The functional reserve of collaterals supplying long-term chronic total coronary occlusions in patients without prior myocardial infarction.
OBJECTIVE
Chronic total coronary occlusions (CTOs) with angiographically well-developed collaterals may be considered to provide sufficient blood supply to the occluded segment, and the indication for revascularization may be questioned. Therefore, the collateral function and functional reserve in patients with a CTO without a prior Q-wave myocardial infarction (MI) were assessed.


RESULTS
Invasive assessment of collateral function was done during successful percutaneous coronary intervention in 107 patients with a CTO and no prior Q-wave MI. Intracoronary Doppler flow velocity and pressure recordings were obtained distal to the occlusion before the first balloon inflation and collateral function indexes calculated. In 62 patients, additional pharmacological stress testing was done by intravenous adenosine (140 microg/kg/min) to assess the collateral flow reserve. Patients with normal and impaired regional dysfunction were compared. Collateral function was similar in patients with and without regional left ventricular (LV) dysfunction. In both groups, 78% collaterals provided a collateral pressure index at baseline > 0.3, sufficient to prevent ischaemia during a balloon occlusion, with a minimum of 0.2 in those with preserved LV function. A Doppler-derived function index showed a wider variation due to the high prevalence of microvascular dysfunction in CTOs. Only 7% of patients had an increase in collateral flow reserve > 2.0 during pharmacological stress, whereas coronary steal occurred in one-third independent of regional LV function.


CONCLUSIONS
A limited increase in collateral flow and the high prevalence of coronary steal during stress underscore the functional limitation of collaterals in CTOs without prior Q-wave MI. Even presumably 'well-collateralized' CTOs may benefit from a revascularization.
Werner
Gerald S
GS
Department of Cardiology and Intensive Care Medicine, Medizinische Klinik I, Klinikum Darmstadt, Grafenstrasse 9, D-64283 Darmstadt, Germany. gerald.werner@klinikum-darmstadt.de
Surber
Ralf
R
Ferrari
Markus
M
Fritzenwanger
Michael
M
Figulla
Hans R
HR
D000241:Adenosine; D000368:Aged; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002908:Chronic Disease; D003097:Collateral Circulation / Q000502:physiology*; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology*; D009204:Myocardial Revascularization / Q000379:methods; D013312:Stress, Physiological / Q000503:physiopathology; D014665:Vasodilator Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
D014665:Vasodilator Agents; D000241:Adenosine