PubMed · 459539
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R H Anderson, A E Becker. 1979. Accessory atrioventricular connections.. https://pubmed.ncbi.nlm.nih.gov/459539/
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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.
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