Principles of Electrophysiology

Extract

[...] The basis for poor propagation of the depolarizing wave front in the heart usually results from pathologic changes in patients with structural heart disease, including coronary artery disease, left ventricular hypertrophy, and heart failure. Fibrotic changes in the heart, with increases in collagen and intracellular matrix as seen in hypertrophy or infarction, can lead to areas of slow conduction and provide portals for reentry. Changes in the gap junction proteins have been noted in hypertrophy with increases of connexin43. These changes typically result from advanced age or the presence of structural heart disease, such as a prior myocardial infarction or a cardiomyopathy. [...]

[...] Variations in the duration and shape of the cardiac action potential exist depending on its location in the heart. Likewise, alterations of ion channel expression and activity in disease states contribute to prolongation of the action potential. The atrial action potential has a typical duration of 100 to 200 msec, whereas the ventricular action potential typically lasts 250 to 300 msec. Different layers of the ventricle exhibit marked changes in the action potential. Epicardial cells have a prominent phase 1 compared with endocardial cells, in which phase 1 is blunted. [...]

[...] Arenito PRINCIPLES OF ELECTROPHYSIOLOGY Introduction The function of the human heart requires rhythmic beatings occurring on the average 70 times a minute hours a day, for 80 or more years. The close to 3 billion contractions of the cardiac musculature that must occur without fail are coordinated by an intricate network of specialized electrically active cells that are integrated with the myocytes that comprise the predominant mass of the heart. Any loss of electrical activity, even for a few seconds, results in syncope; loss of electrical activity for a few minutes may end in death. [...]

[...] Triggered activity is an uncommon mechanism of cardiac arrhythmias. Triggered activity occurs when a preceding depolarization does not repolarize completely before depolarizing again. Early afterdepolarizations (EADs) occur during phase 2 and phase 3 of the action potential. The basis for EADs seems to involve the L-type calcium channel. EADs are facilitated by increased repolarization times, as seen in either congenital or acquired long QT syndromes. With drugs that prolong the QT interval, such as erythromycin, quinidine, sotalol, and procainamide, the block of potassium channels involved in repolarization leads to prolongation of the action potential. [...]

[...] Cardiac Electrophysiology Ion channels are integral membrane-spanning proteins, which allow the rapid movement of specific ions, most importantly Na+ , , Cl- , and Ca2+ , across the cell membrane at rates of 108 ions per second. The opening and closing of the channels occur through a process of gating, whereby changes in the voltage, ligand, or receptor associated with the channel lead to alterations in the conformation of the proteins that activate or inactivate the channel pore. Voltage gating is the predominant method of regulating ion channels in the heart and is found in sodium and various potassium channels. [...]