Systemic inflammation in unstable angina is the result of myocardial necrosis
Michael R Cusack1, Michael S Marber, Pier D Lambiase
1Department of Cardiology, Rayne Institute, St. Thomas' Hospital, London, United Kingdom.
Insights
In unstable angina (UA), an intracardiac inflammatory response, indicated by elevated interleukin-6 (IL-6) and C-reactive protein (CRP), stems from myocardial necrosis, not the ruptured plaque.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Inflammatory response is a key factor in acute coronary syndromes.
- The origin and mechanisms of this inflammation remain incompletely understood.
Purpose of the Study:
- To determine if the acute phase response in unstable angina (UA) originates from the coronary plaque or the myocardium.
- To investigate the relationship between systemic inflammatory markers and atherosclerosis extent.
Main Methods:
- Measured systemic levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and C-reactive protein (CRP) in stable patients and those with UA.
- Assessed the temporal relationship between these markers and troponin T (TnT) in UA patients.
- Measured cytokine levels in the aortic root and coronary sinus of UA patients.
Main Results:
- No correlation was found between stable atherosclerosis and inflammatory markers.
- Patients with UA exhibited elevated IL-6 and CRP levels compared to stable patients.
- Elevated IL-6 and CRP in UA patients correlated with major adverse cardiac events and troponin T appearance.
- Higher TNF-alpha and IL-6 levels were detected in the coronary sinus than the aortic root in UA patients, particularly those with elevated TnT.
- No cytokine gradient was observed across the culprit plaque.
Conclusions:
- Unstable angina involves an intracardiac inflammatory response.
- This inflammation appears to be a consequence of low-grade myocardial necrosis.
- The ruptured coronary plaque is unlikely to be the source of the acute phase response in UA.
Objectives:
We investigated whether the source of the acute phase response in unstable angina (UA) lay within the culprit coronary plaque or distal myocardium.
Background:
An inflammatory response is an important component of the acute coronary syndromes. However, its origin and mechanism remain unclear.
Methods:
In 94 stable patients undergoing coronary angiography, the relationship between systemic levels of tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6) and C-reactive protein (CRP) and extent of atherosclerosis was studied. The temporal relationship between these markers and troponin T (TnT) was determined in 91 patients with UA. Cytokine levels were measured in the aortic root and coronary sinus of 36 unstable patients.
Results:
There was no relationship found between stable coronary atherosclerosis and inflammatory marker levels. Compared with this group, admission levels of IL-6 (3.6 +/- 0.3 ng/ml vs. 10.7 +/- 1.7 ng/ml, p < 0.05) and CRP (2.3 +/- 0.1 mg/l vs. 4.6 +/- 0.6 mg/l, p < 0.05) were elevated in patients with UA. In this group, IL-6 and CRP remained elevated in those who subsequently experienced major adverse cardiac events. This inflammatory response occurred in parallel to the appearance of TnT. Both TNF-alpha (19.2 +/- 3.4 ng/ml vs. 17.1 +/- 3.3 ng/ml, p < 0.001) and IL-6 (10.3 +/- 1.4 ng/ml vs. 7.7 +/- 1.1 ng/ml, p < 0.01) were elevated in the coronary sinus compared with aortic root in patients with UA. This was principally observed in those who were TnT positive. There was no cytokine gradient across the culprit plaque.
Conclusions:
There is an intracardiac inflammatory response in UA that appears to be the result of low-grade myocardial necrosis. The ruptured plaque does not appear to contribute to the acute phase response.
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