urea has been researched along with Cardiac Remodeling, Ventricular in 15 studies
pseudourea: clinical use; structure
isourea : A carboximidic acid that is the imidic acid tautomer of urea, H2NC(=NH)OH, and its hydrocarbyl derivatives.
Excerpt | Relevance | Reference |
---|---|---|
"Landiolol is an ultra-short-acting β-blocker that has less effect on blood pressure, but little is known about its efficacy and safety for patients with AMI undergoing primary percutaneous coronary intervention (PCI)." | 6.77 | Randomized study on the efficacy and safety of landiolol, an ultra-short-acting β1-adrenergic blocker, in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. ( Abe, N; Hanada, K; Higuma, T; Kushibiki, M; Nishizaki, F; Oikawa, K; Okumura, K; Osanai, T; Saito, S; Sukekawa, T; Tomita, H; Yamada, M; Yokota, T, 2012) |
"Omecamtiv mecarbil dosing guided by pharmacokinetics achieved plasma concentrations associated with improved cardiac function and decreased ventricular diameter." | 2.82 | Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure (COSMIC-HF): a phase 2, pharmacokinetic, randomised, placebo-controlled trial. ( Adams, KF; Cleland, JG; Ezekowitz, JA; Felker, GM; Goudev, A; Honarpour, N; Johnston, J; Macdonald, P; Malik, FI; McMurray, JJ; Metra, M; Mitrovic, V; Monsalvo, ML; Ponikowski, P; Serpytis, P; Solomon, SD; Spinar, J; Teerlink, JR; Tomcsányi, J; Vandekerckhove, HJ; Voors, AA, 2016) |
"Landiolol is an ultra-short-acting β-blocker that has less effect on blood pressure, but little is known about its efficacy and safety for patients with AMI undergoing primary percutaneous coronary intervention (PCI)." | 2.77 | Randomized study on the efficacy and safety of landiolol, an ultra-short-acting β1-adrenergic blocker, in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. ( Abe, N; Hanada, K; Higuma, T; Kushibiki, M; Nishizaki, F; Oikawa, K; Okumura, K; Osanai, T; Saito, S; Sukekawa, T; Tomita, H; Yamada, M; Yokota, T, 2012) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 2 (13.33) | 29.6817 |
2010's | 8 (53.33) | 24.3611 |
2020's | 5 (33.33) | 2.80 |
Authors | Studies |
---|---|
Bernier, TD | 1 |
Buckley, LF | 1 |
Biering-Sørensen, T | 1 |
Minamisawa, M | 1 |
Claggett, B | 1 |
Liu, J | 1 |
Felker, GM | 3 |
McMurray, JJV | 1 |
Malik, FI | 3 |
Abbasi, S | 1 |
Kurtz, CE | 1 |
Teerlink, JR | 2 |
Solomon, SD | 2 |
Mann, DL | 1 |
Shen, S | 1 |
Sewanan, LR | 1 |
Campbell, SG | 1 |
Iacoviello, M | 1 |
Palazzuoli, A | 1 |
Gronda, E | 1 |
Saito, T | 1 |
Uchiumi, T | 1 |
Yagi, M | 1 |
Amamoto, R | 1 |
Setoyama, D | 1 |
Matsushima, Y | 1 |
Kang, D | 1 |
Tarone, G | 1 |
Balligand, JL | 1 |
Bauersachs, J | 1 |
Clerk, A | 1 |
De Windt, L | 1 |
Heymans, S | 1 |
Hilfiker-Kleiner, D | 1 |
Hirsch, E | 1 |
Iaccarino, G | 1 |
Knöll, R | 1 |
Leite-Moreira, AF | 1 |
Lourenço, AP | 1 |
Mayr, M | 1 |
Thum, T | 1 |
Tocchetti, CG | 1 |
Roche, C | 1 |
Besnier, M | 1 |
Cassel, R | 1 |
Harouki, N | 1 |
Coquerel, D | 1 |
Guerrot, D | 1 |
Nicol, L | 1 |
Loizon, E | 1 |
Remy-Jouet, I | 1 |
Morisseau, C | 1 |
Mulder, P | 1 |
Ouvrard-Pascaud, A | 1 |
Madec, AM | 1 |
Richard, V | 1 |
Bellien, J | 1 |
Linz, B | 1 |
Hohl, M | 1 |
Reil, JC | 1 |
Böhm, M | 1 |
Linz, D | 1 |
McMurray, JJ | 1 |
Adams, KF | 1 |
Cleland, JG | 1 |
Ezekowitz, JA | 1 |
Goudev, A | 1 |
Macdonald, P | 1 |
Metra, M | 1 |
Mitrovic, V | 1 |
Ponikowski, P | 1 |
Serpytis, P | 1 |
Spinar, J | 1 |
Tomcsányi, J | 1 |
Vandekerckhove, HJ | 1 |
Voors, AA | 1 |
Monsalvo, ML | 1 |
Johnston, J | 1 |
Honarpour, N | 1 |
Li, N | 1 |
Liu, JY | 1 |
Timofeyev, V | 1 |
Qiu, H | 1 |
Hwang, SH | 1 |
Tuteja, D | 1 |
Lu, L | 1 |
Yang, J | 1 |
Mochida, H | 1 |
Low, R | 1 |
Hammock, BD | 1 |
Chiamvimonvat, N | 1 |
Shen, YT | 1 |
Zhao, X | 1 |
Depre, C | 1 |
Dhar, SK | 1 |
Abarzúa, P | 1 |
Morgans, DJ | 1 |
Vatner, SF | 1 |
Hanada, K | 1 |
Higuma, T | 1 |
Nishizaki, F | 1 |
Sukekawa, T | 1 |
Yokota, T | 1 |
Yamada, M | 1 |
Saito, S | 1 |
Kushibiki, M | 1 |
Oikawa, K | 1 |
Abe, N | 1 |
Tomita, H | 1 |
Osanai, T | 1 |
Okumura, K | 1 |
Yoshiyama, M | 1 |
McMahon, AC | 1 |
Greenwald, SE | 1 |
Dodd, SM | 1 |
Hurst, MJ | 1 |
Raine, AE | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
A Double-blind, Randomized, Placebo-controlled, Multicenter, Dose Escalation Study to Select and Evaluate an Oral Modified Release Formulation of Omecamtiv Mecarbil in Subjects With Heart Failure and Left Ventricular Systolic Dysfunction[NCT01786512] | Phase 2 | 544 participants (Actual) | Interventional | 2013-02-26 | Completed | ||
Role of Innate and Adaptive Immunity After Acute Myocardial Infarction BATTLE-AMI Study (B And T Types of Lymphocytes Evaluation in Acute Myocardial Infarction)[NCT02428374] | Phase 4 | 300 participants (Anticipated) | Interventional | 2015-05-31 | Recruiting | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
(NCT01786512)
Timeframe: Day 7 at predose and at 0.5, 1, 2, 3, 4, 6, 8, and 12 hours post-dose
Intervention | ng*hr/mL (Mean) |
---|---|
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F1 | 2030 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F2 | 2000 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg SCT-F2 | 1740 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F1 | 5070 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F2 | 5010 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg SCT-F2 | 6550 |
(NCT01786512)
Timeframe: Day 7 at predose and at 0.5, 1, 2, 3, 4, 6, 8, 12, 24, 48, and 72 hours, and 7 days post-dose.
Intervention | ng/mL (Mean) |
---|---|
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F1 | 193 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F2 | 201 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg SCT-F2 | 171 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F1 | 492 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F2 | 502 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg SCT-F2 | 601 |
(NCT01786512)
Timeframe: Day 7 at predose
Intervention | ng/mL (Mean) |
---|---|
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F1 | 157 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F2 | 137 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg SCT-F2 | 134 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F1 | 376 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F2 | 395 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg SCT-F2 | 476 |
(NCT01786512)
Timeframe: Day 7 at predose and at 0.5, 1, 2, 3, 4, 6, 8, 12, 24, 48, and 72 hours, and 7 days post-dose.
Intervention | hours (Mean) |
---|---|
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F1 | 3.9 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F2 | 2.0 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg SCT-F2 | 4.2 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F1 | 2.6 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F2 | 2.2 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg SCT-F2 | 4.6 |
Heart rate was measured using electrocardiography. Least squares means are from a repeated measures model including treatment group, stratification factor, scheduled visit, interaction of treatment with scheduled visit and the baseline value as covariates. (NCT01786512)
Timeframe: Baseline and week 20
Intervention | bpm (Least Squares Mean) |
---|---|
Expansion Phase: Placebo | 0.57 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | -0.77 |
Expansion Phase: OM PK-based Titration | -2.40 |
LVEDD was measured using echocardiography. Least squares means are from a repeated measures model including treatment group, stratification factor, scheduled visit, interaction of treatment with scheduled visit and the baseline value as covariates. (NCT01786512)
Timeframe: Baseline and week 20
Intervention | cm (Least Squares Mean) |
---|---|
Expansion Phase: Placebo | 0.089 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | 0.023 |
Expansion Phase: OM PK-based Titration | -0.040 |
LVESD was measured using echocardiography. Least squares means are from a repeated measures model including treatment group, stratification factor, scheduled visit, interaction of treatment with scheduled visit and the baseline value as covariates. (NCT01786512)
Timeframe: Baseline and week 20
Intervention | cm (Least Squares Mean) |
---|---|
Expansion Phase: Placebo | -0.242 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | -0.322 |
Expansion Phase: OM PK-based Titration | -0.421 |
Least squares means are from a repeated measures model including treatment group, stratification factor, scheduled visit, interaction of treatment with scheduled visit and the baseline value as covariates. (NCT01786512)
Timeframe: Baseline and week 20
Intervention | pg/mL (Least Squares Mean) |
---|---|
Expansion Phase: Placebo | 502 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | -319 |
Expansion Phase: OM PK-based Titration | -468 |
Stroke volume was measured using echocardiography. Least squares means are from a repeated measures model including treatment group, stratification factor, scheduled visit, interaction of treatment with scheduled visit and the baseline value as covariates. (NCT01786512)
Timeframe: Baseline and week 20
Intervention | mL (Least Squares Mean) |
---|---|
Expansion Phase: Placebo | -1.05 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | 3.53 |
Expansion Phase: OM PK-based Titration | 2.58 |
Systolic ejection time was measured using echocardiography. Least squares means are from a repeated measures model including treatment group, stratification factor, scheduled visit, interaction of treatment with scheduled visit and the baseline value as covariates. (NCT01786512)
Timeframe: Baseline and week 20
Intervention | seconds (Least Squares Mean) |
---|---|
Expansion Phase: Placebo | 0.0000 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | 0.0112 |
Expansion Phase: OM PK-based Titration | 0.0250 |
"An adverse event (AE) is defined as any untoward medical occurrence in a clinical trial participant, including worsening of a preexisting medical condition. The event does not necessarily have a causal relationship with study treatment. Laboratory value changes that required treatment or adjustment in current therapy were considered adverse events.~Each adverse event was graded for severity according to the Common Terminology Criteria for Adverse Events (CTCAE), where Grade 1 = Mild AE, Grade 2 = Moderate AE, Grade 3 = Severe AE, and Grade 4 = life-threatening AE.~A serious adverse event is defined as an adverse event that met at least 1 of the following serious criteria:~fatal~life threatening~required in-patient hospitalization or prolongation of existing hospitalization~resulted in persistent or significant disability/incapacity~congenital anomaly/birth defect~other medically important serious event" (NCT01786512)
Timeframe: From first dose of study drug to 4 weeks after last dose; treatment duration was 7 days in the dose escalation phase.
Intervention | Participants (Count of Participants) | ||||||
---|---|---|---|---|---|---|---|
Any treatment-emergent adverse event (TEAE) | TEAE Grade ≥ 2 | TEAE Grade ≥ 3 | TEAE Grade ≥ 4 | Serious adverse events | TEAE leading to discontinuation of study drug | Fatal adverse events | |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F1 | 2 | 1 | 0 | 0 | 0 | 0 | 0 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg M-F2 | 6 | 1 | 1 | 0 | 1 | 0 | 0 |
Dose-escalation Cohort 1: Omecamtiv Mecarbil 25 mg SCT-F2 | 6 | 1 | 0 | 0 | 0 | 0 | 0 |
Dose-escalation Cohort 1: Placebo | 4 | 0 | 0 | 0 | 0 | 0 | 0 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F1 | 9 | 5 | 2 | 0 | 2 | 2 | 0 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg M-F2 | 3 | 1 | 0 | 0 | 0 | 0 | 0 |
Dose-escalation Cohort 2: Omecamtiv Mecarbil 50 mg SCT-F2 | 5 | 1 | 1 | 0 | 1 | 0 | 0 |
Dose-escalation Cohort 2: Placebo | 1 | 1 | 0 | 0 | 0 | 0 | 0 |
(NCT01786512)
Timeframe: Weeks 2 and 12 at predose and 1, 2, 4, 6, and 8 hours post-dose.
Intervention | ng/mL (Mean) | |
---|---|---|
Week 2 | Week 12 | |
Expansion Phase: OM PK-based Titration | 212 | 318 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | 212 | 200 |
"An adverse event is defined as any untoward medical occurrence in a clinical trial participant, including worsening of a preexisting medical condition. The event does not necessarily have a causal relationship with study treatment. Laboratory value changes that required treatment or adjustment in current therapy were considered adverse events.~Each adverse event was graded for severity according to the Common Terminology Criteria for Adverse Events (CTCAE), where Grade 1 = Mild AE, Grade 2 = Moderate AE, Grade 3 = Severe AE, and Grade 4 = life-threatening AE.~A serious adverse event is defined as an adverse event that met at least 1 of the following serious criteria:~fatal~life threatening~required in-patient hospitalization or prolongation of existing hospitalization~resulted in persistent or significant disability/incapacity~congenital anomaly/birth defect~other medically important serious event" (NCT01786512)
Timeframe: From first dose of study drug until 4 weeks after last dose; treatment duration was 20 weeks in the expansion phase.
Intervention | Participants (Count of Participants) | ||||||
---|---|---|---|---|---|---|---|
Any treatment-emergent adverse event (TEAE) | TEAE Grade ≥ 2 | TEAE Grade ≥ 3 | TEAE Grade ≥ 4 | Serious adverse events | TEAEs leading to discontinuation of study drug | Fatal adverse events | |
Expansion Phase: OM PK-based Titration | 95 | 61 | 31 | 11 | 32 | 12 | 3 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | 92 | 60 | 28 | 8 | 36 | 8 | 1 |
Expansion Phase: Placebo | 91 | 62 | 34 | 5 | 30 | 12 | 4 |
(NCT01786512)
Timeframe: Predose (before morning dose) at weeks 2, 8, 12, 16, and 20
Intervention | ng/mL (Mean) | ||||
---|---|---|---|---|---|
Week 2 | Week 8 | Week 12 | Week 16 | Week 20 | |
Expansion Phase: OM PK-based Titration | 179 | 161 | 263 | 240 | 239 |
Expansion Phase: Omecamtiv Mecarbil 25 mg | 174 | 156 | 165 | 155 | 149 |
4 reviews available for urea and Cardiac Remodeling, Ventricular
Article | Year |
---|---|
Cardiac Myosin Activation for the Treatment of Systolic Heart Failure.
Topics: Animals; Cardiac Myosins; Cardiotonic Agents; Heart Failure, Systolic; Humans; Myocardium; Recovery | 2021 |
Mechanisms and Models in Heart Failure: A Translational Approach.
Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Biphenyl Compounds; Clinical Trials, Phase III as | 2021 |
Recent advances in pharmacological treatment of heart failure.
Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Biphenyl Compounds; Cardiotonic Agents; Drug Combi | 2021 |
Targeting myocardial remodelling to develop novel therapies for heart failure: a position paper from the Working Group on Myocardial Function of the European Society of Cardiology.
Topics: Cell Survival; Cyclosporine; Drugs, Investigational; Heart Failure; Humans; Hypertrophy, Left Ventri | 2014 |
3 trials available for urea and Cardiac Remodeling, Ventricular
Article | Year |
---|---|
Cardiac Myosin Activator Omecamtiv Mecarbil Improves Left Ventricular Myocardial Deformation in Chronic Heart Failure: The COSMIC-HF Trial.
Topics: Aged; Biomarkers; Double-Blind Method; Female; Heart Failure; Heart Rate; Humans; Male; Middle Aged; | 2020 |
Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure (COSMIC-HF): a phase 2, pharmacokinetic, randomised, placebo-controlled trial.
Topics: Administration, Oral; Cardiac Myosins; Dose-Response Relationship, Drug; Heart Failure; Humans; Natr | 2016 |
Randomized study on the efficacy and safety of landiolol, an ultra-short-acting β1-adrenergic blocker, in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention.
Topics: Adrenergic beta-1 Receptor Antagonists; Angioplasty, Balloon, Coronary; Combined Modality Therapy; F | 2012 |
8 other studies available for urea and Cardiac Remodeling, Ventricular
Article | Year |
---|---|
Evidence for synergy between sarcomeres and fibroblasts in an in vitro model of myocardial reverse remodeling.
Topics: Actomyosin; Animals; Animals, Newborn; Benzamides; Benzylamines; Cardiac Myosins; Cell Line; Dioxole | 2021 |
Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses.
Topics: Adaptor Proteins, Signal Transducing; AMP-Activated Protein Kinases; Animals; Cardiomyopathies; Carr | 2017 |
Soluble epoxide hydrolase inhibition improves coronary endothelial function and prevents the development of cardiac alterations in obese insulin-resistant mice.
Topics: Animals; Benzoates; Blood Glucose; Coronary Vessels; Disease Models, Animal; Dose-Response Relations | 2015 |
Inhibition of NHE3-mediated Sodium Absorption in the Gut Reduced Cardiac End-organ Damage Without Deteriorating Renal Function in Obese Spontaneously Hypertensive Rats.
Topics: Animals; Antihypertensive Agents; Blood Pressure; Disease Models, Animal; Genetic Predisposition to | 2016 |
Beneficial effects of soluble epoxide hydrolase inhibitors in myocardial infarction model: Insight gained using metabolomic approaches.
Topics: Animals; Apoptosis; Arrhythmias, Cardiac; Benzoates; Chromatography, Liquid; Cytokines; Disease Mode | 2009 |
Improvement of cardiac function by a cardiac Myosin activator in conscious dogs with systolic heart failure.
Topics: Analysis of Variance; Animals; Cardiac Myosins; Consciousness; Disease Models, Animal; Dobutamine; D | 2010 |
Effect and safety of landiolol in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention.
Topics: Angioplasty, Balloon, Coronary; Female; Humans; Male; Morpholines; Myocardial Infarction; Urea; Vent | 2012 |
Prolonged calcium transients and myocardial remodelling in early experimental uraemia.
Topics: Animals; Blood Pressure; Calcium; Cardiomegaly; Creatinine; Disease Models, Animal; Glomerular Filtr | 2002 |