Subjects -> MEDICAL SCIENCES (Total: 8642 journals)
    - ALLERGOLOGY AND IMMUNOLOGY (218 journals)
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    - CARDIOVASCULAR DISEASES (338 journals)
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CARDIOVASCULAR DISEASES (338 journals)                  1 2 | Last

Showing 1 - 200 of 338 Journals sorted alphabetically
Acta Angiologica     Open Access   (Followers: 5)
Acta Cardiologica     Hybrid Journal   (Followers: 2)
Acute Cardiac Care     Hybrid Journal   (Followers: 8)
Adipositas - Ursachen, Folgeerkrankungen, Therapie     Hybrid Journal  
AJP Heart and Circulatory Physiology     Hybrid Journal   (Followers: 12)
Aktuelle Kardiologie     Hybrid Journal   (Followers: 1)
American Heart Journal     Hybrid Journal   (Followers: 60)
American Journal of Cardiology     Hybrid Journal   (Followers: 68)
American Journal of Cardiovascular Drugs     Hybrid Journal   (Followers: 17)
American Journal of Hypertension     Hybrid Journal   (Followers: 28)
Anales de Cirugia Vascular     Full-text available via subscription   (Followers: 1)
Anatolian Journal of Cardiology     Open Access   (Followers: 6)
Angiología     Full-text available via subscription  
Angiologia e Cirurgia Vascular     Open Access   (Followers: 1)
Angiology     Hybrid Journal   (Followers: 3)
Annales de Cardiologie et d'Angéiologie     Full-text available via subscription   (Followers: 1)
Annals of Circulation     Open Access   (Followers: 2)
Annals of Noninvasive Electrocardiology     Hybrid Journal   (Followers: 1)
Annals of Pediatric Cardiology     Open Access   (Followers: 12)
AORTA     Open Access  
Archives of Cardiovascular Diseases     Full-text available via subscription   (Followers: 5)
Archives of Cardiovascular Diseases Supplements     Full-text available via subscription   (Followers: 3)
Archives of Cardiovascular Imaging     Open Access   (Followers: 2)
Archivos de cardiología de México     Open Access   (Followers: 1)
Argentine Journal of Cardiology (English edition)     Open Access   (Followers: 2)
Arquivos Brasileiros de Cardiologia     Open Access   (Followers: 2)
Arrhythmia & Electrophysiology Review     Open Access   (Followers: 1)
Arteriosclerosis, Thrombosis and Vascular Biology     Full-text available via subscription   (Followers: 32)
Artery Research     Hybrid Journal   (Followers: 4)
ARYA Atherosclerosis     Open Access  
ASAIO Journal     Hybrid Journal   (Followers: 3)
ASEAN Heart Journal     Open Access   (Followers: 2)
Asian Cardiovascular and Thoracic Annals     Hybrid Journal   (Followers: 2)
Aswan Heart Centre Science & Practice Services     Open Access   (Followers: 1)
Atherosclerosis : X     Open Access  
Bangladesh Heart Journal     Open Access   (Followers: 3)
Basic Research in Cardiology     Hybrid Journal   (Followers: 10)
BMC Cardiovascular Disorders     Open Access   (Followers: 22)
Brain Circulation     Open Access   (Followers: 1)
British Journal of Cardiology     Full-text available via subscription   (Followers: 18)
Canadian Journal of Cardiology     Hybrid Journal   (Followers: 18)
Cardiac Cath Lab Director     Full-text available via subscription  
Cardiac Electrophysiology Review     Hybrid Journal   (Followers: 2)
Cardiac Failure Review     Open Access   (Followers: 1)
Cardiocore     Full-text available via subscription   (Followers: 1)
Cardiogenetics     Open Access   (Followers: 3)
Cardiology     Full-text available via subscription   (Followers: 20)
Cardiology and Angiology: An International Journal     Open Access   (Followers: 1)
Cardiology and Therapy     Open Access   (Followers: 12)
Cardiology Clinics     Full-text available via subscription   (Followers: 14)
Cardiology in Review     Hybrid Journal   (Followers: 8)
Cardiology in the Young     Hybrid Journal   (Followers: 34)
Cardiology Journal     Open Access   (Followers: 6)
Cardiology Plus     Open Access   (Followers: 1)
Cardiology Research     Open Access   (Followers: 15)
Cardiology Research and Practice     Open Access   (Followers: 10)
Cardiopulmonary Physical Therapy Journal     Hybrid Journal   (Followers: 8)
Cardiorenal Medicine     Full-text available via subscription   (Followers: 1)
Cardiothoracic Surgeon     Open Access   (Followers: 1)
CardioVasc     Full-text available via subscription   (Followers: 1)
Cardiovascular & Haematological Disorders - Drug Targets     Hybrid Journal   (Followers: 1)
Cardiovascular & Hematological Agents in Medicinal Chemistry     Hybrid Journal   (Followers: 2)
CardioVascular and Interventional Radiology     Hybrid Journal   (Followers: 15)
Cardiovascular and Thoracic Open     Open Access  
Cardiovascular Diabetology     Open Access   (Followers: 10)
Cardiovascular Drugs and Therapy     Hybrid Journal   (Followers: 14)
Cardiovascular Endocrinology & Metabolism     Hybrid Journal   (Followers: 1)
Cardiovascular Engineering     Hybrid Journal   (Followers: 1)
Cardiovascular Engineering and Technology     Hybrid Journal   (Followers: 1)
Cardiovascular Intervention and Therapeutics     Hybrid Journal   (Followers: 5)
Cardiovascular Journal     Open Access   (Followers: 6)
Cardiovascular Journal of Africa     Full-text available via subscription   (Followers: 5)
Cardiovascular Journal of South Africa     Full-text available via subscription   (Followers: 1)
Cardiovascular Medicine in General Practice     Full-text available via subscription   (Followers: 7)
Cardiovascular Pathology     Hybrid Journal   (Followers: 4)
Cardiovascular Regenerative Medicine     Open Access  
Cardiovascular Research     Hybrid Journal   (Followers: 15)
Cardiovascular Revascularization Medicine     Hybrid Journal   (Followers: 1)
Cardiovascular System     Open Access  
Cardiovascular Therapeutics     Open Access   (Followers: 1)
Cardiovascular Toxicology     Hybrid Journal   (Followers: 6)
Cardiovascular Ultrasound     Open Access   (Followers: 5)
Case Reports in Cardiology     Open Access   (Followers: 7)
Catheterization and Cardiovascular Interventions     Hybrid Journal   (Followers: 3)
Cerebrovascular Diseases     Full-text available via subscription   (Followers: 3)
Cerebrovascular Diseases Extra     Open Access  
Chest     Full-text available via subscription   (Followers: 103)
Choroby Serca i Naczyń     Open Access   (Followers: 1)
Circulation     Hybrid Journal   (Followers: 265)
Circulation : Cardiovascular Imaging     Hybrid Journal   (Followers: 15)
Circulation : Cardiovascular Interventions     Hybrid Journal   (Followers: 19)
Circulation : Cardiovascular Quality and Outcomes     Hybrid Journal   (Followers: 11)
Circulation : Genomic and Precision Medicine     Hybrid Journal   (Followers: 16)
Circulation : Heart Failure     Hybrid Journal   (Followers: 26)
Circulation Research     Hybrid Journal   (Followers: 36)
Cirugía Cardiovascular     Open Access  
Clínica e Investigación en Arteriosclerosis     Full-text available via subscription  
Clínica e Investigación en arteriosclerosis (English Edition)     Hybrid Journal  
Clinical and Experimental Hypertension     Hybrid Journal   (Followers: 3)
Clinical Cardiology     Hybrid Journal   (Followers: 11)
Clinical Hypertension     Open Access   (Followers: 5)
Clinical Medicine Insights : Cardiology     Open Access   (Followers: 6)
Clinical Research in Cardiology     Hybrid Journal   (Followers: 6)
Clinical Research in Cardiology Supplements     Hybrid Journal  
Clinical Trials and Regulatory Science in Cardiology     Open Access   (Followers: 4)
Congenital Heart Disease     Hybrid Journal   (Followers: 6)
Congestive Heart Failure     Hybrid Journal   (Followers: 4)
Cor et Vasa     Full-text available via subscription   (Followers: 1)
Coronary Artery Disease     Hybrid Journal   (Followers: 2)
CorSalud     Open Access  
Critical Pathways in Cardiology     Hybrid Journal   (Followers: 4)
Current Cardiology Reports     Hybrid Journal   (Followers: 7)
Current Cardiology Reviews     Hybrid Journal   (Followers: 4)
Current Cardiovascular Imaging Reports     Hybrid Journal   (Followers: 1)
Current Cardiovascular Risk Reports     Hybrid Journal  
Current Heart Failure Reports     Hybrid Journal   (Followers: 5)
Current Hypertension Reports     Hybrid Journal   (Followers: 6)
Current Hypertension Reviews     Hybrid Journal   (Followers: 6)
Current Opinion in Cardiology     Hybrid Journal   (Followers: 14)
Current Problems in Cardiology     Hybrid Journal   (Followers: 3)
Current Research : Cardiology     Full-text available via subscription   (Followers: 1)
Current Treatment Options in Cardiovascular Medicine     Hybrid Journal   (Followers: 1)
Current Vascular Pharmacology     Hybrid Journal   (Followers: 5)
CVIR Endovascular     Open Access   (Followers: 1)
Der Kardiologe     Hybrid Journal   (Followers: 2)
Echo Research and Practice     Open Access   (Followers: 2)
Echocardiography     Hybrid Journal   (Followers: 4)
Egyptian Heart Journal     Open Access   (Followers: 2)
Egyptian Journal of Cardiothoracic Anesthesia     Open Access  
ESC Heart Failure     Open Access   (Followers: 4)
European Cardiology Review     Open Access   (Followers: 1)
European Heart Journal     Hybrid Journal   (Followers: 68)
European Heart Journal - Cardiovascular Imaging     Hybrid Journal   (Followers: 10)
European Heart Journal - Cardiovascular Pharmacotherapy     Full-text available via subscription   (Followers: 2)
European Heart Journal - Quality of Care and Clinical Outcomes     Hybrid Journal  
European Heart Journal : Acute Cardiovascular Care     Hybrid Journal   (Followers: 1)
European Heart Journal : Case Reports     Open Access   (Followers: 1)
European Heart Journal Supplements     Hybrid Journal   (Followers: 8)
European Journal of Cardio-Thoracic Surgery     Hybrid Journal   (Followers: 9)
European Journal of Cardio-Thoracic Surgery Supplements     Full-text available via subscription   (Followers: 2)
European Journal of Cardiovascular Nursing     Hybrid Journal   (Followers: 5)
European Journal of Heart Failure     Hybrid Journal   (Followers: 14)
European Journal of Preventive Cardiology.     Hybrid Journal   (Followers: 6)
European Stroke Organisation     Hybrid Journal   (Followers: 3)
Experimental & Translational Stroke Medicine     Open Access   (Followers: 9)
Expert Review of Cardiovascular Therapy     Full-text available via subscription   (Followers: 3)
Folia Cardiologica     Open Access  
Forum Zaburzeń Metabolicznych     Hybrid Journal  
Frontiers in Cardiovascular Medicine     Open Access   (Followers: 1)
Future Cardiology     Hybrid Journal   (Followers: 6)
General Thoracic and Cardiovascular Surgery     Hybrid Journal   (Followers: 3)
Global Cardiology Science and Practice     Open Access   (Followers: 5)
Global Heart     Hybrid Journal   (Followers: 3)
Heart     Hybrid Journal   (Followers: 48)
Heart and Mind     Open Access  
Heart and Vessels     Hybrid Journal  
Heart Failure Clinics     Full-text available via subscription   (Followers: 2)
Heart Failure Reviews     Hybrid Journal   (Followers: 3)
Heart India     Open Access   (Followers: 2)
Heart International     Full-text available via subscription  
Heart Rhythm     Hybrid Journal   (Followers: 11)
Heart Views     Open Access   (Followers: 2)
HeartRhythm Case Reports     Open Access  
Hellenic Journal of Cardiology     Open Access   (Followers: 1)
Herz     Hybrid Journal   (Followers: 3)
High Blood Pressure & Cardiovascular Prevention     Full-text available via subscription   (Followers: 2)
Hypertension     Full-text available via subscription   (Followers: 23)
Hypertension     Open Access   (Followers: 2)
Hypertension in Pregnancy     Hybrid Journal   (Followers: 9)
Hypertension Research     Hybrid Journal   (Followers: 4)
Ibrahim Cardiac Medical Journal     Open Access  
IJC Heart & Vessels     Open Access   (Followers: 1)
IJC Heart & Vasculature     Open Access   (Followers: 1)
IJC Metabolic & Endocrine     Open Access   (Followers: 1)
Indian Heart Journal     Open Access   (Followers: 5)
Indian Journal of Cardiovascular Disease in Women WINCARS     Open Access  
Indian Journal of Thoracic and Cardiovascular Surgery     Hybrid Journal  
Indian Pacing and Electrophysiology Journal     Open Access   (Followers: 1)
Innovations : Technology and Techniques in Cardiothoracic and Vascular Surgery     Hybrid Journal   (Followers: 1)
Insuficiencia Cardíaca     Open Access  
Interactive CardioVascular and Thoracic Surgery     Hybrid Journal   (Followers: 7)
International Cardiovascular Forum Journal     Open Access  
International Journal of Angiology     Hybrid Journal   (Followers: 2)
International Journal of Cardiology     Hybrid Journal   (Followers: 18)
International Journal of Cardiology Hypertension     Open Access   (Followers: 1)
International Journal of Cardiovascular and Cerebrovascular Disease     Open Access   (Followers: 2)
International Journal of Cardiovascular Imaging     Hybrid Journal   (Followers: 2)
International Journal of Cardiovascular Research     Hybrid Journal   (Followers: 6)
International Journal of Heart Rhythm     Open Access  
International Journal of Hypertension     Open Access   (Followers: 8)
International Journal of Hyperthermia     Open Access  
International Journal of Stroke     Hybrid Journal   (Followers: 32)
International Journal of the Cardiovascular Academy     Open Access  
Interventional Cardiology Clinics     Full-text available via subscription   (Followers: 2)
Interventional Cardiology Review     Open Access  
JACC : Basic to Translational Science     Open Access   (Followers: 5)
JACC : Cardiovascular Imaging     Hybrid Journal   (Followers: 18)
JACC : Cardiovascular Interventions     Hybrid Journal   (Followers: 19)
JACC : Heart Failure     Full-text available via subscription   (Followers: 14)
JAMA Cardiology     Hybrid Journal   (Followers: 30)

        1 2 | Last

Similar Journals
Journal Cover
Cardiovascular Drugs and Therapy
Journal Prestige (SJR): 1.349
Citation Impact (citeScore): 3
Number of Followers: 14  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1573-7241 - ISSN (Online) 0920-3206
Published by Springer-Verlag Homepage  [2626 journals]
  • Statin Controversies: Response to the Letter from Tomlinson et al.
    • PubDate: 2020-06-01
       
  • A Reconciliation Attempt of the Acute Coronary Syndrome Clinical Trials on
           Clopidogrel, Prasugrel, and Ticagrelor
    • PubDate: 2020-06-01
       
  • The Melatonin Receptor Agonist Ramelteon Induces Cardioprotection that
           Requires MT2 Receptor Activation and Release of Reactive Oxygen Species
    • Abstract: Purpose The melatonin receptor (MT) agonist ramelteon has a higher affinity to MT1 than for MT2 receptors and induces cardioprotection by involvement of mitochondrial potassium channels. Activation of mitochondrial potassium channels leads to release of free radicals. We investigated whether (1) ramelteon-induced cardioprotection is MT2 receptor specific and (2) if free radicals are involved in ramelteon-induced cardioprotection. Methods Hearts of male Wistar rats were randomized, placed on a Langendorff system, and perfused with Krebs-Henseleit buffer at a constant pressure of 80 mmHg. All hearts were subjected to 33 min of global ischemia and 60 min of reperfusion. Before ischemia hearts were perfused with ramelteon (Ram) with or without the MT2 receptor inhibitor 4-phenyl-2-propionamidotetralin (4P-PDOT+Ram, 4P-PDOT). In subsequent experiments, ramelteon was administered together with the radical oxygen species (ROS) scavenger N-2-mercaptopropionylglycine (MPG+Ram). To determine whether the blockade of ramelteon-induced cardioprotection can be restored, we combined ramelteon and MPG with mitochondrial permeability transition pore (mPTP) inhibitor cyclosporine A (CsA) at different time points. Infarct size was determined by triphenyltetrazolium chloride (TTC) staining. Results Ramelteon-induced infarct size reduction was completely blocked by 4P-PDOT and MPG. Ramelteon and MPG combined with CsA before ischemia were not cardioprotective but CsA at the onset of reperfusion could restore infarct size reduction. Conclusions This study shows for the first time that despite the higher affinity to MT1 receptors, (1) ramelteon-induced cardioprotection involves MT2 receptors, (2) cardioprotection requires ROS release, and (3) inhibition of the mPTP can restore infarct size reduction.
      PubDate: 2020-06-01
       
  • A Common Missense Variant in OMA1 Associated with the Prognosis of Heart
           Failure
    • Abstract: Purpose Mitochondrial dysfunction plays a vital role in the pathophysiologic process of heart failure (HF). As a quality control system, mitochondrial fusion and fission are under control of mitochondrial fusion and fission-related proteins. The objective of this study was to investigate the effects of common variants in mitochondrial fusion and fission-related genes on the prognosis of HF. Methods We performed whole exome sequencing (WES) with 1000 HF patients; the statistically significant variant was further genotyped in the replicated population with 2324 HF patients. A series of function analysis including western blot, cell proliferation assay, and in vitro OMA1 activity assay were conducted to illuminate the underlying mechanism. Results We identified a missense variant rs17117699 associated with the prognosis of HF in group without β-blocker use rather than with β-blocker use in two-stage population: adjusted P = 0.79, HR = 0.88 (0.36–2.13) in group with β-blocker use and adjusted P = 0.016, HR = 1.43 (1.07–1.91) in group without β-blocker in first-stage population; adjusted P = 0.42, HR = 0.85 (0.56–1.28) in group with β-blocker use and adjusted P = 0.015, HR = 1.39 (1.06–1.82) in group without β-blocker in replicated stage. Functional analysis indicated that rs17117699-G allele increased the activity of OMA1 assessed by the ratio of S-OPA1 to L-OPA1 and suppressed cells proliferation under ISO treatment when compared with rs17117699-T allele. Furthermore, OMA1 functioned downstream of β-adrenergic receptor signaling and ISO-induced OPA1 cleavage is dependent on OMA1. Conclusions Our findings demonstrate that rs17117699T>G in OMA1 increases the risk of HF mortality via enhancing its OPA1 cleavage activity. It is a promising potential treatment target for HF. Clinical Trial Registration NCT03461107. https://www.clinicaltrials.gov/ct2/show/NCT03461107'term=03461107&cond=Heart+Failure&cntry=CN&rank=1
      PubDate: 2020-06-01
       
  • Dihydromyricetin Prevents Diabetic Cardiomyopathy via miR-34a Suppression
           by Activating Autophagy
    • Abstract: Purpose The pro-aging miRNA, miR-34a, is hyperactivated in the cardiac myocardial tissues of patients and mice with diabetes, leading to diabetic cardiomyopathy (DCM). Increasing evidence suggests that dihydromyricetin (DHM) can be used to effectively treat cardiomyopathy. In this study, we investigated whether DHM affects the expression of miR-34a in DCM. Methods The expression of miR-34a in high-glucose-induced cardiomyocytes and in the heart tissue of diabetic mice was determined by microRNA isolation and quantitative reverse transcription-polymerase chain reaction. Lipofectamine 3000 was used to transfect cardiomyocytes with miR-34a inhibitor, miR-34a mimics, and miR-control. These agents were intravenously injected into the tail vein of streptozotocin-induced diabetic mice. Autophagy and apoptosis were assessed in high-glucose-induced cardiomyocytes and cardiac tissue in diabetic mice by western blotting, immunofluorescence, Masson staining, hematoxylin and eosin staining (H&E), and electron microscopy. Results DHM clearly ameliorated the cardiac dysfunction in the diabetic mice. The expression of miR-34a was up-regulated in high-glucose-induced cardiomyocytes and in the hearts of diabetic mice, thus impairing autophagy. Treatment with DHM decreased the expression of miR-34a and rescued the impairment of autophagy in high-glucose-induced cardiomyocytes and in the heart tissue of diabetic mice, while the miR-34a mimic offset the effect of DHM with respect to the development of DCM by inhibiting autophagy. Conclusions By decreasing the expression of miR-34a, DHM restores impaired autophagy, and thus ameliorates DCM. Therefore, DHM may potentially be used in the treatment of DCM.
      PubDate: 2020-06-01
       
  • Real-World Dual Antiplatelet Therapy Following Polymer-Free
           Sirolimus-Eluting Stent Implantations to Treat Coronary Artery Disease
    • Abstract: Objectives The objective of this post hoc analysis was to analyze real-world dual antiplatelet therapy (DAPT) regimens following polymer-free sirolimus-eluting stent (PF-SES) implantations in an unselected patient population. Methods Patient-level data from two all-comers observational studies (ClinicalTrials.gov Identifiers: NCT02629575 and NCT02905214) were pooled and analyzed in terms of their primary endpoint. During the data verification process, we observed substantial deviations from DAPT guideline recommendations. To illuminate this gap between clinical practice and guideline recommendations, we conducted a post hoc analysis of DAPT regimens and clinical event rates for which we defined the net adverse event rate (NACE) consisting of target lesion revascularization (TLR, primary endpoint of all-comers observational studies) all-cause death, myocardial infarction (MI), stent thrombosis (ST), and bleeding events. A logistic regression was utilized to determine predictors why ticagrelor was used in stable coronary artery disease (CAD) patients instead of the guideline-recommended clopidogrel. Results For stable CAD, the composite endpoint of clinical, bleeding, and stent thrombosis, i.e., NACE, between the clopidogrel and ticagrelor treatment groups was not different (5.4% vs. 5.1%, p = 0.745). Likewise, in the acute coronary syndrome (ACS) cohort, the NACE rates were not different between both DAPT strategies (9.2% vs. 9.3%, p = 0.927). There were also no differences in the accumulated rates for TLR, myocardial infarction ([MI], mortality, bleeding events, and stent thrombosis in elective and ACS patients. The main predictors for ticagrelor use in stable CAD patients were age < 65 years, smaller vessels, treatment of ostial and calcified lesions, and in-stent restenosis. Conclusion Within the framework of a post hoc analysis based on a real-world, large cohort study, there were no differences in the combined endpoint of major adverse cardiac events (MACE), bleeding and thrombotic events for clopidogrel and ticagrelor in stable CAD or ACS patients. Despite the recommendation for clopidogrel by the European Society of Cardiology (ESC), real-world ticagrelor use was observed in subgroups of stable CAD patients that ought to be explored in future trials.
      PubDate: 2020-06-01
       
  • Cardiac Cyclic Nucleotide Phosphodiesterases: Roles and Therapeutic
           Potential in Heart Failure
    • Abstract: Abstract The cyclic nucleotides cyclic adenosine-3′,5′-monophosphate (cAMP) and cyclic guanosine-3′,5′-monophosphate (cGMP) maintain physiological cardiac contractility and integrity. Cyclic nucleotide–hydrolysing phosphodiesterases (PDEs) are the prime regulators of cAMP and cGMP signalling in the heart. During heart failure (HF), the expression and activity of multiple PDEs are altered, which disrupt cyclic nucleotide levels and promote cardiac dysfunction. Given that the morbidity and mortality associated with HF are extremely high, novel therapies are urgently needed. Herein, the role of PDEs in HF pathophysiology and their therapeutic potential is reviewed. Attention is given to PDEs 1–5, and other PDEs are briefly considered. After assessing the role of each PDE in cardiac physiology, the evidence from pre-clinical models and patients that altered PDE signalling contributes to the HF phenotype is examined. The potential of pharmacologically harnessing PDEs for therapeutic gain is considered.
      PubDate: 2020-06-01
       
  • Effects of Sodium–Glucose Co-transporter 2 Inhibition with Empaglifozin
           on Renal Structure and Function in Non-diabetic Rats with Left Ventricular
           Dysfunction After Myocardial Infarction
    • Abstract: Background The use of sodium–glucose co-transporter 2 inhibitors (SGLT2i) is currently expanding to cardiovascular risk reduction in non-diabetic subjects, but renal (side-)effects are less well studied in this setting. Methods Male non-diabetic Sprague Dawley rats underwent permanent coronary artery ligation to induce MI, or sham surgery. Rats received chow containing empagliflozin (EMPA) (30 mg/kg/day) or control chow. Renal function and electrolyte balance were measured in metabolic cages. Histological and molecular markers of kidney injury, parameters of phosphate homeostasis and bone resorption were also assessed. Results EMPA resulted in a twofold increase in diuresis, without evidence for plasma volume contraction or impediments in renal function in both sham and MI animals. EMPA increased plasma magnesium levels, while the levels of glucose and other major electrolytes were comparable among the groups. Urinary protein excretion was similar in all treatment groups and no histomorphological alterations were identified in the kidney. Accordingly, molecular markers for cellular injury, fibrosis, inflammation and oxidative stress in renal tissue were comparable between groups. EMPA resulted in a slight increase in circulating phosphate and PTH levels without activating FGF23–Klotho axis in the kidney and bone mineral resorption, measured with CTX-1, was not increased. Conclusions EMPA exerts profound diuretic effects without compromising renal structure and function or causing significant electrolyte imbalance in a non-diabetic setting. The slight increase in circulating phosphate and PTH after EMPA treatment was not associated with evidence for increased bone mineral resorption suggesting that EMPA does not affect bone health.
      PubDate: 2020-06-01
       
  • Phase 3 Multicenter Study of Revusiran in Patients with Hereditary
           Transthyretin-Mediated (hATTR) Amyloidosis with Cardiomyopathy (ENDEAVOUR)
           
    • Abstract: Purpose The Phase 3 ENDEAVOUR study evaluated revusiran, an investigational RNA interference therapeutic targeting hepatic transthyretin (TTR) production, for treating cardiomyopathy caused by hereditary transthyretin-mediated (hATTR) amyloidosis. Methods Patients with hATTR amyloidosis with cardiomyopathy were randomized 2:1 to receive subcutaneous daily revusiran 500 mg (n = 140) or placebo (n = 66) for 5 days over a week followed by weekly doses. Co-primary endpoints were 6-min walk test distance and serum TTR reduction. Results Revusiran treatment was stopped after a median of 6.71 months; the study Sponsor prematurely discontinued dosing due to an observed mortality imbalance between treatment arms. Eighteen (12.9%) patients on revusiran and 2 (3.0%) on placebo died during the on-treatment period. Most deaths in both treatment arms were adjudicated as cardiovascular due to heart failure (HF), consistent with the natural history of the disease. A post hoc safety investigation of patients treated with revusiran found that, at baseline, a greater proportion of those who died were ≥ 75 years and showed clinical evidence of more advanced HF compared with those who were alive throughout treatment. Revusiran pharmacokinetic exposures and TTR lowering did not show meaningful differences between patients who died and who were alive. Revusiran did not deleteriously affect echocardiographic parameters, cardiac biomarkers, or frequency of cardiovascular and HF hospitalization events. Conclusions Causes for the observed mortality imbalance associated with revusiran were thoroughly investigated and no clear causative mechanism could be identified. Although the results suggest similar progression of cardiac parameters in both treatment arms, a role for revusiran cannot be excluded. Clinical Trial Registration NCT02319005.
      PubDate: 2020-06-01
       
  • Beneficial Effect of Flecainide Controlled Release on the Quality of Life
           of Patients with Atrial Fibrillation—the REFLEC-CR Study
    • Abstract: Purpose Atrial fibrillation (AF) is the most common cardiac arrhythmia with a considerable impact on patients’ quality of life (QoL). Methods This prospective, multicenter, observational study aimed to evaluate the effect of oral treatment with controlled-release (CR) flecainide on AF patients’ QoL and treatment compliance during a 12-week period. A total of 70 sites enrolled consecutive patients with paroxysmal (PAF) or persistent AF (PerAF), treated with flecainide CR in the context of a rhythm control strategy. The effect on QoL was assessed by the Canadian Cardiovascular Society Severity of Atrial Fibrillation scale (CCS-SAF). Results In total, 679 patients (53.2% females, 66 ± 11.7 years, 86.9% PAF) were included. Prior antiarrhythmic medication had been administered in 43.8% of patients. A daily dose of 200 mg was administered to 66.4% of patients by the end of study. Flecainide CR resulted in a significant reduction in the CCS-SAF score (mean (SD)) at the end of the study as compared with baseline (1.32 (0.57) vs 1.64 (0.73), p < 0.0001). Flecainide CR significantly reduced the CCS-SAF score both in PAF (1.27 (0.52) vs 1.61 (0.72), p < 0.0001) as well as in PerAF (1.63(0.77) vs 1.84(0.81), p = 0.017). Overall, 4 (0.6%) patients experienced a total of 6 adverse events during the study period. The compliance to flecainide CR treatment was very high with 93.6% of patients responding that they had not missed any dose during the study period. Conclusion Treatment with flecainide CR significantly improves QoL in both paroxysmal as well as persistent AF patients, with an excellent safety profile and associated patient compliance.
      PubDate: 2020-06-01
       
  • Interrupted or Uninterrupted Oral Anticoagulants in Patients Undergoing
           Atrial Fibrillation Ablation
    • Abstract: Background and Purpose The safety and efficacy of uninterrupted, minimally interrupted (one dose skipped) or completely interrupted (24 h skipped) oral anticoagulant therapy in patients with atrial fibrillation (AF) ablation are poorly defined. We conducted a network meta-analysis to explore the effect of interrupted or uninterrupted oral anticoagulants in patients with AF undergoing ablation. Methods The Cochrane Library, PubMed and Embase databases were systematically searched for studies comparing uninterrupted, minimally interrupted or completely interrupted non-vitamin K antagonist oral anticoagulants (NOACs) with continuous or interrupted warfarin in patients undergoing AF ablation. Results Twelve randomized clinical trials (RCTs) with a total of 5597 patients with AF undergoing catheter ablation were included. For thromboembolism, minimally interrupted NOACs (OR 0.03, 95% CI 0.01–0.35), uninterrupted NOACs (OR 0.04, 95% CI 0.01–0.23) and continuous VKAs (OR 0.05, 95% CI 0.01–0.21) were better than interrupted warfarin. The risk of total bleeding appeared higher in the completely interrupted NOAC group compared with the minimally interrupted NOACs (OR 2.74, 95% CI 1.18–6.37), uninterrupted NOACs (OR 2.15, 95% CI 1.05–4.38) and uninterrupted warfarin (OR 2.04, 95% CI 1.02–4.08). To reduce the risk of total bleeding, minimally interrupted NOACs (OR 0.15, 95% CI 0.08–0.27), uninterrupted NOACs (OR 0.19, 95% CI 0.14–0.42) and uninterrupted warfarin (OR 0.24, 95% CI 0.15–0.39) were better than interrupted warfarin. In the event of major bleeding, there was no significant difference in the interrupted NOAC, uninterrupted NOAC, interrupted VKA and uninterrupted VKA groups. Conclusions These three NOAC strategies may have similar safety and efficacy in terms of thromboembolism and major bleeding complications. The total bleeding risk of completely interrupted oral anticoagulants is higher than that of uninterrupted and minimally interrupted NOACs. For thromboembolism, minimally interrupted NOACs, uninterrupted NOACs and continuous VKAs were better than interrupted warfarin.
      PubDate: 2020-06-01
       
  • Non-Vitamin K Antagonist Oral Anticoagulants Versus Warfarin in Patients
           with Atrial Fibrillation and Peripheral Artery Disease: a Systematic
           Review and Meta-Analysis
    • Abstract: Background The efficacy and safety of non-vitamin K antagonist oral anticoagulants (NOACs) compared with warfarin in patients with atrial fibrillation (AF) and peripheral artery disease (PAD) remain largely unknown. Therefore, we conducted a meta-analysis to explore the effects of NOACs versus warfarin in this population. Methods We systematically searched the PubMed and Embase databases, with no linguistic restrictions, until December 2019 for relevant randomized controlled trials (RCTs) and observational studies. A random-effects model using an inverse variance method was selected to pool the risk ratios (RRs) and 95% confidence intervals (CIs). Results A total of six studies (three post hoc analyses of RCTs and three cohort studies) were included in this meta-analysis. Among AF patients treated with NOACs and warfarin, individuals with PAD had increased rates of all-cause death (RR = 1.26, 95% CI 1.07–1.48) and cardiovascular death (RR = 1.32, 95% CI 1.06–1.64) compared with those without PAD. In AF patients with PAD, we observed a similar risk of thromboembolic events, bleeding, and death with NOACs as with warfarin. In addition, there were no interactions between PAD and non-PAD subgroups regarding any of the reported outcomes of NOACs versus warfarin in AF patients (all Pinteraction > 0.05). Conclusions Based on current evidence, AF patients with PAD are at a higher risk of death than those without PAD. Efficacy and safety outcomes with NOACs are comparable to those with warfarin, suggesting that the use of NOACs has effects similar to warfarin in AF patients with concomitant PAD.
      PubDate: 2020-06-01
       
  • Exendin-4 Attenuates Remodeling in the Remote Myocardium of Rats After an
           Acute Myocardial Infarction by Activating β-Arrestin-2, Protein
           Phosphatase 2A, and Glycogen Synthase Kinase-3 and Inhibiting β-Catenin
    • Abstract: Purpose This study tested if the protective anti-remodeling effect of GLP-1 agonist Exendin-4 after an acute myocardial infarction (MI) in rats involves inhibition of the Wnt1/β-catenin signaling pathway. Methods Rats were divided into sham, sham + Exendin-4 (10 μg/day, i.p), MI, and MI + Exendin-4. MI was introduced to rats by permanent left anterior descending coronary artery (LAD) ligation. Results On day 7 post-infraction, MI rats showed LV dysfunction with higher serum levels of cardiac markers. Their remote myocardia showed increased mRNA and protein levels of collagen I/III with higher levels of reactive oxygen species (ROS) and inflammatory cytokines, as well as protein levels of Wnt1, phospho-Akt, transforming growth factor (TGF-β1), Smad, phospho-Smad3, α-SMA, caspase-3, and Bax. They also showed higher protein levels of phospho-glycogen synthase kinase-3β (p-GSK3β), as well as total, phosphorylated, and nuclear β-catenin with a concomitant decrease in the levels of cyclic adenosine monophosphate (cAMP), mRNA of manganese superoxide dismutase (MnSOD), and protein levels of Bcl-2, β-arrestin-2, and protein phosphatase-2 (PP2A). Administration of Exendin-4 to MI rats reduced the infarct size and reversed the aforementioned signaling molecules without altering protein levels of TGF-1β and Wnt1 or Akt activation. Interestingly, Exendin-4 increased mRNA levels of MnSOD, protein levels of β-arrestin-2 and PP2A, and β-catenin phosphorylation but reduced the phosphorylation of GSK3β and Smad3, and total β-catenin levels in the LV of control rats. Conclusion Exendin-4 inhibits the remodeling in the remote myocardium of rats following acute MI by attenuating β-catenin activation and activating β-arrestin-2, PP2A, and GSK3β. Graphical A graphical abstract that illustrates the mechanisms by which Exendin-4 inhibits cardiac remodeling in remote myocardium of left ventricle MI-induced rats. Mechanisms are assumed to occur in the cardiomyocytes and/or other resident cells such as fibroblast. Β-catenin activation and nuclear translocation are associated with increased synthesis of inflammatory cytokines and transforming growth factor β-1 (TGF-β1). GSK3β is inhibited by phosphorylation at Ser9. Under normal conditions, β-catenin is degraded in the cytoplasm by the active GSK3β-dependent degradation complex (un-phosphorylated) which usually phosphorylates β-catenin at Ser33/37/Thr41. After MI, TGF-β1, and Wnt 1 levels are significantly increased, the overproduction of Wnt1 induces β-catenin stabilization and nuclear translocation through increasing the phosphorylation of disheveled (DVL) protein which in turn phosphorylates and inhibits GSK3β. TGF-β1 stimulates the phosphorylation of Smad-3 and subsequent nuclear translocation to activate the transcription of collage 1/III and α-smooth muscle actin (α-SMA). Besides, TGF-β1 stabilizes cytoplasmic β-catenin levels indirectly by phosphorylation of Akt at Thr308-induced inhibition of GSK3β by increasing phosphorylation of Ser9. Exendin-4, and possibly through G protein-coupled receptors (GPCRs), increases levels of cAMP and upregulates β-arrestin-2 levels. Both can result in a positive inotropic effect. Besides, β-arrestin-2 can stimulate PP2A to dephosphorylation Smad3 (inhibition) and GSK3β (activation), thus reduces fibrosis and prevents the activation of β-catenin and collagen deposition.
      PubDate: 2020-05-30
       
  • Tailoring Dual Antiplatelet Therapy for the Complex PCI Patient: Current
           Status and Perspectives
    • Abstract: Abstract Dual antiplatelet therapy (DAPT) duration in patients undergoing percutaneous coronary intervention (PCI) has long been considered a matter of controversy. Complex-PCI (C-PCI) is considered to be associated with an increased ischemic risk that tends to be greater with progressively higher procedural complexity. Thus, with a view to balance ischemic versus bleeding risks, high complexity of PCI intuitively represents an advocate of prolonged DAPT duration. However, the optimal DAPT strategy in this high ischemic risk subset of patients remains unclear, a fact that is exacerbated by the absence of a universal definition of C-PCI, resulting in a significant between-study heterogeneity. The aim of this review is to highlight the increased risks associated with C-PCI, compare long- versus short-term DAPT regimens regarding safety and efficacy endpoints as well as investigate outcomes in special C-PCI cohorts, such as patients with bifurcation, left main or chronic total occlusion lesions. Furthermore, controversial issues, such as antithrombotic regimens in C-PCI patients with atrial fibrillation, and future perspectives are addressed.
      PubDate: 2020-05-29
       
  • CD38: A Potential Therapeutic Target in Cardiovascular Disease
    • Abstract: Abstract Substantial research has demonstrated the association between cardiovascular disease and the dysregulation of intracellular calcium, ageing, reduction in nicotinamide adenine dinucleotide NAD+ content, and decrease in sirtuin activity. CD38, which comprises the soluble type, type II, and type III, is the main NADase in mammals. This molecule catalyses the production of cyclic adenosine diphosphate ribose (cADPR), nicotinic acid adenine dinucleotide phosphate (NAADP), and adenosine diphosphate ribose (ADPR), which stimulate the release of Ca2+, accompanied by NAD+ consumption and decreased sirtuin activity. Therefore, the relationship between cardiovascular disease and CD38 has been attracting increased attention. In this review, we summarize the structure, regulation, function, targeted drug development, and current research on CD38 in the cardiac context. More importantly, we provide original views about the as yet elusive mechanisms of CD38 action in certain cardiovascular disease models. Based on our review, we predict that CD38 may serve as a novel therapeutic target in cardiovascular disease in the future.
      PubDate: 2020-05-29
       
  • Attenuation of atrial remodeling by aliskiren via affecting oxidative
           stress, inflammation and PI3K/Akt signaling pathway
    • Abstract: Introduction Atrial fibrillation (AF) is the most common type of arrhythmia. Atrial remodeling is a major factor to the AF substrate. The purpose of the study is to explore whether aliskiren (ALS) has a cardioprotective effect and its potential molecular mechanisms on atrial remodeling. Methods In acute experiments, dogs were randomly assigned to Sham, Paced and Paced+aliskiren (10 mg kg−1) (Paced+ALS) groups, with 7 dogs in each group. Rapid atrial pacing (RAP) was maintained at 600 bpm for 2 h for paced and Paced+ALS groups and atrial effective refractory periods (AERPs), inducibility of AF (AFi) and average duration time (ADT) were measured. In chronic experiments, there were 5 groups: Sham, Sham+ALS, Paced, Paced+ALS and Paced+ALS+PI3K antagonist wortmannin (WM) (70 μg kg−1 day−1). RAP at 500 beats/min was maintained for 2 weeks. Inflammation and oxidative stress indicators were measured by ELISA assay, echocardiogram and pathology were used to assess atrial structural remodeling, phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathways were studied by RT-PCR and western blotting to evaluate whether the cardioprotective effect of ALS works through PI3K/Akt signaling pathway. Results The electrophysiological changes were observed after 2-h pacing. The AERP shortened with increased AFi and ADT, which was attenuated by ALS (P < 0.05). After pacing for 2 weeks, oxidative stress and inflammation markers in the Paced group were significantly higher than those in the Sham group (P < 0.01) and were reduced by ALS treatment (P < 0.01). The reduced level of antioxidant enzymes caused by RAP was also found to be elevated in ALS-treated group (P < 0.01). The results of pathology and echocardiography showed that RAP can cause atrial enlargement, fibrosis (P < 0.01), and were attenuated in ALS treatment group. The PI3K/Akt signaling pathway were downregulated induced by RAP. ALS could upregulate the PI3K/Akt pathway expression (P < 0.05). Furthermore, the cardioprotective effects in structural remodeling of ALS were suppressed by WM. Conclusions ALS may offer cardioprotection in RAP-induced atrial remodeling, which may partly be ascribed to its anti-inflammatory and anti-oxidative stress action and the regulation of PI3K/Akt signaling pathway.
      PubDate: 2020-05-27
       
  • Factor Xa Inhibition with Apixaban Does Not Influence Cardiac Remodelling
           in Rats with Heart Failure After Myocardial Infarction
    • Abstract: Background Heart failure (HF) is considered to be a prothrombotic condition and it has been suggested that coagulation factors contribute to maladaptive cardiac remodelling via activation of the protease-activated receptor 1 (PAR1). We tested the hypothesis that anticoagulation with the factor Xa (FXa) inhibitor apixaban would ameliorate cardiac remodelling in rats with HF after myocardial infarction (MI). Methods and Results Male Sprague-Dawley rats were either subjected to permanent ligation of the left ascending coronary artery (MI) or sham surgery. The MI and sham animals were randomly allocated to treatment with placebo or apixaban in the chow (150 mg/kg/day), starting 2 weeks after surgery. Cardiac function was assessed using echocardiography and histological and molecular markers of cardiac hypertrophy were assessed in the left ventricle (LV). Apixaban resulted in a fivefold increase in anti-FXa activity compared with vehicle, but no overt bleeding was observed and haematocrit levels remained similar in apixaban- and vehicle-treated groups. After 10 weeks of treatment, LV ejection fraction was 42 ± 3% in the MI group treated with apixaban and 37 ± 2 in the vehicle-treated MI group (p > 0.05). Both vehicle- and apixaban-treated MI groups also displayed similar degrees of LV dilatation, LV hypertrophy and interstitial fibrosis. Histological and molecular markers for pathological remodelling were also comparable between groups, as was the activity of signalling pathways downstream of the PAR1 receptor. Conclusion FXa inhibition with apixaban does not influence pathological cardiac remodelling after MI. These data do not support the use of FXa inhibitor in HF patients with the aim to amend the severity of HF. Graphical
      PubDate: 2020-05-26
       
  • A TOR2A Gene Product: Salusin-β Contributes to Attenuated Vasodilatation
           of Spontaneously Hypertensive Rats
    • Abstract: Purpose Attenuated vasodilatation of small arteries is a hallmark feature of hypertension. Salusin-β, which is a TOR2A gene product and an important vasoactive peptide, has a close relationship with cardiovascular disease. This study aimed to determinate the roles of salusin-β in vasodilatation, and its signal pathways in Wistar–Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Methods Isometric tension experiments were performed. Vasodilatation was induced by acetylcholine (ACh) or sodium nitroprusside (SNP). Results Plasma salusin-β levels and their protein expressions in coronary artery (CA), mesenteric artery (MA), and pulmonary artery (PA) of SHR were much higher than that of WKY. Intravenous injection of salusin-β increased arterial blood pressure in SHR, while anti-salusin-β IgG decreased it. Salusin-β further deteriorated, while anti-salusin-β IgG improved, the attenuated ACh-induced relaxation, the decreased nitric oxide (NO) level, and endothelial nitric oxide synthase (eNOS) activity in arteries of SHR, and salusin-β had no significant effect on SNP-induced relaxation. The NAD(P)H oxidase activity and reactive oxygen species (ROS) level in arteries of SHR were much higher than that of WKY, which was further increased by salusin-β but reduced by anti-salusin-β IgG. ROS scavenger NAC or antioxidant apocynin significantly inhibited, while SOD inhibitor DETC aggravated, the effects of salusin-β, and the eNOS inhibitor L-NAME inhibited the effects of anti-salusin-β IgG. Conclusions These results indicated that enhanced salusin-β activity is involved in attenuated endothelium-dependent vasodilatation pathogenesis in SHR by activating NAD(P)H oxidase derived ROS generation and inhibiting eNOS activation and NO release.
      PubDate: 2020-05-26
       
  • Sodium-Glucose Co-transporter 2 Inhibitors in the Failing Heart: a Growing
           Potential
    • Abstract: Abstract Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are a new drug class designed to treat patients with type 2 diabetes (T2D). However, cardiovascular outcome trials showed that SGLT2i also offer protection against heart failure (HF)–related events and cardiovascular mortality. These benefits appear to be independent of glycaemic control and have recently been demonstrated in the HF population with reduced ejection fraction (HFrEF), with or without T2D. This comprehensive, evidence-based review focuses on the published studies concerning HF outcomes with SGLT2i, discussing issues that may underlie the different results, along with the impact of these new drugs in clinical practice. The potential translational mechanisms behind SGLT2i cardio-renal benefits and the information that ongoing studies may add to the already existing body of evidence are also reviewed. Finally, we focus on practical management issues regarding SGLT2i use in association with other T2D and HFrEF common pharmacological therapies. Safety considerations are also highlighted. Considering the paradigm shift in T2D management, from a focus on glycaemic control to a broader approach on cardiovascular protection and event reduction, including the potential for wide SGLT2i implementation in HF patients, with or without T2D, we are facing a promising time for major changes in the global management of cardiovascular disease.
      PubDate: 2020-04-30
       
  • Ibutilide Reduces Ventricular Defibrillation Threshold and Organizes
           Ventricular Fibrillation Activation in Canine Heart Failure Model
    • Abstract: Purpose To compare the effects of class III antiarrhythmic agents (amiodarone vs. ibutilide) on ventricular fibrillation (VF) and hemodynamic status in a canine heart failure (HF) model. Methods A total of 12 beagles were used to establish the HF model by rapid pacing for 4 consecutive weeks. These canines were randomly divided into two groups based on the administration of ibutilide and amiodarone. A 12 × 12 unipolar electrode plaque was used for ventricular epicardial mapping, and a 6-electrode plunge needle was inserted for ventricular transmural mapping. The restitution curve was estimated from activation recovery intervals (ARIs) by pacing from the plaque electrodes before and after drug administration. The defibrillation threshold (DFT) and VF activation patterns, including the activation rate, cycle length (VF-CL) and the transmural dispersion of the activation rate, were evaluated and the hemodynamic parameters were mearsured and compared before and after drug administration. Results Compared to HF baseline, ibutilide administration has markedly decreased the DFT by 28% (18 ± 2 J vs. 13 ± 2.7 J, P < 0.01) without affecting the canine’s hemodynamics (mean arterial pressure 91 ± 15 mmHg vs. 92 ± 17 mmHg, P > 0.05). Furthermore, VF activation pattern became more organized, and spontaneous termination was observed only after ibutilide administration. Conversely, amiodarone has significantly compromised the hemodynamic status (mean arterial pressure 92 ± 6.1 mmHg vs. 52 ± 11.6 mmHg, P < 0.05), but did not alter the DFT (17 ± 2.3 J vs. 16 ± 2.0 J, P > 0.05). Compared to pre-medication, both ibutilide and amiodarone have significantly prolonged the VERP (178 ± 9.6 ms vs. 208 ± 8.9 ms, P < 0.05; 185 ± 10.5 ms vs. 202 ± 7.5 ms, P < 0.05, respectively) and reduced the dispersion of refractoriness, the maximal slope of restitution curve, and the epicardial dispersion during pacing. Additionally, both drugs have significantly increased the VF-CL and reduced the transmural dispersion of the VF activation rate. Conclusions Ibutilide had potential antifibrillatory properties, which was shown by decreasing the DFT and organizing the VF activation in HF, and with no apparent impact on the hemodynamic status. In contrast, intravenous amiodarone administration demonstrated prominent negative effects on the hemodynamic status possibly by affecting the myocardial contractility before and after defibrillation but did not alter the DFT.
      PubDate: 2020-04-15
       
 
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