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In Vivo and In Vitro Cardiac Preparations Used in Antiarrhythmic Assays
Published in John H. McNeill, Measurement of Cardiovascular Function, 2019
Two major determinants of the incidence and severity of ischemia-induced arrhythmias are the size of the ischemic zone and serum potassium concentration.4,15,16 It is not surprising that, within limits, the larger the ischemic insult the greater the number and severity of arrhythmias. Elevated serum potassium levels reduce arrhythmias and vice versa. It is therefore important to ensure that animals have similar size occluded zones and serum potassium levels. For a detailed review of the methods using coronary occlusion, particularly in rats, see reviews by Curtis et al. (1987) and Cheung et al. (1993).4,17
Morphologic features and pathology of the elderly heart
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Atsuko Seki, Gregory A. Fishbein, Michael C. Fishbein
The morphologic appearance of MI is dependent on the acuity of the event. Myocardial necrosis is clearly evident within 2 days of infarction (47). Histologically, findings are apparent within a few hours of coronary occlusion. Wavy fibers indicative of ischemic injury appear first. Then, necrotic fibers show increased eosinophilia, loss of cross-striation, loss of cytoplasmic granularity, and nuclear pyknosis or karyolysis. Within hours, neutrophils “marginate” in capillaries in the necrotic zone. Wavy fibers may be seen in infarcts only minutes old. By one week, fibroblastic proliferation and collagen deposition are evident, although it is not until the third week that proliferation of connective tissue is the dominant feature. The fibrotic (or healed) MI looks the same, whether it is months or years old. If reperfusion occurs related to thrombolytic therapy or angioplasty, infarcts may become hemorrhagic.
Cardiovascular system
Published in Brian J Pollard, Gareth Kitchen, Handbook of Clinical Anaesthesia, 2017
Redmond P Tully, Robert Turner
Modern treatment of myocardial infarction following coronary occlusion is early reperfusion therapy, using either primary percutaneous coronary intervention (PPCI) or thrombolytic therapy. This has been demonstrated to reduce the infarct size, although not to eliminate myocardial ischaemia completely (Figure 2.3). This is because paradoxically, the reperfusion essential to myocardial salvage can induce myocardial damage itself – this phenomenon is termed ‘myocardial reperfusion injury’. It can be categorized clinically into myocardial stunning and reperfusion arrhythmias, microvascular obstruction (MVO) and lethal myocardial reperfusion injury.
Therapeutic angiogenesis in coronary artery disease: a review of mechanisms and current approaches
Published in Expert Opinion on Investigational Drugs, 2021
Bharat Narasimhan, Harish Narasimhan, Marta Lorente-Ros, Francisco Jose Romeo, Kirtipal Bhatia, Wilbert S. Aronow
Angiogenesis results in increased capillary density, and is often driven by hypoxia-inducible factor (HIF-1), a key mediator during periods of ischemic insult. Arteriogenesis on the other hand is triggered by both hemodynamic forces (shear stress) [10] and inflammation [11], resulting in arterial development over longer periods of days or even weeks. Occlusion of the coronary artery results in increased shear stress across the collateral endothelium, triggering changes in gene expression driven by the sensing of deformations within the cell membrane [12]. The extent of endothelial activation is directly proportional to the pressure changes across the blockade and hence the degree of occlusion. Studies indicate that total coronary occlusion is likely the most effective in promoting arteriogenesis [13]. Furthermore, the release of several collateral growth factors including bFGF, MCP-1, and TGF-B has been found to be directly correlated with the extent and duration of the occlusion [14]. Finally, vasculogenesis relies on the migration and replication of EPCs or endothelial colony forming cells (ECFCs), which serve as the backbone of newly formed vessels [15,16]. Mesenchymal stem and progenitor cells (MSPCs) function as pericytes which serve to support vessel growth and maintain microvessel stability [17,18]. A summary of these mechanisms is provided in Table 1 and Figure 1.
Predicting and improving outcomes of transcatheter aortic valve replacement in older adults and the elderly
Published in Expert Review of Cardiovascular Therapy, 2020
Antonio Giulio Bruno, Laura Santona, Tullio Palmerini, Nevio Taglieri, Cinzia Marrozzini, Gabriele Ghetti, Mateusz Orzalkiewicz, Nazzareno Galiè, Francesco Saia
In one of the largest registries available, the incidence of coronary occlusion was 0.7% (44/6688 TAVR patients), with a mortality rate of 40.9% at 30-day and 45% at 1-year. Fatality rate was close to 100% when attempts to reopen the occluded coronary failed, 22% in patients successfully treated with ostial stenting (feasible in 81% of the patients), and 50% in patients in which emergency coronary bypass was needed because of stenting failure [115]. Coronary occlusion was more frequent in women and it was related to anatomic risk factors: in 80% of the cases coronary height was <12 mm,, and in 64% of the subjects, sinus of Valsalva diameter was <30 mm [115]. The risk of coronary occlusion is higher after valve in valve (VIV) procedures (ranging from 1.9% to 2.4%) [116]. The highest risk is associated with stentless surgical valves (including homograft) and pericardial surgical valves with leaflets sutured outside the stent (i.e. Mitroflow; Trifecta; St. Jude Medical). With these types of surgical prosthesis, more than with others, the leaflets of the dysfunctioning valve may extend outwards and reach the coronary ostia or the sino-tubular junction, thus compromising coronary flow [114,116]. While acute coronary compromise seems more frequent with BE valves, delayed coronary occlusion (which occurs hours or days after the index procedure) seems more frequent with SE prostheses [117,118].
Bioprosthetic valve fracture during valve-in-valve transcatheter aortic valve replacement
Published in Baylor University Medical Center Proceedings, 2020
Mohanad Hamandi, Ikenna Nwafor, Katherine R. Hebeler, Alexander Crawford, Allison T. Lanfear, Justin Schaffer, Karim Al-Azizi, Srinivasa Potluri, William T. Brinkman, Katherine Harrington, Molly Szerlip, J. Michael DiMaio
In our case series, the mean preoperative aortic valve gradient was 44 mm Hg, which was reduced to 14.9 mm Hg following VIV TAVR, then to 7.3 mm Hg following BVF. However, at 30-day follow-up, the mean aortic valve gradient was 15.0 mm Hg, similar to the mean post-VIV TAVR gradient. This is likely because intraoperative gradients were obtained with Doppler echocardiogram while the patient was in supine position, which may yield different results compared to measurements taken when patients can be optimally positioned on their side. Also, intraoperative gradients may be lower after pacing and due to the effects of sedation. Furthermore, there were two cases of coronary occlusion in our case series, one that was the suspected cause of our only case of operative mortality and another that was successfully surgically repaired. Coronary obstruction is a clinically significant complication of VIV TAVR, with rates as high as 2.3%.16 It more commonly occurs in externally mounted leaflet or stentless bioprosthetic valves.16 Overall, available studies show that BVF VIV TAVR is a safe and feasible treatment method that yields clinical improvements in certain subsets of high-risk patients. However, in future studies, we recommend the use of a more uniform system of reporting valve gradients and areas to aid in the comparison of results.