Teasing Death in Acute Inferior Infarct

The acute inferior infarct has certain characteristics that separate it from other infarcts. It is fair to say that no two acute infarcts are the same. Each acute infarct is unique in its own way. Several variables determine each infarction and affect the degree of muscle damage, the acute complications, and the long-term effects on the myocardium, which indirectly affect other systems and the general health of the individual patient. Independent variables in each acute infarction include the duration of vessel occlusion before revascularization, the presence or absence of revascularization, the pre-conditioning of the affected myocardium with prior ischemia, the presence of collaterals, the extent/location of previous cardiac injury, the medications given before and during the infarction, vessel size, location of occlusion, thrombus burden, previous coronary artery bypass surgery, anatomy of other non-culprit coronaries, the age/gender/size of the patient, and any other co-morbidity. In the 1980’s, acute myocardial infarctions were mainly treated with thrombolytics. The percutaneous transluminal coronary angioplasty (PTCA) procedure was occasionally complicated by acute vessel closure resulting in de novo, acute injury in the hospital or in the cardiac catheterization laboratory. In the past two decades, percutaneous coronary intervention (PCI) for acute ST-elevation myocardial infarction (STEMI) has become the standard of care. This has become quite effective and relatively safe due to the availability of thrombus extraction devices, IIb/IIIa antiplatelet agents and undoubtedly, stents. An acute vessel closure following PCI, in 2010, is very rare, in contrast to frequent vessel closure following PTCA in 1985. Despite the wide variability in acute injury, one can find a common thread in inferior infarctions that is distinctly different from other infarctions. In the past 25 years of treating and intervening on acute infarctions, both in the emergency department/intensive care unit or in the cardiac catheterization laboratory, it has become apparent that inferior infarctions are tricky and frightening to the healthcare provider early in their course. Yet, they are benign in the long run. Therefore, the term “teasing death in acute inferior infarction” is appropriate. The inferior injury manifests itself in various ways; each one is deadly if the cardiologist is unavailable, but all are easily treated and rendered harmless by a treating cardiologist. The inferior injury presents itself as a myriad of life-threatening manifestations that are usually easy to treat and equally easy to prevent in the catheterization laboratory. The vengeance of inferior injury includes recurrent ventricular tachycardia/fibrillations, bradycardia/various degrees of atrioventricular (AV) heart block, atrial arrhythmia (atrial fibrillation), and hypotension/shock. As serious and deadly as they seem, these complications can be effectively treated in the setting of inferior injury. The inferior injury presents itself as a deadly acute infarction, but in fact it is much less malignant than its counterpart, anterior injury. It has a deadly-looking façade, but with proper management, it renders very little harm. The patient with acute inferior injury is at risk to encounter death, but in reality, this is more of a tease and once the patient is done with teasing death, he or she is quite well, has a good long-term prognosis, and has a healthy outlook. In contrast, when a patient with acute anterior injury encounters the same life-threatening complications like arrhythmia, heart block or shock, it is an ominous sign and the patient is not teasing death. He or she is actually dying and if the patient survives, long-term prognosis is poor and the patient will never be healthy again. One can speculate on why the acute complications of inferior injury are more benign than other infarcts. The ventricular arrhythmia in acute inferior infarction is mostly due to few irritable individual myocardial cells in the right ventricle rather than extensive area of necrotizing myocardial cells in the septum, apex, anterior or lateral wall. The heart block is due to a localized transient ischemia to the AV node and usually resolves shortly after reperfusing the AV node artery (with thrombolytics or PCI). It is very rare nowadays to see permanent, complete AV node block following inferior infarct. In the acute setting, the initial transient heart block is often seen immediately after reperfusing the vessel in the catheterization lab and can be easily treated with back-up temporary pacing for few hours. The bradycardia/hypotension phenomenon is also due to an autonomic reflex and does not correlate with the extent of damage. The same reflex can be triggered equally, by a small or a large inferior injury. The potency of the reflex reaction is dependent on the individual patient and does not correlate with the severity of infarction. The hypotension and bradycardia in inferior infarct is benign, short-lived and easily treated with dopamine and temporary pacing. It is commonly seen immediately after reperfusing the coronary artery in the catheterization lab. One can be ahead of the game and start IV fluid/dopamine before an acute inferior infarct patient is brought to the cardiac catheterization lab, and can insert a temporary pacemaker in the catheterization lab prior to PCI. This also explains why these patients are so volume-dependent and are sensitive to nitrates. On the other hand, hypotension in other acute infarctions is a sign of severe pump failure and is often times irreversible. The ventricular arrhythmia, bradycardia, heart block, and transient shock in acute inferior infarction should be treated immediately (defibrillation, anti-arrhythmic therapy, temporary pacing, IV fluid, dopamine). When treated early or implemented prior to reperfusing the culprit vessel, these acute complications are benign and have no bearing on the long-term prognosis. The patients with inferior injury and all or some of the acute complications (those who teased death) who have a successful PCI should do just as well as the patients with none of the acute complications (those who do not tease death). Having ventricular fibrillation, bradycardia, heart block or shock in other acute infarction is a sign that death is imminent and it is not just a tease! Dr. Bitar has been an interventional cardiologist since 1989. He can be contacted at jbbitar@aol.com