Reversible high rate atrial fibrillation dilated cardiomyopathy.
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Biomedical subjects
Publications and source records attributed to J O Lazzari.
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Four cases of pacemaker-related SVC obstruction or syndrome are reported. While two of them lacked any symptom suggestive of SVC obstruction, the other two presented with mild symptoms. None of them received any treatment. One died from a cause unrelated to SVC obstruction, while the others presented no change in their clinical status. A review of the literature suggests that neither thrombotic nor fibrotic obstruction in patients with pacemaker leads is strictly related to the number of abandoned leads, the presence of severed leads, or the time elapsing from pacemaker implant. The diagnosis is clinically made and is confirmed by venography. Only one of the reported deaths is attributable to SVC obstruction. The remaining cases from the literature responded to treatment with heparin, thrombolytic agents, angioplasty, or surgery.
A 22-year-old man who engaged in intense and regular physical exercise complained of atypical chest pain. The only remarkable abnormality found in the routine clinical work-up was a left posterior hemiblock. The echocardiogram and the magnetic resonance imaging (MRI) study showed a tumour in the posterior and superior aspect of the interventricular septum where the posterior fascicle of the left bundle is located. It was interpreted that the left posterior hemiblock was produced by the tumour.
Use-dependent effect is characteristic of certain antiarrhythmic drugs, mainly those included in Group I of Vaughan-Williams classification. There is an increasing interest in the study of this phenomenon in order to correlate it with the potential arrhythmogenic effect of currently used antiarrhythmic drugs. Use-dependent effect produces widening of the QRS ECG complex as the heart rate is increased. Thus, to produce the necessary changes in heart rate to clinically disclose this phenomenon, endocardial stimulation of the right ventricle is usually done both in control condition and under the effect of the tested drug. As this is an invasive method, the amount of information collected on this important aspect of the antiarrhythmic drug effects has been limited. Hence, we decided to confirm whether transesophageal cardiac pacing is a suitable method to produce controlled changes of the heart rate in order to analyse the use-dependent phenomenon. In this study we included 14 patients, 9 women and 5 men aged 47.85 +/- 13.91 years and ejection fraction of 54.64 +/- 7.19%. Transesophageal stimulation was performed up to the Wenckebach point and the previous rate producing 1:1 A-V response was considered. ECG was recorded in an ink-jet three-channel electrocardiograph at 100 mm/sec chart speed and QRS duration was measured. All patients were studied in the basal unsedated state, free of any medication and after the administration of 3.13 +/- 0.74 mg/kg of flecainide during 4.07 +/- 1.4 days. Atrial capture was obtained with pulses of 15 mA and 18 msec. Heart rate attained before treatment was 150 +/- 21.83 bpm and 144.28 +/- 19.88 bpm under the effect of flecainide (p = NS) (Table 1).(ABSTRACT TRUNCATED AT 250 WORDS)
The accepted variation of 80-120 ms in the coupling interval of non-parasystolic ventricular premature beats has been linked to the duration of the preceding cycle length, but a lack of correlation between these factors has often been found. As a result, there is no explanation for variations in the coupling interval of such ventricular premature beats. To analyze the influence of the preceding cycle length on the coupling interval of isolated ventricular premature beats throughout an entire day, 10 otherwise healthy patients with frequent monofocal non-parasystolic isolated ventricular premature beats were studied with Holter recordings. A sample of the electrocardiogram was obtained at the beginning of each quarter of an hour and coupling intervals as well as preceding cycle lengths of ventricular premature beats not belonging to a bigeminy or trigeminy sequence were measured. Preceding cycle lengths changed in a way similar to the prevailing heart rate, with a marked prolongation during sleep. Coupling intervals showed an irregular pattern during the waking period but increased consistently from the first to the last hour of sleep. The average coupling interval during sleep was significantly longer than during waking (439 +/- 74 vs 466 +/- 80, p less than 0.01). In each patient a similar preceding cycle length within a narrow range of 40 ms was searched for during waking as well as during sleep and the corresponding coupling intervals were significantly longer during sleep (446 +/- 80 vs 466 +/- 85, p = 0.009).(ABSTRACT TRUNCATED AT 250 WORDS)
To assess the short-term behavior of the right ventricle anterior papillary muscle extrasystoles (APME) based on Holter recording and exercise data, 20 subjects (age 31.5 +/- 13.7 years) with otherwise normal electrocardiogram were studied. APME was diagnosed when it resembled LBBB morphology, with downward oriented AQRS in the frontal plane, slurred r wave in lead V1, and an R/S ratio less than 1 in this same lead. Except for palpitations in ten patients, there were no other symptoms related to the arrhythmia. Two Holter recordings, 30 to 330 days apart, were performed and their results compared. In the first Holter recording, the average rate of VPB/minute was 9.9 +/- 2.5 (xg +/- SD). Half of the patients had couplets and five had ventricular tachycardia. In the second Holter recording, the average rate of VPB/minute was 8.7 +/- 3. In eight cases, couplets were recorded, in half of which one or more episodes of ventricular tachycardia were also noted. Six patients showed another VPB morphology distinct from APME. Stress test suppressed VPB in 10/13 patients, couplets in 2/3 and ventricular tachycardia in the only one with this arrhythmia at the start of the test. Repetitive forms vs APME frequency and vs heart rate exhibited an inverse relationship. We conclude that APME is a clinical condition with both high and stable VPB levels, which can be found in subjects with otherwise normal hearts and in the short-term has a spontaneous uncomplicated outcome.
Clinical evaluation of a 64-year-old male patient with a permanent pacemaker showed a right bundle branch block in his ECG that led to the suspicion of catheter misplacement. A two-dimensional echocardiogram and bilateral venogram demonstrated that the pacemaker lead was not in the venous system and that its course was from the axillary artery to the left ventricle passing through the aortic valve. Thirty-three days after implant, replacement of the pacemaker lead through the venous system to stimulate the right ventricular endocardium was performed. At 7 month follow-up the patient has had no complication from his previous arterial pacemaker implantation.
Twenty asthmatic patients clinically free of heart disease were studied for the possible arrhythmogenic action of albuterol (salbutamol). Two puffs of either albuterol or placebo were inhaled four times per day on two consecutive days and continuous ECG recordings obtained during each 24-hour period. Sixteen patients had atrial extrasystoles, four with albuterol, one with placebo, and 11 with both drugs. The extrasystoles/hour were 6.55 (23.75 SD) with albuterol and 8.37 (33.82) with placebo, a nonsignificant difference. Ventricular extrasystoles were shown in 11 patients, two with albuterol, two with placebo, and seven during both treatments. The extrasystoles/hour were 2.57 (6.36) and 3.10 (7.61) with albuterol and placebo, respectively. This difference was not significant. These findings suggest that therapeutic doses of albuterol aerosol in asthmatic patients without evidence of heart disease and severe hypoxemia should not be considered a cause of cardiac arrhythmias.
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The presence of cellular reactivity against homologous tissues and subcellular fractions of Trypanosoma cruzi was investigated in Chagas' disease patients (CDP). CDP were grouped in asymptomatic (CDP-1) and with probable (CDP-2) and overt (CDP-3) cardiomyopathy. Healthy and non-Chagasic cardiomyopathic subjects were studied as controls. Lymphoproliferative reactions against heart tissue extracts were detected in 42% of 72 CDP studied, with similar prevalence of positive reactions in all groups, and correlated with reactivity to both liver and kidney homologous tissues (P less than 0.001). These results confirm the existence of cellular immune reactivity against tissues in CDP, and indicate the lack of organ specificity of this reaction as well as the absence of relation with the clinical state of patients. Cellular reactivity to subcellular fractions of T. cruzi showed a definite pattern according to the clinical status of CDP. Although prevalence of T. cruzi stimulation appeared similar in all groups (70% in CDP-1, 82% in CDP-2 and 75% in CDP-3), CDP-3 showed a significantly higher reactivity to flagellar (69%) and cytosol (63%) fractions than CDP-1 (38 and 27%, respectively). These findings suggest a variable modulation of immune response according to the clinical state of T. cruzi infected subjects.
Phase 4 or phase 3 block or both occurred in the His bundle branch system of 11 patients with intermittent bundle branch block and in the anomalous bundle of 6 of 46 patients with the Wolff-Parkinson-White syndrome (13%). Administration of a single dose of ajmaline (50 mg intravenously) in these patients caused a similar response: expansion of the range of phase 3 and phase 4 block at the expense of the intermediate normal conduction range and total interruption of conduction in the affected fascicle when the effect of the drug was maximal. The great similarity in physiologic behavior and pharmacologic response in these groups of patients suggests that the anomalous bundle was probably diseased or abnormal in the six patients with Wolff-Parkinson-White conduction. In addition, ajmaline caused the first appearance of phase 4 or phase 3 block, or both, but not total interruption of conduction in 26 of the 46 patients with Wolff-Parkinson-White conduction (56.5%). Ajmaline does not cause fascicular block in normal subjects; thus this finding suggests either that the anomalous bundle is diseased or that the safety margin for conduction in the anomalous bundle is much narrower than in the bundle branch system. The conduction-depressing action of ajmaline may be greater at relatively rapid or relatively slow rates of stimulation, and smaller or absent at intermediate rates.
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