Ewa Makowska

The incidence of asymptomatic paroxysmal atrial fibrillation in patients treated with propranolol or propafenone

Anti-arrhythmic therapy for paroxysmal atrial fibrillation leads to complete symptomatic relief in a number of patients. The elimination of symptoms may be associated either with a complete elimination of arrhythmia or with a conversion of symptomatic atrial fibrillation into asymptomatic episodes of arrhythmia. The aim of the study was to evaluate the occurrence of asymptomatic paroxysmal atrial fibrillation in 52 patients treated with propafenone (35 drug trials) or propranolol (34 drug trials) by means of ambulatory ECG Holter monitoring. Propafenone was clinically effective (complete relief of symptoms) in 26 (74%) patients. However, in 7 cases (27%) asymptomatic episodes of arrhythmia were still recorded when awake. In patients treated with propranolol clinical symptoms were absent in 18 (53%). However, in 4 (22%) patients attacks of paroxysmal atrial fibrillation were present. The mechanism of drug-induced conversion of symptomatic episodes of atrial fibrillation into asymptomatic spells of arrhythmia was a marked shortening in duration of episodes in 7 patients (from 2215 +/- 3843 s to 16 +/- 10 s, N.S.) or by a significant slowing of ventricular response during atrial fibrillation in 4 patients (from 125 +/- 27 to 84 +/- 8 beats/min, P = 0.05). In conclusion, in a significant proportion of patients with symptomatic paroxysmal atrial fibrillation asymptomatic episodes of arrhythmia may occur while on anti-arrhythmic drug therapy. Some of these patients, particularly those with other risk factors for stroke such as advanced age or the presence of organic heart disease, may require anti-coagulant therapy or change in anti-arrhythmic treatment, and can be selected on the basis of ambulatory ECG monitoring.

QT Interval Dispersion in Ventricular Beats: A Noninvasive Marker of Susceptibility to Sustained Ventricular Arrhythmias

KULAKOWSKI, P., et al.: QT Interval Dispersion in Ventricular Beats: A Noninvasive Marker of Susceptibility to Sustained Ventricular Arrhythmias. Increased QT dispersion (QTd) calculated from sinus beats has been shown to identify patients prone to sustained VT. However, predictive accuracy of this parameter is limited. Electrophysiological properties of the myocardium may be altered by a premature ventricular beats, which is a well‐established trigger for sustained VT. Therefore, the author hypothesised that QTd in spontaneous or paced ventricular beats may improve identification of patients with inducible sustained VT. In 28 consecutive patients (men, mean age 61 ± 13 years) who underwent programmed ventricular stimulation, the values of QTd calculated in sinus and ventricular beats were compared between inducible and noninducible patients. The mean QTd values obtained using three different methods differed significantly, QTd in paced ventricular beats being the highest, QTd in spontaneous ventricular beats was intermediate, and QTd in sinus beats was the lowest (83.9 ± 30 vs 63.0 ± 29 ms vs 53.9 ± 27 ms, P < 0.0001 and P < 0.004, respectively). In 13 (46%) patients sustained VT was induced. QTd values were significantly higher in inducible than noninducible patients (QTd sinus beats: 67.5 ± 31 vs 42.1 ± 11 ms, P = 0.02; QTd spontaneous ventricular beats: 79.3 ± 35 vs 46.7 ± 13 ms, P = 0.008, and QTd‐paced ventricular beats: 104.8 ± 32 vs 65.9 ± 9 ms, P = 0.0009). The receiver operator characteristic curves showed that at a sensitivity level of 100%, the highest specificity for identification of inducible patients had QTd measured in paced ventricular beats (87%) followed by QTd in spontaneous ventricular beats (45%), and QTd in sinus beats (40%). In conclusion, (1) QTd in ventricular beats is greater than in sinus beats, and (2) QTd calculated from paced ventricular beats identifies patients with inducible sustained VT better than QTd measured during sinus rhythm.

Twiddler's syndrome in a patient with a single-chamber implantable cardioverter defibrillator

A 67-year-old, obese, Caucasian female with a history of ischaemic dilated cardiomyopathy and ventricular fibrillation, underwent a single-chamber implantable cardioverter defibrillator (ICD) with a screw, in ventricular lead implantation. Appropriate sensing, pacing, and defibrillation thresholds were obtained at implantation. A …

Evaluation of Patients with Palpitations: Cardiac Event Recorder Versus 48‐hour Holter Monitoring

Objectives: (1) To compare a diagnostic yield of cardiac event recorders with that of 48‐hour Holler monitoring, (2) to determine the etiologies of palpitations, and (3) to assess an optimal duration of using an event recorder by a patient.

Cardiac arrest due to ineffective pacing caused by metabolic disorders and ischaemia

In patients with an implanted pacemaker, an increase of pacing threshold is one of the most dangerous complications, which may lead to syncope, cardiac arrest, or death in pacemaker-dependent patients. The increase of pacing threshold may be caused by electrolyte disturbances, acid-base disorders, hyperglycaemia, or hypothyroidism. In some cases it may also occur due to ischaemia or myocardial infarction in the area near the tip of the electrode. However, it is uncommon because pacing leads are usually implanted in the apex of the right ventricle where ischaemia is relatively rare. We present an illustrative case of an 84-year-old man with a dual-chamber pacemaker implanted due to complete atrioventricular block 10 years ago, hypertension, diabetes mellitus, chronic kidney disease, and hyperlipidaemia, without previous history of coronary artery disease, who was admitted to our hospital after sudden cardiac arrest due to ineffective pacing with no escape rhythm (Fig. 1). Interrogation of the pacemaker was performed and an increase of pacing threshold to 7.5 V at 1.0 ms was found. The chest radiograph and transthoracic echocardiography showed no pacing lead dislocation. Blood tests showed hyperglycaemia (330 mg/dL) and mild metabolic acidosis (pH 7.2). The level of serum troponin T increased, but without growth typical for myocardial infarction. After compensation of metabolic disorders (pH 7.45, glycaemia 171 mg/dL) a decrease in the pacing threshold was observed to 1.25 V at 1.0 ms, but it still remained elevated in comparison to the baseline parameters obtained at the last scheduled visit (1.0 V at 0.4 ms). Transthoracic echocardiography showed regional wall motion abnormalities near the tip of the ventricular pacing lead (Fig. 2). Next, coronary angiography was performed and showed significant stenosis of the left anterior descending artery with TIMI-2 flow (Fig. 3), requiring angioplasty and stent implantation with the final TIMI-3 effect. After percutaneous coronary intervention, an interrogation of the pacemaker was performed and a decrease in the pacing threshold was found 1.0 V at 1.0 ms (the trend of pacing threshold is shown in Fig. 4). This case report shows that metabolic disturbances and ischaemia may elevate the pacing threshold to very high values and should be considered as a possible and treatable cause of ineffective pacing.