Subjects -> MEDICAL SCIENCES (Total: 8665 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: 59)
American Journal of Cardiology     Hybrid Journal   (Followers: 67)
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: 33)
Artery Research     Hybrid Journal   (Followers: 4)
ARYA Atherosclerosis     Open Access  
ASAIO Journal     Hybrid Journal   (Followers: 4)
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: 9)
BMC Cardiovascular Disorders     Open Access   (Followers: 22)
Brain Circulation     Open Access   (Followers: 1)
British Journal of Cardiology     Full-text available via subscription   (Followers: 17)
Canadian Journal of Cardiology     Hybrid Journal   (Followers: 17)
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: 19)
Cardiology and Angiology: An International Journal     Open Access   (Followers: 1)
Cardiology and Therapy     Open Access   (Followers: 11)
Cardiology Clinics     Full-text available via subscription   (Followers: 13)
Cardiology in Review     Hybrid Journal   (Followers: 8)
Cardiology in the Young     Hybrid Journal   (Followers: 34)
Cardiology Journal     Open Access   (Followers: 5)
Cardiology Plus     Open Access   (Followers: 1)
Cardiology Research     Open Access   (Followers: 14)
Cardiology Research and Practice     Open Access   (Followers: 10)
Cardiopulmonary Physical Therapy Journal     Hybrid Journal   (Followers: 9)
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: 35)
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: 10)
Clinical Hypertension     Open Access   (Followers: 5)
Clinical Medicine Insights : Cardiology     Open Access   (Followers: 6)
Clinical Research in Cardiology     Hybrid Journal   (Followers: 5)
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: 3)
CorSalud     Open Access  
Critical Pathways in Cardiology     Hybrid Journal   (Followers: 5)
Current Cardiology Reports     Hybrid Journal   (Followers: 6)
Current Cardiology Reviews     Hybrid Journal   (Followers: 3)
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: 13)
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: 1)
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: 67)
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: 7)
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: 13)
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: 5)
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: 2)
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: 17)
International Journal of Cardiology Hypertension     Open Access   (Followers: 1)
International Journal of Cardiovascular and Cerebrovascular Disease     Open Access   (Followers: 3)
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 Toxicology
Journal Prestige (SJR): 0.836
Citation Impact (citeScore): 2
Number of Followers: 6  
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1559-0259 - ISSN (Online) 1530-7905
Published by Springer-Verlag Homepage  [2626 journals]
  • Rho Kinase Inhibition by Fasudil Attenuates Adriamycin-Induced Chronic
           Heart Injury
    • Abstract: Abstract Adriamycin (ADR)-induced chronic heart injury (CHI) is a serious complication of chemotherapy. The present study was designed to assess the ability of fasudil, a Rho kinase inhibitor, to prevent ADR-induced CHI. Forty male 6-week-old C57BL6 mice were randomly divided into the following four groups: (1) control group, (2) CHI induced by adriamycin (ADR group), (3) CHI plus low dose fasudil (ADR + L group), and (4) CHI plus high dose fasudil (ADR + H group). Animals from groups 2–4 received ADR (2.5 mg/kg, i.p.) once a week for 8 weeks, and the control group received saline. Meanwhile, the animals in groups 3–4 received 2 mg/kg/day or 10 mg/kg/day fasudil, respectively. After measurement of cardiac functions, blood samples were collected for biochemical assays. The hearts were excised for histological, immunohistochemistry and western blot study, respectively. Adriamycin produced evident cardiac damage revealed by cardiac functions changes: decreased left ventricular fractional shortening (FS), left ventricular ejection fraction (EF), increased left ventricular volume, cardiac injury marker changes (increased creatine kinase, lactate dehydrogenase), antioxidant enzymes activity changes (decreased superoxide dismutase), and lipid peroxidation (elevated malondialdehyde) to the control group. Fasudil treatment notably ameliorated ADR-induced cardiac damage, restored heart function, suppressed cell apoptosis and senescence, ameliorated redox imbalance, and DNA damage. Fasudil has a protective effect on ADR-induced chronic heart injury, which partially attributed to its antioxidant, anti-apoptotic effects of inhibiting the RhoA/Rho kinase (ROCK) signaling pathway.
      PubDate: 2020-08-01
  • Cardioprotective Effect of Paricalcitol on Amitriptyline-Induced
           Cardiotoxicity in Rats: Comparison of [ 99m Tc]PYP Cardiac Scintigraphy
           with Electrocardiographic and Biochemical Findings
    • Abstract: Abstract Taking an overdose of AMT, a commonly prescribed tricyclic antidepressant drug, has an increased risk of sudden cardiac death. The cardiotoxicity of amitriptyline (AMT) is a commonly observed toxicity with high morbidity and mortality rates in emergency departments (ED). Nevertheless, there are still no effective treatment options for AMT-induced cardiotoxicity. The aim of the present study was to evaluate the effects of paricalcitol (PRC), a Vitamin D receptor agonist, using electrocardiographic (ECG), biochemical, and scintigraphic methods. Twenty-eight male Wistar rats were randomly divided into four groups: untreated control (CON), amitriptyline-induced cardiotoxicity (AMT), paricalcitol (PRC), and amitriptyline + paricalcitol (AMT + PRC). Cardiotoxicity was induced by intraperitoneal (i.p) injection of a single-dose AMT (100 mg/kg). PRC was administered as 10 μg/kg (i.p.) after the injection of AMT. We examined ECG, biochemical, and scintigraphic results of PRC administration on AMT-induced changes. Cardiotoxicity of AMT was characterized by conduction abnormalities (increased QRS complex, T wave, and QT interval duration and elevation of ST segment amplitude), elevated 99mTechnetium Pyrophosphate ([99mTc]PYP) uptake, and increased cardiac troponin T (cTnT) levels. Treatment with PRC significantly decreased all AMT-associated conduction abnormalities in ECG (p < 0.001), and decreased [99mTc]PYP uptake (p < 0.001) and serum cTnT level (p < 0.001). The present study indicated that the vitamin D receptor agonist paricalcitol could decrease the AMT-induced cardiotoxicity. This suggests [99mTc]PYP as a non-invasive method for the evaluation of myocardial injury induced by AMT. According to the results of the present study, PRC has beneficial effects on AMT-induced cardiotoxicity.
      PubDate: 2020-08-01
  • Human Amnion Membrane Proteins Prevent Doxorubicin-Induced Oxidative
           Stress Injury and Apoptosis in Rat H9c2 Cardiomyocytes
    • Abstract: Abstract Doxorubicin (DOX) is widely used as an effective chemotherapy agent in cancer treatment. Cardiac toxicity in cancer treatment with DOX demand urgent attention and no effective treatment has been established for DOX-induced cardiomyopathy. It has been well documented that human amniotic membrane proteins (AMPs), extracted from amnion membrane (AM), have antioxidant, anti-apoptotic, and cytoprotective properties. Therefore, in this study, we aimed to investigate the protective effects of AMPs against cardiotoxicity induced by DOX in cultured rat cardiomyocyte cells (H9c2). DOX-induced cell injury was evaluated using multi-parametric assay including thiazolyl blue tetrazolium bromide (MTT), the release of lactic dehydrogenase (LDH), intracellular Ca2+ , reactive oxygen species (ROS) levels, cellular antioxidant status, mitochondrial membrane potential (ΔΨm), malondialdehyde (MDA), and NF-κB p65 DNA-binding activity. Moreover, expression profiling of apoptosis-related genes (P53, Bcl-2, and Bax) and Annexin V by flow cytometry were used for cell apoptosis detection. It was shown that AMPs pretreatment inhibited the cell toxicity induced by DOX. AMPs effectively attenuated the increased levels of LDH, Ca2+ , ROS, and MDA and also simultaneously elevated the ΔΨm and antioxidant status such as superoxide dismutase (SOD) and Catalase (CAT) in pretreated H9c2 cardiomyocytes. Besides, the activity of NF-kB p65 was reduced and the p53 and Bax protein levels were inhibited in these myocardial cells subjected to DOX. These findings provide the first evidence that AMPs potently suppressed DOX-induced toxicity in cardiomyocytes through inhibition of oxidative stress and apoptosis. Thus, AMPs can be a potential therapeutic agent against DOX cardiotoxicity.
      PubDate: 2020-08-01
  • Various Manifestations of 5-Fluorouracil Cardiotoxicity: A Multicenter
           Case Series and Review of Literature
    • Abstract: Abstract 5-Fluorouracil is a key element to the treatment of colon cancer. But it is also one of the most cardiotoxic chemotherapies, and the management of those that experience cardiotoxicity can be challenging. We present three cases of 5-FU cardiac toxicity that manifested as myocardial infarction, cardiogenic shock, and ventricular fibrillation. Additionally, we discuss the current literature regarding 5-fluorouracil cardiotoxicity mechanisms as well as management.
      PubDate: 2020-08-01
  • Exendin-4 Ameliorates Cardiac Remodeling in Experimentally Induced
           Myocardial Infarction in Rats by Inhibiting PARP1/NF-κB Axis in A
           SIRT1-Dependent Mechanism
    • Abstract: Abstract Sirt1 is a potent inhibitor of both poly(ADP-ribose) polymerases1 (PARP1) and NF-kB. This study investigated the cardioprotective effect of exendin-4 on cardiac function and remodeling in rats after an expreimentally-induced myocardial infarction (MI) and explored if this protection involves SIRT1/PARP1 axis. Rats were divided into five groups (n = 10/each): sham, sham + exendin-4 (25 nmol/kg/day i.p.), MI (induced by LAD occlusion), MI + exendin-4, and sham + exendin-4 + EX527 (5 mg/2×/week) (a SIRT1 inhibitor). All treatments were given for 6 weeks post the induction of MI. In sham-operated and MI-induced rats, exendin-4 significantly upregulated Bcl-2 levels, enhanced activity, mRNA, and levels of SIRT1, inhibited activity, mRNA, and levels of PARP1, and reduced ROS generation and PARP1 acetylation. In MI-treated rats, these effects were associated with improved cardiac architectures and LV function, reduced collagen deposition, and reduced mRNA and total levels of TNF-α and IL-6, as well as, the activation of NF-κB p65. In addition, exendin-4 inhibited the interaction of PARP1 with p300, TGF-β1, Smad3, and NF-κB p65 and signficantly reduced mRNA and protein levels of collagen I/III and protein levels of MMP2/9. In conclusion, exendin-4 is a potent cardioprotective agent that prevents post-MI inflammation and cardiac remodeling by activating SIRT1-induced inhibition of PARP1.
      PubDate: 2020-08-01
  • Mechanisms of the Cardiac Myocyte-Damaging Effects of Dasatinib
    • Abstract: Abstract The anticancer drug dasatinib (Sprycel) is a BCR-ABL1-targeted tyrosine kinase inhibitor used in treating chronic myelogenous leukemia that has been shown in clinical trials to display cardiovascular toxicities. While dasatinib potently inhibits BCR-ABL1, it is not a highly selective kinase inhibitor and may have off-target effects. A neonatal rat cardiac myocyte model was used to investigate potential mechanisms by which dasatinib damaged myocytes. The anthracycline cardioprotective drug dexrazoxane was shown to be ineffective in preventing dasatinib-induced myocyte damage. Dasatinib treatment increased doxorubicin accumulation in myocytes and doxorubicin-induced myocyte damage, likely through its ability to bind to one or more ABC-type efflux transporters. Dasatinib induced myocyte damage either after a brief treatment that mimicked the clinical situation, or more potently after continuous treatment. Dasatinib slightly induced apoptosis in myocytes as evidenced by increases in caspase-3/7 activity. Dasatinib treatment reduced pERK levels in myocytes most likely through inhibition of RAF, which dasatinib strongly inhibits. Thus, inhibition of the RAF/MEK/ERK pro-survival pathway in the heart may be, in part, a mechanism by which dasatinib induces cardiovascular toxicity.
      PubDate: 2020-08-01
  • Electropharmacological Characterization of Aciclovir in the
           Halothane-Anesthetized Dogs: A Proposal of Evaluation Method for
           Cardiovascular Safety Pharmacology of Anti-virus Drugs
    • Abstract: Abstract Given limited information regarding the pathophysiology underlying aciclovir-associated, clinically observed cardiovascular adverse events including chest pain, tachycardia, bradycardia, palpitation, arrhythmia, hypertension and hypotension, we investigated its electropharmacological effects using the halothane-anesthetized beagle dogs. Aciclovir in doses of 2 and 20 mg/kg was sequentially infused over 10 min with an interval of 20 min (n = 4), which would achieve sub-therapeutic to supra-therapeutic levels of plasma concentrations. Aciclovir decreased the total peripheral vascular resistance along with the blood pressure in a dose-related manner, which increased the heart rate, ventricular contraction and atrioventricular nodal conduction speed probably via a reflex-mediated increase of sympathetic tone. No significant change was detected in the intra-atrial or intra-ventricular conduction, indicating that aciclovir may not inhibit atrial or ventricular INa. Aciclovir prolonged the repolarization period in a dose-related as well as in a reverse frequency-dependent manners, indicating that aciclovir may inhibit IKr, which was supported by the Tpeak − Tend prolongation. Aciclovir transiently prolonged the J − Tpeakc possibly through a reflex-mediated increase of sympathetic tone, indicating an increase of net inward current in the early repolarization phase. Thus, aciclovir may directly inhibit IKr, and also have the potential to indirectly induce Ca2+ overload leading to early afterdepolarization. These in vivo electropharmacological profile of aciclovir would partly explain the onset mechanism of clinical adverse events.
      PubDate: 2020-08-01
  • The Effect of High Lactate Level on Mortality in Acute Heart Failure
           Patients With Reduced Ejection Fraction Without Cardiogenic Shock
    • Abstract: Background We aimed to determine the effect of blood lactate levels on cardiovascular (CV) death and hospitalization for heart failure (HF) in acute HF patients with reduced left ventricular ejection fraction (EF). Methods Eighty-five acute HF patients with reduced ejection fraction were divided into two groups according to admission blood lactate levels. 48 of them had low blood lactate levels (< 2 mmol/l) and 37 of them had high blood lactate levels (≥ 2 mmol/l). Patients with acute coronary syndrome, cardiogenic shock, sepsis and low blood pressure at admission were excluded from the study. Primary endpoint is the composite of cardiovascular (CV) death and hospitalization for heart failure (HHF) in 6-month follow-up. Secondary endpoint is the change in NT-proBNP levels from admission to 72 h. Results Baseline characteristics of patients were similar in two groups. On baseline echocardiographic evaluation; patients with high lactate revealed a higher mitral E/A ratio (2.34 [0.43–3.31], p = 0.008) and a lower TAPSE ratio (14 [10–27], p = 0.008) than patients with low lactate levels. Over a median follow-up period of 6 months, the primary end point occurred in 28 (75.7%) of 37 patients assigned to high lactate group and in 20 (41.7%) of 48 patients assigned to low lactate group (p = 0.006). High lactate levels significantly increased the risk of CV death and HHF at 6 months by nearly 5.35-fold in acute HF patients with reduced EF. The change in NT-proBNP levels at 72nd hour after admission were similar between two groups. Conclusion Higher lactate levels at admission related with higher HHF at 6 months and may be related with higher risk of CV death in acute HF patients with reduced EF.
      PubDate: 2020-08-01
  • How the Deuteration of Dronedarone Can Modify Its Cardiovascular Profile:
           In Vivo Characterization of Electropharmacological Effects of Poyendarone,
           a Deuterated Analogue of Dronedarone
    • Abstract: Abstract Since deuterium replacement has a potential to modulate pharmacodynamics, pharmacokinetics and toxicity, we developed deuterated dronedarone; poyendarone, and assessed its cardiovascular effects. Poyendarone hydrochloride in doses of 0.3 and 3 mg/kg over 30 s was intravenously administered to the halothane-anesthetized dogs (n = 4), which provided peak plasma concentrations of 108 ± 10 and 1120 ± 285 ng/mL, respectively. The 0.3 mg/kg shortened the ventricular repolarization period. The 3 mg/kg transiently increased the heart rate at 5 min but decreased at 45 min, and elevated the total peripheral vascular resistance and left ventricular preload, whereas it reduced the mean blood pressure at 5 min, left ventricular contractility and cardiac output. The transient tachycardic action is considered to be induced by the hypotension-induced, reflex-mediated increase of sympathetic tone. The 3 mg/kg delayed both intra-atrial and intra-ventricular conductions, indicating Na+ channel inhibitory action. Moreover, the 3 mg/kg transiently shortened the ventricular repolarization period at 5 min. No significant change was detected in the late repolarization by poyendarone, indicating it might not hardly significantly alter rapidly activating delayed-rectifier K+ current (IKr). Poyendarone prolonged the atrial effective refractory period greater than the ventricular parameter. When compared with dronedarone, poyendarone showed similar pharmacokinetics of dronedarone, but reduced β-adrenoceptor blocking activity as well as the cardio-suppressive effect. Poyendarone failed to inhibit IKr and showed higher atrial selectivity in prolonging the effective refractory period of atrium versus ventricle. Thus, the deuteration may be an effective way to improve the cardiovascular profile of dronedarone. Poyendarone is a promising anti-atrial fibrillatory drug candidate.
      PubDate: 2020-08-01
  • Evolution of Electrocardiographic Repolarization Parameters During
           Antiandrogen Therapy in Patients with Prostate Cancer and Hypogonadism
    • Abstract: Abstract We assessed the effects of antiandrogen therapy on ECG parameters of ventricular repolarization related to arrhythmic risk in 35 patients aged 70.3 ± 7 years with advanced prostate cancer treated with degarelix associated with enzalutamide (group A, 26 patients) or degarelix monotherapy (group B, 9 patients). We analyzed Fridericia corrected Q-T interval (QTc), Q-T dispersion (QTd), J-Tpeak interval (JTp), mean and maximum Tpeak-Tend interval (Tpe) and Tpe/QT ratio, Tpeak-Tend dispersion (Tped), index of cardio-electrophysiological balance (iCEB) from ECG tracings, and occurrence of ventricular premature beats (VPB) recorded by Holter ECG, before initiation of medication (M0) and after 6 months of treatment (M1). The groups had similar demographics except for a higher prevalence of prior myocardial infarction in group B (p = 0.01). All patients had low serum testosterone at M1. Baseline QTc, QTd, maxTpe/QT, meanTpe, maxTpe, Tped values were higher in B compared to A. They had a significant prolongation at M1 only in A. 20 patients in A and 6 in B had a 10% prolongation or decrease of iCEB (p = 0.66). In 5 patients, VPB severity increased from non-complex to complex: 3 in A and 2 in B (p = 0.31), but no sustained ventricular arrhythmia was registered. In conclusion, after 6 months of treatment, patients with hypogonadism on degarelix associated with enzalutamide had significant prolongation of QTc, QTd, maxTpe, meanTpe/QT, maxTpe/QT, Tped compared to patients on degarelix alone. The proportion of patients with 10% iCEB variation was similar between groups. There was no record of severe arrhythmias during the first 6 months of treatment.
      PubDate: 2020-08-01
  • Calcium Oxalate Monohydrate is Associated with Endothelial Cell Toxicity
           But Not with Reactive Oxygen Species Accumulation
    • Abstract: Abstract One characteristic of ethylene glycol overdose is a cardiopulmonary syndrome including hypertension and pulmonary edema with pathology indicating damage to the endothelium of heart, lung and brain vessels. The mechanism of the cardiopulmonary toxicity is unknown, but has been linked with accumulation of the metabolite calcium oxalate monohydrate (COM) in the endothelium. These studies have evaluated the hypothesis that COM or the oxalate ion produces endothelial damage in vitro and that damage is linked with induction of reactive oxygen species (ROS). In cultured human umbilical vein endothelial cells (HUVEC), COM, but not the oxalate ion, produced cytotoxicity in a dose- and time-dependent manner. Using three ROS-sensitive dyes, HUVEC exposed to COM did not significantly increase ROS production. Additionally, co-treatment with three antioxidants that operate by different mechanisms did not reduce COM cytotoxicity. As such, an increase in ROS production does not explain cell death in endothelial cells. Aluminum citrate, uniquely among citrate compounds, significantly reduced COM cytotoxicity to endothelial cells and thus may act as an adjunct therapy for ethylene glycol poisoning to reduce endothelial damage. These results imply that accumulation of COM in endothelial cells is an important aspect of the cardiopulmonary toxicity from ethylene glycol.
      PubDate: 2020-06-25
  • Modulation of Paraoxonase-1 and Apoptotic Gene Expression Involves in the
           Cardioprotective Role of Flaxseed Following Gestational Exposure to Diesel
           Exhaust Particles and/or Fenitrothion Insecticide
    • Abstract: Abstract The developmental exposure to a single chemical may elicit apoptosis in the different fetal organs, while the combined effects are restricted. We have examined the protective role of flaxseed (FS) against diesel exhaust particles (DEPs)- and/or fenitrothion (FNT)-induced fetal cardiac oxidative stress and apoptosis. A total of 48 timed pregnant rats were divided into eight groups (n = 6). The first group was saved as the control and the second fed on 20% FS diet. Animals in the third, fourth, and fifth groups were administered with DEPs (2.0 mg/kg), FNT (3.76 mg/kg), and their combination, respectively, while the sixth, seventh, and eighth groups were supplemented with 20% FS through intoxication with DEPs, FNT, and their combination, respectively. Our results revealed that DEPs and/or FNT significantly elevated the level of protein carbonyl and superoxide dismutase activity in the fetal cardiac tissues. However, the catalase activity and total thiol level were decreased; besides the histopathological alterations were remarked. Moreover, DEPs and/or FNT exhibited significant down-regulation in the anti-apoptotic (Bcl-2) and paraoxonase-1 gene expression, and up-regulation in the apoptotic (Bax and caspase-3) gene expression along with DNA fragmentation. Remarkably, FS supplementation significantly ameliorated the fetal cardiac oxidative injury, down-regulated the expression of the apoptotic genes, up-regulated the anti-apoptotic and paraoxonase-1 gene expression, reduced DNA fragmentation, and alleviated the myocardial cell architectures. These findings revealed that FS attenuates DEPs- and/or FNT-induced apoptotic cell death by repairing the disturbance in the anti-apoptotic/pro-apoptotic gene balance toward cell survival in the fetal myocardial cells.
      PubDate: 2020-06-22
  • Delayed-type Hypersensitivity to Metals in Newly Diagnosed Patients with
           Nonischemic Dilated Cardiomyopathy
    • Abstract: Abstract The causes of nonischemic dilated cardiomyopathy are classified as genetic or nongenetic, but environmental factors such as metal pollutants may interact with genetic susceptibility. The presence of metal particles has been detected in the myocardium, including in those patients with dilated cardiomyopathy. It is also known that hypersensitivity reactions can induce inflammation in tissue. The present study aimed to verify if metal-induced delayed-type hypersensitivity is present in patients with nonischemic dilated cardiomyopathy. The patient group consisted of 30 patients with newly diagnosed dilated cardiomyopathy; the control group comprised 41 healthy subjects. All patients and control subjects provided blood samples for lymphocyte transformation testing (MELISA®) to assess possible hypersensitivity to seven common metals. Specific exposure to metals was based on interview data. Results showed that exposure to cadmium and lead (p = 0.0002), aluminum (p = 0.0006), nickel (p = 0.0012), and chromium (p = 0.0065) was more often reported by patients than controls. The patients also had significantly more frequent hypersensitivity reactions to mercury (26.7% vs. 7.3%, p = 0.014624), nickel (40% vs. 12.2%, p = 0.02341), and silver (20% vs. 4.8%, p = 0.025468) than the control group. Patients with dilated cardiomyopathy had greater exposure to certain metals compared with healthy controls. Hypersensitivity to metals was more frequent in patients with dilated cardiomyopathy, suggesting a possible association that warrants further investigation.
      PubDate: 2020-06-15
  • Speckle-Tracking Echocardiography for Cardioncological Evaluation in
           Bevacizumab-Treated Colorectal Cancer Patients
    • Abstract: Abstract Angiogenesis inhibitor Bevacizumab (BVZ) may lead to the development of adverse effects, including hypertension and cardiac ischemia. Whether assessment of changes in myocardial strain by two-dimensional speckle-tracking echocardiography (2D-STE) can be of value in detecting BVZ-mediated cardiotoxicity at an earlier stage is not known. We investigated whether 2D-STE can non-invasively detect early evidence of cardiotoxicity in metastatic colorectal cancer (mCRC) patients treated with BVZ. Between January and June 2019, 25 consecutive patients (71.8 ± 7.5 year/old, 17 males) with mCRC were prospectively enrolled. Patients underwent physical examination, blood tests, and conventional 2D-transthoracic echocardiography implemented with 2D-STE analysis, at baseline and at 3 and 6 months following treatment with BVZ (15 mg/kg every 15 days) + 5-fluorouracil/folinic acid plus oxaliplatin (FOLFOX i.v.). At 6-month follow-up, we assessed occurrence of global longitudinal strain (GLS) impairment (> 15% decrease in GLS compared with baseline) as primary end-point and a new-onset systemic hypertension (secondary end-point). On average, GLS showed a progressive significant impairment after BVZ, from − 17.4 ± 3.2% at baseline to − 16 ± 2.9% (p = 0.003) at 6-month follow-up; > 15% decrease in GLS (primary end-point) was detected in 9 patients (36%). All other strain parameters remained unchanged. New-onset systemic hypertension (secondary end-point) was diagnosed in five patients (20%). No significant changes were observed in serial high-sensitivity cardiac troponin I measurements. No patient developed significant changes in LV size or LV ejection fraction; no case of clinically symptomatic HF was observed during BVZ-treatment. Measurement of GLS by 2D-STE analysis can effectively detect BVZ-mediated cardiotoxicity at an early stage.
      PubDate: 2020-06-09
  • Effects of Extracellular Matrix Softening on Vascular Smooth Muscle Cell
    • Abstract: Abstract Vascular smooth muscle cells (VSMCs) shift from a physiological contractile phenotype to an adverse proliferative or synthetic state, which is a major event leading to aortic disease. VSMCs are exposed to multiple mechanical signals from their microenvironment including vascular extracellular matrix (ECM) stiffness and stretch which regulate VSMC contraction. How ECM stiffness regulates the function and phenotype of VSMCs is not well understood. In this study, we introduce in vitro and in vivo models to evaluate the impact of ECM stiffnesses on VSMC function. Through unbiased transcriptome sequencing analysis, we detected upregulation of synthetic phenotype-related genes including osteopontin, matrix metalloproteinases, and inflammatory cytokines in VSMCs cultured using soft matrix hydrogels in vitro, suggesting VSMC dedifferentiation toward a synthetic phenotype upon ECM softening. For the in vivo model, the lysyl oxidase inhibitor β-aminopropionitrile monofumarate (BAPN) was administrated to disrupt the cross-linking of collagen to induce ECM softening. Consistently, decreased ECM stiffnesses promoted VSMC phenotypic switching to a synthetic phenotype as evidenced by upregulation of synthetic phenotype-related genes in the aortas of mice following BAPN treatment. Finally, BAPN-treated mice showed severe expansion and developed aortic dissection. Our study reveals the pivotal role of ECM softening in regulating the VSMC phenotype switch and provides a potential target for treating VSMC dysfunction and aortic dissection disease.
      PubDate: 2020-06-04
  • Disruption of the Keap1/Nrf2-Antioxidant Response System After Chronic
           Doxorubicin Exposure In Vivo
    • Abstract: Abstract Doxorubicin (DOX) is a widely prescribed anthracycline antineoplastic drug for treating human solid tumors and leukemias. However, DOX therapy is limited by a cumulative, dose-dependent, and irreversible cardiomyopathy that occurs with repeated administration. Presumably, a pivotal initiating event of DOX-induced cardiotoxicity is the production of reactive oxygen species (ROS) and oxidation of lipids, DNA, and proteins. We recently identified activation of the Keap1/Nrf2-antioxidant response system—a major cellular defense mechanism against such oxidative stress—as an important response to acute DOX exposure in vitro. In the present study, we address the hypothesis that dysregulation of this pathway in cardiac tissue is also manifested in vivo following chronic DOX administration. Male, Sprague–Dawley rats received 6 weekly injections of 2 mg/kg (s.c.) DOX or saline followed by a 5-week drug-free period prior to analysis of cardiac tissue transcripts and proteins. In contrast to in vitro findings, the Keap1/Nrf2-antioxidant response system was suppressed in hearts of DOX-treated animals and consistent with the observed decrease in protein abundance for Nrf2 and PGAM5, both of which are substrates for Keap1. Although this shift in Keap1/Nrf2 suppresses the antioxidant pathway, the concurrent loss of PGAM5 could function as a signal for disposal of damaged mitochondria from the cell, thus removing the source of ROS. These findings identify the Keap1/Nrf2 and Keap1/PGAM5 pathways as important responses to DOX-induced cardiac injury in vivo; disruption of this system for mitochondrial hormesis may be an important contributing factor to cardiotoxicity after chronic drug administration.
      PubDate: 2020-06-04
  • Concomitant Treatment with Proton Pump Inhibitors and Cephalosporins Does
           Not Enhance QT-Associated Proarrhythmia in Isolated Rabbit Hearts
    • Abstract: Abstract Recent results from data mining analyses and reports of adverse drug events suggest a QT-prolonging drug–drug interaction resulting from the combination of distinct proton pump inhibitors and cephalosporins. Therefore, this study aimed at investigating the effect of the suspected QT-prolonging combinations of lansoprazole + ceftriaxone and esomeprazole + cefazolin, respectively. 26 hearts of New Zealand White rabbits were retrogradely perfused and paced at different cycle lengths. After generating baseline data, the hearts were assigned to two groups: In group 1, hearts were treated with 5 µM lansoprazole. Thereafter, 200 µM ceftriaxone was infused additionally. Group 2 was perfused with 10 µM esomeprazole followed by 250 µM cefazolin. In group 1, lansoprazole did not significantly alter QT intervals and APD90. Additional treatment with ceftriaxone significantly shortened QT interval, APD90 and slightly reduced dispersion of repolarization compared to sole lansoprazole infusion. In group 2, esomeprazole led to a significant shortening of the QT interval without altering APD90 or dispersion. Additional treatment with the antibiotic cefazolin further shortened QT interval, APD90 and reduced the dispersion of repolarization. Incidence of ventricular arrhythmias was not significantly altered in both groups. This is the first experimental whole-heart study that investigated the impact of a concomitant treatment with proton pump inhibitors and cephalosporins. In contrast to previous reports, the combination of both agents did not cause QT prolongation but instead shortened QT interval and action potential duration. As a consequence, no triggered activity occurred in the presence of a stable dispersion of repolarization.
      PubDate: 2020-06-04
  • The Effects of Neuropeptide Y Overexpression on the Mouse Model of
           Doxorubicin-Induced Cardiotoxicity
    • Abstract: Abstract Doxorubicin is a potent anticancer drug with cardiotoxicity hampering its use. Neuropeptide Y (NPY) is the most abundant neuropeptide in the heart and a co-transmitter of the sympathetic nervous system that plays a role in cardiac diseases. The aim of this work was to study the impact of NPY on doxorubicin-induced cardiotoxicity. Transgenic mice overexpressing NPY in noradrenergic neurons (NPY-OEDβH) and wild-type mice were treated with a single dose of doxorubicin. Doxorubicin caused cardiotoxicity in both genotypes as demonstrated by decreased weight gain, tendency to reduced ejection fraction, and changes in the expression of several genes relevant to cardiac pathology. Doxorubicin resulted in a tendency to lower ejection fraction in NPY-OEDβH mice more than in wild-type mice. In addition, gain in the whole body lean mass gain was decreased only in NPY-OEDβH mice, suggesting a more severe impact of doxorubicin in this genotype. The effects of doxorubicin on genes expressed in the heart were similar between NPY-OEDβH and wild-type mice. The results demonstrate that doxorubicin at a relatively low dose caused significant cardiotoxicity. There were differences between NPY-OEDβH and wild-type mice in their responses to doxorubicin that suggest NPY to increase susceptibility to cardiotoxicity. This may point to the therapeutic implications as suggested for NPY system in other cardiovascular diseases.
      PubDate: 2020-06-01
  • Chronic Mercury Exposure in Prehypertensive SHRs Accelerates Hypertension
           Development and Activates Vasoprotective Mechanisms by Increasing NO and H
           2 O 2 Production
    • Abstract: Abstract Mercury is a heavy metal associated with cardiovascular diseases. Studies have reported increased vascular reactivity without changes in systolic blood pressure (SBP) after chronic mercury chloride (HgCl2) exposure, an inorganic form of the metal, in normotensive rats. However, we do not know whether individuals in the prehypertensive phase, such as young spontaneously hypertensive rats (SHRs), are susceptible to increased arterial blood pressure. We investigated whether chronic HgCl2 exposure in young SHRs accelerates hypertension development by studying the vascular function of mesenteric resistance arteries (MRAs) and SBP in young SHRs during the prehypertensive phase. Four-week-old male SHRs were divided into two groups: the SHR control group (vehicle) and the SHR HgCl2 group (4 weeks of exposure). The results showed that HgCl2 treatment accelerated the development of hypertension; reduced vascular reactivity to phenylephrine in MRAs; increased nitric oxide (NO) generation; promoted vascular dysfunction by increasing the production of reactive oxygen species (ROS), such as hydrogen peroxide (H2O2); increased Gp91Phox protein levels and in situ levels of superoxide anion (O2·−); and reduced vasoconstrictor prostanoid production compared to vehicle treatment. Although HgCl2 accelerated the development of hypertension, the HgCl2-exposed animals also exhibited a vasoprotective mechanism to counterbalance the rapid increase in SBP by decreasing vascular reactivity through H2O2 and NO overproduction. Our results suggest that HgCl2 exposure potentiates this vasoprotective mechanism against the early establishment of hypertension. Therefore, we are concluding that chronic exposure to HgCl2 in prehypertensive animals could enhance the risk for cardiovascular diseases.
      PubDate: 2020-06-01
  • Effects of Hyperbaric Oxygen Therapy on Acute Myocardial Infarction
           Following Carbon Monoxide Poisoning
    • Abstract: Abstract Carbon monoxide poisoning (COP) may increase the risk of myocardial infarction. We conducted a study to investigate the effects of hyperbaric oxygen therapy (HBOT) on the risk. We used the Nationwide Poisoning Database in Taiwan to identify COP patients diagnosed between 1999 and 2012. We compared the risk for myocardial infarction between patients with and without HBOT by following up through 2013 and identified the independent predictors of myocardial infarction. The risk of myocardial infarction in the 7278 patients with HBOT was lower than in the 18,459 patients without HBOT, but this difference did not reach statistical significance [adjusted hazard ratio (AHR): 0.69; 95% confidence interval (CI) 0.45–1.07]. Stratified analyses showed that the reductions in the risk associated with HBOT for myocardial infarction reached statistical significance in male patients (AHR: 0.45; 95% CI 0.24–0.83) and during the first 2 weeks of follow-up (AHR: 0.22; 95% CI 0.05–0.96). In patients without HBOT, independent predictors of myocardial infarction were old age, male sex, and the underlying comorbidities of hypertension, diabetes, coronary artery disease, and congestive heart failure. In patients with HBOT, however, old age, male sex, and the underlying comorbidities of diabetes, coronary artery disease, and congestive heart failure were not independent predictors. HBOT was associated with a reduced risk of myocardial infarction in male patients and within 2 weeks following COP. These results may provide important reference for using HBOT in treating COP.
      PubDate: 2020-06-01
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
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