Myocardial infarction pathophysiology

St. John Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction. Pathophysiology and therapy. Circulation 2000 101 2981-2988. 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

One of the most important chronic alterations in the heart is the chronic phase after myocardial infarction. The postinfarction period is known to be associated with an increased risk for sudden cardiac death and for the occurrence of cardiac arrhythmia. Changes in conduction properties have been identified [Dillon et al., 1988], although the cells exhibit normal or near normal action potential characteristics [Wit and Janse, 1992]. Thus, cellular electrophysiology does not explain the complete pathophysiology of the arrhythmogenic substrate. Thus, other factors, for example structural changes and passive electrical properties, have to be taken into account. 

Several experimental studies have provided support for the hypothesis that coronary spasm plays a major role in the pathophysiology of myocardial infarction during the administration of sulprostone. However, the possibility of myocardial infarction is not mentioned in the product information. 

Stringer KA, Lopez LM. Uncomplicated myocardial infarction. In DiPiro JT, et al, eds. Pharmacotherapy A Pathophysiologic Approach. 5th ed. New York McGraw-Hill 2002. 

To understand the evolution of therapy of the acute coronary syndrome (ACS), which includes unstable angina, acute myocardial infarction, and interventional therapy— percutaneous coronary intervention (PCI), it is most useful to trace the historical events that provided a rationale for the use of anticoagulant and antiplatelet drugs, The focus of this chapter is upon the explosion in knowledge of the physiology of the hemostatic mechanism and will trace the rational development of therapy based upon the pathophysiology of the ACS over the past 40 years. 

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... 

Topaz O, Taylor AL, Interventricular septal rupture complicating acute myocardial infarction from pathophysiologic features to the role of invasive and noninvasive diagnostic modalities in current management. Am J Med 1992 93(6) 683-688. Review. 

Roberts R, Morris D, Pratt CM (1994) Pathophysiology, recognition, and treatment of acute myocardial infarction and its complications. In Schlant RC, Alexander RW (eds) Hurst s the heart arteries and veins, 8th edn. McGraw Hill, New York, NY, pp 1107-1184... 

FIGURE 14-4. Key components of the pathophysiology of cardiac remodeling. Myocardial injury (e.g., myocardial infarction) results in the activation of a number of hemodynamic and neurohormonal compensatory responses in an attempt to maintain circulatory homeostasis. Chronic activation of the neurohormonal systems results in a cascade of events that affect the myocardium at the molecular and cellular levels. These events lead to the changes in ventricular size, shape, structure, and function known as ventricular remodeling. The alterations in ventricular function result in further deterioration in cardiac systolic and diastolic function, which further promotes the remodeling process. 

Electrophysiological Dysfunction During Myocardial Infarction A Pathophysiological Process Mediated by Alterations in Cellular Lipid Metabolism 355... 

ELECTROPHYSIOLOGICAL DYSFUNCTION DURING MYOCARDIAL INFARCTION A PATHOPHYSIOLOGICAL PROCESS MEDIATED BY ALTERATIONS IN CELLULAR LIPID METABOLISM... 

Hiccup is a forceful, involuntary inspiration commonly experienced by fetuses, children, and adults. Its purpose is unknown, and its pathophysiology still poorly understood. Short hiccup bouts are mostly associated with gastric distention or alcohol intake. They resolve spontaneously or with simple folk remedies and do not require medical attention. In contrast, prolonged hiccup is a rare but disabling condition that can induce depression, weight loss, and sleep deprivation. A wide variety of pathological conditions can cause chronic hiccup myocardial infarction, brain tumor, renal failure, prostate cancer, and abdominal surgery are only a few of these conditions. 

Loussouam G, Sternberg D, Nicole S et al (2016) Physiological and pathophysiological insights of Navl.4 and Navl.5 comparison. Front Pharmacol 6 314 Lu ML, De Venecia T, Patnaik S, Figueredo VM (2016) Atrial myocardial infarction a tale of the forgotten chamber. Int J Cardiol 202 904-909... 

Burke, A. and Virmani, R. (2007) Pathophysiology of acute myocardial infarction., Med. Clin. 

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