Arterial pulsatile hemodynamic load induced by isometric exercise strongly predicts left ventricular mass in hypertension.
Although resting hemodynamic load has been extensively investigated as a determinant of left ventricular (LV) hypertrophy, little is known about the relationship between provoked hemodynamic load and the risk of LV hypertrophy. We studied central pressure-flow relations among 40 hypertensive and 19 normotensive adults using carotid applanation tonometry and Doppler echocardiography at rest and during a 40% maximal voluntary forearm contraction (handgrip) maneuver. Carotid-femoral pulse wave velocity (CF-PWV) was measured at rest. Hypertensive subjects demonstrated various abnormalities in resting and induced pulsatile load. Isometric exercise significantly increased systemic vascular resistance, aortic characteristic impedance (Zc), induced earlier wave reflections, increased augmentation index, and decreased total arterial compliance (TAC; all P < or = 0.01). In hypertensive subjects, CF-PWV was the strongest resting predictor of LV mass index (LVMI) and remained an independent predictor after adjustment for age, gender, systemic vascular resistance, reflection magnitude, aortic Zc, and TAC (beta = 2.52 m/s; P < 0.0001). Age, sex, CF-PWV, and resting hemodynamic indexes explained 48% of the interindividual variability in LVMI. In stepwise regression, TAC (beta = -17.85; P < 0.0001) during handgrip, Zc during handgrip (beta = -150; P < 0.0001), and the change in the timing of wave reflections during handgrip (beta = -0.63; P = 0.03) were independent predictors of LVMI. A model that included indexes of provoked hemodynamic load explained 68% of the interindividual variability in LVMI. Hemodynamic load provoked by isometric exercise strongly predicts LVMI in hypertension. The magnitude of this association is far greater than for resting hemodynamic load, suggesting that provoked testing captures important arterial properties that are not apparent at rest and is advantageous to assess dynamic arterial load in hypertension.
Chirinos
Julio A
JA
University of Pennsylvania, Philadelphia Veterans Affairs Medical Center, Philadelphia, PA 19104, USA. Julio.chirinos@uphs.upenn.edu
Segers
Patrick
P
Raina
Amresh
A
Saif
Hassam
H
Swillens
Abigail
A
Gupta
Amit K
AK
Townsend
Raymond
R
Emmi
Anthony G
AG
Kirkpatrick
James N
JN
Keane
Martin G
MG
Ferrari
Victor A
VA
Wiegers
Susan E
SE
St John Sutton
Martin G
MG
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001794:Blood Pressure / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D002339:Carotid Arteries / Q000503:physiopathology*; D016022:Case-Control Studies; D019560:Echocardiography, Three-Dimensional; D015444:Exercise / Q000502:physiology*; D005221:Fatigue / Q000503:physiopathology; D005260:Female; D018737:Hand Strength / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008365:Manometry; D008875:Middle Aged; D011237:Predictive Value of Tests; D012039:Regional Blood Flow / Q000502:physiology*; D013318:Stroke Volume / Q000502:physiology