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Myocardial ischemia pathophysiology

Silent Myocardial Ischemia Pathophysiology and Perioperative Management Anders G. Hedman... [Pg.525]

Over the past years, research in the cardiovascular field has been fruitful and experimental work has contributed to better understanding of the pathophysiology of myocardial ischemia, enabling new therapeutic treatments to emerge. In this book some important conceptual advances are highlighted in self- contained mini- reviews. [Pg.199]

Calcium overload as a pathogenic mechanism of cell injury has been incriminated in various disorders of cardiac and skeletal muscle including catecholamine-induced cardiac necrosis (8, 13), myocardial ischemia (8, 13), myopathies (9, 17), and malignant hyperthermia (18). Of interest is that in the majority of these pathophysiological entities calcium antagonists effectively suppress calcium accumulation and cell necrosis (8, 13, 18). [Pg.183]

Acute myocardial ischemia Adrenaline administration is the gold standard for anaphylaxis treatment but it may cause acute myocardial ischemia. This pathophysiology is a different entity from Kounis syndrome [19 ]. [Pg.183]

Given the understanding that release of cardiac troponin into the circulation reflects myocardial cell death, it is understandable why, clinically, therapies are oriented toward inhibiting the pathophysiologic processes of thrombosis, fibrinolysis, platelet aggregation, and inflammation leading to ischemia and, ultimately, myocardial cell death. Several markers of ischemia have been proposed [2], and research and development studies are underway to adequately validate their clinical usefulness or lack of evidence. These include the topic of this chapter (ischemia-modified albumin [IMA]), as well as choline, unbound free fatty acids, and nourin. [Pg.2]

Sildenafil was the first oral treatment for ED and is the most extensively evaluated (35). Overall success rates in patients with cardiovascular disease of 80% or greater have been recorded with no evidence of tolerance, Patients with diabetes with or without additional risk factors, with their more complex, and extensive pathophysiology, have an average success rate of 60%. In randomized trials to date, open-label or outpatient monitoring studies the use of sildenafil is not associated with any excess risk of myocardial infarction, stroke, or mortality (38-40), In patients with stable angina pectoris there is no evidence of an ischemic effect due to coronary steal, and in one large, double-blind, placebo-controlled, exercise study sildenafil 100 mg increased exercise time and diminished ischemia (41), A study of the hemodynamic effects in men with severe CAD identified no adverse cardiovascular effects and a potentially beneficial effect on coronary blood flow reserve (42), Studies in patients with and without diabetes have demonstrated improved endothelial function acutely and after long-term oral dose administration, which may have implications beyond... [Pg.509]

Figure 5-3. Complete spectrum of acute coronary pathophysiological process from initiation of atherosclerosis to cell death. Biomarkers released at different stages include interleukin 6 (IL-6), myeloperoxidase (MPO), soluble CD40 ligand (sCD40L), high-sensitivity C-reactive protein (Hs-CRP), ischemia-modified albumin (IMA), cardiac troponins I and T (cTnT and cTnl, respectively), B-type natriuretic peptide (BNP), and N-terminal proBNP (NT-proBNP). Of these, only the troponins and BMPs are myocardial specific. Figure 5-3. Complete spectrum of acute coronary pathophysiological process from initiation of atherosclerosis to cell death. Biomarkers released at different stages include interleukin 6 (IL-6), myeloperoxidase (MPO), soluble CD40 ligand (sCD40L), high-sensitivity C-reactive protein (Hs-CRP), ischemia-modified albumin (IMA), cardiac troponins I and T (cTnT and cTnl, respectively), B-type natriuretic peptide (BNP), and N-terminal proBNP (NT-proBNP). Of these, only the troponins and BMPs are myocardial specific.
R. Bolli, M. Zughaib, X.Y. Li, X.L. Tang, J.Z. Sun, J.F. Triana and P.B. McCay, Recurrent ischemia in the canine heart causes recurrent bursts of free radical production that have a cumulative effect on contractile function. A pathophysiological basis for chronic myocardial stunning. J. Clin. Invest. 96, 1066 1084 (1995). [Pg.67]

The pathophysiology that underlies this disease process is dynamic, evolutionary, and complex. An understanding of the determinants of myocardial oxygen demand (MVO2), regulation of coronary blood flow, the effects of ischemia on the mechanical and metabolic function of the myocardium, and how ischemia is recognized is important in understanding the rationale for the selection and use of pharmacotherapy for IHD. [Pg.263]


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See also in sourсe #XX -- [ Pg.528 , Pg.529 ]




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