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At least 271 records · Page 15Linked to original sources
PubMed1989

Chloroquine abuse and heart block in Africans.

Twelve of 30 Africans with heart block gave a history of chronic chloroquine abuse. Eleven of these had evidence of chloroquine retinopathy whereas four of the 18 nonabusers had abnormal ophthalmologic findings, thought to be senile changes. The chronic chloroquine abusers were all male and were younger (mean age 51.6 years) than the non-abusers (mean age 61.2), nine of whom were female. Serum chloroquine levels were not helpful diagnostically. In the absence of other etiological factors, chronic chloroquine toxicity is important in the causation of heart block in Africans.

Adult↗
PubMed1988

Stokes-Adams attacks in congenital complete heart block.

Stokes-Adams attacks are a well-known complication of congenital complete heart block. Although they are generally felt to be precipitated by either bradycardia or tachycardia, this is poorly documented. A case is presented in which a 23 month old with congenital complete heart block and an intermittently prolonged QT interval had a Stokes-Adams attack during a spontaneous episode of ventricular tachycardia. The combination of congenital complete heart block and a prolonged QT interval carries a significant risk of ventricular tachycardia.

Adams-Stokes Syndrome↗
PubMed1995

In utero identification and therapy of congenital heart block.

To determine the feasibility and effectiveness of prenatal therapy of congenital heart block (CHB), information was sought regarding the timing of identification of CHB in 72 pregnancies and the outcome of those pregnancies in which the mothers were administered corticosteroids. Mailed questionnaires with telephone follow-up, data from primary physicians and chart review were utilized. In 38 (53%) of affected pregnancies CHB was identified between 16 and 24 weeks of gestation, in 17 (24%) between 25 and 30 weeks of gestation, in 8 (11%) between 31 and 37 weeks, and in 5 (7%) between 38 and 40 weeks. In four pregnancies the timing was unknown. Five women were taking prednisone for disease activity prior to the discovery of CHB and in six other women prednisone therapy was initiated at or about the time CHB was identified. In 19 pregnancies, women were given fluorinated steroids (available to the fetus in an active form) as attempted therapy after the discovery of CHB. Of these, one fetus with second degree block reverted to sinus rhythm and two with third degree block exhibited an improvement in the degree of block. In eight fetuses pleural and/or pericardial effusions resolved. In conclusion, the gestational period of heightened fetal vulnerability for the development of heart block is in the mid second to early third trimester. Although there is no evidence that maternal prednisone should be used prophylactially, fluorinated steroids may be efficacious after the identification of heart block, particularly with regard to an associated myocarditis.

Dexamethasone↗
PubMed1982

Heart block in children. Evaluation of subsidiary ventricular pacemaker recovery times and ECG tape recordings.

To evaluate subsidiary ventricular pacemaker function in 20 children with congenital or surgically induced complete heart block, we measured recovery times following overdrive ventricular pacing. Long-term ECG tape recordings were performed in eight of these children. Ages ranged from 1 month to 17 years. The resting R-R intervals ranged from 595 to 1,740 msec. The ventricles were paced at various cycle lengths of 400 to 1,000 msec with either transvenous electrode catheters or surgically implanted epicardial electrodes. His bundle recordings showed that the site of block did not allow separation of patients with symptoms from those without symptoms. Prolonged recovery times were present in patients with block above the His bundle recording site who had symptoms of syncope or dizziness, as well as in patients who had a wide QRS. However, some asymptomatic patient with heart block above the His bundle recording site also had long recovery times. None of the asymptomatic patients who had ECG tape recordings had paroxysmal tachycardia in more than 300 hours of recordings. However, one symptomatic patient with congenital heart block and a prolonged recovery time had brief episodes of paroxysmal ventricular tachycardia that produced no symptoms at the time of recording. The results suggest that the coexistence of prolonged recovery times and paroxysmal tachycardia may be predisposing factors to the development of symptoms in patients with complete heart block. We believe that further electrophysiologic investigation of this possibility is warranted in patients with heart block.

Adolescent↗
PubMed1981

Disopyramide-induced heart block.

A 57-year-old woman with right bundle branch block +LPH and ventricular premature contractions developed complete heart block (CHB) following administration of disopyramide phosphate (Norpace). The ECG at the onset of CHB suggested block to have occurred in the trifascicular conduction system. On rechallenging the patient with the drug following the implantation of a permanent pacemaker, intermittent complete heart block developed. This case suggests that disopyramide should be used with caution in patients with bifascicular block patterns on ECG.

Bundle-Branch Block↗
PubMed1996

Apoptosis as a possible cause of gradual development of complete heart block and fatal arrhythmias associated with absence of the AV node, sinus node, and internodal pathways.

BACKGROUND: Gradually progressive development of complete heart block in young people often is associated with cardiac arrhythmia and sudden death, but the pathogenesis remains unexplained. METHODS AND RESULTS: A young woman with complete heart block died suddenly. Her mother had serological but no clinical evidence of antiphospholipid syndrome. Five brothers of another family had arrhythmia and heart block. Three died suddenly; the other two have automatic defibrillators and are alive. The hearts from the young woman and two of the three brothers who died were available for our histological examination of their cardiac conduction systems. In two of the three hearts, the AV node was absent; in the third heart, only fragments of the AV node remained. In all three hearts, the sinus node was nearly destroyed by a noninflammatory degeneration with no abnormal fibrosis or infiltrate. In each heart, the interatrial and internodal pathways were similarly involved, and in the young woman, there were no myocardial cells in which these pathways normally exist. CONCLUSIONS: In these three subjects with progressive development of complete heart block and various arrhythmias, all of whom died suddenly, the histological abnormalities of their cardiac conduction systems are best interpreted as resulting from apoptosis. Programmed cell death is a logical explanation for the pathogenesis of this puzzling clinical picture.

Adolescent↗
PubMed1999

Heart block after induction of anesthesia in a child.

A case of complete heart block occurred after induction of halothane anesthesia in a previously healthy child. The patient underwent repair of an umbilical hernia under general anesthesia. After a standard halothane, nitrous oxide, and oxygen mask induction, complete heart block was noted on the electrocardiographic monitor. Atropine and 100% oxygen were administered, and sinus tachycardia resulted. With the immediate stabilization of the patient's condition, the surgical team agreed to proceed with the case. After deepening of the level of anesthesia, first with halothane and then with desflurane and easy intubation of the trachea, complete heart block again was noted. Oxygen was administered at 100%, sinus tachycardia resumed, the case was canceled, and the patient emerged from anesthesia without further incident. The patient had an uneventful recovery and was discharged to home.

Anesthetics, Inhalation↗
PubMed1978

The surface electrocardiogram in complete intra-his heart block.

In some cases, the surface ECG may be useful in predicting that the level of heart block is intra-His rather than supra-His. In five patients with third degree heart block the level of block was documented to be within the His bundle. In all five, the surface ECG showed an escape rhythm with QRS complexes of less than 0.10s. duration. The initial QRS forces were abnormal in that "septal" q waves were not present in leads 1 and V6. Two of the five patients had occasional conducted beats with normal "septal" q waves. Thus, heart block associated with an escape rhythm of narrow QRS morphology but abnormal septal depolarization may indicate that the level of the block is intra-His rather than supra-His.

Aged↗
PubMed2003

Selective atrionodal input ablation for induction of proximal complete heart block with stable junctional escape rhythm in patients with uncontrolled atrial fibrillation.

BACKGROUND: The study tests the hypothesis that ablating all inputs to the atrioventricular (AV) node can result in complete heart block with stable junctional escape rhythm. METHODS AND RESULTS: We attempted atrionodal input ablation in 76 consecutive patients with uncontrolled atrial fibrillation. Fast and slow pathways were first ablated. If there was no AV block, additional energy applications were done between fast and slow pathway locations. The patients were followed for 42 +/- 11 months. Group I (n = 57) comprised patients with complete heart block and junctional escape rhythm (53 +/- 4 beats/min) at the end of the procedure. The escape rhythm remained stable throughout follow-up. Group II (n = 15) were patients who failed the stepwise atrionodal input ablation and required AV junctional ablation guided by His bundle potential to achieve complete heart block. Four patients showed a slow escape rhythm after ablation (33 +/- 4 beats/min). Others had no escape rhythm. All 15 pts remained pacemaker dependent. The total death rate of groups I and II was 18/57 (31.6%) vs 10/15 (66.7%), respectively (p < 0.02). These differences could not be explained by a difference of left ventricular ejection fraction (0.42 +/- 0.07 vs 0.41 +/- 0.04, respectively, p = NS). CONCLUSIONS: (1) In most patients, ablation of both fast and slow pathways did not result in complete heart block, indicating the presence of multiple atrionodal inputs. (2) Ablation of all atrionodal inputs may result in complete heart block with stable junctional escape rhythm. (3) As compared with AV junctional ablation, atrionodal input ablation was associated with a lower mortality rate on long-term follow up.

Aged↗
PubMed2001

Treatment of fetal congenital complete heart block with maternal administration of beta-sympathomimetics (terbutaline): a case report.

We report a case of fetal congenital heart block treated with maternal administration of beta-sympathomimetics. The case was diagnosed as fetal complete heart block associated with maternal anti-Ro/SS-A antibody at 22 weeks of gestation. By fetal sonography, the ventricular rate was revealed to be 60 beats/min and mild cardiomegaly was shown. We initiated maternal administration of a sympathomimetic, specifically terbutaline, to prevent fetal heart failure. An increase in the fetal ventricular rate and an improvement in cardiac function were both achieved during the treatment. A viable infant was delivered by an elective cesarean section without complications at term. Maternal administration of the beta-adrenergic agent terbutaline is suggested to be effective for improving fetal congenital heart block in order to prevent heart failure in utero.

Adult↗
PubMed1989

Congenital complete heart block in patients without anatomic cardiac defects.

Forty-three patients with congenital complete heart block and an otherwise structurally normal heart were reviewed in an effort to better define the profile of an anatomically homogenous group and to identify factors that may predict the need for pacing. Fourteen patients (32%) developed "symptoms" during follow-up, including two with out-of-hospital cardiac arrest. Heart rate on electrocardiogram or Holter monitor did not clearly distinguish this subgroup. The presence of alternate "risk factors," such as atrial enlargement seen on electrocardiogram, cardiomegaly seen on x-ray film, or prolonged QT interval were independent predictors of symptoms and poor outcome (p less than 0.05). Ventricular ectopy determined on Holter monitoring was also common among the symptomatic group, although this finding was inconsistent. Prophylactic pacing is indicated in select patients with congenital complete heart block and otherwise normal anatomy. Surveillance for rick factors beyond rate criteria alone may refine this selection process.

Adolescent↗
PubMed1982

Delayed maternal lupus after delivery of offspring with congenital heart block.

An association between maternal connective tissue disease, especially lupus, and congenital complete heart block in the offspring has been recently recognized. In general, maternal lupus is clinically or serologically manifest by the time the infant with heart block is born, although in some cases the appearance of maternal disease may be delayed for some time. Systemic lupus erythematosus occurred in the mother of three children with congenital heart block 16 years after delivery of her first affected child. To our knowledge this represents the longest latency period for the appearance of maternal disease on record.

Adult↗
PubMed1984

Peri-operative management and administration of anaesthesia in children with congenital complete heart block. A case report and review.

The clinical presentation and natural history of congenital complete heart block (CHB) differ from those of acquired third-degree heart block. Although perioperative prophylactic cardiac pacing is considered mandatory in patients with acquired CHB, it is not usually necessary in children with asymptomatic congenital heart block. The anaesthetist should be able to identify which patients require temporary perioperative pacing, and should modify his anaesthetic technique appropriately for patients who do not. An 8-year-old patient with congenital CHB who required emergency surgery for acute appendicitis is presented and the anaesthetic management, including the indications for pacing, is discussed.

Anesthesia, General↗
PubMed1994

Sleep apnea and complete heart block.

Sleep apnea has been associated with various types of cardiac dysrhythmias; however, complete heart block has not been reported to occur in this condition. This brief report describes the case of a patient who developed episodes of prolonged complete heart block during sleep apnea. Nasal continuous positive airway pressure resulted in complete resolution of the heart block.

Electrocardiography↗
PubMed1998

Development of a model of complete heart block in rats.

Atrioventricular (AV) block is a useful substrate for the study of cardiac physiology. The objective of this investigation was to develop a straightforward and reproducible model of permanent AV block in rats. Working through a sternotomy, we used an epicardial fat pad between the aortic root and the right atrial wall of the rat as a landmark for the site for injection of 70% ethanol (5-10 microl) into the myocardium 3 mm below the epicardial surface. Stable, complete heart block was produced in 23 of 28 rats (82%) with a success rate of 100% in the last 16 rats of the series. Saline injection produced no heart block in 15 rats. A separate group of 14 animals was allowed to recover. Chronic heart block was achieved in all ethanol-injected animals for up to 7 days before death. The survival rate in the recovered rats was 90% in the ethanol-injected group and 100% in the saline-injected control group. Acute hemodynamic changes following the production of heart block consisted of an increase in central venous pressure, a decrease in systolic blood pressure, a decrease in left ventricular pressure, and a decrease in change in pressure over time. Chronic hemodynamic changes demonstrated a return to baseline of the central venous pressure, a persistent decrease in systolic blood pressure, and a decrease in left ventricular pressure. After the rats were killed and the hearts were dissected, discrete areas of myocardial damage were identified histologically in the atrial septum near the AV conduction axis tissue in the ethanol-injected hearts. Complete heart block was associated only with lesions extending into the specialized muscle of the AV node or His bundle. Focal mild hemorrhage, inflammation, and damaged myocardial fibers were observed in the acute stage, whereas healing lesions were characterized by granulation tissue and fibrosis replacing conduction tissue. The simple technique described provides a reproducible model for permanent, complete heart block and the study of cardiac function.

Adipose Tissue↗
PubMed1982

Long-term follow-up of young adults following permanent pacemaker placement for complete heart block.

Young adults with nonsurgically induced complete heart block (CHB) do not necessarily have a benign prognosis and pacemaker (PM) implantation may be necessary. No one has reported long-term PM follow-up in young adults with CHB. We studied 13 patients aged 15 to 37 years (mean 24 years) at PM implantation. There were nine female and four male patients. All were functional class II or III (NYHA) before PM implantation. Syncope, dizziness, fatigue, shortness of breath, and dyspnea on exertion were the most common symptoms. Cardiac catheterization findings (11 of 13 patients) were normal in five, and additional cardiac anomalies were present in six. His bundle studies (9 of 13 patients) showed absent AH intervals in all patients, with HV intervals not identified in two, 20 to 30 msec in one, and 30 to 50 msec in six patients. Holter monitor recordings (8 of 13 patients) demonstrated CHB in all eight with intermittent second- to third-degree block in two of three patients. Two patients had occasional premature ventricular contractions. Stress exercise tests (9 of 13 patients) demonstrated increased ventricular rate response (although subnormal in some patients); symptoms developed in seven. One patient had ventricular ectopy. All 13 patients were contacted 3 months to 7 years (mean 4 years) after PM implantation. Two patients had died, but the deaths were not related to PM dysfunction. All patients who are currently alive had marked improvement in functional symptomatology and all are currently functional class I. CHB is not a benign condition in young adults and may require PM implantation, which improves symptoms and allows the patient to lead a normal life.

Adult↗
PubMed2005

Anesthetic management of the neonate with congenital complete heart block: a 16-year review.

BACKGROUND: Anesthesia for patients with complete heart block can be associated with significant hemodynamic instability. The aim of this study is to review our anesthetic experience of neonates with congenital complete heart block (CCHB) who underwent placement of either a temporary epicardial pacing system or a permanent epicardial pacemaker. METHODS: The anesthetic management of neonates with CCHB who underwent pacemaker placement at a single institution over a 16-year period was reviewed. RESULTS: Twenty-four neonates were identified, 17 with a structurally normal heart (NL) and seven with associated congenital heart defects (CHD). Median (range) gestational age was 36.9 (26-41) weeks, birth weight 2.9 (1.0-4.1) kg, and baseline heart rate 47 (38-80) b.min(-1). A temporary epicardial pacing system was placed in six patients (four CHD, two NL; P = 0.003) following institution of mechanical ventilation and inotropic support for a low cardiac output state, and a permanent epicardial pacemaker was placed in 18 patients. Atropine 0.02 mg.kg(-1) IV prior to induction (n = 5) increased heart rate less than 20%. Intraoperative hypotension was documented in nine neonates, five of seven with CHD and four of 17 with NL (P = 0.02). In four patients (44%) hypotension occurred despite concurrent inotropic support. Intraoperative cardiac arrest occurred in one neonate, necessitating institution of extracorporeal membrane oxygenation. Two patients (8.3%) died in hospital from complex CHD and complications of prematurity. CONCLUSIONS: Early institution of mechanical ventilation, inotropic support and pacing are necessary in the neonate with CCHB and poor hemodynamic function, particularly with coexisting CHD or prematurity.

Anesthesia↗