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Specialized Circulations in Susceptible Tissues
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
These hemodynamic factors provide complexities to the measurement and interpretation of coronary blood flow under different conditions. As already pointed out, it is still possible to discuss mean pressure and mean flow as coronary resistance, “steal” and coronary reserve, but one must be more circumspect in interpretation of pressure–flow relationships with respect to microvascular change. These principles are of crucial importance for the interpretation of coronary flow in disease states and under conditions where cardiac function is altered. Takotsubo cardiomyopathy (O'Rourke et al., 2019c), discussed in this chapter, is a case in point. An even broader spectrum on coronary thrombosis and myocardial infarction is added in this book to explain advances in clinical management of coronary disease over the last 100 years.
Coronary Artery Disease
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Treatment of CAD is focused on reducing the cardiac workload. This is achieved by decreasing oxygen demand while improving blood flow through the coronary artery. Over time, the goal is to stop and reverse atherosclerosis. Percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) can improve coronary artery blood flow. Fibrinolytic drugs may be used to dissolve an acute coronary thrombosis, for some patients. The medical treatments for CAD are based on cardiac function, present symptoms, and underlying disorders. Antiplatelet drugs are recommended to stop clot formation. Statins are used to lower LDL cholesterol, improving outcomes in part by stabilizing atheromatous plaques and also by causing better endothelial function. Beta-blockers can reduce angina symptoms by decreasing myocardial oxygen demand and reducing heart rate and contractility. Calcium channel blockers are often effective, especially when used with beta-blockers to manage angina and hypertension. Nitrates slightly dilate the coronary arteries to decrease venous return. For patients with CAD and LV dysfunction, the angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are the preferred medications.
The Cardiovascular System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
The root cor- also refers to the heart, as in coronary thrombosis, a blockage of a coronary artery by a blood clot. The root actually comes from the Latin word corona, which means crown; with only a little imagination, one can see in Figure 5.1 that the two coronary arteries sit atop the heart and circle it somewhat like a crown.
Association between serum SCUBE1 levels and thrombus burden in patients with ST-segment elevation myocardial infarction
Published in Acta Cardiologica, 2021
Arafat Yıldırım, Mehmet Kücükosmanoglu, Nermin Yildiz Koyunsever, Yusuf Cekici, Mustafa Dogdus, Erhan Saracoglu, Salih Kilic
ST-segment elevation myocardial infarction (STEMI) is currently one of the major causes of cardiovascular mortality and morbidity [1]. Coronary thrombosis is unequivocally the most important pathophysiological process underlying STEMI. High thrombus burden in the coronary artery responsible for STEMI (infarct related artery, IRA) was shown to be associated with distal emboli, stent thrombosis, no-reflow phenomenon and long-term mortality and morbidity [2–5]. No-reflow phenomenon is an important problem in STEMI patients undergoing primary percutaneous coronary intervention (PPCI) and is associated with a high coronary thrombus burden [2]. In addition, no-reflow phenomenon is known to be associated with long-term mortality and morbidity in STEMI patients [2]. Platelet and endothelial adhesion molecules play an important pathological role in intracoronary thrombus formation.
Subacute stent thrombosis in a patient with COVID-19 pneumonia
Published in Baylor University Medical Center Proceedings, 2021
Mohamed Ayan, Swathi Kovelamudi, Malek Al-Hawwas
COVID-19 may predispose to both venous and arterial thromboembolic disease due to excessive inflammation, hypoxia, and diffuse intravascular coagulation.3–5 Although these patients are at risk of acute coronary events from de novo coronary thrombosis, COVID-19 may increase the incidence of stent thrombosis, as shown in this and other reports.6–8 Most patients with severe COVID-19 have laboratory evidence of severe inflammatory response, similar to cytokine release syndrome, with persistent fevers, elevated inflammatory markers (e.g., D-dimer, ferritin), and elevated proinflammatory cytokines.9,10 This severe inflammatory response with massive release of tissue factors and interleukin-6 may promote the coagulation cascade and platelet activation. Additionally, there is evidence of direct invasion of endothelial cells by the virus, potentially leading to cell injury and promotion of a procoagulable state.10
Investigational drugs for the treatment of acute myocardial infarction: focus on antiplatelet and anticoagulant agents
Published in Expert Opinion on Investigational Drugs, 2019
Srikanth Yandrapalli, Gabriela Andries, Shashvat Gupta, Abdel Rahman Dajani, Wilbert S. Aronow
High-risk plaque rupture is the most frequent cause of coronary thrombosis and advances in our understanding the pathophysiology of plaque development and rupture led to the development of drugs which are currently being used to treat an AMI. Biological changes related to platelet hyperreactivity, increased coagulability, and inflammation has been identified as important factors which can accentuate thrombotic responses in vulnerable atherosclerotic plaques [4–9]. Reperfusion is the goal in AMI and is achieved by either mechanical revascularization with percutaneous coronary interventions (PCI) and coronary artery bypass grafting (CABG), or pharmacologic revascularization using fibrinolytic agents to dissolve the obstructive thrombus [10,11].