Low coronary driving pressure is associated with subendocardial remodelling and left ventricular dysfunction in

Maria C Guido1, Clovis de Carvalho Frimm, Márcia K Koike

  • 1Laboratory of Medical Investigation, LIM-51, Department of Emergency Medicine, University of São Paulo Medical School, São Paulo, Brazil.

Insights

Low coronary driving pressure in volume overload hypertrophy damages the heart's subendocardium. This early damage negatively impacts overall left ventricular function, highlighting a critical factor in cardiac remodeling.

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Remodeling
  • Hemodynamics

Background:

  • Left ventricular remodeling in volume overload hypertrophy is not well understood.
  • Low diastolic blood pressure and high filling pressures may impair subendocardial perfusion.
  • The impact on global left ventricular remodeling remains unclear.

Purpose of the Study:

  • To investigate the role of coronary driving pressure in subendocardial remodeling.
  • To assess the effects of coronary driving pressure on cardiac function.
  • Utilized a rat model of aortocaval fistula (ACF).

Main Methods:

  • Wistar rats underwent ACF or sham operations.
  • Hemodynamic measurements (coronary driving pressure, dP/dt) were taken at 1 and 8 weeks.
  • Assessed cytokine expression, myeloperoxidase activity, metalloproteinase activity, and fibrosis in subendocardial and non-subendocardial layers.

Main Results:

  • ACF group had lower coronary driving pressure and cardiac function (+dP/dt, -dP/dt).
  • Initial coronary driving pressure independently predicted subendocardial fibrosis and cardiac function.
  • Matrix metalloproteinase-2 and inflammatory cytokines (IL-6, IL-1beta) were elevated in the subendocardium of ACF rats, correlating with low coronary driving pressure.

Conclusions:

  • Low coronary driving pressure early in ACF is a key determinant of subendocardial damage.
  • This subendocardial damage negatively influences left ventricular function.
  • Coronary driving pressure is a critical factor in the pathophysiology of volume overload-induced cardiac remodeling.

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