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Last Updated: February 15, 2025

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.
NCT00578617 ↗ Ablation vs Drug Therapy for Atrial Fibrillation - Pilot Trial Completed St. Jude Medical 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
Hypertension 1
Idiopathic Pulmonary Arterial Hypertension 1
Arrhythmia 1
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Condition MeSH

Condition MeSH for Cardizem Cd
Intervention Trials
Atrial Fibrillation 4
Hypertension 2
Heart Failure 1
Blood Loss, Surgical 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
Norway 1
Canada 1
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Trials by US State

Trials by US State for Cardizem Cd
Location Trials
Minnesota 2
Tennessee 2
West Virginia 1
Florida 1
Texas 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
Withdrawn 1
Not yet recruiting 1
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Clinical Trial Sponsors for Cardizem Cd

Sponsor Name

Sponsor Name for Cardizem Cd
Sponsor Trials
Mayo Clinic 2
St. Jude Medical 1
Medtronic 1
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Sponsor Type

Sponsor Type for Cardizem Cd
Sponsor Trials
Other 10
Industry 5
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Cardizem CD: Clinical Trials, Market Analysis, and Projections

Introduction

Cardizem CD, a formulation of diltiazem hydrochloride, is a calcium channel blocker used to treat hypertension and angina. Here, we will delve into the clinical trials, market analysis, and projections for this medication.

Clinical Trials for Cardizem CD

Angina Studies

Clinical trials have demonstrated the efficacy of Cardizem CD in managing angina. In a double-blind, parallel, dose-response study, patients received doses ranging from 60 mg to 480 mg once daily. The results showed a linear increase in the time to termination of exercise across all doses. Specifically, the improvement in time to termination of exercise using a Bruce exercise protocol was 29, 40, 56, 51, 69, and 68 seconds for placebo, 60 mg, 120 mg, 240 mg, 360 mg, and 480 mg, respectively. This study also noted a significant decrease in overall angina frequency as the doses of Cardizem CD increased[1][4][5].

Hypertension Studies

For hypertension, another double-blind, parallel dose-response study evaluated the efficacy of Cardizem CD at doses from 90 mg to 540 mg once daily. The results indicated a linear reduction in supine diastolic blood pressure across the entire dose range. The changes in diastolic blood pressure were –2.9, –4.5, –6.1, –9.5, and –10.5 mmHg for placebo, 90 mg, 180 mg, 360 mg, and 540 mg, respectively. Cardizem CD also decreased vascular resistance, increased cardiac output, and had a slight decrease or no change in heart rate[1][4][5].

Adverse Effects Observed in Clinical Trials

While Cardizem CD has shown significant therapeutic benefits, it is not without side effects. Common adverse effects include gastrointestinal issues such as anorexia, constipation, diarrhea, dry mouth, and vomiting. Dermatological side effects like petechiae, photosensitivity, pruritus, and urticaria have also been reported. Other notable side effects include amblyopia, CPK increase, dyspnea, epistaxis, eye irritation, hyperglycemia, hyperuricemia, impotence, muscle cramps, nasal congestion, nocturia, osteoarticular pain, polyuria, and sexual difficulties[1][4].

Market Analysis for Diltiazem

Market Size and Growth

The diltiazem market, which includes Cardizem CD, is projected to grow significantly. As of 2021, the market size was approximately $369.95 million, and it is expected to reach $832.51 million by 2028, growing at a Compound Annual Growth Rate (CAGR) of 12.3% from 2021 to 2028[2].

Driving Factors

The growth of the diltiazem market is driven by several factors, including an increase in the incidence of cardiovascular diseases and an aging population. Cardiovascular diseases are more prevalent among the elderly due to weakened immunity and other health issues. The stiffening of heart and blood vessels with age contributes to higher systolic blood pressure, leading to cardiovascular conditions such as coronary artery disease and heart failure[2].

Market Challenges

Despite the growth potential, the market faces challenges, particularly related to the side effects of diltiazem. These side effects can hamper the market growth as they may lead to patient non-compliance and seek alternative treatments[2].

Mechanisms of Action and Therapeutic Effects

Hypertension

Diltiazem produces its antihypertensive effect primarily by relaxing vascular smooth muscle, which results in a decrease in peripheral vascular resistance. This mechanism leads to a reduction in blood pressure, especially in hypertensive individuals, with minimal effect on normotensive individuals[5].

Angina

For angina, diltiazem reduces myocardial oxygen demand by lowering heart rate, blood pressure, and cardiac contractility. It also induces coronary and peripheral vasodilation, which is beneficial in relieving coronary artery spasm associated with variant angina[2][5].

Pharmacokinetics of Cardizem CD

Absorption and Elimination

Cardizem CD capsules ensure more than 95% absorption of the drug, with detectable plasma levels within 2 hours and peak plasma levels between 10 and 14 hours. The apparent elimination half-life is 5 to 8 hours, and the absorption is not affected by a high-fat content breakfast[5].

Key Takeaways

  • Clinical Efficacy: Cardizem CD has demonstrated efficacy in managing angina and hypertension through various clinical trials.
  • Market Growth: The diltiazem market is expected to grow at a CAGR of 12.3% from 2021 to 2028, driven by increasing cardiovascular disease incidence and an aging population.
  • Side Effects: While effective, Cardizem CD is associated with several side effects that need to be monitored.
  • Mechanisms of Action: Diltiazem works by relaxing vascular smooth muscle and reducing myocardial oxygen demand.

FAQs

What is Cardizem CD used for?

Cardizem CD is used to treat hypertension and angina by relaxing blood vessels and reducing heart rate.

What are the common side effects of Cardizem CD?

Common side effects include gastrointestinal issues, dermatological problems, and other systemic effects such as amblyopia, CPK increase, and hyperglycemia.

How does Cardizem CD work?

Cardizem CD works by inhibiting the cellular influx of calcium ions, leading to relaxation of vascular smooth muscle and a decrease in peripheral vascular resistance.

What is the projected market size for diltiazem by 2028?

The diltiazem market is projected to reach $832.51 million by 2028, growing at a CAGR of 12.3% from 2021 to 2028.

What are the driving factors for the growth of the diltiazem market?

The growth is driven by an increase in cardiovascular disease incidence and an aging population.

Sources

  1. eMPR.com: CARDIZEM CD Prescription & Dosage Information.
  2. The Insight Partners: Diltiazem Market Size, Share & Growth Analysis by 2028.
  3. AstraZeneca Clinical Trials: Open label study, assessing the effect of Diltiazem or Ketoconazole.
  4. FDA: Cardizem CD (diltiazem hydrochloride) capsule label.
  5. Drugs.com: Cardizem CD: Package Insert / Prescribing Information.

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