High incidence of atrial fibrillation after successful catheter ablation of atrioventricular nodal reentrant tachycardia: a 15.5-year follow-up.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common type of supraventricular tachycardia. Slow pathway (SP) ablation is the treatment of choice with a high acute success rate and a negligible periprocedural risk. However, long-term outcome data are scarce. The aim of this study was to assess long-term outcome and arrhythmia free survival after SP ablation. In this study, 534 consecutive patients with AVNRT, who underwent SP ablation between 1994 and 1999 were included. During a mean follow-up of 15.5 years, 101 (18.9%) patients died unrelated to the procedure or any arrhythmia. Data were collected by completing a questionnaire and/or contacting patients. Clinical information was obtained from 329 patients (61.6%) who constitute the final study cohort. During the electrophysiological study, sustained 1:1 slow AV nodal pathway conduction was eliminated in all patients. Recurrence of AVNRT was documented in 9 patients (2.7%), among those 7 patients underwent a successful repeat ablation procedure. New-onset atrial fibrillation (AF) was documented in 39 patients (11.9%) during follow-up. Pre-existing arterial hypertension (odds ratio 2.61, 95% CI 1.14-5.97, p = 0.023), age (odds ratio 1.05, 95% CI 1.02-1.09, p = 0.003) and the postinterventional AH interval (odds ratio 1.02, 95% CI 1.00-1.04, p = 0.038) predicted the occurrence of AF. The present long-term observational study after successful SP ablation of AVNRT confirms its clinical value reflected by low recurrence and complication rates. The unexpectedly high incidence of new-onset AF (11.9%) may impact long-term follow-up and requires further clinical attention.

Ablation of atrial tachycardia originating from the vicinity of the atrioventricular node: significance of mapping both sides of the interatrial septum.

OBJECTIVES: The purpose of the study was to examine the value of right- and left-sided mapping to identify the site of tachycardia origin. BACKGROUND: Focal atrial tachycardia may originate from the vicinity of the atrioventricular node from either side of the interatrial septum. METHODS: In 16 patients undergoing radiofrequency catheter ablation of perinodal atrial tachycardia, activation mapping of the right and left side of the interatrial septum was performed. RESULTS: Atrial tachycardia originated from the right side of the interatrial septum in 10 patients (group A) and from the left side in 6 patients (group B). On the right side, earliest atrial activity preceded the onset of the P-wave by 49 +/- 15 ms in group A and by 38 +/- 8 ms in group B (NS), and it preceded the signal recorded from the right atrial appendage by 59 +/- 19 ms in group A and by 60 +/- 13 ms in group B (NS). On the left side, earliest activity preceded the onset of the P-wave by 27 +/- 16 ms in group A and by 51 +/- 6 ms in group B (<0.01), and it preceded the signal obtained from the right atrial appendage by 38 +/- 19 ms in group A and by 73 +/- 9 ms in group B (<0.01). Atrial tachycardias were successfully eliminated in all patients without impairment of atrioventricular conduction. During follow-up, two patients had a recurrence of tachycardia. CONCLUSIONS: Mapping of only the right side cannot exclude a left-sided origin. Therefore, mapping of both sides of the interatrial septum is required prior to ablation of focal atrial tachycardia originating from the vicinity of the atrioventricular node.

Significance of left-sided heart disease for the detection of patent foramen ovale by transesophageal contrast echocardiography.

Detection of patent foramen ovale by contrast echocardiography is based on transient inversion (right atrial pressure higher than left atrial pressure) of the interatrial pressure gradient. Therefore, the presence of left-sided heart disease with potential elevation of left atrial pressure might obscure the diagnosis of patent foramen ovale. Accordingly, 150 patients (88 men, 62 women; mean age 51.7 +/- 15.2 years) were evaluated for a patent foramen ovale by transesophageal contrast echocardiography. Additionally, atrial septal motion during normal respiration and during the Valsalva maneuver was analyzed. Patency of the foramen ovale was observed in 20 (27%) of 74 patients without left-sided heart disease and with previous arterial embolism, in none (0%) of 25 patients with left-sided heart disease and embolism, in 7 (39%) of 18 patients without left-sided heart disease and without embolism and in 3 (9%) of 33 patients with left-sided heart disease and without embolism. The detection rate of patent foramen ovale was lower in patients with than without left-sided heart disease (5% vs. 29%, p = 0.0007) but was similar in patients with and without embolism (20% vs. 19.5%, p = NS). Abnormal atrial septal motion was more frequently observed in patients with left-sided heart disease (p = 0.0003) and was inversely correlated to detection of patent foramen ovale (p = 0.0003). Multivariate analysis revealed an independent association between the absence of left-sided heart disease and the detection of patent foramen ovale (p = 0.0003). These data suggest that in patients with left-sided heart disease, patency of the foramen ovale may be missed even by transesophageal contrast echocardiography.

Demographic and perioperative factors associated with initial and prolonged sinus node dysfunction after orthotopic heart transplantation. The impact of ischemic time.

The etiology of sinus node (SN) dysfunction after orthotopic heart transplantation as assessed by the origin of rhythm, heart rate (HR), and, provided the origin of rhythm was sinus, by corrected sinus node recovery time (CSNRT) was studied in 50 patients. The possible influences on postoperative donor SN function of donor age, recipient age, underlying pretransplant heart disease, pretransplant amiodarone (AMIO) treatment, date of surgery, ischemic time, surgical technique of atrial incision, the use of different cardioplegic solutions during the study period, and rejection were evaluated. The results thus obtained indicate that SN dysfunction is common after cardiac transplantation and pinpoint to a different etiology of transient (restoration of normal SN function within 4 postoperative weeks) and persistent (SN function still impaired at 3 months) SN dysfunction. Of the several demographic and perioperative variables evaluated, only ischemic time had an influence on postoperative SN function in that ischemic times were significantly longer in patients with impaired SN function when compared with patients exhibiting normal SN function (148 +/- 39 min vs. 110.5 +/- 36 min, respectively, P = 0.001). Further stratification according to the duration of SN dysfunction revealed significantly longer ischemic times in patients with transiently impaired SN function only (156.3 +/- 35 min vs. 110.5 +/- 36 min, P = 0.0026). No relation to persistent SN dysfunction of ischemic time (130.5 +/- 36 min vs. 110.5 +/- 36 min, P = ns) or any other factor investigated was found.

Impaired fibrinolytic capacity predisposes for recurrence of venous thrombosis.

The fibrinolytic capacity of 121 patients with a history of venous thrombosis and/or pulmonary embolism was studied by venous occlusion technique, at earliest 3 months after the last thromboembolic episode. After discontinuation of oral anticoagulation treatment the clinical course of the patients was followed and new thromboembolic episodes were noted. During the observation period of 56 +/- 18.8 months 45 of 121 patients experienced recurrence of thrombosis. The recurrence-rate was significantly lower in patients with a post-occlusion ELT shorter than 60 min (4.8%/year) than in patients with an ELT longer than 60 min (10.3%/year). It is concluded that the fibrinolytic capacity is a useful parameter for determining the risk of recurrence in patients with venous thrombosis.

Prevention of arterial and pulmonary embolism by oral anticoagulants in patients with dilated cardiomyopathy.

The incidence of arterial embolism (AE) and pulmonary embolism (PE) during treatment with oral anticoagulants (OA) or without OA therapy was studied in 38 patients with dilated cardiomyopathy (DCMP). AE/PE occurred in 17 patients (44.7%) before initiation of OA treatment. The severity of DCMP was a risk factor for AE/PE, but not the presence of atrial fibrillation or intracardial thrombi. No AE/PE episodes occurred during the period of OA therapy. No major bleeding complications were seen, probably due to the moderate intensity of OA therapy (therapeutic range 5-15% Thrombotest [TT], 2.1-4.8 International Normalized Ratio [INR], median TT value 11%, median INR 2.6). Recurrence of AE was observed in 4 of 5 patients in whom treatment with OA had been discontinued.

Evidence for an increased generation of prostacyclin in the microvasculature and an impairment of the platelet alpha-granule release in chronic renal failure.

The formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the microvasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the alpha-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is--at least partially--due to an acquired defect of the platelet alpha-granule release and an increased generation of PGI2 in the microvasculature.

Improvement in left ventricular systolic function after successful radiofrequency His bundle ablation for drug refractory, chronic atrial fibrillation and recurrent atrial flutter.

Incessant supraventricular tachyarrhythmia may lead to a reversible impairment of left ventricular (LV) function. This issue was investigated in 10 patients (aged 64 +/- 13 years) who underwent radiofrequency His bundle ablation for control of drug refractory, chronic atrial fibrillation (n = 9) and recurrent atrial flutter (n = 1). LV function was assessed by 2-dimensional guided M-mode echocardiography within 24 hours (baseline) and 49 +/- 18 days (follow-up) after successful ablation, both during VVI pacing at 70 beats/min. Fractional shortening increased from 28 +/- 9% at baseline to 35 +/- 8% at follow-up (p = 0.006). This increase in fractional shortening was due to a significant reduction of end-systolic diameter from 41 +/- 10 to 36 +/- 10 mm (p = 0.02), whereas there was no appreciable change in end-diastolic diameter (56 +/- 7 to 55 +/- 10 mm; p = 0.5). These changes were substantially greater in patients with baseline impairment of LV function (fractional shortening less than 27%). Fractional shortening increased by 12% (p = 0.14) in patients with normal LV function (n = 5) and by 44% (p = 0.02) in those with impaired LV function at baseline (n = 5). The greater increase in fractional shortening in patients with preexisting LV impairment was due to a more pronounced decline in end-systolic dimensions (-11.9%; p = 0.08) compared with that of patients with normal LV function at baseline (-9.21%; p = 0.2). End-diastolic diameter showed no significant change in either group (-3.53% [p = 0.8] and -0.58% [p = 0.4]).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic determinants of recurrent atrial flutter after successful termination by overdrive pacing.

The potential ability of electrophysiologic abnormalities to predict recurrence of atrial flutter was evaluated. Twenty-five patients with chronic atrial flutter resistant to combined digitalis and quinidine therapy were studied electrophysiologically after restoration of sinus rhythm by overdrive pacing or by eventual direct current cardioversion. Recurrence of atrial flutter was observed in 12 patients during a mean follow-up period of 17 months (range 3 to 50). Electrophysiologic testing included programmed high right atrial stimulation at a paced drive cycle length of 600 ms and incremental pacing up to 200-ms paced intervals. When coupling intervals of 90% of the drive cycle length were compared to coupling intervals of 48% of the drive cycle length, the increase in S1A1 interval, defined as the interval between the stimulus artifact and the atrial activation near the atrioventricular junction, was greater in patients with subsequent recurrence of atrial flutter (47 +/- 11 vs 21 +/- 18 ms). Stepwise logistic regression analysis identified the S1A1 increase to be the sole independent predictor of recurrence (p = 0.0082) while previous episodes of atrial flutter or the presence of organic heart disease were identified as dependent variables. Reclassification showed a 91% sensitivity and a 92% specificity. Correct classification was achieved in 92% of patients. The initiation of atrial dysrhythmia had no predictive value. The assessment of the S1A1 interval by programmed atrial stimulation appears helpful in delineating the patient risk of recurrent atrial flutter after termination by overdrive pacing.

Different risk factor profiles in young and elderly stroke patients with special reference to cardiac disorders.

The risk factors of ischemic cerebrovascular disorders in 77 young patients (< or = 40 years) were compared to those in 138 older patients (> 40 years). The risk factor profile of patients with juvenile stroke was considerably different from that of older patients. Migrainous headache and mitral valve prolapse occurred more frequently in the younger age group, whereas hypertension, diabetes mellitus, high levels of cholesterol and triglycerides were found more often in older patients with stroke. 65% of the women under the age of 40 took oral contraceptives which compares to the baseline community value of 28% of women in childbearing age in this country. Cardiac disorders such as atrial fibrillation, left ventricular hypertrophy, coronary heart disease including a history of myocardial infarction, as well as mitral valve disease were demonstrated more often in the group of elderly patients. 7 out of 77 younger patients (9.1%), and 59 out of 138 older patients (42.8%) were considered to belong to a group with "high cardiac risk for stroke". The results of this study indicate that electrocardiographic screening is of prime importance for detecting cardiac risk factors. However, echocardiographic examination often yields additional diagnostic information, particularly in younger patients. The conflicting opinions concerning the relevance of certain risk factors for ischemic stroke could partly be explained by the fact that these risk factors are distributed unevenly depending on age.

Postoperative sinus node dysfunction in the transplanted heart. Impaired automaticity but normal refractoriness.

We describe the use of the extrastimulus technique to define the range of sinus node (SN) effective refractoriness (SNERP) in the denervated transplanted human heart. SNERP could be successfully determined in 18 of 28 patients corresponding to 25 of 43 SN studies and ranged from 210 to 360 ms at a basic pacing cycle length of 500 ms (95 percent confidence limits: 252.5 to 296.2 ms), which is shorter than reported in the innervated native heart. Sixteen data sets in 12 patients showed normal SN function and nine sets of measurements in seven patients showed abnormal SN function (corrected SN recovery time greater than 520 ms). While recovery time was profoundly abnormal (279.7 +/- 94 vs 7,284.8 +/- 10,454, p less than 0.001), the SNERP did not differ significantly between the groups (274.3 +/- 40 vs 286 +/- 42 ms at 500 ms, p = 0.5) and was normal at a range of 220 to 340 ms even in those patients with grossly impaired SN recovery (SNERP in patients with normal SN function: 210 to 360 ms at 500 ms). This study demonstrates that SN refractoriness in the transplanted human heart is shorter than previously reported in innervated controls and suggests that posttransplantation SN dysfunction is characterized by impaired automaticity rather than impaired refractoriness.

Inducible atrial flutter and fibrillation after orthotopic heart transplantation.

Inducible atrial flutter (two patients) and fibrillation (two patients) were observed in a series of 35 heart transplant patients who underwent evaluation of sinus node function including premature atrial stimulation. The sinus node function was entirely normal in both patients with inducible atrial flutter. In contrast it was profoundly abnormal in the patients with inducible atrial fibrillation. Atrial fibrillation was no longer inducible as the sinus node function became borderline normal. These observations suggest extensive electrical atrial abnormality, including the sinus node, in patients with atrial fibrillation, and temporary pacing should be available when considering cardioversion in patients with atrial fibrillation early after heart transplantation. Atrial flutter, in contrast, may be inducible in the absence of any sinus node abnormality and without any evidence of rejection.

Evoked potentials in severe herpes simplex encephalitis.

Diagnostic and prognostic value of evoked potentials (EP) were studied in 5 patients with severe herpes simplex encephalitis (HSE). Latency of the third negative cortical N70 peak, elicited by median nerve stimulation, was prolonged in 3 survivors with Glasgow coma score of less than or equal to 6 (115 vs 71 ms in controls, p less than 0.05), but normal after improvement of the acute disease. N70 right to left interhemisphere difference was increased initially in the 4 survivors (26 vs 3 ms in controls, p less than 0.05) indicating focal brain involvement, a crucial finding in HSE. The first cortical N20 peak was preserved in all survivors even during deep coma where evaluation of brain function is difficult. Auditory brainstem EP were normal in all patients and useful to exclude brainstem death. In severe HSE, somatosensory long-latency EP are an effective monitor of the level of impaired consciousness and can detect brain focal signs. Short-latency N20 components may be predictive of the outcome.

Combined sotalol and flecainide given at low dosage in patients with the Wolff-Parkinson-White syndrome.

We determined the effects of combined sotalol (160 mg/day) and flecainide (200 mg/day) in 15 patients with the Wolff-Parkinson-White syndrome. After medication given for 3 days, the plasma levels were 0.8 +/- 0.3 micrograms/ml for sotalol and 232 +/- 104 ng/ml for flecainide. Electrophysiologic testing showed complete blockade of the accessory pathway in 4 patients and a decrease in the anterograde conduction capacity by 27% in the remainder. The effect on the accessory pathway was unrelated to the resting conduction properties. Initiation of circus movement tachycardia was prevented in 5 of 11 patients. During a median period of 28 months of follow-up, 87% of patients were either free of tachycardia or satisfactorily improved. No proarrhythmic or adverse drug effects were observed.

Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia.

We studied the prognostic relevance of inducible ventricular tachycardia in 32 patients with dilated cardiomyopathy and spontaneous nonsustained asymptomatic ventricular tachycardia. Programmed ventricular stimulation included basic drive cycle lengths of 600, 500, 430, 370, 330 and 300 msec at single, double, and triple extrastimuli. Ventricular tachycardia (greater than or equal to 6 beats) was initiated in 7 patients (22%), with sustained monomorphic ventricular tachycardia being seen in 4 of them. During median follow-up of 21 months (13-44), 14 patients died. Sudden cardiac death occurred in two of the seven patients with inducible tachycardia and in only one of the 25 patients in whom it was not possible to induce tachycardia. Although patients with inducible tachycardia did not differ clinically from those in whom tachycardia could not be induced, the projected mean survival time was significantly shorter in those with inducible tachycardia (10 months vs. 32 months, P = 0.04). For late sudden cardiac death, the positive predictive value of inducible tachycardia was 28%. The negative predictive value was 96%. We conclude that induction of ventricular tachycardia by programmed stimulation might indicate poorer prognosis in patients with dilated cardiomyopathy.

Irregularity of the ventricular rhythm during atrial fibrillation: effect of slow atrioventricular nodal pathway ablation.

BACKGROUND: The contribution of dual atrioventricular (AV) nodal pathway physiology to the irregularity of the ventricular rhythm during atrial fibrillation has not been clarified. HYPOTHESIS: This study was performed to assess the effects of slow AV nodal pathway ablation on the irregularity of the ventricular rhythm during atrial fibrillation. METHODS: Irregularity of the ventricular rhythm was quantified using analysis of heart rate variability. In 20 patients with AV nodal reentrant tachycardia, absolute heart rate variability during atrial fibrillation was quantified before and after slow AV nodal pathway ablation by the standard deviation of all NN intervals (SDNN). Relative heart rate variability was determined by computing the coefficient of variation, SDNN normalized for the standard deviation of the mean ventricular cycle length (MVCL-AF). RESULTS: The slope of the regression between MVCL-AF and SDNN was significantly more gradual after slow pathway ablation (slope 0.39 vs. 0.23, p < 0.001). Coefficient of variation increased in 12 patients with heart rates > 120 beats/min at baseline (18.6 +/- 3.9 vs. 22.1 +/- 2.7% MVCL-AF, p < 0.05), but decreased in 8 patients with heart rates < 120 beats/min at baseline (25.6 +/- 3.1 vs. 22.2 +/- 2.2% MVCL-AF, p = 0.05). Furthermore, coefficient of variation correlated with MVCL-AF only at baseline (slope 0.034, r = 0.66), but no relation was found after slow pathway ablation (slope 0, r = 0). CONCLUSIONS: Slow AV nodal pathway ablation alters the relation between absolute heart rate variability and mean ventricular rate during atrial fibrillation and eliminates cycle length dependency of relative heart rate variability. These data indicate that dual AV nodal pathway physiology contributes to the irregularity of the ventricular rhythm during atrial fibrillation.

Day to day reproducibility of Doppler sonographic measurements in patients with valvular aortic stenosis.

High reproducibility of Doppler gradient measurements is necessary for both the reliable noninvasive assessment of the severity of aortic stenosis and for repeated follow-up examinations in individual patients. We therefore studied day to day reproducibility of Doppler sonographically measured peak pressure drops in 46 patients with valvular aortic stenosis. Clinically stable patients were examined twice within 29 +/- 18.2 days by the same examiner. Peak pressure drop (PPD) and peak flow velocity differed between the two examinations by 8.6 +/- 7.0 (range 0-29) mmHg and by 0.25 +/- 0.18 (range 0-0.7) m/s, respectively. Reproducibility was comparable in patients with excellent, good, and moderate quality examinations, but was lower in the 6 patients with poor quality examination. Variability of PPD, but not of peak flow velocity was higher (p less than 0.05) in patients with severe (PPD greater than 60 mmHg) stenosis. Reproducibility was comparable in patients with or without concomitant aortic incompetence and in patients with normal or reduced left ventricular function. Similar reproducibility was obtained in patients with heart rate changes below or above 10 beats/min between the two examinations. It is concluded that good reproducibility of Doppler measurements in patients with aortic stenosis allows reliable noninvasive assessment of the severity of the stenosis. In follow-up studies of patients with mild to moderate aortic stenosis increases in peak flow velocity in excess of 15% (mean day to day variability +2 SD) are highly indicative of the true progress of the stenosis.

Pacing-induced myocardial ischemia does not affect the endothelial release of coagulant and fibrinolytic factors into the coronary circulation.

The present study addresses the potential effects of pacing-induced myocardial ischemia on the secretion of coagulant and fibrinolytic factors within the coronary circulation. In 6 patients undergoing programmed ventricular stimulation with repeated induction of clinical ventricular tachycardia, the coronary release of tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI) capacity, von Willebrand factor antigen (WF:Ag), and prostacyclin (6-keto-PGF 1a) was measured. Blood samples were collected simultaneously from the ascending aorta and the coronary sinus at baseline and immediately after the induction of ventricular tachycardia. The occurrence of pacing-induced myocardial ischemia was established by myocardial net lactate production. Myocardial ischemia was induced in every patient by repeated pacing trials. Pacing-induced ischemia did not affect the coronary release of any of the above factors. Consequently, there was no alteration of transcardiac gradients of thrombin-antithrombin complexes and D-dimer. The present results indicate that pacing-induced myocardial ischemia does not affect the release of coagulant and fibrinolytic endothelial factors or prostacyclin into the coronary circulation.

Asystole during dipyridamole infusion in patients without coronary artery disease or beta-blocker therapy.

The authors report two patients without coronary artery disease who experienced asystole during the IV infusion of dipyridamole on routine TI-201 myocardial perfusion imaging and review the literature for possible explanations of this rare side effect. Until now, this side effect was only reported in patients with coronary artery disease or beta-blocker therapy. Yet, the cases lacked both concomitant factors and autonomic dysregulation is suggested as a cause for asystole.

[Poisoning with clonidin hydrochloride in children and adults]. / Die Intoxikation mit Clonidinhydrochlorid im Kindes- und Erwachsenenalter.

In this study clinical findings are presented of 31 patients with clonidinee intoxication and the therapeutic measures taken in these cases are discussed. In toddlers poisoning is seen after ingestion of a single tablet of 150 micrograms clonidine, whilst in adults poisoning may occur already at a dosage just exceeding the therapeutic limit, which is subject to wide individual variation (1 to 3 tablets). Primary elimination procedures must be instituted at these dosages, but, because of the rapid absorption of clonidine, gastric lavage and induced emesis provide no benefit to patients with complete symptomatology or those who took the overdose several hours before. Chlorpromazine-like effects, hypotension and bradycardia proved to be the outstanding features. Respiratory depression, disturbances of myocardial conduction or hypertension were less frequent. Symptoms lasted for a mean of 15.5 +/- 8.6 hours, with a range of 4 to 36 hours. Fluid therapy and, as necessary, dopamine for hypotension, phentolamine for hypertension and atropine for bradycardia caused prompt improvement in addition to essential measures such as meticulous control of respiratory function, body temperature and of ECG changes. There was no need to implement the central clonidine antagonist, tolazoline in any of these cases.