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[Left ventricular hypertrophy: physiopathological signs using a hemodynamic and cardio-autonomic approach]
Insights
Left ventricular hypertrophy (LVH) may stem from sympathetic nervous system overactivity, not just high blood pressure. Normotensive individuals with LVH show prolonged autonomic reactivity, suggesting a hyper-adrenergic state contributes to this cardiac change.
Area of Science:
- Cardiology
- Autonomic Nervous System Physiology
- Hypertension Research
Background:
- Left ventricular hypertrophy (LVH) is an anatomic cardiac change observed in both hypertensive and normotensive individuals.
- The exact mechanisms driving LVH are not fully understood, with factors beyond blood pressure, such as neural and endocrine influences, potentially playing a role.
Purpose of the Study:
- To investigate the role of sympathetic nervous system dys-reactivity in the development of LVH.
- To determine if autonomic function differs in normotensive individuals with LVH compared to hypertensive individuals with LVH and normotensive individuals without LVH.
Main Methods:
- Studied three groups: hypertensive with LVH, normotensive with LVH, and normotensive without LVH.
- Utilized computer-interfaced equipment to measure beat-to-beat hemodynamic and autonomic functions during stressor tests (Mental Arithmetic, Stroop, Cold Pressure, Handgrip).
- Assessed autonomic response using the Percentual Total Activity Index (PTAI), reflecting changes and recovery in autonomic activity.
Main Results:
- Normotensive individuals with LVH exhibited significantly higher PTAI for skin conductance level (SCL), photoplethysmography (PHT), heart rate (HR), stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) compared to the other two groups.
- These findings indicate a prolonged autonomic reactivity in normotensive individuals with LVH.
Conclusions:
- LVH can be associated with a hyper-adrenergic state characterized by sympathetic dys-reactivity, independent of elevated blood pressure.
- These results support the hypothesis that autonomic nervous system imbalances contribute to the pathogenesis of LVH in normotensive subjects.
Abstract:
The presence of left ventricular hypertrophy (LVH) in either hypertensives -H- or in normotensives -N-, suggests that not only blood pressure is determining this anatomic change, but various factors, as neural or endocrine ones, could be involved in its genesis. In order to evaluate the role of sympathetic dys-reactivity on LVH, we studied three groups of subjects: a) 12 -H- (SBP 159+/-9; DBP 99.6+/-7; FC 80+/-7) with LVH, diagnosed by echocardiogram. b) 12 -N- (SBP 138.2+/-8; DBP 83+/-2; FC 75.6+/-4) with LVH. c) 12 -N- (SBP 136.6+/-11; DBP 81.8+/-5; FC 76.3+/-5) without LVH. Using computer interfaced equipment, we measured beat to beat, hemodynamic and extra-cardiovascular autonomic functions, during a session of stressors (Mental Arithmetic, Color Word Stroop, Cold Pressure and Handgrip Tests), preceded and followed by 10' of observation. Among the various considered indexes, we evaluated the Percentual Total Activity Index (PTAI), as percentual total activity change + percentual total recovery change. Our findings point out that the PTAI of N with LVH is significantly higher for SCL, PHT, HR, SV, CO, TPR than either in H with LVH or N without LVH. These data seem to demonstrate a prolonged reactivity in N without LVH and are according to the hypothesis that LVH could also be supported by a hyper-adrenergic state with sympathetic dys-reactivity, independently from high blood pressure values.