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A survey of current literature suggests an increasing interest in both the desirable and undesirable implications of a prolonged QT interval, the former perceived to be the beneficial effect of antiarrhythmic drugs that prolong the duration of ventricular action potential, and the latter considered to be a potential marker for sudden cardiac death in patients with ischemic heart disease. In addition, there has been an increasing interest in the congenital long QT syndrome associated with an apparent dysfunction of the autonomic nervous system and serious, potentially lethal ventricular arrhythmias. Circumstantial evidence suggests that these arrhythmias are due to increased dispersion of repolarization which may be aggravated by psychologic and emotional perturbations. In this review, the associations between the long QT interval, autonomic nervous system, dispersion of repolarization, antiarrhythmic drugs and ventricular arrhythmias are examined. Attention is directed to the difficulties of accurate QT measurement, problems related to the correction of the QT interval for heart rate and sex (QTc), the wide range of normal values and the modest QT alterations after various manipulations of the autonomic nervous system. Clinical conditions associated with marked, moderate and occasional QT lengthening are listed and discussed briefly in relation to the disturbances of nervous system, dispersion of ventricular repolarization and ventricular arrhythmias. It is proposed that the absence of relevant animal models of neurogenic or psychogenic QT prolongation hinders the investigation of the neurogenic factors associated with QT lengthening. QT prolongation is most often induced by antiarrhythmic drugs and ischemic heart disease. However, it is not known whether the occurrence of torsade de pointes type of ventricular tachycardia in patients treated with antiarrhythmic drugs is related to a critical drug dose or a critical degree of QTc prolongation. There is no conclusive evidence that QT lengthening has any predictive value either during the acute phase or during convalescence after myocardial infarction. Also, a serious deficiency in current knowledge is the lack of an established relation between the prolonged QT interval and the dispersion of ventricular repolarization. It is concluded that the number of unanswered questions discussed in this review still makes it difficult to judge when a prolonged QT interval is good, bad or indifferent.

Wall thicknesses were measured and echo densities were evaluated from the left ventricular echograms of 182 patients. The echogram was considered to reflect scar tissue when 1) either the interventricular septum, the posterior left ventricular wall or the anterior left ventricular wall was less than 7 mm thick in mid-diastole and was more echo-producing than its opposing wall or another area of the same wall in a sector scan, or 2) an area of myocardium was 30% less thick than an adjacent area within a sector scan. Myocardial scarring was diagnosed by echocardiography in 52 of the 182 patients. The echocardiographic presence or absence of scarring was confirmed in 95% (173 of 182) of cases, 34 cases by microscopic examination and 139 by surgical appearance. This study shows that M-mode echocardiography is both a sensitive and specfic method for detecting myocardial scar tissue.

The purpose of this study was to determine whether a quantitative relationship existed between a reduction in regional myocardial blood flow, measured by radiolabeled microspheres, and the degree and type of changes in myocardial activation recorded in bipolar left ventricular subepicardial and subendocardial electrograms, in open-chest dogs following acute coronary artery occlusion. We found that the degree of regional myocardial ischemia was related quantitatively to the reduction in amplitude recorded with bipolar electrograms in the subepicardium and subendocardium, and to the increase in duration of subepicardial electrograms. Other characteristics measured in electrograms did not relate to the degree of ischemia. Despite a comparable reduction in regional myocardial blood flow, subepicardial conduction delay exceeded that recorded in the subendocardium, which often exhibited accelerated conduction.

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