Left ventricular wall stress normalization in chronic pressure-overloaded heart: a mathematical model study

Area of Science:

• Cardiovascular Physiology
• Computational Biology
• Biomedical Engineering

Background:

• Left ventricular hypertrophy (LVH) is a common response to chronic pressure overload in hypertension.
• Traditionally, LVH is thought to normalize systolic wall stress (sigma(s)).
• An alternative hypothesis suggests LVH may also normalize end-diastolic wall stress (sigma(d)) by increasing LV filling pressure (P(v)).

Purpose of the Study:

• To investigate ventricular-arterial interaction in hypertension-induced LVH using a computational model.
• To test hypotheses regarding the normalization of systolic (sigma(s)) and diastolic (sigma(d)) wall stress in LVH.
• To compare model predictions with in vivo human data.

Main Methods:

• Coupled LV time-varying elastance and a four-element arterial lumped-parameter model.
• Simulated arterial changes in hypertension (increased resistance, decreased compliance).
• Assessed three scenarios: no cardiac adaptation, sigma(s) normalization, and sigma(s) & sigma(d) normalization with increased P(v).

Main Results:

• Scenarios without P(v) increase predicted only minor blood pressure rise and significant cardiac output drop.
• LVH with sigma(s) normalization alone resulted in modest wall thickness increase.
• The scenario including P(v) increase aligned with clinical observations of elevated blood pressure, preserved cardiac output, and impaired diastolic function.

Conclusions:

• LVH contributes to elevated blood pressure in hypertension.
• Cardiac adaptations in LVH involve increased P(v), normalization of sigma(s), and preservation of cardiac output.
• These adaptations occur despite impaired diastolic function, highlighting a complex interplay between cardiac remodeling and hemodynamics.