China
Africa
Explore chapters and articles related to this topic
What Is Plugging Your Heart Arteries? Plaque Formation, Types of Plaque, and Plaque Rupture
Published in Mark C Houston, The Truth About Heart Disease, 2023
Atherosclerosis is a hardening and narrowing of your arteries due to obstruction with plaque, which is made up of fatty material, oxidized cholesterol and fats, inflammatory cells, white blood cells, immune cells, T lymphocytes, activated smooth muscle cells, cell debris, and other substances. As the plaque grows, it blocks the artery, thereby threatening blood flow. The severity of the blockage will determine the distal blood flow from the area of plaque obstruction. This blockage can be up to 99% and patients may have minimal symptoms of chest pain or shortness of breath (unless they are engaged in heavy exercise). This is referred to as atherosclerosis or atherosclerotic cardiovascular disease (Figure 15.1). Atherosclerosis is a slow process that starts very early in life (Figure 15.2). The older you become, the more likely you are to have CHD with plaque formation. This can be evaluated with many different tests, such as a coronary computerized tomographic angiogram (CTA), cardiac magnetic resonance imaging or angiogram (MRI or MRA), or coronary arteriogram. Another type of test is an ultrasound of the coronary arteries, called intravascular ultrasound (IVUS) (Figures 15.2 and 15.3). The IVUS has shown us a lot of new information about the natural history of CHD. It can determine the age of onset, presence, location, and severity of CHD both in the lumen and in the subendothelial layer of the coronary arteries (Figure 15.3). By the age of 50, over 85% of patients will have CHD to some extent.
Valvular Heart Disease and Heart Failure
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Kali Polytarchou, Constantina Aggeli
Treatment of AS includes surgical aortic valve replacement (SAVR), transcatheter aortic valve implantation (TAVI), balloon angioplasty, and medical therapy. The latter includes treatment of risk factors for atherosclerosis. When symptoms of HF occur, treatment with angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, diuretics, or digoxin is indicated. Statins are not recommended, as there is no clear evidence of benefit in AS.18,19
Omega-3 Fatty Acids and NO from Flax Intervention in Atherosclerosis and Chronic Systemic Inflammation
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
It is also generally understood that diet and lifestyle factors play a key role in atherosclerosis. The emphasis is usually on saturated fats in the diet and on alcohol use, smoking and physical inactivity. But there is now a common understanding that atherosclerosis is an inflammatory disease, and there is substantial scientific literature on the role of reactive oxygen species (ROS) in plaque formation, and these arise largely from mitochondria metabolic activity. In fact, ROS have been shown to promote atherosclerotic plaque formation. (5)
Understanding the role of alternative macrophage phenotypes in human atherosclerosis
Published in Expert Review of Cardiovascular Therapy, 2022
Kenji Kawai, Aimee E. Vozenilek, Rika Kawakami, Yu Sato, Saikat Kumar B Ghosh, Renu Virmani, Aloke V. Finn
Atherosclerotic lesions develop over time and hamper blood flow to vital organs. Narrowing of coronary and peripheral vessels due to atherosclerosis causes clinical symptoms (i.e. chest pain/angina pectoris for coronary arterial disease and claudication for peripheral arterial disease). A sudden rupture of an otherwise non-flow limiting coronary atherosclerotic plaque can cause thrombosis, which itself can lead to ischemia [1]. Rupture of coronary plaque is the leading cause of myocardial infarction, a major cause of death [2]. In 2019, as reported by the World Health Organization (WHO), ischemic heart disease was the leading cause of death and accounted for 16% of all deaths. The incidence of ischemic heart disease is expected to continue increasing in coming years, due to increasing prevalence of co-morbidities such as obesity, diabetes, and metabolic syndrome [3].
Achieving coronary plaque regression: a decades-long battle against coronary artery disease
Published in Expert Review of Cardiovascular Therapy, 2022
Venkat S. Manubolu, Matthew J. Budoff
For years, scientific experts have sought to reverse and prevent atherosclerosis from occurring. Significant resources have been invested to prevent atherosclerosis through risk factor management, including dietary and behavioral alterations as well as medicinal interventions. Numerous studies indicate that the majority of myocardial infarctions (MI) occur in lesions with less than 50% stenosis [2]. Contemporary data from large-scale registries, such as CONFIRM and PROMISE, suggest that the global atherosclerotic plaque burden and high-risk plaque features on cardiac computed tomography angiography (CCTA) are prognostically relevant for adverse cardiac events beyond stenosis severity or clinical risk scores [3–5]. Furthermore, CCTA is now the preferred technique to risk-stratify patients with low and intermediate risk chest pain in the 2021 guidelines [6]. When it comes to treating coronary artery disease (CAD), and identifying coronary atherosclerosis, recent data suggest that we need to reshape our treatment framework, especially with regard to nonobstructive CAD. The focus now encompasses therapies that target inflammation, metabolic activity, susceptibility to vascular thrombosis, and other factors involved in atherogenesis.
Citrullinated and homocitrullinated low- density lipoprotein in rheumatoid arthritis
Published in Scandinavian Journal of Rheumatology, 2021
A Rajamohan, B Heit, E Cairns, L Barra
To our knowledge, there are no prior studies investigating citrullination of LDL. In our study, LDL incubated with PAD2 resulted in a high proportion of ApoB100 citrullinated residues (35% of arginines). ApoB100 has fewer arginines than lysines and the degree of modified amino acids in CitLDL is lower than in HomoCitLDL, which would lead to a lower frequency of epitopes and may explain the lack of detectable anti-CitLDL antibodies in our study population. Despite the differences in the degree of modified amino acids, we found that CitLDL and HomoCitLDL were equally potent inducers of foam cell formation. Given the structural similarity of citrulline to homocitrulline, it is possible that LDL modified in either fashion interacts with the same receptors, therefore accounting for the similar effect of CitLDL and HomoCitLDL on foam cell formation. HomoCitLDL is known to exhibit atherogenic receptor binding properties with low affinity for hepatic LDL receptor, impairing LDL metabolism (30), but high macrophage scavenger receptor binding, including to CD36, SR-A1, and LOX-1, leading to cholesterol accumulation and foam cell formation (19, 30). HomoCitLDL has also been shown to promote smooth muscle cell proliferation and to affect endothelial cell function by increasing interactions with monocytes, the production of reactive oxygen species, and cell death (30). These effects are important contributors to the progression of atherosclerosis and its complications.