Related Experiment Video
Updated: Jul 19, 2026

Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
Published on: September 11, 2018
The sympathetic drive after acute myocardial infarction in hypertensive patients
Andrew J Hogarth1, Alan F Mackintosh, David A S G Mary
1The Department of Cardiology, St James's University Hospital, Leeds, UK. hogarth2003@yahoo.co.uk
Insights
Following acute myocardial infarction (AMI), hypertensive patients exhibit prolonged sympathetic nervous system activation compared to normotensive individuals. This sustained sympathetic hyperactivity may contribute to the worse prognosis observed in hypertensive patients after AMI.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Myocardial Infarction Studies
Background:
- Sympathetic activation is a known risk factor in hypertension (HT) and acute myocardial infarction (AMI).
- Patients with both conditions (AMI-HT) face higher cardiovascular risks than those without antecedent HT (AMI-NT).
Purpose of the Study:
- To investigate if sympathetic activation and its duration are elevated after AMI in patients with pre-existing hypertension compared to normotensive individuals.
Main Methods:
- Muscle sympathetic nerve activity (MSNA) was measured in 68 subjects across four groups: AMI-HT, AMI-NT, HT, and normotensive (NT).
- MSNA was assessed using multiunit (m-MSNA) and single-unit (s-MSNA) burst frequencies.
- Measurements in AMI groups were taken shortly after infarction and at 3-month intervals until MSNA normalized.
Main Results:
- Patients with AMI-HT showed significantly higher s-MSNA (99 ± 3.5 impulses/100 cardiac beats) compared to AMI-NT (84 ± 2.8 impulses/100 cardiac beats).
- s-MSNA hyperactivity persisted in AMI-HT throughout the 9-month follow-up, returning to baseline HT and NT levels later.
- Similar trends were observed for m-MSNA.
Conclusions:
- Acute myocardial infarction exacerbates sympathetic hyperactivity in hypertensive patients, with elevated MSNA levels persisting for at least 6 months longer than in normotensive individuals.
- This prolonged sympathetic activation in AMI-HT could be a key factor contributing to their poorer clinical outcomes.
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.
Related Concept Videos
Disorders of the Autonomic Nervous System
Raynaud's disease, also known as Raynaud's phenomenon, is a...
Heart Failure II: Pathophysiology
Sympathetic Activation
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antihypertensive Drugs: Action of β1 Blockers
Hypertension II: Pathophysiology