Page last updated: 2024-11-07

spironolactone and Cardiomyopathy, Hypertrophic

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).

Research Excerpts

ExcerptRelevanceReference
"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."9.27Effect 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."7.91Adding 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."5.27Effect 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."3.91Adding 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)

Research

Studies (5)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's2 (40.00)29.6817
2010's2 (40.00)24.3611
2020's1 (20.00)2.80

Authors

AuthorsStudies
Stătescu, C1
Enachi, Ș1
Ureche, C1
Țăpoi, L1
Anghel, L1
Șalaru, D1
Pleșoianu, C1
Bostan, M1
Marcu, D1
Ovanez Balasanian, M1
Sascău, RA1
Maron, MS1
Chan, RH1
Kapur, NK1
Jaffe, IZ1
McGraw, AP1
Kerur, R1
Maron, BJ1
Udelson, JE1
Kajimoto, K1
Otsubo, S1
Tsybouleva, N1
Zhang, L1
Chen, S1
Patel, R1
Lutucuta, S1
Nemoto, S1
DeFreitas, G1
Entman, M1
Carabello, BA1
Roberts, R1
Marian, AJ1
de Resende, MM1
Kriegel, AJ1
Greene, AS1

Clinical Trials (2)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Clinical and Therapeutic Implications of Fibrosis in Hypertrophic Cardiomyopathy[NCT00879060]Phase 453 participants (Actual)Interventional2007-11-30Completed
Evaluating the Effect of Spironolactone on Hypertrophic Cardiomyopathy-- a Multicenter Randomized Control Trial[NCT02948998]Phase 4260 participants (Anticipated)Interventional2018-05-14Not yet recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Absolute Change in Serum Markers of Collagen Turnover (Micrograms/L) Over a One-year Follow-up Period in the Spironolactone Group Compared to Placebo.

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).

,
Interventionmicrograms/L (Mean)
Baseline (PINP)12 Months (PINP)Baseline (PIIINP)12 Months (PIIINP)Baseline (ICTP)12 Months (ICTP)
Placebo Control2.10.64.51.62.5-2.3
Spironolactone2.10.74.72.02.22.7

Assessment of Cardiac Mass and Fibrosis by Cardiac Magnetic Resonance Imaging (CMR) - Left Atrial Dimension (in mm)

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)

,
Interventionmillimeters (Mean)
Left Atrial Dimension (Baseline)Left Atrial Dimension (12-Month Follow-Up)
Placebo Control4140
Spironolactone4040

Assessment of Cardiac Mass and Fibrosis by Cardiac Magnetic Resonance Imaging (CMR) - Left Ventricular End-Diastolic (LVED) Cavity Size (in mm/m^2)

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)

,
Interventionmm/m^2 (Mean)
LVED Cavity Size (Baseline)LVED Cavity Size (12-Month Follow-Up)
Placebo Control145146
Spironolactone133129

Assessment of Cardiac Mass and Fibrosis by Cardiac Magnetic Resonance Imaging (CMR) - Maximum Left Ventricular Wall Thickness (in mm)

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).

,
Interventionmillimeters (Mean)
Maximum Left Ventricular Wall Thickness (Baseline)Maximum Left Ventricular Wall Thickness (12-Month Follow-Up)
Placebo Control2119
Spironolactone2222

Assessment of Cardiac Mass and Fibrosis by Cardiac Magnetic Resonance Imaging (CMR) - Percentage of Left Ventricular Mass (%LV)

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).

,
InterventionPercentage of Total LV Mass (Mean)
LGE Assessment of Myocardial Fibrosis (Baseline)LGE Assessment of Myocardial Fibrosis (12-Month Follow-Up)
Placebo Control2.52.8
Spironolactone1.11.8

Measure of Functional Capacity: Peak Oxygen Consumption With Exercise

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).

,
Interventionml/kg/min (Mean)
Peak VO2 (Baseline)Peak VO2 (12-Month Follow-Up)
Placebo Control2829
Spironolactone3029

Measure of Heart Failure Symptoms According to the New York Heart Association Functional Class

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)

,
Interventionscore on a scale (Mean)
NYHA Class (Baseline)NYHA Class (12-Month Follow Up)
Placebo Control1.51.6
Spironolactone1.61.7

Measure of Indices of Diastolic Function by Tissue Doppler Echocardiography (Septal E/e')

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).

,
InterventionRatio (Mean)
Diastolic Function (Baseline)Diastolic Function (12-month Follow-Up)
Placebo Control1513
Spironolactone1413

Reviews

1 review available for spironolactone and Cardiomyopathy, Hypertrophic

ArticleYear
Pushing the Limits of Medical Management in HCM: A Review of Current Pharmacological Therapy Options.
    International journal of molecular sciences, 2021, Jul-05, Volume: 22, Issue:13

    Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Calcium Channel Blockers; Cardiomyopathy, Hypertro

2021

Trials

1 trial available for spironolactone and Cardiomyopathy, Hypertrophic

ArticleYear
Effect of Spironolactone on Myocardial Fibrosis and Other Clinical Variables in Patients with Hypertrophic Cardiomyopathy.
    The American journal of medicine, 2018, Volume: 131, Issue:7

    Topics: Adult; Biomarkers; Cardiomyopathy, Hypertrophic; Collagen Type I; Double-Blind Method; Fibrosis; Hea

2018

Other Studies

3 other studies available for spironolactone and Cardiomyopathy, Hypertrophic

ArticleYear
Adding High-Dose Spironolactone to Tolvaptan Improves Acute Decompensated Heart Failure Due to Obstructive Hypertrophic Cardiomyopathy and Aortic Stenosis: A Case Report.
    The American journal of case reports, 2019, Jul-12, Volume: 20

    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.
    Circulation, 2004, Mar-16, Volume: 109, Issue:10

    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.
    Circulation, 2004, Mar-16, Volume: 109, Issue:10

    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.
    Circulation, 2004, Mar-16, Volume: 109, Issue:10

    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.
    Circulation, 2004, Mar-16, Volume: 109, Issue:10

    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.
    Journal of cardiovascular pharmacology, 2006, Volume: 48, Issue:6

    Topics: Administration, Oral; Aldosterone; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals

2006