spironolactone has been researched along with Cardiomyopathy, Hypertrophic in 5 studies
Spironolactone: A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827)
spironolactone : A steroid lactone that is 17alpha-pregn-4-ene-21,17-carbolactone substituted by an oxo group at position 3 and an alpha-acetylsulfanyl group at position 7.
Cardiomyopathy, Hypertrophic: A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).
Excerpt | Relevance | Reference |
---|---|---|
"These findings do not support the use of spironolactone in hypertrophic cardiomyopathy to improve left ventricular remodeling by mitigating myocardial fibrosis or altering clinical course." | 9.27 | Effect of Spironolactone on Myocardial Fibrosis and Other Clinical Variables in Patients with Hypertrophic Cardiomyopathy. ( Chan, RH; Jaffe, IZ; Kapur, NK; Kerur, R; Maron, BJ; Maron, MS; McGraw, AP; Udelson, JE, 2018) |
"BACKGROUND In the setting of acute decompensated heart failure (ADHF), tolvaptan, a selective V₂ receptor antagonist, did not alter plasma renin activity or angiotensin II level, but significantly increased plasma aldosterone by the activation of V₁ₐ receptor, suggesting that a high-dose mineralocorticoid receptor antagonist (MRA) combined with a V₂ receptor antagonist might be of interest, especially in ADHF patients." | 7.91 | Adding High-Dose Spironolactone to Tolvaptan Improves Acute Decompensated Heart Failure Due to Obstructive Hypertrophic Cardiomyopathy and Aortic Stenosis: A Case Report. ( Kajimoto, K; Otsubo, S, 2019) |
"These findings do not support the use of spironolactone in hypertrophic cardiomyopathy to improve left ventricular remodeling by mitigating myocardial fibrosis or altering clinical course." | 5.27 | Effect of Spironolactone on Myocardial Fibrosis and Other Clinical Variables in Patients with Hypertrophic Cardiomyopathy. ( Chan, RH; Jaffe, IZ; Kapur, NK; Kerur, R; Maron, BJ; Maron, MS; McGraw, AP; Udelson, JE, 2018) |
"BACKGROUND In the setting of acute decompensated heart failure (ADHF), tolvaptan, a selective V₂ receptor antagonist, did not alter plasma renin activity or angiotensin II level, but significantly increased plasma aldosterone by the activation of V₁ₐ receptor, suggesting that a high-dose mineralocorticoid receptor antagonist (MRA) combined with a V₂ receptor antagonist might be of interest, especially in ADHF patients." | 3.91 | Adding High-Dose Spironolactone to Tolvaptan Improves Acute Decompensated Heart Failure Due to Obstructive Hypertrophic Cardiomyopathy and Aortic Stenosis: A Case Report. ( Kajimoto, K; Otsubo, S, 2019) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 2 (40.00) | 29.6817 |
2010's | 2 (40.00) | 24.3611 |
2020's | 1 (20.00) | 2.80 |
Authors | Studies |
---|---|
Stătescu, C | 1 |
Enachi, Ș | 1 |
Ureche, C | 1 |
Țăpoi, L | 1 |
Anghel, L | 1 |
Șalaru, D | 1 |
Pleșoianu, C | 1 |
Bostan, M | 1 |
Marcu, D | 1 |
Ovanez Balasanian, M | 1 |
Sascău, RA | 1 |
Maron, MS | 1 |
Chan, RH | 1 |
Kapur, NK | 1 |
Jaffe, IZ | 1 |
McGraw, AP | 1 |
Kerur, R | 1 |
Maron, BJ | 1 |
Udelson, JE | 1 |
Kajimoto, K | 1 |
Otsubo, S | 1 |
Tsybouleva, N | 1 |
Zhang, L | 1 |
Chen, S | 1 |
Patel, R | 1 |
Lutucuta, S | 1 |
Nemoto, S | 1 |
DeFreitas, G | 1 |
Entman, M | 1 |
Carabello, BA | 1 |
Roberts, R | 1 |
Marian, AJ | 1 |
de Resende, MM | 1 |
Kriegel, AJ | 1 |
Greene, AS | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
Clinical and Therapeutic Implications of Fibrosis in Hypertrophic Cardiomyopathy[NCT00879060] | Phase 4 | 53 participants (Actual) | Interventional | 2007-11-30 | Completed | ||
Evaluating the Effect of Spironolactone on Hypertrophic Cardiomyopathy-- a Multicenter Randomized Control Trial[NCT02948998] | Phase 4 | 260 participants (Anticipated) | Interventional | 2018-05-14 | Not yet recruiting | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
Specific variables of collagen turnover markers that will be evaluated include markers of collagen synthesis (PINP, PIIINP), and marker of collagen degradation (ICTP). A two-sample t-test was used to compare the differences between these collagen turnover markers at baseline and the absolute differences in change from baseline to 12 months of follow-up. (NCT00879060)
Timeframe: The time points measured were at Baseline and at 12 Months (Follow-Up).
Intervention | micrograms/L (Mean) | |||||
---|---|---|---|---|---|---|
Baseline (PINP) | 12 Months (PINP) | Baseline (PIIINP) | 12 Months (PIIINP) | Baseline (ICTP) | 12 Months (ICTP) | |
Placebo Control | 2.1 | 0.6 | 4.5 | 1.6 | 2.5 | -2.3 |
Spironolactone | 2.1 | 0.7 | 4.7 | 2.0 | 2.2 | 2.7 |
CMR will be utilized as it has superior reproducibility (as compared to 2-D echocardiography). Late Gadolinium Enhancement (LGE) Assessment of myocardial fibrosis by CMR will be expressed as a percentage of left ventricular mass (%LV), maximum left ventricular wall thickness (in mm), left ventricular end-diastolic cavity size (in mm/m^2), and left atrial dimension (in mm). (NCT00879060)
Timeframe: The time points measured were at Baseline and at 12 Months (Follow-Up)
Intervention | millimeters (Mean) | |
---|---|---|
Left Atrial Dimension (Baseline) | Left Atrial Dimension (12-Month Follow-Up) | |
Placebo Control | 41 | 40 |
Spironolactone | 40 | 40 |
CMR will be utilized as it has superior reproducibility (as compared to 2-D echocardiography). Late Gadolinium Enhancement (LGE) Assessment of myocardial fibrosis by CMR will be expressed as a percentage of left ventricular mass (%LV), maximum left ventricular wall thickness (in mm), left ventricular end-diastolic (LVED) cavity size (in mm/m^2), and left atrial dimension (in mm). (NCT00879060)
Timeframe: The time points measured were at Baseline and at 12 Months (Follow-Up)
Intervention | mm/m^2 (Mean) | |
---|---|---|
LVED Cavity Size (Baseline) | LVED Cavity Size (12-Month Follow-Up) | |
Placebo Control | 145 | 146 |
Spironolactone | 133 | 129 |
CMR will be utilized as it has superior reproducibility (as compared to 2-D echocardiography). Late Gadolinium Enhancement (LGE) Assessment of myocardial fibrosis by CMR will be expressed as a percentage of left ventricular mass (%LV), maximum left ventricular wall thickness (in mm), left ventricular end-diastolic cavity size (in mm/m^2), and left atrial dimension (in mm). (NCT00879060)
Timeframe: The time points measured were at Baseline and at 12 Months (Follow-Up).
Intervention | millimeters (Mean) | |
---|---|---|
Maximum Left Ventricular Wall Thickness (Baseline) | Maximum Left Ventricular Wall Thickness (12-Month Follow-Up) | |
Placebo Control | 21 | 19 |
Spironolactone | 22 | 22 |
CMR will be utilized as it has superior reproducibility (as compared to 2-D echocardiography). Late Gadolinium Enhancement (LGE) Assessment of myocardial fibrosis by CMR will be expressed as a percentage of left ventricular mass (%LV), maximum left ventricular wall thickness (in mm), left ventricular end-diastolic cavity size (in mm/m^2), and left atrial dimension (in mm). (NCT00879060)
Timeframe: The time points measured were at Baseline and at 12 Months (Follow-Up).
Intervention | Percentage of Total LV Mass (Mean) | |
---|---|---|
LGE Assessment of Myocardial Fibrosis (Baseline) | LGE Assessment of Myocardial Fibrosis (12-Month Follow-Up) | |
Placebo Control | 2.5 | 2.8 |
Spironolactone | 1.1 | 1.8 |
This data was collected at baseline, prior to drug administration, and again at 12-months of follow-up to determine if spironolactone improves a subject's functional capacity during exercise (peak oxygen consumption levels/peak VO2). Peak VO2 levels were measured in ml/kg/min. (NCT00879060)
Timeframe: The time points measured were at Baseline and at 12 Months (Follow-Up).
Intervention | ml/kg/min (Mean) | |
---|---|---|
Peak VO2 (Baseline) | Peak VO2 (12-Month Follow-Up) | |
Placebo Control | 28 | 29 |
Spironolactone | 30 | 29 |
This data was collected at baseline, prior to drug administration, and again at 12-months of follow-up to assess heart failure symptoms according to the New York Heart Association (NYHA) functional class, which is an estimate of a patients functional ability. The NYHA functional classes include: Class I (no limitation of physical activity), Class II (slight limitation of physical activity), Class III (marked limitation of physical activity), and Class IV (unable to carry out any physical acitivity without discomfort). (NCT00879060)
Timeframe: Time points were measured at Baseline and again at 12 months (follow-up)
Intervention | score on a scale (Mean) | |
---|---|---|
NYHA Class (Baseline) | NYHA Class (12-Month Follow Up) | |
Placebo Control | 1.5 | 1.6 |
Spironolactone | 1.6 | 1.7 |
This data was collected at baseline, prior to drug administration, and again at 12-months of follow-up to measure indices of diastolic function by Tissue Doppler Echocardiography using the Septal E/e' ratio. (NCT00879060)
Timeframe: The time points measured were at Baseline and at 12 Months (Follow-Up).
Intervention | Ratio (Mean) | |
---|---|---|
Diastolic Function (Baseline) | Diastolic Function (12-month Follow-Up) | |
Placebo Control | 15 | 13 |
Spironolactone | 14 | 13 |
1 review available for spironolactone and Cardiomyopathy, Hypertrophic
Article | Year |
---|---|
Pushing the Limits of Medical Management in HCM: A Review of Current Pharmacological Therapy Options.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Calcium Channel Blockers; Cardiomyopathy, Hypertro | 2021 |
1 trial available for spironolactone and Cardiomyopathy, Hypertrophic
Article | Year |
---|---|
Effect of Spironolactone on Myocardial Fibrosis and Other Clinical Variables in Patients with Hypertrophic Cardiomyopathy.
Topics: Adult; Biomarkers; Cardiomyopathy, Hypertrophic; Collagen Type I; Double-Blind Method; Fibrosis; Hea | 2018 |
3 other studies available for spironolactone and Cardiomyopathy, Hypertrophic
Article | Year |
---|---|
Adding High-Dose Spironolactone to Tolvaptan Improves Acute Decompensated Heart Failure Due to Obstructive Hypertrophic Cardiomyopathy and Aortic Stenosis: A Case Report.
Topics: Acute Disease; Aged, 80 and over; Antidiuretic Hormone Receptor Antagonists; Aortic Valve Stenosis; | 2019 |
Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy.
Topics: Aged; Aldosterone; Animals; beta Catenin; Biomarkers; Cadherins; Cardiomyopathy, Hypertrophic; Cells | 2004 |
Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy.
Topics: Aged; Aldosterone; Animals; beta Catenin; Biomarkers; Cadherins; Cardiomyopathy, Hypertrophic; Cells | 2004 |
Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy.
Topics: Aged; Aldosterone; Animals; beta Catenin; Biomarkers; Cadherins; Cardiomyopathy, Hypertrophic; Cells | 2004 |
Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy.
Topics: Aged; Aldosterone; Animals; beta Catenin; Biomarkers; Cadherins; Cardiomyopathy, Hypertrophic; Cells | 2004 |
Combined effects of low-dose spironolactone and captopril therapy in a rat model of genetic hypertrophic cardiomyopathy.
Topics: Administration, Oral; Aldosterone; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals | 2006 |