Relationship between left ventricular mass and hemodynamic responses to physical and mental stress

Objective: Increased left ventricular mass (LVM) is predictive of future ca rdiac morbidity and mortality. Although casual and ambulatory blood pressur e (BP) predict LVM, other hemodynamic determinants of LVM are incompletely understood. The present study examines laboratory-induced hemodynamic respo nses (to exercise, cold: and mental stress) and 24-hour ambulatory measures as predictors of LVM. Methods: Thirty-six healthy non-hypertensive subject s (mean age 33.9 +/- 9.4 years; 23 women, 13 men) were tested with mental s tress, cold presser, and treadmill exercise in the laboratory and 24-hour a mbulatory BP monitoring. LVM was measured using two-dimensional targeted M- mode echocardiography and indexed for body surface area (LVMI). Results: Al l laboratory tasks produced significant hemodynamic responses (p's < 0.01). Systolic blood pressure responses to mental stress (r = 042, p < 0.01) and cold presser (r = 0.34, p < 0.05) were significantly related to LVM. After adjusting for body size, the mental stress-induced SEP responses was the o nly significant predictor of LVMI (r = 0.32, p < 0.05). Exercise SEP respon ses 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 SEP dur ing mental stress was significantly predictive of LVMI (beta = 0.65, p = 0. 05), independent of baseline SEP, 24-hour ambulatory SEP, and other control variables. Conclusion: The present results indicate that-SEP responses to mental stress are significantly related to LVM among healthy individuals, i ndependently of baseline SEP, 24-hour ambulatory BP, age, body size, and se x. Blood pressure responses to exercise show a robust association with LVM in men but not in women. Hemodynamic responses elicited during laboratory t asks may therefore reveal important information about the pathophysiologica l processes involved in the development of cardiac end-organ damage. (C) 20 00 Elsevier Science Inc. All rights reserved.