Time-varying myocardial stress and systolic pressure-stress relationship: role in myocardial-arterial coupling in hypertension.
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.
Chirinos
Julio A
JA
University of Pennsylvania, Philadelphia, USA. julio.chirinos@uphs.upenn.edu
Segers
Patrick
P
Gupta
Amit Kumar
AK
Swillens
Abigail
A
Rietzschel
Ernst R
ER
De Buyzere
Marc L
ML
Kirkpatrick
James N
JN
Gillebert
Thierry C
TC
Wang
Yan
Y
Keane
Martin G
MG
Townsend
Raymond
R
Ferrari
Victor A
VA
Wiegers
Susan E
SE
St John Sutton
Martin
M
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
D000959:Antihypertensive Agents