title: LV peak instantaneous wall stress versus time-stress-integral as measures of afterload in aortic stenosis.
abstract: BACKGROUND
  LV pressure overload triggers biological events leading to LV hypertrophy, and the severity of LV pressure overload has been represented by LV wall stress (LVWS). However, duration of exposure to the given LVWS has not been considered as a factor leading to LV hypertrophy.
  
  
  METHODS
  In 20 patients with severe aortic stenosis, LV pressure, with a Millar catheter, and LV dimensions, with echocardiography, were simultaneously obtained. By synchronising LV pressure waveform and LV dimensions, the instantaneous peak LVWS (IP-LVWS) and systolic LV wall time-stress-integral (LV TSI), which is the LVWS integrated during the systolic period and physically implies LV wall impulse per unit area, were obtained. These measurements were obtained at rest, during right atrial pacing at an HR of 10% higher than resting HR, and after esmolol infusion.
  
  
  RESULTS
  IP-LVWS cannot be predicted from the peak LV pressure or peak dp/dt. There were no significant differences in peak IP-LVWS at rest, during pacing or after esmolol infusion. However, systolic LV TSI after esmolol infusion was significantly higher compared to that at rest or during pacing. Only LV TSI correlated with LV wall thickness or LV mass at rest (r=0.64, p=0.002 and r=0.54, p=0.014, respectively), while correlations between IP-LVWS and LV wall thickness or LV mass at rest were not statistically significant (r=0.32, p=0.173 and r=0.32, p=0.168, respectively).
  
  
  CONCLUSIONS
  As IP-LVWS cannot be predicted from the peak LV pressure or peak dp/dt, one should be cautious in interpreting the data regarding peak LV pressure as the parameter representing LV afterload. Based on the current results, the systolic LV TSI might be more important than IP-LVWS in LV hypertrophy. In addition, as LV TSI is affected by the systolic duration, factors prolonging systolic duration might exert adverse effects on LV hypertrophy.
authors: Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors: Dae-Won
authors: DW
authors: Sohn
authors: Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors: Seung-Pyo
authors: SP
authors: Lee
authors: Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors: Hyung-Kwan
authors: HK
authors: Kim
authors: Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors: Yong-Jin
authors: YJ
authors: Kim
authors: Department of Biomedical Engineering, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors: Byeong-Wook
authors: BW
authors: Yoo
authors: Department of Biomedical Engineering, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors: Hee Chan
authors: HC
authors: Kim
mesh_terms: D000368:Aged; D001024:Aortic Valve Stenosis / Q000150:complications / Q000503:physiopathology*; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology*