Morphologic features and pathology of the elderly heart
Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich in Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Gender and age discrepancies are striking. Females comprise 90%–95% of reported cases. Most patients are elderly and postmenopausal (96,115–119). Common symptoms include abrupt onset of angina-like chest pain and dyspnea resembling acute coronary syndrome (108,112,115,116). Symptoms are usually preceded by emotional or physical stress, such as family death, abuse, a harsh argument, exhausting work, or an earthquake (108,112,115). Sympathetic hyperactivity and increased catecholamine levels may play a role in myocardial stunning and contractile dysfunction (120). Plasma catecholamine levels are elevated in patients with takotsubo cardiomyopathy (108,116,119), and the histological findings are similar to catecholamine-induced changes, including contraction-band necrosis (120). Neurologic or psychiatric disorders are more prevalent in takotsubo cardiomyopathy (118). There is also an increased prevalence of migraine headaches and affective disorders (121). A multimodal MRI study demonstrated structural and functional alterations in regions primarily involved in cardiac control and emotional processing such as the amygdala and hippocampus (122).
Coronary Artery Disease
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
An acute coronary syndrome is usually caused by an acute thrombus in an atherosclerotic coronary artery. The plaque can become unstable or inflamed, then rupture or split. Thrombogenic material is exposed, activating platelets and the coagulation cascade, resulting in an acute thrombus. Cross-linking and aggregation of platelets occurs. Even with slight obstruction, atheromas can rupture and cause thrombosis. In more than half of all cases, pre-syndrome stenosis is less than 40%. While stenosis severity predicts the symptoms that will occur, it cannot always be predictive of acute thrombotic events. The thrombus quickly slows blood flow to areas of the myocardium. In most cases, spontaneous thrombolysis occurs. However, the obstruction does remain for long enough to cause tissue necrosis.
Acute Aortic Dissection
Stephen M. Cohn, Matthew O. Dolich, Kenji Inaba in Acute Care Surgery and Trauma, 2016
Early and accurate diagnosis of AAD is critical. A careful history and physical examination, along with a high degree of clinical suspicion, should suggest the diagnosis. The most common symptoms for patients presenting with AAD are chest, back, and/or abdominal pain. Pain is almost invariably present and may be sharp or tearing in nature. Many patients also have a history of hypertension, and a personal or family history of aneurysm or connective tissue disorder should raise suspicion. Possible physical examination abnormalities include a murmur of aortic regurgitation and an abnormal pulse exam. A plain chest radiogram may show a widened mediastinum, irregular aortic contour, deviated trachea, enlarged cardiac silhouette, or pleural effusion, but is not diagnostic of AAD. An electrocardiogram should be obtained to evaluate for acute coronary syndrome. Be aware that as an ascending dissection may involve the coronary ostia, myocardial ischemia may be present. Therefore both entities, myocardial infarction and aortic dissection, may need to be evaluated if clinically indicated.
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
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- Coronary Arteries