aldosterone has been researched along with Cardiomyopathy, Hypertrophic in 9 studies
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).
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 1 (11.11) | 18.7374 |
1990's | 1 (11.11) | 18.2507 |
2000's | 3 (33.33) | 29.6817 |
2010's | 3 (33.33) | 24.3611 |
2020's | 1 (11.11) | 2.80 |
Authors | Studies |
---|---|
Mendes, LC | 1 |
de Oliveira Magalhães, R | 1 |
Pereira Dos Santos, RK | 1 |
Araújo, RS | 1 |
Ramchand, J | 1 |
Sampaio Rodrigues, T | 1 |
Yudi, MB | 1 |
Burrell, LM | 1 |
Orenes-Piñero, E | 1 |
Hernández-Romero, D | 1 |
Romero-Aniorte, AI | 1 |
Martínez, M | 1 |
García-Honrubia, A | 1 |
Caballero, L | 1 |
Garrigos-Gómez, N | 1 |
Andreu-Cayuelas, JM | 1 |
González, J | 1 |
Feliu, E | 1 |
Climent, V | 1 |
Nicolás-Ruiz, F | 1 |
De La Morena, G | 1 |
Valdés, M | 1 |
Lip, GY | 1 |
Marín, F | 1 |
Tarjus, A | 1 |
Martínez-Martínez, E | 1 |
Amador, C | 1 |
Latouche, C | 1 |
El Moghrabi, S | 1 |
Berger, T | 1 |
Mak, TW | 1 |
Fay, R | 1 |
Farman, N | 1 |
Rossignol, P | 1 |
Zannad, F | 1 |
López-Andrés, N | 1 |
Jaisser, F | 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 |
Chai, W | 1 |
Hoedemaekers, Y | 1 |
van Schaik, RH | 1 |
van Fessem, M | 1 |
Garrelds, IM | 1 |
Saris, JJ | 1 |
Dooijes, D | 1 |
ten Cate, FJ | 1 |
Kofflard, MM | 1 |
Danser, AH | 1 |
Brilla, CG | 1 |
Rupp, H | 1 |
Funck, R | 1 |
Maisch, B | 1 |
Kohyama, J | 1 |
Watanabe, S | 1 |
Fukuda, C | 1 |
Shimozawa, K | 1 |
Saitoh, K | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
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 | ||
Clinical and Therapeutic Implications of Fibrosis in Hypertrophic Cardiomyopathy[NCT00879060] | Phase 4 | 53 participants (Actual) | Interventional | 2007-11-30 | Completed | ||
[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 aldosterone and Cardiomyopathy, Hypertrophic
Article | Year |
---|---|
The renin-angiotensin-aldosterone system and myocardial collagen matrix remodelling in congestive heart failure.
Topics: Adult; Aldosterone; Cardiomyopathy, Hypertrophic; Cell Division; Collagen; Connective Tissue; Corona | 1995 |
8 other studies available for aldosterone and Cardiomyopathy, Hypertrophic
Article | Year |
---|---|
Pseudohypoaldosteronism associated with hypertrophic cardiomyopathy, hypertension and thrombocytosis due to mutation in the ELAC2 gene: a case report.
Topics: Aldosterone; Cardiomyopathy, Hypertrophic; Child; Humans; Hypertension; Mutation; Neoplasm Proteins; | 2022 |
Further studies needed before using renin-angiotensin-aldosterone system blockade for atrial fibrillation prevention in hypertrophic cardiomyopathy.
Topics: Aldosterone; Angiotensins; Atrial Fibrillation; Cardiomyopathy, Hypertrophic; Humans; Renin; Renin-A | 2018 |
Prognostic value of two polymorphisms in non-sarcomeric genes for the development of atrial fibrillation in patients with hypertrophic cardiomyopathy.
Topics: Adult; Aged; Aldosterone; Atrial Fibrillation; Cardiomyopathy, Hypertrophic; Case-Control Studies; C | 2014 |
Neutrophil Gelatinase-Associated Lipocalin, a Novel Mineralocorticoid Biotarget, Mediates Vascular Profibrotic Effects of Mineralocorticoids.
Topics: Acute-Phase Proteins; Aldosterone; Animals; Aorta; Cardiomyopathy, Hypertrophic; Cells, Cultured; Cy | 2015 |
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 |
Cardiac aldosterone in subjects with hypertrophic cardiomyopathy.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Aldosterone; Cardiomyopathy, Hypertrophic; Cytochrome P- | 2006 |
Adrenocorticotropic hormone unresponsiveness associated with hypertrophic cardiomyopathy.
Topics: 17-Ketosteroids; Adrenal Glands; Adrenocorticotropic Hormone; Aldosterone; Cardiomyopathy, Hypertrop | 1989 |