Peripheral hemorheological and vascular correlates of coronary blood flow.
The slow coronary flow phenomenon (SCF), a condition described by the presence of inappropriate delay in the progression of intracoronary contrast during angiography in the absence of stenoses, has been shown in some patients presenting with chest pain. While several conditions leading to "secondary" slow flow are known, there are no definitive conclusions regarding the exact pathogenesis of "primary" SCF. The present paper outlines the mechanisms that may lead to SCF, emphasizing the role of hemorheological and vascular factors in the pathogenesis of this phenomenon. Small vessel dysfunction has been proposed in the pathogenesis of SCF since the first description of this syndrome in 1972. Abnormalities in coronary microvascular function result from increased microvascular resistances and impaired endothelial release of vasoactive substances, especially in production and bioavailability of endothelium derived NO. Inflammatory conditions (increased levels of C-reactive protein, interleukin-6 and adhesion molecules) and metabolic abnormalities such as impaired glycemic control, hyperuricemia and elevated serum gamma-glutamyltransferase were also found to contribute to microvascular dysfunction in patients with SCF. New studies have also indicated that increased blood viscosity and one of its major determinants, erythrocyte aggregation, is associated with the SCF. Rheological variables play a role in the control of shear stress and contribute to blood flow velocity changes. Although platelets do not have a significant influence on blood viscosity, it has been demonstrated that they are involved in the development of SCF. Increased mean platelet volume (MPV), an indicator of platelet activation and platelet aggregability is also significantly higher in patients with SCF compared with patients with normal coronary flow.
Medical Clinic and Policlinic, University Medical Center Mainz, Mainz, Germany.
Ana
A
Damaske
Selina
S
Muxel
Federica
F
Fasola
Marie Christine
MC
Radmacher
Sarina
S
Schaefer
Alexander
A
Jabs
Dörte
D
Orphal
Philipp
P
Wild
John D
JD
Parker
Massimo
M
Fineschi
Thomas
T
Munzel
Sandro
S
Forconi
Tommaso
T
Gori
D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D001783:Blood Flow Velocity / Q000502:physiology*; D002637:Chest Pain / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D003937:Diagnosis, Differential; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D018056:Hemorheology; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology; D008297:Male; D055806:Microvessels / Q000187:drug effects / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000175:diagnosis / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D015539:Platelet Activation; D013577:Syndrome; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology / Q000627:therapeutic use
D014665:Vasodilator Agents; D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D001120:Arginine