Does Montelukast Have an Affect on the Function of the Artery in Patients With Heart Disease

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT00351364
Recruitment Status : Terminated (Diffic;ulty recruiting)
First Posted : July 12, 2006
Last Update Posted : December 3, 2014
Foothills Interventional Cardiology Group
Information provided by (Responsible Party):
Todd Anderson, University of Calgary

Brief Summary:
To evaluate the effect of the drug Montelukast on the brachial artery's function. By giving a drug like Montelukast, which blocks the effects of inflammation in the lungs arteries and controls asthma, we hope to see positive effects in other arteries such as in the heart.

Condition or disease Intervention/treatment Phase
Coronary Artery Disease Acute Coronary Syndrome Drug: Montelukast Sodium Phase 4

Detailed Description:
To measure the benefit of cysteinyl leukotriene blockade in favourably altering the pathophysiology of coronary artery disease. We hypothesize that patients admitted to hospital with acute coronary syndromes will have markedly abnormal endothelial function as measured by peripheral vasomotor responses to forearm ischemia. Patients with myocardial infarction and unstable angina have markedly increased renal excretion of the cysteinyl leukotriene metabolite LTE4 as observed in patients with asthma. Observations that coronary vessel tone is negatively affected by leukotrienes C4,D4 and E4 which influences the atherosclerotic process in these arteries. Studies that isolated the epicardial coronary arteries and challenged the vessels with an LTC4 and LTD4 concentration showed that coronary arterial myocytes were found to produce cysteinyl leukotrienes which lead to responsive vasoconstriction. The continued stimulus of vasoconstriction over time leads to endothelial dysfunction and disruption of the endothelium integrity which then leads to stressors that encourage a disease state and atherosclerosis.In this study we will specifically assess peripheral endothelial function by measuring brachial artery diameter changes and PAT responses to temporary forearm ischemia in patients that have had an acute coronary event before and after receiving Montelukast. As well we will measure leukotriene assays both in blood and urine .

Study Type : Interventional  (Clinical Trial)
Actual Enrollment : 40 participants
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Single (Investigator)
Primary Purpose: Treatment
Official Title: The Effect of Leukotriene Receptor Blockade on Endothelial Function in Acute Coronary Syndrome Patients
Study Start Date : July 2006
Actual Primary Completion Date : July 2010
Actual Study Completion Date : July 2010

Resource links provided by the National Library of Medicine

U.S. FDA Resources

Arm Intervention/treatment
Active Comparator: Montelukast sodium
Drug arm - Montelukast as a single dose 100 mg. To test the hypothesis of leukotriene inhibition.
Drug: Montelukast Sodium
100 mg P.O. One time only
Other Name: singular
Placebo Comparator: 2
No drug given - no placebo available. To compare with active drug.
Drug: Montelukast Sodium
100 mg P.O. One time only
Other Name: singular

Primary Outcome Measures :
  1. The degree of brachial artery flow mediated dilation achieved compared between the control and interventional conditions. [ Time Frame: 2 hours between baseline and follow up ]

Secondary Outcome Measures :
  1. The degree of RH-PAT mediated dilation as a ratio of PVA during reactive hyperemia/ baseline PVA index will be compared between the control and Interventional conditions. [ Time Frame: 2 hours between baseline and followup ]

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Ages Eligible for Study:   18 Years to 80 Years   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No

Inclusion Criteria:

  • male or female age 18-80 years, diagnosis of acute coronary syndrome with one increased Troponin assay,chest pain or chest pain syndrome, stable on initial medical therapy, painfree x 6 hours prior to enrollment

Exclusion Criteria:

  • STEMI, Q-wave MI, < 18years, women of childbearing potential, new LBBB, recurrent chest pain since hospitalization, IV nitroglycerine drip, hemodynamically unstable, history of asthma, history of liver disease or abnormal liver enzymes

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT00351364

Canada, Alberta
Foothills Medical Center
Calgary, Alberta, Canada, T2N 2T9
Sponsors and Collaborators
University of Calgary
Foothills Interventional Cardiology Group
Principal Investigator: David Goodhart, MD Foothills Medical Center

Responsible Party: Todd Anderson, Director Libin Cardiovascular Institute, University of Calgary Identifier: NCT00351364     History of Changes
Other Study ID Numbers: 18169
First Posted: July 12, 2006    Key Record Dates
Last Update Posted: December 3, 2014
Last Verified: December 2014

Keywords provided by Todd Anderson, University of Calgary:
leukotriene blockade
endothelial function

Additional relevant MeSH terms:
Coronary Artery Disease
Myocardial Ischemia
Coronary Disease
Acute Coronary Syndrome
Pathologic Processes
Heart Diseases
Cardiovascular Diseases
Arterial Occlusive Diseases
Vascular Diseases
Anti-Asthmatic Agents
Respiratory System Agents
Leukotriene Antagonists
Hormone Antagonists
Hormones, Hormone Substitutes, and Hormone Antagonists
Physiological Effects of Drugs
Cytochrome P-450 CYP1A2 Inducers
Cytochrome P-450 Enzyme Inducers
Molecular Mechanisms of Pharmacological Action