title: Incremental value of pulse wave velocity in the determination of coronary microcirculatory dysfunction in never-treated patients with essential hypertension.
abstract: BACKGROUND
  Coronary microcirculation is disturbed in essential hypertension. We investigated whether arterial stiffness determines coronary flow reserve (CFR) in hypertensive patients.
  
  
  METHODS
  We examined 100 never-treated hypertensives and 20 healthy controls. We measured (i) carotid-to-femoral pulse wave velocity (PWV); (ii) Systolic (V (s)) and diastolic (V (d)) coronary flow velocity, time integral (V (TI)-V (d)) of diastolic velocity and CFR after adenosine by transthoracic echocardiography; (iii) ratio of E wave from mitral inflow to Em of mitral annulus, as an index of left ventricular (LV) diastolic pressures using tissue Doppler; (iv) carotid intima-media thickness (IMT), as an index of vascular damage; and (v) 24-h blood pressure parameters using ambulatory blood pressure monitoring.
  
  
  RESULTS
  Patients had abnormal PWV, IMT, E/Em, resting V (d)/V (s), and CFR than controls (P < 0.05). In hypertensives, PWV was related to abnormal IMT and E/Em which in turn were related to reduced CFR (P < 0.05). PWV and E/Em were independent determinants of CFR and V (d)/V (s) (P < 0.05) in hypertensives. When added to a model including age, sex, smoking, LV mass (LVM), heart rate, 24-h systolic blood pressure (SBP), and E/Em, PWV had an incremental value in the determination of CFR (r (2) change from 0.25 to 0.46, P < 0.01). PWV >10.7 m/s predicted a CFR <2 with 79 and 75% and a CFR <2.6 with 83 and 82% sensitivity and specificity, respectively, using adjusted-receiver operating characteristic curve (ROC) analysis.
  
  
  CONCLUSIONS
  Elevated LV diastolic compressive forces on coronary microcirculation and the presence of generalized vascular damage may explain the association between PWV and CFR. PWV has an incremental value in the determination of impaired coronary microcirculation in hypertensive patients.
authors.affiliation: Second Cardiology Department, Attikon Hospital, University of Athens, Greece. ignoik@otenet.gr
authors.forename: Ignatios
authors.initials: I
authors.lastname: Ikonomidis
authors.forename: John
authors.initials: J
authors.lastname: Lekakis
authors.forename: Costas
authors.initials: C
authors.lastname: Papadopoulos
authors.forename: Helen
authors.initials: H
authors.lastname: Triantafyllidi
authors.forename: Ioannis
authors.initials: I
authors.lastname: Paraskevaidis
authors.forename: Georgia
authors.initials: G
authors.lastname: Georgoula
authors.forename: Stavros
authors.initials: S
authors.lastname: Tzortzis
authors.forename: Ioanna
authors.initials: I
authors.lastname: Revela
authors.forename: Dimitrios Th
authors.initials: DT
authors.lastname: Kremastinos
mesh_terms: D000241:Adenosine; D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000209:etiology* / Q000503:physiopathology; D003326:Coronary Circulation; D018618:Echocardiography, Doppler, Color; D004548:Elasticity; D005260:Female; D005263:Femoral Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D053805:Fractional Flow Reserve, Myocardial; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D008875:Middle Aged; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D011446:Prospective Studies; D012372:ROC Curve; D013997:Time Factors; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D000241:Adenosine