Nicorandil improves myocardial function by regulating plasma nitric oxide and endothelin-1 in coronary slow flow

Zuoyuan Chen1, Xiuhua Chen, Shan Li

  • 1Departments of aCardiology bCardiac Ultrasound, The Affiliated Hospital of Qingdao University cDepartment of Internal Medicine, Qingdao Commercial Hospital dDepartment of Cardiology, Qingdao Fifth People's Hospital, Qingdao eDepartment of Cardiology, Dezhou People's Hospital, Dezhou, Shandong, China.

Coronary Artery Disease
|October 18, 2014
PubMed

Insights

Nicorandil treatment improved left ventricular function and reduced chest pain in patients with coronary slow flow (CSF) by increasing nitric oxide (NO) and decreasing endothelin-1 (ET-1). This highlights nicorandil as a potential therapy for CSF.

Area of Science:

  • Cardiology
  • Vascular Biology
  • Pharmacology

Background:

  • Coronary slow flow (CSF) is a microvascular disorder with unclear causes and treatments.
  • Left ventricular (LV) function in CSF patients requires further evaluation.
  • Investigating therapeutic options for CSF is crucial.

Purpose of the Study:

  • To assess global and regional LV function in patients with CSF.
  • To evaluate the efficacy of nicorandil in treating CSF.
  • To explore the impact of nicorandil on nitric oxide (NO) and endothelin-1 (ET-1) levels.

Main Methods:

  • Echocardiography (Doppler and speckle tracking) assessed LV function in 36 CSF patients and 20 controls.
  • Plasma levels of NO and ET-1 were measured.
  • Patients received nicorandil (15 mg/day) for 90 days, with pre- and post-treatment assessments.

Main Results:

  • CSF patients showed lower E, E/A ratio, and NO levels, and higher A and ET-1 levels compared to controls.
  • LV longitudinal strain rate was significantly reduced in CSF patients.
  • Nicorandil treatment improved LV function markers (E, E/A, longitudinal strain rate), increased NO, decreased ET-1, and relieved chest pain in 75% of patients.

Conclusions:

  • Nicorandil may alleviate chest pain and improve impaired LV function in CSF.
  • The mechanism may involve increasing NO and reducing ET-1.
  • Nicorandil shows promise as a therapeutic agent for coronary slow flow.
Abstract

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