Radiofrequency catheter ablation of posteroseptal accessory pathways--results of a step-by-step ablation approach.

INTRODUCTION: Transcatheter radiofrequency ablation of posteroseptal accessory pathways (AP) is challenging. A number of different interventional approaches have been suggested by different groups. The selection of the initial approach is crucial in order to reduce radiation exposure and the number of unsuccessful lesions applied. We present our ablation technique as guided by a simplified electrocardiographic analysis of the delta wave polarity and the electrophysiologic mapping results. METHODS AND RESULTS: Out of 35 manifest APs encountered in the right (n=17) or the left posteroseptum (n=18) in 35 patients, 34 were successfully ablated. Despite their left sided location, 7 of the 18 "left" sided APs were ablated after switching from an initial arterial to a venous approach looking for an appropriate target site in the right posteroseptal space or within the coronary sinus network. The other 11 left sided APs were ablated in the mitral ring, on 2 occasions, on their atrial aspect through a retrograde transmitral approach. On the contrary, 16 of the 17 "right" sided APs were successfully ablated exclusively through a venous approach. Fourteen of these were ablated in the right posteroseptum, in 2 cases, only after reaching their ventricular aspect. Two right sided APs were interrupted in the coronary sinus os and the middle cardiac vein respectively. CONCLUSION: It appears that even though the electrocardiographic and electrophysiologic location of the AP in the posteroseptal space helps select the appropriate initial approach, it does not always guarantee a successful ablation procedure in the expected site of the corresponding atrioventricular ring. Not uncommonly, it will be necessary to look after intermediate target sites within the coronary sinus to improve the overall ablation success rate.

Mild left ventricular hypertrophy in essential hypertension: is it really arrhythmogenic?

Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 +/- 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.

Right posterior atrioventricular ring: a location for different types of atrioventricular accessory connections.

We present an unusual case of a 28-year-old female patient with recurrent episodes of tachycardias due to participation of two accessory connections located in the posterior tricuspid annulus. Both connections were of the atrioventricular type, the one with non decremental fast conducting properties at the right posteroseptal area, the other with node-like properties at the posterolateral tricuspid ring. Both pathways were successfully ablated transvenously with radiofrequency energy application at the same session. Implications about a common embryological origin of the two pathways as well as review of the literature for similar cases are presented.

Von Willebrand factor in patients evolving Q-wave versus non-Q-wave acute myocardial infarction.

We assessed the changes in plasma von Willebrand factor level concentration in 10 patients with Q-myocardial infarction and in six patients with non-Q-myocardial infarction who did not receive thrombolytic treatment. Concentrations of von Willebrand factor antigen were measured by an enzyme-linked immunoassay method in plasma samples obtained twice daily for 4 consecutive days. In patients with Q-wave myocardial infarction, a significant rise in von Willebrand factor antigen levels (P < 0.05) occurred after admission and persisted for 3 days. No significant changes were found in plasma concentration of fibrinogen. In conclusion, von Willebrand factor antigen levels were greater in patients with Q-wave compared to patients with non-Q-wave myocardial infarction.

t-Plasminogen activator and von Willebrand factor in patients with unstable angina.

We investigated whether the clinical evolution of symptoms in patients admitted with unstable angina is associated with changes in t-plasminogen activator antigen (t-PA) and von Willebrand (vW) factor levels. Concentrations of vW factor antigen and t-PA antigen were measured by an enzyme-linked immunoassay method in 10 patients who became clinically stable within 24 h of admission and remained so for 5 days. A significant rise in morning t-PA plasma level occurred 24 h after the admission (15.15 +/- 2.1 ng/ml, P < 0.05), whereas the vW factor remained unchanged. No significant changes were found in the night concentration in t-PA and vW factor during the 5 day period. Thus t-PA level is significantly raised 24 h after admission in patients with unstable angina who stabilize in response to medical treatment.

Sex differences in the anatomy of coronary artery disease.

In a prospective study, the extent and severity of coronary artery disease (CAD) as well as the location of coronary stenoses were studied comparatively, in relation to age and sex, in 192 consecutive women vs 543 selected men, who all underwent coronary angiography during the same time period, and who were found to have significant CAD. Overall, the age of women (59 +/- 8 years) was higher than that of men (55 +/- 8 years), p < 0.001. Also, the prevalence of smoking was higher in men (81% vs 31%, p = 0.0000) and that of diabetes mellitus in women (29% vs 12%, p = 4 x 10(-6)). In addition, women over 50 years old had a higher incidence of hypertension (51% vs 32%, p = 6 x 10(-5)). Although in both sexes the prevalence of multivessel CAD increased with age, the prevalence of one-vessel CAD was significantly more and that of three-vessel CAD significantly less common in women than in men, both overall (35% vs 16%, p = 4 x 10(-8) and 36% vs 54%, p = 2 x 10(-5), respectively) and in all age subgroups. However, the location of coronary stenoses did not show important differences between men and women with the left anterior descending being the most frequently involved artery. Furthermore, the calculated Gensini index, which reflects cumulatively the extent, severity and location of coronary stenoses, was significantly higher in men (59.2 +/- 34.6 vs 52.2 +/- 36.2, p = 0.03), implying more severe and extensive CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Polymorphic ventricular tachycardia induced during tilt table testing in a patient with syncope and probable dysfunction of the sinus node.

We present a case of life-threatening arrhythmia occurring during tilt table testing in a 44-year-old man with syncope. Polymorphic ventricular tachycardia occurred while the patient was tilted up under the intravenous infusion of isoproterenol (2 micrograms/min). No ischemia, QTc prolongation, or electrolyte abnormality preceded this event. The arrhythmia was not induced by programmed ventricular stimulation or exercise testing. Based on electrophysiological and clinical data, the diagnosis of sick sinus syndrome was entertained.

45,X Turner syndrome with normal ovarial function and multiple malformations of the aorta.

We present a case of a female patient with monosomy of X chromosome in peripheral lymphocytes and skin fibroblasts, normal ovarian function and associated multiple congenital abnormalities of the aorta: bicuspid aortic valve, dilatation of the ascending aorta and multiple cystic structures of the aortic wall, complicated by endarteritis. We review the literature on fertile women with 45,X karyotype and the possible pathogenetic mechanisms of the aortic defects described as 'cystic medial necrosis of the aorta'.

Effects of ketanserin on epicardial coronary arteries after coronary angioplasty in patients with stable angina.

Previous studies have demonstrated the development of vasoconstriction immediately after percutaneous coronary angioplasty (PTCA), distal to the dilated stenosis, presumably resulting from endothelial injury. We have investigated the role of 5-HT2 receptors in mediating vasomotor changes in proximal and distal coronary segments and coronary stenoses, immediately after successful PTCA in patients with chronic stable angina. We compared the effects of the intracoronary infusion of 1 mg ketanserin (5-HT2 receptor antagonist) on proximal and distal coronary arterial segments immediately after PTCA in both vessels subjected to PTCA and control vessels. Coronary diameters, before and after angioplasty and after ketanserin administration, of proximal and distal segments and coronary stenoses were measured by computerized quantitative coronary angiography (CAAS system) in 12 patients (10 male, two female; mean age 54 +/- 6 years) with stable angina subjected to PTCA. After coronary angioplasty, vasoconstriction was observed in the segment distal to the dilated stenosis but not in the distal segments of control vessels (-0.12 +/- 0.04 and -0.02 +/- 0.02 mm respectively; P < 0.05). After ketanserin infusion significant dilatation was found in the distal segments of both PTCA vessels and control vessels, but the dilatation was greater in the PTCA vessels (P < 0.05). No significant changes were found in the proximal segments of either PTCA or control vessels, or at the PTCA site. In conclusion, the vasoconstriction distal to the site of PTCA is mediated, at least in part, via 5-HT2 receptors.

Endarteritis of the aortic arch in Turner's syndrome with cystic degeneration of the aorta.

We present a case of a 36-year-old 45 XO Turner syndrome with bicuspid aortic valve, dilatation of the ascending aorta and of the major branches of the aortic arch and multiple cysts of the aortic wall. This was complicated by endarteritis of the base of the aortic arch and production of an intraluminal structure (intra-aortic debris). She also presented reactive pleural effusion and involvement of the pulmonary artery which was complicated by pulmonary embolism. Possible aetiological mechanisms are discussed.