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Biomedical subjects

P Denes

Publications and source records attributed to P Denes.

At least 55 records · Page 3Linked to original sources

Prevalence of late potentials in patients undergoing Holter monitoring.

UNLABELLED: High-frequency, low-amplitude signals detected in the terminal portion of the surface QRS, called late potentials (LP), have been shown to correlate with inducible sustained ventricular tachycardia and to be absent in normal subjects. We studied LP in 152 patients without a history of sustained ventricular tachycardia who underwent 24-hour Holter monitoring for varying clinical indications (chest pain 21%, syncope 17%, palpitations 32%, dizziness 20%, other 10%). Twenty-one patients (14%) had a positive test. Of the 152 patients, 84 (55%) had complex ventricular arrhythmias and 68 (45%) had simple or no ventricular arrhythmias. Complex ventricular arrhythmias were present in 71% of patients with and in 52% of those without LP. IN CONCLUSION: patients without history of sustained ventricular tachycardia who demonstrate complex nonsustained ventricular arrhythmias on Holter monitoring have a low prevalence of LP; the presence of LP on signal-averaged ECG indicates an electrical property of the heart, which is distinct from complex ventricular arrhythmias detected on Holter monitoring.

Arrhythmias, Cardiac↗

Tachycardia- and bradycardia-dependent atrioventricular block: observations regarding the mechanism of block.

A case of paroxysmal bradycardia- and tachycardia-dependent atrioventricular (AV) block is described in a patient with right bundle branch block. The His bundle recordings demonstrated the site of the AV block to be distal to the His bundle recording site (probably in the left bundle branch). Whereas AV block distal to the His bundle occurred at an atrial paced cycle length of 700 ms, intact ventriculoatrial (VA) conduction was present up to a ventricular paced cycle length of 400 ms. Resumption of AV conduction was dependent on a critical HH or RH (in case of escapes) interval. These findings suggest that the bradycardia-dependent block is related to a time-dependent decrease in the amplitude of the current intensity of the proximal segment during late diastole. Spontaneous diastolic depolarization during late diastole resulted in impaired anterograde (AV) conduction but facilitated retrograde (VA) conduction. These findings are consistent with experimental "in vitro" observation in the sucrose gap model of AV block.

Bradycardia↗

Cardiac arrhythmias--update 1987.

Arrhythmias may result from abnormalities of impulse initiation (automaticity), conduction (slow conduction, block, reentry), or a combination. The central and peripheral nervous systems have an important influence on the genesis of cardiac arrhythmias. Sympathetic and parasympathetic fibers innervate both atria and ventricle. The study of clinical cardiac arrhythmias includes the use of invasive and noninvasive testing procedures. The ECG, ambulatory monitoring, esophageal recording, exercise testing, and signal averaging techniques are the currently used noninvasive tests. Intracardiac electrophysiologic studies and endocardial catheter mapping are invasive techniques. The treatment of cardiac arrhythmias includes the use of antiarrhythmic drugs, cardiac pacing (antibradycardia, antitachycardia), implantable automatic defibrillator, cardiac fulguration, and antitachycardiac surgery. Clinical cardiac arrhythmias are of two types, the bradyarrhythmias and the tachyarrhythmias. The tachyarrhythmia, in turn, may be supraventricular or ventricular. There are clinical syndromes specifically related to arrhythmias: preexcitation syndromes are associated with supraventricular tachyarrhythmias, long Q-T syndromes with ventricular tachyarrhythmias, and sick sinus syndrome with bradyarrhythmias. The "tachycardia-bradycardia syndrome" is a combination of atrial tachyarrhythmias and sinus node dysfunction (some of the patients may also have ventricular tachyarrhythmias). Specific arrhythmias are recognized by their ECG characteristics. These arrhythmias also have specific electrophysiologic features which can be defined during invasive electrophysiologic studies. Cardiac arrhythmias may or may not be accompanied by underlying organic heart disease. Their treatment is related to the specific diagnosis and mechanism of the rhythm disturbance. The presence and extent of underlying organic heart disease is an important factor in the selection of antiarrhythmic therapy (drug, pacemaker, or surgery).

Arrhythmia, Sinus↗

Multiple reentry tachycardia in patients with ventricular preexcitation: report of three cases.

The electrophysiologic studies of three patients with accessory pathways and multiple reentrant circuits are reported. The first patient had two atrioventricular accessory pathways: a left posterior capable of bidirectional conduction and a right paraseptal with retrograde conduction only. Four atrioventricular reentry circuits were documented: left and right orthodromic circuits and a left antidromic circuit with retrograde conduction over the right paraseptal accessory pathway. The second patient had a left lateral atrioventricular accessory pathway with type A preexcitation. Two reentrant tachycardias were noted: an atrial tachycardia where the accessory pathway remained concealed and an orthodromic atrioventricular tachycardia. The third patient had dual atrioventricular nodal pathways and a right nodofascicular accessory pathway. The accessory pathway became manifest only when a critical atrioventricular delay was reached, indicating its association with the slow atrioventricular nodal pathway. Wide QRS tachycardia with left bundle branch block contour was documented, by means of the slow atrioventricular nodal pathway and nodofascicular fiber antegradely, and the proximal right bundle branch, the His bundle, and the fast atrioventricular nodal pathway retrogradely.

Adult↗

Emergency treatment of tachyarrhythmias.

The diagnosis, clinical aspects, and emergency treatment of the most common cardiac arrhythmias, including atrial flutter and fibrillation, paroxysmal supraventricular tachycardia, the Wolff-Parkinson-White syndrome, ventricular tachycardia, and torsades de pointes, are discussed. The use of the antiarrhythmic drugs most frequently utilized in clinical practice is described.

Anti-Arrhythmia Agents↗

Significance of ventricular pauses of three seconds or more detected on twenty-four-hour Holter recordings.

The natural history of patients with asymptomatic prolonged ventricular pauses and the indications for permanent pacing are controversial. To examine this problem, 6,470 consecutive 24-hour Holter recordings were reviewed between 1979 and 1983 for the presence of ventricular pauses of at least 3 seconds. Fifty-two patients (0.8% of total), 22 men and 30 women, were identified with an average longest pause duration of 4.1 seconds. Holter recordings were requested to evaluate syncope in 14 patients (27%), dizziness in 9 (17%) and other reasons in 29 (56%). Causes of the pauses were sinus arrest in 22 patients, atrial fibrillation with slow ventricular response in 18 patients and atrioventricular block in 12. Holter recordings were also evaluated for the presence of tachyarrhythmias. Six patients had nonsustained ventricular tachycardia and 7 had supraventricular tachycardia. Five of the 52 patients (10%) had dizziness or syncope during pauses. Twenty-six patients (50%) received permanent pacemakers. The paced (26 patients) and unpaced (26 patients) groups were similar in the length and etiology of pause, associated tachyarrhythmias, presence of bradycardia-related symptoms, prevalence of organic heart disease, medications and length of follow-up. Four patients in the paced group and 2 in the unpaced group died, yielding 3-year actuarial survival probabilities of 78% and 85%, respectively. It is concluded that ventricular pauses of 3 seconds or longer are uncommon, these pauses usually do not cause symptoms, and the presence of these pauses does not necessarily portend a poor prognosis or the need for pacing in asymptomatic patients.

Aged↗

Ventricular arrhythmia induced by programmed ventricular stimulation after acute myocardial infarction.

The prevalence, characteristics and clinical significance of ventricular electrical instability with programmed ventricular stimulation was studied in 50 hemodynamically stable patients 17 to 40 days after acute myocardial infarction (AMI) using double extrastimuli at 2- and 10-mA intensity and from 2 right ventricular sites. Ventricular electrical instability was defined as induction of 10 or more consecutive intraventricular reentrant beats. Of 50 patients, 23 (46%) had ventricular electrical instability (10 of these had sustained ventricular tachycardia [VT] induced). No significant differences were observed between patients with and without ventricular electrical instability with respect to age, site of AMI, coronary prognostic index, maximal level of CK, number of narrowed coronary arteries and presence of severe wall motion abnormalities. During a mean follow-up of 11.2 months no patient died suddenly. During repeated Holter recordings patients with ventricular electrical instability had a higher incidence of nonsustained VT than did patients without ventricular electrical instability.

Adult↗

Unexpected coexistence of supraventricular and ventricular tachycardia in patients with syncope.

The incidence of multiple, inducible sustained arrhythmias during electrophysiologic studies is unknown. We have identified five patients who had several sustained tachycardias, some of which were not previously recognized clinically. Three patients had documented sustained supraventricular tachycardia (one of these also had nonsustained ventricular tachycardia) and two had documented sustained ventricular tachycardia. The clinically documented tachycardia was successfully reproduced in all cases; however, the three cases of supraventricular tachycardia also had sustained ventricular tachycardia initiated, and the two cases of ventricular tachycardia also had sustained supraventricular tachycardia, which had not previously been seen. The underlying common denominators for all five patients were poor left ventricular function due to ischemic heart disease and a history of syncope. In one case of clinical supraventricular tachycardia, the second sustained tachycardia appeared following drug therapy (procainamide), which seemed to convert nonsustained to sustained ventricular tachycardia. In another patient with clinical ventricular tachycardia, the supraventricular tachycardia was also initiated following drug therapy (indecainide). We conclude that: (1) patients with syncope may have multiple arrhythmic etiologies and (2) complete electrophysiologic evaluation, during control studies as well as serial drug studies, are important in the management of these patients.

Bradycardia↗

The role of electrophysiologic studies in the management of patients with unexplained syncope.

We evaluated the frequency and type of electrophysiologic abnormalities in an unselected population of consecutive patients with unexplained syncope. Fifty patients were entered in the study; all had 24-hour dynamic electrocardiographic (Holter) recordings and underwent complete electrophysiological studies. An abnormal electrophysiologic study was found in 74% of the patients. Sinus node abnormality was observed in 30%, abnormal AV node function in 14%, long HV in 10%, block distal to H during rapid atrial pacing in 6%, paroxysmal supraventricular tachycardia in 12%, ventricular tachycardia/fibrillation in 8%, and hypersensitive carotid sinus syndrome in 24%. There was no correlation between Holter and electrophysiologic study findings except for the presence of paroxysmal sustained supraventricular tachycardia. Based on clinical, Holter monitoring, and electrophysiologic findings, 38% were treated by antiarrhythmic drugs, 40% received permanent pacemakers, and 22% were not treated at all. During follow-up (23 +/- 13 months), 9 patients (18%) experienced recurrent syncope or death.

Adolescent↗

Determinants of arrhythmogenic ventricular activity detected on the body surface QRS in patients with coronary artery disease.

The prevalence of arrhythmogenic ventricular activity (AVA) was investigated in 166 patients with coronary artery disease. Thirty patients had documented ventricular tachycardia (VT)/ventricular fibrillation (VF). Bipolar X, Y, Z leads were signal-averaged and filtered with a 40-Hz, bidirectional, high-pass digital filter. The filtered QRS signals were analyzed for the amplitude of the last 40 and 50 ms; duration of low-amplitude potentials (less than 40 microV) in the terminal portion; and duration of the filtered QRS. A positive AVA test result was defined as the presence of 2 or more abnormal indexes. Of the 30 patients with VT/VF, 66% had positive AVA test results (AVA-positive patients). Of the 136 patients without VT/VF, 25% had positive AVA test results. The following univariate variables showed significant correlation with an AVA-positive test: age, previous myocardial infarction, previous VT/VF, left ventricular wall motion abnormalities and left ventricular ejection fraction. Multivariate stepwise discriminant function analysis revealed that the presence of previous myocardial infarction and history of sustained VT/VF were the only independent determinants of AVA. During electrophysiologic studies, sustained VT/VF could be induced in 77% of the AVA-positive patients (24 of 31) and in 30% of the AVA-negative patients (3 of 10). The survival probabilities for 6, 12 and 18 months of follow-up were 92%, 85% and 85% for the AVA-positive and 97%, 92% and 90% for the AVA-negative patients. Our findings support the concept that a positive AVA test result reflects areas of delayed ventricular activation. The areas of delayed ventricular activation are associated with previous myocardial injury and scar tissue and serve as an anatomic basis for reentry.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Relation of ventricular premature beats to underlying heart disease.

The relation between ventricular premature beats (VPBs) and physiologic disease was investigated in 305 patients who had 24-hour Holter monitoring tests, cardiac catheterization and angiography. Both frequency and Lown class of VPBs were measured. Analyses showed that occurrence of VPBs at an average frequency of more than 2 per hour or occurrence of complex VPBs (Lown class greater than 2) have the highest association with the presence and severity of cardiac disease. Using these criteria, VPB severity was then compared with extent of ventricular wall motion abnormality (right anterior oblique projection segments), ejection fraction, end-diastolic pressure, category of disease (normal, coronary artery disease [CAD], valvular heart disease, dilated cardiomyopathy), age and severity of CAD (major coronary arteries with greater than 75% diameter reduction). Severe VPBs defined either by complexity or frequency were significantly correlated with extent of wall motion abnormality, ejection fraction, category of disease and age. Severe VPBs were not significantly correlated with end-diastolic pressure or severity of CAD. Discriminant analysis then showed that in addition to wall motion abnormality and ejection fraction, category of disease and age are independently correlated with VPB severity.

Arrhythmias, Cardiac↗

The role of Holter monitoring in patients with recurrent sustained ventricular tachycardia: an electrophysiologic correlation.

The significance of spontaneous ventricular premature depolarization (VPD) frequency and severity in patients with sustained ventricular tachycardia undergoing serial electrophysiologic studies (EPS) are unknown. Nineteen patients with sustained ventricular tachycardia were studied with 24-hour Holter recordings prior to control EPS and prior to each drug trial. Successful drug or surgical treatment (with the exception of amiodarone) was based upon noninducibility of ventricular tachycardia in the laboratory. Among the eight noninducible and nonamiodarone medically treated patients, two (25%) had significant VPD reduction and/or Lown class improvement. The remaining six (75%) had no change or worsening of Holter findings, despite noninducibility of sustained VT. Among the six amiodarone-treated patients, five of whom were persistently inducible prior to discharge, four (66%) had improved and two (33%) had worsened Holter findings compared to control. None of the five (100%) surgically managed patients were inducible postoperatively, and three of the five (60%) had no change or worsening of Holter findings. We conclude that (1) EPS are superior to Holter findings in assessing successful management; and (2) Holter findings may be concordant or discordant during EPS serial drug trials or following surgery and therefore cannot predict the success or failure of the intervention.

Aged↗

Short PR interval and narrow QRS complex associated with pheochromocytoma: electrophysiologic observations.

A patient with a short (0.10 second) PR interval, narrow QRS complex and palpitation is described. Electrophysiologic studies demonstrated the presence of accelerated atrioventricular (AV) nodal conduction. Subsequently, a pheochromocytoma was found. Surgical removal of the tumor resulted in normalization of the PR interval. These findings suggest that the short PR interval and the accelerated AV nodal conduction were due to the effect of excess catecholamines on the AV conduction system.

Adrenal Gland Neoplasms↗

The effect of cycle length on the atrial refractory period.

The effect of cycle length upon refractory period of the atria was measured in 34 patients. The effect of abrupt change in paced cycle length on atrial refractory period was measured by introducing after every eighth paced cycle (CLP) a test cycle (CLT) at an interval which was either 100 ms longer (CLT = CLP + 100 ms) or shorter (CLT = CLP - 100 ms) than the paced cycle. These findings confirm that: (1) atrial refractory periods shorten with decreasing cycle length during steady state pacing; (2) an abrupt change in paced cycle length results in a change in refractory period. This change is similar in direction but smaller in magnitude than the change which occurs in response to steady state pacing; and (3) there is no correlation between intraatrial conduction time and refractoriness.

Atrial Function↗

Sleep and ventricular arrhythmias.

Sleep is usually associated with a reduction in the frequency of ventricular arrhythmias. We analyzed 1260 24-hour Holter recordings exhibiting ventricular ectopy and identified 50 patients who had significant increases in sleep-related ectopy. This study group was compared to an age, sex, and 24-hour ventricular ectopic frequency matched control group. There were 21 females and 29 males with a mean age of 64 years in each group. During sleep, the study patients had more frequency of ventricular ectopy per hour than did controls (mean +/- SEM; 143.2 +/- 30.7 vs 62.9 +/- 16.3; p less than 0.005). The study group had fewer daytime ventricular premature beats per hour than did the control patients (45.2 +/- 13.6 vs 67.7 +/- 13.8; p less than 0.05). The study patients also exhibited a significant sleep-related increase in complexity of ventricular arrhythmias (chi 2 = 22.1; p less than 0.001) and the control group a decrease (chi 2 = 19.1; p less 0.001). Nocturnal heart rates were slower than daytime rates in both the study (69.4 +/- 14.5 vs 79.2 +/- 12.2 bpm; p less than 0.005) and control groups (75.5 +/- 15.8 vs 82.6 +/- 16.4 bpm; p less than 0.005), without significant differences between the two groups. No significant differences in clinical and ECG characteristics of the study and control groups were found regarding presence or type of organic heart disease, pulmonary disease, hypertension, medication use, intraventricular conduction delay, abnormal Q waves, ventricular hypertrophy, or QT prolongation. Neurologic abnormalities (60% vs 28%; chi 2 = 9.38 p less than 0.005), in particular cerebrovascular disease (30% vs 14%; chi 2 = 7.56; p less than 0.01), were significantly more common in the study group. We have identified a subgroup of individuals with ventricular ectopy who increase the frequency and complexity of premature ventricular beats during sleep. The higher prevalence of neurologic disease in these individuals suggests a neurologic or neurohumoral mediation of these arrhythmias.

Aged↗