Mathias Forkmann

Fluoroscopy integrated 3D mapping significantly reduces radiation exposure during ablation for a wide spectrum of cardiac arrhythmias

AIMS Despite the use of established 3D-mapping systems, invasive electrophysiological studies and catheter ablation require high radiation exposure of patients and medical staff. This study investigated whether electroanatomic catheter tracking in prerecorded X-ray images on top of an existing 3D-mapping system has any impact on radiation exposure. METHODS AND RESULTS Two hundred and ninety-five consecutive patients were either ablated with the guidance of the traditional CARTO-3 system (c3) or with help of the CARTO-UNIVU system (cU): [typical atrial flutter (AFL) n = 58, drug refractory atrial fibrillation (AF) n = 81, ectopic atrial tachycardia (EAT) n = 37, accessory pathways (APs) n = 22, symptomatic, idiopathic premature ventricular complexes (PVCs) n = 56, ventricular tachycardias (VTs) n = 41]. The CARTO-UNIVU allowed a reduction in radiation exposure: fluoroscopy time: AFL c3: 8.6 ± 0.8 min vs. cU: 2.9 ± 0.3 min, P < 0.001; AF c3: 16.0 ± 1.3 min vs. cU: 6.4 ± 0.9 min, P < 0.001; EAT c3: 23.4 ± 3.1 min vs. cU: 9.7 ± 1.7 min, P < 0.001; AP c3: 7.1 ± 1.2 min vs. cU: 6.0 ± 1.5 min, P = 0.59; PVCs c3: 17.6 ± 2.3 min vs. cU: 15.2 ± 2.8 min, P = 0.52; VT c3: 31.4 ± 3.4 min vs. cU: 17.5 ± 2.4 min, P = 0.003. Corresponding to the fluoroscopy time the fluoroscopy dose was also reduced significantly. These advantages were not at the cost of increased procedure times, periprocedural complications, or decreased acute ablation success rates. CONCLUSION In a wide spectrum of cardiac arrhythmias, and especially in AF and VT ablation, fluoroscopy integrated 3D mapping contributed to a dramatic reduction in radiation exposure without prolonging procedure times and compromising patients safety. That effect, however, could not be maintained in patients with APs and PVCs.

Reduction of radiation exposure during atrial fibrillation ablation using a novel fluoroscopy image integrated 3-dimensional electroanatomic mapping system: A prospective, randomized, single-blind, and controlled study

OBJECTIVE We explored whether the use of a novel fluoroscopy image integrated 3-dimensional electroanatomic mapping (F-EAM) system could result in a reduction of overall fluoroscopy time and radiation doses during the whole procedure of atrial fibrillation (AF) ablation. METHODS Eighty patients (44 men (55%); mean age 63 ± 10 years) who underwent catheter ablation due to paroxysmal AF were recruited consecutively in the present study. Patients were randomized (1:1) into 2 arms for AF ablation: one using a conventional 3-dimensional electroanatomical mapping (EAM) system and the other using the F-EAM system. RESULTS Fluoroscopy time (10:42 [interquartile range {IQR} 8:45-12:46] minutes:seconds vs 1:45 [IQR 1:05-2:22] minutes:seconds; P < .001) and radiation doses (2440 [IQR 1593-3091] cGy·cm(2) vs 652 [IQR 326-1489] cGy·cm(2); P < .001) in the EAM group were significantly greater than those in the F-EAM group. The majority of reduction of radiation exposure was achieved after transseptal puncture, which was near-zero fluoroscopic exposure. In total, approximately 84% of fluoroscopy time and 73% of radiation doses have been reduced during the AF ablation procedure using the F-EAM system compared to using the conventional EAM system. However, procedure time did not differ significantly (1:39 [IQR 1:18-2:10] hours:minutes vs 1:37 [IQR 1:17-1:50] hours:minutes; P = .362). During follow-up (5.9 ± 1.3 months), 61 patients (76.3%) had no recurrence of atrial arrhythmias. The recurrence rate between the 2 groups did not differ. CONCLUSION AF catheter ablation using the F-EAM system was safe and resulted in a significant reduction of radiation exposure to patients and staff without complicating the workflow of the procedure. A near-zero fluoroscopic catheter ablation procedure could be performed without compromising acute/mid-term efficacy and safety.

Intra-aortic balloon pump (IABP) counterpulsation improves cerebral perfusion in patients with decreased left ventricular function

Background: The current goal of treatment after acute ischemic stroke is the increase of cerebral blood flow (CBF) in ischemic brain tissue. Intra-aortic balloon pump (IABP) counterpulsation in the setting of cardiogenic shock is able to reduce left ventricular afterload and increase coronary blood flow. The effects of an IABP on CBF have not been sufficiently examined. We hypothesize that the use of an IABP especially enhances cerebral blood flow in patients with pre-existing heart failure. Methods: In this pilot study, 36 subjects were examined to investigate the effect of an IABP on middle cerebral artery (MCA) transcranial Doppler (TCD) flow velocity change and relative CBF augmentation by determining velocity time integral changes (ΔVTI) in a constant caliber of the MCA compared to a baseline measurement without an IABP. Subjects were divided into two groups according to their left ventricular ejection fraction (LVEF): Group 1 LVEF >30% and Group 2 LVEF ≤30%. Results: Both groups showed an increase in CBF using an IABP. Patients with a LVEF ≤30% showed a significantly higher increase of ΔVTI in the MCA under IABP augmentation compared to patients with a LVEF >30% (20.9% ± 3.9% Group 2 vs.10.5% ± 2.2% Group 1, p<0,05). The mean arterial pressure (MAP) increased only marginally in both groups under IABP augmentation. Conclusions: IABP improves cerebral blood flow, particularly in patients with pre-existing heart failure and highly impaired LVEF. Hence, an IABP might be a treatment option to improve cerebral perfusion in selected patients with cerebral misperfusion and simultaneously existing severe heart failure.

Epicardial Ventricular Tachycardia Ablation in a Patient With Brugada ECG Pattern and Mutation of PKP2 and DSP Genes

The Brugada syndrome (BS) and arrhythmogenic right ventricular cardiomyopathy (ARVC) are currently seen as 2 distinct clinical entities. However, several genetic mutations linked to reduced sodium transmembrane flow and disrupted integrity of the desmosome with resulting fatty infiltration have been identified, corresponding to BS and ARVC, respectively.1 A 22-year-old male patient was admitted to our hospital with repeated discharges of the implantable cardioverter defibrillator caused by pleomorphic ventricular tachycardia. He had a previous history of survived sudden cardiac death and an implanted single-chamber implantable cardioverter defibrillator in 2010. No data on work-up of genetic arrhythmias had been available to date. On current clinical presentation in echocardiography, normal ejection fraction and heart diameter could be determined. Because of abnormal ECG pattern in a sense of an incomplete right bundle branch block with slightly elevated ST-segments and T-wave inversions in the right precordial leads, an ajmaline test was conducted (Figure A). This resulted in prominent coved-type Brugada ECG (Figure B). Figure. A , Baseline …

Heart-type fatty acid-binding protein and myocardial creatine kinase enable rapid risk stratification in normotensive patients with pulmonary embolism

BACKGROUND Risk assessments of hemodynamically stable patients with pulmonary embolisms (PE) remain challenging. In this context heart-type fatty acid-binding protein (H-FABP), creatine kinase isoenzyme MB (CK-MB), and troponin I (TnI) may hold prognostic utility for patients with pulmonary embolism. METHODS We included 161 consecutive normotensive (systolic blood pressure above 90 mm Hg) patients with confirmed PE to study the combined utility of echocardiographic signs of right ventricular dysfunction and several biomarkers (TnI, CK-MB, H-FABP). The primary endpoint was defined as death within 30 days after admission to the hospital. RESULTS Elevated biomarkers were measured in 26 patients (16.1%) for HFABP, in 66 (41%) for TnI and in 41 (25.5%) for CK-MB. Echocardiography revealed right ventricular dysfunction (RVD) in 99 (61.5%) patients. Overall, 16 patients (9.9%) died within the study period. In the H-FABP positive group 15 (57.7%) patients died compared to 13 (19.7%) patients in the TnI positive group and 15 (37.5%) patients in the CK-MB positive group (H-FABP positive vs TnI positive patients, P< .001; H-FABP positive vs CK-MB positive patients P= .13; CK-MB positive vs TnI positive patients P= .07). All elevated biomarkers correlated with the primary endpoint with H-FABP being strongly, CK-MB intermediately and TnI weakly associated with short term death (H-FABP r= 0.701, P< .001; CK-MB r= 0.486, P< .001; TnI r= 0.272, P= .001). In multivariate logistic regression analysis, a positive H-FABP test (OR 27.1, 95% CI 2.1-352.3, P= .001), elevated CK-MB levels (OR 5.3, 95% CI 1.3-23.3, P= .002) and a low systolic blood pressure on admission (OR 0.8, 95% CI 0.8-0.9, P< .001) emerged as independent predictors of 30-day mortality. CONCLUSIONS Both H-FABP and CK-MB are associated with short term mortality in normotensive PE patients and could be advantageous for risk stratification in this intermediate risk group.

Dexrazoxane prevents the development of the impaired cardiac phenotype in caveolin-1-disrupted mice.

Abstract: Caveolin-1-deficient (cav1−/−) mice display a severely diseased cardiac phenotype with systolic and diastolic heart failure. Accumulating evidence supports a causative role of uncoupled endothelial nitric oxide synthase in the development of these abnormalities. Interestingly, a similar molecular mechanism was proposed for anthracycline-induced cardiomyopathy. Currently, dexrazoxane is approved for the prevention of anthracycline-induced cardiomyopathy. Given the molecular similarities between the anthracycline-induced cardiomyopathy and the cardiomyopathy in cav1−/− mice, we questioned whether dexrazoxane may also prevent the evolution of the cardiac pathologies in cav1−/− mice. We evaluated dexrazoxane treatment for 6 weeks in cav1−/− mice and wild-type controls. This study provides the first evidence for a reduced reactive oxygen species formation in the vessels of dexrazoxane-treated cav1−/− mice. This reduced oxidative stress resulted in a markedly reduced rate of apoptosis, which finally was translated into a significantly improved heart function in dexrazoxane-treated cav1−/− mice. These hemodynamic improvements were accompanied by significantly lowered proatrial natriuretic peptide levels. Notably, these protective properties of dexrazoxane were not evident in wild-type animals. Taken together, these novel findings indicate that dexrazoxane significantly reduces vascular reactive oxygen species formation cav1−/−. Because this is paralleled by an improved cardiac performance in cav1−/− mice, our data suggest dexrazoxane as a novel therapeutic strategy in this specific cardiomyopathy.

Association of platelet activation markers with recurrence of atrial fibrillation after pulmonary vein isolation

Abstract Atrial fibrillation (AF) is known to cause platelet activation. AF and its degree of thrombogenesis could be associated with monocyte-platelet aggregates (MPAs). We investigated on whether the content of MPAs or other platelet activation markers is associated with the recurrence of AF after pulmonary vein isolation (PVI). A total of 73 patients with symptomatic AF underwent PVI. After 6 months, all patients were evaluated for episodes of AF recurrence. At the same time, flow-cytometric quantification analyses were performed to determine the content of MPAs. Further platelet activation parameters were detected by using either cytometric bead arrays or quantitative immunological determination. Patients with recurrent AF (n = 20) compared to individuals without AF relapse (n = 53) were associated with an increased content of MPAs (43 ± 3% vs. 33 ± 2%, p = 0.004), as well as an increased CD41 expression on monocytes (191 ± 20 vs. 113 ± 6, p = 0.001). The level of the soluble platelet activation markers such as D-dimer, sCD40L, and sP-selectin did not differ between these groups. The content of MPAs correlated weakly with the level of sCD40L (r = 0.26, p = 0.03), but not with sP-selectin and D-dimer, whereas sP-selectin and sCD40L correlated with each other (r = 0.38, p = 0.001). Only the cellular marker of platelet activation, the content of MPAs, was increased in patients with recurrent AF after PVI. In contrast, soluble markers remained unaltered. These data indicate a distinct mechanism and level of platelet activation in AF. The clinical relevance of MPAs in identifying AF recurrence or in guiding the therapy with anticoagulants remains to be elucidated.

Reduction of atrial fibrillation burden by pulmonary vein isolation leads to a decrease of CD11b expression on inflammatory cells

Aims It is hypothesized that inflammation could promote structural and electrical remodelling processes in atrial fibrillation (AF). Atrial infiltration of monocytes and granulocytes has been shown to be dependent on CD11b expression. The aim of this study was to investigate whether treatment of AF by pulmonary vein isolation (PVI) may lead to reduced inflammation, as indicated by a decrease of CD11b expression on monocytes and granulocytes. Methods and results Flow-cytometric quantification analysis and determination of systemic inflammatory markers of peripheral blood were performed in 75 patients undergoing PVI 1 day before and 6 months after PVI. The extent of activation of monocytes and granulocytes was measured by quantifying the cell adhesion molecule CD11b. The mean expression of CD11b on monocytes (20.9 ± 2.5 vs. 10.2 ± 1.4; P < 0.001) and granulocytes (13.9 ± 1.6 vs. 6.8 ± 0.5; P < 0.001), as well as the relative count of CD11b-positive monocytes (P < 0.05) and CD11b-positive granulocytes (P < 0.01) were significantly reduced when comparing the identical patients before and 6 months after PVI. Systemic inflammatory parameters showed only a declining tendency after 6 months. Patients with unsuccessful PVI and ongoing AF on the day of follow-up showed no decrease in CD11b expression. Conclusions A significant reduction of CD11b expression on monocytes and granulocytes, as a sign of reduced cellular inflammation, was achieved by treatment of AF using PVI. These data strongly support that AF is not only a consequence of but also a cause for inflammatory processes, which, in turn, may contribute to atrial remodelling.

Stored red blood cells impair vascular function in vivo

We have read with great interest the recent results of progressive impairments in nitric oxide (NO)–mediated vasodilation through stored red blood cells (RBCs). Because of their in vitro studies, Alexander and colleagues concluded that RBC-mediated vasoinhibitory mechanism did not work by NO scavenging. Although they recognize that their results do not specifically argue against vasoconstriction caused by cell-free hemoglobin (Hb), they arrive at the conclusion that the RBC-derived inhibitory activity appears much more potent than the vasoconstrictive activity of cell-free Hb. In view of these findings, the results of an in vivo study recently finished by our group may add valuable additional insight on the vasoinhibitory activity of stored RBCs. After transfusion of stored RBCs (older than 14 days) we found indications for enhanced scavenging of vasodilating nitric oxide by cell-free Hb. We conducted detailed hemodynamic and biochemical studies in 16 patients requiring transfusion of RBCs. The arterial function was studied noninvasively. In particular, we determined the pulse wave velocity as well as the aortic augmentation index as indicators of arterial stiffness. Patients (n = 8) who received stored RBCs showed a significantly increased aortic augmentation index (27.67% vs. 20.67%, p = 0.04) as well as an enhanced pulse wave velocity (13.46 m/sec vs. 11.45 m/sec, p = 0.004). Additionally, stored RBCs increased the nitrosylhemoglobin concentration (0.061 μmol/L vs. 0.018 μmol/L, p = 0.048) in transfusion recipients, possibly due to increased reaction between cell-free Hb (released because of agedepended RBC hemolysis) and nitric oxide. The described hemodynamic and biochemical alterations were absent in patients (n = 8) who received fresh RBCs (younger than 14 days). These data document that transfusion of aged RBCs has profound effects on arterial function in patients and show that the vasoconstrictive activity of free Hb may exceed what Alexander and colleagues assume in their studies. In addition to large clinical meta-analyses our results provide further evidence of the mechanism of deleterious transfusion outcomes in patients with stored RBCs. CONFLICT OF INTEREST