Heme oxygenase-1 gene promoter polymorphism and the risk of pediatric nonalcoholic fatty liver disease.

BACKGROUND AND OBJECTIVES: Oxidative stress and the insulin-resistant state are thought to be key components in the pathogenesis of pediatric nonalcoholic fatty liver disease (NAFLD). Heme oxygenase (HO) is important in the defense against oxidative stress. This study aimed to assess the association of HO-1 gene promoter polymorphism and insulin resistance with NAFLD among obese children. METHODS: A total of 101 obese children aged 6-17 years were recruited. Anthropometric, serum biochemical variables and biomarkers for glucose and insulin metabolism were measured. We screened the allelic frequencies of (GT)n repeats in the HO-1 gene promoter among these obese children. NAFLD was determined through liver ultrasonography. Because the distribution of numbers of (GT)n repeats was bimodal, we divided the alleles into two classes: class S included shorter (27) repeats, and class L included longer (⩾27) repeats. We assessed the effects of the length of (GT)n repeats in HO-1 gene promoter on pediatric NAFLD. RESULTS: Of the 101 obese subjects, 27 (26.7%) had NAFLD. The alanine aminotransferase level was higher in patients carrying L alleles (L/L and L/S) than patients with S alleles (S/S) (46.2±49.3 IU|(-1) versus 30.2±20.1 IU|(-1); P=0.027). The significant risk factors for pediatric NAFLD were patients carrying L alleles (L/L and L/S) (odds ratio (OR)=18.84; 95% confidence interval (CI): 1.45-245.22; P=0.025), homeostasis model assessment of insulin resistance (OR=1.40; 95% CI: 1.07-1.83; P=0.014) and age (OR=1.24; 95% CI: 1.03-1.50; P=0.025). CONCLUSION: In this hospital-based study, the obese children with longer GT repeats in the HO-1 gene promoter and insulin resistance were susceptible to NAFLD.

Orolingual angioedema after alteplase therapy of acute ischaemic stroke: incidence and risk of prior angiotensin-converting enzyme inhibitor use.

BACKGROUND AND PURPOSE: Orolingual angioedema (OA) is an uncommon but potentially life-threatening complication of treatment with recombinant tissue plasminogen activator (rt-PA; alteplase) during acute ischaemic stroke. This study aimed to determine the incidence of rt-PA-related OA in an Asian stroke population and the risk of pre-stroke anti-hypertensive drug use for development of this complication. METHODS: A multi-center stroke registry was used to identify the pre-stroke medications of acute ischaemic stroke patients receiving intravenous rt-PA from January 2002 to December 2013. The clinical manifestations of rt-PA-related OA were recorded and the incidence of this complication was determined. The risks of pre-stroke use of different anti-hypertensive agents for the occurrence of rt-PA-related OA were determined from this study and from a meta-analysis. RESULTS: A total of 559 patients received intravenous rt-PA over a 12-year period. Five patients (two males) developed OA after rt-PA administration. The incidence of OA amongst these patients was 0.89% (95% confidence interval 0.29%-2.09%), which was lower than that obtained by meta-analysis (1.9%). Amongst pre-stroke anti-hypertensive medications, angiotensin-converting enzyme (ACE) inhibitors were found in this study to have the highest relative risk for rt-PA-related OA (17.1; 95% confidence interval 3.0-96.9). Meta-analysis also revealed that pre-stroke use of ACE inhibitors was associated with a high relative risk of OA after intravenous rt-PA (12.9; 95% confidence interval 4.5-37.0). CONCLUSIONS: The incidence of rt-PA-related OA in the Asian population is lower than that in the Caucasian population. Pre-stroke use of ACE inhibitors significantly increases the risk of this complication.

Pre-ICH warfarin use, not antiplatelets, increased case fatality in spontaneous ICH patients.

BACKGROUND AND PURPOSE: Anticoagulant and antiplatelets for prevention of ischaemic stroke and cardiovascular diseases may increase the risk of intracerebral hemorrhage (ICH). This study aimed to investigate the influence of pre-ICH use of anticoagulant and antiplatelets on ICH patients. METHODS: Consecutive patients with acute spontaneous ICH registered in a single-center stroke registry during 2001 to 2010 were analyzed and categorized according to their pre-ICH use of warfarin (Group I), antiplatelets (Group II), or neither (Group III). Survival analysis and the Cox proportional hazard model were used to compare between the three groups and the predictors. RESULTS: Of 2021 ICH patients (male, 63.3%; mean age, 62.6 ± 14.4 years) included, there were 94 (4.7%) in Group I, 232 (11.4%) in Group II, and 1695 (83.9%) in Group III. Warfarin users had larger hematoma volume, more intraventricular extension, higher frequencies of lobar ICH, and higher case fatality than non-warfarin users (Groups II and III). The Cox proportional hazard model showed increased 6-month case fatality in pre-ICH warfarin users (adjusted hazard ratio 2.75, 95% confidence interval 2.04-3.72, P < 0.001), but not in pre-ICH antiplatelet users (adjusted hazard ratio 0.95, 95% confidence interval 0.72-1.26). CONCLUSIONS: Intracerebral hemorrhage patients with prior warfarin use, but not antiplatelet use, had significantly higher case fatality at 6 months.

Screen for intracranial dural arteriovenous fistulae with carotid duplex sonography.

OBJECTIVES: Early diagnosis and management of intracranial dural arteriovenous fistulae (DAVF) may prevent the occurrence of stroke. This study aimed to identify the best carotid duplex sonography (CDS) parameters for screening DAVF. METHODS: 63 DAVF patients and 170 non-DAVF patients received both CDS and conventional angiography. The use of seven CDS haemodynamic parameter sets related to the resistance index (RI) of the external carotid artery (ECA) for the diagnosis of DAVF was validated and the applicability of the best CDS parameter set in 20 400 patients was tested. RESULTS: The CDS parameter set (ECA RI (cut-off point = 0.7) and internal carotid artery (ICA) to ECA RI ratio (cut-off point = 0.9)) had the highest specificity (99%) for diagnosis of DAVF with moderate sensitivity (51%). Location of the DAVF was a significant determinant of sensitivity of detection, which was 70% for non-cavernous DAVF and 0% for cavernous sinus DAVF (p<0.001). The above parameter set detected abnormality in 92 of 20 400 patients. These abnormalities included DAVF (n = 25), carotid stenosis (n = 32), vertebral artery stenosis (n = 7), intracranial arterial stenosis (n = 6), head and neck tumour (n = 3) and unknown aetiology (n = 19). CONCLUSION: Combined CDS parameters of ECA RI and ICA to ECA RI ratio can be used as a screening tool for the diagnosis of DAVF.

Antibody response to murine anti-GD2 monoclonal antibodies: correlation with patient survival.

Clinical strategies which modulate the human anti-mouse antibody response (HAMA) in patients may have a profound influence on the idiotype network inducible by murine monoclonal antibodies (MoAb). Prior to myeloablative chemotherapy (ABMT), 9 patients with Stage IV neuroblastoma were imaged with 131I-3F8, a MoAb specific for the ganglioside GD2. Their serum HAMA, anti-idiotypic, anti-GD2, and anti-anti-idiotypic antibodies were assayed by enzyme-linked immunosorbent assay prior to, and at 3 and 6 months postimaging. HAMA and anti-idiotypic levels remained low, in contrast to the high levels in 10 patients imaged with 131I-3F8 without ABMT. Five of the 9 patients are long-term survivors; all had elevated anti-GD2 and anti-anti-idiotypic levels, significantly higher than those who died of disease. Although 131I-3F8 imaging prior to ABMT detected abnormal sites in 4 of 9 patients, 3 of the 4 patients have continued in remission for 24-63 months after ABMT, and all 3 mounted anti-GD2 and anti-anti-idiotypic antibody responses. We conclude that myeloablative therapy strongly suppressed the HAMA/anti-idiotypic response to murine MoAb and that the prognostic significance of host immune response to ganglioside GD2 MoAb deserves further investigation.

Anti-G(D2) antibody treatment of minimal residual stage 4 neuroblastoma diagnosed at more than 1 year of age.

PURPOSE: To eradicate minimal residual disease with anti-G(D2) monoclonal antibody 3F8 in stage 4 neuroblastoma (NB) diagnosed at more than 1 year of age. PATIENTS AND METHODS: Thirty-four patients were treated with 3F8 at the end of chemotherapy. Most had either bone marrow (n=31) or distant bony metastases (n=29). Thirteen patients were treated at second or subsequent remission (group I) and 12 patients in this group had a history of progressive/persistent disease after bone marrow transplantation (BMT); 21 patients were treated in first remission following N6 chemotherapy (group II). RESULTS: Before 3F8 treatment, 23 patients were in complete remission CR, eight in very good partial remission (VGPR), one in partial remission (PR), and two had microscopic foci in marrow. Twenty-five had evidence of NB by at least one measurement of occult/minimal tumor (iodine 131[(131)I]-3F8 imaging, marrow immunocytology, or marrow reverse-transcriptase polymerase chain reaction [RT-PCR]). Acute self-limited toxicities of 3F8 treatment were severe pain, fever, urticaria, and reversible decreases in blood counts and serum complement levels. There was evidence of response by immunocytology (six of nine), by GAGE RT-PCR (seven of 12), and by (131)I-3F8 scans (six of six). Fourteen patients are alive and 13 (age 1.8 to 7.4 years at diagnosis) are progression-free (40 to 130 months from the initiation of 3F8 treatment) without further systemic therapy, none with late neurologic complications. A transient anti-mouse response or the completion of four 3F8 cycles was associated with significantly better survival. CONCLUSION: Despite high-risk nature of stage 4 NB, long-term remission without autologous (A)BMT can be achieved with 3F8 treatment. Its side effects were short-lived and manageable. The potential benefits of 3F8 in consolidating remission warrant further investigations.

Double atrial responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways.

Electrophysiologic studies were performed in two patients. In one patient (Case 1) with ventricular pre-excitation and paroxysmal supraventricular tachycardia, studies after diltiazem administration showed two QRS responses to a single atrial stimulus during atrial pacing at a cycle length of 300 ms. The first QRS response with full pre-excitation and short PR interval was consistent with accessory pathway conduction, while the second QRS response with a normal duration and an atrio-His bundle interval of 350 ms was consistent with normal pathway conduction. The second QRS response was followed by initiation of supraventricular tachycardia. Studies after verapamil administration on a separate day disclosed two atrial responses to a single QRS complex during ventricular pacing at cycle lengths between 330 and 280 ms, suggesting simultaneous retrograde accessory and normal pathway conduction. In Case 2 with a supraventricular tachycardia using a fast atrioventricular nodal pathway for anterograde and a slow ventriculoatrial pathway for retrograde conduction, two atrial responses to a single QRS complex were observed during ventricular pacing at cycle lengths between 500 and 400 ms. The first atrial response showed a stimulus to atrial interval of 120 ms and an atrial activation sequence with the low septal right atrium being earlier than other atrial sites, suggesting retrograde fast pathway conduction. The second atrial response showed a stimulus to atrial interval of 505 ms and an atrial activation sequence with low septal right atrium being simultaneous with the proximal coronary sinus, suggesting retrograde slow pathway conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.

Atrioventricular block in the atypical form of junctional reciprocating tachycardia: evidence supporting the atrioventricular node as the site of reentry.

Serial electrophysiologic studies were performed in 19 patients with the atypical form of supraventricular tachycardia having a long RP and short PR interval. In all 19 patients, supraventricular tachycardia was found to have a 1:1 P-QRS relation during initial control electrophysiologic studies, and in all 19 patients, electrophysiologic studies suggested that junctional reentry was the mechanism of supraventricular tachycardia. Seven of the 19 patients developed atrioventricular (AV) block during initiation of supraventricular tachycardia or after induction of supraventricular tachycardia following various drug administrations in subsequent studies. In three patients, second degree block within the His bundle or block distal to the His bundle recording site occurred after administration of quinidine. In one patient it occurred after procainamide, and in another patient it occurred after atropine. In one patient, 2:1 block proximal to the His deflection occurred after verapamil. In the remaining patient, a transient Wenckebach block proximal to the His deflection was noted after adenosine triphosphate. In this latter patient, 2:1 AV block was also noted after propranolol and digoxin. The site of reentry in these seven patients with AV block during supraventricular tachycardia was confined to the AV node area. Their supraventricular tachycardia did not involve a slowly conducting paraseptal accessory pathway because the distal AV node, His bundle and ventricle were not found to be necessary links in the tachycardia circuit.

Pseudosimultaneous fast and slow pathway conduction: a common electrophysiologic finding in patients with dual atrioventricular nodal pathways.

Two ventricular responses following termination of rapid atrial pacing were noted in 24 of 87 patients with dual atrioventricular (AV) nodal pathways and supraventricular tachycardia. In all 24 patients, the AH intervals of the first and second ventricular responses were comparable with those of the fast and slow pathways, respectively. Careful analysis of the whole pacing sequence revealed that, in 21 patients, this phenomenon resulted from sustained slow pathway conduction with long AH intervals. In these patients, as the AH interval of each paced beat was progressively lengthened during pacing, the corresponding His bundle and ventricular responses were pushed one cycle behind the current atrial paced beat, so that the last paced beat was followed by two His bundle and ventricular responses. In only three patients did double ventricular responses result from simultaneous fast and slow pathway conduction. One of these three patients also showed two ventricular responses resulting from sustained slow pathway conduction. Several factors predispose to the occurrence of this phenomenon in patients with dual AV nodal pathways. These include an ability to sustain slow pathway conduction, a longer slow pathway AH interval, a shorter sinus AH interval (fast pathway) and a shorter atrial paced cycle length that sustains slow pathway conduction. In conclusion, sustained slow pathway conduction with resultant long AH intervals is the mechanism of two ventricular responses following termination of atrial pacing in most patients with dual AV nodal pathways. This phenomenon should be distinguished from the rare occurrence of double ventricular responses to an atrial impulse due to simultaneous fast and slow pathway conduction.

Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 +/- 2.8 s (mean +/- SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional sinoatrial block. Group II consisted of 22 patients with either 1:1 sinoatrial conduction (group IIa = 13 patients) or second degree sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to greater than 14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 +/- 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 +/- 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patients with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 +/- 1,121). Thus, abnormalities in both sinus node automaticity and sinoatrial conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive sinoatrial exit block plays a major role in producing posttachycardia pauses.

Nature of dual atrioventricular node pathways and the tachycardia circuit as defined by radiofrequency ablation technique.

OBJECTIVES: A comprehensive electrophysiologic study followed by selective radiofrequency ablation from three sites was performed in patients with atrioventricular (AV) node reentrant tachycardia to better delineate the nature of the tachycardia circuit. BACKGROUND: We postulated that the retrograde fast pathway is the anterior superficial group of transitional cells and the slow pathway is the compact node with its posterior input of transitional cells. Twenty-three consecutive patients were studied. In nine, the atria could be dissociated from the tachycardia by delivery of an atrial extrastimulus during tachycardia. METHODS: Radiofrequency ablation was performed with three approaches. The anterior approach was designed to interrupt the anterior superficial atrial input to the compact node, the posterior approach to interrupt the posterior atrial input to the compact node and the inferior approach to destroy the compact node itself. RESULTS: Selective ablation of the retrograde fast pathway was achieved in seven patients, six with the anterior and one with the inferior approach. Anterograde fast pathway conduction was not affected, whereas retrograde fast pathway conduction was either abolished or markedly depressed. None had induction of echoes or tachycardia after ablation. Selective ablation of the slow pathway was successful in 13 patients, 1 with anterior, 3 with posterior and 9 with inferior approaches. In these 13 patients, both anterograde and retrograde fast pathway conduction were not affected, the dual pathway physiology was abolished and the tachycardia was not inducible after ablation. Ablation of both the retrograde fast pathway and the slow pathway occurred with the inferior approach in three patients. CONCLUSIONS: We conclude that the retrograde fast pathway is likely to be the anterior superficial group of transitional cells, whereas the slow pathway is the compact node and its posterior input of transitional cells. A barrier seems to exist between the atrium and the tachycardia circuit. In a broad view of the AV node structure, the tachycardia circuit is confined to the node.

Repetitive sinoatrial exit block as the major mechanism of drug-provoked long sinus or atrial pause.

Prolonged sinus or atrial pause occurred in six patients with paroxysmal supraventricular tachycardia after drug administration. All six patients had normal sinus node function during control electrophysiologic study; the sinus cycle length ranged from 510 to 900 ms (mean 743 +/- 141) and the longest sinus node recovery time ranged from 800 to 1,230 ms (mean 1,018 +/- 168). A long sinus or atrial pause occurring at the termination of tachycardia or cessation of atrial pacing, ranging from 3,100 to 8,200 ms (mean 6,270 +/- 1,674), was provoked by the administration of various drugs. These included an intravenous bolus injection of adenosine triphosphate (5 mg; one patient), intravenous bolus injection of verapamil (5 mg; one patient), a combination of a single oral dose of diltiazem (120 mg) and propranolol (20 to 40 mg; three patients), oral diltiazem (240 mg/day; one patient) and a combination of oral diltiazem (240 mg/day) and propranolol (160 mg/day; one patient). In five patients, low frequency deflections suggestive of sinus node activity with a cycle length between 620 and 3,500 ms were recorded during pauses. These findings suggest that repetitive sinoatrial exit block was responsible for the pause. Sinus slowing with a long arrest suggesting suppression of sinus automaticity was also noted in three of these five patients; the longest sinus arrest in these three patients was 4,160, 4,800 and greater than 4,910 ms, respectively. The remaining patient with a pause of 6,840 ms had no recordable sinus activity, either reflecting suppression of sinus automaticity or technical failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Successful radiofrequency ablation of idiopathic left ventricular tachycardia at a site away from the tachycardia exit.

OBJECTIVES: This study sought to assess the possibility of ablating verapamil-responsive idiopathic left ventricular tachycardia at a site distant from the tachycardia exit and thus to define the tachycardia circuit. BACKGROUND: The nature of the reentry circuit in idiopathic left ventricular tachycardia is unclear. If the circuit is of considerable size, then it should be possible to ablate the tachycardia at a site distant from the exit site. METHODS: Electrophysiologic studies and radiofrequency ablation were performed in 27 consecutive patients with verapamil-responsive idiopathic left ventricular tachycardia. In all 27 patients, the tachycardia exit site was defined as the site where the earliest Purkinje potential was recorded > or = 25 ms before the onset of the QRS complex during the tachycardia and where the pace map QRS complex resembled that during the tachycardia. A potential ablation site other than the exit site was then sought around the midseptum, proximal to the exit site. At such sites the tachycardia could be terminated transiently by pressure applied to the catheter tip, without induction of ventricular ectopic beats. RESULTS: The potential ablation site, other than the tachycardia exit site, was identified in seven male patients (mean [+/-SD] age 31 +/- 12 years, range 13 to 52). Application of the radiofrequency current at this site resulted in termination of the tachycardia within 1 to 5 s (mean 2.9 +/- 1.6), and successful ablation of the tachycardia was achieved in all seven patients (success rate 100%, 95% exact confidence interval 0.5898 to 1). The mean distance between the ablation site and the tachycardia exit site was 3.1 +/- 0.7 cm (range 2.0 to 4.0). A presystolic Purkinje spike was recorded 14 +/- 5 ms (range 8 to 20) before the onset of the QRS complex during the tachycardia. During the follow-up period of 24 +/- 11 months (range 12 to 39), there was no recurrence of tachycardia in these seven patients. CONCLUSIONS: Successful ablation of idiopathic left ventricular tachycardia can be achieved at sites away from the tachycardia exit site in some patients. This finding suggests that the reentry circuit is likely to be of considerable size, encompassing the middle, inferior and lower aspects of the left interventricular septum.

Adenosine-sensitive ventricular tachycardia from the anterobasal left ventricle.

OBJECTIVES: This study demonstrates that exercise-provocable tachycardia resembling right ventricular outflow tract tachycardia may originate from the anterobasal left ventricle. BACKGROUND: Reentry is the operative mechanism of idiopathic left ventricular tachycardia, with a QRS complex of right bundle branch block and superior axis that is responsive to verapamil but not adenosine. Whether some mechanism other than reentry is operative in some idiopathic left ventricular tachycardias is unclear. METHODS: In 4 of 53 consecutive patients with idiopathic left ventricular tachycardia, the tachycardia was sensitive to adenosine. These four patients were women 63, 61, 61 and 31 years old and were the subjects of the present study. RESULTS: In all four patients, spontaneous tachycardia was related to exercise or emotional stress. The tachycardia displayed atypical left (one patient) or right (three patients) bundle branch block with an inferior axis and marked variation in cycle length. An intravenous bolus of adenosine triphosphate (10 to 20 mg) terminated tachycardia in all four patients. Tachycardia was terminated or prevented in three patients given intravenous or oral verapamil. Atrial or ventricular incremental or extrastimulus testing induced tachycardia in all four patients (three with, one without isoproterenol infusion). Electrically induced tachycardia also demonstrated marked variation in cycle length, which ranged from 230 to 390 ms. Entrainment was not demonstrable with overdrive pacing from multiple sites. Endocardial mapping during tachycardia revealed that the earliest activations were registered 25, 40, 35 and 50 ms before onset of the QRS complex, respectively, from the anterior aspect of the left ventricle just below the mitral annulus, adjacent to the left ventricular outflow tract. High frequency Purkinje spikes were not recorded at this site. Radiofrequency current delivered to this site successfully ablated the tachycardia in three of the four patients. CONCLUSIONS: Exercise-provocable, catecholamine-mediated, verapamil-responsive, adenosine-sensitive ventricular tachycardia may arise from the anterobasal left ventricle adjacent to the outflow tract.

A simple technique for selective radiofrequency ablation of the slow pathway in atrioventricular node reentrant tachycardia.

OBJECTIVES: A simple technique was designed for radiofrequency ablation therapy of atrioventricular (AV) node reentrant tachycardia. BACKGROUND: This technique was based on the hypothesis that slow pathway conduction reflects conduction through the compact node and its posterior atrial input. METHODS: A total of 100 consecutive patients were studied; there were 37 men and 63 women, with a mean age of 48 +/- 15 years. All 100 patients had induction of sustained tachycardia with (51 patients) or without (49 patients) administration of isoproterenol or atropine, or both. The ablation catheter was initially manipulated to record the largest His bundle deflection from the apex of Koch's triangle. It was then curved downward and clockwise to the area of the compact node when His deflection was no longer visible and the ratio of atrial to ventricular electrogram was < 1. The radiofrequency current was delivered from the 4-mm tip electrode a mean of 5 +/- 7 times at a power of 25 +/- 4 W for a duration of 21 +/- 4 s. The total fluoroscopic time was 19 +/- 11 min. RESULTS: Selective ablation (56 patients) or modification (26 patients) of the slow pathway without affecting anterograde and retrograde fast pathway conduction was achieved in 82 patients. Ablation or modification of both the retrograde fast pathway and the slow pathway but with preservation of anterograde fast pathway conduction was noted in 12 patients. Ablation or modification of the retrograde fast pathway alone or both anterograde and retrograde fast pathway conduction was noted in three patients. Complete AV node block occurred in three patients. Seventy-three patients had no induction of echo beats or tachycardia and 24 patients had induction of a single echo beat after ablation. Follow-up study was performed in 62 patients 76 +/- 18 days after ablation. Thirty-nine patients had no induction of echo beats or tachycardia, 22 had induction of echo beats alone and 1 patient had induction of sustained tachycardia. CONCLUSION: Selective ablation of the slow AV node pathway can be achieved by a simple procedure with a high success rate and few complications.

Variation of P-QRS relation during atrioventricular node reentry tachycardia.

OBJECTIVES: The main objective of this study was to characterize the phenomenon of variation in the P-QRS relation during atrioventricular node reentry tachycardia. BACKGROUND: Variation of P-QRS relation during tachycardia has been observed occasionally in atrioventricular node reentry tachycardia. However, the incidence, the characteristics and the mechanisms of this phenomenon have not been investigated previously. METHODS: Retrospective analysis was performed in 311 consecutive patients with slow-fast form and 108 patients with atypical or multiple form of atrioventricular node reentry tachycardia to examine whether variation of P-QRS relation with changes in AH, HA and AH/HA (A = atria; H = His bundle) ratio occurred during tachycardia. RESULTS: A total of 28 patients, 8 with slow-fast and 20 with atypical or multiple tachycardias, were found to manifest this phenomenon. There were 6 males and 22 females, with an average age of 38+/-16 years. In 10 patients, this phenomenon occurred transiently following electrical induction of the tachycardia. In 15 patients, changes in AH, HA and AH/HA ratio were associated with the occurrence of Wenckebach or 2:1 block proximal to the His bundle (H) recording site without interruption of the tachycardia. In nine patients, three with nonsustained tachycardia and six after administration of adenosine triphosphate, this phenomenon was observed at the termination of the tachycardia. This phenomenon was usually accompanied by a mild lengthening of the tachycardia cycle length. CONCLUSIONS: Variation of P-QRS relation with or without block may occur during atrioventricular node reentry tachycardia, especially in atypical or multiple-form tachycardias. It was postulated that decremental conduction in the distal common pathway, which exists between the distal link of the reentry circuit and the H, is primarily responsible for this phenomenon.

Effects of isoproterenol on accessory pathway conduction in intermittent or concealed Wolff-Parkinson-White syndrome.

The effects of isoproterenol on accessory pathway conduction were evaluated in 24 patients with intermittent and 60 patients with concealed pre-excitation, using atrial and ventricular incremental and extrastimulus testing techniques. The atrial paced cycle length that induced block in the accessory pathway could be compared in 11 of the 24 patients with intermittent preexcitation before and after isoproterenol; it decreased from 622 +/- 212 ms to 408 +/- 128 ms (mean +/- standard deviation) after isoproterenol (p less than 0.01). The anterograde effective refractory period of the accessory pathway could be compared in 5 patients before and after isoproterenol; it decreased from 460 +/- 131 to 310 +/- 48 ms after isoproterenol (p less than 0.01). None of the 60 patients with concealed preexcitation showed ventricular preexcitation with isoproterenol infusion. Eighty-one of the 84 patients had clinically documented supraventricular tachycardia, suggesting the accessory pathway was capable of retrograde conduction. Retrograde study was performed in all 84 patients; 83 had retrograde conduction and the other had no retrograde conduction before and after isoproterenol. The ventricular paced cycle length that induced block in the accessory pathway could be compared in 38 patients before and after isoproterenol; it decreased from 342 +/- 71 to 296 +/- 39 ms after isoproterenol (p less than 0.001). The retrograde effective refractory period of the accessory pathway could be compared in 56 patients; it decreased from 293 +/- 76 to 238 +/- 36 ms after isoproterenol (p less than 0.001). In conclusion, isoproterenol facilitates anterograde and retrograde accessory pathway conduction, but the facilitation of anterograde conduction occurs only in those capable of spontaneous conduction.

Effects of oral diltiazem in paroxysmal supraventricular tachycardia.

Electrophysiologic studies were performed before and 2 hours after the oral administration of 270 mg of diltiazem in 3 divided doses at 8-hour intervals in 36 patients with paroxysmal supraventricular tachycardia (SVT). Before diltiazem, all 36 patients had induction of sustained SVT: 24 with atrioventricular (AV) reentrance incorporating an accessory pathway (Group 1) and 12 with AV nodal reentrance (Group 2). After diltiazem, 20 patients in Group 1 lost the ability to induce or sustain SVT because of increased anterograde normal pathway refractoriness in 19 patients and increased retrograde accessory pathway refractoriness in 1. Eight patients in Group 2 could no longer induce or sustain SVT because of increased anterograde slow pathway refractoriness in 2 patients and increased retrograde fast pathway refractoriness in 6. Diltiazem concentration in the blood, measured in 29 patients, was 156 +/- 75 ng/ml (mean +/- standard deviation). Fifteen patients, 2 with and 13 without induction of sustained SVT after diltiazem, were discharged on the same dosage of diltiazem and followed up 5 +/- 3 months. The former 2 patients had attacks of sustained SVT, whereas the latter 13 have been free of sustained SVT. In conclusion, oral diltiazem prevents induction and sustenance of paroxysmal SVT in most patients and may be used as an alternative agent for the prophylaxis of SVT.

Usefulness of intravenous diltiazem in predicting subsequent electrophysiologic and clinical responses to oral diltiazem.

Diltiazem, 0.25 mg/kg, was given intravenously during induced tachycardias in 6 patients with atrioventricular (AV) nodal reentrant tachycardia (group I) and in 24 patients with AV reentrant tachycardia incorporating a retrogradely conducting accessory pathway (group II). In all 6 group I and in 15 of 24 group II patients, tachycardias terminated within 1 minute after diltiazem administration, with a weak link in the anterograde direction. In 3 other patients in group II, tachycardias were terminated by a premature ventricular complex within 1 minute. In the remaining 6 patients in group II, in whom tachycardias failed to terminate, rates of tachycardias decreased as a result of suppression of anterograde AV nodal conduction by diltiazem. Electrophysiologic studies were performed subsequently 2 hours after the third dose of 90 mg of diltiazem, which was given orally at 8-hour intervals. In 18 responders to intravenous diltiazem who were subjected to oral diltiazem testing, sustained supraventricular tachycardia (SVT) could be induced in only 2. Of the 6 nonresponders, sustained tachycardias could not be induced in 3. Twelve patients, including 11 responders and 1 nonresponder to intravenous diltiazem who responded to oral diltiazem testing, were discharged with oral diltiazem therapy, 90 mg every 8 hours, with follow-up periods of 2 to 13 months (mean 7 +/- 4 [+/- standard deviation]). The frequency of recurrent SVT decreased significantly; 8 patients were free of tachycardias and 4 had occasional recurrences of SVT that required no hospital visit. In conclusion, intravenous diltiazem is effective in terminating SVT. Termination of SVT by intravenous diltiazem predicts subsequent electrophysiologic and clinical responses to oral diltiazem.