Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

162
Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
162
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

173
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
173
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

159
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
159
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

580
In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
580
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

500
Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
500
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

516
Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
516

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

[Hepatosplenic T-cell lymphoma with pancytopenia and massive splenomegaly].

[Rinsho ketsueki] The Japanese journal of clinical hematology·2026
Same author

Addition of High-Dose Cytarabine to Fludarabine, Busulfan, and Melphalan Conditioning for Cord Blood Transplantation in Adult Acute Myeloid Leukemia.

Transplantation and cellular therapy·2026
Same author

Percutaneous Coronary Intervention for Coronary Events during Tyrosine Kinase Inhibitor Therapy in Leukemia Patients.

International heart journal·2026
Same author

Integration of peripheral blood lymphocyte count kinetics and bone marrow hematogones for stratifying B-cell recovery and clinical outcomes after cord blood transplantation: a retrospective study.

Leukemia & lymphoma·2026
Same author

Cord Blood Transplantation versus Other Donor Sources in High-Risk Acute Myeloid Leukemia.

Transplantation and cellular therapy·2026
Same author

Evaluation of Exercise Tolerance in Cancer Patients With Cardiovascular Complications: A Japanese Single-Center Retrospective Study Using Cardiopulmonary Exercise Testing.

Circulation reports·2026

Related Experiment Video

Updated: Jun 29, 2025

Scaled-Up Preparation of an Intermediate of Upatinib, ACT051-3
08:36

Scaled-Up Preparation of an Intermediate of Upatinib, ACT051-3

Published on: April 7, 2023

1.1K

Ponatinib-Related Vasospastic Angina.

Michiho Shindo1,2, Chinatsu Komiyama1, Tetsuo Yamaguchi1

  • 1Department of Cardiology, Toranomon Hospital.

International Heart Journal
|March 31, 2024
PubMed
Summary

Tyrosine kinase inhibitors (TKIs) can cause vasospastic angina. Prophylactic nitrates or calcium channel blockers effectively managed this side effect in three leukemia patients.

Keywords:
Cardio-oncologyChronic myeloid leukemiaOnco-cardiologyTyrosine kinase inhibitorVasospasm

More Related Videos

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
10:28

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

5.0K
Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery
09:41

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

Published on: December 23, 2014

16.4K

Related Experiment Videos

Last Updated: Jun 29, 2025

Scaled-Up Preparation of an Intermediate of Upatinib, ACT051-3
08:36

Scaled-Up Preparation of an Intermediate of Upatinib, ACT051-3

Published on: April 7, 2023

1.1K
Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
10:28

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

5.0K
Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery
09:41

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

Published on: December 23, 2014

16.4K

Area of Science:

  • Oncology
  • Cardiology
  • Pharmacology

Background:

  • Tyrosine kinase inhibitors (TKIs) are crucial for treating chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia.
  • Cardiovascular and arteriothrombotic adverse events are known risks associated with TKI therapy.
  • Vasospastic angina is a serious cardiovascular complication that can occur in patients receiving TKIs.

Purpose of the Study:

  • To report three cases of vasospastic angina associated with Ponatinib, a specific TKI.
  • To evaluate the efficacy of prophylactic treatment for Ponatinib-induced vasospastic angina.

Main Methods:

  • Case series reporting three patients who developed vasospastic angina while on Ponatinib treatment.
  • Review of medical records to assess the clinical presentation and management of the adverse events.
  • Analysis of the effectiveness of prophylactic nitrates and calcium channel blockers.

Main Results:

  • All three patients experienced vasospastic angina during Ponatinib therapy.
  • Prophylactic administration of nitrates and/or calcium channel blockers was initiated.
  • The prophylactic treatments were effective in preventing or managing the vasospastic angina episodes.

Conclusions:

  • Ponatinib can induce vasospastic angina, a significant cardiovascular adverse event.
  • Prophylactic use of nitrates and calcium channel blockers may be a beneficial strategy to mitigate this risk.
  • Further research is warranted to understand the mechanisms and optimal management of TKI-associated vasospastic angina.