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Last Updated: March 28, 2024

CLINICAL TRIALS PROFILE FOR CARDIZEM CD


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All Clinical Trials for Cardizem Cd

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.
NCT00313157 ↗ RATe Control in Atrial Fibrillation Completed Asker & Baerum Hospital Phase 3 2006-04-01 The purpose of this study is to compare the effect of metoprolol, verapamil, diltiazem and carvedilol on ventricular rate, working capacity and quality of life in patients with chronic atrial fibrillation.
NCT00578617 ↗ Ablation vs Drug Therapy for Atrial Fibrillation - Pilot Trial Completed Abbott Medical Devices N/A 2006-09-01 The CABANA pilot study is designed to test the hypothesis that the treatment strategy of percutaneous left atrial catheter ablation for the purpose of the elimination of atrial fibrillation (AF) is superior to current state-of-the-art therapy with either rate control or anti-arrhythmic drugs for reducing AF recurrences at 1 year follow-up.
NCT00578617 ↗ Ablation vs Drug Therapy for Atrial Fibrillation - Pilot Trial Completed Duke Clinical Research Institute N/A 2006-09-01 The CABANA pilot study is designed to test the hypothesis that the treatment strategy of percutaneous left atrial catheter ablation for the purpose of the elimination of atrial fibrillation (AF) is superior to current state-of-the-art therapy with either rate control or anti-arrhythmic drugs for reducing AF recurrences at 1 year follow-up.
>Trial ID >Title >Status >Phase >Start Date >Summary

Clinical Trial Conditions for Cardizem Cd

Condition Name

Condition Name for Cardizem Cd
Intervention Trials
Atrial Fibrillation 4
Healthy 1
Heart Failure 1
Hypertension 1
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Condition MeSH

Condition MeSH for Cardizem Cd
Intervention Trials
Atrial Fibrillation 4
Hypertension 2
Pulmonary Arterial Hypertension 1
Hypertension, Pulmonary 1
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Clinical Trial Locations for Cardizem Cd

Trials by Country

Trials by Country for Cardizem Cd
Location Trials
United States 21
Canada 1
Norway 1
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Trials by US State

Trials by US State for Cardizem Cd
Location Trials
Tennessee 2
Minnesota 2
Maryland 1
Massachusetts 1
Ohio 1
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Clinical Trial Progress for Cardizem Cd

Clinical Trial Phase

Clinical Trial Phase for Cardizem Cd
Clinical Trial Phase Trials
Phase 4 2
Phase 3 2
Phase 1 3
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Clinical Trial Status

Clinical Trial Status for Cardizem Cd
Clinical Trial Phase Trials
Completed 6
Unknown status 1
Withdrawn 1
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Clinical Trial Sponsors for Cardizem Cd

Sponsor Name

Sponsor Name for Cardizem Cd
Sponsor Trials
Mayo Clinic 2
Kowa Research Institute, Inc. 1
Vanderbilt University 1
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Sponsor Type

Sponsor Type for Cardizem Cd
Sponsor Trials
Other 10
Industry 5
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