title: Relationship between left ventricular mass and hemodynamic responses to physical and mental stress.
abstract: OBJECTIVE
  Increased left ventricular mass (LVM) is predictive of future cardiac morbidity and mortality. Although casual and ambulatory blood pressure (BP) predict LVM, other hemodynamic determinants of LVM are incompletely understood. The present study examines laboratory-induced hemodynamic responses (to exercise, cold, and mental stress) and 24-hour ambulatory measures as predictors of LVM.
  
  
  METHODS
  Thirty-six healthy non-hypertensive subjects (mean age 33.9 +/- 9.4 years; 23 women, 13 men) were tested with mental stress, cold pressor, and treadmill exercise in the laboratory and 24-hour ambulatory BP monitoring. LVM was measured using two-dimensional targeted M-mode echocardiography and indexed for body surface area (LVMI).
  
  
  RESULTS
  All laboratory tasks produced significant hemodynamic responses (p's < 0.01). Systolic blood pressure responses to mental stress (r = 0.42, p < 0.01) and cold pressor (r = 0.34, p < 0.05) were significantly related to LVM. After adjusting for body size, the mental stress-induced SBP responses was the only significant predictor of LVMI (r = 0.32, p < 0.05). Exercise SBP responses were associated to LVMI in men (r = 0.63, p = 0.02), but not in women (r = 0.02, p = n.s.). Multivariate regression analyses revealed that SBP during mental stress was significantly predictive of LVMI (beta = 0.65, p = 0.05), independent of baseline SBP, 24-hour ambulatory SBP, and other control variables.
  
  
  CONCLUSIONS
  The present results indicate that SBP responses to mental stress are significantly related to LVM among healthy individuals, independently of baseline SBP, 24-hour ambulatory BP, age, body size, and sex. Blood pressure responses to exercise show a robust association with LVM in men but not in women. Hemodynamic responses elicited during laboratory tasks may therefore reveal important information about the pathophysiological processes involved in the development of cardiac end-organ damage.
authors.affiliation: Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. wjkop@mxb.usuhs.mil
authors.forename: W J
authors.initials: WJ
authors.lastname: Kop
authors.forename: J S
authors.initials: JS
authors.lastname: Gottdiener
authors.forename: S M
authors.initials: SM
authors.lastname: Patterson
authors.forename: D S
authors.initials: DS
authors.lastname: Krantz
mesh_terms: D000223:Adaptation, Psychological; D000328:Adult; D000367:Age Factors; D018660:Blood Pressure Monitoring, Ambulatory; D003080:Cold Temperature; D015986:Confounding Factors, Epidemiologic; D004562:Electrocardiography; D005080:Exercise Test; D005260:Female; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology* / Q000503:physiopathology*; D008297:Male; D015999:Multivariate Analysis; D011237:Predictive Value of Tests; D011379:Prognosis; D012016:Reference Values; D012494:Sampling Studies; D012737:Sex Factors; D013315:Stress, Psychological / Q000503:physiopathology*; D013599:Systole