients typically include: diabetes, heart failure, stroke, peripheral arterial disease, and arthritis (Table 1) [51], all of which can individually and collectively benefit from a lifestyle management and prevention programme. Exercise adaptations for those with diabetes is now a key consideration as they make up 25% (and increasing) of patients attending CR [57]. The National Audit for Cardiac Rehabilitation in the UK, reports that those attending rehabilitation typically have at least two co-morbidities [50]. With programmes increasingly having to adapt to these co-morbidities, it may be both clinically- and cost-effective to combine rehabilitation and prevention with other key chronic diseases illustrated in Figure 2. Examples including lower functioning or older patients with heart failure, pulmonary disease, peripheral arterial disease and falls prevention could participate in the same exercise sessions as they will likely be working at similar intensities with similar symptoms, and where combined endurance, strength and balance activities are becoming more prominent; they have been shown to better enhance function and endurance compared to only aerobic endurance activities [58].
Study on the relationship between SLCO1B1 and ApoE gene polymorphisms and the risk of coronary heart disease in the Mongolian population
Published in Clinical and Experimental Hypertension, 2021
Rui-Bing Niu, Xiao-Xian Dong, Li-Ping Guo, Li Pan, Yue-Qin Hai, Xiao-Xiao Chen, Bao-Sheng Duan
Coronary atherosclerotic heart disease, commonly known as coronary heart disease, is a heart disease resulting from either coronary artery stenosis or myocardial ischemia, hypoxia, or necrosis caused by functional changes in the coronary artery. Epidemiological studies have shown that this disease is affected by a variety of factors, which are generally considered to be the result of a combination of genetic and environmental factors (1–3). Multiple studies have proved that many genes affect the occurrence and development of coronary heart disease. The risk of getting coronary heart disease may be different in various regions and races due to discrepancies in gene distribution. This could be the result of genetic polymorphism, which affects the metabolism and the efficacy of statins for managing blood lipids, thereby affecting the occurrence and development of coronary heart disease (1234,5). The polymorphisms 388A>G and 521T>C are two common single nucleotide polymorphisms (SNP) of the SLC01B1 gene, the polymorphisms rates of which show differences between regions and races. The ApoE gene has two main SNPs, 526C>T and 388T>C, which is related to the efficacy of statins. This gene is considered to be a predictor of the early onset of coronary disease and may participate in the occurrence and development of atherosclerosis as a genetic factor (6–8).