Endothelial and non-endothelial coronary blood flow reserve and left ventricular dysfunction in systemic hypertension.
OBJECTIVE
We evaluated the impairment of endothelium-dependent and endothelium-independent coronary blood flow reserve after administration of intracoronary acetylcholine and adenosine, and its association with hypertensive cardiac disease.


BACKGROUND
Coronary blood flow reserve reduction has been proposed as a mechanism for the progression of compensated left ventricular hypertrophy to ventricular dysfunction.


METHODS
Eighteen hypertensive patients with normal epicardial coronary arteries on angiography were divided into two groups according to left ventricular fractional shortening (FS). Group 1 (FS > or =0.25): n=8, FS=0.29 +/- 0.03; Group 2 (FS <0.25): n=10, FS= 0.17 +/- 0.03.


RESULTS
Baseline coronary blood flow was similar in both groups (Group 1: 80.15 +/- 26.41 mL/min, Group 2: 100.09 +/- 21.51 mL/min, p=NS). In response to adenosine, coronary blood flow increased to 265.1 +/- 100.2 mL/min in Group 1 and to 300.8 +/- 113.6 mL/min (p <0.05) in Group 2. Endothelium-independent coronary blood flow reserve was similar in both groups (Group 1: 3.31 +/- 0.68 and Group 2: 2.97 +/- 0.80, p=NS). In response to acetylcholine, coronary blood flow increased to 156.08 +/- 36.79 mL/min in Group 1 and to 177.8 +/- 83.6 mL/min in Group 2 (p <0.05). Endothelium-dependent coronary blood flow reserve was similar in the two groups (Group 1: 2.08 +/- 0.74 and group Group 2: 1.76 +/- 0.61, p=NS). Peak acetylcholine/peak adenosine coronary blood flow response (Group 1: 0.65 +/- 0.27 and Group 2: 0.60 +/- 0.17) and minimal coronary vascular resistance (Group 1: 0.48 +/- 0.21 mmHg/mL/min and Group 2: 0.34 +/- 0.12 mmHg/mL/min) were similar in both groups (p= NS). Casual diastolic blood pressure and end-systolic left ventricular stress were independently associated with FS.


CONCLUSIONS
In our hypertensive patients, endothelium-dependent and endothelium-independent coronary blood flow reserve vasodilator administrations had similar effects in patients with either normal or decreased left ventricular systolic function.
Rocha
Aloísio Marchi
AM
Heart Institute, Hospital das Clínicas, da Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil.
Salemi
Vera Maria Cury
VM
Lemos Neto
Pedro Alves
PA
Matsumoto
Afonso Yoshikiro
AY
Pereira
Valéria Fontenelle Angelim
VF
Fernandes
Fábio
F
Nastari
Luciano
L
Mady
Charles
C
D000109:Acetylcholine / Q000494:pharmacology; D000241:Adenosine / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*
D014665:Vasodilator Agents; D000241:Adenosine; D000109:Acetylcholine