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Coupling of the Left Ventricle with the Systemic Circulation
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Intra-aortic balloon counterpulsation (IABP) was introduced in 1968 (Kantrowitz et al., 1968) for treatment of cardiogenic shock complicating acute coronary occlusion with extensive evolving myocardial infarction. With present emphasis on early aggressive management of acute myocar-dial infarction, patients with angioplasty or coronary artery bypass surgery, use of IABP as a routine measure in such situations has decreased, and its use is questioned unless further mechanical complications such as free-wall heart rupture (O'Rourke, 1973; Windsor et al., 1976), ventricular septal rupture or papillary muscle rupture have occurred and urgent surgical correction is scheduled (Thiele et al., 2012, 2018; Zeymer and Thiele, 2017; Zeymer et al., 2017). In their most recent contribution, Thiele et al. (2018) question any use of IABP in acute ischemic heart syndromes. One obvious indication, however, is Takotsubo cardiomyopathy, which typically presents as acute ST segment elevation myocardial infarction in older females following unaccustomed physical exercise or profound fright with tachycardia. At diagnostic angiography, coronary arteries are either completely normal or show minor hemodynamically insignificant coronary lesions. This is discussed in Chapter 14.
Adult Autopsy
Published in Cristoforo Pomara, Vittorio Fineschi, Forensic and Clinical Forensic Autopsy, 2020
Cristoforo Pomara, Monica Salerno, Vittorio Fineschi
There are several ways to examine the heart of an infant, and each has adherents. No matter which method is chosen, the external description of the heart is very important. Cardiac enlargement may indicate the presence of hypertrophic cardiomyopathy, hypertension, or even maternal drug abuse. Hypertrophic cardiomyopathy occurs as a consequence of many different polymorphisms, some of which do not produce obvious changes that are macroscopically obvious, whereas others, like LAMP2 cardiomyopathy (lysosomal-associated membrane protein 2), manifest anatomical changes that are diagnostic. When suspicion of inheritable cardiomyopathy is strong, DNA testing must be requested, if for no other reason than to determine whether the rest of the family must be screened. The normal heart is vaguely cone-shaped. If its shape is globular or irregular, as in the case of ventricular aneurysm, then extensive sampling for subsequent histological examination is necessary. If the subepicardium has a grayish tinge, this suggests congenital heart disease. In the case of preexisting heart failure and chronic anemia, the myocardium may appear pale, spotted, or even hemorrhagic when there is acute heart failure or heart rupture. The consistency of the left ventricle can be hard (suggesting hypertrophy, fibrosis, amyloidosis, calcification, or rigor mortis) or soft (due to acute myocardial infarct, myocarditis, dilated cardiopathy, or decomposition). Most of the older methods of dissection are not practical for routine diagnostic purposes, which is why only the inflow–outflow and the “short-axis” methods have survived.
The Pericardium
Published in P. Chopra, R. Ray, A. Saxena, Illustrated Textbook of Cardiovascular Pathology, 2013
Hemopericardium As the name indicates there is collection of pure blood in the pericardial sac consequent to penetrating injury to the heart, rupture of the heart due to full thickness myocardial infarction, rupture of thoracic aneurysm of aorta into pericardial cavity, extensive tumor metastasis, bleeding diathesis, etc. The pericardium may appear shaggy, hemorrhagic and irregular (Fig. 11.10).
Cardiac fibrosis: emerging agents in preclinical and clinical development
Published in Expert Opinion on Investigational Drugs, 2021
Roberto Spoladore, Giulio Falasconi, Giorgio Fiore, Silvana Di Maio, Alberto Preda, Massimo Slavich, Alberto Margonato, Gabriele Fragasso
Another open question is timing of action, in particular whether it is better to aim to prevent fibrosis formation completely or to just modulate its deposition. For example, contrasting fibrotic scar development during the early acute phase of myocardial infarction is object of concern about the risk of heart rupture, since in this specific setting fibrosis is actually a reparative process.
A review on the current literature regarding the value of exosome miRNAs in various diseases
Published in Annals of Medicine, 2023
Senjie Li, Dongqing Lv, Hong Yang, Yan Lu, Yongping Jia
The most common cardiovascular disease worldwide is coronary atherosclerotic heart disease (CHD), which is mainly caused by myocardial hypoxia and ischaemia due to the accumulation of lipid plaques and thrombosis [32]. The characteristic plaque formation and aggregation of CHD can be controlled by inhibiting the early inflammatory response; therefore, reducing the inflammatory reaction and the resulting damage is the key to protecting the vascular intima [33,34]. Studies have found that MSC-derived exosome miR-133 regulates inflammation levels by controlling the snail 1 gene [35]. Exosomal miR-34a, miR-124 and miR-135b can suppress inflammation through polarization of M2 macrophages [36]. Serum-derived exosomal miR-126 can inhibit atherosclerosis and reduce the risk of stable coronary heart disease [37]. Adipose-derived stem cell (ADSCs)-derived exosome miR-146a reduces cellular inflammation and fibrosis [38]. One study of myocardial infarction found that the MSC-derived exosomes miR-19a and miR-144 protected the myocardium by reducing the apoptosis of cardiomyocytes mediated through the PTEN/AKT pathway [39,40]. MiR-125 also plays a cardioprotective role by regulating autophagic flux [41,42]. Clathrin is a highly conserved protein, which mainly plays a major role in transport in the human body. Exosome miR-214 from ADRCs has been proven to inhibit cell death through clathrin endocytosis and reduce the risk of heart rupture in acute myocardial infarction [43]. Myocardial ischaemia–reperfusion injury (MIRI) increases the difficulty of follow-up treatment. Thus, the smaller the degree of reperfusion injury, the better the prognosis and recovery of the myocardium. Exosomes from MSCs – such as miR-132, miR-21 and miR-210 – can improve myocardial health by promoting vascular regeneration [44–46]. Additionally, miR-25-3p and miR-486-5p can play a cardioprotective role by regulating myocardial apoptosis and necrosis, thereby reducing the area of myocardial infarction [47,48]. The exosomes miR-211/222 of ADSCs and miR-133a-3p of macrophage migration inhibitory factor-engineered umbilical cord MSCs (MIF-ucMSCs) regulate MIRI by reducing fibrosis and inhibiting apoptosis [49,50]. The abovementioned studies indicate a close relationship between exosomal miRNAs and the cardiovascular system (Table 1).