title: [Paradoxic changes in the morphology of blood pressure wave in hypertensive heart diseases].
abstract: The objective is to study the relation between left ventricular (LV) effect (index of LV mass (LVMI) and index of inotropic state) and arterial compliance determined but the proximal aortic pressure waveform and by the carotid femoral pulse wave velocity.
  
  
  METHODS
  72 untreated hypertensives; systolic blood pressure (SBP) 170 +/- 18 mmHg/diastolic blood pressure (DBP); heart rate: 69 +/- 9 batt/min; age: 48 +/- 13 years; duration of hypertension 4.6 +/- 4.8 years; sex ratio 49 M/23 F.
  
  
  OBJECTIVE
  Proximal aortic pressure waveform (carotid artery) was studied by applanation tonometry. We derived the index of amplification (AI = Pmax-Pinflex)/PP, %), pulse pressure (PP), the maximum rate of rise of pressure (dpdt, mmHg.s-1). Echocardiography was used to define the index of LV mass (VLMI), end systolic volume (ESV), end systolic stress (ESS), myocardial contractile force (ESS/ESV), inotropic state (SBP/ESV). Carotid-femoral pulse wave velocity was determined by mechanogram (PWW m/s).
  
  
  RESULTS
  1. Relationship of physiological changes of AI and SDA to age, height, PP, DBP, PWV, and LVMI were observed in table I (r-Pearson cor. coefficient, * < p 0.05; **: p < 0.001). [table: see text] In stepwise regression analysis, even allowing for BP, age, and height, there was no relationship between LVMI and the index of aortic amplification (AI). 2. In the subjects with LVH (LVMI > 110 g/m2) we found a bimodal distribution of the AI which defines two groups in agreement with the Murgo Classification. [table: see text] In type B, where AI is weaker, the indices of aortic rigidity are reduced, there is an increased ESS and a paradoxal fall in LV performances.
  
  
  CONCLUSIONS
  Analysis of proximal aortic pressure waveform don't allow to predict index of LV mass. These results suggest that in the sphere of LV aortic compiling the reduction of LV function contributes to modification of the BP waveform with diminution of dpdt and the index of amplification.
authors.affiliation: Service de médecine interne et cardiologie, CHU, Grenoble.
authors.forename: M
authors.initials: M
authors.lastname: Chevallier
authors.forename: J P
authors.initials: JP
authors.lastname: Siche
authors.forename: F
authors.initials: F
authors.lastname: Tremel
authors.forename: R
authors.initials: R
authors.lastname: de Gaudemaris
authors.forename: S
authors.initials: S
authors.lastname: Boutelant
authors.forename: J M
authors.initials: JM
authors.lastname: Mallion
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D015150:Echocardiography, Doppler; D005260:Female; D006331:Heart Diseases / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013599:Systole
vernacular_title: Modifications paradoxales de la morphologie de l'onde de pression dans la cardiopathie hypertensive évoluée.