Cushing's Syndrome CardiomyopathyPhase 2ERGONCT02611258
Endocrine Cardiomyopathy in Cushing Syndrome: Response to Cyclic GMP PDE5 inhibitOrs
A Phase 2 study testing Tadalafil in people with Cushing's Syndrome Cardiomyopathy, run by Andrea M. Isidori at 1 site in Italy.
Trial summary
Pathophysiology of Cushing's Syndrome (CS) cardiomyopathy is yet unclear and a specific treatment have not been indicated. It was already demonstrated the positive impact of phosphodiesterase type 5A (PDE5A) inhibition in several models of cardiomyopathy and in a model of endocrine cardiomyopathy due to type 2… Read more about this study
- Who is it for?
- Ages 18 to 75 years
- Conditions the study is for
- Cushing's Syndrome Cardiomyopathy
- What is being tested?
- Tadalafil
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 18 participants
- Where
- 1 siteItaly
- Study dates
- Jul 2016to Jun 2021
- Phase
- Phase 2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 75 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- age>18 yrs;
- patients (men and women) with previous diagnosis of Cushing Syndrome (CS), surgically and/or clinically treated according to current guidelines, with stable parameters of CS disease in the last 3 months, and with concomitant cardiac hypertrophy and/or diastolic dysfunction developed independently of CS care and detected by 2D echocardiography;
- urinary free cortisol (UFC) levels in the normal range for sex and age;
- normal blood pressure or controlled hypertension
Who cannot join
- use of thiazolidinediones, or spironolactone; nitrates, doxazosin, terazosin e prazosin;
- current use of PDE5 inhibitors or previous (wash out of two months at least);
- congenital or valvular cardiomyopathy;
- recent ischemic heart disease or revascularization after a myocardial infarction (MI);
- contraindications to tadalafil use (hypersensitivity to tadalafil, nitrates use, severe cardiovascular disorders such as unstable angina or severe heart failure, severe hepatic impairment, blood pressure <90/50 mmHg, recent history of stroke or myocardial infarction and known hereditary degenerative retinal disorders such as retinitis pigmentosa);
- contraindications to CMR.
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Study on New Insights in Remodeling of Endocrine Cardiomyopathies: Intramyocardial, Molecular and Neuroendocrine Assessment in Response to Chronic Inhibition of Cyclic GMP Phosphodiesterase 5A in Cushing's Syndrome
Pathophysiology of Cushing's Syndrome (CS) cardiomyopathy is yet unclear and a specific treatment have not been indicated. It was already demonstrated the positive impact of phosphodiesterase type 5A (PDE5A) inhibition in several models of cardiomyopathy and in a model of endocrine cardiomyopathy due to type 2 diabetes mellitus. In this patients with diabetic cardiomyopathy it was demonstrated an improvement in cardiac kinetic, geometry and performance parameters and reduction of the ambulatory measurement of waist circumference.
This represents the first study that evaluate heart remodeling and performance changes and metabolic/immunological/molecular parameters after 5-months of Tadalafil 20 mg in Cushing's Syndrome cardiomyopathy. The proposed research will test whether phosphodiesterase 5A inhibition could become a new target for anti-remodeling drugs and to discover molecular pathways affected by this class of drugs and a network of circulating markers (miRNA) for the early diagnosis of Cushing's Syndrome cardiomyopathy.
Read more
The investigators hypothesize that:
- the signal molecules cGMP and cAMP could underlie the hypertrophic/profibrotic triggers related to this model of endocrine cardiomyopathy and that chronic inhibition of PDE5, activating cGMP signaling pathways, could improve cardiac remodeling due to CS;
- PDE5 inhibition could have a role in lipolytic regulation;
- neuroendocrine (e.g. natriuretic peptides) and metabolic markers and chemokines (e.g. MCP-1, TGF-ß) might relate with left ventricular remodeling in CS;
- there are neuroendocrine (e.g. natriuretic peptides), metabolic markers and chemokines (e.g. MCP-1, TGF-ß) related to cardiac disease in CS;
- miRNA expression [miR-208a, 499, 1, 133, 126, 29, 233, 222, 4454] might relate with left ventricular remodeling in CS;
Read the detailed description
Mechanisms of action and evolutionary progression of Cushing's Syndrome (CS) cardiomyopathy are not yet been well elucidated and a specific treatment has not been identified. Our study aims to characterize the CS cardiomyopathy in terms of measuring the cardiac kinetic and performance parameters (tagged Cardiac Magnetic Resonance Imaging), fibrosis (T1-mapping technique). Our study will evaluate if PDE5A inhibition could become a new target for antiremodeling drugs in CS treated patients that developed cardiac hypertrophy and/or diastolic dysfunction independently of CS care accorded by current guidelines. The investigators also will explore the potential mechanisms of action of PDE5Ai: if exerted on cardiac tissue directly and contemporary also on other secondary pathways (analyzing vascular, endothelial, or metabolic markers).
A multidisciplinary approach will allow identifying a cluster of cardiovascular (NT-ProBNP, TGFb, MCP1) and metabolic indices, oxidative stress markers (iNOS, COX2, ROS, RANTES) and miRNAs, whose variations will analyze together with the CS cardiomyopathy parameters measured at CMR and 2D-echocardiography.
The Primary Objective is to evaluate the effects of PDE5Ai on Left Ventricular (LV) remodeling (kinetic and geometry parameters) at cine cardiac magnetic resonance (CMR) with tagging technique and contrast-enhanced and/or at 2D echocardiography with Tissue Doppler Imaging and speckle tracking in patients with CS cardiomyopathy
Secondary Objectives :
- to measure the effect of PDE5Ai on LV fibrosis at T1-mapping CMR at baseline and after PDE5Ai administration.
- to measure the effect of PDE5Ai on cardiac performance at cine CMR and at 2D echocardiography with Tissue Doppler Imaging and speckle tracking at baseline and after PDE5Ai administration.
- to measure the effect PDE5Ai of circulating cardiac-inflammatory-metabolic-endothelial molecular markers
- to measure the effect on bone and body composition
Patients will be screened at time 0. Follow up visits will take place every 4 weeks during treatment for 5 months and 1 month after the end of treatment.
Diagnostic procedures will include:
- physical examination with measurement of anthropometric parameters (weight, waist circumference, hip circumference) and vital signs (blood pressure, heart rate);
- blood sampling for assessing glucose and lipid metabolism, liver, renal, hematopoietic and coagulative function, thyroid and androgen hormones, ACTH and UFC, inflammatory parameters (cytokines, monocyte subpopulations) and microRNA;
- SF36, FSFI (in women), IEFF e IPSS (in men) questionnaires;
- cardiac exam, electrocardiogram and echocardiogram;
- MOC with DEXA;
- magnetic resonance imaging (MRI) with contrast-enhanced cardiac: T1-mapping for assessing cardiac fibrosis; tagging for evaluating kinetic parameters (torsion);
This is a pilot study proof-of-concept, then 10 patients are sufficient to detect the effect of PDE5Ai on cardiac remodeling in CS cardiomyopathy. Estimating a 80% drop-out of the study due to the complexity of CS and the related neuro-psychiatric involvement, 18 CS patients will be enrolled.
All variables will be tested for normality. Statistical analyzes will be performed using SPSS 18.0. The comparison before and after treatment will be made by non parametric Wilcoxon test. The investigators will calculate the confidence interval for the prevalence of the effect measured by χ2 test or Fisher exact test. The correlation was perfomed by Rho di Spearman.
- Conditions
- Cushing's Syndrome Cardiomyopathy
- Being tested
- Tadalafil
- Keywords
- Left Ventricular Hypertrophy, Diastolic Dysfunction, Myocardial Fibrosis, Cushing's Syndrome
- Medical subject headings
- Hypertrophy, Left Ventricular, Cushing Syndrome
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
TadalafilDrug
Also called Cialis
Tadalafil 20 mg to be taken orally once daily, for 3 months
| Study group | Role | What they receive |
|---|---|---|
| Tadalafil | Experimental | Tadalafil 20 mg to be taken orally once daily, for 3 months Receives: Drug: Tadalafil |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change of Left ventricular torsion (°)
Change of Left ventricular torsion (°) evaluated through Cardiac Magnetic Resonance
Measured: Baseline and 3 months after treatment
Secondary outcomes (12)
Change of cardiac strain (σ - longitudinal shortening: strain %)
Change of cardiac strain (σ - longitudinal shortening: strain %) evaluated through Cardiac Magnetic Resonance
Measured: Baseline and 3 months after treatment
Quantification of Myocardial fibrosis
Quantification of Myocardial fibrosis assessed with T1-mapping through Cardiac Magnetic Resonance
Measured: Baseline and 3 months after treatment
Inflammatory indices
Assessment of inflammatory indices (e.g. TGF-beta, MCP1)
Measured: Baseline and 3 months after treatment
Assessment of endothelial function markers Assessment of endothelial function markers
Assessment of endothelial function markers (e.g ET-1, VEGF)
Measured: Baseline and 3 months after treatment
NT-proBNP
Assessment of NT-proBNP
Measured: Baseline and 3 months after treatment
Assessment of oxidative stress markers
Assessment of oxidative stress markers (eg iNOS, COX2, ROS, P Selectin, ICAM1)
Measured: Baseline and 3 months after treatment
cGMP
Assessment of plasmatic levels of cGMP
Measured: Baseline and 3 months after treatment
Correlation analysis
Correlation of biochemical parameters with cardiac parameters assessed through Cardiac Magnetic Resonance
Measured: Baseline and 3 months after treatment
Assessment of circulating microRNAs
Assessment of circulating microRNAs from plasma and white blood cells (miR208, 499, 1, 133, 29, 223, 222, 4454) and correlation of their levels to basal torsion, strain and fibrosis.
Measured: Baseline
Changes of circulating miRNAs
Changes of circulating miRNAs from plasma and white blood cells (miR208, 499, 1, 133, 29, 223, 222, 4454)
Measured: Baseline and 3 months after treatment
Assessment of circulating pro-fibrotic and pro-inflammatory chemokines
Assessment of circulating pro-fibrotic and pro-inflammatory chemokines (MCP-1 and TGF-beta) and correlation to torsion, strain and fibrosis
Measured: Baseline and 3 months after treatment
Body composition
Change of parameters of body composition evaluated by MOC with total body DEXA scan
Measured: Baseline and 3 months after treatment
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted20 Nov 2015 (estimated)
- Study startJul 2016
- Primary completionJan 2021
- Study completionJun 2021
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (6)Papers the sponsor has linked to this study.
- Other trials for Cushing's Syndrome CardiomyopathyStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 2
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 18 participants (actual)
Sponsor and investigators
- Lead sponsor
- Andrea M. Isidori
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor-investigator, Andrea M. Isidori, University of Roma La Sapienza
- Investigators
- Elisa Giannetta, MD - Phd, Principal investigator, Sapienza University of Rome, Policlinico Umberto I, Department of Experimental Medicine
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02611258
- Sponsor's protocol ID
- ERGO
- Other IDs
- 2015-004497-15, 2015
- Acronym
- ERGO
- Status last verified
- May 2023
- First submitted
- 16 Nov 2015
- Last updated
- 16 May 2023
- Results posted
- No
Publications
Giannetta E, Isidori AM, Galea N, Carbone I, Mandosi E, Vizza CD, Naro F, Morano S, Fedele F, Lenzi A. Chronic Inhibition of cGMP phosphodiesterase 5A improves diabetic cardiomyopathy: a randomized, controlled clinical trial using magnetic resonance imaging with myocardial tagging. Circulation. 2012 May 15;125(19):2323-33. doi: 10.1161/CIRCULATIONAHA.111.063412. Epub 2012 Apr 11.
PubMed 22496161Bernardo BC, Weeks KL, Pretorius L, McMullen JR. Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. Pharmacol Ther. 2010 Oct;128(1):191-227. doi: 10.1016/j.pharmthera.2010.04.005. Epub 2010 May 12.
PubMed 20438756Montgomery RL, Hullinger TG, Semus HM, Dickinson BA, Seto AG, Lynch JM, Stack C, Latimer PA, Olson EN, van Rooij E. Therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure. Circulation. 2011 Oct 4;124(14):1537-47. doi: 10.1161/CIRCULATIONAHA.111.030932. Epub 2011 Sep 6.
PubMed 21900086Fichtlscherer S, Zeiher AM, Dimmeler S. Circulating microRNAs: biomarkers or mediators of cardiovascular diseases? Arterioscler Thromb Vasc Biol. 2011 Nov;31(11):2383-90. doi: 10.1161/ATVBAHA.111.226696.
PubMed 22011751Baseler WA, Thapa D, Jagannathan R, Dabkowski ER, Croston TL, Hollander JM. miR-141 as a regulator of the mitochondrial phosphate carrier (Slc25a3) in the type 1 diabetic heart. Am J Physiol Cell Physiol. 2012 Dec 15;303(12):C1244-51. doi: 10.1152/ajpcell.00137.2012. Epub 2012 Oct 3.
PubMed 23034391De Leo M, Pivonello R, Auriemma RS, Cozzolino A, Vitale P, Simeoli C, De Martino MC, Lombardi G, Colao A. Cardiovascular disease in Cushing's syndrome: heart versus vasculature. Neuroendocrinology. 2010;92 Suppl 1:50-4. doi: 10.1159/000318566. Epub 2010 Sep 10.
PubMed 20829618
Study at a glance
From the registry record, last updated by the sponsor on 16 May 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Study on New Insights in Remodeling of Endocrine Cardiomyopathies: Intramyocardial, Molecular and Neuroendocrine Assessment in Response to Chronic Inhibition of Cyclic GMP Phosphodiesterase 5A in Cushing's Syndrome
- ClinicalTrials.gov ID
- NCT02611258
- Acronym / sponsor ID
- ERGO / ERGO
- Conditions
- Cushing's Syndrome Cardiomyopathy
- Keywords
- Left Ventricular Hypertrophy, Diastolic Dysfunction, Myocardial Fibrosis, Cushing's Syndrome
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 18 participants (actual)
- Lead sponsor
- Andrea M. IsidoriUniversity, hospital or other
- Study start
- Jul 2016 (actual)
- Primary completion
- Jan 2021 (actual)
- Study completion
- Jun 2021 (actual)
- First posted
- 20 Nov 2015 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Pathophysiology of Cushing's Syndrome (CS) cardiomyopathy is yet unclear and a specific treatment have not been indicated. It was already demonstrated the positive impact of phosphodiesterase type 5A (PDE5A) inhibition in several models of cardiomyopathy and in a model of endocrine cardiomyopathy due to type 2 diabetes mellitus. In this patients with diabetic cardiomyopathy it was demonstrated an improvement in cardiac kinetic, geometry and performance parameters and reduction of the ambulatory measurement of waist circumference.
This represents the first study that evaluate heart remodeling and performance changes and metabolic/immunological/molecular parameters after 5-months of Tadalafil 20 mg in Cushing's Syndrome cardiomyopathy. The proposed research will test whether phosphodiesterase 5A inhibition could become a new target for anti-remodeling drugs and to discover molecular pathways affected by this class of drugs and a network of circulating markers (miRNA) for the early diagnosis of Cushing's Syndrome cardiomyopathy.
The investigators hypothesize that:
- the signal molecules cGMP and cAMP could underlie the hypertrophic/profibrotic triggers related to this model of endocrine cardiomyopathy and that chronic inhibition of PDE5, activating cGMP signaling pathways, could improve cardiac remodeling due to CS;
- PDE5 inhibition could have a role in lipolytic regulation;
- neuroendocrine (e.g. natriuretic peptides) and metabolic markers and chemokines (e.g. MCP-1, TGF-ß) might relate with left ventricular remodeling in CS;
- there are neuroendocrine (e.g. natriuretic peptides), metabolic markers and chemokines (e.g. MCP-1, TGF-ß) related to cardiac disease in CS;
- miRNA expression [miR-208a, 499, 1, 133, 126, 29, 233, 222, 4454] might relate with left ventricular remodeling in CS;
Detailed description
Mechanisms of action and evolutionary progression of Cushing's Syndrome (CS) cardiomyopathy are not yet been well elucidated and a specific treatment has not been identified. Our study aims to characterize the CS cardiomyopathy in terms of measuring the cardiac kinetic and performance parameters (tagged Cardiac Magnetic Resonance Imaging), fibrosis (T1-mapping technique). Our study will evaluate if PDE5A inhibition could become a new target for antiremodeling drugs in CS treated patients that developed cardiac hypertrophy and/or diastolic dysfunction independently of CS care accorded by current guidelines. The investigators also will explore the potential mechanisms of action of PDE5Ai: if exerted on cardiac tissue directly and contemporary also on other secondary pathways (analyzing vascular, endothelial, or metabolic markers).
A multidisciplinary approach will allow identifying a cluster of cardiovascular (NT-ProBNP, TGFb, MCP1) and metabolic indices, oxidative stress markers (iNOS, COX2, ROS, RANTES) and miRNAs, whose variations will analyze together with the CS cardiomyopathy parameters measured at CMR and 2D-echocardiography.
The Primary Objective is to evaluate the effects of PDE5Ai on Left Ventricular (LV) remodeling (kinetic and geometry parameters) at cine cardiac magnetic resonance (CMR) with tagging technique and contrast-enhanced and/or at 2D echocardiography with Tissue Doppler Imaging and speckle tracking in patients with CS cardiomyopathy
Secondary Objectives :
- to measure the effect of PDE5Ai on LV fibrosis at T1-mapping CMR at baseline and after PDE5Ai administration.
- to measure the effect of PDE5Ai on cardiac performance at cine CMR and at 2D echocardiography with Tissue Doppler Imaging and speckle tracking at baseline and after PDE5Ai administration.
- to measure the effect PDE5Ai of circulating cardiac-inflammatory-metabolic-endothelial molecular markers
- to measure the effect on bone and body composition
Patients will be screened at time 0. Follow up visits will take place every 4 weeks during treatment for 5 months and 1 month after the end of treatment.
Diagnostic procedures will include:
- physical examination with measurement of anthropometric parameters (weight, waist circumference, hip circumference) and vital signs (blood pressure, heart rate);
- blood sampling for assessing glucose and lipid metabolism, liver, renal, hematopoietic and coagulative function, thyroid and androgen hormones, ACTH and UFC, inflammatory parameters (cytokines, monocyte subpopulations) and microRNA;
- SF36, FSFI (in women), IEFF e IPSS (in men) questionnaires;
- cardiac exam, electrocardiogram and echocardiogram;
- MOC with DEXA;
- magnetic resonance imaging (MRI) with contrast-enhanced cardiac: T1-mapping for assessing cardiac fibrosis; tagging for evaluating kinetic parameters (torsion);
This is a pilot study proof-of-concept, then 10 patients are sufficient to detect the effect of PDE5Ai on cardiac remodeling in CS cardiomyopathy. Estimating a 80% drop-out of the study due to the complexity of CS and the related neuro-psychiatric involvement, 18 CS patients will be enrolled.
All variables will be tested for normality. Statistical analyzes will be performed using SPSS 18.0. The comparison before and after treatment will be made by non parametric Wilcoxon test. The investigators will calculate the confidence interval for the prevalence of the effect measured by χ2 test or Fisher exact test. The correlation was perfomed by Rho di Spearman.
Study design
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Tadalafil | Experimental | Drug: TadalafilTadalafil 20 mg to be taken orally once daily, for 3 months |
Who may qualify
- Ages
- 18 to 75 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (4 listed)
- age>18 yrs;
- patients (men and women) with previous diagnosis of Cushing Syndrome (CS), surgically and/or clinically treated according to current guidelines, with stable parameters of CS disease in the last 3 months, and with concomitant cardiac hypertrophy and/or diastolic dysfunction developed independently of CS care and detected by 2D echocardiography;
- urinary free cortisol (UFC) levels in the normal range for sex and age;
- normal blood pressure or controlled hypertension
Key exclusion criteria (6 listed)
- use of thiazolidinediones, or spironolactone; nitrates, doxazosin, terazosin e prazosin;
- current use of PDE5 inhibitors or previous (wash out of two months at least);
- congenital or valvular cardiomyopathy;
- recent ischemic heart disease or revascularization after a myocardial infarction (MI);
- contraindications to tadalafil use (hypersensitivity to tadalafil, nitrates use, severe cardiovascular disorders such as unstable angina or severe heart failure, severe hepatic impairment, blood pressure <90/50 mmHg, recent history of stroke or myocardial infarction and known hereditary degenerative retinal disorders such as retinitis pigmentosa);
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| TadalafilAlso: CialisTadalafil 20 mg to be taken orally once daily, for 3 months | Drug | Tadalafil |
Primary outcome
Change of Left ventricular torsion (°)
Time frame: Baseline and 3 months after treatment
Change of Left ventricular torsion (°) evaluated through Cardiac Magnetic Resonance
12 secondary outcomes
Change of cardiac strain (σ - longitudinal shortening: strain %)
Time frame: Baseline and 3 months after treatment
Quantification of Myocardial fibrosis
Time frame: Baseline and 3 months after treatment
Inflammatory indices
Time frame: Baseline and 3 months after treatment
Assessment of endothelial function markers Assessment of endothelial function markers
Time frame: Baseline and 3 months after treatment
NT-proBNP
Time frame: Baseline and 3 months after treatment
Assessment of oxidative stress markers
Time frame: Baseline and 3 months after treatment
cGMP
Time frame: Baseline and 3 months after treatment
Correlation analysis
Time frame: Baseline and 3 months after treatment
Assessment of circulating microRNAs
Time frame: Baseline
Changes of circulating miRNAs
Time frame: Baseline and 3 months after treatment
Assessment of circulating pro-fibrotic and pro-inflammatory chemokines
Time frame: Baseline and 3 months after treatment
Body composition
Time frame: Baseline and 3 months after treatment
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 16 May 2023.
- Background: PubMed 22496161Giannetta E, Isidori AM, Galea N, Carbone I, Mandosi E, Vizza CD, Naro F, Morano S, Fedele F, Lenzi A. Chronic Inhibition of cGMP phosphodiesterase 5A improves diabetic cardiomyopathy: a randomized, controlled clinical trial using magnetic resonance imaging with myocardial tagging. Circulation. 2012 May 15;125(19):2323-33. doi: 10.1161/CIRCULATIONAHA.111.063412. Epub 2012 Apr 11.
- Background: PubMed 20438756Bernardo BC, Weeks KL, Pretorius L, McMullen JR. Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. Pharmacol Ther. 2010 Oct;128(1):191-227. doi: 10.1016/j.pharmthera.2010.04.005. Epub 2010 May 12.
- Background: PubMed 21900086Montgomery RL, Hullinger TG, Semus HM, Dickinson BA, Seto AG, Lynch JM, Stack C, Latimer PA, Olson EN, van Rooij E. Therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure. Circulation. 2011 Oct 4;124(14):1537-47. doi: 10.1161/CIRCULATIONAHA.111.030932. Epub 2011 Sep 6.
- Background: PubMed 22011751Fichtlscherer S, Zeiher AM, Dimmeler S. Circulating microRNAs: biomarkers or mediators of cardiovascular diseases? Arterioscler Thromb Vasc Biol. 2011 Nov;31(11):2383-90. doi: 10.1161/ATVBAHA.111.226696.
- Background: PubMed 23034391Baseler WA, Thapa D, Jagannathan R, Dabkowski ER, Croston TL, Hollander JM. miR-141 as a regulator of the mitochondrial phosphate carrier (Slc25a3) in the type 1 diabetic heart. Am J Physiol Cell Physiol. 2012 Dec 15;303(12):C1244-51. doi: 10.1152/ajpcell.00137.2012. Epub 2012 Oct 3.
- Background: PubMed 20829618De Leo M, Pivonello R, Auriemma RS, Cozzolino A, Vitale P, Simeoli C, De Martino MC, Lombardi G, Colao A. Cardiovascular disease in Cushing's syndrome: heart versus vasculature. Neuroendocrinology. 2010;92 Suppl 1:50-4. doi: 10.1159/000318566. Epub 2010 Sep 10.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Elisa Giannetta, MD - Phd principal investigator
Sapienza University of Rome, Policlinico Umberto I, Department of Experimental Medicine
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Tadalafil in people with Cushing's Syndrome Cardiomyopathy, run by Andrea M. Isidori at 1 site in Italy.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 6 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 16 May 2023. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Italy. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change of Left ventricular torsion (°) (time frame: Baseline and 3 months after treatment). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02611258, which also lists 6 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 16 May 2023.