Ablation of atrial fibrillation with the Epicor system: a prospective observational trial to evaluate safety and efficacy and predictors of success

<p>Abstract</p> <p>Background</p> <p>High intensity focused ultrasound (HIFU) energy has evolved as a new surgical tool to treat atrial fibrillation (AF). We evaluated safety and efficacy of AF ablation with HIFU and analyzed predictors of success in a prospective clinical study.</p> <p>Methods</p> <p>From January 2007 to June 2008, 110 patients with AF and concomitant open heart surgery were enrolled into the study. Main underlying heart diseases were aortic valve disease (50%), ischemic heart disease (48%), and mitral valve disease (18%). AF was paroxysmal in 29%, persistent in 31%, and long standing persistent in 40% of patients, lasting for 1 to 240 months (mean 24 months). Mean left atrial diameter was 50 ± 7 mm. Each patient underwent left atrial ablation with the Epicor system prior to open heart surgery. After surgery, the patients were treated with amiodarone and coumadin for 6 months. Follow-up studies including resting ECG, 24 h Holter ECG, and echocardiography were obtained at 6 and 12 months.</p> <p>Results</p> <p>All patients had successful application of the system on the beating heart prior to initiation of extracorporeal circulation. On average, 11 ± 1 ultrasound transducer elements were used to create the box lesion. The hand-held probe for additional linear lesions was employed in 83 cases. No device-related deaths occurred. Postoperative pacemaker insertion was necessary in 4 patients. At 6 months, 62% of patients presented with sinus rhythm. No significant changes were noted at 12 months. Type of AF and a left atrial diameter > 50 mm were predictors for failure of AF ablation.</p> <p>Conclusion</p> <p>AF ablation with the Epicor system as a concomitant procedure during open heart surgery is safe and acceptably effective. Our overall conversion rate was lower than in previously published reports, which may be related to the lower proportion of isolated mitral valve disease in our study population. Left atrial size may be useful to determine patients who are most likely to benefit from the procedure.</p

Transient cortical blindness after diagnostic cerebral angiography – A single center report

Background: Transient cortical blindness (TCB) has been reported as a complication after diagnostic cerebral angiography in 0.3–1% of cases. Our aim was to observe the frequency of TCB after diagnostic cerebral angiography over a period of 11 years using only hypo-osmolar, nonionic contrast agents and following a protocol to reduce both the total volume of injected contrast agent and the number of angiography series obtained. Methods: We retrospectively included all 2431 patients who received diagnostic cerebral angiographies at our institution. Primary outcome measure was the occurrence of TCB after diagnostic cerebral angiography, hypothesizing that the occurrence of TBC depends on the volume of contrast agent and angiography of the vertebrobasilary arteries. Results: Over the analyzed time period of 11 years, we did not observe a single case of TCB following diagnostic cerebral angiography. The median contrast volume used was 100 ml (IQR, 100–200), ranging from 15 ml to 500 ml. In our cohort, 61.5% of patients received a selective catheterization of the vertebrobasilary territory. In 99.8% of angiographies iopamidol was used a contrast agent. Conclusion: Our results indicate that following to certain aspects of the angiography protocol (using the hypoosmolar, non-ionic contrast agent iopamidol and reducing the number of catheterized vessels and angiography series to a diagnostic minimum) the frequency of transient cortical blindness as a complication of diagnostic cerebral angiography considerably can be very low

Sacubitril/valsartan for the treatment of non-obstructive hypertrophic cardiomyopathy: An open label randomized controlled trial (SILICOFCM)

\ua9 2024 The Authors. European Journal of Heart Failure published by John Wiley &amp; Sons Ltd on behalf of European Society of Cardiology.Aim: Sacubitril/valsartan treatment reduces mortality and hospitalizations in heart failure with reduced ejection fraction but has limited application in hypertrophic cardiomyopathy (HCM). The aim of this study was to evaluate the effect of sacubitril/valsartan on peak oxygen consumption (VO2) in patients with non-obstructive HCM. Methods and results: This is a phase II, randomized, open-label multicentre study that enrolled adult patients with symptomatic non-obstructive HCM (New York Heart Association class I–III) who were randomly assigned (2:1) to receive sacubitril/valsartan (target dose 97/103 mg) or control for 16 weeks. The primary endpoint was a change in peak VO2. Secondary endpoints included echocardiographic measures of cardiac structure and function, natriuretic peptides and other cardiac biomarkers, and Minnesota Living with Heart Failure quality of life. Between May 2018 and October 2021, 354 patients were screened for eligibility, 115 patients (mean age 58 years, 37% female) met the study inclusion criteria and were randomly assigned to sacubitril/valsartan (n = 79) or control (n = 36). At 16 weeks, there was no significant change in peak VO2 from baseline in the sacubitril/valsartan (15.3 [4.3] vs. 15.9 [4.3] ml/kg/min, p = 0.13) or control group (p = 0.47). No clinically significant changes were found in blood pressure, cardiac structure and function, plasma biomarkers, or quality of life. Conclusion: In patients with HCM, a 16-week treatment with sacubitril/valsartan was well tolerated but had no effect on exercise capacity, cardiac structure, or function

Genetic determinants of clinical phenotype in hypertrophic cardiomyopathy

© 2020, The Author(s). Background: Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disease that affects approximately one in 500 people. HCM is a recognized genetic disorder most often caused by mutations involving myosin-binding protein C (MYBPC3) and β-myosin heavy chain (MYH7) which are responsible for approximately three-quarters of the identified mutations. Methods: As a part of the international multidisciplinary SILICOFCM project (www.silicofcm.eu) the present study evaluated the association between underlying genetic mutations and clinical phenotype in patients with HCM. Only patients with confirmed single pathogenic mutations in either MYBPC3 or MYH7 genes were included in the study and divided into two groups accordingly. The MYBPC3 group was comprised of 48 patients (76%), while the MYH7 group included 15 patients (24%). Each patient underwent clinical examination and echocardiography. Results: The most prevalent symptom in patients with MYBPC3 was dyspnea (44%), whereas in patients with MYH7 it was palpitations (33%). The MYBPC3 group had a significantly higher number of patients with a positive family history of HCM (46% vs. 7%; p = 0.014). There was a numerically higher prevalence of atrial fibrillation in the MYH7 group (60% vs. 35%, p = 0.085). Laboratory analyses revealed normal levels of creatinine (85.5 ± 18.3 vs. 81.3 ± 16.4 µmol/l; p = 0.487) and blood urea nitrogen (10.2 ± 15.6 vs. 6.9 ± 3.9 mmol/l; p = 0.472) which were similar in both groups. The systolic anterior motion presence was significantly more frequent in patients carrying MYH7 mutation (33% vs. 10%; p = 0.025), as well as mitral leaflet abnormalities (40% vs. 19%; p = 0.039). Calcifications of mitral annulus were registered only in MYH7 patients (20% vs. 0%; p = 0.001). The difference in diastolic function, i.e. E/e′ ratio between the two groups was also noted (MYBPC3 8.8 ± 3.3, MYH7 13.9 ± 6.9, p = 0.079). Conclusions: Major findings of the present study corroborate the notion that MYH7 gene mutation patients are presented with more pronounced disease severity than those with MYBPC3

Coronary angiography with synchrotron radiation

Worldwide several systems for Digital Subtraction Angiography in energy subtraction mode (dichromography) are developed. One of the systems which allows investigations of patients - the system NIKOS in the Hamburger Synchrotronstrahlungslabor HASYLAB at DESY is described. The system consists out of six main parts : The 20 pole wiggler HARWI in the beamline W2 of the storage ring DORIS, the two beam monochromator for the two 12.5 cm wide monochromatic X-ray beams, the safety system, the fast scanning device, the fast low-noise two-line ionization chamber and the computer system. Since 1990 patients were investigated with the system NIKOS. Aim of the work is to visualize coronary arteries down to 1 mm diameter with an iodine mass density of 1 mg/cm2, thus allowing non-invasive investigations by intravenous application of the contrast medium. The two images for subtraction are simultaneously taken with photon energies just below and above the iodine K-edge (33.17 keV) in a line scan mode. Intravenous angiograms from investigations with version III of the system NIKOS are presented and the next steps for getting an increased image quality are described

A dual line multicell ionization chamber for transvenous coronary angiography with synchrotron radiation

A position sensitive one‐dimensional x‐ray detector with a large dynamic range (≳214:1) for high photon fluxes with fast image recording sequence (300 ms per frame) has been developed for transvenous coronary angiography with synchrotron radiation. A position resolution of 1 LP/mm and a detection quantum efficiency (DQE) of at least 58% (for 11 000 photons per pixel) has been achieved for 33 keV photons in a Xe‐CO2 gas mixture at 20 bars. The use of Kr‐CO2 as conversion gas provides a better contrast of the weak iodine signal than Xe‐CO2 or Si, respectively, for a fraction of 2% of the second harmonics of the synchrotron beam used

Sacubitril/valsartan for the treatment of non-obstructive hypertrophic cardiomyopathy:An open label randomized controlled trial (SILICOFCM)

Aim: Sacubitril/valsartan treatment reduces mortality and hospitalizations in heart failure with reduced ejection fraction but has limited application in hypertrophic cardiomyopathy (HCM). The aim of this study was to evaluate the effect of sacubitril/valsartan on peak oxygen consumption (VO2) in patients with non-obstructive HCM. Methods and results: This is a phase II, randomized, open-label multicentre study that enrolled adult patients with symptomatic non-obstructive HCM (New York Heart Association class I–III) who were randomly assigned (2:1) to receive sacubitril/valsartan (target dose 97/103 mg) or control for 16 weeks. The primary endpoint was a change in peak VO2. Secondary endpoints included echocardiographic measures of cardiac structure and function, natriuretic peptides and other cardiac biomarkers, and Minnesota Living with Heart Failure quality of life. Between May 2018 and October 2021, 354 patients were screened for eligibility, 115 patients (mean age 58 years, 37% female) met the study inclusion criteria and were randomly assigned to sacubitril/valsartan (n = 79) or control (n = 36). At 16 weeks, there was no significant change in peak VO2 from baseline in the sacubitril/valsartan (15.3 [4.3] vs. 15.9 [4.3] ml/kg/min, p = 0.13) or control group (p = 0.47). No clinically significant changes were found in blood pressure, cardiac structure and function, plasma biomarkers, or quality of life. Conclusion: In patients with HCM, a 16-week treatment with sacubitril/valsartan was well tolerated but had no effect on exercise capacity, cardiac structure, or function.</p