title: The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension.
abstract: BACKGROUND
  The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively.
  
  
  OBJECTIVE
  Myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN).
  
  
  METHODS
  Fractional shortening (%) and end-systolic stress (10(3) x dyn x cm(-2)) were determined using echocardiography, and coronary reserve was calculated using transesophageal Doppler echocardiography. Coronary reserve/stress (cm2 x dyn(-1)) was utilized as a measure of supply-demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening > or = 30), HTN2 (19 patients, 20 < or = fractional shortening < 30), and HTN3 (21 patients, fractional shortening < 20) were constituted.
  
  
  RESULTS
  Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end-systolic stress (NL = 72 +/- 16, HTN1 = 72 +/- 23, HTN2 = 143 +/- 32, HTN3 = 186 +/- 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 +/- 0.6, HTN1 = 3.4 +/- 1.0, HTN2 = 3.1 +/- 1.0, HTN3 = 2.6 +/- 1.1), but coronary reserve/stress was reduced in both HTN2 and HTN3 (NL = 50 +/- 12, HTN1 = 53 +/- 21, HTN2 = 22 +/- 7, HTN3 = 15 +/- 7). Stepwise regression analysis identified diastolic internal dimension, end-systolic stress, and coronary reserve/stress as independently associated with fractional shortening.
  
  
  CONCLUSIONS
  The imbalance between supply-demand explains the severity of hypertensive cardiac dysfunction and adds information to cardiac enlargement and elevated wall stress.
authors.affiliation: Emergências Clínicas (LIM 51), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil. frimm@emercli.fm.usp.br
authors.forename: Clovis de Carvalho
authors.initials: Cde C
authors.lastname: Frimm
authors.forename: Valéria F A
authors.initials: VF
authors.lastname: Pereira
authors.forename: Ana Clara T
authors.initials: AC
authors.lastname: Rodrigues
authors.forename: Jeane M
authors.initials: JM
authors.lastname: Tsutsui
authors.forename: Mariana
authors.initials: M
authors.lastname: Cúri
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology*; D016022:Case-Control Studies; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D013312:Stress, Physiological / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D013318:Stroke Volume / Q000502:physiology; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology*