Arrhythmias pathophysiology

In the following paragraphs several types of arrhythmia will be discussed with regard to the underlying mechanisms. Since it would be out of the scope of this book on gap junction channels to discuss all possible mechanisms of arrhythmia in detail, readers interested in a complete detailed review of the pathophysiology and clinics of arrhythmia are referred to the reviews by Janse and Wit [1989] and Pogwizd and Corr [1987, 1990] and to the specialized literature. 

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. 

Besides acute arrhythmia, chronic arrhythmia is a common and important clinical problem and chronification of arrhythmia is only poorly understood, although this might be the basis for new antiarrhythmic treatments from a more pathophysiological viewpoint. 

Bauman JL, Schoen MD. Arrhythmias. In DiPiro JT, et al, eds. Pharmacotherapy A Pathophysiologic Approach. 5th ed New York McGraw-Hill 2002. 

Noble, D. and Noble, P. J. Late sodium current in the pathophysiology of cardiovascular disease consequences of sodium-calcium overload. Heart 2006, 92 ivl-iv5. Noble, D. and Varghese, A. Modeling of sodium-calcium overload arrhythmias and... 

Wollnik B, Schroeder BC, Kubisch C, Es-perer HD, Wieacker P, Jentsch TJ. 1997. Pathophysiological mechanisms of dominant and recessive KVLQT1 K+ channel mutations found in inherited cardiac arrhythmias. Hum. Mol. Genet. 6 1943-49... 

This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features - arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve -, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein Ilb/IIIa antagonism. 

International Symposium, Pathophysiology and Drug Treatment of Cardiac Arrhythmias. Preliminary Experience with a New Antiarrhythmlc Drug (Aprindlne), Acta Cardiol., Suppl. 18, 1 (1974). 

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