Time-varying Myocardial Stress and Systolic Pressure-Stress Relationship: Role in Myocardial-Arterial Coupling in Hypertension

Circulation. 2009 Jun 2;119(21):2798-807. doi: 10.1161/CIRCULATIONAHA.108.829366. Epub 2009 May 18.

Abstract

Background: Myocardial afterload depends on left ventricular (LV) cavity size, pressure, and wall thickness, all of which change markedly throughout ejection. We assessed the relationship between instantaneous ejection-phase pressure and myocardial stress and the effect of arterial wave reflections on myocardial stress in hypertensive and normotensive adults.

Methods and results: We studied 42 untreated hypertensive, 42 treated hypertensive, and 42 normotensive adults with normal LV ejection fraction. Time-resolved central pressure, flow, and LV geometry were measured with carotid tonometry, Doppler, and speckle-tracking echocardiography for computation of arterial load and time-varying circumferential and longitudinal myocardial stress. In all 3 groups, peak myocardial stress typically occurred in early systole (within the first 100 milliseconds of ejection), followed by a marked midsystolic shift in the pressure-stress relationship, which favored lower late systolic stress values (P<0.001) relative to pressure. The mean magnitude of this midsystolic shift was quantitatively important in all 3 groups (circumferential stress, 144 to 148 kdynes/cm(2)) and was independently predicted by a higher LV ejection fraction and ratio of LV end-diastolic cavity to wall volume. Time of peak myocardial stress independently correlated with time of the first systolic but not with time of the second systolic central pressure peak.

Conclusions: Peak myocardial stress occurs in early systole, before important contributions of reflected waves to central pressure. In the presence of normal LV ejection fraction, a midsystolic shift in the pressure-stress relationship protects cardiomyocytes against excessive late systolic stress (despite pressure augmentation associated with wave reflections), a coupling mechanism that may be altered in various disease states.

MeSH terms

  • Adult
  • Aged
  • Antihypertensive Agents / therapeutic use
  • Arteries / physiopathology*
  • Echocardiography / methods
  • Female
  • Heart Ventricles / diagnostic imaging
  • Heart Ventricles / physiopathology
  • Humans
  • Hypertension / drug therapy
  • Hypertension / physiopathology*
  • Male
  • Manometry
  • Middle Aged
  • Models, Cardiovascular*
  • Myocardial Contraction*
  • Stress, Mechanical
  • Stroke Volume
  • Systole
  • Vascular Resistance
  • Ventricular Remodeling / physiology

Substances

  • Antihypertensive Agents