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Aims: The purpose of this study was to evaluate a retrograde approach for radiofrequency (RF) ablation of ectopic atrial tachycardias (EATs) with an early atrial activation at the His site., Methods and Results: This study included 12 patients with EAT. During tachycardia, earliest atrial activation was recorded at the His site at a standard catheter setting. Activation mapping was performed in the right atrium and along the mitral annulus and at the aortic root after retrograde insertion of the ablation catheter over the ascending aorta. In five patients, earliest atrial activation was recorded at the mitral annulus (in two patients at the superior-lateral annulus and in three patients at the inferior-medial annulus). In four of these patients, EAT could be successfully treated by RF ablation through the retrograde approach, whereas in one patient, a transseptal puncture was performed in order to achieve a stable catheter position. In seven patients, RF ablation at the non-coronary aortic sinus eliminated the tachycardia. During a follow-up period of 14 +/- 8 months, there was no tachycardia recurrence., Conclusion: In patients with EATs and early atrial activation at the His site, tachycardia may arise in the non-coronary aortic sinus or from the mitral annulus. Radiofrequency energy ablation can be performed through a retrograde approach in the majority of these patients and is safe and effective in eliminating this type of tachycardia.

Advances in medical imaging now make it possible to investigate any patient with cardiovascular disease using multiple methods which vary widely in their technical requirements, benefits, limitations, and costs. The appropriate use of alternative tests requires their integration into joint clinical diagnostic services where experts in all methods collaborate. This statement summarises the principles that should guide developments in cardiovascular diagnostic services.

Advances in medical imaging now make it possible to investigate any patient with cardiovascular disease using multiple methods which vary widely in their technical requirements, benefits, limitations, and costs. The appropriate use of alternative tests requires their integration into joint clinical diagnostic services where experts in all methods collaborate. This statement summarizes the principles that should guide developments in cardiovascular diagnostic services.

Aims: Because of its high spatial resolution and tissue contrast, magnetic resonance imaging (MRI) was used to assess cardiac structure and function in a large population of patients with acute myocardial infarction (AMI)., Methods and Results: One hundred and ten patients were studied by MRI 6.1 +/- 2.2 days after AMI. Infarct size (IS), persistent microvascular obstruction (PMO), left and right ventricular (LV/RV) volumes, and functions were measured. The same MRI measurements were repeated in 89 patients after a mean follow-up period of 225 +/- 92 days. IS was 11.9 +/- 7.3% of total LV muscle mass. PMO was detected in 51/110 (46.4%) patients and comprised 15.6 +/- 8.5% of IS and 2.8 +/- 2.3% of LV muscle mass. Papillary muscle infarct was seen in 26%, RV infarction in 16%, pericarditis in 40%, and pericardial effusion in 66% of the patients. During follow-up, there were 16 major adverse cardiac events (MACE) including seven deaths. IS, PMO, and amount of transmural infarction were predictive for LV adverse remodelling defined as > 20% increase in LV end-diastolic volume. Multivariable analysis revealed LV end-diastolic volume, LV ejection fraction, and PMO as significant predictors for the occurrence of MACE., Conclusion: MRI is a highly sensitive and reliable tool to detect morphologic and functional sequelae of AMI providing baseline MRI parameters with relevant predictive power for LV adverse remodelling and occurrence of MACE.

Aims: Heparin coating of stents is thought to reduce stent thrombosis and restenosis rates. However, clinical data comparing coated and uncoated stents of the same model are lacking. We compared the heparin coated (C) and the uncoated (U) version of the Jostent stent with regard to the clinical and angiographic outcome after 6 months., Methods and Results: Provisional stenting was done in 277 patients and 306 lesions; only 40 were Benestent-II like lesions. Delivery success rate was 98.4%. Both groups (C/U: n=156/150 lesions) were comparable in clinical and procedural data. Post stenting, reference diameter (C/U: 2.68+/-0.56/2.66+/-0.53 mm) and minimal lumen diameter did not differ (C/U: 2.48+/-0.47/2.48+/-0.52 mm). During follow-up the rate of subacute stent thrombosis (C/U: 1.9%/1.3%) and myocardial infarction did not differ. Angiography at the 6-month follow-up (79.4%) revealed no difference in restenosis rate (C/U: 33.1%/30.3%). Risk factors for restenosis were a type B2/C lesion (P<0.02), a stented segment longer than 16 mm (P<0.006) and a stent inflation pressure <14 bar (P<0.0063)., Conclusion: Corline heparin coating of the Jostent has no impact on the in-hospital complication rate, stent thrombosis or restenosis. The Jostent design gives a high procedural success rate and satisfying result at 6 months in an everyday patient population undergoing provisional stenting., (Copyright 2001 The European Society of Cardiology.)

Aims: To compare the value of the proximal flow convergence method and the jet area method for the determination of the severity of tricuspid regurgitation., Methods and Results: The proximal isovelocity surface area radius and the jet area/length were measured in 71 consecutive patients with angiographically graded (grade 0/I-III) tricuspid regurgitation. Rank correlation coefficients with the angiographic grade were 0.71 (P < 0.001) for the proximal isovelocity surface area radius (aliasing border of 28 cm.s-1), 0.66 (P < 0.001) for the jet area, and 0.63 (P < 0.001) for the jet length. The proximal isovelocity surface area radius was significantly correlated with the jet area/length (correlation coefficients 0.82/0.77, P < 0.001). Correct differentiation between mild to moderate (grade I-II) and severe (grade III) tricuspid regurgitation was achieved in 62 of 71 patients (87%) by means of the proximal isovelocity surface area radius, in 61 of 71 (86%) by the jet area, and in 62 of 71 (87%) by the jet length. Grade III tricuspid regurgitation was not identified in five of 21 patients (24%) by means of the proximal isovelocity surface area radius, in six of 21 (29%) by the jet area, and in seven of 21 (33%) by the jet length., Conclusion: The flow convergence method and the jet area method are of similar value for the determination of the severity of tricuspid regurgitation. Both methods differentiated mild to moderate from severe tricuspid regurgitation in most patients. However, underestimation of severe tricuspid regurgitation in 20-30% of the cases represents a serious limitation of both methods.

In 84 patients mitral regurgitation was quantified by angiography. The mechanism of regurgitation was determined by echocardiography (organic, n = 54, functional, n = 30). The radii of the proximal isovelocity surface areas in the flow convergence region for 28 and 41 cm.s-1 blood flow velocity and the area and length of the regurgitant jet were measured using colour flow Doppler imaging. The radii of the proximal isovelocity surface areas correlated more closely with the angiographic grade than the jet parameters irrespective of the mechanism of regurgitation. In more than 90% of the patients, grades I-II mitral regurgitation were correctly differentiated from grades III-IV by means of the radii of the proximal isovelocity surface areas. Using the jet parameters, the differentiation was correct in 50-90% of the patients depending on the mechanism of regurgitation. The jet area method particularly failed to identify grades III-IV organic mitral regurgitation due to a high prevalence of eccentric jets in these patients. It is concluded that the proximal flow convergence method was suitable for the quantification of mitral regurgitation irrespective of the mechanism of mitral regurgitation. On the other hand, the value of the jet area method depended largely on the regurgitation mechanism.

The Long QT syndrome (LQTS) is a relatively rare disorder. It has a major clinical impact as affected individuals are prone to syncope and sudden arrhythmogenic cardiac death. The LQTS comprises three groups of patients. The Jervell-Lange-Nielsen syndrome is characterized by an autosomal recessive pattern of inheritance and congenital neural deafness. The Romano-Ward syndrome shows an autosomal dominant pattern of inheritance and normal hearing. Patients with the sporadic form of LQTS have no evidence of familial transmission and have normal hearing. Imbalance of sympathetic cardiac innervation with predominance of the left stellate ganglion and an intrinsic myocardial defect leading to early afterdepolarization are the two pathogenetic mechanisms of LQTS discussed today. More recently a genetic basis for the Romano-Ward LQTS has been reported. The genetic linkage to the Harvey ras-1 gene provides the basis for a new hypothesis that an impairment of guanine nucleotide binding proteins is responsible for symptoms observed in LQTS. This paper discusses the genetic basis, pathology and pathophysiology of LQTS and tries to unify the different theories.

Unlabelled: It is well known that patients with coronary heart disease and ventricular tachycardia show a high incidence of arrhythmogenic complications and sudden cardiac death. The best predictor of spontaneous ventricular tachycardia and sudden death in these patients is programmed ventricular stimulation, but this invasive method is limited to specialized institutions. The purpose of our study was to assess the predictive value of Holter monitoring, late potentials and heart rate variability as markers for these high-risk patients. We investigated 20 patients (18 m, 2 f, age range 31-79 years) with coronary artery disease documented angiographically (6 patients with single vessel disease (vd), nine patients with 2 vd, five patients with 3 vd) and previous myocardial infarction. Each patient underwent 24-h ambulatory monitoring with analysis of rhythm of heart rate variability (24-h spectral and non-spectral analysis) and a signal-averaged ECG with late potential measurement. In all patients, sustained ventricular tachycardia was inducible during programmed ventricular stimulation. Late potentials were recorded in 12 out of the 20 patients (60%). Ventricular arrhythmias of Lown classes IVa, IVb or V were recorded in 12 patients. Analysis of heart rate variability compared to 20 age- and sex-matched healthy controls revealed a loss of parasympathic activity and increased sympathic activity in 16 of the 20 patients (80%)., Conclusion: in this study, heart rate variability was the most sensitive method with which to recognize patients at a high risk of arrhythmogenic complications. Evaluation of the above parameters in large controlled clinical trials may help predict arrhythmogenic complications and sudden cardiac death.

The aim of this study was to assess variability of ventricular late potentials (VLP) in patients with and without inducible ventricular tachycardia (VT), and the effects of antiarrhythmic drugs on VLP variability in the high-resolution electrocardiogram (HRECG). In 27 patients 90 s of unaveraged HRECGs were analysed before and 2 h after oral administration of 200 mg disopyramide, 400 mg mexiletine, 300 mg propafenone and 160 mg DL-sotalol. The duration of the QRS (QRSD) and the duration of the terminal low amplitude signal (LASD) was measured from each beat. Beat-to-beat variability was defined as standard deviation of the differences between consecutive beats. Patients with inducible sustained VT (n = 9) showed higher LASD variability than patients without inducible VT (12.3 vs 9.3 ms.beat-1, P < 0.01). Patients with VLP (n = 17), as defined by the signal averaged ECG, also had higher QRSD and LASD variability (11.8 vs 9.5 ms.beat-1, P < 0.05; 11.5 vs 8.2 ms.beat-1, P < 0.01, respectively) compared to those without VLP. All class I drugs lengthened QRSD and LASD in terms of the absolute values, but only propafenone increased QRSD and LASD variability (9.7 to 12.0 ms.beat-1, P < 0.01; 8.9 to 11.9 ms.beat-1, P < 0.01, respectively). In patients with inducible VT, sotalol decrease LASD variability from 14.3 to 9.3 ms.beat-1 (P < 0.05). We conclude that beat-to-beat VLP variability is increased in patients at a high risk of malignant arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to detect ventricular late fields recorded by a biomagnetic multichannel system in patients with ventricular late potential and to determine the site of these ventricular late fields non-invasively in three dimensions. Biomagnetic signals of sinus beats during a 5-min acquisition period simultaneously recorded by a 37-channel system Krenikon were averaged in all channels. Ventricular late fields were determined in each channel according to the algorithm of Simson for ECG data. For the localization process, baseline correction from the averaged non-filtered signals was performed at the end of the QRS complex under visual control. The single current dipole model within the homogeneous half-space was applied. Eight patients post myocardial infarction with ventricular late potentials (four with recurrent sustained ventricular tachycardia) and four healthy individuals were examined. In the normal subjects, no ventricular late fields were detected. However, ventricular late fields were found in all patients, and were localized in six patients within the border zone of myocardial infarction. In the four patients with ventricular tachycardia, a spatial coincidence of the site of origin of ventricular late fields and the site of origin of ventricular tachycardia determined by catheter mapping was found in two. It is concluded that magnetocardiography is able to detect ventricular late fields and can be used to determine their site of origin.

Different patho-anatomical and functional factors are considered to be involved in patients with unstable angina pectoris. Among these are a pre-existing plaque based on coronary atherosclerosis, the development of fissures or dissections of the plaque (often combined with thrombus formation at the site of the plaque) coronary vascular tone, and theoretically primary aggregation of platelets at a site of apparently normal vascular endothelium. Several comprehensive studies on patients who died from acute myocardial infarction or unstable angina, have convincingly shown that complications of an atherosclerotic plaque like fissures, dissections and thrombus formation may be present in 60 to 90% of cases. In addition, two groups of investigators, who have applied coronary angioscopy for direct visualization of offending coronary arteries, have confirmed these results, since in about 60-80% of patients with unstable angina complicated atheromata, i.e. rupture, ulceration, thrombus formation, could be documented, whereas in all patients with stable angina an uncomplicated atheroma was seen angioscopically. On the basis of these results a hypothetical sequence of events in patients with stable angina, unstable angina and acute myocardial infarction has been proposed. Stable angina pectoris may be seen in patients with uncomplicated atheroma in one of the major coronary artery branches. When dissections, ulcerations and thrombus formation occur as a complication of a formerly smooth plaque, patients show the clinical syndrome of unstable angina. If an occlusive thrombus develops, the patient will run into a fresh myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

The analysis of ST segment changes during Holter monitoring is one important diagnostic method for detection and diagnosis of silent myocardial ischaemia. To assess the specificity and sensitivity of ST segment alterations as a diagnostic tool, 106 healthy medical students (43 females, 57 males, aged 18-36 years, mean age 26 +/- 4 years) and 26 children (14 females, 12 males, aged 12-17 years, mean 14 +/- 3 years) with no history of heart disease and normal findings during physical examination were studied by exercise stress test and Holter monitoring. Criteria for exclusion were a history of hypertension, diabetes mellitus and ST segment alterations during conventional 12-lead ECG. Due to these criteria, eight volunteers had to be excluded from the study. The exercise stress test (maximum work load protocol) revealed no pathological ST segment depressions. During Holter monitoring seven episodes of ST segment depressions (greater than or equal to 1.0 mm planar or downsloping, duration greater than or equal to 1.0 min) were found. Typical ST segment depressions detected by Holter monitoring may be found in healthy subjects. Therefore this finding has to be considered cautiously as a diagnostic tool for evaluation of patients with suspected coronary heart disease.