Atrioventricular block development

Complete atrioventricular block developed 60 hours after the start of an octreotide infusion 50 micrograms/hour for the treatment of vari-ceal bleeding in a patient with hepatic cirrhosis and resolved 6 days after withdrawal of octreotide. The presence or absence of other drugs was not reported. Atropine and saline increased heart rate without a change in rhythm. 

When adenosine (70 micrograms/kg/minute) was given by intravenous infusion to 45 patients with acute myocardial infarction preceding balloon angioplasty, one patient developed persisting hypotension in conjunction with a large inferolateral myocardial infarction (18). Transient hypotension in three other patients resolved with a reduction in dosage. There were no cases of atrioventricular block. 

Amiodarone and carvedilol have been used in combination in 109 patients with severe heart failure and left ventricular ejection fractions of 0.25 (16). They were given amiodarone 1000 mg/week plus carvedilol titrated to a target dose of 50 mg/day. A dual-chamber pacemaker was inserted and programmed in back-up mode at a basal rate of 40. Significantly more patients were in sinus rhythm after 1 year, and in 47 patients who were studied for at least 1 year the resting heart rate fell from 90 to 59. Ventricular extra beats were suppressed from 1 to 0.1/day and the number of bouts of tachycardia over 167 per minute was reduced from 1.2 to 0.3 episodes per patient per 3 months. The left ventricular ejection fraction increased from 0.26 to 0.39 and New York Heart Association Classification improved from 3.2 to 1.8. The probability of sudden death was significantly reduced by amiodarone plus carvedilol compared with 154 patients treated with amiodarone alone and even more so compared with 283 patients who received no treatment at all. However, the study was not randomized, and this vitiates the results. The main adverse effect was s)mptomatic bradycardia, which occurred in seven patients two of those developed atrioventricular block and four had sinoatrial block and/or sinus bradycardia one patient developed slow atrial fibrillation. 

A 59-year-old man developed third-degree atrioventricular block after using an extract of Nerium oleander transdermally to treat psoriasis (24). A fatality due to drinking a herbal tea prepared from N. oleander leaves, erroneously believed to be eucalyptus leaves, has been reported (25). 

Clonidine causes sinus bradycardia and atrioventricular block, as illustrated by two cases, one a 10-year-old boy (6) and the other a 71-year-old woman (7), who developed Wenckebach s phenomenon. Clonidine was also studied in seven patients subjected to electrophysiological studies after 5 weeks of therapy (8). It slowed the sinus rate and increased the atrial pacing rate, producing Wenckebach s phenomenon, indicating depressed function of the sinus and AV nodes. 

A 47-year-old man taking furosemide for hypertension was given diltiazem 300 mg/day to achieve better blood pressure control 1 month later he developed atrioventricular block, resolved by atropine. 

A 62-year-old hypertensive man with renal artery stenosis, an adrenal adenoma, peripheral artery disease, and an abdominal aortic aneurysm developed a hypertensive crisis with chest pain. He was treated with nitrates, heparin, aspirin, and nicardipine, which were afterwards replaced by diltiazem 200 mg/day, because of persistent chest pain. He developed atrioventricular block 2 hours after the second dose of diltiazem, and was successfully treated with a pacemaker. 

Doxapram is used to treat idiopathic apnea in premature infants. Second-degree atrioventricular heart block developed after its administration to three neonates (6). 

Five patients with acute accidental poisoning with V. album rapidly developed nausea, vomiting, abdominal pain, hypotension, and bradycardia (26). In four cases the electrocardiogram showed sinus bradycardia and in one there was complete atrioventricular block with an ectopic atrial bradycardia and an intermittent idioventricular rhythm. Symptomatic treatment and/or atropine led to recovery within a few hours. 

A 22-year-old woman took an overdose of propafenone (amount unknown) and developed tetany and then generalized convulsions requiring intravenous clonazepam (44). She had a low blood pressure and first-degree atrioventricular block associated with prolonged intraventricular conduction. She was intubated and given intravenous fluids, equimolar sodium lactate, dopamine, and adrenaline. Her cardiac conduction returned to normal. 

An 86-year-old Japanese man received a pacemaker for atrioventricular block, and 2 months later developed a scaly erythema over the implantation site and later widespread nummular eczema. Histologically, the lesions showed slight spongiosis, intracellular edema, moderate acanthosis in the epidermis, and perivascular infiltration with thickened capillary walls in the dermis. The pacemaker contained titanium and a variety of other metals, but patch tests were all negative. However, titanium sensitivity was demonstrated by intracutaneous and lymphocyte stimulation tests. 

A 79-year-old white woman developed extreme fatigue and dizziness (34). Her heart rate was 40/minute and her blood pressure 80/40 mmHg. An electrocardiogram showed complete atrioventricular block, an escape rhythm at 50/minute, and QT interval prolongation to 583 milliseconds. This event was attributed to concomitant treatment with verapamil 480 mg/day and erythromycin 2000 mg/day, which had been prescribed 1 week before admission. 

Symptoms of intoxication include (1) bradycardia, (2) prolongation of the QRS interval, (3) atrioventricular block, and (4) induced arrhythmias. These symptoms occur at blood concentrations of procainamide and NAPA exceeding 30[ig/mL. Hypotension sometimes encountered in procainamide therapy is not related to excessive plasma concentration. The development of systemic lupus erythematosus associated with procainamide therapy is not related to plasma concentration but is associated with the acetyla-tor status of the patient slow acetylators predominate in the group in whom the syndrome develops. 

After taking rimonabant for 3 weeks a man developed dizziness, palpitation, and exertional dyspnea. He had atrial fibrillation, for which no other causes were found. Rimonabant was withdrawn and 10 days later the rhythm had reverted to sinus rhythm with first-degree atrioventricular block. 

A 57-year-old woman developed acute mental status changes. Her serum lithium concentration was 2.2 mmol/l and the creatinine 187 (imol/1. She was hypotensive (70/ 45 mmHg) and bradycardic (37/minute). An electrocardiogram showed complete atrioventricular block. Her hemodynamic status normalized when she cleared the lithium. 

Patients with impaired function of the sinus node or impaired atrioventricular conduction can develop sinus bradycardia, sinus arrest, heart block, hypotension and shock, and even asystole, with verapamil (139) or diltiazem. These drugs should not be given to patients with aberrant conduction pathways associated with broad-complex tachydysrhythmias, and they can cause severe conduction disturbances in hypertrophic cardiomyopathy. 

Most side effects of /3-blockers are an extension of their ability to antagonize /3-adrenoceptors. /3-Blockade in the myocardium can be associated with bradycardia, atrioventricular conduction abnormalities (e.g., second- or third-degree heart block), and the development of acute heart failure. The decreases in heart rate actually may benefit certain patients with atrial arrhythmias (e.g., atrial fibrillation and atrial flutter) and hypertension by both providing rate control and lowering BP. /3-Blockers usually only produce heart failure if... 

---