title: Mechanism of coronary flow reserve reduction in systemic sclerosis: insight from intracoronary pressure wire studies.
abstract: OBJECTIVE
  Functional impairment of coronary microcirculation is thought to be a major pathway in the development of primary cardiac involvement in SSc; however, the underlying mechanism is not fully understood. We aimed to investigate the mechanisms of coronary flow reserve (CFR) reduction in patients with SSc.
  
  
  METHODS
  Seventeen SSc patients and 17 gender- and age-matched controls were enrolled. Coronary angiography and determination of coronary flow parameters including index of myocardial resistance (IMR) using intracoronary pressure wire at basal conditions and during vasodilator-induced maximal hyperaemia were performed. Transit times of repeated intracoronary saline injection were measured to evaluate the role of cold exposure.
  
  
  RESULTS
  SSc patients with decreased CFR had accelerated basal coronary flow velocity (P < 0.05), and their IMR in hyperaemia (IMR(hyp)) did not differ from either SSc patients with normal CFR or from the controls (P = 0.292 and P =  0.308). The coronary flow velocity of SSc patients correlated with the IMR at baseline (IMR(bas)) (r  = 0.56, P  = 0.019). Injection of room temperature saline did not provoke changes in coronary transit times.
  
  
  CONCLUSIONS
  The lack of decrease in the maximal vasodilatation response indicates that there is no irreversible functional damage at the level of the coronary arterioles. In patients with reduced CFR, the decreased basal IMR and higher velocity reflect compensatory vasodilatory mechanisms probably triggered by ischaemic signals deriving from abnormal myocardial microcirculation.
authors.affiliation: Heart Institute, University of Pécs, H-7624 Pécs, Ifjúság 13, Hungary.
authors.forename: Tünde
authors.initials: T
authors.lastname: Pintér
authors.forename: Réka
authors.initials: R
authors.lastname: Faludi
authors.forename: Balázs
authors.initials: B
authors.lastname: Magyari
authors.forename: András
authors.initials: A
authors.lastname: Vorobcsuk
authors.forename: Gábor
authors.initials: G
authors.lastname: Kumánovics
authors.forename: Tünde
authors.initials: T
authors.lastname: Minier
authors.forename: László
authors.initials: L
authors.lastname: Czirják
authors.forename: András
authors.initials: A
authors.lastname: Komócsi
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology; D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D016022:Case-Control Studies; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000503:physiopathology*; D004452:Echocardiography; D057510:Endovascular Procedures / Q000295:instrumentation / Q000379:methods*; D005260:Female; D006321:Heart / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology*; D012595:Scleroderma, Systemic / Q000503:physiopathology*; D014664:Vasodilation / Q000502:physiology