Coronary left main and non-left main bifurcation angles: how are the angles modified by different bifurcation stenting techniques?

BACKGROUND: Investigation of the correlation between bifurcation angles and outcomes is limited with discordant results. The aim of this study is to investigate left main (LM) and non-left main (N-LM) bifurcation angles and their modification after percutaneous coronary intervention (PCI). Measurement of all three angles adds to our understanding of bifurcation anatomy and the resultant effect of different stenting techniques. METHODS AND RESULTS: All three bifurcation angles were described according to the European Bifurcation Club definition: the A (proximal bifurcation angle), the B (distal bifurcation angle) and the C (main branch angle). Measurements were performed in 75 LM and 140 N-LM bifurcations. In LM bifurcations baseline mean values of C, A, and B were 151 degrees +/- 28 degrees, 131 degrees +/- 32 degrees, and 78 +/- 28 degrees, respectively. In bifurcations with 2 stents the B significantly decreased by a mean of 10 degrees (P = 0.003) and A increased by 10 degrees (P = 0.006). Crush stenting significantly decreased B (A - 14 degrees ; P = 0.020) and increased A (A + 21 degrees; P = 0.005), particularly non-true bifurcations. In N-LM bifurcations mean values for C, A, and B were 156 degrees +/- 19 degrees , 144 degrees +/- 22 degrees, and 60 degrees +/- 20 degrees, respectively. Similar to LM bifurcations, the B became narrower mainly at the expense of the A, which became wider. In both types of bifurcations the greatest variation in A and B was found following 2-stent techniques performed in T-shaped (> or =70 degrees) bifurcations. CONCLUSIONS: In both LM and N-LM bifurcations we found a significant difference in A and B pre- and post-PCI. This difference was driven by the 2-stent technique and was most evident with a baseline bifurcation angle > or =70 degrees. The Crush technique caused the largest angle variation post-procedure, particularly in non-true LM bifurcations.

Noninvasive evaluation of flow reserve in the left anterior descending coronary artery in patients with cardiac syndrome X.

Data on coronary flow reserve (CFR) in patients with syndrome X are still controversial. Further, noninvasive evaluation of epicardial and microvascular flow reserves in these patients has never been performed. In 17 patients with syndrome X and in 17 age- and gender-matched control subjects, CFR in the mid left anterior descending coronary artery (LAD) was evaluated by transthoracic color and pulse-wave Doppler using a 7-mHz probe (Sequoia, Siemens). Peak diastolic LAD flow was calculated at rest and at peak adenosine (140 microg/kg/min intravenously in 90 seconds). Myocardial contrast echocardiography (MCE) was performed at rest and during adenosine use by real-time cadence pulse sequencing and intravenous SonoVue (Bracco; 5 ml at 1 ml/min) and microvascular blood volume (A), velocity (beta), and flow (Axbeta) by replenishing curves (y = A[1 - e(betat)]). CFR was measured by Doppler echocardiography as an adenosine/rest velocity ratio and by MCE as a microvascular volume, velocity, and flow adenosine/rest ratio. Compared with controls, patients with syndrome X demonstrated lower LAD CFR and velocity and flow microvascular flow reserves (p <0.01, <0.005, and <0.005, respectively). In patients with syndrome X, those with angina and ST-segment depression during adenosine testing had even lower LAD CFR and velocity and flow microvascular flow reserves compared with those with no symptoms (p <0.0001, <0.0001, and <0.005, respectively). LAD CFR demonstrated a significant linear correlation with velocity microvascular flow reserve (r = 0.92, p <0.0001) and flow microvascular flow reserve (r = 0.77, p <0.0001). In conclusion, CFR in the LAD, successfully evaluated by transthoracic Doppler echocardiography and MCE, is significantly decreased in patients with syndrome X and even more in those with angina pectoris and ST-segment depression during adenosine testing. Thus, noninvasive evaluation of CFR by echocardiography is feasible and provides information on the severity of microvascular impairment.