The heart
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella in Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Acute coronary syndromes are a continuum of conditions that includes unstable angina, non-ST elevation myocardial infarction (non-STEMI) and ST elevation myocardial infarction (STEMI). It begins when a previously stable atherosclerotic plaque in a coronary artery destabilizes and loses its protective fibrous cap. When a plaque destabilizes, the necrotic core is exposed, which allows platelets to attach to form a platelet plug. Formation of the platelet plug is accompanied by activation of the clotting cascades, leading to the rapid formation of a blood clot in the coronary artery. This forming clot rapidly occludes blood flow to the myocardium to cause ischemia and angina pain at rest. If the clot resolves or breaks up quickly, no permanent damage will occur to the myocardium. However, if the occlusion of blood flow persists, myocardial injury and necrosis will begin to occur. Initially, the injury will only involve the subendocardial layer of muscle and is characterized by ST depression and T wave inversion without ST elevation (hence the term non-STEMI) on an ECG. Prolonged occlusion of coronary blood flow will result in myocardial injury that involves the full thickness of the heart wall (transumral) and is characterized by marked elevation of the ST segments (STEMI) on the ECG.
Coronary Artery Disease
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
Acute coronary syndromes cause a variety of symptoms. Stimuli from the heart and other thoracic organs cause discomfort. This is described as pressure, burning, indigestion, aching, sharp pain, or stabbing pain. It is difficult to assess the amount of ischemia present only by symptoms, unless the infarction is very large. The symptoms often mimic those of angina. Complications of acute coronary syndromes may involve electrical dysfunction, myocardial dysfunction, or valvular dysfunction. Electrical defects include arrhythmias and conduction defects. Myocardial effects include heart failure, free wall rupture, interventricular septum rupture, pseudoaneurysm, ventricular aneurysm, cardiogenic shock, and formation of a mural thrombus. Valvular defects usually involve mitral regurgitation. Additional complications of acute coronary syndromes include recurring ischemia and pericarditis. If pericarditis occurs 2–10 weeks after an MI, it is called post-MI syndrome, also known as Dressler syndrome.
Clinical syndromes in acute coronary syndrome
K Sarat Chandra, AJ Swamy in Acute Coronary Syndromes, 2020
Virtually all acute coronary syndromes are caused by thrombosis developing on a culprit coronary atherosclerotic plaque, resulting in acute reduction of coronary blood flow. If it results in total obstruction it may cause infarction with corresponding regional myocardial necrosis. The occurrence of infarct with subtotal obstruction as in NSTEMI, is due to distal embolisation of thrombi (usually platelet thrombi). Rarely, total obstruction may not result in infarct, because of the presence of rich collaterals. The vast majority of myocardial infarctions occurs in patients with coronary atherosclerosis with more than 90% associated with superimposed luminal thrombi. Arbustini et al. [13] found coronary thrombi in 298 of patients dying with clinically documented acute myocardial infarction. Of these thrombi, 74 were caused by plaque erosion. The proximate cause of this luminal thrombus – ruptured plaque or plaque erosion – is variable and is influenced by age and gender.
Acute right ventricular myocardial infarction
Published in Expert Review of Cardiovascular Therapy, 2018
Arif Albulushi, Andreas Giannopoulos, Nikolaos Kafkas, Stylianos Dragasis, Gregory Pavlides, Yiannis S. Chatzizisis
Coronary artery disease remains the main cause of morbidity and mortality globally [1]. Acute coronary syndrome occurs when there is a decreased blood flow or complete cessation of flow in one of coronary arteries. Acute right ventricular myocardial infarction (RVMI) was first described in the literature in 1974 in a series of six patients [2]. RVMI occurs in one-third to one-half of patients presenting with inferior myocardial infarction (MI) [3–5], and it significantly contributes to the clinical and hemodynamic instability that these patients are presented with [6–8]. Occasionally, RVMI can accompany anterior wall MI, and very rarely it can occur in isolation [9]. Right ventricle (RV) involvement in the setting of inferior MI increases the inhospital morbidity and mortality [10]. Almost, half of RVMI patients have poor outcomes secondary to electrical or hemodynamic instability [11]. Effective fluid resuscitation aiming to restore the preload, and subsequently maintain adequate cardiac output, along with percutaneous or pharmacological revascularization is first-line therapy of acute RVMI [12]. It is very important to early recognize the RV involvement in a patient presenting with acute MI, not only for prognosis, but also to choose the specific therapy, including aggressive primary percutaneous coronary intervention (PCI), with particular attention to RV branch revascularization, all in order to avoid any unwanted detrimental complications associated with this diagnosis.
Differential value of eosinophil count in acute coronary syndrome among elderly patients
Published in The Aging Male, 2020
Isa Sincer, Yilmaz Gunes, Asli Kurtar Mansiroglu, Gulali Aktas
Acute coronary syndrome is a clinical condition that causes significant mortality. Acute coronary syndrome develops because of thrombus formation over ruptured or eroded coronary plaque. Coronary plaque instability have multiple underlying mechanisms [9]. The most common pathway causing acute coronary syndrome is plaque rupture with systemic signs of inflammatory activation and local inflammatory cell infiltration [9,10]. Inflammatory cells, such as macrophages, lymphocytes, and neutrophils, have been extensively studied in the pathogenesis of acute coronary syndromes [9]. Eosinophils, basophils, and mast cells, as cellular mediators of allergic inflammatory responses, may also play a pathogenetic role in subgroup of ACS patients [11]. The thrombus formation and coronary vasoconstriction were found to be associated with eosinophils [12–14]. Eosinophil degranulation was supposed to be related with the pathogenesis of ACS [11]. Ingredients of eosinophilic granules may interfere with inflammatory cell activation. It has been shown that eosinophilic granule proteins led to platelet activation and thrombus formation by inhibition of thrombomodulin [15]. In addition, proinflammatory and prothrombotic state in endothelial cells were induced by activated eosinophils, which release potent peroxidase products [16]. Eosinophils are also the source of circulating IL-17, which has a role in coronary instability [17]. A greater eosinophil infiltration was found in large red thrombi rather than the underlying atherosclerotic plaques. This finding suggests that activation of eosinophils in coronary plaque is not local but systemic [18].
Cardiac sarcoidosis – an expert review for the chest physician
Published in Expert Review of Respiratory Medicine, 2019
Jamie S. Y. Ho, Edwin R. Chilvers, Muhunthan Thillai
Patients with sarcoidosis have been shown to be at increased risk of cardiovascular events compared to age- and sex-matched controls with an overall hazard ratio of 1.65 after adjusting for risk factors such as smoking status, diabetes and hypertension [8]. One explanation for this may be common inflammatory pathways between atherosclerosis and sarcoidosis. The true risk of acute coronary syndrome is difficult to ascertain, partly due to the active exclusion of subjects with evidence of previous cardiovascular disease in many studies but also as true CS may present similarly to acute coronary syndrome with symptoms of angina-like chest pain and shortness of breath, further complicating disease presentation [9]. Sarcoidosis has been shown to cause myocardial infarction through direct infiltration of coronary arteries [10] and is also associated with increased risk of pulmonary embolism [11].
Related Knowledge Centers
- Chest Pain
- Diabetes
- Necrosis
- Perspiration
- Syndrome
- Nausea
- Cardiac Muscle
- Hemodynamics
- Signs & Symptoms
- Coronary Arteries