Peter Rakovec

Late cardiac damage of anthracycline therapy for acute lymphoblastic leukemia in childhood.

Long-termleukemia survivors (46) underwent cardiac evaluation, including physical examination, ECG, exercise testing, and echocardiography. They were 2-17 years old at diagnosis and 5-23 years old aftertreatment. Thirty-four survivors received anthracyclines (AC) (mean 203 mg/m2), 12 of them had also alkylating agents (AA) and 12 had no AC. Exercise tolerance was bellow predicted valuesin 21 (48%) survivors and 21 survivors had ECG abnormalities, which were more frequent in those treated with AC. Concomitant AC with AA was correlated with prolonged isovolumic relaxation time (IVRT) and influenced significantly the volume of left atrium (p = .02). Sixteen (52%) survivors had IVRT 90 ms. There were no significant differences in other parameters of diastolic orsystolic function. Despite the lack of clinical symptoms in the survivors treated with lower doses of AC, subtile abnormalities in myocardial function were found, mainly manifest as abnormal diastolic function. Prolonged IVRT may be a sensitive indicator for early detection of AC cardiotoxicity.

Unusual ECG variations in left-sided pneumothorax

A patient with spontaneous left-sided pneumothorax and unusual, phasic voltage variations in the electrocardiogram (ECG), which fluctuated depending on respiration, was observed. After intercostal tube drainage, these variations disappeared. The respiratory changes in the thorax seem to be a cause of these ECG findings.

Role of endogenous adenosine in vasovagal syncope.

Adenosine may be a potential mediator in the pathogenesis of vasovagal syncope. Intravenous adenosine increases sympathetic discharge and provokes vasovagal syncope in sensitive subjects. No data are available for endogenous adenosine. The authors compared the results of head-up tilt-table testing (HUT) (45 minutes at 60°) of three arbitrary groups of subjects: sensitive (n=25, age 34 y, vasovagal syncope, positive HUT), moderately sensitive (n=28, age 34 y, vasovagal syncope, negative HUT), and nonsensitive (n=19, age 30 y). A positive test result produced syncopal symptoms with hypotension and/or bradycardia. Single-lead electrocardiogram (ECG) was recorded, and arterial pressure was measured noninvasively. Fourier transform was used for power-spectral heart rate variability (HRV) analysis of 5-minute ECG data. In the nonsensitive and moderately sensitive groups, HUT was repeated with intravenous dipyridamole, and adenosine transport blocker. In the sensitive group, HUT was repeated with oral theophylline, an adenosine receptor blocker, or placebo. In the moderately sensitive group, a third HUT was performed with dipyridamole and oral theophylline. If adenosine plays a role in vasovagal syncope, then dipyridamole would induce more positive HUT responses, a positive HUT response would be prevented by theophylline, and hemodynamic and HRV data in positive HUT responses induced by dipyridamole should reproduce those observed during spontaneous positive HUT responses. Dipyridamole induced positive HUT responses in 57% of the moderately sensitive group and 21% of the nonsensitive group (p<0.05). Theophylline treatment was not efficient in preventing HUT-induced syncope in sensitive subjects; however, it prevented dipyridamole-induced syncope in 75% of the moderately sensitive group. Dipyridamole immediately increased arterial pressure, heart rate, and total HRV in all (p<0.05). In sensitive subjects, these responses were different: small for arterial pressure and for total and low-frequency HRV, and large for heart rate. It is concluded that endogenous adenosine, like exogenous adenosine, may induce vasovagal syncope. However, the mechanism of adenosine-induced syncope is probably different from that of HUT-induced vasovagal syncope.Adenosine may be a potential mediator in the pathogenesis of vasovagal syncope. Intravenous adenosine increases sympathetic discharge and provokes vasovagal syncope in sensitive subjects. No data are available for endogenous adenosine. The authors compared the results of head-up tilt-table testing (HUT) (45 minutes at 60°) of three arbitrary groups of subjects: sensitive (n=25, age 34 y, vasovagal syncope, positive HUT), moderately sensitive (n=28, age 34 y, vasovagal syncope, negative HUT), and nonsensitive (n=19, age 30 y). A positive test result produced syncopal symptoms with hypotension and/or bradycardia. Single-lead electrocardiogram (ECG) was recorded, and arterial pressure was measured noninvasively. Fourier transform was used for power-spectral heart rate variability (HRV) analysis of 5-minute ECG data. In the nonsensitive and moderately sensitive groups, HUT was repeated with intravenous dipyridamole, and adenosine transport blocker. In the sensitive group, HUT was repeated with oral theophylline, an adenosine receptor blocker, or placebo. In the moderately sensitive group, a third HUT was performed with dipyridamole and oral theophylline. If adenosine plays a role in vasovagal syncope, then dipyridamole would induce more positive HUT responses, a positive HUT response would be prevented by theophylline, and hemodynamic and HRV data in positive HUT responses induced by dipyridamole should reproduce those observed during spontaneous positive HUT responses. Dipyridamole induced positive HUT responses in 57% of the moderately sensitive group and 21% of the nonsensitive group (p<0.05). Theophylline treatment was not efficient in preventing HUT-induced syncope in sensitive subjects; however, it prevented dipyridamole-induced syncope in 75% of the moderately sensitive group. Dipyridamole immediately increased arterial pressure, heart rate, and total HRV in all (p<0.05). In sensitive subjects, these responses were different: small for arterial pressure and for total and low-frequency HRV, and large for heart rate. It is concluded that endogenous adenosine, like exogenous adenosine, may induce vasovagal syncope. However, the mechanism of adenosine-induced syncope is probably different from that of HUT-induced vasovagal syncope.

Effects of Systolic Atrial Function on Plasma Renin Activity and Natriuretic Peptide Secretion after High Rate Atrial and Ventricular Pacing in Dogs

Rapid atrial rates cause electrical, structural remodeling, and neuro‐humoral changes. This study compares the effects of mechanical remodeling on plasma renin activity (PRA) and atrial natriuretic peptide (ANP) secretion. Eight beagles were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Left atrial systolic maximal dimension (LAmax) and left atrial appendage (LAA) peak late emptying velocity (LAA‐E) were assessed by echocardiography. Blood samples were taken from the right atrium and from the peripheral vein. LAmax after AP and VP enlarged significantly (2.16 ± 0.21 cm vs 2.41 ± 0.23 cm, P = 0.002). Compared with baseline, LAA‐E velocities were significantly reduced (0.65 ± 0.12 m/s vs 0.26 ± 0.16 m/s, P = 0.001) after AP only. AP caused a significant elevation of PRA in right atrial (9.28 ± 4.23 nmol/L per hour) and peripheral samples compared with baseline values (4.82 ± 2.53 nmol/L per hour, P = 0.04). ANP levels increased after AP (1117.12 ± 252.21 fmol/L) with respect to baseline values (824.37 ± 159.08 fmol/L, P = 0.001). There was no difference in PRA and ANP levels between atrial and peripheral samples. Atrial size and impaired systolic appendage function play an important role in secretion of PRA and ANP. Both neuro‐humoral pathways may be therapeutic targets in the treatment of patients with AF.

Transition of orthodromic tachycardia into atrioventricular nodal tachycardia during radiofrequency ablation of an accessory pathway

We report a patient with Wolff-Parkinson-White syndrome, in whom orthodromic atrioventricular reciprocating tachycardia directly passed over to atrioventricular nodal re-entrant tachycardia during radiofrequency ablation of the accessory pathway. After the accessory pathway ablation, there were no tachycardia recurrences.

Left atrial systolic function in relation to electrical and mechanical remodeling in a canine model

Abstract Rapid atrial activation causes electrical remodeling that promotes the occurrence and maintenance of atrial fibrillation. The aim of this research was to compare the relationship between mechanical remodeling and atrial electrophysiology. Eight dogs (beagles) were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After a complete recovery of electrical variables and left ventricular function evaluated by echocardiography, they underwent high-rate ventricular pacing (VP) at 240 beats/min of equal duration. In half of them, the study was started by VP and in the other half by AP. Left atrial systolic function was assessed by transesophageal echocardiography. Atrial effective refractory period (AERP) at a basic cycle length of 400 ms decreased significantly after either type of pacing (AP: 115 ± 17 ms, VP: 136 ± 22 ms) compared with baseline values (153 ± 23 ms); the difference between tachycardias was significant too (p < 0.02). Significant increases (p < 0.05) in left atrial dimensions (LA-A) (AP: 2.41 ± 0.23 cm , VP: 2. 43 ± 0. 34 cm vs. basal: 2. 16 ± 0. 21 cm) indicated atrial dilatation after either type of pacing, the differences between two groups being insignificant. Atrial reversal pulmonary venous flow (AR velocity) decreased in AP (−0. 13 ± 0. 02 m/s) and VP (−0. 17 ± 0. 04 m/s). The difference was highly significant as compared to basal values (-0.25 ± 0.05 m/s) and also with respect to both tachycardias (p<0.01). In both groups, atrial remodeling occurred in a relatively short period of time. The echocardiographic findings suggested that left atrial systolic function was significantly more disturbed in the AP group than in the VP group. Mechanical changes are an important substrate of electrical remodeling, yet the deterioration of electrical variables was more pronounced in AP than in VP.

Spontaneous shifts in the sinus node pacemaker complex.

Shifts in sinus node pacemaker complex may occur spontaneously, but occurrence of clinically relevant shifts is very rare. In this report, three patients (2 are siblings) with a history of palpitations and nearly permanent shifts in sinus node pacemaker complex are presented. Often, but not always, the pacemaker shifts followed spontaneous sinoatrial exit blocks. The shifts were probably related to varying vagal tone, since they were eliminated by atropine and exercise. The experience with these patients suggests that sinus pacemaker shifts can be a cause of symptomatic nonrespiratory sinus arrhythmia. A 4-year follow-up period showed no changes in symptoms or in heart rhythm; therefore, a benign course of the disease can be expected.

Electrophysiological and clinical characteristics of atrioventricular nodal reentrant tachycardia and longterm success of radiofrequency catheter ablation

Background: Diff erent reentry circuits within A-V node region are able to sustain A-V nodal reentrant tachycardia (AVNRT). On this basis, electrophysiological criteria for at least three AVNRT types – slow/fast, fast/slow, and slow/ slow–have been proposed. Th e aim was to reevaluate these criteria in a group of our patients. In addition, clinical profi le and long-term success rate of catheter ablation procedure were studied. Methods: All consecutive patients referred for catheter ablation of AVNRT from September 2004 to December 2006 were prospectively recruited. Th e informed consent was signed by all and the study had been approved by the competent state’s ethics committee. A standard electrophysiological study with programmed single or double extrastimuli or high-rate electrostimulation until the development of refractoriness or tachycardia induction was performed. Orciprenaline i.v. was used to facilitate AVNRT induction and to test the ablation result. Slow-pathway electrograms at inferoposteroseptal right atrium and ablation-induced nodal rhythm were ablation targets. Th e radiofrequency energy of 30–50 W for a duration of at least 20 seconds was used. Non-inducibility of AVNRT and of echo-beats was the procedure end point. In addition, antegrade and retrograde A-V junction conduction times were measured and analysed manually. Patients underwent a detailed re-evaluation aft er at least 1 year of follow-up. Th e descriptive statistic was used to present the data. Results: One hundred and four patients, 72 % female, mean age 53 years, were included. Th ey had their fi rst tachycardia episode at a mean age of 35 years with an average recurrence rate of 1- to 3-times a year. Syncope was experienced in 9.5 % of patients. Familial tachycardias were reported in 4 % of patients. One third (34 %) were hypertensive (≥ 140/90 mmHg). In majority, slow/fast AVNRT type (98/104–94 %) was induced. Th e fast/slow and slow/slow types were rare (3/104 each). Th e mean heart rate of induced AVNRT was 166 beats/min. Measurements were available for 92 patients. Our best diagnostic criteria were: V-A’interval ( 150 fast/slow, 70–120 slow/slow), H-A’interval ( 200 fast/slow; 120–170 slow/ slow), and A’-H/H-A’ ratio (> 2,3 slow/fast, < 1 fast/slow, 1–2,3 slow/slow). Th e slow/fast type was generally induced from the atrium, while the fast/slow and slow/slow also from the ventricle. In the slow/fast type, the earliest retrograde atrial activation was recorded from the His bundle position in 95 % (proximal coronary sinus (CS) in 5 %). Th e earliest retrograde atrial activation was recorded from proximal CS in the fast/slow type, but from CS or His in the slow/slow. A transient A-V block was documented in 6 patients during ablation procedure. None of them needed a permanent pacemaker implantation. Aft er 16 months of follow-up, 96 % of our patients were free of tachycardia recurrences. Conclusions: Electophysiologic criteria for three AVNRT types, clinical characteristics, and AVNRT long-term radiofrequency catheter ablation success rate are consistent with data reported in the literature.

Atrial Tachycardia with Atypical Wenckebach Atrioventricular Block after Slow Pathway Ablation

A case of a patient with dual supraventricular tachycardias, atrioventricular nodal tachycardia, and atrial tachycardia is presented. The former was successfully ablated, whereas the latter was inducible after the ablation of the former, but without clinical importance during follow‐up. However, this tachycardia showed interesting characteristics, including dual atrioventricular Wenckebach periodicity, presumably due to multiple slow pathways.

Ventricular Tachycardia as a Consequence of a Suicidal Stabbing Injury to the Heart

Twenty-one years ago. a 25-year-old woman attempted suicide by stabbing herself witb a knife. Her life was saved by emergency surgery, during which time a wound to the right ventricle was sutured. At the age of 43 years, she experienced episodes of nonsustained ventricular tachycardia. Bicycle ergometry was normal. At the age of 46, she was admitted to our hospital with sustained ventricular tachycardia with a right bundle branch block morphology. At electrophysiologic study.