Lupus · 2012
Pathophysiology of Q waves in II, III, avF in systemic lupus erythematosus. Evaluation using cardiovascular magnetic resonance imaging.
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Mavrogeni S, Bratis K, Kolovou G
Аннотация
OBJECTIVES: To investigate the pathophysiology of Q waves in II, III, avF in systemic lupus erythematosus (SLE) by cardiovascular magnetic resonance (CMR).
METHODS: Inflammation evaluation by CMR using T2, early (EGE) and late gadolinium enhanced images (LGE) was performed in 20 SLE patients with mild cardiac symptoms and Q in leads II, III, avF of ECG. Their results were compared with 20 SLE patients with the same symptoms and normal ECG.
RESULTS: In both groups, T2, EGE and left ventricular ejection fraction were normal. However, in 3/20 with Q in II, III, avF, CMR revealed lesions indicative of acute myocarditis. In the rest of them, CMR documented transmural LGE, due to past inferior myocardial infarction in 4/20 and epicardial LGE due to past myocarditis in 8/20 (4/8 in the inferior and 4/8 in the lateral wall of left ventricle). No LGE was found in 5/20 and the Q was attributed to the position of the heart. In 3/20 with normal ECG, CMR detected past myocarditis in 2/3 and myocardial infarction in 1/3. Coronary angiography assessed coronary artery disease in all SLE with evidence of myocardial infarction and normal coronaries in 9/10 patients with past myocarditis.
CONCLUSION: Q in II, III, avF in SLE may indicate myocardial infarction, acute or past inflammation or be a positional finding. The lack of Q does not exclude the possibility of infarction or inflammation. CMR is the best tool to reveal the pathophysiology of Q waves in SLE and guide treatment of heart involvement in these patients.
METHODS: Inflammation evaluation by CMR using T2, early (EGE) and late gadolinium enhanced images (LGE) was performed in 20 SLE patients with mild cardiac symptoms and Q in leads II, III, avF of ECG. Their results were compared with 20 SLE patients with the same symptoms and normal ECG.
RESULTS: In both groups, T2, EGE and left ventricular ejection fraction were normal. However, in 3/20 with Q in II, III, avF, CMR revealed lesions indicative of acute myocarditis. In the rest of them, CMR documented transmural LGE, due to past inferior myocardial infarction in 4/20 and epicardial LGE due to past myocarditis in 8/20 (4/8 in the inferior and 4/8 in the lateral wall of left ventricle). No LGE was found in 5/20 and the Q was attributed to the position of the heart. In 3/20 with normal ECG, CMR detected past myocarditis in 2/3 and myocardial infarction in 1/3. Coronary angiography assessed coronary artery disease in all SLE with evidence of myocardial infarction and normal coronaries in 9/10 patients with past myocarditis.
CONCLUSION: Q in II, III, avF in SLE may indicate myocardial infarction, acute or past inflammation or be a positional finding. The lack of Q does not exclude the possibility of infarction or inflammation. CMR is the best tool to reveal the pathophysiology of Q waves in SLE and guide treatment of heart involvement in these patients.