Objective: To compare total left ventricular mass assessment using steady state free precession (SSFP) and inversion recovery fast gradient echo (IR GRE) imaging and further to assess the influence of contrast dosage on mass by IR GRE and its implications on relative infarct size assessment with both methods. Methods: Forty-three patients with first documented myocardial infarction and single vessel disease underwent measurement of total myocardial mass using SSFP technique and an IR GRE sequence. As part of a Phase 2 multi-center dose ranging study for infarct identification patients received 1 of 4 possible dosages (0.05, 0.1, 0.2 or 0.3 mmol/kg body weight) of the contrast agent gadoversetamide (OptiMARK, Tyco Healthcare Mallinckrodt, St. Louis, MO, USA). Results: Left ventricular mass assessment using IR GRE resulted in a slightly greater detection of myocardial mass than from the SSFP images (160.1 and 156.4 g, respectively, p < 0.001). The overall good correlation of both methods (R-2 = 0.97 for the total study group, p < 0.001) was further improved by using gadoversetamide at doses of 0.2 or 0.3 mmol/kg (R-2= 0.99, p < 0.001), mainly as a result of a considerably higher blood-myocardial contrast-to-noise ratio (CNR) in the IR GRE images. Bland-Altman analysis in these subgroups showed very little scatter of the residuals over the mean (3.5 +/- 5.4 g and 1.3 +/- 6.9 g respectively, 95% confidence interval). The observed differences in total mass calculation, while statistically significant, were not correlated with clinically relevant differences in estimation of relative infarct size. Conclusion: Total LV mass calculations using SSFP and IR GRE techniques are interchangeable when using appropriate contrast media, such as gadoversetamide. Late gadolinium enhancement results in good blood myocardial CNR. Hence, for relative infarct size assessment either method for calculation of total myocardial mass can be used.

Background: Different substrate based ablation strategies have been developed for ablation of ventricular tachycardia (VT) after myocardial infarction (MI). We investigated the “Dynamic Substrate Mapping (DSM)”, a tool integrated into the noncontact mapping (NCM) system. Methods: An electrophysiologic study (EPS) was performed 96 ± 10 days after experimental anteroseptal MI in 19 female sheep. Scar was defined by NCM during sinus rhythm. The area of scar was determined using the DSM tool with a cut-off of 50 %, 40%, 30% and 20% of the largest deflection of the unipolar electrogram. The scar was determined by either magnetic resonance imaging (MRI, n=9) or pathology (n=10). Areas determined by MRI or pathology and by DSM were compared. In 11 patients referred for ablation of VT simultaneous electroanatomical mapping and NCM was performed. The location of the low voltage area in the bipolar voltage map and the DSM were compared. Results: For all 19 animals a low voltage area was delineated with a cut off of 50% of the largest unipolar deflection. The low voltage area determined with DSM was greater then the scar determined by pathology or MRI (29,32 ± 28,83 cm 2 vs 8,52 ± 3,48 cm 2 . p < 0,05). Infarct scar determined by MRI or pathology was always located within the low voltage area determined by DSM. There was no correlation between the sizes of the low voltage area determined by pathology/MRI and DSM. Delineation of a low voltage area was not possible in all animals with a cut off of 40%, 30%, and 20%. In 11 patients, locations of the low voltage areas determined by bipolar voltage maps and DSM corresponded well. The area defined by DSM was larger then the area defined by bipolar voltage map. there was a good correlation between the size of the low voltage areas determined by bipolar voltage map and DSM for cut off values of 50% and 40% (r 2 = 0,66 and r 2 = 0,61; p<0,05). With a cut off of 30% and 20% of the largest unipolar deflection a low voltage area could not be defined for all patients. Conclusion: Sizes of abnormal myocardium defined by DSM do not correlate with scar areas determined by pathology or MRI. Areas of abnormal myocardium delineated by DSM are greater then areas defined with bipolar voltage map. A detailed description of the scar border zone with DSM during sinus rhythm alone is not feasible.

Ein bislang anerkanntes pathophysiologisches Konzept des Vorhofflimmerns basiert auf der Vorstellung, dass Vorhofflimmern durch das gleichzeitige Vorhandensein multipler atrialer Reentry-Kreise aufrechterhalten wird. Die hierdurch hervorgerufene ungeordnete elektrische atriale Aktivierung verhindert eine geordnete mechanische Vorhofkontraktion [51], [102]. Neben der zumeist akzeptierten Vorstellung, dass multiple, instabile Reentry-Kreise zum Vorhofflimmern führen, gibt es auch Modelle, in denen Vorhofflimmern durch fokale, hochfrequente Ektopie bzw. durch einen einzelnen stabilen Reentry-Kreis und konsekutiver irreguläre Ausbreitung von sekundären Erregungsfronten aufrechterhalten wird [93], [95], [110]. Diese Befunde lassen den Schluss zu, dass Vorhofflimmern nicht zwangsläufig auf einer einzelnen pathophysiologischen Grundlage beruht, sondern die zugrunde liegenden Mechanismen individuell verschieden sein können.

Ventricular response (VR) during atrial fibrillation (AF) is a complex process, which is modulated by the autonomic nervous system (ANS). The purpose of this study was to characterize VR to both exercise as ANS stimulus and flecainide which is also supposed to have effects on the ANS. RR series were analyzed by means of time domain parameters and non-linear methods. In 15 patients (10 male, aged 55 plusmn 13 years) with persistent AF (mean AF duration 13 plusmn24 months), time domain parameters and indexes assessing the predictability of the time series, (regularity index, approximate entropy and an index for linear predictability) were evaluated. VR during exercise resulted modulated by adrenergic stimulation. Flecainide exhibited vagolytic activity especially during exercise. Thus, monitoring of exercise- induced and antiarrhythmic drug effects on ANS is possible with parameters derived from time domain and non-linear analysis.

A new passive cardiomyoplasty device, the Paracor ventricular support system (Paracor Medical Inc., Sunnyvale, California, USA) is being evaluated in heart failure patients to assess its ability to halt or reverse the disease process of dilated cardiomyopathy. During a minimal invasive surgical procedure the mesh is placed around the heart, and is intended to reduce wall stress by …

BACKGROUND:The C826A mutation in the fukutin-related protein (FKRP) gene is typically associated with autosomal recessive limb-girdle muscular dystrophy 2I (LGMD2I) but oligosymptomatic phenotypes and patients with predominant cardiac involvement are also described.OBJECTIVE:To assess cardiac involvement in patients with LGMD2I.PATIENTS:Nine patients from 5 families (2 female, 7 male) homozygous for the 826C > A FKRP mutation were included.METHODS:Additional to conventional cardiac investigations (electrocardiography and echocardiography) the patients underwent cardiovascular magnetic resonance imaging (CMR).RESULTS/CONCLUSION:Cardiac involvement was detected by CMR in eight of nine patients (reduced left ventricular ejection fraction in 6, enlargement of left ventricular end-diastolic volume in 2 and left ventricular mass in 2) and in four patients by conventional cardiac diagnostic investigations. Two of the nine patients showed no muscle weakness or atrophy but suffered myalgias; both had cardiac manifestation of the disease. CMR is a sensitive method for detecting cardiac abnormalities in patients with LGMD2I and can be used for early detection of mild or subclinical cardiac involvement.

AIMS:The CARTO electrophysiological mapping system has demonstrated accurate results for end-diastolic ventricular volumes in casts and animals. However, in humans, a comparison with cardiac magnetic resonance (CMR), the non-invasive gold standard for volumetric analysis, has not yet been performed.METHODS AND RESULTS:A total of 34 (29 male) heart failure patients (NYHA class III/IV) underwent an electrophysiological mapping procedure with the CARTO system in the left ventricle (LV) (n = 34) and right ventricle (RV) (n = 12) and CMR for RV and LV end-diastolic volume (RVEDV and LVEDV) measurements another day. Mean LVEDV was comparable between CMR and CARTO (328 +/- 95 and 320 +/- 92 mL, respectively; P = NS), whereas RV volumes measured by CARTO were larger (CMR 140 +/- 48 vs. CARTO 176 +/- 47 mL; P < 0.01). Overall, we found a good correlation between CMR and CARTO measurements for both chambers; however, the Bland-Altman analysis showed a non-interchangeability of these methods. Measurement differences were independent of chamber size, but significantly affected by the number of acquired mapping points.CONCLUSION:Although CMR and CARTO showed a good correlation in the measurement of RVEDV and LVEDV in a group of heart failure patients, the clinical interchangeability of the two methods may be questioned.

Atrial tachyarrhythmia (AF) alters intracellular calcium homeostasis and induces cellular hypertrophy of atrial myocytes. The impact of the calcium-dependent calcineurin pathway on the development of AF-induced atrial hypertrophy has not yet been analyzed. In this study, atrial tissue samples from patients with sinus rhythm and chronic persistent atrial fibrillation (CAF) were used to determine changes in expression and activity of calcineurin A (CnA), and its relation to CnA-regulated transcription factors NFATc1-4, and hypertrophic markers ANP, troponin I, and beta-MHC. CnA phosphatase activity and CnAbeta protein contents were significantly upregulated in patients with CAF. Calcineurin activation led to dephosphorylation, redistribution, and subsequent accumulation of NFATc3 in nuclei during CAF, and expression of hypertrophic genes was increased. CAF-dependent changes were reproduced by ex vivo pacing (2-4 Hz) of human atrial tissue slices. FK506 abolished the hypertrophic response induced by electrical-field stimulation. Atrial tachyarrhythmia causes atrial hypertrophy by activation of the CnA signal pathway, which thereby contributes to structural remodeling of human atria.

2/2005) were screened in 22 centers for cardiac rehabilitation in Germany (76% male, 62 12 yrs). 75% of pts had the last MI 4 to 8 weeks prior to inclusion, in 90% it was their first MI. 90% of the pts had revascularization before inclusion, mainly PCI (74%) and/or CABG (25%). Additional diseases: hypertension, diabetes, renal insufficiency, atrial fibrillation in 72%, 25%, 5% and 3% of pts respectively. Medication at discharge from rehabilitation consisted of -blockers (95%), ACE-inhibitors (90%), statins and antiplatelet agents in 96% of pts. Mean LVEF: 56 12%. Pts were classified according to their LVEF at inclusion: group 1 with LVEF 30%, group 2 with 30% LVEF 40%, and control group 3 with LVEF 40%. All pts are followed-up during 3 years to document cause of death, cardiac events and interventions. Results: 216 pts (2.6%) out of 8.430 ( 100%) had a LVEF 30%, 557 pts (6.7%) had 30% LVEF 40%. Only 47 pts (22%) of group 1 received an ICD either early during the rehabilitation phase (25 pts,12 %) or later initiated by their local practitioners (12 pts,10%). The reasons for 78% of the pts not receiving ICD implant are diverse (details will be presented). Conclusions: The incidence of pts after MI with severely impaired LVEF 30% (2.6%) is smaller than expected from data of the 1990s. Although the vast majority of these pts were medicated according to guidelines, only 22% received ICD therapy in line with randomized studies despite the small incidence of this pt type.

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study