BACKGROUND: Sympathetic activation occurs in hypertension (HT) and after acute myocardial infarction (AMI) and is related to greater cardiovascular risk. Also, AMI in patients with HT (AMI-HT) carries greater risk than that in normal subjects (AMI-NT). We therefore planned to determine whether the sympathetic activation and its duration after AMI are greater in patients with antecedent HT than in patients with normal arterial pressure (NT). METHODS: In 68 matched subjects with uncomplicated AMI-HT (n = 17), AMI-NT (n = 17), HT (n = 17), and NT (n = 17), we measured resting muscle sympathetic nerve activity (MSNA) as the mean frequency of multiunit bursts (m-MSNA) and single units (s-MSNA). In AMI groups data were obtained 2 to 4 days after AMI and then at 3-month intervals until MSNA returned to levels found in HT and NT. RESULTS: The AMI-HT had greater (at least P < 0.05; ANOVA) s-MSNA (99 +/- 3.5 impulses/100 cardiac beats) than AMI-NT (84 +/- 2.8 impulses/100 cardiac beats). During follow up, s-MSNA hyperactivity in AMI-HT was always greater than in AMI-NT, and returned to values found in HT and NT (84 +/- 3.5 impulses/100 cardiac beats and 62 +/- 4.4 impulses/100 cardiac beats, respectively) 9 months after AMI. Similar results were obtained for m-MSNA. CONCLUSIONS: AMI in hypertensives resulted in greater MSNA levels lasting at least 6 months longer than AMI in normotensives. This indicates that AMI further augmented the MSNA hyperactivity of HT and that this could be one mechanism involved in the reported worse prognosis in AMI-HT.
BACKGROUND: Sympathetic activation occurs in hypertension (HT) and after acute myocardial infarction (AMI) and is related to greater cardiovascular risk. Also, AMI in patients with HT (AMI-HT) carries greater risk than that in normal subjects (AMI-NT). We therefore planned to determine whether the sympathetic activation and its duration after AMI are greater in patients with antecedent HT than in patients with normal arterial pressure (NT). METHODS: In 68 matched subjects with uncomplicated AMI-HT (n = 17), AMI-NT (n = 17), HT (n = 17), and NT (n = 17), we measured resting muscle sympathetic nerve activity (MSNA) as the mean frequency of multiunit bursts (m-MSNA) and single units (s-MSNA). In AMI groups data were obtained 2 to 4 days after AMI and then at 3-month intervals until MSNA returned to levels found in HT and NT. RESULTS: The AMI-HT had greater (at least P < 0.05; ANOVA) s-MSNA (99 +/- 3.5 impulses/100 cardiac beats) than AMI-NT (84 +/- 2.8 impulses/100 cardiac beats). During follow up, s-MSNA hyperactivity in AMI-HT was always greater than in AMI-NT, and returned to values found in HT and NT (84 +/- 3.5 impulses/100 cardiac beats and 62 +/- 4.4 impulses/100 cardiac beats, respectively) 9 months after AMI. Similar results were obtained for m-MSNA. CONCLUSIONS: AMI in hypertensives resulted in greater MSNA levels lasting at least 6 months longer than AMI in normotensives. This indicates that AMI further augmented the MSNA hyperactivity of HT and that this could be one mechanism involved in the reported worse prognosis in AMI-HT.