scholarly journals Alcohol Intake Is a Predictive Factor of Developing Heart Failure Among Patients With Infective Endocarditis

2016 ◽  
Vol 3 (suppl_1) ◽  
Author(s):  
Fujiko Morita ◽  
Yuji Hirai ◽  
Kiyozumi Suzuki ◽  
Yuki Uehara ◽  
Kazunori Mitsuhashi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Infective Endocarditis ◽  
Predictive Factor ◽  
Alcohol Intake ◽  
Developing Heart

scholarly journals Clinical and echocardiographic trends in percutaneous balloon mitral valvuloplasty

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Ofir Koren ◽  
Asaf Israeli ◽  
Ehud Rozner ◽  
Nassem Darawshy ◽  
Yoav Turgeman
Keyword(s):  
Heart Failure ◽  
Medical Center ◽  
Success Rates ◽  
Mitral Valvuloplasty ◽  
Percutaneous Balloon Mitral Valvuloplasty ◽  
Developing Heart ◽  
Percutaneous Balloon ◽  
Study Population ◽  
Procedural Success ◽  
Over Time

Abstract Background The prevalence of Rheumatic Mitral Stenosis (MS) has significantly changed over the last decades. We intend to examine patient demographics, Echocardiographic characteristics, procedural success rates, and complications throughout 30-years. Methods We conducted a single-center descriptive observational study. The study population consists of patients undergone percutaneous balloon mitral valvuloplasty (PBMV) at Emek Medical Center in Israel from January 1990 to May 2019. Results Four hundred seventeen patients underwent PBMV during the study period and were eligible for the study. Age did not change significantly over time (p = 0.09). The prevalence of Male and patients who were smoking and had multiple comorbidities such as hypertension, dyslipidemia, ischemic heart disease, and chronic kidney disease became increases over time (p = 0.02, p = 0.02, p = 0.001, p = 0.01, p = 0.02, and p = 0.001, respectively). Wilkins score and all its components increased over time, and the total score was higher in females (p = 0.01). Seventy-nine (18.9%) patients had complications. The rate of complications did not change over decades. Patients with Wilkins score > 8, post-procedural MR of ≥2, and post-procedural MVA < 1.5 had the highest risk for the need of Mitral valve replacement (MVR) surgery in 2 years following PBMV (3.64, 4.03, 2.44, respectively, CI 95%, p < .0001 for all). The median time in these patients was 630 days compared to 4–5 years in the entire population. Patients with Post-procedural MR of ≥2 and post-procedural MVA < 1.5 had ten times risk for developing heart failure (HR 9.07 and 10.06, respectively, CI 95%, P < .0001). Conclusion Our research reveals trends over time in patients’ characteristics and echocardiographic features. Our study population consists of more male patients with multiple comorbidities and more complex and calcified valvular structures in the last decade. Wilkins score > 8, post-procedural MR of ≥2, and post-procedural MVA < 1.5 cm2 were in-depended predictors for the time for surgery and heart failure hospitalization.

The effect of oestrogen withdrawal on cardiac Ca2+ regulation and the influence of GPER1

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A.J Francis ◽  
J.M Firth ◽  
N Islam ◽  
J Gorelik ◽  
K.T MacLeod
Keyword(s):  
Heart Failure ◽  
Structural Integrity ◽  
Left Ventricular ◽  
Funding Source ◽  
Hormonal Changes ◽  
Ion Conductance ◽  
Developing Heart ◽  
Rapid Stimulation ◽  
Post Menopausal

Abstract Background Post-menopausal women have an enhanced risk of developing heart failure, attributed to declining oestrogen levels during menopause. However, the signalling mechanisms remain undetermined. Purpose We aim to determine the role of G-protein coupled oestrogenic receptor 1 (GPER1) in intracellular Ca2+ regulation and the consequences of hormonal changes that may exacerbate the pathophysiology of heart failure. Methods Ovariectomy (OVx) (mimics menopausal hormone changes) or sham surgeries were conducted on female guinea pigs. Left ventricular cardiomyocytes were isolated 150-days post-operatively for experimental use. Cellular t-tubule network and structural integrity was measured using fluorescent di-8-ANEPPs staining and scanning ion conductance microscopy. GPER1 expression and localisation was measured by Western blot and immunostaining. The role of GPER1 activation was measured using selective agonist G-1 in electrophysiological and Ca2+-sensitive dye fluorescence experiments. Results Following oestrogen withdrawal, the t-tubule network density decreased by 13% and z-groove index reduced by 15%. GPER1 predominantly localised to the peri-nuclear endoplasmic reticulum and its expression increased by 32% in OVx. Action potential duration (APD) prolonged in OVx and following GPER1 activation, APD90 shortened by 11% and 25% in sham and OVx respectively. OVx cells had larger peak inward Ca2+ current (ICaL) (by 22%) and sarcoplasmic reticulum (SR) Ca2+ content (by 13%), compared with sham. While GPER1 activation had little effect on peak ICaL or SR content, it reduced Ca2+ transient amplitude (by 20%), SR fractional release (by 11%) in OVx cells. The frequency of occurrence of spontaneous Ca2+ waves evoked by periods of rapid stimulation reduced by 40% and wave-free survival time prolonged in OVx cells following GPER1 activation. Conclusions In the hearts of an animal species whose electrophysiology and intracellular Ca2+ regulation is akin to humans, we show that following oestrogen deficiency, the t-tubule network is down-regulated and becomes disorganised, GPER1 expression is increased and its activation induces negative inotropic responses in cardiomyocytes. This may limit the adverse changes to Ca2+ signalling reported in OVx that could be pro-arrhythmic and exacerbate the progression to heart failure. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation

Low-to-Moderate Alcohol Intake and Health Status in Heart Failure Patients

2005 ◽  
Vol 11 (5) ◽  
pp. 323-328 ◽  
Author(s):  
Adam C. Salisbury ◽  
John A. House ◽  
Mark W. Conard ◽  
Harlan M. Krumholz ◽  
John A. Spertus
Keyword(s):  
Heart Failure ◽  
Health Status ◽  
Alcohol Intake ◽  
Heart Failure Patients ◽  
Moderate Alcohol Intake

Early Surgical Intervention for Infective Endocarditis

2002 ◽  
Vol 10 (4) ◽  
pp. 298-301 ◽  
Author(s):  
Hong Sheng Zhu ◽  
Pei Yan Yao ◽  
Jia Hao Zheng ◽  
A Thomas Pezzella
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Heart Disease ◽  
Infective Endocarditis ◽  
Complex Disease ◽  
Surgical Intervention ◽  
Elective Surgery ◽  
Postoperative Bleeding ◽  
Arterial Embolization ◽  
Early Surgical Intervention

Infective endocarditis remains a serious and complex disease with significant morbidity and mortality. Sixty cases of infective endocarditis were retrospectively reviewed, consisting of 41 males and 19 females aged 7 to 50 years (mean, 30 years). Congenital heart disease was diagnosed in 19 of the patients and rheumatic heart disease in 41. Congestive heart failure occurred in 36 and systemic embolism in 8 cases. Blood cultures were positive in only 21.7% of the cases, while vegetations were detected by 2-dimensional echocardiography in 70%. Elective surgery was performed in 57 patients and emergent operation for systemic arterial embolization and/or intractable congestive heart failure in 3 patients. Two patients required reoperation for postoperative bleeding. All but 2 patients had been followed up for 6 to 160 months with no evidence of reinfection. Three patients with mechanical valve implantation later died of intracranial bleeding due to over-anticoagulation. The remaining 55 resumed normal activity. The encouraging outcomes were the result of an aggressive diagnostic approach and early surgical intervention.

Abstract 350: Atorvastatin Attenuates Pressure Overload-induced Cardiac Hypertrophy and Dysfunction Through Enhanced Autophagy

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Zhuo Zhao ◽  
Wei Wang ◽  
Hua-Ting Wang ◽  
Qing-Xin Geng ◽  
Di Zhao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Mrna Level ◽  
Mammalian Target Of Rapamycin ◽  
Pressure Overload ◽  
Oral Gavage ◽  
Atorvastatin Treatment ◽  
Developing Heart ◽  
Phosphorylated Akt

Aims: Cardiac hypertrophy is a maladaptive change in response to pressure overload and is also an important risk for developing heart failure. We previously demonstrated that atorvastatin inhibits cardiac hypertrophy and remodeling in a mouse model of transverse aorta constriction (TAC). This study was designed to determine the regulation of atorvastatin on cardiac autophagy and its association with the development of cardiac hypertrophy and dysfunction in the mice TAC model. Methods and results: TAC or sham operations were performed in male C57/L6 mice at 8 weeks of age. Atorvastatin (50 mg/kg/day) or vehicle (normal saline) were administered daily by oral gavage to TAC mice (n=10 per group). Echocardiography and real-time PCR data showed that chronic atorvastatin treatment for four weeks significantly attenuated pressure overload-induced cardiac hypertrophy and dysfunction, as well as cardiac mRNA level of atrial natriuretic factor (ANF), a biomarker of cardiac hypertrophy and heart failure. After 4 weeks of TAC, results from electron microscopy and Western blot showed that cardiac autophagy was activated, evidenced by the increased expression of microtubule-associated protein-1 light chain 3-II (LC3-II), Beclin-1, caspase-3, and the formation of autophagosomes. Interestingly, cardiac autophagy was further increased by the treatment of atorvastatin for 4 weeks. Western blot analysis showed phosphorylated Akt and mammalian target of rapamycin (p-mTor) decreased in the heart of TAC versus sham mice, which were further decreased by atorvastatin treatment. Conclusions: These findings suggest that atorvastatin attenuates cardiac hypertrophy and dysfunction in TAC mice probably through its regulation on cardiac autophagy via Akt/mTor pathways.

Impaired HDL Function Predicts Subclinical Myocardial Necrosis in Patients at Risk of Developing Heart Failure

2011 ◽  
Vol 17 (8) ◽  
pp. S24
Author(s):  
Zhili Shao ◽  
Yuping Wu ◽  
Yi Lu ◽  
Stanley L. Hazen ◽  
W.H. Wilson Tang
Keyword(s):  
Heart Failure ◽  
At Risk ◽  
Myocardial Necrosis ◽  
Hdl Function ◽  
Developing Heart ◽  
Patients At Risk

scholarly journals Drug-Induced Heart Failure (Part 2: Mechanisms of Development, Clinical Signs, Differential Diagnosis, Risk Factors, Treatment and Prevention)

2020 ◽  
Vol 8 (2) ◽  
pp. 57-65
Author(s):  
O. D. Ostroumova ◽  
I. V. Goloborodova
Keyword(s):  
Heart Failure ◽  
Beta Blockers ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Left Ventricular ◽  
Clinical Syndrome ◽  
Channel Blockers ◽  
Drug Induced ◽  
Treatment And Prevention ◽  
Developing Heart

Heart failure is a complex clinical syndrome caused by an impaired pumping function of the heart muscle, etiologically associated with cardiovascular disease and, in the vast majority of cases, requiring complex therapeutic regimens and simultaneous prescription of several drugs. To date, we know several classes of drugs (including those used for heart failure) which can induce development/progression of heart failure in both patients with left ventricular dysfunction, and in patients who do not have cardiovascular diseases. The aim of the study was to analyse and systematize data on development mechanisms, as well as methods of prevention and treatment of drug-induced heart failure when using diff erent groups of drugs. It has been established that drug-induced heart failure is most often associated with the use of calcium channel blockers (verapamil, diltiazem, nifedipine), beta-blockers, antiarrhythmic drugs (disopyramide, fl ecainide, propafenone, amiodarone, ibutilide, dofetilide, dronedarone), anthracyclines (doxorubicin) and other antitumor drugs (trastuzumab, bevacizumab, infl iximab), hypoglycemic drugs (thiazolidinediones, saxagliptin, alogliptin), and nonsteroidal anti-infl ammatory drugs, including selective cyclooxygenase-2 inhibitors. The study revealed various mechanisms of heart failure development following drug treatment. In some patients, heart failure development is associated with the cardiotoxic eff ect of a particular drug, in others with adverse eff ects on hemodynamics. Much depends on risks of developing heart failure, including specifi c risks attributable to groups of drugs and individual drugs. The identifi cation of drugs that can contribute to the development/ progression of heart failure, and possible clinical manifestations of drug-induced heart failure, as well as provision of timely information to physicians, and engagement of clinical pharmacologists with the aim of optimizing treatment of patients can facilitate timely diagnosis, treatment and prevention of drug-induced heart failure. 

scholarly journals The risk of developing chronic heart failure in patients with hypertension depending on the actual arterial stiffness

2020 ◽  
Vol 35 (2) ◽  
pp. 98-105
Author(s):  
A. I. Chernyavina ◽  
N. A. Koziolova
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Arterial Stiffness ◽  
Left Ventricular ◽  
Myocardial Mass ◽  
Developing Heart ◽  
Group 2 ◽  
Lv Volume ◽  
Lv Diastolic Function ◽  
Group 1

Objective. To determine the risk of developing chronic heart failure (CHF) in patients with hypertension (HTN) depending on the actual arterial stiffness.Material and Methods. The study included 175 patients with HTN without a verified diagnosis of heart failure. The average age was 48.5 ± 6.8 years. Patients underwent general clinical examination, volume sphygmoplethysmography assessments of cardio-ankle vascular index (CAVI), echocardiography study (left ventricular (LV) ejection fraction, LV diastolic function, LV myocardial mass index, indexed LV volume by echocardiography), and tests for serum N-terminal pro-B-type natriuretic peptide (NT-proBNP). Patients were divided into two groups depending on CAVI. Group 1 included 141 (80.6%) patients with CAVI < 9; group 2 included 34 (19.4%) patients with CAVI > 9.Results. In patients of group 1, the level of NT-proBNP was 0.008 [0.006; 5.770], which was significantly lower than the corresponding value in group 2, where the level of NT-proBNP was 13.08 [0.01; 350.65] ng/mL (p = 0.041). Indicators of odds ratio (OR) and relative risk (RR) were also significant. The chance of developing CHF with CAVI > 9 increased by almost 7 times (OR = 6.9; 95% CI = 2.8–16.8), and OR of CHF onset was 4.1 (95% CI = 2.2–7.6). Sensitivity and specificity rates were 55.9% and 84.4%, respectively. Correlation analysis revealed a medium degree of dependence and direct relationships between NT-proBNP level and CAVI values (r = 0.35; p <0.05).Conclusion. Serum level of NT-proBNP depended on the actual arterial stiffness. Patients with CAVI > 9 indicative of an increase in true arterial stiffness had a greater risk of developing heart failure assessed based on the level of NT-proBNP in the blood. Further studies are required to assess the effects of arterial stiffness, registered within the intermediate values of CAVI index, on the risk of heart failure onset. 

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