Reflections on reentry and focal activity

Abstract

Initiation and maintenance of reentrant arrhythmias, such as ventricular tachycardia and fibrillation in the acute phase of myocardial ischemia, may be due to different mechanisms. The characteristics of circus movement reentry, both with and without involvement of an anatomic obstacle, are discussed. The concept of wavelength of a reentrant circuit as calculated by the product of refractory period and conduction velocity is emphasized. To maintain circus movement tachycardia in an acutely ischemic myocardium, the ischemic tissue mass must be larger than the wavelength. For maintenance of fibrillation, several independent reentrant wavelets must be simultaneously present. Agents that prolong wavelength (by lengthening refractory period, increasing conduction velocity or both) may prevent reentry. Experiments are described that show the effectiveness of lidocaine, which depresses action potentials of ischemic myocardial cells, in preventing ventricular fibrillation when administered before coronary artery occlusion in isolated pig hearts. Ventricular premature depolarizations or beats are usually necessary to initiate reentrant rhythms. They may be caused by reflection, a type of reentrant excitation involving slow conduction, or by electronic transmission over short segments of depressed or unexcitable tissue. An example of microreentry in a 4 mm segment of papillary muscle exposed to elevated extracellular K + concentrations, resulting in a ventricular premature beat, is shown. Focal mechanisms, such as abnormal automaticity or triggered activity, may also be responsible for premature impulses. Agents that suppress premature depolarizations may be effective against reentrant arrhythmias, even when they do not affect the reentrant mechanism itself. Experiments are described, showing that moricizine HCl suppresses abnormal automaticity in isolated papillary muscle, partially depolarized by application of electric current.