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Congestive heart failure remains associated with substantial morbidity and mortality. A common finding in advanced heart failure is abnormal electrical activation of the ventricles or electrical ventricular dyssynchrony. In the early 90s, standard dual-chamber pacing with short AV delay was proposed as a supplementary treatment of drug-resistant heart failure. Initial results were encouraging but were never confirmed. These studies however made it possible to select a population of potentially responsive patients, especially those with a prolonged PR interval reflecting major atrioventricular asynchrony in the left heart. That relative failure of standard dual-chamber pacing could be linked to the fact that by capturing the ventricle from the right apex, it increases, or at least it cannot correct the marked asynchrony of activation, contraction and relaxation, which characterizes a number of patients with chronic left ventricular dysfunction. Such is the case in particular in patients with important QRS enlargement linked to major intraventricular conduction delay. Biventricular pacing, which simultaneously activates both ventricles, may contribute to correcting the asynchrony and thus improve cardiac performance.

A case of 80-year-old woman with marked hyperkalemia in the course of chronic treatment with angiotensin converting enzyme (ACE) inhibitors and spironolactone is presented. AAI pacemaker was implanted three months ago. The ECG revealed a nodal rhythm, ineffective AAI pacing and other typical features of hyperkalemia. After normalisation of potassium level the ECG changes disappeared. Potential mechanism of the nodal rhythm during ineffective atrial pacing is discussed.

The follow-up of 22 patients (out of 31 patients after artificial aortic valve and pacemaker implantation between 1982 and 2001) have been evaluated. There were 15 men aged 30-76 (x=55) and 7 women aged 43-69 (x=59). Aortic valve replacement (AVR) was subsequently followed by pacemaker implantation (PI) after approximately 16 days. Indication for permanent stimulation were: atrio-ventricular complete block in 18 patients and atrial fibrillation with slow ventricular response in the remaining 4. There were implanted 15 devices of VVI type and 7 of VDD type. The duration of follow up was 9-196 (x=56) months. All these patients remained in good general state (II degree--19 patients or II/III degree--3 patients acc. to NYHA classification). In 21 out of 22 patients, atrioventricular conduction disturbances and bradyarrhythmia remained for the entire follow-up duration with permanent stimulation (VVI or VAT). In one patient the postoperative complete atrio-ventricular block disappeared during follow up, 24 months after AVR.1. The main indication for PI after AVR was complete atrio-ventricular block, persisting 2-3 weeks after surgery, without accompanying atrial fibrillation. 2. In long term follow up after AVR and PI (VVI or VDD) the dominance of 100% capture ventricular pacing have been recorded in almost all cases, which holds the decision of early postoperative PI.

Passive-fixation of ventricular lead was implanted through left superior vena cava (LSVC) and DDD pacing system replaced AAI in a young patient with II degree A-V block. Good mechanical stability and proper bioelectrical parameters obtained in short-lasting, uncomplicated procedure does not stay in line with world-wide approach. It is preferential for active fixation of leads in the right ventricle through the LSVC.

We describe a case of a 59-year-old female with paroxysmal atrial fibrillation and arterial hypertension who had syncopal attacks due to polymorphic ventricular tachycardia (PMVT) with a short coupling interval of an initiating beat (280 msec). We excluded structural heart disease. In the resting ECG the QTc interval was 420 msec. During Holter monitoring a slight changes of the ST-T segment in V1 were observed (from positive T wave with ST elevation of 1 mm to flat or negative T wave without ST elevation). Additionally, after PMVT a large U-wave (4 mm of amplitude) with the QTU interval of 600 msec and QTUc interval of 662 msec were observed. The U wave disappeared 9 minutes afterwards. The ajmaline test was positive for the Brugada syndrome. The patient received ICD and sotalol, and during 6-month follow-up she remains asymptomatic.

Radiofrequency catheter ablation (RFCA) may cause myocardial injury.To assess changes in myocardial enzymes levels following RFCA.Creatine kinase (CK), CK-MB, aspartate aminotransferase (GOT), alanine aminotransferase (GPT), troponin I and myoglobin levels were assessed in 53 patients (33 females, 20 males, mean age 53 years, range 23-78 years) before and 20 hours after successful RFCA (WPW type A = 13, WPW type B = 10, atrio-ventricular nodal tachycardia n = 17, atrial fibrillation or flutter n = 5, atrial tachycardia n = 2 and complex arrhythmias n = 6).The mean number of RF applications was 10.4, cumulative energy - 22 671 J, duration of application - 468 sec, and temperature - 58 degrees C. A significant post-RFCA increase in the troponin I and myoglobin levels was found whereas the changes in CK and GOT levels were less pronounced. A significant correlation between troponin I elevation and RFCA energy, particularly in males, was documented. There was a trend towards a decrease in the GPT and CK-MB levels. Troponin I and myoglobin levels increased regardless of the site of RF energy application.Troponin I and myoglobin are useful for the assessment of RFCA-induced myocardial injury, regardless of the site of RFCA application.

The left atrial appendage (LAA) has been implicated as a potential trigger for atrial fibrillation (AF). Catheter ablation to isolate the LAA with catheter ablation has been successful, but is limited by the risk of tamponade and the potential for mechanical standstill & thrombus formation. We

Eleven resting patients with an implanted DDD pacemaker were studied. After 30 minutes of AV sequentiai pacing at a rate of 80 beats/min with three consecutive atrioventricular delays (AVDs; 100, 150, and 200 msec) peripheral venous blood was drawn for further analyses by specific radioimmunoassays of atrial natriuretic peptide (ANP) and the ANP second messenger, cyclic guanosine monophosphate (cGMP). Relative changes in left ventricular (LV) stroke volume following alterations of AVD were assessed by means of pulsed-Doppler echocardiography through measurement of LV outflow time-velocity integrals (TVI). The optimal AVD (oA VD) was defined in individual patients as that which was associated with the greatest TVI and with improvement over both other AVDs of more than 4%. The oA VD was found in nine patients. For these nine patients no significant differences in either plasma ANP or cGMP between various AVDs were observed. However, we found such differences with respect to values measured at oAVD; both ANP and cGMP levels were lowest at oAVD. Pooling together the data obtained in 11 patients at three AVDs, a positive correlation between ANP and cGMP levels was found (r = 0.7, P < 0.0001. n = 33). Moreover, changes of plasma ANP and cGMP induced by every A VD increment of 50 msec were also correlated (r = 0.6, P < 0.01, n = 22). It is concluded that in AV sequential pacing at rest piasma ANP reaches minimal levels at the AVD, which provides the best LV performance. Although levels of cGMP changed in parallel with those of ANP, low relative values of cGMP differences may limit the usefulness of cGMP assays in optimization of the AVD.