Left Anterior Descending Artery Location Research Articles

Visual-Functional Mismatch Between Coronary Angiography and Fractional Flow Reserve

The goal of this study was to identify clinical and lesion-specific local factors affecting visual-functional mismatch. Although lesion severity determined by coronary angiography has not been well correlated with physiological significance, the mechanism of the discordance remains poorly understood. The authors assessed quantitative coronary angiography, intravascular ultrasound (IVUS), and fractional flow reserve (FFR) in a prospective cohort of 1,000 patients with 1,129 coronary lesions. Three-dimensional computational simulation studies were performed. Lesions with angiographic diameter stenosis (DS) ≥50% and FFR >0.80 ("mismatches") were seen in 57% of non-left main lesions and in 35% of the left main lesions, respectively (p = 0.032). Conversely, among the lesions with DS <50% and FFR <0.80 ("reverse mismatches") 16% were found in the non-left main lesions and 40% in the left main lesions (p < 0.001). The independent predictors for mismatch were advanced age, non-left anterior descending artery location, absence of plaque rupture, short lesion length, large minimal lumen area, smaller plaque burden, and greater minimal lumen diameter. Conversely, reverse mismatch was independently associated with younger age, left anterior descending artery location, the presence of plaque rupture, a smaller minimal lumen area, and larger plaque burden. In a computational simulation study, FFR was influenced by DS, lesion length, different lesion shape, plaque eccentricity, surface roughness, and various shapes of plaque rupture. There were high frequencies of visual-functional mismatch between angiography and FFR. The discrepancy was related to the clinical and lesion-specific factors frequently unrecognizable by angiography, thus suggesting that coronary angiography cannot accurately predict FFR. (Natural History of FFR-Guided Deferred Coronary Lesions [IRIS FFR-DEFER]; NCT01366404).

VALIDATION OF INTRAVASCULAR ULTRASOUND DERIVED PARAMETERS WITH FRACTIONAL FLOW RESERVE FOR ASSESSMENT OF CORONARY STENOSIS SEVERITY

Background—We assessed optimal intravascular ultrasound (IVUS) criteria for predicting functional significance of intermediate coronary lesions. Methods and Results—Overall, 201 patients with 236 coronary lesions underwent IVUS and invasive physiological assessment before intervention. Fractional flow reserve (FFR) was measured at maximal hyperemia induced by intravenous adenosine infusion. FFR <0.80 at maximum hyperemia was seen in 49 (21%) of the overall 236 lesions. The independent determinants of FFR were minimal lumen area (MLA; β=0.020; 95% confidence interval [CI], 0.008 to 0.031; P=0.032), plaque burden (β=−0.002; 95% CI, −0.003 to 0.001; P=0.001), lesion length with a lumen area <3.0 mm2 (β=−0.003; 95% CI, −0.005 to −0.001; P=0.005), and left anterior descending artery location (β=−0.035; 95% CI, −0.055 to −0.016; P=0.001). The best cutoff value (with a maximal accuracy) of the MLA to predict FFR <0.80 was <2.4 mm2, with a diagnostic accuracy of 68% (90% sensitivity, 60% specificity, and area und...

Validation of Intravascular Ultrasound–Derived Parameters With Fractional Flow Reserve for Assessment of Coronary Stenosis Severity

We assessed optimal intravascular ultrasound (IVUS) criteria for predicting functional significance of intermediate coronary lesions. Overall, 201 patients with 236 coronary lesions underwent IVUS and invasive physiological assessment before intervention. Fractional flow reserve (FFR) was measured at maximal hyperemia induced by intravenous adenosine infusion. FFR <0.80 at maximum hyperemia was seen in 49 (21%) of the overall 236 lesions. The independent determinants of FFR were minimal lumen area (MLA; β=0.020; 95% confidence interval [CI], 0.008 to 0.031; P=0.032), plaque burden (β=-0.002; 95% CI, -0.003 to 0.001; P=0.001), lesion length with a lumen area <3.0 mm(2) (β=-0.003; 95% CI, -0.005 to -0.001; P=0.005), and left anterior descending artery location (β=-0.035; 95% CI, -0.055 to -0.016; P=0.001). The best cutoff value (with a maximal accuracy) of the MLA to predict FFR <0.80 was <2.4 mm(2), with a diagnostic accuracy of 68% (90% sensitivity, 60% specificity, and area under the curve=0.800; 95% CI, 0.742 to 0.848; P<0.001). The cutoff value of plaque burden to predict FFR <0.80 was ≥79% (69% sensitivity, 72% specificity, and area under the curve=0.756; 95% CI, 0.696 to 0.810; P<0.001). The cutoff value of lesion length with a lumen area <3.0 mm(2) was 3.1 mm (84%sensitivity, 63%specificity, and area under the curve=0.765; 95% CI, 0.706 to 0.818; P<0.001). Among 117 lesions with an MLA ≥2.4 mm(2), 112 (96%) had an FFR ≥0.80,; and all but 1 showed FFR ≥0.75. Conversely, 44 (37%) lesions with an MLA <2.4 mm(2) had an FFR <0.80. IVUS-derived MLA ≥2.4 mm(2) may be useful to exclude FFR <0.80, but poor specificity limits its value for physiological assessment of lesions with MLA <2.4 mm(2). Thus, FFR or stress tests may be necessary to accurately identify ischemia-inducible intermediate stenoses.

Comparison of Effects of Bare Metal Versus Drug-Eluting Stent Implantation on Biomarker Levels Following Percutaneous Coronary Intervention for Non–ST-Elevation Acute Coronary Syndrome

Drug-eluting stents (DESs) deliver biphasic (early and late) elution of anti-inflammatory compounds. We therefore hypothesized that DESs would be associated with early reductions in inflammatory biomarker release after percutaneous coronary intervention (PCI). A total of 741 patients with non-ST-elevation acute coronary syndrome underwent PCI in the Randomized Trial to Evaluate the Relative PROTECTion against Post-PCI Microvascular Dysfunction and Post-PCI Ischemia among Anti-Platelet and Anti-Thrombotic Agents (PROTECT) Thrombolysis In Myocardial Infarction 30 study of eptifibatide and reduced-dose antithrombin compared with bivalirudin. Serial biomarkers C-reactive protein, troponin, creatine kinase-MB, soluble CD40 ligand, interleukin-6, prothrombin fragment F1.2, and RANTES (regulated on activation, normal T-cell expressed and secreted) were assessed through 24 hours after PCI. DES use was at the investigator's discretion. Patients treated with DESs (n = 665) versus bare metal stents (n = 139) were more likely to have patent arteries before PCI (92.0% vs 86.6%, p = 0.04), Thrombolysis In Myocardial Infarction myocardial perfusion grade 3 (57.9% vs 47.7%, p = 0.033), and the left anterior descending artery as the culprit artery (38.5% vs 18.3%, p <0.001). The increase in C-reactive protein and troponin was lower among patients undergoing DES implantation (median 2.1 vs 3.5 mg/L for C-reactive protein, median 0.11 vs 0.41 ng/ml for troponin), even after adjustment for randomized treatment, clopidogrel before treatment, diabetes mellitus status, epicardial patency, left anterior descending artery location, and myocardial perfusion (p = 0.036 and p = 0.039, respectively). Interleukin-6 was lower with DESs on univariate analysis but not multivariate analysis. Creatine kinase-MB, soluble sCD40 ligand, prothrombin fragment F1.2, and RANTES did not differ by DES use. In conclusion, patients undergoing DES implantation achieved more reductions in periprocedural markers of inflammation and necrosis than patients receiving bare metal stents among those with non-ST-elevation acute coronary syndrome.

Time for contrast material to traverse the epicardial artery and the myocardium in ST-Segment elevation acute myocardial infarction versus unstable angina pectoris/non–ST-elevation acute myocardial infarction

Although the time for contrast material to fill the epicardial artery in the setting of acute coronary syndromes has been studied extensively, the time for contrast material to fill the myocardium has not been evaluated. We compared differences in myocardial contrast material transit among patients with unstable angina pectoris/non–ST-elevation acute myocardial infarction (UAP/NSTEAMI) with patients with ST-elevation acute myocardial infarction (STEAMI). The time it took for contrast material to first appear and to arrive at peak intensity in the myocardium was compared in 224 patients with STEAMI enrolled in the LIMIT-AMI study versus 430 patients with UAP/NSTEAMI enrolled in the TACTICS-TIMI 18 trial. In patients with STEAMI, there was a delay in both the time for contrast material to first enter the myocardium (5,619 ± 1,789 vs 4,663 ± 1,626 ms, p <0.0001) and the time from entrance to peak blush intensity (2,387 ± 1,359 vs 1,959 ± 1,244 ms, p = 0.003) compared with patients with UAP/NSTEAMI. STEAMI remained significantly associated with impaired entrance of contrast material into the myocardium (p <0.0001) in a multivariate model controlling for known correlates of impaired epicardial flow (presence of thrombus, percent diameter stenosis, left anterior descending artery location, and contrast material inflow in the epicardial artery [corrected TIMI frame count]). The time for contrast material to enter the myocardium is impaired to a greater degree in STEAMI compared with UAP/NSTEAMI, even after adjusting for other variables known to delay flow in the epicardial artery. These data provide insight into potential mechanistic differences between these 2 clinical syndromes.

Effect of prior coronary restenosis on the risk of subsequent restenosis after stent placement or directional atherectomy

Lesions that have developed restenosis after a prior intervention may be more likely to develop restenosis after subsequent percutaneous interventions. To determine if this is an independent effect, the clinical characteristics and immediate angiographic outcomes of 179 prior restenosis lesions were compared with those of 254 primary lesions after stenting or directional atherectomy. Six-month angiographic follow-up was obtained for 79% of successfully treated lesions. Univariable and muttivariable logistic regression was used to determine how binary restenosis (defined as $ ̆ -50% diameter stenosis at follow-up) was influenced by postprocedure luminal diameter, left anterior descending artery location, diabetes mellitus, as well as prior restenosis. At 6-month follow-up, prior restenosis lesions had a significantly smaller late diameter (1.77 vs 2.18 mm, p < 0.001), more absolute late loss (1.35 vs 1.14 mm, p = 0.051), a higher loss index (0.58 vs 0.45, p < 0.02), and a higher binary restenosis rate (37.3% vs 24.4%, p = 0.01). Whereas univariable analysis revealed that left anterior descending artery location, diabetes mellitus, postprocedure luminal diameter < 3.1 mm, and prior restenosis were each strong predictors of binary restenosis (all p < 0.02), muttivariable analysis showed that after adjustment for left anterior descending artery location, diabetes, and postprocedure luminal diameter, prior restenosis was no longer an independent predictor of restenosis (odds ratio 1.57, 95% confidence interval 0.95–2.60, p = 0.073). In conclusion, although prior restenosis lesions do show more restenosis than primary lesions, much of this effect is due to preselection of a population enriched in other known factors that predispose to restenosis.

Prior restenosis predicts restenosis after coronary angioplasty of a new significant narrowing

To determine the influence of a history of restenosis on subsequent restenosis after percutaneous transluminal coronary angioplasty (PTCA) of a new significant narrowing, the records of 100 patients who underwent successful PTCA at another site (“new narrowing PTCA”) ≥2 months after successful initial PTCA were retrospectively reviewed. Patients were grouped according to whether initial PTCA resulted in restenosis, which was determined by angiographic follow-up ≥3 months after initial PTCA. Patients in group 1 did not have restenosis after initial PTCA (n = 50), whereas patients in group 2 did (n = 40). All patients were followed for recurrent symptoms, with serial exercise tests, for ≥6 months after new narrowing PTCA. Clinically suspected and angiographically confirmed restenosis occurred in 11 of 50 (22%) patients and 12 of 63 (19%) narrowings in group 1, and in 20 of 40 (50%) patients and 22 of 48 (46%) narrowings in group 2 (p < 0.01 for patients, p < 0.002 for narrowings). Multivariate analysis identified that prior restenosis (p < 0.02, odds ratio 3.4), left anterior descending artery location of stenosis (p < 0.04, odds ratio 3.0), and severity of stenosis before PTCA (p < 0.02, odds ratio 1.8) were independently associated with restenosis after new narrowing PTCA. In conclusion, prior restenosis is an independent risk factor for subsequent restenosis after new narrowing PTCA.

Restenosis after coronary angioplasty: A multilvariate statistical model to relate lesion and procedure variables to restenosis

The Multi-Hospital Eastern Atlantic Restenosis Trial group obtained follow-up angiography in 510 patients with 598 successfully dilated coronary lesions who were enrolled in a controlled trial of the effects of a single dose of 1 g of methylprednisolone on restenosis after coronary angioplasty. The overall restenosis rate was 39.6%. The strongest univariate relations to the restenosis rate were found for lesion location (saphenous vein graft, 68%; left anterior descending artery, 45%; left circumflex artery and right coronary artery, 32%; p = 0.002); lesion length (≤4.6 mm, 33%; >4.6 mm, 45%; p = 0.001); percent stenosis before angioplasty (≤73%, 25%; >73%, 43%; p = 0.005), percent stenosis after angioplasty (≤21%, 33%; >21%, 46%; p = 0.017) and arterial diameter (<2.9 mm, 44%; ≥ 2.9 mm, 34%; p = 0.036).Two multivariate models to predict restenosis probability were developed with use of stepwise logistic regression. The preprocedural model, which included only variables whose values were known before angioplasty, entered lesion length, vein graft location, left anterior descending artery location, percent stenosis before angioplasty, eccentric lesion and arterial diameter. The postprocedural model, which also included variables whose values were known after angioplasty was performed, was similar to the preangioplasty model except that it also entered postangioplasty percent stenosis and “optimal” balloon sizing but did not enter eccentric lesion.These data indicate that the probability of restenosis after angioplasty is determined predominantly by the characteristics of the lesion being dilated. They are consistent with the known intimal proliferative mechanism of restenosis, offer a means of identifying lesions at unusually high or low risk of restenosis, and of predicting the likelihood that a particular lesion will restenose after angioplasty and provide a rationale for stratification by restenosis probability in the design of future studies of restenosis.