The mechanisms of left septal and anterior wall reentrant atrial tachycardias analyzed with ultrahigh resolution mapping: The role of functional block in the circuit

Importance of anatomo-topographic peculiarities for endoscopic diagnosis and treatment of Sphenoiditis

Kazan medical journal ◽

10.17816/kazmj82714 ◽

1995 ◽

Vol 76 (1) ◽

pp. 38-40

Author(s):

M. K. Mikhailov ◽

L. G. Svatko ◽

V. N. Krasnozhen ◽

S. B. Mosikhin

Keyword(s):

Surgical Intervention ◽

Anterior Wall ◽

Endoscopic Diagnosis ◽

Diagnosis And Treatment ◽

Case Record ◽

Endoscopic Method

The results of anatomo-topographic investigation of 100 clinoid sinuses obtained in autopsy of 50 dead persons are given. The relations of clinoid sinuses with posterior cells of ethmoidal labyrinth are found, the location of natural anastomoses of sinuses on the anterior wall is defined. The case record of the patient with sphenoiditis after endoscopic surgical intervention is given. The role of endoscopic method for diagnosis and treatment of sphenoiditis is shown.

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Abstract 15632: Phenotypic Overlap Between Left Ventricular Noncompaction and Hypertrophic Cardiomyopathy: A Case Report

Circulation ◽

10.1161/circ.142.suppl_3.15632 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Ethan Senser ◽

Madison Hawkins ◽

Eric M Williams ◽

Lauren Gilstrap

Keyword(s):

Hypertrophic Cardiomyopathy ◽

Cardiac Mri ◽

Genetic Diagnosis ◽

Lateral Wall ◽

Anterior Wall ◽

Left Ventricular ◽

Ventricular Noncompaction ◽

History Of ◽

Clinically Significant

Introduction: Left ventricular non-compaction (LVNC) is characterized by extensively trabeculaed myocardium adjacent to normal compacted myocardium of the left ventricle (LV). Hypertrophic cardiomyopathy (HCM) typically appears as diffuse or segmental LV hypertrophy, with or without outflow tract obstruction. Cardiac sarcomere mutations are present in most HCM cases and have also been identified in LVNC. Whether or not there is clinically significant phenotypic overlap between the two diseases is less well understood. We present a case of known HCM that met criteria for both LVNC and HCM by cardiac MRI. Case: A 49-year old man with HCM due to a c.3742_3759dup variant in MYBPC3 presented to clinic after an episode of syncope and ICD firing. In clinic, the device was interrogated and he was found to have had ventricular flutter which was successfully treated with one shock and a new, high (>20%) burden of premature ventricular beats. An echocardiogram showed a stable ejection fraction at 42%, mild concentric LV hypertrophy without obstruction and a newly dilated LV with an end diastolic diameter of 7.1cm (previously 6.2cm). A cardiac MRI was performed ( Figure ) and showed LV noncompaction and diffuse transmural and mid myocardial hyperenhancement/fibrosis of the septum, basilar lateral wall, anterior wall, and distal right ventricle consistent with patient's long-standing history of hypertrophic cardiomyopathy. Discussion: This case highlights the phenotypic overlap between HCM and LVNC by cardiac MRI. Had this patient not already carried a genetic diagnosis of HCM, he would likely have been diagnosed with LVNC based on this cardiac MRI. The phenotypic overlap in these diseases raises questions about ICD guidelines, the role of anticoagulation and prognosis.

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Selection of Critical Isthmus in Scar-Related Atrial Tachycardia Using a New Automated Ultrahigh Resolution Mapping System

Circulation Arrhythmia and Electrophysiology ◽

10.1161/circep.116.004510 ◽

2017 ◽

Vol 10 (1) ◽

Cited By ~ 60

Author(s):

Decebal Gabriel Laţcu ◽

Sok-Sithikun Bun ◽

Frédéric Viera ◽

Tahar Delassi ◽

Mohammed El Jamili ◽

...

Keyword(s):

Atrial Tachycardia ◽

Ultrahigh Resolution ◽

Mapping System ◽

Resolution Mapping ◽

Selection Of

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The role of local impedance drop in the acute lesion efficacy during pulmonary vein isolation performed with a new contact force sensing catheter—A pilot study

PLoS ONE ◽

10.1371/journal.pone.0257050 ◽

2021 ◽

Vol 16 (9) ◽

pp. e0257050

Author(s):

Nándor Szegedi ◽

Zoltán Salló ◽

Péter Perge ◽

Katalin Piros ◽

Vivien Klaudia Nagy ◽

...

Keyword(s):

Pilot Study ◽

Pulmonary Vein ◽

Pulmonary Vein Isolation ◽

Contact Force ◽

Posterior Wall ◽

Anterior Wall ◽

Force Sensing ◽

Lesion Formation ◽

Force Time

Introduction Our pilot study aimed to evaluate the role of local impedance drop in lesion formation during pulmonary vein isolation with a novel contact force sensing ablation catheter that records local impedance as well and to find a local impedance cut-off value that predicts successful lesion formation. Materials and methods After completing point-by-point radiofrequency pulmonary vein isolation, the success of the applications was evaluated by pacing along the ablation line at 10 mA, 2 ms pulse width. Lesions were considered successful if loss of local capture was achieved. Results Out of 645 applications, 561 were successful and 84 were unsuccessful. Compared to the unsuccessful ablation points, the successful applications were shorter (p = 0.0429) and had a larger local impedance drop (p<0.0001). There was no difference between successful and unsuccessful applications in terms of mean contact force (p = 0.8571), force-time integral (p = 0.0699) and contact force range (p = 0.0519). The optimal cut-point for the local impedance drop indicating successful lesion formation was 21.80 Ohms on the anterior wall [AUC = 0.80 (0.75–0.86), p<0.0001], and 18.30 Ohms on the posterior wall [AUC = 0.77 (0.72–0.83), p<0.0001]. A local impedance drop larger than 21.80 Ohms on the anterior wall and 18.30 Ohms on the posterior wall was associated with an increased probability of effective lesion creation [OR = 11.21, 95%CI 4.22–29.81, p<0.0001; and OR = 7.91, 95%CI 3.77–16.57, p<0.0001, respectively]. Conclusion The measurement of the local impedance may predict optimal lesion formation. A local impedance drop > 21.80 Ohms on the anterior wall and > 18.30 Ohms on the posterior wall significantly increases the probability of creating a successful lesion.

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Large-Scale Analysis of Apolipoprotein CIII Glycosylation by Ultrahigh Resolution Mass Spectrometry

Frontiers in Chemistry ◽

10.3389/fchem.2021.678883 ◽

2021 ◽

Vol 9 ◽

Author(s):

Daniel Demus ◽

Annemieke Naber ◽

Viktoria Dotz ◽

Bas C. Jansen ◽

Marco R. Bladergroen ◽

...

Keyword(s):

Cardiovascular Disease ◽

Lipid Metabolism ◽

Large Scale ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Sinapinic Acid ◽

Chemical Oxidation ◽

Ultrahigh Resolution ◽

Apolipoprotein Ciii

Apolipoprotein-CIII (apo-CIII) is a glycoprotein involved in lipid metabolism and its levels are associated with cardiovascular disease risk. Apo-CIII sialylation is associated with improved plasma triglyceride levels and its glycosylation may have an effect on the clearance of triglyceride-rich lipoproteins by directing these particles to different metabolic pathways. Large-scale sample cohort studies are required to fully elucidate the role of apo-CIII glycosylation in lipid metabolism and associated cardiovascular disease. In this study, we revisited a high-throughput workflow for the analysis of intact apo-CIII by ultrahigh-resolution MALDI FT-ICR MS. The workflow includes a chemical oxidation step to reduce methionine oxidation heterogeneity and spectrum complexity. Sinapinic acid matrix was used to minimize the loss of sialic acids upon MALDI. MassyTools software was used to standardize and automate MS data processing and quality control. This method was applied on 771 plasma samples from individuals without diabetes allowing for an evaluation of the expression levels of apo-CIII glycoforms against a panel of lipid biomarkers demonstrating the validity of the method. Our study supports the hypothesis that triglyceride clearance may be regulated, or at least strongly influenced by apo-CIII sialylation. Interestingly, the association of apo-CIII glycoforms with triglyceride levels was found to be largely independent of body mass index. Due to its precision and throughput, the new workflow will allow studying the role of apo-CIII in the regulation of lipid metabolism in various disease settings.

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Abstract 083: Macrophages Dictate the Progression and Manifestation of Hypertensive Heart Disease in Rat

Circulation Research ◽

10.1161/res.113.suppl_1.a083 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

DAVID KAIN ◽

Chana Yagil ◽

Natalie Landa-Rouben ◽

Yoram Yagil ◽

Jonathan Leor

Keyword(s):

Heart Disease ◽

Significant Role ◽

Hypertensive Heart Disease ◽

Treated Group ◽

Anterior Wall ◽

Wall Thickening ◽

Macrophage Depletion ◽

Strain And Strain Rate ◽

Lv Remodeling

Introduction: Inflammation has been implicated in the initiation, progression and manifestation of hypertension. However, the role of macrophages in hypertension-induced LV remodeling has yet to be determined. Hypothesis: We assessed the hypothesis that macrophages play a significant role in the initiation and progression of hypertension-induced LV remodeling. Methods and Results: Hypertension was induced in male Sabra salt-sensitive (SBH/y) rats with high salt diet (8%NaCl) over 6 weeks. Hypertensive SBH/y developed LV hypertrophy, hyper-contractility and a higher LV ejection fraction (EF). Notably, the number of macrophages, particularly cardiac macrophages was significantly greater in hypertensive SBH/y than in controls. Macrophage depletion was induced after induction of hypertension by intravenous administration of clodronate liposomes at 3-day intervals over 4 weeks (n=9) and was validated by FACS analysis and ED1 (CD68) staining of heart sections. Control hypertensive rats (n=9) were treated with PBS liposomes. Surprisingly, macrophage depletion attenuate the progression of hypertension in the clodronate-treated group (from 177±2 to 179±2 mmHg) compared with controls (from 179±2 to 184 ± 5mmHg; p=0.01).Serial echocardiography studies before and 30 days after initiation of macrophage depletion or control showed that LV systolic diameter and volume were smaller; anterior wall thickening, fractional shortening and EF were higher in the macrophage-depletion group (p<0.05). LV strain and strain rate were significantly higher in the macrophage depletion group (p=0.04). Furthermore, 1 month after BP elevation, the expression of miR-31, which has been implicated in the pathogenesis of cardiac hypertrophy, was decreased (4.6-fold) in the macrophage-depleted hearts compared to controls, suggesting that macrophages control miR-31 expression in LV hypertrophy. Conclusion: Our findings suggest a significant role of macrophages in the initiation and progression of salt-sensitive hypertension and the related heart disease. Targeting macrophages, therefore, could be a potential therapeutic target for the treatment of hypertension and prevention of LV remodeling and dysfunction.

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