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

Identification of individuals at increased risk of sudden cardiac death is an important but difficult problem, especially in persons without clinically apparent heart disease. The ability of the electrocardiogram (ECG) to predict sudden death was determined in a study of 3983 men who were 30.8 years of age (mean) at entry and who had been followed with regular examinations, including ECGs. During the 30-year observation period, 70 cases of sudden death occurred in men without previous clinical manifestations of heart disease. Electrocardiographic abnormalities were detected before sudden death in 71.4% of cases. The abnormalities were, in decreasing order of frequency, ST segment and T-wave abnormalities, ventricular extrasystoles, left ventricular hypertrophy, complete left bundle branch block, and pronounced left axis deviation. When these electrocardiographic findings in men without clinical manifestations of heart disease were related prospectively to the incidence of sudden death, ST segment and T-wave abnormalities, ventricular extra-systoles, left ventricular hypertrophy and complete left bundle branch block were significant predictors of sudden death, while left axis deviation and right bundle branch block were not significant predictors of sudden death. Increased severity of primary T-wave abnormalities and the association of ST segment and T-wave abnormalities with increased QRS voltage further increased the sudden death risk. The combination of ventricular extrasystoles with either ST-T abnormalities or left ventricular hypertrophy considerably increased the risk of sudden death. Thus, these data indicate that electrocardiographic abnormalities detected on routine examination in men without clinical evidence of heart disease identify men at an increased risk of sudden death.
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PMID:Electrocardiographic abnormalities in apparently healthy men and the risk of sudden death. 620 83

During the past 5 years, we have seen six patients who met inclusion criteria of exertional palpitations, reproducible treadmill (TM) provocable ventricular tachycardia (VT), and performance of electrophysiologic (EP) studies including isoproterenol (ISO) infusion. There were five males and one female, aged 15 to 55 years (mean +/- SD, 31 +/- 18 years). Three patients were trained athletes, two patients had mitral valve prolapse, three had enlarged right ventricular (RV) volumes (all trained athletes), and two had no evidence of organic heart disease. TM testing in all patients demonstrated reproducible exercise-provocable VT of at least 20 beats' duration. TM VT was characterized by left bundle branch block pattern ORS morphology and rates of 150 to 230 bpm (186 +/- 30 bpm). EP did not reproduce VT in five of six patients while ISO at a dose of 2 to 4 micrograms/min (2.5 +/- 0.8 micrograms/min) reproduced VT in all patients. ISO VT was characterized by QRS morphology identical to TM VT and rates of 165 to 230 bpm (191 +/- 26 bpm). Endocardial mapping of ISO VT revealed earliest activity in RV outflow tract. Serial TM testing revealed suppression of TM VT in all six patients on propranolol therapy. Responses to class I drugs were variable and less successful. In summary, we describe a group of patients with common clinical, ECG, and electrophysiologic features who may share a common pathophysiology of VT. Possible mechanisms are discussed.
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PMID:Exercise provocable right ventricular outflow tract tachycardia. 621 41

Forty-nine cases of Wolff-Parkinson-White syndrome (WPW) were diagnosed out of 10 750 patients with cardiac disease (0.45 p. 100), 24 cases out of 3 761 congenital malformations and 25 cases in the 6 989 patients with acquired heart disease. Right ventricular pre-excitation was recorded in 31 cases; 13 in the lateral zone, 12 in the posterior paraseptal zone and 6 in the anterior paraseptal zone. Left ventricular pre-excitation was recorded in 18 cases: 8 in the lateral zone, 5 in the anterior paraseptal and 5 in the posterior paraseptal zones. WPW and congenital heart disease: Out of 20 cases of Ebstein's anomaly, 5 cases of WPW were observed: 4 right posterior and 1 right lateral pre-excitations. Out of 218 cases of hypertrophic obstructive cardiomyopathy, 7 cases of WPW were observed, 4 of which were congenital. Three cases of WPW were recorded in 699 patients with ventricular septal defects. Out of 1 348 cases of atrial septal defect, 5 cases of pre-excitation were recorded, including 3 right posterior pre-excitations associated with an ostium primum defect. Pre-excitation was also observed in isolated cases of corrected transposition of the great arteries, supravalvular aortic stenosis, aortic incompetence and patent ductus arteriosus. Pre-excitation and acquired heart disease: Five cases of pre-excitation were recorded out of 305 cases of dilated cardiomyopathy (1.62 p. 100). Eleven cases of pre-excitation were recorded in a total of 3 471 cases of valvular heart disease (0.31 p. 100): 9 in rheumatic valve disease and 2 in mitral valve prolapse. Nine cases of pre-excitation were observed in 2 850 cases of coronary artery disease. Intermittent Wolff-Parkinson-White syndrome: Ventricular pre-excitation masks the ECG changes of complete right bundle branch block in Ebstein's anomaly, complete left bundle branch block in aortic incompetence and dilated cardiomyopathy, and the in-complete right bundle branch block often seen in mitral valve prolapse. The characteristic appearances of WPW depend on the zone of pre-excitation. Right ventricular hypertrophy observed in ventricular septal defect with pulmonary stenosis and mitral stenosis may be masked by right lateral pre-excitation. Changes of inferior wall myocardial infarction may be masked by left anterior wall pre-excitation. On the other hand, the effects of WPW on left ventricular hypertrophy are variable, high amplitudes of the resultant forces seeming to depend on late and isolated activation of one of the left ventricular walls.
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PMID:[Wolff-Parkinson-White syndrome and cardiopathies]. 624 Feb 36

The clinical and electrophysiologic characteristics of 6 patients who had repetitive monomorphic ventricular tachycardia (VT) after a remote myocardial infarction (group A) were compared with those of 22 patients who had this arrhythmia without structural heart disease (group B). VT had a right bundle branch block morphologic pattern in 5 of 6 group A patients and a left bundle branch block morphologic pattern in all group B patients. Endocardial catheter activation mapping was performed in 4 group A patients and in 9 group B patients during VT. In all group A patients, the site of VT origin was on the border of the previous infarction; in all group B patients VT originated at the right ventricular outflow tract. Pacing and programmed stimulation induced VT in 5 of 6 group A patients and 7 of 22 group B patients (p = 0.03). Isoproterenol infusion provoked VT in 4 group A patients and 9 group B patients. Type I antiarrhythmic agents suppressed VT in 4 group A patients and in 14 group B patients, whereas propranolol suppressed VT in 3 of 3 group A patients tested and in 12 of 20 group B patients. Verapamil suppressed spontaneous VT in 1 group A patient and in 4 group B patients. During a mean follow-up of 19 months for group A and 40 months for group B, no patient had died suddenly or had cardiac arrest.
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PMID:Repetitive, monomorphic ventricular tachycardia: clinical and electrophysiologic characteristics in patients with and patients without organic heart disease. 649 64

A slight middle slurring in V1 and/or V2 with rS morphology (R less than S) in these leads, without right or left bundle branch block is a nearly ignored electrocardiographic finding. The purpose of this work is to provide a prospective and electrocardiographic analysis of this finding. We followed 200 subjects with middle slurring in V1 and/or V2, in the absence of bundle branch block (study group), (age: 41.5 +/- 19 years, follow-up period: 5.7 +/- 2.5 years) and 200 subjects with rS morphology in V1-V2 without the middle slurring (control group), (age: 39.8 +/- 20 years, follow-up period: 5.2 +/- 2 years). The age, sex, prevalence of organic heart disease, QRS duration and follow-up period did not show significant differences between the two group. In the study group there was a higher prevalence of vertical axis (P less than 0.001), of S1S2S3 morphology (P less than 0.001) and of terminal r wave in a VR (P less than 0.05) compared to control group. During the follow-up period, a right bundle branch block appeared in 19 subjects of study group (incomplete in 15 and complete in 4) and in 2 (complete) of control group (P less than 0.001). A left bundle branch block appeared only in one patient of study group and in one of control group. We conclude that the isolated slight middle slurring in V1-V2 expresses an initial involvement of the right bundle branch system and increases the likelihood of appearance of right bundle branch block.
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PMID:Slight middle slurring in V1-V2 without bundle branch block. An electrocardiographic and follow-up study. 651 Jun 18

Endocardial catheter mapping was performed in 18 patients with left bundle branch block (LBBB). Four patients had no organic heart disease (group I), six had cardiomyopathy (group II), and eight had coronary artery disease and previous infarction (group III). Twelve patients had one septal site of left ventricular endocardial breakthrough, while six had two left ventricular endocardial breakthrough sites, with one site always being septal. There was no significant difference among the groups with respect to time of left ventricular breakthrough (group I, 44 msec after the onset of the QRS complex; group II, 58 msec; and group III, 51 msec). Total left ventricular endocardial activation time was significantly longer in group III (119 msec) than group I (81 msec; p less than .05) and group II (61 msec; p less than .001). Duration of total right ventricular endocardial activation was 36 msec (seven patients). The final site of right ventricular activation was at 44 msec after the onset of the QRS complex. We conclude that (1) right ventricular activation occurs before initiation of left ventricular activation in patients with LBBB, (2) left ventricular endocardial activation in patients with LBBB most likely occurs as a result of right-to-left transseptal activation, (3) left ventricular endocardial activation sequence in patients with LBBB is heterogeneous, and (4) patients with coronary artery disease and LBBB have significantly longer total left ventricular endocardial activation times than patients with no organic heart disease or those with cardiomyopathies.
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PMID:Endocardial activation of left bundle branch block. 670 67

Twenty-nine patients with apparent ventricular tachycardia (VT) of left bundle branch block (LBBB) morphology were evaluated. Tachycardia was associated with an organic basis in 24 of 29 patients: 7 had Mahaim fibers of the nodoventricular type, 7 had arrhythmogenic right ventricular dysplasia, 5 had coronary heart disease, 3 had biventricular cardiomyopathy, and 2 had associated congenital heart disease. In many patients the underlying cardiac disease was not readily apparent. In the patients with a Mahaim fiber, the electrocardiogram taken during sinus rhythm was frequently normal. A reentry tachycardia with anterograde conduction over the nodoventricular fiber could mimic VT as diagnosed by the usual criteria; nodoventricular fibers were, therefore, often unsuspected before electrophysiologic evaluation. In patients with arrhythmogenic right ventricular dysplasia, cineangiography demonstrated abnormalities of the right ventricle, but only minor or no abnormalities of the left ventricle. Clinical and electrocardiographic features were not distinctive. Of the 29 patients, 22 had serious symptoms accompanying the tachyarrhythmia or had required cardioversion. Patients were followed up for an average of 20 months: 4 patients died. Thus, VT exhibiting an LBBB morphology is not uncommon and is frequently associated with organic heart disease, serious symptoms, and significant mortality. Right ventricular angiography and electrophysiologic study may clarify the diagnosis in these patients.
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PMID:Clinical spectrum of ventricular tachycardia with left bundle branch morphology. 684 49

A review of the electrocardiogram in the aged and the comparison of prevalence of ECG abnormalities in the young and aged suggest that: 1. The same criteria for normal ECG should be applied to both groups. Some minor changes in advancing age can be accepted as normal and reflecting physiologic changes attending growth, changes in anteroposterior diameter of the chest and lung volume, and so on. 2. The abnormal ECG is most likely a marker of anatomic heart disease or clinical heart disease, or both. 3. The incidence of abnormal electrocardiograms increases with age and heart disease. 4. The specific ECG abnormalities which have a high degree of correlation with clinically evident heart disease include atrial fibrillation, left bundle branch block, intraventricular conduction defects, and ST segment and T wave changes. 5. Myocardial infarction, left anterior hemiblock and right bundle branch block did not correlate with presence of clinical disease, but strong evidence suggests that these findings reflect anatomic disease.
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PMID:The electrocardiogram in the aged. 728 46

To investigate the right ventricular activation, filtered bipolar recordings (1 cm interelectrode distance) of Apex (RVA), Inflow tract (RVIT) and Outflow tract (RVOT) of the right ventricle were obtained in 4 groups of subjects. 1st group: 25 cases with normal QRS; 2nd group: 7 cases with left ventricular conduction disturbances (4 LBBB and 3 LAH patterns); 3rd group: 20 cases with chronic coronary heart disease (CCHD) and RBBB alone (5 cases) or combined with LAH (15 cases); 4th group: 9 young subjects without heart disease (7 cases) or ostium secundum atrial septal defect (2 cases) and RBBB pattern. The activation times were calculated from the beginning of the QRS in the first endocavitary rapid deflection. The data obtained (average +/- s.d.) for QRS duration (QRSd), RVA, RVIT and RVOT were respectively: 1st group: 97 +/- 9, 23 +/- 9, 36 +/- 9, 39 +/- 8; 2nd group: 133 +/- 43, 20 +/- 14, 25 +/- 9, 42 +/- 6; 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. Activation times as expected were similar in 1st and 2nd groups. Significant differences were noted between 1st and 3rd groups (p less than 0.001) in activation times of RVA, RVIT and RVOT. Between 1st and 4th group significant differences were noted in activation times of RVA and RVIT (p less than 0.001) while no significant differences were observed for RVOT (p greater than 0.05). In 2 cases of the third group (CCHD) and in the 2 cases of atrial septal defect the activation time of RVA was within the normal range suggesting a peripheral block. In the cases of the 3rd group with troncular RBBB activation times of RVIT and RVOT were significantly related to the QRSd (r = 0.79 and 0.65, p less than 0.001 and less than 0.01 respectively), while there was no significant correlation between the activation time of RVA and the QRSd. In accordance with other Authors our study demonstrates that: 1) the RBBB pattern in ASD has a peripheral electrogenesis; 2) the RBBB pattern in CCHD is generally due to a troncular block but our study also suggests the possibility of a distal block in these patients. In contrast with some Authors the RBBB pattern in young people without heart disease was due to a troncular and not to a peripheral block. Finally, the absence of correlation observed in the cases with troncular block of the 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. QRSd and RVIT and RVOT activation times might be explained as follows: 1) in high degree troncular block the RVA activation time is due to the time employed byt the wave front to cross the septum which is probably similar in all the cases; 2) the QRSd depends on the activation time of the peripheral areas which depends on the variable spread of activation of the right ventricle probably due to a variable participation of the specialized conduction system.
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PMID:[The right ventricular activation in ventricular activation delays. An endocardial mapping study (author's transl)]. 732 20

Cardiac arrhythmias, investigated in 1000 persons subjects to a submaximal exercise test, showed an incidence of 6%. The most frequent were the ventricular premature beats, related in more than half of the cases to an organic, probably ischemic, heart disease. Left bundle branch block and ventricular tachycardia were rare and indicated an organic heart disease. Several other rare arrhythmias are discussed. In patients with exercise-induced cardiac arrhythmias, an increased ratio of the tension-time index to maximal oxygen consumption indicates an uneconomical and less efficient cardiac work. The increase of the PEP and of the PEP/LEVT ratio during recovery, in the subjects exhibiting exercise-induced ventricular premature beats, also suggests a lowered cardiac efficiency. These findings support the view that cardiac arrhythmias frequently coexist with an organic, especially ischemic, heart disease.
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PMID:Cardiac arrhythmias and submaximal exercise test. 741 39


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