CLINICAL TRIALS PROFILE FOR CAPOTEN
✉ Email this page to a colleague
All Clinical Trials for CAPOTEN
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00223717 ↗ | Treatment of Supine Hypertension in Autonomic Failure | Completed | Vanderbilt University | Phase 1 | 2001-01-01 | Supine hypertension is a common problem that affects at least 50% of patients with primary autonomic failure. Supine hypertension can be severe, and complicates the treatment of orthostatic hypotension. Drugs used for the treatment of orthostatic hypotension (eg, fludrocortisone and pressor agents), worsen supine hypertension. High blood pressure may also cause target organ damage in this group of patients. The pathophysiologic mechanisms causing supine hypertension in patients with autonomic failure have not been defined. In a study, we, the investigators at Vanderbilt University, examined 64 patients with AF, 29 with pure autonomic failure (PAF) and 35 with multiple system atrophy (MSA). 66% of patients had supine systolic (systolic blood pressure [SBP] > 150 mmHg) or diastolic (diastolic blood pressure [DBP] > 90 mmHg) hypertension (average blood pressure [BP]: 179 ± 5/89 ± 3 mmHg in 21 PAF and 175 ± 5/92 ± 3 mmHg in 21 MSA patients). Plasma norepinephrine (92 ± 15 pg/mL) and plasma renin activity (0.3 ± 0.05 ng/mL per hour) were very low in a subset of patients with AF and supine hypertension. (Shannon et al., 1997). Our group has showed that a residual sympathetic function contributes to supine hypertension in patients with severe autonomic failure and that this effect is more prominent in patients with MSA than in those with PAF (Shannon et al., 2000). MSA patients had a marked depressor response to low infusion rates of trimethaphan, a ganglionic blocker; the response in PAF patients was more variable. At 1 mg/min, trimethaphan decreased supine SBP by 67 +/- 8 and 12 +/- 6 mmHg in MSA and PAF patients, respectively (P < 0.0001). MSA patients with supine hypertension also had greater SBP response to oral yohimbine, a central alpha2 receptor blocker, than PAF patients. Plasma norepinephrine decreased in both groups, but heart rate did not change in either group. This result suggests that residual sympathetic activity drives supine hypertension in MSA; in contrast, supine hypertension in PAF. It is hoped that from this study will emerge a complete picture of the supine hypertension of autonomic failure. Understanding the mechanism of this paradoxical hypertension in the setting of profound loss of sympathetic function will improve our approach to the treatment of hypertension in autonomic failure, and it could also contribute to our understanding of hypertension in general. |
| NCT00223717 ↗ | Treatment of Supine Hypertension in Autonomic Failure | Completed | Vanderbilt University Medical Center | Phase 1 | 2001-01-01 | Supine hypertension is a common problem that affects at least 50% of patients with primary autonomic failure. Supine hypertension can be severe, and complicates the treatment of orthostatic hypotension. Drugs used for the treatment of orthostatic hypotension (eg, fludrocortisone and pressor agents), worsen supine hypertension. High blood pressure may also cause target organ damage in this group of patients. The pathophysiologic mechanisms causing supine hypertension in patients with autonomic failure have not been defined. In a study, we, the investigators at Vanderbilt University, examined 64 patients with AF, 29 with pure autonomic failure (PAF) and 35 with multiple system atrophy (MSA). 66% of patients had supine systolic (systolic blood pressure [SBP] > 150 mmHg) or diastolic (diastolic blood pressure [DBP] > 90 mmHg) hypertension (average blood pressure [BP]: 179 ± 5/89 ± 3 mmHg in 21 PAF and 175 ± 5/92 ± 3 mmHg in 21 MSA patients). Plasma norepinephrine (92 ± 15 pg/mL) and plasma renin activity (0.3 ± 0.05 ng/mL per hour) were very low in a subset of patients with AF and supine hypertension. (Shannon et al., 1997). Our group has showed that a residual sympathetic function contributes to supine hypertension in patients with severe autonomic failure and that this effect is more prominent in patients with MSA than in those with PAF (Shannon et al., 2000). MSA patients had a marked depressor response to low infusion rates of trimethaphan, a ganglionic blocker; the response in PAF patients was more variable. At 1 mg/min, trimethaphan decreased supine SBP by 67 +/- 8 and 12 +/- 6 mmHg in MSA and PAF patients, respectively (P < 0.0001). MSA patients with supine hypertension also had greater SBP response to oral yohimbine, a central alpha2 receptor blocker, than PAF patients. Plasma norepinephrine decreased in both groups, but heart rate did not change in either group. This result suggests that residual sympathetic activity drives supine hypertension in MSA; in contrast, supine hypertension in PAF. It is hoped that from this study will emerge a complete picture of the supine hypertension of autonomic failure. Understanding the mechanism of this paradoxical hypertension in the setting of profound loss of sympathetic function will improve our approach to the treatment of hypertension in autonomic failure, and it could also contribute to our understanding of hypertension in general. |
| NCT01292694 ↗ | Contribution of Angiotensin II to Supine Hypertension in Autonomic Failure | Terminated | Vanderbilt University | Phase 1 | 2011-03-01 | The purpose of this study is to test the hypothesis that angiotensin II plays a role in the supine hypertension of primary autonomic failure. To determine the contribution of angiotensin II to renin and blood pressure regulation in autonomic failure, patients with multiple system atrophy [MSA] or pure autonomic failure [PAF] and supine hypertension will undergo medication testing with the angiotensin II receptor blocker losartan. The investigators will compare the biochemical and hemodynamic effects between MSA and PAF patients. In a subset of patients, the investigators will also give the ACE inhibitor captopril. Our primary endpoint will be changes in plasma renin activity, and subsequent components of the circulating renin-angiotensin system, in response to angiotensin II blockade. Our secondary outcome will be changes in hemodynamic measures during administration of these drugs. |
| NCT01669434 ↗ | Chronic Angiotensin Converting Enzyme Inhibitors in Intermediate Risk Surgery | Completed | University of Nebraska | Phase 4 | 2015-06-01 | Primary research hypothesis: Patients who continue their chronic ACEI therapy up to and including the morning of a non-cardiac, non-vascular surgery will experience more intraoperative hypotension than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #1: Patients who continue their chronic ACEI up to and including the morning of a non-cardiac, non-vascular surgery will experience better postoperative control of hypertension than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #2: Patients who continue their chronic ACEI up to and including the morning of a non-cardiac, non-vascular surgery will experience less acute renal failure than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #3: In the subgroup of patients with a preoperative systolic blood pressure less than 110 mmHg, those who continue their chronic ACEI therapy up to and including the morning of a non-cardiac, non-vascular surgery will experience more intraoperative hypotension than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #4: In the subgroup of patients above the age of 64, those who continue their chronic ACEI therapy up to and including the morning of a non-cardiac, non-vascular surgery will experience more intraoperative hypotension than those who transiently hold their chronic ACEI preoperatively. |
| NCT03389724 ↗ | Prevention of Chemotherapy Induced Cardiotoxicity in Children With Bone Tumors and Acute Myeloid Leukemia | Recruiting | Children's Cancer Hospital Egypt 57357 | Phase 3 | 2017-11-14 | Prevention and early detection of chemotherapy-induced cardiotoxicity in children with bone tumors and Acute Myeloid Leukemia by giving capoten |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
Clinical Trial Conditions for CAPOTEN
Condition Name
Clinical Trial Locations for CAPOTEN
Trials by Country
Clinical Trial Progress for CAPOTEN
Clinical Trial Phase
Clinical Trial Sponsors for CAPOTEN
Sponsor Name
