Ivabradine improves all aspects of quality of life assessed with the 36-item short form health survey in subjects with chronic ischemic heart disease compared with beta-blockers.

No published studies have evaluated quality of life (QOL) with the 36-item Short Form Health Survey (SF-36) in subjects with chronic stable angina pectoris (CSAP). We evaluated whether a 1-month treatment with 10 mg ivabradine (IVA) or ß-blockers (bisoprolol 2.5 mg/day, carvedilol 12.5 mg/day, atenolol 50 mg/day) improves the QOL in patients with CSAP. The SF-36 was administered to 238 patients randomized in two groups. QOL and heart rate (HR) results after 1 month of therapy with IVA and ß-blockers (T1) were compared with basal values (T0). Treatments in both groups significantly reduced HR (-11 bpm at T1 compared with T0 in the IVA group, -7 bpm at T1 compared with T0 in the ß-blocker group), but IVA demonstrated a more significant (p < 0.001) reduction in HR than ß-blocker treatment (p < 0.01). We observed a significant improvement in all QOL dimensions in the group treated with IVA, in particular in the sections regarding physical functioning, physical role, and general health (p < 0.001). In the group treated with ß-blockers, we found statistically significant improvement only in the physical functioning and physical role sections (p < 0.01). With ß-blocker treatment, many questionnaire sections showed no statistically significant improvement (body pain, social functioning, emotional role, and mental component summary). IVA treatment significantly improves all aspects of QOL in patients with CSAP, unlike ß-blocker treatment. This improvement is associated with a greater reduction in HR.

Usefulness of transesophageal atrial pacing in hyperkalemia-induced impulse formation and conduction disturbances.

This report describes the usefulness of transesophageal atrial pacing in the treatment of five patients with hyperkalemia-induced bradycardias. Three patients had marked sinus bradycardia while the other two had a regular rhythm with QRS of left bundle branch block morphology, with no P waves visible on the surface electrocardiogram. Four patients were in chronic hemodialysis three times a week, and one had severe post-traumatic hemorrhage. In three patients, hyperkalemia had been precipitated by food intoxication. In one case the cause was unknown while, in the last case, hyperkalemia was due to rapid infusion of stored blood and solutions containing high concentrations of potassium. Transesophageal atrial pacing was performed in all cases utilizing a bipolar catheter introduced into the esophagus and a constant current generator delivering square wave pulses of 10 msec duration and 19-28 mA intensity. Atrial capture, followed by impulse conduction to the ventricles, was constant in all cases, being performed for between 15 and 35 minutes until a normal sinus rhythm was restored. The procedure was well tolerated. The advantages of this procedure as opposed to invasive ventricular pacing are discussed.

High doses of L-carnitine in acute myocardial infarction: metabolic and antiarrhythmic effects.

Fatty acids accumulate in the muscle cells in some carnitine deficiency syndromes due to a variety of genetic defects in intermediary metabolism. L-Carnitine administration may relieve this excess by transporting acyl compounds out of the cell as acylcarnitine. Similar fatty acid accumulation occurs during myocardial ischaemia because of the decreased rate of beta-oxidation, and this has been put forward as a cause of ventricular arrhythmias. This study was carried out to investigate whether administration of high doses of i.v. L-carnitine in patients with acute myocardial infarction could increase urinary excretion of acylcarnitine and reduce early ventricular arrhythmias. Fifty-six patients suffering from acute myocardial infarction, admitted to the Coronary Unit between 3 and 12 h after the onset of symptoms, were included in the study. The design of the study was double blind, parallel and placebo controlled. Allocation of treatment to patients was done randomly after stratification (time from onset of pain and site of infarction). The first group (28 patients) received intravenous L-carnitine at a dose of 100 mg kg-1 b.w. every 12 h for 36 h while the second group (28 patients) received placebo intravenously. Immediately before starting treatment two blood samples were taken (at 5-min intervals) and a further 16 samples were taken at regular intervals over the following 48 h. Patients' urine was collected over the same period of time. Concentrations of free carnitine, short chain acylcarnitine esters and long chain acylcarnitine esters in serum and urine were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Incidence of 'dual A-V nodal pathways' in first- and second-degree type I supra-His A-V block.

The incidence of 'dual A-V nodal pathways', diagnosed on the basis of spontaneous or induced modifications in the PR interval, has been assessed in a group of 168 consecutive patients with first- (77) and second-degree (91) type I supra-His block. 'Dual A-V nodal pathways' were found in 12 cases (16%) with first-degree and in 7 cases (7.7%) with second-degree type I supra-His A-V block. His bundle recording confirmed the hypothesis that PR interval variations observed in these cases are due to modifications in the AH interval and thus to changes in A-V nodal conduction velocity. The electrophysiologic study also showed that the phenomenon was easily reproduced by atrial stimulation. The frequent association between 'dual A-V nodal pathways' and supra-His blocks suggests that the block mechanism should be studied in depth as it could have prognostic and therapeutic implications.

Role of QT prolongation secondary to a postextrasystolic pause as a possible mechanism for the induction of ventricular fibrillation. Report of two cases.

Two patients developed ventricular fibrillation (VF) while undergoing continuous electrocardiographic monitoring. Analysis showed that VF appeared only when a particular combination of circumstances occurred: a postextrasystolic pause, QT prolongation of the subsequent beat and a premature ventricular beat that did not have a short coupling interval. The relevance of this sequence as a trigger mechanism of VF is discussed.

Ventricular fibrillation induced by transesophageal atrial pacing in hypertrophic cardiomyopathy.

Sudden death is a rather frequent occurrence in patients with hypertrophic cardiomyopathy, yet the mechanism is uncertain in most cases. We describe a case of an 18 years old patient with a family history of hypertrophic cardiomyopathy and sudden death in whom ventricular fibrillation could be repeatedly induced by means of transesophageal atrial stimulation with 1:1 AV conduction at a rate of 200 beats min-1 and prevented by pharmacological depression of AV node. The not particularly high ventricular rate at which VF occurred could suggest that in hypertrophic cardiomyopathy a major role in favouring VF induction is played by the electrophysiological properties of the myocardium and that sudden death can occur as a consequence of different atrial tachyarrhythmias.

Effect of adenosine and adenosine-5'-triphosphate on atrioventricular conduction in patients.

This study was carried out to further elucidate the effects of adenosine and adenosine-5'-triphosphate (ATP) on atrioventricular (AV) conduction in patients. Adenosine (0.24 mg/kg) and ATP (0.28 mg/kg) were administered intravenously to 37 patients undergoing intracardiac electrophysiologic evaluation. Both adenosine and ATP depressed AV conduction by lengthening the atrial to His bundle (AH) interval. The effects of adenosine and ATP after rapid intravenous bolus administration were fast in onset (15 +/- 0.5 and 15 +/- 1.5 s, respectively), but transient in duration (10.5 +/- 0.5 s for ATP and 17 +/- 3 s for adenosine). Although muscarinic blockade with 0.04 mg/kg atropine shortened the AH interval from a control value of 123 +/- 12 to 74 +/- 4 ms, it did not modify the effects of adenosine or ATP, or both (that is, latency and duration of the effects were not significantly different from before atropine administration). In contrast, aminophylline, a competitive antagonist of adenosine, completely prevented the effects of adenosine and ATP. Aminophylline alone also shortened the AH interval from a control value of 98 +/- 9 to 74 +/- 9 ms. This decrease was blocked by propranolol (0.1 mg/kg), whereas propranolol did not influence the ability of aminophylline to antagonize the effects of adenosine or ATP, or both. Thus, the catecholamines released by aminophylline are unlikely to account for the ability of aminophylline to antagonize the effects of adenosine and ATP. In conclusion, these findings indicate that intravenously administered adenosine and ATP are equally effective in producing AV block that is antagonized by aminophylline but not by atropine.

[Complicated ventricular arrhythmias in angina at rest]. / Le aritmie ventricolari complicate in corso di angina a riposo.

To assess the incidence of serious ventricular arrhythmias (SVA) during transient ischemic attacks (IA), 27 patients with severe angina at rest were submitted to Holter monitoring for a total period of 1344 hours. The recorded IA's were 565. To evaluate the time/relation between SVA and ST segment changes, the IA's complicated by SVA were divided in 2 parts: one for the upstroke and plateau phase of ST changes; Hse other for the period of resolution of ST changes and the first 3 minutes after ST return to baseline. SVA's were found in 12 of the 27 patients (44.4%), but only in 29 of the 565 IA's (5.1%). The recorded arrhythmias consisted of: frequent ventricular premature beats (VPB) (greater than or equal to 5/min) in 8 patients, multifocal VPB in 6, paired VPB in 10, ventricular tachycardia in 5, R on T phenomenon in 2. No correlations were found between the occurrence of SVA during IA and type of ST changes, location of ST changes, occurrence of the same arrhythmias outside the IA's. SVA's were significantly more frequent during IA associated with pain than during silent IA. When considering only IA associated with ST elevation, a relation was found between the occurrence of SVA and amplitude and duration of ST displacement. The same relation was not observed when IA's associated with ST depression were taken in consideration. Among the 29 IA's complicated by SVA, 22 showed the arrhythmias during the first phase (3.8% of all IA's) and 7 during the second phase (1.3% of all IA's); 6 of these 7 IA's were associated with ST elevation.