Arrhythmias developing after 48 hours post-myocardial infarction are associated with adverse outcomes, unlike those occurring in the peri-infarction period.
Despite considerable progress in management over the recent years, coronary artery disease (CAD) remains the leading cause of death in the industrialised world. It is estimated that CAD is responsible for causing 152,000 deaths per year in the UK and one in eight deaths world-wide. Many of these deaths are attributed to the development of ventricular tachyarrhythmias during periods of myocardial ischaemia or infarction. Myocardial ischaemia is characterised by ionic and biochemical alterations, creating an unstable electrical substrate capable of initiating and sustaining arrhythmias, and infarction creates areas of electrical inactivity and blocks conduction, which also promotes arrhythmogenesis. The purpose of this chapter is to review some of the metabolic changes associated with cardiac ischaemia, their relevance to electrophysiological instability, and the clinical manifestation and management of some of the more common arrhythmias that follow cardiac ischaemia. Particular attention is given to the peri-infarction period (arbitrarily accepted as within 48 h of the index myocardial infarction) as arrhythmias are most likely to be seen around this time, and are considered to be non-indicative of long-term prognosis. In contrast, arrhythmias developing in the post-infarction period (after 48 h) have been demonstrated to be associated with an adverse outcome. Regardless of the anti-arrhythmic therapy used in treating peri- and post-infarction arrhythmias, it is presumed that patients who had a myocardial infarction or who have left ventricular dysfunction will also receive other appropriate therapies, such as aspirin, ss-blockers, cholesterol lowering agents and angiotensin converting enzymes inhibitors.
Ghuran et al. (Mon,) studied this question.