Ventricular Premature Systoles Research Articles

Using Three-Dimensional Lorenz Scatter Plots to Detect Patients with Atrioventricular Node Double Path Caused by Interpolated Ventricular Premature Systoles: A Case Study

A series of related electrophysiology phenomena can be caused by the occurrence of interpolated ventricular premature contraction. In our recent three-dimensional Lorenz R-R scatter plot research, we found that atrioventricular node double path caused by interpolated ventricular premature contraction imprints a specific pattern on three-dimensional Lorenz plots generated from 24-hour Holter recordings. We found two independent subclusters separated from the interpolated premature beat precluster, the interpolated premature beat cluster, and the interpolated premature beat postcluster, respectively. Combined with use of the trajectory tracking function and the leap phenomenon, our results reveal the presence of the atrioventricular node double conduction path.

Lipomatöse Hypertrophie des Vorhofseptums: Kardial bedingte Synkope bei Hamartom des rechten Herzvorhofs

A previously well 40-year-old woman suddenly collapsed and had to be resuscitated by an emergency physician. Admitted to hospital she remained unconscious and needed artificial respiration. Diagnostic tests failed to find evidence for pulmonary embolism, myocardial infarction or myocarditis. ECG monitoring in the intensive care unit merely revealed occasional unifocal ventricular premature systoles. Echocardiography was within normal limits. She remained in coma without spontaneous respiration. Cranial computed tomography and serial electroencephalograms indicated brain death. Autopsy revealed lipomatous hypertrophy (hamartoma) of the atrial septum with extensive bleeding into it as the most likely cause of (unrecorded) malignant cardiac arrhythmias.

Electrocardiographic ischemic ST-T changes and ventricular premature systoles

41928 consecutive electrocardiograms were statistically analyzed for the presence of ventricular premature systoles (VPSs) and ischemic ST-T changes in different age groups. VPSs were found in 2314 tracings, whereas signs of myocardial ischemia were noted in 10448 records. VPSs appeared to be more prevalent in the presence of ischemic changes than in the absence of ischemia, and those VPSs in cases with ischemic changes showed a higher correlation with aging. 456 electrocardiograms were then selected to correlate the morphology of VPSs and the areas of myocardial ischemia based on the following criteria: (1) VPSs with the same morphology were present in both limb and precordial leads, and (2) only one representative record was used on each patient who had more than one tracing showing VPSs. It was found that, especially in cases with inferior or anterolateral wall ischemia, right bundle branch block (RBBB) type VPSs appeared to arise from these ischemic areas, whereas such a correlation was less evident in left bundle branch block (LBBB) type VPSs. Although LBBB type VPSs were generally considered benign, those with superiorly oriented QRS axes appeared to be more closely associated with organic cardiac lesions than those with inferiorly oriented axes. Clinical significance of the morphology of VPSs may thus be substantiated.

Mobitz II atrioventricular block due to infra-Hisian block and bundle branch extrasystoles

An asymptomatic elderly male presented with complete right bundle branch block, left anterior fascicular block and Mobitz Type II second degree atrioventricular block. In addition, he was noted to have ventricular premature systoles. Electrophysiologic studies demonstrated two apparently different mechanisms for the second degree A-V block--infra-Hisian block and A-V block due to bundle branch extrasystoles arising in the affected right bundle branch. Concealed conduction of the bundle branch extrasystoles as the proximate cause of infra-Hisian block could not be excluded. However, both forms of A-V block were evidently dependent upon significant distal conduction system disease; this consideration was felt to warrant permanent pacemaker implantation.

Effects of intraventricular conduction disturbances on the incidence and characteristics of ventricular premature systoles.

Effects of intraventricular conduction disturbances on the incidence and characteristics of ventricular premature systoles.

Role of intraventricular conduction disturbances in ventricular premature systoles

Ten thousand electrocardiograms were reviewed with reference to intraventricular conduction and ventricular premature systoles. Ventricular premature systoles were found in 444 electrocardiograms, an overall incidence of 4.44 percent. The incidence was small in the presence of normal intraventricular conduction (3.73 percent) and greater in the groups with abnormal intraventricular conduction (9.80 percent), increasing in parallel with the degree of conduction delay. The coupling interval was significantly longer in tracings revealing intraventricular conduction disturbances than in normal tracings. Studies of QRS configuration and mean frontal QRS axis of the dominant and ectopic beats disclosed: (1) a positive correlation between the QRS duration of sinus and premature beats; (2) a significantly greater angle between the QRS axes of sinus and ectopic beats in the presence of abnormal intraventricular conduction; and (3) in groups with intraventricular conduction delay, a QRS axis of premature systoles commonly either directed away from the region of the blocked bundle or suggesting an additional delay in the remaining nonblocked fascicles. From these data we conclude that (1) ventricular premature systoles are more likely to originate from the area of intraventricular conduction delay, and (2) the ectopic impulse seems to invade and at least partially utilize the other fascicles of the Purkinje system for ventricular excitation. The clinical significance of more frequent ventricular premature systoles in patients with cardiac disorders than in normal subjects should be reemphasized.

The effect of bretylium tosylate on the normal and digitalis-sensitized dog heart

Investigations were made of the effect of bretylium tosylate, an antiarrhythmic drug, on automaticity, atrioventricular conduction time, intraventricular conduction time, and sinus rate in the digitalis-sensitized and normal, intact dog heart. Bretylium and acetylstrophanthidin decreased sinus rate 27 and 18 per cent, respectively. Acetylstrophanthidin given after bretylium pretreatment caused a 36 per cent decrease in sinus rate. Bretylium and acetylstrophanthidin each increased atrioventricular conduction time (P-H interval). With right atrial pacing at a constant rate, bretylium increased atrioventricular conduction time 36 per cent while acetylstrophanthidin increased this time by 25 per cent. Together, bretylium and acetylstrophanthidin increased conduction time 111 per cent, chiefly in the A-V-H subinterval. Bretylium initially increased then subsequently decreased automaticity. The average ventricular escape time increased 190 per cent by bretylium. Acetylstrophanthidin, given after bretylium, decreased ventricular escape time 50 per cent, as compared to 80 per cent when given alone. Bretylium produced ventricular premature systoles and ventricular tachycardia in 7 of 17 dogs during the short period of increased automaticity. This finding as well as the effect to decrease sinus rate and to increase atrioventricular conduction time may limit the clinical usefulness of bretylium.

Antazoline in the treatment of cardiac arrhythmias

Antazoline was administered in sixty-five episodes of various types of cardiac arrhythmia. A complete suppression of the ectopic beats was achieved in five out of six episodes of premature atrial systoles and in twenty-one of the twenty-four episodes of ventricular premature systoles. Conversion to sinus rhythm was observed in seven out of ten and four out of five episodes of paroxysmal atrial and nodal tachycardia respectively. Six out of ten episodes of ventricular tachycardia were controlled by intravenous therapy. However, the drug proved to be ineffective in cases of atrial fibrillation. The side-effects were few and transitory, consisting of nausea, vomiting and drowsiness.

Recognition and therapy of digitalis toxicity

Complicating the recognition of digitalis toxicity are certain electrophysiological phenomena which may result in arrhythmias which mimic toxic effects of the glycosides. In particular, the “rule of bigeminy”, aberrancy of intraventricular conduction, ”concealed” toxicity, concealed conduction into the AV junction, and exit block complicate the diagnosis of excessive digitalization. Of the various arrhythmias indued by digitalis, atrial tachycardia with block, nonparoxysmal junctional tachycardia, bidirectional “ventricular” tachycardia, ventricular premature systoles, ventricular tachycardias, multiple ectopic arrhythmias, AV dissociation, and the coexistance of conduction defects with ectopic beats or rhythms are of particular interest either (1) because of a high degree of correlation with digitalis toxicity or (2) because the recognition of the arrhythmia may present complexities which need consideration. The discussion in this review focuses on these complexities of arrhythmia interpretation as a manifestation of digitalis toxicity.

Cardiocirculatory effects of glucagon in patients with congestive heart failure and cardiogenic shock

Cardiocirculatory Effects of Glucagon in Patients with Congestive Heart Failure and Cardiogenic Shock EZRA A. AMSTERDAM, MD/ROBERT ZELIS, MD/JAMES F. SPANN, Jr., MD, FACC EDWARD J. HURLEY, MD, FACC and DEAN T. MASON, MD, FACC Davis, California Although the powerful inotropic property of glucagon is well established in isolated heart muscle and experimentd animals, the efficacy of the agent in patients with severe cardiac malfunction has not been determined. The purpose of this study was to define the cardiocirculatory effects of glucagon in patients with congestive heart failure or cardiogenie shock. Accordingly, the hemodynamic actions of intravenously administered glucagon (50 k there was a small but significant (P < 0.05) rise in heart rate (93 to 99). In the 5 patients of both groups whose cardiac output rose, the maximal increase was 14%. In the 3 patients with cardiogenic shock whose blood pressure increased, the increases were 5, 11 and 30%, respectively. These data suggest that glucagon, as administered in these studies, produces inconsistent hemodynamic improvement in patients with congestive heart failure and cardiogenic shock ahd that when favorable changes occur, they are usually of small magnitude. Signs and Symptoms of the Different Causes of Endocarditis Dr. FELIX ANSCHOTZ Dafmstadt, West Germany Knowledge of the causative inflammable process of the heart valves is important to understanding of the origin, progress, prognosis and treatment of the valvular disease. It is impossible to describe valvular heart disease with the aid of hemodynamic studies alone. The origin of the endocarditis is the central problem because of the consequences in therapy and prophylaxis. The differential diagnosis of endocarditis is described by our own studies in which the signs and symptoms are related in each case to the autopsy findings (137 cases of rheumatic heaxt disease, 85 cases of subacute bacterial endocarditis, 44 cases of acute bacterial endocarditis and 40 cases of rafe causes of endocarditis) . It is easier to recognize carditis in acute rheumatic fever than in cases of chronic valvular disease in which the inflammation doubtless influences the progress of the valvular damage. In these cases other possible explanations of inflammation must be considered. Subacute bacterial endocarditis, too, will be easy to recognize, particularly if the bacterial culture is positive. Often abacterial endocarditis may be hard to diagnose because of its indistinct symptoms. The central problem is to find the strains, which is difficult because many patients have already been given antibiotics. In some cases it is impossible to diagnose the cause of the endocarditis definitely even with the help of the most modern clinical studies. Hemodynamic Effects of Glucagon in Patients with Fixed-Rate Pacemakers WILLIAM W. ASHLEY, MD/DAVID M KAMINSKY, MD/JANET I. LIPSKI, MD ARTHUR C. WEISENSEEL, Jr., MD/EPHRAIM DONOSO, MD, FACC and CHARLES K. FRIEDBERG, MD, FACC New York, New York The effects of glucagon (50 clg/kg) on cardiac output (dye dilution) and brachial arterial pressure were studied in 7 patients, aged 57 to 73, with fixed-rate pacemakers. Mean cardiac index at rest increased 0.8 + 0.07 liters/ min per m2 (9% confidence interval) without significant change in braehial arterial pressures. Exercise performed by 5 patients, without glucagon, increased the cardiac index. During the same amount of exercise with glucagon, there was no aignifioant further increase in cardiac index (0.5 + 0.06 liters/min per m*). One additional patient with congestive heart failure did not show an increased cardiac index with glucagon at rest or during exercise. Isoproterenol administered to 2 patients increased cardiac index by 1.91 and 1.90 liters/min per ma compared to 1.02 and 0.75, respectively, with glucagon. Six of 8 patients experienced nausea and lightheadedness, and in 2 patients ventricular premature systoles developed after administration of glucagon. Mean serum potassium in 9 patients decreased from 82 The Amodem JoounMl of CARDlOLOaY

The Advantages of Demand Over Fixed-Rate Pacing: Report of Clinical Experience

Clinical experience with both fixed rate and demand pacing suggests that the latter mode should probably be utilized in patients with second degree or intermittent high grade A-V block. Instances of ventricular tachycardia and fibrillation following a propagated pacemaker beat, competition between sinus rhythm and fixed rate pacing, and rapid ventricular rates due to coupled ventricular premature systoles also suggest pertinent arguments in favor of demand pacing. Although it is probably too early to advise demand pacing for ail patients, inferential reasoning from clinical experience is offered to identify more clearly the advantages of demand over fixed rate pacing.

Ventricular arrhythmias after precordial electric shock

New cardiac arrhythmias occurred 43 times in 50 patients who underwent 55 elective precordial applications of synchronized D.C. shock for the control of cardiac arrhythmias. Ventricular arrhythmias were seen after 27 procedures. There were unifocal ventricular premature systoles in 11, multifocal ventricular premature systoles in 15, and ventricular bigeminy in 17. Three of these patients developed runs of ventricular tachycardia, and 2 developed ventricular fibrillation. One patient with ventricular fibrillation received additional D.C. shock to control this arrhythmia. Except for this one patient, all arrhythmias were transient and self-limited. All patients survived the procedure, and there were no complications due to the new arrhythmias. Although there were only 7 patients who were not receiving digitalis, 3 of these 7 patients developed new ventricular arrhythmias (bigeminy, unifocal and multifocal premature systoles). This suggests that, in these patients, electric shock acted to increase ventricular irritability, even though there were no cases of ventricular fibrillation or tachycardia in this small group. Furthermore, in those patients who were not receiving toxic doses of digitalis, the dose of digitalis being used did not appear to be an important factor in determining which patients would develop new ventricular arrhythmias. Ventricular arrhythmias were more frequent after multiple shocks and high levels of energy. This may have been due either to a dose-dependent pro-arrhythmic effect of electric shock or to the severity of the underlying heart disease that necessitated multiple shocks of high energy, or to both.

Hemodynamic features of extrasystoles in newborn and older infants

The hemodynamic features of catheter-induced supraventricular and ventricular extrasystoles of 30 newborn infants, aged 47 minutes to 10 hours, and of 25 older infants 2 days to 9 months of age were studied.The hemodynamic changes produced by ventricular and atrial extrasystoles in infants over 2 weeks of age generally resembled those observed in adult subjects and in animal studies. The extrasystolic beat was followed by a compensatory pause which was inversely related to coupling. The pressure of the ectopic beat was consistently low, and its amplitude varied directly with coupling, i.e., inversely with its prematurity. The pressure of the postextrasystolic beat was always greater than that of the preceding normal beats, and this increase was inversely related to coupling of the ectopic beat.In newborn infants up to 2 weeks of age, a prolonged compensatory pause also followed the ectopic beat. In the case of ventricular premature beats, the compensatory pause was inversely related to coupling; in atrial premature beats, no definite relation was observed. The extrasystolic contraction was also weaker than that of the normal beat as in older infants. However, for relatively identical degrees of extrasystolic prematurity, the amplitude of the right ventricular or pulmonary arterial systolic pressures was significantly higher in the newborn infants than in the older ones. A striking finding in this age group was the absence of postextrasystolic pressure increase typically observed in the older infants. In the instances of simultaneous ventricular and atrial tracings recorded at the time of the ventricular premature systoles, evidence of atrioventricular regurgitation during the ectopic beat was observed.It is suggested that the potentiating effect of extrasystolic contraction upon myocardial contractility may still be poorly developed in the immediate newborn period.

Ventricular tachycardia

Although ventricular tachycardia (VT) was previously considered to be an uncommon arrhythmia, the use of electrocardiographic monitors has revealed a much higher incidence of this arrhythmia. As many as 60 per cent of patients with acute myocardial infarction may have VT at some time during their course. VT is also seen during cardiac catheterization and selective ventriculography. Rarely it may occur after precordial electric shock and with malfunction of a cardiac pacemaker. There has been an increasing awareness that supraventricular tachycardias may satisfy all the usual criteria of VT: (1) rapid, bizarre, widened QRS complexes; (2) independent atrial activity; and (3) ventricular premature systoles whose configuration is similar to those of the tachycardia. A definitive diagnosis is possible only when fusion and/or capture beats are demonstrated. The antiarrhythmic drugs procaine amide and quinidine remain the treatment of choice for most cases except where the availability of anesthesia and the appropriate equipment make precordial electric shock the preferred therapy. Lidocaine has gained favor as an antiarrhythmic agent because of the ease of administration and the lesser incidence of hypotension. Betaadrenergic blockade with propranolol appears to be useful in the management of repetitive VT and digitalis induced ventricular arrhythmias. In selected cases suppresive therapy with an internal cardiac pacemaker has proved useful.

Clinical and physiologic effects of antazoline, a new antiarrhythmic agent

1.Intravenous antazoline caused a transient reduction in cardiac output and stroke volume. Blood pressure was maintained while peripheral vascular resistance increased.2.Antazoline exhibited both direct myocardial depressant effects and anti-acetylcholine actions.3.There was a complete suppression of atrial premature systoles in all 15 subjects studied. Atrial tachycardia was promptly terminated in 12 of 13 patients. However, antazoline proved to be ineffective in the presence of atrial flutter and fibrillation.4.All but 7 of 68 patients with frequent ventricular premature systoles had an adequate response to antazoline. Ventricular tachycardia was terminated by intravenous antazoline in 6 of 10 patients.5.Antazoline proved to be effective in terminating ventricular tachycardia, multifocal ventricular premature systoles, and nonparoxysmal nodal tachycardia due to digitalis excess. However, 1:1 conduction resulted in 2 cases of paroxysmal atrial tachycardia with block engendered by digitalis excess.6.Antazoline is an effective, well-tolerated antiarrhythmic agent which may be used in the therapy of ectopic beating of atrial, nodal, or ventricular origin.

Multiple pathways of conduction and reciprocal rhythm with interpolated ventricular premature systoles

Multiple pathways of conduction and reciprocal rhythm with interpolated ventricular premature systoles

Atrial parasystole with interpolation Observations on prolonged sinoatrial conduction

1. 1. We have reported an unusual case of sinus rhythm with atrial premature systoles due to an independent ectopic pacemaker (atrial parasystole). 2. 2. Marked variations in the duration of the returning cycle (P′-P) after the ectopic atrial beats, in spite of a fairly regular rate of the sinus pacemaker, are accounted for in the following manner: (a) A P′-P interval longer than the P-P cycle indicates discharge of the sinus pacemaker by the ectopic impulse. This is seen with P′ occurring in the middle portion of the cycle. (b) P′-P intervals about equal to the P-P cycle indicate interference of the ectopic with the next sinus impulse (fully compensatory pause). This is seen with P′ occurring late in the cycle. (c) P′-P intervals shorter than the P-P cycle indicate interpolation of P′ with postextra-systolic prolongation of S-A conduction time. This is seen with P′ occurring early in the cycle. 3. 3. Events subsequent to interpolation of the ectopic atrial impulse indicate that the sinus impulse which follows the postextrasystolic sinus impulse is blocked rather than interfered with. Thus, the mechanism is that of a pseudointerpolation with postponed compensatory pause, analogous to the same phenomenon which occurs after nodal or ventricular premature systoles. 4. 4. Comparison of a single atrial cycle (P-P) with one which contains an interpolated atrial premature systole (P-P′-P) permits determination of the delay in S-A conduction of the postextrasystolic beat.

Ventricular asynchronism in the dog.

Dissociation of electrical and mechanical asynchronism in the canine right and left ventricles has been studied by simultaneous registration of right and left ventricular pressure and strain gauge arch curves and the electrocardiogram. Observations were made during sinus rhythm and during acetylstrophanthidin-induced ventricular premature beats with widened aberrant QRS complexes. The data demonstrate only limited mechanical asynchronism during the asynchronous electrical depolarization of ventricular premature systoles. Submitted on October 19, 1961

Bidirectional tachycardia

A case of bidirectional tachycardia is presented. It is suggested that it represents atrial fibrillation with nodal rhythm and variable forward block. The illusion of bidirectional tachycardia is created by bigeminy with ventricular premature systoles or with aberrant conduction simulating ectopic impulse formation.

The supernormal phase of ventricular excitation in man. Its bearing on the genesis of ventricular premature systoles, and a note on atrioventricular conduction

Artificially produced ventricular premature beats apparently due to a supernormal phase of ventricular excitation in man is demonstrated. This phase occurs within 0.04 second of the beginning of the descent of the T wave. Subthreshold stimuli can produce parasystole with constant coupling and may explain some hitherto obscure A-V arrhythmias.