Search

It is not well established the importance of 50 Hz alternating current (AC) (that supplies most of house appliances) as a source of inappropriate inhibition of today cardiac pacemakers (PM). This problem has been studied in 58 consecutive patients permanently paced (VVI unipolar) for AV block with 27 different PM models from 11 manufacturers. Under ECG monitoring, 50 Hz AC was applied through a pair of electrodes set at both patient's wrists using a battery powered external source, with voltage ranging between 0 and 45 V. Inappropriate inhibition was considered if PM pauses longer than twice the programmed escape interval of the PM were observed during interference. This happened in 46 patients (79.3%), with PM from all 11 manufacturers, with voltages ranging from 3 to 28 V. In each case, inhibition was seen with a narrow voltage window between no interference detection and interference reversion of the PM. Only 3 patients (5.2%) referred perception of electrical current during the study. Three of the patients studied had complained, prior to the study, about dizziness or presyncope related to touching electrical devices and in all of them inappropriate inhibition was observed during interference. We conclude that: 1) it is possible to demonstrate inappropriate inhibition caused by 50 Hz AC galvanic interference in a high percentage of unipolar PM; 2) This inhibition occurs at current levels that in most cases are not sensed by the cutaneous nerves, and 3) although the problem seems to have little clinical significance it should be investigated in paced patients with symptoms attributable to inappropriate inhibition of their PM.

Serial signal-averaged electrocardiograms were recorded every 72 hours in 60 patients admitted to the coronary care unit with acute myocardial infarction. The prevalence of late potentials was 61.6% (37 patients) during hospitalization. Of these 37 patients, late potentials appeared transiently in 20 (54%), while in 9 patients (24%), once late potentials had appeared, they tended to persist. No specific clinical characteristics were related to the development of late potentials (site of infarction, peak creatine kinasa activity, Killip class, thrombolytic therapy). The presence of late potentials did not identify patients who developed clinically significant ventricular tachyarrhythmias (primary ventricular fibrillation, ventricular tachycardia). The abnormal late potentials were modified by the administration of lidocaine. This lack of correlations suggests that the abnormal signal averaged electrocardiogram and complex ventricular arrhythmias during acute myocardial infarction have different electrophysiological bases. Late potentials could be only a bystander electrophysiological phenomenon without clinical correlation in this clinical phase.

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

A study was made of nodal conduction times of atrial stimuli with fixed coupling intervals, in 23 patients divided into two groups according to their atrial stimulus test response: Group I (continuous AV node function curve; 17 cases) and Group II (dual AV node pathway; six cases). The stimulation protocol involved the delivery of 75 stimuli with a fixed coupling interval 20 ms greater than the effective refractory period (ERP) of the AV node (Group I) or fast pathway (Group II). The atrial coupling intervals (A1A2) and node conduction times (A2H2) were measured. An evaluation was made of the dispersion of intervals with range (R) and of the distribution of A2H2 times (X2 test). In both Groups, R (A2H2) was greater than R(A1A2) (P less than 0.05); R(A2H2) in Group II was greater than R(A2H2) in Group I (P less than 0.001). In Group I the distribution of A2H2 was non-normal in four cases and bimodal in five; in Group II the distribution was non-normal and bimodal in all cases. It is concluded that: (1) the AV node generates a dispersion in its conduction times in the vicinity of its ERP, although the nodal conduction curve is continuous; and (2) the so-called dual pathway may constitute an exaggeration of AV node response inhomogeneity.

We report the appearance of concealed conduction and fatigue phenomenon in the accessory pathway of a patient with WPW syndrome. Both phenomena were demonstrated by the loss of delta wave during and after rapid atrial pacing. The mechanisms involved in these unusual properties of accessory pathways are discussed.

Two cases of bidirectional tachycardia are presented. The ventricular origin of these arrhythmias was assessed by His bundle recordings. Because of the V1 morphology of the ventricular complexes during tachycardia in one case and the unknown etiology in the other, these arrhythmias were considered to be atypical. The involved mechanisms and the causes inducing these tachycardias are discussed. Whatever the involved mechanism, our cases reaffirm the opinion that the terminology bidirectional tachycardia should be used only to describe an electrocardiographic pattern that may be caused by different electrophysiological mechanisms.

Three hundred hospital patients with syncope (193 males and 107 females, mean age 61 +/- 17 years) were prospectively evaluated with a standard protocol. Associated diseases were found in 76.7% of cases. The incidence of heart diseases was 50.8% in males vs 32.7% in females (p less than 0.003). The cause of syncope was diagnosed in 250 patients (84%). The diagnosis was made at initial evaluation in 101 patients (group A); in the remaining patients (group B), no diagnosis was made in 25% (16.6% of the overall series) despite a wide array of investigations. Syncope due to arrhythmia was diagnosed in 57.6% (group A: 91.1% group B: 40.7; p less than 0.0001); cardiac syncope not due to arrhythmia was diagnosed in 4%, and other types of syncope in 21.6% (group A; 6.9%; group B: 29.1%; p less than 0.0001). It is concluded that a) the hospital population of patients with syncope represents a subgroup of advanced age and a high incidence of associated diseases; b) one third of patients were diagnosed at the initial evaluation, whereas in 25% of the remaining ones no diagnosis was obtained, and c) in these patients, arrhythmia is the most likely cause of syncope.