title: Time-varying myocardial stress and systolic pressure-stress relationship: role in myocardial-arterial coupling in hypertension.
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.
  
  
  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.
authors.affiliation: University of Pennsylvania, Philadelphia, USA. julio.chirinos@uphs.upenn.edu
authors.forename: Julio A
authors.initials: JA
authors.lastname: Chirinos
authors.forename: Patrick
authors.initials: P
authors.lastname: Segers
authors.forename: Amit Kumar
authors.initials: AK
authors.lastname: Gupta
authors.forename: Abigail
authors.initials: A
authors.lastname: Swillens
authors.forename: Ernst R
authors.initials: ER
authors.lastname: Rietzschel
authors.forename: Marc L
authors.initials: ML
authors.lastname: De Buyzere
authors.forename: James N
authors.initials: JN
authors.lastname: Kirkpatrick
authors.forename: Thierry C
authors.initials: TC
authors.lastname: Gillebert
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Martin G
authors.initials: MG
authors.lastname: Keane
authors.forename: Raymond
authors.initials: R
authors.lastname: Townsend
authors.forename: Victor A
authors.initials: VA
authors.lastname: Ferrari
authors.forename: Susan E
authors.initials: SE
authors.lastname: Wiegers
authors.forename: Martin
authors.initials: M
authors.lastname: St John Sutton
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001158:Arteries / Q000503:physiopathology*; D004452:Echocardiography / Q000379:methods; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008365:Manometry; D008875:Middle Aged; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D013314:Stress, Mechanical; D013318:Stroke Volume; D013599:Systole; D014655:Vascular Resistance; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D000959:Antihypertensive Agents