Systemic inflammation in unstable angina is the result of myocardial necrosis
Michael R. Cusack, MB, MRCP*,
Michael S. Marber, PhD, FACC*,
Pier D. Lambiase, BA, MRCP*,
Clifford A. Bucknall, MD, FRCP* and
Simon R. Redwood, MD, FACC*,*
* Department of Cardiology, Rayne Institute, St. Thomas’ Hospital, London, United Kingdom
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Figure 1 The levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and C-reactive protein (CRP) are shown for the stable patients undergoing angiography. No consistent relation was found between the level of these inflammatory markers and the extent of angiographic coronary disease. A = normal coronary arteries; B = single vessel disease; C = double vessel disease; D = triple vessel disease.
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Figure 2 The levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and C-reactive protein (CRP) are shown for the stable patients and the unstable angina patients divided according to the subsequent occurrence of major adverse cardiac events (MACE). The levels of IL-6 and CRP are substantially higher in those with unstable angina compared with those with stable symptoms (*p < 0.05). A = stable patients; B = unstable patients without MACE; C = unstable patients with MACE.
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Figure 3 The levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, C-reactive protein (CRP) and troponin T are shown for the patients with unstable angina for the first seven days after admission. The systemic inflammatory response exhibited in the patients who subsequently experienced major adverse cardiac events (MACE) occurs in parallel to a rise in troponin T. Open circle = patients who experienced MACE; solid box = patients who did not experience MACE.
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Figure 4 The levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha present in the aortic root and coronary sinus on simultaneous sampling in patients with unstable angina undergoing cardiac catheterization are shown. A rise in the levels of these cytokines is observed across the coronary circulation. When these patients were divided according to their troponin T (TnT) status, this transcardiac cytokine gradient is found to occur primarily in those with evidence of myocardial necrosis. Solid bar = coronary sinus; open bar = aortic root. **p < 0.01.
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Figure 5 Shown are the changes in the level of interleukin (IL)-6 between the aortic root and the distal coronary artery and between aortic root and coronary sinus in the unstable patients undergoing percutaneous coronary intervention (n = 9). There is minimal change in IL-6 across the culprit plaque but a significant rise across the myocardial bed (p < 0.05).
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