Hugo Roesler

Transient electrocardiographic changes identical with those of acute myocardial infarction accompanying attacks of angina pectoris.

Abstract During spontaneous attacks of angina pectoris, which were observed in two patients, transient changes of the electrocardiogram occurred, such as are usually associated with myocardial infarction. The changes disappeared rapidly. The electrocardiographic features usually held diagnostic of myocardial infarction, namely, significant Q deflections associated with elevation of the S-T segment or inversion of T, do not invariably represent dependable evidence of myocardial infarction. Transient coronary insufficiency, if it is of great magnitude, may in rare instances cause similar temporary changes of the electrocardiogram.

Transient bundle branch block and other electrocardiographic changes in pulmonary embolism

Abstract Transitory electrocardiographic changes which have their onset in right bundle branch block and occur in association with pulmonary embolism are described and their diagnostic significance discussed. The importance of the very early conduction disturbance, occurring within a few hours of the onset of the condition, and the rapidity with which this disturbance regresses are emphasized.

Electrocardiographic changes in funnel chest.

Abstract Thirteen patients with funnel chest were studied. In eight adults (60 per cent) the electrocardiogram showed inversion or notching of the T deflection in multiple precordial leads in association with the right ventricular pattern. In one instance where an unusually deep depression of the sternum caused marked dislocation of the heart to the left, the electrocardiogram in Lead I showed features similar to those associated with dextrocardia. In patients with funnel chest who often complain of precordial pain, inversion of T in right-side precordial leads should not be mistaken for a sign of coronary artery disease. Reading electrocardiograms without knowledge of the chest configuration of the patient might lead to erroneous interpretation.

The occurrence in paroxysmal ventricular tachycardia of ventricular complexes transitional in shape to sinoauricular beats: A diagnostic aid

Abstract Six instances of paroxysmal ventricular tachycardia are reported, which show variations of the ventricular complexes transitional in shape to sinoauricular beats. The variations are caused by transmission of atrial excitations to the ventricles, which mostly results in ventricular fusion beats. The regularity of the ventricular rhythm is only exceptionally disturbed by conduction of atrial excitations. In the presence of paroxysmal ventricular tachycardia, dissociation with interference develops infrequently because of the shortness of the ventricular cycle. When it does occur, the ventricular rate is usually less than 150 per minute. The finding of ventricular complexes which are transitional in configuration to sinoauricular beats may be an aid in the diagnosis of paroxysmal ventricular tachycardia when an independent atrial rhythm is not readily recognizable.

An electrocardiographic pattern of infarction of the interventricular septum, extending from the anterior to the posterior aspect of the heart

Abstract Five cases are reported which presented in the limb leads signs of posterior wall infarction and, simultaneously, in the precordial leads, signs of anteroseptal infarction. Post-mortem examination showed in all cases infarction of the interventricular septum that extended from the anterior to the posterior aspect of the heart and involved variable portions of the anterior or posterior wall adjacent to the septum. Similar cases are quoted from the literature. It is suggested that extensive infarction of the interventricular septum, reaching from the anterior to the posterior aspect of the heart, be considered when the electrocardiogram shows a Q 3 -T 3 pattern and diagnostic signs of infarction in leads from the right side of the precordium, and when the changes in the limb and chest leads indicate the same stage of acute or subacute infarction. A similar electrocardiographic pattern sometimes is observed when infarction in the apical region extends from the anterior to the posterior aspect of the heart.

An electrocardiographic study of high take-off of the R(R′)-T segment in right precordial leads: Altered repolarization∗

Abstract An abnormal electrocardiographic pattern of altered repolarization is described in eight cases. The common finding is an elevation of the R(R′)-T segment over the right side of the precordium, with varying shapes and with varying degrees of extension to the left. While some degree of delay in the excitation of the right ventricular free wall is frequently noted, this is not always the case. The abnormal findings are constant and they are associated with a normal morphologic and functional status of the heart. The abnormal electrocardiographic finding may be misinterpreted as evidence for acute myocardial injury.

Dissociation with interference in the presence of 2:1 atrioventricular block

Abstract Two cases are reported which present dissociation with interference in the presence of 2:1 atrioventricular block. This arrhythmia differs from ordinary dissociation with interference in that the automatic ventricular rhythm is slower than the sinus rhythm, but is faster than the sinoauricular half rhythm. Dissociation with interference combined with 2:1 atrioventricular block is a well-defined arrhythmia which shows the following characteristic features: 1. 1. Dissociated action of the atria and ventricles. The regular ventricular rhythm is occasionally interrupted by shorter ventricular cycles. 2. 2. The ventricular complexes which conclude the shorter cycles show a fixed relationship to a preceding atrial wave, thus suggesting that they are due to conducted atrial excitations. They may or may not differ in shape from the regular ventricular beats. 3. 3. The P wave of the conducted beats show a distinct time relationship to the preceding automatic ventricular beat. Only those atrial impulses are conducted which fall late in diastole after the refractory state of the bundle, caused by transmission of an automatic ventricular excitation, has ended. 4. 4. The refractory period of the bundle can be estimated from the shortest R-P interval of the conducted sinoauricular beats. This “critical” R-P interval may be close to, but is mostly longer than, one sinus period. Complete atrioventricular dissociation develops instead of dissociation with interference when the critical R-P interval plus the time required for conduction of a sinoauricular excitation is longer than the automatic ventricular period. Complete atrioventricular dissociation of this type should not be mistaken for complete atrioventricular block.

Premature beats in atrioventricular rhythm

Abstract Premature beats of atrial and ventricular origin disturbing A-V rhythm in man are reported and compared with observations made by others in the experimental animal. All premature beats were followed by noncompensatory pauses. In one instance evidence was obtained that the atrium was activated by the premature ventricular excitation. In a case of upper A-V rhythm the restored beat after a premature ventricular contraction showed merging of the P wave and the QRS complex. An identical phenomenon was observed in the experimental animal and interpreted as due to temporary improvement in the conductivity of Hiss bundle secondary to retrograde transmission of the premature ventricular impulse to the A-V pacemaker. Upright P waves in Leads II and III were observed in a case in which the sequence of ventricular and atrial contractions indicated the presence of lower A-V rhythm.

High chest leads and minor myocardial infarctions.

Electrocardiographic studies in patients with either a suspected or clear-cut anginal history may reveal a wide variety of findings ranging from altogether normal or borderline normal through patterns compatible with so-called coronary insufficiency, anoxia, ischvmia, injury, to frank infarction. Abnormal findings may appear or may become more outspoken when a tracing is taken during an anginal seizure, whether it be spontaneous or induced. This study is limited to electrocardiographic abnormalities of relatively minor degree, essentially affecting the T deflections only, that emphasize in particular the use of exploring chest leads at a higher level. That the incidence of omissions and commissions in electrocardiographic interpretation is considerable, due to the widespread use of the method by inadequately trained, inadequately experienced, and uncritical physicians, is known. Some of what one may call finer diagnostic points may be overlooked by men otherwise competent in this field; this, as the author has repeatedly noted, refers to the abnormal findings described in this study. It is usually the office patient with a suspected or clear-cut anginal history whose electrocardiogram is likely to reveal only minor changes, in contrast to that of the patient who, obviously ill, is admitted to the hospital and submitted to a study. All our patients, and they are described later in detail, were seen in the office except one: this one was referred, while in the hospital for electroshock therapy, for cardiac evaluation. None of the patients had had a heavy meal or a cold drink nor had any of them smoked just .prior totthe examination. None had received digitalis, quinidine, or adrenaline. None had thyroid dysfunction or anmmia. Three were diabetic. Five were heavy tobacco smokers. None had suffered chest trauma; and none had experienced paroxysmal rapid heart action. One of the patients had a minor degree of aortic regurgitation and showed slight left ventricular hypertrophy. All the others showed normal heart size and sounds and rhythm. Only one exhibited a mild degree of diastolic hypertension. Except for one, a diabetic who also revealed evidence of occlusive arterial disease in the lower limbs, all had the anginal syndrome. One patient was seen but once, all others repeatedly, at intervals of from two weeks to eight years. All electrocardiographic studies were done by the author personally. The high chest leads were taken at the level of the third rib. None of the tracings were obtained during an anginal seizure.

Variations in the deviations of S-T in anterior wall infarction

Abstract Reciprocal deviations of S-T in chest leads from right- and left-side positions occur in clinical cases of anterior wall infarction. They conform to changes observed in experimentally produced ischemia of the heart muscle. When myocardial infarction is of anteroseptal location, elevation of S-T in leads from the right side of the precordium may be accompanied by depression of S-T in chest leads from the left side. Then Lead I may also show depression of S-T, and the resulting features may resemble those sometimes seen in the presence of lateral wall infarction. When myocardial infarction is of lateral location, elevation of S-T in leads from the left side of the precordium may be associated with depression of S-T in leads from the right side. However, when infarction fails to include the superficial muscle layers, or when it is located close to the base of the heart, depression instead of elevation of S-T may be present in leads from the left side of the precordium at the customary level. There is great variability in the deviations of S-T in limb and chest leads in clinical cases of myocardial infarction. One determining factor is the site and extension of infarction. Another important factor is that the the chest leads, unlike direct leads used in the experimental animal, record changes of potential from a far greater area than that covered by an electrode placed directly upon the myocardium, that is, from an area which may include damaged and undamaged myocardium. Thus, positive and negative changes of potential may be mixed and the resultant deviation of S-T will depend on whether the positive or negative potential variation prevails. Therefore, reciprocal deviations of S-T in the chest leads are not invariably observed with anteroseptal or lateral wall infarction. Also, in limb leads, in the presence of anterior wall infarction, elevation of S-T may be inconspicuous in Lead I while marked depression of S-T is noted in Leads II and III. On the other hand, in infarction of posterior site, positive and negative changes in S-T potential which originate in damaged and undamaged parts of the posterior wall may neutralize each other. Thus, Lead III may show no deviation of S-T, while marked depression of S-T is present in Lead I.