Precordial electrocardiographic mapping. A technique to assess the efficacy of interventions designed to limit infarct size.

Abstract

THE QUANTITY OF MYOCARDIUM which becomes necrotic following coronary occlusion has been shown to influence both the acute and long-term consequences of myocardial infarction.1 2 Fortunately, experiments now indicate that the size of a myocardial infarct is not irrevocably determined immediately following a coronary occlusion, but can be altered substantially by a number of interventions.3-1-However, the clinical assessment of interventions designed to protect ischemic myocardium has posed considerable difficulty. Precordial electrocardiographic mapping, including analysis of both the ST segment and the QRS complex, which has been developed over the past several years, is now being used in studies on patients with acute myocardial infarction. In this review evidence will be presented which indicates that electrocardiographic mapping, when employed properly and with appropriate awareness of its limitations, can yield valid results and indicate whether or not an intervention modifies either the severity of ischemia itself or the eventual size of an infarction. Epicardial Electrocardiographic MappingThe electrocardiogram has been used in the study of myocardial ischemia and infarction for half a century. In 1918, in an effort to establish the utility of the electrocardiogram as an aid in the diagnosis of myocardial infarction, Smith conducted a systematic study in dogs of the changes in the electrocardiogram following coronary occlusion.12 These experiments demonstrated conclusively that STsegment elevation appears following coronary occlusion; Q waves appeared in tracings recorded five days postocclusion but were not discussed. A detailed description of the epicardial QRS changes of infarction was then provided by Wilson and his colleagues,'3 14 who postulated that a QS wave results from transmission of the negative cavity potential through necrotic myocardium. This theory of Q wave genesis was confirmed by Prinzmetal for some infarcts, but it was found that in other instances a QS complex resulted simply from a balance of vectors directed away from the injured area.'5 '1 Prinzmetal also noted that an epicardial QR complex was produced by a mixture of living and necrotic myocardium in the subjacent tissue.

The relationship between the electrocardiographically estimated infarct size and 1 ‐ and 2‐year survival in acute myocardial infarction

“…Electrocardiographic methods constitute one subgroup, but these methods possess several disadvantages (Lekven et al , 1980). The electrocardiographically estimated infarct size can be expressed in different ways (Muller et al, 1978). The relationship between electrocardiographically estimated infarct size, morbidity and 3-month mortality in this series has previously been described (Herlitz and Hjalmarson, 1984a-c).…”

Body surface distributions of repolarization potentials after acute myocardial infarction. II. Relationship between isopotential mapping and ST-segment potential summation methods.

“…10 The quantitative basis for this is expressed in figures 1-3. First, percentages of total thoracic positivity sensed by left precordial grids varied from 45-70%, related to the distribution of positive potential on the chest surface.…”

Prediction of left ventricular function in acute anterior myocardial infarction by serum creatine kinase activity and precordial ECG mapping

“…Precordial ECGs were recorded ( 1 mV = 10 mm; paper speed 50 mm/s) by a 35-lead blanket (Maroko ct ul., 1972;Muller et a/. , 1978) connected through a switch box with a Siemens-Elema Mingograf 32 recorder.…”