Variable procedural strategies adapted to anatomical characteristics in catheter ablation of the cavotricuspid isthmus using a preoperative multidetector computed tomography analysis.

OBJECTIVES: This study aimed to investigate the anatomical characteristics complicating cavotricuspid isthmus (CTI) ablation and the effectiveness of various procedural strategies. METHODS AND RESULTS: This study included 446 consecutive patients (362 males; mean age 60.5 ± 10.4 years) in whom CTI ablation was performed. A total of 80 consecutive patients were evaluated in a preliminary study. The anatomy of the CTI was evaluated by multidetector row-computed tomography (MDCT) prior to the procedure. A multivariate logistic regression analysis revealed that the angle and mean wall thickness of the CTI, a concave CTI morphology, and a prominent Eustachian ridge, were associated with a difficult CTI ablation (P < 0.01). In the main study, 366 consecutive patients were divided into 2 groups: a modulation group (catheter inversion technique for a concave aspect, prominent Eustachian ridge, and steep angle of the CTI or increased output for a thicker CTI) and nonmodulation group (conventional strategy). The duration and total amount of radiofrequency energy delivered were significantly shorter and smaller in the modulation group than those in the nonmodulation group (162.2 ± 153.5 vs 222.7 ± 191.9 seconds, P < 0.01, and 16,962.4 ± 11,545.6 vs 24,908.5 ± 22,804.2 J, P < 0.01, respectively). The recurrence rate of type 1 atrial flutter after the CTI ablation in the nonmodulation group was significantly higher than that in the modulation group (6.3 vs 1.7%, P = 0.02). CONCLUSION: Changing the procedural strategies by adaptating them to the anatomical characteristics improved the outcomes of the CTI ablation.

Pulmonary artery mapping for differential diagnosis of left-sided atrial tachycardia.

BACKGROUND: Distinguishing left-and right-sided atrial tachycardia (AT) is often challenging. The coronary sinus (CS) provides information only concerning the anterior left atrium (LA). Potentials recorded in the pulmonary artery (PA) have been substituted for those of the upper posterior LA because of their anatomical relationship. METHODS AND RESULTS: Three patterns were designed, using potentials in the PA, right atrium (RA) and CS, to predict the side of AT. Two patterns were for left-sided AT and 1 pattern was for right-sided AT. Ten left-sided and 11 right-sided ATs were investigated regardless of mechanism. Electrode catheters were inserted in the RA, His bundle region, and CS, and an ablation catheter was inserted into the left and/or right PA. The sequences from these catheters were analyzed before detailed electroanatomical mapping. Patterns were obtained for 20 of 21 ATs. The mechanism was focal in 16 ATs and macroreentry in 5. The method predicted left-sided AT with a sensitivity of 78%, a specificity of 100%, a positive predictive value of 100%, a negative predictive value of 84%, and an accuracy of 90%. CONCLUSIONS: The use of potentials in PA combined with conventional RA and CS electrograms is useful for distinguishing left-sided AT from right-sided AT, regardless of mechanism.

Left atrial thickness under the catheter ablation lines in patients with paroxysmal atrial fibrillation: insights from 64-slice multidetector computed tomography.

A detailed understanding of the left atrial (LA) anatomy in patients with atrial fibrillation (AF) would improve the safety and efficacy of the radiofrequency catheter ablation. The objective of this study was to examine the myocardial thickness under the lines of the circumferential pulmonary vein isolation (CPVI) using 64-slice multidetector computed tomography (MDCT). Fifty-four consecutive symptomatic drug-refractory paroxysmal AF patients (45 men, age 61 ± 12 years) who underwent a primary CPVI guided by a three-dimensional electroanatomic mapping system (Carto XP; Biosense-Webster, Diamond Bar, CA, USA) with CT integration (Cartomerge; Biosense-Webster) were enrolled. Using MDCT, we examined the myocardial thickness of the LA and pulmonary vein (PV) regions in all patients. An analysis of the measurements by the MDCT revealed that the LA wall was thickest in the left lateral ridge (LLR; 4.42 ± 1.28 mm) and thinnest in the left inferior pulmonary vein wall (1.68 ± 0.27 mm). On the other hand, the thickness of the posterior wall in the cases with contact between the esophagus and left PV antrum was 1.79 ± 0.22 mm (n = 30). After the primary CPVI, the freedom from AF without any drugs during a 1-year follow-up period was 78 % (n = 42). According to the multivariate analysis, the thickness of the LLR was an independent positive predictor of an AF recurrence (P = 0.041). The structure of the left atrium and PVs exhibited a variety of myocardial thicknesses in the different regions. Of those, only the measurement of the LLR thickness was associated with an AF recurrence.

A specific sign for differential diagnosis of atypical atrioventricular nodal reentrant tachycardia from atrial tachycardia.

Narrow QRS tachycardia with atrial activation occurring before ventricular activation was induced in a 34-year-old woman with dilated cardiomyopathy. During tachycardia late ventricular extrastimulus delivered when His bundle was refractory failed to reset the tachycardia while early ventricular extrastimulus caused paradoxical delay of the subsequent atrial response and terminated the tachycardia with a QRS not being followed by an atrial response. This is a rare but specific sign for excluding atrial reentry as the mechanism of tachycardia when P wave or atrial activation is registered before QRS response.

A spontaneous Type 1 electrocardiogram pattern in lead V2 is an independent predictor of ventricular fibrillation in Brugada syndrome.

AIM: Risk stratification for Brugada syndrome remains controversial. We investigated the relationships between episodes of ventricular fibrillation (VF) and various clinical, electrocardiographic, electrophysiologic, and genetic parameters both retrospectively and prospectively. METHODS AND RESULTS: Fifty-two patients with Brugada syndrome (49 men, average age 42 +/- 3 years) were studied. In the Brugada patients with a VF history, the frequency of a spontaneous Type 1 electrocardiogram (ECG) pattern in lead V2 was significantly higher and the STJ amplitude in the V1 and V2 leads was also higher than in those without a VF history. Multivariate analyses revealed that the spontaneous Type 1 ECG pattern in lead V2 (but not lead V1) was the only independent predictor of a VF history. During a mean follow-up period of 39 +/- 4 months, 38.8% of the patients with a VF history and 2.9% of those without experienced an appropriate implantable cardioverter-defibrillation owing to VF. A multivariate analysis using a Cox's proportional hazard model showed that a VF history and spontaneous Type 1 ECG pattern in lead V2 were independent predictors of subsequent VF events. CONCLUSION: A spontaneous Type 1 Brugada ECG pattern in lead V2 (but not lead V1) was both a prospective and retrospective independent predictor of VF episodes in Brugada syndrome.

Is structural remodeling of fibrillated atria the consequence of tissue hypoxia?

BACKGROUND: Matrix metalloproteinases (MMPs) play an important role in degradation of the extracellular matrix of injured tissue. MMP-9 expression increases in fibrillating atrial tissue; however, the mechanism for this increase has not been clarified. METHODS AND RESULTS: Changes in the expression of vascular endothelial growth factor (VEGF), VEGF receptors, and hypoxia-induced transcription factor-1alpha (HIF-1alpha) in fibrillating atrial tissue were investigated. Atrial tissue samples were obtained from 13 patients with atrial fibrillation (AF) and 25 patients without a history of AF (regular sinus rhythm, RSR) undergoing cardiac operations. Western blot, real-time polymerase chain reaction, and immunofluorescence analyses of the expression of VEGF, VEGF receptors, and HIF-1alpha were performed. The VEGF mRNA and protein levels increased significantly in the AF group compared with the RSR group (P<0.05), and the expression of HIF-1alpha protein was also significantly higher in the AF group. VEGF receptor-1 mRNA, a high-affinity receptor for VEGF, but not VEGF receptor-2 mRNA, was upregulated in the atria of the AF group (P<0.05). Immunofluorescence staining revealed excess production and co-localization of HIF-1alpha, VEGF and MMP-9 in the endothelium of the atrial arteries in the AF group. CONCLUSIONS: It is possible that upregulation of HIF-1/VEGF is involved in the enhancement of MMP-9 expression under hypoxic conditions.

Long-term effects of quinapril with high affinity for tissue angiotensin-converting enzyme after coronary intervention in Japanese.

BACKGROUND: Angiotensin-converting enzyme inhibitors have been shown experimentally to prevent restenosis after balloon injury. We previously reported that quinapril reduced the 6-month restenosis (percent diameter stenosis >or=50%) rate after percutaneous coronary intervention (PCI). However, it was not established whether this favorable outcome was maintained for longer periods. METHODS: This study was a prospective, randomized, open, and non-placebo controlled trial. Patients with coronary artery disease were enrolled after successful coronary balloon angioplasty or stenting. Two hundred and fifty-three patients were randomly assigned to the quinapril (10-20 mg per day) or control groups. The major clinical end points included death, myocardial infarction, cerebrovascular accident, or revascularization (either coronary artery bypass grafting or repeat PCI). These were tabulated according to the intention-to-treat principle. RESULTS: Long-term follow-up was available with a median of 4.8 (interquartile range 4.2-5.1) years after the procedure. The incidence of combined end points of mortality and morbidity (myocardial infarction and cerebrovascular accident) in the quinapril group was lower than that in the control group (6.1% vs 14.8%; relative risk [RR] 0.42, 95% CI 0.18-0.96, P =.033). The overall incidence of end-point events in patients with quinapril also occurred less frequently (29.8% vs 46.7%; RR 0.58, 95% CI 0.38-0.86, P =.007). CONCLUSIONS: These clinical outcomes show that the benefit of quinapril in patients following PCI is maintained for 4 years.

Disopyramide for transient high-degree atrioventricular block in a young patient with a history of syncope.

Although high-degree atrioventricular (AV) block in patients with a history of syncope usually requires pacemaker implantation, therapeutic strategies should also be considered. A 35-year-old man presented with complaints of palpitations, nausea and dysgeusia. Since aged 30, the patient had experienced three episodes of syncope. Holter monitoring showed transient high-degree AV block (up to 5:4 block) associated with nausea, eructation and dysgeusia irrelevant to posture as well as ventricular ectopic beats with palpitation. A head-up tilt test revealed neurally mediated vasodepression but electrophysiological study showed no abnormalities. These results indicated that his transient high-degree AV block was functional, and syncope would have been because of neurally mediated vasodepression, not bradycardia. After administration of disopyramide at 300 mg daily, the symptoms subsided and ventricular ectopic beats and AV block disappeared. He has been well for 20 months.

Catheter ablation of atrioventricular nodal reentrant tachycardia in a patient with complete situs inversus, atrial septal defect and "inverse" persistent left superior vena cava.

We report a case of successful radiofrequency ablation for atypical atrioventricular nodal reentrant tachycardia in a patient with complete situs inversus, secundum atrial septal defect and an "inverse" persistent left superior vena cava. The procedure was performed under the monoplane fluoroscopic guidance using the inferior approach.

Non-SCN5A related Brugada syndromes: verification of normal splicing and trafficking of SCN5A without exonic mutations.

Recently, it has been reported that under 20% of Brugada syndrome cases are linked to SCN5A mutations. The purpose of this study was to clarify whether abnormalities other than exonic mutations, such as splicing disorders, decreased mRNA expression levels, or membrane transport abnormalities of SCN5A, play a role in the pathogenesis of Brugada syndrome. We analyzed all SCN5A exons and splice sites using genomic DNA from 23 Brugada syndrome patients. We also analyzed the mRNA obtained from RV cardiomyocytes using real time PCR and sequencing, to study the expression levels and splicing patterns of SCN5A. The localization of SCN5A was examined by immunofluorescence analysis. A de novo heterozygous G to A transversion in a 5' splice junction of the intron between exons 21 and 22 was detected in 1 patient. In the mRNA analysis of Brugada syndrome patients without a mutation of SCN5A no splicing abnormalities were detected, and the SCN5A mRNA levels were similar to those of normal controls. Immunofluorescence analyses revealed that SCN5A is located on the surface membrane not only in the RV cardiomyocytes of normal controls but also in those with Brugada syndrome. We can confirm that some Brugada syndrome patients without exonic mutations in SCN5A had no other SCN5A abnormalities, including any involving the location of the SCN5A protein. These results suggest the involvement of other proteins in the pathogenesis in Brugada syndrome.

Hemodynamic consequences of a swinging, infarcted ventricular septum.

Noonan syndrome presents with dysmorphic facial features, short stature, and cardiac abnormalities (most commonly pulmonic stenosis and hypertrophic cardiomyopathy). This report describes a rare case accompanied by a secundum atrial septal defect (ASD) and a ventricular septal aneurysm causing right ventricular (RV) pressure gradient. A 29-year-old mentally retarded man was admitted to hospital with exertional dyspnea. His somatic features included short stature (148 cm), hypertelorism, a shield chest, and thoracic scoliosis. Echocardiogram showed a secundum ASD with bidirectional shunting and a ventricular septum bulging toward the left ventricle in diastole, and then toward the RV in systole causing obliteration of the RV. The peak pressure gradient measured across the RV outflow by continuous wave Doppler was 30 mmHg. Cardiac catheterization revealed an elevated RV pressure without pulmonary hypertension and confirmed the pressure gradient. Right ventriculography revealed the septal excursion toward the RV in systole, leaving only a small residual cavity in the inflow and outflow regions of the RV. The ASD was closed with an autologous pericardial patch. A thin, fibrous portion of the ventricular septum was resected and replaced with a Dacron patch. From the histological examination, the RV cavity obliteration turned out to be produced by the excursion of the infarcted ventricular septum.