Elevation of asymmetric dimethylarginine in patients with unstable angina and recurrent cardiovascular events
Tanja K Krempl1, Renke Maas, Karsten Sydow
1Institute of Experimental and Clinical Pharmacology, University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. t.krempl@uke.uni-harburg.de
European Heart Journal
|April 30, 2005
Summary
Asymmetric dimethylarginine (ADMA) is elevated in unstable angina patients. Lowering ADMA levels after PCI may signal reduced cardiovascular event risk, aiding clinical outcome prediction.
Area of Science:
- Cardiovascular Medicine
- Biomarkers
- Clinical Chemistry
Background:
- Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase.
- Elevated ADMA levels are associated with endothelial dysfunction and cardiovascular disease.
- The clinical significance of ADMA in unstable angina (UA) requires further investigation.
Purpose of the Study:
- To investigate the association between ADMA levels and clinical outcomes in patients with unstable angina.
- To determine if changes in ADMA levels after percutaneous coronary intervention (PCI) correlate with cardiovascular event recurrence.
Main Methods:
- Prospective study including 36 UA patients, 45 stable angina (SA) patients, and 40 controls.
- ADMA levels measured at baseline and 6 weeks post-PCI using ELISA.
- 1-year follow-up for major adverse cardiovascular events (MACE).
Main Results:
- Baseline ADMA was significantly higher in CAD patients than controls (0.76 vs. 0.59 μmol/L).
- UA patients had higher baseline ADMA than SA patients (0.82 vs. 0.73 μmol/L; P=0.01).
- UA patients without recurrent events showed a significant ADMA reduction post-PCI (0.81 to 0.73 μmol/L).
- Persistently elevated ADMA correlated with a higher MACE rate.
Conclusions:
- ADMA is significantly elevated in patients with unstable angina.
- A decrease in ADMA levels 6 weeks after PCI may indicate a lower risk of recurrent cardiovascular events.
- ADMA serves as a potential biomarker for predicting clinical outcomes in UA patients.
More Related Videos
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
1.9K
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
1.9K
Aortic Regurgitation III: Medical Management
598
Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
598
Acute Coronary Syndrome I: Introduction
2.1K
Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
2.1K
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
943
The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
943
Angina II: Classification
709
Angina, also known as angina pectoris, is a chest pain resulting from diminished blood flow to the heart muscle and is often a symptom of coronary artery disease. Angina presents several variants with distinctive attributes, etiologies, and therapeutic approaches. The main types of angina include stable, unstable, variant (Prinzmetal's), microvascular, intractable, and silent ischemia.Stable angina is caused by atherosclerosis, which leads to the formation of plaques that narrow the coronary...
709
Angina IV: Management
493
IntroductionThe management of angina requires a comprehensive approach that includes pharmacological therapies, medical procedures, and lifestyle modifications.Pharmacological TherapiesAntiplatelet agents, such as aspirin, clopidogrel, prasugrel, and ticagrelor, play a pivotal role in preventing thrombus formation in patients with angina. These medications inhibit platelet aggregation and reduce the likelihood of myocardial infarction and other cardiovascular events.Anticoagulants, including...
493


