SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
First degree atrioventricular block occurred in a 68 year old man with a large right atrial myxoma. This conduction abnormality resolved within three months of successful surgical removal of the tumour. It is suggested that mechanical compression by the myxoma on either the underlying conduction tissue or the interventricular septum is likely to have caused this phenomenon.
A family of complete atrioventricular block (FCAVB) of adult onset was reported. A 36-year-old-female had 1 degree AH block, atrial and ventricular premature beats and mild sinus node dysfunction. Her father had complete AV block and died of it. A 57-year-old uncle and a 52 years-old uncle had bradycardia from 44, 5 years of age and 51 years of age, respectively, and their ECG showed complete AV block with narrow QRS waves. They were implanted with permanent pacemakers. Her grandmother died a sudden death of Adams-Stokes attack. Acquired heart diseases were not seen in any of the family Thus, this family was thought a FCAVB of adult onset.
Sixty-five patients with congenital complete atrioventricular block have been studied. The median age at time of diagnosis was 7 months with 26 infants being diagnosed prior to 1 month of age. Anatomic heart disease was present in 25/65 (39%) infants, with ventricular inversion/L-transposition of great arteries complex occurring in 20/25 infants (80%). The site of block was above the bundle of His in 11 of 18 (61%) patients studied, in the bundle of His in three of 18 (17%), and below the bundle of His in two of 18 (11%). Permanent pacemakers were implanted in 17 (26%). Ten patients (15%) have died. The highest risk was in patients with anatomic heart disease and patients diagnosed early in life.
BACKGROUND: Paroxysmal atrial tachyarrhythmias have been frequently detected in patients paced for atrioventricular block. However, it is not yet clear which is the actual incidence of such arrhythmias and if they were preexisting but not recognized, or if they could be related to the device. METHODS: One hundred and forty-five patients with a diagnosis of second or third degree atrioventricular block were enrolled into the study. One hundred and twenty-four received a pacemaker Medtronic Thera DDD and 21 a Medtronic Thera VDD. High rate atrial episodes were evaluated for 3 months after enrollment. Atrial electrograms documenting paroxysmal atrial fibrillation (AF) were stored and programming of atrial sensitivity and pacemaker diagnostics was very strict in order to exclude short and false positive AF episodes. RESULTS: Thirty-six patients (35%) in the DDD group and 8 (42%) in the VDD group presented with AF (p = NS). The mean number o
A 25-year-old male was admitted to hospital with a 3-day history of worsening faintness. The electrocardiogram showed complete atrioventricular block. Echocardiography showed generalized hypokinesis and prominent trabeculations ranged from the apex to the mid-ventricular lateral wall of the left ventricle as well. Furthermore, trabeculations in the left ventricle were seen in his sister and brother. Thus, isolated ventricular noncompaction (IVNC) was diagnosed and a permanent pacemaker was implanted. Common clinical symptoms of IVNC are heart failure, ventricular arrhythmias, and embolic events. This is the first reported adult case of IVNC disclosed by the presence of complete atrioventricular block.
We report on four elderly women in whom carbamazepine was suspected of inducing sinus node dysfunction (3 patients) and atrioventricular block (1 patient). Patients were treated with carbamazepine, 200 to 600 mg a day, for trigeminal neuralgia (n = 3) or epilepsy (n = 1). After 1 to 16 months of carbamazepine therapy, these patients were admitted to our emergency room because of bradyarrhythmia. Their conduction disturbances on electrocardiographic monitoring disappeared immediately after the cessation of carbamazepine intake. Provocation tests were performed on three patients. Because of renal insufficiency, one patient could not undergo the provocation test. Her carbamazepine clearance was markedly decreased. Carbamazepine induced sinus arrest in two patients within 48 hours after intake, but did not induce atrioventricular block in the remaining patient. In two patients, computer simulation of carbamazepine pharmacokinetics was performed and disclosed a clear-cut relationship between the plasma concentration of carbamazepine and the frequency of sinus arrest. During the test, the maximum plasma carbamazepine concentration in these two patients did not exceed the therapeutic range. However, it did exceed the range in the one with a negative test. Our results suggest that careful monitoring of ECG and plasma drug concentration is required with carbamazepine therapy, especially in elderly women.
OBJECTIVES: The goal of this study was to determine how often atrioventricular (AV) block is really caused by medications. BACKGROUND: Beta-blockers, verapamil, and diltiazem are considered a cause of AV block for which pacemaker implantation is not indicated. However, it is not known if such patients can expect a benign course after discontinuation of the culprit medication. METHODS: Consecutive patients with II or III degree AV block not related to acute myocardial infarction, digitalis toxicity, or vasovagal syncope were studied. The level of AV block (AV-nodal or infranodal) was defined by electrocardiographic criteria. The cause and effect relation between AV block and drugs was defined according to the response to drug discontinuation. RESULTS: Of 169 patients with AV block, 92 (54%) were receiving beta-blockers and/or verapamil or diltiazem. Patients receiving medications had similar clinical and electrocardiographic characteristics with patients who had AV block in the absence of drugs. Drug discontinuation was followed by resolution of AV block in 41% of cases, whereas spontaneous improvement of AV conduction occurred in 23% of patients who had AV block in the absence of drugs. However, 56% of the patients for whom drug discontinuation led to resolution of AV block had recurrence of AV block in the absence of therapy. Atrioventricular block that was "truly caused by drugs" was found in only 15% of patients who had II or III degree AV block during therapy with beta-blockers, verapamil, or diltiazem. CONCLUSIONS: Atrioventricular block is commonly "related to drugs" but is rarely "caused by drugs."
Swallow or deglutition syncope is a very unusual but treatable disorder. A 44-year-old male presented with multiple, recurrent episodes of complete atrioventricular block associated with swallowing. Over a 24-hour period, 92 episodes of complete atrioventricular block occurring with meals were recorded by Holter monitoring. Evaluation did not demonstrate any underlying esophageal or cardiac disease. A trial of anticholinergic medications was unsuccessful. The patient's symptoms resolved following placement of a demand cardiac pacemaker. This is a rare but potentially lethal disorder that can be successfully treated if recognized. Physicians should be alerted to symptoms of lightheadedness or syncope during meals.
OBJECTIVES: We sought to determine the incidence, nature, and predisposing factors of atrioventricular block (AVB) associated with closure of atrial septal defects (ASDs) using the Amplatzer septal occluder (ASO). BACKGROUND: In our institution, 162 patients underwent ASD closure using ASO between December 1997 and December 2001. This includes small children with large defects. METHODS: Electrocardiographic tracings during ASO implantation and at follow-up visits were reviewed. Anatomic characteristics and device size were assessed as potential risk factors for AVB. RESULTS: Ten patients (6.2%) presented with new-onset (n = 9) or aggravation of preexisting (n = 1) AVB. Atrioventricular block occurred during the procedure (n = 3) or was first noted one day to one week later (n = 7). Patients had first-degree (n = 4), second-degree Wenckebach (n = 4), or third-degree (n = 2) AVB, with no symptoms or hemodynamic compromise. First-degree AVB persisted in two patients at 12 and 33 months of follow-up, whereas most recovered normal AV conduction within one (n = 7) or six months (n = 1). A larger shunt (Qp/Qs ratio 2.8 +/- 0.9 vs. 2.1 +/- 0.8, p < 0.01) and device size (24 +/- 5 vs. 19 +/- 6 mm, p < 0.01) were the only determinant factors for AVB. A device size > or =19 mm was used in 90% (9 of 10) of patients who developed AVB, as compared with 49% of those without AVB (p < 0.02). CONCLUSIONS: Closure of ASDs using the large ASO can be associated with the development of AV block and mandate a closer follow-up. In our series, however, all AVBs resolved or improved spontaneously, with no recurrence at mid-term follow-up.
The influence of heart rate on the maximal work capacity was investigated in 18 patients (mean age 55 years) with a physiological pacemaker implanted on account of chronic complete atrioventricular block of different aetiology. Twelve patients with a dominating atrial sinus activity had a dual chamber DDD pacemaker and six patients with dominating atrial fibrillation or flutter had a single chamber QTVVIR pacemaker. The exercise test was made on a bicycle ergometer using three stimulation regimes in randomized order and without the patient's knowledge of the programmed mode of pacing: 1. VVI pacing with frequency of 30/min exercise on AV block, 2. VVI pacing with a frequency of 70/min, 3. Uhysiological DDD or QT pacing. Patients with atrioventricular block attained an average heart rate of 54 + 9/min and a work capacity of 81 + 31 W. During VVI pacing a mean frequency of 73 +/- 9/min was achieved (+35%, P less than 0.002) and a work capacity of 100 +/- 45 W (+24%, P less than 0.008). The load during physiological stimulation led to an increased heart rate, i.e. to 140 +/- 15/min (+169%, P less than 0.002) and work capacity to 130 +/- 52 W (+61%, P less than 0.002). The increment of work capacity was thus 2.5 times greater during physiological than during standard ventricular pacing (P less than 0.005), when compared with the work capacity of patients during AV block. A more extensive investigation is needed to identify patients who will benefit maximally from physiological pacing.
Two patients who had univentricular heart presented with complaints of recurrent nausea and vomiting during exertion. Exercise study revealed 1:1 atrioventricular conduction and no symptoms at rest; at peak exercise, both patients experienced progressive, high grade, second degree atrioventricular block and nausea. Both patients underwent permanent pacemaker implantation, with relief of symptoms. Exercise testing is important in evaluating patients who are at increased risk of spontaneous atrioventricular block, and exertion-induced nausea may be a clue to its presence.
A randomised study was performed to assess the influence of prophylactic permanent pacing on the incidence of late sudden death in patients surviving transient complete atrioventricular block with acute anterior myocardial infarction. Fourteen patients were studied, of whom ten died within two years, confirming the high overall late mortality in this group. The deaths included eight of the nine paced patients, of whom seven died suddenly. We conclude that prophylactic permanent pacing is not warranted in patients surviving transient complete atrioventricular block with acute anterior myocardial infarction.
OBJECTIVE: We compare the profiles of heart rate variability (HRV) during sleep stages in 9 healthy controls and one subject with second degree atrioventricular blocks (AVB), investigating the role of sympathovagal balance in such pathology. METHOD: Sleep and cardiac records were taken for one night in 9 male subjects from 21:00 to 07:00 h and for two nights in a male subject with AVB. Time and frequency domain indexes of HRV were calculated over 5 min-periods. RESULTS: In one subject without any daytime heart disease, 253 and 318 AVB of type 2 (Mobitz 2) were observed during the two experimental nights, predominantly during rapid eye movement (REM) sleep and the surrounding sleep stage 2 in the second half of the night. In the 9 control subjects, absolute HRV indexes and low frequency (LF)/(LF+high frequency, HF) (where LF and HF are low frequency and high frequency power) were low during slow wave sleep, and significantly increased during REM sleep and the preceding sleep stage 2. In the subject with AVB, these HRV indexes were abnormally low during all sleep stages, with a predominant increase in parasympathetic activity as inferred from low LF/(LF+HF). During wake, however, LF/(LF+HF) normally increased, and the tachycardia observed with the arousal that terminates SWS was preserved in the subject with AVB. CONCLUSION: These results suggest that in the subject with second degree atrioventricular blocks, sleep processes, particularly during REM sleep, create a specific neurological background that prevents an increase in sympathetic tone and triggers cardiac pauses.
Explore the source record for details and available documents.
BACKGROUND: Complete heart block is dreaded perioperatively in patients with chronic bifascicular or left bundle branch block (LBBB) and additional first-degree A-V block. Our aim was to investigate the necessity as well as the efficacy and safety of transcutaneous pacing in the perioperative setting. METHODS: Thirty-nine consecutive patients with asymptomatic chronic bifascicular block or LBBB and prolongation of the P-R interval scheduled to undergo surgery under anesthesia were prospectively enrolled in the study. Preoperatively, a transcutaneous pacemaker (PACE 500 D, Osypka Co.) was applied; its efficacy was checked with intra-arterial blood pressure measurement; the pain level was recorded. Additionally, 24-h Holter monitoring (CM2, CM5) was applied. Occurrences of a block progression or a bradycardia of <40 beats/min with hemodynamic impairment were the defined end points. RESULTS: Thirty-seven of the 39 patients (95%) could be successfully stimulated with a median current strength of 70 mA; whereby 33 of the 39 patients felt moderate to severe pain. There was no perioperative block progression. Three cases of brady-cardia of <40 beats/min with a critical drop in blood pressure occurred; but these patients were successfully treated with drug therapy without pacemaker stimulation. CONCLUSION: The perioperative application and testing of the pacemaker was safe and could be performed in nearly all patients successfully. However, we do not consider a routine prophylactic transcutaneous placement in patients with chronic bifascicular or LBBB and additional first-degree A-V block justified. Nevertheless, appropriate drugs and temporary pacemaker equipment should be easily accessible.
Explore the source record for details and available documents.
Two-dimensional echocardiography, cardiac catheterization, electrophysiologic studies, and biopsies of cardiac and skeletal muscle were performed in a patient with complete atrioventricular block as the initial manifestation of restrictive cardiomyopathy. The patient also showed distal myopathy with rimmed vacuoles. Weakness of the distal leg muscles occurred several years after the initial cardiac manifestations and the patient developed congestive heart failure 1 year before the second admission. Endomyocardial biopsy showed patchy myocardial fibrosis without endomyocardial fibrosis or any other specific findings of myocardial disease. Histochemical examination of skeletal muscle showed the typical features of distal myopathy with rimmed vacuoles. In some patients with atrioventricular block as the initial manifestation of restrictive cardiomyopathy, the cardiomyopathy may be just 1 manifestation of a more generalized disorder affecting both cardiac and skeletal muscle.
The purpose of this study was to examine the histopathological findings of right ventricular endomyocardial biopsies from ten patients less than 60 years of age (47 +/- 9.8 (mean +/- SD) years) with documented atrioventricular block but without apparent heart disease. They underwent electrophysiological testing, echocardiography, coronary angiography, and right ventricular endomyocardial biopsy. Biopsy specimens were assessed for morphologic changes in myocyte diameter, fibrosis, disarray, and degeneration. Electrophysiological testing demonstrated atrioventricular nodal block in 2, intra-His bundle block in 2, and infra-His bundle block in 6 patients. Histology revealed evidence of myocardial fibrosis with either myocyte hypertrophy or disarray in 7 of the 10 patients. The results of electrophysiological testing did not correlate with the histopathological findings or severity. In one patient, heart failure appeared during the follow-up period. We conclude that patients with atrioventricular block of unknown etiology have histological abnormalities of the ventricular endomyocardium in addition to the conduction system disturbances. We consider such cases as constituting one of the disease groups of cardiomyopathy, and suggest that it is necessary to follow up the clinical course in these patients.