Abstract 14740: Sympathetic Down-regulation With Zamicastat Reduces Arrhythmogenicity in Isolated Hearts From Rats With Pulmonary Hypertension

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nuno Pires ◽  
Bruno Igreja ◽  
Luis Magalhaes ◽  
Maria-Joao Bonifacio ◽  
eric chevalier ◽  
...  
Keyword(s):  
Recovery Time ◽  
Sham Group ◽  
Cardiac Tissue ◽  
Fold Increase ◽  
Sympathetic Nerves ◽  
Premature Ventricular Contractions ◽  
Isolated Hearts ◽  
System A ◽  
Bundle Branch Blocks ◽  
The Right

Introduction: Pulmonary arterial hypertension (PAH) is a disease often causing right ventricular failure and death. During disease progression, structural and electrical remodeling of the right ventricle creates proarrhythmic substrates and triggers for arrhythmias. Studies of PAH patients show a hyperstimulation of the sympathetic nervous system (SNS) indicating that PAH may be mediated by SNS hyperactivation. Zamicastat (ZAM) is a reversible dopamine β-hydroxylase inhibitor that modulates SNS by reducing the biosynthesis of norepinephrine in peripheral sympathetic nerves. ZAM improves survival in the monocrotaline (MCT) rat model of PAH. Hypothesis: To evaluate the effect of ZAM on electrophysiological parameters in isolated hearts from MCT-treated rats. Methods: Male Wistar Han rats were randomized in 3 groups, Sham (n=6), MCT (n=15) and MCT+ZAM (n=17). On day zero, MCT and MCT+ZAM groups received MCT (60 mg/kg, SC) and Sham group received saline. Starting on day 12, MCT+ZAM rats were daily administered ZAM (30 mg/kg, PO) while all other animals were given vehicle. On day 28, hearts were excised and mounted on a Langendorff system. A bipolar circuit of two electrodes was placed on the epicardium for ECG recording. Provoked arrhythmias were induced with a burst pacing protocol (50Hz, 1 second) and the recovery time was measured as the time needed to reach 3 consecutive stable R-R intervals. Results: MCT increased the proportion of hearts exhibiting bundle branch blocks, 3 rd degree atrioventricular (AV) blocks, atrial fibrillation (AF), ventricular fibrillation (VF) and premature ventricular contractions (PVCs) when compared to Sham group. ZAM treatment suppressed 3 rd degree AV blocks, AF and VF. In addition, PVCs were less frequent in hearts from MCT+ZAM animals as compared to MCT group. Isolated hearts naturally entered a pause following overpacing-induced VF. MCT hearts showed a non-significant 1.7-fold increase in recovery time compared to Sham group. Hearts from MCT+ZAM animals had a significant ≈50% reduction in post-fibrillation pause. Conclusions: These data suggest that treatment with Zamicastat yields a lower proarrhythmic cardiac tissue decreasing the incidence of cardiac arrhythmias.

scholarly journals Prevention of postoperative intrapericardial adhesion by dextrin hydrogel

2021 ◽  
Author(s):  
Satoshi Kikusaki ◽  
Kazuyoshi Takagi ◽  
Takahiro Shojima ◽  
Kosuke Saku ◽  
Tomofumi Fukuda ◽  
...  
Keyword(s):  
Crystal Violet ◽  
Proliferative Response ◽  
Sham Group ◽  
Cardiac Tissue ◽  
Crystal Violet Staining ◽  
Pericardial Cavity ◽  
Uptake Assay ◽  
Surgically Induced ◽  
Observation Period

Abstract Objective Postoperative intrapericardial adhesion increases the risk of complications in patients undergoing reoperation. We investigated the effect of a bioabsorbable dextrin hydrogel (DHG) on the formation of intrapericardial adhesions. Methods Intrapericardial adhesion was surgically induced in Japanese white rabbits with DHG treatment (Adh + DHG) or without DHG treatment (Adh). The sham group was not treated with DHG and intrapericardial adhesion was not induced. The extent of intrapericardial adhesion was assessed by adhesion scoring and crystal violet staining of the pericardial cavity. Bromodeoxyuridine (BrdU) uptake assay was performed to assess the proliferative response to the injury in the tissue beneath the intrapericardial adhesion. Results The Adh + DHG group showed looser intrapericardial adhesions compared to the Adh group. The adhesion area of the Adh + DHG group was 4.6 ± 2.2%, whereas that of the Adh group was 32.6 ± 6.4% at the end of the 28-day observation period (p < 0.01). The induction of intrapericardial adhesion resulted in a proliferative response mainly in the cardiac tissue just beneath the adhesion. There were 48.6 ± 10.7 cells/0.1 mm2 BrdU-positive cells in the Adh + DHG group and 135.7 ± 23.8 cells/0.1 mm2 BrdU-positive cells in the Adh group on day 28 (p < 0.05). Conclusion These findings indicate that DHG effectively prevented intrapericardial adhesion in this model.

Peritricuspid annular prostate pellet

2021 ◽  
Vol 14 (2) ◽  
pp. e238076
Author(s):  
Bryan O'Sullivan ◽  
Richard Tanner ◽  
Peter Kelly ◽  
Gerard Fahy
Keyword(s):  
Right Ventricle ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Prostate Adenocarcinoma ◽  
Left Ventricular ◽  
Premature Ventricular Contractions ◽  
Left Ventricular Outflow ◽  
Metallic Object ◽  
The Right

A 75-year-old was treated for prostate adenocarcinoma with brachytherapy in September 2018. A routine follow-up chest radiograph 3 months later revealed a metallic object of the same dimensions as a brachytherapy pellet located in the right ventricle. Further imaging showed the brachtherapy pellet was located in the anterobasal right ventricular endocardium close to the tricuspid valve. Frequent asymptomatic premature ventricular contractions were observed with likely origin from the left ventricular outflow tract, an area remote from the site of the pellet. The patient remains asymptomatic and subsequent imaging shows that the position of the pellet has not changed.

Abstract 15607: Right Atrial Reservoir Strain Predicts Survival in Patients With Cardiac Amyloidosis

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Peter Huntjens ◽  
Kathleen Zhang ◽  
Yuko Soyama ◽  
Maria Karmpalioti ◽  
Daniel Lenihan ◽  
...  
Keyword(s):  
Cardiac Amyloidosis ◽  
Ventricular Hypertrophy ◽  
Cardiac Tissue ◽  
Fold Increase ◽  
Left Ventricular ◽  
Right Atrial ◽  
Chamber View ◽  
All Cause Mortality ◽  
And Function

Introduction: Myofibril deposition in amyloidosis diffusely may affect cardiac structure and function. Right ventricular involvement has been associated with adverse clinical outcome. However, the utility of right atrial (RA) function assessment by echocardiographic strain imaging is unclear. Hypothesis: We hypothesize that right atrial stain has prognostic value in cardiac amyloidosis. Methods: We studied 121 consecutive patients with cardiac amyloidosis: 18% had transthyretin and 79% had light chain amyloidosis. Cardiac amyloidosis was either confirmed by endocardial biopsy (36%) or by a combination of non-cardiac tissue biopsy and proof of left ventricular hypertrophy (64%). Speckle tracking peak RA reservoir strain was assessed based on 6 segments from the apical 4-chamber view. All-cause mortality was tracked over a median of 5 years. Results: Echocardiographic peak longitudinal RA strain was feasible in 109 patients (90%). 60 CA patients died during follow-up period. Peak longitudinal RA strain was reduced in cardiac amyloidosis non-survivors (8.1%) in comparison to survivors (18.3%, p<0.01), showing RA involvement in cardiac amyloidosis. Peak RA strain was significantly associated with survival (using median 12.5%) (p<0.001). Low peak longitudinal RA strain was associated with a 3.3-fold increase in mortality risk (95% confidence interval: 1.83 - 5.96). Conclusions: Reduced peak longitudinal RA strain was significantly associated with survival in patients with cardiac amyloidosis. RA reservoir function assessed by strain appears to be useful as a new means to predict prognosis in cardiac amyloidosis patients and has promise for clinical application.

Local bone injections of LPS and M-CSF increase bone resorption by different pathways in vivo in rats

1993 ◽  
Vol 264 (3) ◽  
pp. E391-E397 ◽  
Author(s):  
P. Orcel ◽  
M. Feuga ◽  
J. Bielakoff ◽  
M. C. De Vernejoul
Keyword(s):  
Bone Resorption ◽  
Fold Increase ◽  
Tartrate Resistant Acid Phosphatase ◽  
Normal Female ◽  
Local Bone ◽  
Macrophage Colony ◽  
The Right ◽  
And Function ◽  
Marrow Cells

We investigated the local in vivo action of lipopolysaccharide (LPS), a potent monocyte activator, and of macrophage colony-stimulating factor (M-CSF), a hemopoietic growth factor influencing monocyte differentiation, on bone resorption in normal female 8-wk-old rats. LPS (2 injections of 0.5 microgram), M-CSF (2 injections of either 12.5, 25, 100, or 500 ng), or vehicle was injected into bone marrow space through a thin catheter implanted, under hydrochloride anesthesia, in the distal end of the right femur. Histomorphometry was performed after staining of the tartrate-resistant acid phosphatase (TRAP). The number of osteoclasts and of TRAP-positive marrow cells (considered as osteoclast precursors) were counted in the secondary spongiosa. LPS caused a 3-fold increase in osteoclast surface, a 4.5-fold increase in the number of osteoclasts, but no change in the number of TRAP-positive marrow cells. M-CSF induced a striking dose-dependent biphasic effect on the number of TRAP-positive marrow cells and on bone resorption (no change with the lowest or with the highest concentrations, although the two intermediate doses significantly increased resorption surfaces and the number of osteoclasts). Our results demonstrate a local in vivo effect of LPS and of M-CSF on bone resorption and suggest that these substances act at different stages of osteoclast development and function.

scholarly journals A mouse model of ankle-subtalar joint complex instability induced post-traumatic osteoarthritis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Peixin Liu ◽  
Kaiwen Chen ◽  
Shuo Wang ◽  
Chunzhuo Hua ◽  
Hongtao Zhang ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Subtalar Joint ◽  
Sham Group ◽  
Step Length ◽  
Ligament Injury ◽  
Deltoid Ligament ◽  
Balance Beam ◽  
Post Traumatic ◽  
Time Required ◽  
The Right

Abstract Background Ankle-subtalar joint complex instability is not uncommonly presented in the clinic, but symptoms and signs similar to other conditions can easily lead to its misdiagnosis. Due to the lack of appropriate animal models, research on ankle-subtalar joint complex instability is limited. The aims of the present study were to establish an animal model of ankle-subtalar joint complex instability in mice and to explore its relationship with post-traumatic osteoarthritis (PTOA). Methods Twenty-one male C57BL/6J mice were randomly divided into three groups: SHAM group (sham surgery group), transected cervical ligament + anterior talofibular ligament (CL+ATFL) group, and transected cervical ligament + deltoid ligament (CL+DL) group. Two weeks after surgery, all mice underwent cage running training. Balance beam and gait tests were used to evaluate the changes in self-movement in the mice after ankle-subtalar ligament injury. Micro-CT and histological staining were used to evaluate the progress of PTOA. Results Compared with the SHAM group, balance and gait were affected in the ligament transection group. Twelve weeks after surgery, the time required to cross the balance beam in the CL+ATFL group was 35.1% longer and the mice slipped 3.6-fold more often than before surgery, and the mean step length on the right side was 7.2% smaller than that in the SHAM group. The time required to cross the balance beam in the CL+DL group was 32.1% longer and the mice slipped 3-fold more often than prior to surgery, and the average step length on the right side was 5.6% smaller than that in the SHAM group. CT images indicated that 28.6% of the mice in the CL+DL group displayed dislocation of the talus. Tissue staining suggested that articular cartilage degeneration occurred in mice with ligament transection 12 weeks after surgery. Conclusions Transected mice in the CL+ATFL and CL+DL groups displayed mechanical instability of the ankle-subtalar joint complex, and some mice in the CL+DL group also suffered from talus dislocation due to ligament injury leading to loss of stability of the bone structure. In addition, as time progressed, the articular cartilage displayed degenerative changes, which affected the ability of animals to move normally.

Abstract 16663: Premature Ventricular Contractions and Incident Heart Failure: Identifying Risk Factors via Interaction Analyses

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Vratika Agarwal ◽  
Eric Vittinghoff ◽  
Isaac R Whitman ◽  
Thomas A Dewland ◽  
Jonathan Dukes ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Case Reports ◽  
Large Population ◽  
Premature Ventricular Contraction ◽  
Fold Increase ◽  
Population Based ◽  
P Value ◽  
Premature Ventricular Contractions ◽  
Younger Patients

Introduction: Premature ventricular contraction (PVC)-induced cardiomyopathy is a potentially reversible cause of heart failure (HF). The association between PVCs and HF has been limited to case reports and small observational studies. Our objective was to leverage a large population-based database to examine interactions that might prove clinically useful in risk stratification. Methods: We included adult patients free of structural heart disease in the California Healthcare Cost and Utilization Project (HCUP) database from 2005-2009. After excluding patients with prevalent cardiomyopathy or heart failure, we identified patients with a diagnosis of PVCs. The primary outcome was incident systolic HF. Results: Among 16.8 million patients experiencing 48.1 million hospitalizations, 35,817 (0.2%) had a PVC diagnosis, and 198,818 (1.2%) developed systolic HF during study follow-up. After adjustment for age, sex, race, income & known HF risk factors, PVCs were an independent predictor of systolic HF [Hazard Ratio (HR) 1.57, 95% CI 1.51-1.63, p-value<0.001]. Interaction analyses revealed that relationship between PVCs and incident systolic HF was especially strong among younger patients and in those without coronary artery disease (CAD), hypertension (HTN), diabetes mellitus (DM) or atrial fibrillation (AF) [Table 1]. In patients <65 years without HTN, DM, CAD or AF, a PVC diagnosis was associated with an over 6-fold increase in incident HF risk (HR 6.5, 95% CI 5.5-7.7, p<0.001). Conclusion: Using a large population-based database, we found that a diagnosis of PVCs predicts incident systolic HF even after adjusting for conventional risk factors. This effect is most pronounced in younger patients, and those without HTN, DM, CAD or AF, suggesting that PVCs impart the greatest risk for heart failure when other cardiac comorbidities are absent.

Abstract 81: End-Stage Human Failing Heart Increases Functional Cardiac Progenitor Cells

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Rachana Mishra ◽  
David Simpson ◽  
Sudhish Sharma ◽  
Evan Colletti ◽  
Sunjay Kaushal
Keyword(s):  
Progenitor Cells ◽  
Fold Increase ◽  
Myosin Heavy Chain Isoforms ◽  
Functional Improvement ◽  
Cardiac Progenitor Cells ◽  
Failing Heart ◽  
Normal Human ◽  
Fetal Reprogramming ◽  
The Right ◽  
End Stage

Background: Human cases of end-stage heart failure provide the rare opportunity to test whether the cells within these hearts exhibit different phenotypic characteristics than those in healthy hearts. We tested whether the failing heart, as it reverses to a well-known fetal reprogramming state, also compensates by increasing the number of functional cardiac progenitor cells. Methods and Results: We examined samples from end-stage human failing hearts and also normal human hearts to quantitate the expression of various cardiac progenitor markers, by immunofluorescence, flow cytometry and RT-PCR. We further tested whether the cardiac progenitor cells were functional in a rodent model of myocardial infarction. All the failing end-stage hearts (N=13) reversed to a fetal state by switching their myosin heavy chain isoforms from beta to alpha. Additionally, atrial natriuretic factor was increased. Compared to normal congenital myocardium, failing end-stage hearts had a 2 to 5 fold increase in the number of C-kit+ and ISL-1+ cardiac progenitor cells (P<0.5). The numbers of cardiac progenitor cells was highest in the right atria as compared to other chambers of the end-stage heart. Cardiac progenitor cells isolated from failing hearts expressed several stemness markers that were upregulated compared to normal human hearts. FACS and IF analysis demonstrated significantly (P<0.5) higher c-kit expression in CDCs derived from end stage patients compare to normal congenital myocardium. Also, there was a tendency for increased FLK1 and Sca-1 expression in CM patients respectively. Transplanted cardiac progenitor cells from end-stage hearts promoted greater myocardial regeneration and functional improvement in the infarcted rat myocardium than transplanted cardiac progenitor cells derived from normal congenital patients (EF=57+3 vs. 41.5±3, P<0.05). Conclusion: Our results show an increase of progenitor cells within the end-stage heart that have the functional potential to regenerate the myocardium. Stimulating the differentiation and increasing the population of cardiac progenitor cells may provide a novel therapeutic strategy for these end-stage hearts.

P1603Nicorandil suppresses ischemia-induced cardiac interstitial norepinephrine enhancement and ventricular arrhythmia in hypertrophic hearts

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kobara ◽  
N Naseratun ◽  
Y Watanabe ◽  
H Toba ◽  
T Nakata
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Ventricular Arrhythmias ◽  
Sham Group ◽  
Cardiac Tissue ◽  
Norepinephrine Release ◽  
Norepinephrine Concentration ◽  
Ischemic Period

Abstract Background Myocardial infarction (MI) is a major cause of death in western countries and Japan, and hypertension is a major risk factor of MI. In hypertensive heart, acute myocardial infarction often leads to lethal ventricular arrhythmia. Nicorandil, an ATP sensitive potassium channel (KATP) opener, is usually used in the treatment of acute myocardial infarction. The effects of nicorandil on ischemic myocyte are fully defined. On the other hand, KATP in neuroterminals is known to regulate norepinephrine release, but the effect of nicorandil on ischemic norepinephrine release in cardiac tissue has remained unexplored. Purpose We examined whether nicorandil suppressed norepinephrine release via neuronal KATP and ventricular arrhythmia during acute ischemia in pressure overload-induced hypertrophic hearts. Methods SD Rats were divided into two groups; abdominal aortic constriction (AAC) group and sham-operated (Sham) group. Four weeks after constriction, cardiac geometry and function were examined using echocardiography. Then, myocardial ischemia was induced by the left anterior descending artery occlusion for 100 minutes in the presence or absence of intravenous infusion of nicorandil. Cardiac interstitial norepinephrine concentration in ischemic region was measured using the microdialysis method and concentration of cyclic AMP, a second messenger of norepinephrine, in cardiac tissue was measured by ELISA. Ventricular arrhythmias were monitered by ECG during whole ischemic period. Results Four weeks after constriction, remarkable left ventricular wall thickening was observed in AAC group. Before ischemia, ventricular arrhythmia was not found in both groups. Number of ventricular arrhythmia, including ventricular tachycardia and ventricular fibrillation, was increased in early ischemic period (- 40 min) in both groups, and was grater in AAC group. Before ischemia, interstitial norepinephrine concentration in cardiac tissue was higher level in AAC group than in Sham group. Ischemia obviously increased norepinephrine concentration in both groups time dependently and AAC further increased norepinephrine than Sham group. Concentration of cyclic AMP in cardiac tissue was raised in early ischemic period (- 40 min) and then gradually decreased. Nicorandil significantly suppressed the number of ventricular arrhythmias, and abolished the ventricular tachycardia and fibrillation without hemodynamic alterations. Nicorandil also attenuated norepinephrine and cAMP enhancement in acute ischemic period in both groups. Conclusion Ischemia-induced ventricular arrhythmia was more frequent and severe in hypertrophic hearts and interstitial norepinephrine enhancement may play a role in this ischemic arrhythmia. Nicorandil suppressed ischemia-induced interstitial norepinephrine release by neuronal KATP opening, which attenuated ventricular arrhythmias in normal and hypertrophic hearts.

scholarly journals Endoscopic incision of protruding right ureterocele in a single collecting system: a case report

2017 ◽  
Vol 25 (4) ◽  
pp. 240-44
Author(s):  
Rinto Hariwibowo ◽  
Harrina E. Rahardjo
Keyword(s):  
External Genitalia ◽  
Excretory Urography ◽  
Voiding Cystourethrography ◽  
System A ◽  
Grade 5 ◽  
Grade Ii ◽  
The Right ◽  
Collecting System ◽  
Endoscopic Incision

Protruding ureterocele is a very rare case found in the literature. We are reporting a 21 year-old female with an intermittent protruding mass from urethra, accompanied by dysuria, hematuria, and recurrent urinary tract infection. Inspection of the external genitalia revealed a protruding mass from the urethra which could be reduced manually. Excretory urography showed bilateral single collecting systems, grade II hydronephrosis of the right kidney, and a cobra head appearance of the lower right pelvis. The patient was diagnosed with a protruding right ureterocele in a single collecting system, and thus, endoscopic incision of a ureterocele was performed. Ultrasonography which was carried out three weeks after the procedure confirmed no residual hydronephrosis or ureterocele in the bladder. Voiding cystourethrography (VCUG) underwent at a three-month-follow up revealed a grade 5 vesico-ureteral reflux (VUR) on the right side. Surgical reimplantation was then considered. In conclusion, endoscopic incision was safe and yielded good result for protruding ureteroceles, but the need for secondary surgery in several conditions should be considered.

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