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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-four patients with a prolonged A-H interval (group I) and 26 with A-V nodal Wenckebach block (group II) were studied in the basal state and after autonomic blockade (propranolol 0.2 mg kg-1 and atropine 0.04 mg kg-1 in order to assess the role of autonomic system in A-V nodal conduction disturbances. In group I, the A-H intervals did not change significantly after autonomic blockade, whereas pacing cycle length for Wenckebach block, effective and functional refractory periods of the A-V node decreased significantly (P less than 0.05). In the 22 patients with organic heart disease these variables did not change significantly after autonomic blockade, whereas in the 12 without underlying heart disease, they decreased in all cases (P less than 0.001). In the former, the variables of intrinsic A-V nodal conduction were normal in only 9% of patients, whereas in the latter they were normal in 66%. Also in group II, the intrinsic A-H intervals were normal in only 6% of patients with cardiac disease but were normal in 63% without underlying heart disease. These data suggest that in the patients with first and second degree A-V nodal block and organic heart disease, the conduction disturbance is predominantly related to intrinsic involvement of A-V node, whereas in the subjects without underlying heart disease the A-V nodal blocks appear mainly related to autonomic alterations.
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PMID:Role of the autonomic nervous system in the genesis of first and second degree atrio-ventricular nodal block. 379 56

The clinical, electrocardiographic and electrophysiologic determinants and effects of antiarrhythmic agents on sustained sinus node reentrant tachycardia remain poorly defined. Of 65 consecutive men undergoing electrophysiologic studies for symptomatic paroxysmal supraventricular tachycardia over a 4 year period, 11 (16.9%), who ranged in age from 39 to 76 years, demonstrated sustained sinus node reentrant tachycardia. On the surface electrocardiogram, before electrophysiologic studies, the following diagnoses were considered in the 11 patients: sinus node reentrant tachycardia on the basis of an RP'/P'R ratio of greater than 1 and P wave configuration similar to that of sinus P waves (7 patients); atrioventricular (AV) nodal reentrant tachycardia on the basis of an RP'/P'R ratio of less than 1 (3 patients); and paroxysmal atrial tachycardia with AV block (1 patient). All 11 patients had a history of recurrent palpitation, 4 had syncope, 2 had dizzy spells and 9 had organic heart disease. Sustained sinus node reentrant tachycardia could be reproducibly induced in all 11 patients during atrial pacing or premature atrial stimulation, or both, over a wide echo zone. The tachycardia could be terminated by carotid sinus massage, atrial pacing and premature atrial stimulation. Characteristics of tachycardia included: high-low activation sequence; cycle lengths of 250 to 590 ms with wide fluctuations of 20 to 180 ms in individual patients; RP'/P'R ratio of greater than 1 in 8 (73%) of the 11 patients and a ratio of less than 1 in 3 (27%). Induction of sustained sinus node reentrant tachycardia was prevented by intravenous ouabain (0.01 mg/kg body weight) in two of two patients, by intravenous verapamil (10 mg) in two of two patients and by intravenous amiodarone (5 mg/kg body weight) in four of four patients. In contrast, intravenous propranolol (0.1 mg/kg body weight) did not affect induction of sustained sinus node reentrant tachycardia in two of two patients. It is concluded that sustained sinus node reentrant tachycardia, seen in 16.9% of the study patients with paroxysmal supraventricular tachycardia, is not as benign as previously believed; it is frequently associated with organic heart disease; it demonstrates wide variations in cycle length, unlike other forms of paroxysmal supraventricular tachycardia; it can masquerade as AV nodal reentrant tachycardia and paroxysmal atrial tachycardia with AV block on the surface electrocardiogram in 36% of patients; and it is responsive to intravenous administration of ouabain, verapamil or amiodarone.
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PMID:Sustained symptomatic sinus node reentrant tachycardia: incidence, clinical significance, electrophysiologic observations and the effects of antiarrhythmic agents. 396 8

Associated electrophysiologic abnormalities and site of delay were studied in 20 patients, aged 1.5 to 16.5 years, with congenital heart disease and first-degree atrioventricular (AV) block (PR interval above the 98th percentile for age and heart rate). Eight of the 20 patients with first-degree AV block were studied after 1 or more cardiovascular operations. Refractory periods of the atrium, AV node, His-Purkinje system and ventricle were determined. As a further test for AV nodal integrity, rapid atrial pacing was performed and the cycle at which Wenckebach periodicity occurred was noted. Four groups were identified. Group I included 4 patients (20%) with intraatrial conduction delay (long PA interval). Three patients had depressed sinus nodal function and 1 had depressed AV nodal function. Group II included 7 patients (35%) with AV nodal delay (long AH interval). One patient had sinus nodal depression and 2 had AV nodal depression (prolonged AV nodal refractory period or Wenckebach at a long paced cycle length). Group III included 3 patients (15%) with His-Purkinje delay (long HV interval). Measured functions were normal in all patients. Group IV included 6 patients (30%) with normal or high normal intracardiac intervals with long PR. One patient had sinus nodal dysfunction, 2 patients had long atrial refractory periods, 1 had AV nodal depression; 2 had long refractory period of the His-Purkinje system, and 1 had long ventricular refractory period. Atrial flutter was induced in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Site of conduction delay and electrophysiologic significance of first-degree atrioventricular block in children with heart disease. 399 64

A prospective study examined the diagnostic yield and therapeutic efficacy of electrophysiologic studies in patients with SUO. We defined SUO as those syncopal or near-syncopal events remaining unexplained after a standardized, noninvasive evaluation that included a history, physical examination, routine laboratory screening, EEG, nuclear brain scan or CAT scan, 12-lead ECG, chest x-ray, orthostatic vital signs, bedside carotid sinus massage, and at least 24 hours of continuous ECG monitoring. The 150 SUO patients included 95 men and 55 women (mean age 62.0 years); 35 had recurrent SUO, 75 (50%) had organic heart disease, and 129 (86%) had abnormal ECGs. There were 162 abnormal electrophysiologic findings that could explain the SUO uncovered in 112 patients, a diagnostic yield of 75%: one finding in 71 patients, two findings in 32, and three findings in nine. These findings were: His-Purkinje disease in 49 patients (30%), inducible ventricular arrhythmias in 36 (22%), AV nodal disease in 20 (12%), sinus node disease in 19 (12%), inducible supraventricular arrhythmias in 18 (11%), carotid sinus hypersensitivity (not elicited by carotid sinus massage prior to electrophysiologic studies) in 15 (9%), and hypervagotonia in five (3%). When electrophysiologic study findings were classified as clearly abnormal or borderline, 54 patients had at least one clearly abnormal finding, a diagnostic yield of 36%. Subgroups of patients presenting with only a single SUO event, no evidence of organic heart disease, or normal baseline ECGs all had substantial diagnostic yields during electrophysiologic studies. Follow-up data in 137 patients (91%) (mean 31 months) showed recurrences in 16 of 34 patients (47%) without and 15 of 103 patients (15%) with electrophysiologic findings despite therapy directed by electrophysiologic testing (p less than 0.0005). This study and a review of the literature indicate that electrophysiologic testing is useful in elucidating the causes of SUO and directing therapy. A significant number of patients benefit from electrophysiologic studies, even when only clearly abnormal findings are considered diagnostic, when only a single syncopal event has occurred, or whether or not organic heart disease or an abnormal ECG is present.
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PMID:The value of electrophysiologic studies in syncope of undetermined origin: report of 150 cases. 402 22

The implications of the minor ECG abnormalities that I have dealt with may be categorized as follows. Innocent: 1. Sinus arrhythmia, with or without nodal escape beats 2. Atrial extrasystoles 3. Incomplete right bundle-branch block 4. Parabolic depression of the ST segment in association with a rapid heart rate 5. Elevation of the ST segment in the right precordial leads 6. Positive/negative T waves in the transitional zone. Not necessarily indicating disease: 1. Ventricular indicating disease: 1. Ventricular extrasystoles 2. Complete right bundle-branch block 3. Left anterior or posterior hemiblock 4. Abnormally directed T-wave vectors. Probably indicating disease: 1. Plane or downward-sloping ST depression, at rest or on exercise, of more than 1 mm 2. Pyramidal arrowhead T waves, with or without an abnormally directed T-wave vector 3. Negative/positive T waves in leads facing the left ventricle 4. Inverted U waves. It is clear that careful assessment must be made before minor ECG abnormalities in presumptively normal individuals are accepted as indicators of the presence of heart disease.
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PMID:Symptomless abnormalities. Minor ECG abnormalities. 618 Jul 89

We examined the chronic electrophysiologic, systemic, and pharmacologic effects of chronic oral amiodarone therapy in 24 patients with refractory ventricular tachycardia and organic heart disease. Chronic amiodarone therapy resulted in significant increases in R-R interval (from 798 +/- 182 msec to 912 +/- 100 msec; P less than 0.01), P-R interval (from 205 +/- 66 msec to 221 +/- 87 msec; P less than 0.02), QRS duration (from 103 +/- 24 msec to 115 +/- 28 msec; P less than 0.001), and Q-Tc interval (from 413 +/- 48 msec to 470 +/- 46 msec; P less than 0.001). Significant increases were also noted in P-A interval (from 36 +/- 14 msec to 45 +/- 13 msec; P less than 0.05), A-H interval (from 119 +/- 61 msec to 141 +/- 87 msec; P less than 0.02), and H-V interval (from 52 +/- 12 msec to 64 +/- 11 msec; P less than 0.001). Electrophysiologic parameters showing changes included corrected sinus node recovery time (from 271 +/- 140 msec to 425 +/- 122 msec; P less than 0.01), the effective refractory period of the atrium (from 263 +/- 32 msec to 321 +/- 47 msec; P less than 0.01), the effective refractory period of the atrioventricular node (from 348 +/- 109 msec to 478 +/- 157 msec; P less than 0.001), the effective refractory period of the ventricle (from 253 +/- 21 msec to 291 +/- 28 msec; P less than 0.001), the atrial pacing cycle length producing A-V nodal Wenckebach (from 436 +/- 109 msec to 531 +/- 95 msec; P less than 0.001), and the functional refractory period of the A-V node (from 422 +/- 68 msec to 499 +/- 95 msec; P less than 0.001). Programmed electrical stimulation performed after 21-88 (mean 31) days of treatment was highly predictive of long-term results if suppression of arrhythmia induction was demonstrated (12 patients) or if the spontaneous arrhythmia was reinduced (5 patients). Induction of morphologically new ventricular tachyarrhythmias was frequent (42%) but had a low spontaneous recurrence rate (10%) during follow-up. Systemic parameters on chronic amiodarone therapy showed significant increases in total T4 and reverse T3, with no change in pulmonary function tests or left ventricular ejection fraction. Serum amiodarone levels at chronic electrophysiologic study ranged from 0.44-4.10 (mean 1.3) micrograms/ml. Long-term follow-up (2.5 to 20 months) demonstrated a marked improvement in clinical symptoms and mortality, but a significant recurrence rate of a well-tolerated slower arrhythmia persisted. Adverse effects on chronic amiodarone therapy were frequent (10 patients) and often disabling but required drug discontinuation in only 1 patient.
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PMID:Chronic effects of amiodarone in patients with refractory ventricular tachycardia. 634 14

Seven patients with short episodes of parasystolic ventricular tachycardia, in the absence of organic heart disease, and in good healthy state, are presented. The tachycardic episodes were analyzed through simultaneous esophageal and standard electrocardiographic recordings. The persistent fetal dispersion of nodal and Hiss bundle fragments within the ventricular septum is proposed as a possible explanation.
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PMID:Parasystolic ventricular tachycardias in young healthy patients. 649 66

Sinus nodal dysfunction (SND) and complete heart block (CHB) in congenital heart disease (CHD) are commonly associated with congestive heart failure, syncopal attacks, and sudden death. Permanent cardiac pacing (PCP) is required to avoid these manifestations which are frequently associated with a high rate of complications, particularly in the younger age group. Twenty patients with CHD aged 4 months to 46 years underwent pacemaker implantation. Twelve (60%) were less than 20 years of age. CHB was present in 15 patients: in 10 it developed 1 week to 11 years following surgery, in two it was congenital, and in three patients it developed spontaneously with previous conduction disturbances. SND was present in 5 patients: it was congenital in two patients and developed post-operatively in three. Seventeen patients are alive and no syncopal attacks or bradyarrhythmias were recorded 2.5 to 12.5 years following the initiation of PCP. Improvement in the cardiac output was noted in most patients with heart failure. The three patients who died had adequately functioning pacemakers. Only nine re-implantations were needed, seven of them in adult patients after closure of an atrial septal defect. Our experience indicates a favourable outcome for patients with CHD needing PCP.
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PMID:Permanent cardiac pacing in congenital heart disease: a follow-up study of 20 patients. 649 55

Extrastimulus-induced intraatrial conduction delays were measured in 12 patients with documented episodes of atrial fibrillation (AF) by recording atrial electrograms at the high right atrium, His bundle region, and coronary sinus. Seventeen patients with and without heart disease, but without atrial arrhythmias served as the control group. During baseline-paced atrial rhythms, a conduction delay zone could be delineated, near the atrial effective refractory period, during which all extrastimuli produced conduction delays. When compared at the same paced cycle lengths (500 to 650 ms), the patients with AF had shorter atrial effective refractory periods (mean +/- standard deviation 206 +/- 24.1 versus 233 +/- 28.2 in control patients, p less than 0.02), wider conduction delay zones (79 +/- 21.7 ms versus 52 +/- 21 in control patients, p less than 0.01), and longer conduction delays both to the His bundle region (64 +/- 18.3 ms versus 35 +/- 21.7 in control patients, p less than 0.005) and the coronary sinus (76 +/- 18.9 ms versus 35 +/- 16.1 in control patients, p less than 0.001). Repetitive atrial responses were recorded in 6 patients with AF and in 9 control subjects. Sinus nodal function abnormalities were detected in 6 of the patients with fibrillation. Patients with AF had a higher tendency than control subjects to develop slow intraatrial conduction, as well as shorter effective refractory periods. Since both features would favor reentry, they may be the electrophysiologic manifestations of the abnormalities making these patients prone to atrial reentrant arrhythmias. Repetitive atrial responses were of no predictive value. Sinus nodal dysfunction was frequently found, but was not essential for the occurrence of AF.
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PMID:Electrophysiologic studies in atrial fibrillation. Slow conduction of premature impulses: a possible manifestation of the background for reentry. 684 50

Ten patients are described with two discrete discontinuities in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean +/- SD, 48 +/- 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion, triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.
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PMID:Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia. 705 52


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