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Abnormal Muscle Vasodilatation during Mental Stress in Patients with Myocardial Infarction
Author(s) -
Rondon Maria Urbana Pinto Brandão,
Martinez Daniel G,
Nicolau José C,
Lage Rony,
Matos Luciana,
Laterza Mateus C,
Barel Matheus,
Trombetta Ivani C,
Negrao Carlos E
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.816.7
We tested the hypothesis that patients with myocardial infarction (MI) would have exaggerated muscle sympathetic nerve activity (MSNA) response and decreased skeletal muscle vasodilatation during mental stress (MS). We studied 23 patients (48±1 years; ejection fraction= 56±2%), 30‐days after MI, and 12 age‐matched healthy controls (C, 44±1 years). MSNA was measured by microneurography technique and forearm blood flow by venous occlusion plethysmography. MS was induced by Stroop Color Word Test. Baseline MSNA was higher (66±3 vs. 32±2 bursts/100HB, P<.001), and forearm vascular conductance (FVC) was lower (1.67±0.1 vs. 3.15±0.3 units, P<.001) in MI patients when compared with C. During MS, MSNA increased in both groups (P<.001). However, the absolute levels of MSNA were higher in MI patients than in C (62±4 vs. 39±1 bursts/100HB, P<.001). FVC increased during MS in C (2.88±0.8 vs. 4.11±1.2 units, P<.02), but not in MI patients in whom FVC was not significantly changed (1.40±0.3 vs. 1.95±0.4 units, P=.48). In conclusion, despite of augmented baseline sympathetic activation, MSNA in response to MS is preserved in patients with MI. Muscle vasodilatation in response to MS is blunted in patients with MI patients. This abnormal vascular control during MS in patients with MI may contribute to cardiovascular events in patients with MI.