Prognostic Values of Fractional Flow Reserve Based on Clinical Outcomes in Patients on Chronic Hemodialysis.

The fractional flow reserve (FFR) cut-off values of 0.75 or 0.8 have been widely used; however, whether they apply to patients on hemodialysis remains unknown. We aimed to investigate the cut-off value of FFR associated with clinical outcomes in patients on hemodialysis. Using the Japanese multicenter registry, we analyzed data of patients on hemodialysis with measured FFR between January 2010 and December 2016. Survival classification and regression tree analysis for the composite primary outcome of cardiovascular mortality, myocardial infarction, and target vessel revascularization revealed a threshold FFR of 0.83. Multivariate Cox regression analyses were performed for the clinical outcomes. Additionally, the primary outcome was analyzed using propensity score matching by dividing the patients into complete and incomplete revascularization groups according to the presence of residual lesions with an FFR of ≤0.83 after the intervention. Of the 212 included patients, 112 (52.8%) had lesions with an FFR of ≤0.83. After adjusting for confounders, an FFR of ≤0.83 was associated with a higher risk for the primary outcome (adjusted hazard ratio 2.01, 95% confidence interval 1.11 to 3.66, p = 0.021). Propensity score matching showed that complete revascularization for lesions with an FFR of ≤0.83 was associated with a reduced risk for the primary outcome compared with incomplete revascularization (hazard ratio 0.38, 95% confidence interval 0.20 to 0.71, log-rank p = 0.0016). In conclusion, an FFR of ≤0.83 was an independent predictor of clinical events in patients on hemodialysis. Furthermore, complete revascularization was associated with better clinical outcomes. Thus, this population may require a distinct FFR cut-off value.

Liver fibrosis index as a novel prognostic factor in patients with pulmonary arterial hypertension.

Liver dysfunction is an important determinant of the prognosis of left heart failure patients. However, few studies have reported on cardiohepatic interactions in right heart failure patients, a condition that is an important prognostic factor in pulmonary arterial hypertension (PAH). This study aimed to evaluate the existence and extent of hepatic fibrosis and its contribution as a prognostic factor in PAH. This prospective study enrolled 60 consecutive patients with PAH in the International University of Health and Welfare Mita Hospital from June 2016 to December 2017. After the application of the exclusion criteria, 35 patients were assessed for hepatic fibrosis, using real-time tissue elastography, and for clinical deterioration. Sixteen healthy controls were also assessed for comparison. The liver fibrosis index (LFI) was significantly higher in PAH patients than in healthy controls (1.214 ± 0.047 vs. 0.911 ± 0.059, P < 0.001), suggesting that PAH patients exhibited mild liver fibrosis. However, patients with deterioration (vs. no deterioration) had significantly higher LFI values (1.507 ± 0.078 vs. 1.080 ± 0.034, P < 0.001), independent from other established liver function parameters. A receiver operating characteristic curve analysis identified that an LFI ≥ 1.275 indicated a significant probability of clinical deterioration (hazard ratio: 8.4 (95% CI 1.5-45.4, P = 0.012), independent from other known PAH prognostic factors. PAH patients may exhibit subclinical liver fibrosis associated with chronic right heart failure. The LFI can serve as both a non-invasive evaluation of liver fibrosis and a predictive marker for the deterioration of PAH patients.

Successful transition from Treprostinil to Selexipag in patient with severe pulmonary arterial hypertension.

BACKGROUND: In this report, we describe the first successful case of transition from subcutaneous administration of treprostinil to selexipag in a patient with severe pulmonary arterial hypertension (PAH), by evaluating hemodynamic changes and exercise tolerance. CASE PRESENTATION: A 38-year-old female with idiopathic PAH (IPAH) had received initial triple combination therapy (macitentan PO, tadalafil PO, and treprostinil SC) and achieved excellent improvement in hemodynamics. Afterwards, due to the development of side effects from subcutaneous administration, we replaced treprostinil therapy with oral selexipag, resulting in stable hemodynamic parameters and exercise capacities. CONCLUSIONS: We report the first case of successful replacement of treprostinil (20.1 ng/kg/min) with selexipag (1600 µg BID) as a component of triple combination therapy, which provides incentive to perform a larger, prospective exchange study.

Vasospastic angina resulting in sudden cardiac arrest, initially misdiagnosed as a psychiatric disorder.

A 51-year-old-woman with a history of ablation therapy due to Wolff-Parkinson-White syndrome had been suffering from ambiguous chest pain, prompting investigation by several cardiologists. After being dissatisfied with a psychiatric disorder diagnosis, she was admitted to our hospital for further investigation. She lost her consciousness due to a sudden cardiac arrest shortly after admission. A provocation test indicated vasospastic angina associated with a diffuse spastic pattern of her left anterior descending artery. .

Intravascular ultrasound-guided bail-out therapy in a case of acute myocardial infarction with iatrogenic coronary artery spiral dissection.

A 54-year-old man with suspected vasospastic angina returned to the hospital 2 weeks later with symptoms of acute myocardial infarction. Emergent coronary angiography (CAG) showed an occlusive lesion just beyond the bend of the proximal right coronary artery segment. The selected 7F AL1.0 guiding catheter may have injured the vessel surface and the guide wire might have entered the pseudo-lumen. Balloon dilatation of the pseudo-lumen resulted in a spiral dissection. We were able to provide bail out with therapy under guidance of combined CAG and intravascular ultrasound, which provided structural 3D images of coronary artery anatomy. .

Detection of attenuated plaque in stable angina with 64-multidetector computed tomography: a comparison with intravascular ultrasound.

BACKGROUND: To clarify multidetector computed tomography (MDCT) findings of attenuated plaque detected by intravascular ultrasound (IVUS). METHODS AND RESULTS: One hundred and fifty-four patients with stable angina underwent MDCT before IVUS. The attenuated plaque was identified in the targeted artery with IVUS, and the same artery was analyzed with MDCT for the presence of a high density area (HDA) >130 Hounsfield units (HU), and a low density area (LDA) <30 HU. A HDA in attenuated plaque was compared with that in calcified plaque. Ten attenuated plaques and 15 calcified plaques were identified in 9 of 154 patients (males=9, 66.2 ± 9.5 years). Eight of the 10 attenuated plaques and all 15 calcified plaques were accompanied with a HDA on MDCT. The HDA ranged from 174 to 667 HU (mean 389.0 ± 148.3 HU) in the 8 attenuated plaques, and from 545 to 1,205 HU (mean 920.9 ± 215.9 HU) in 15 calcified plaques. There was a significant difference in CT density of the HDA between the attenuated and calcified plaque (P<0.001). All attenuated plaques contained LDA <30 HU in the portions without HDA. CONCLUSIONS: MDCT has the ability to demonstrate attenuated plaque as the combination of HDA (approximately 400 HU on average) and LDA <30 HU. The HDA can be differentiated from calcified plaque by its lower CT density value.

Can intravascular ultrasound guidance modify the efficacy of drug-eluting stent over bare-metal stent in an aorto-ostial lesion?

PURPOSE: We compared the efficacy of drug-eluting stents (DESs) versus bare-metal stents (BMSs) in de novo and native aorto-ostial lesions (AOLs) guided by intravascular ultrasound (IVUS). METHOD: Thirty-eight patients underwent DES implantation for 38 AOLs; 35 with sirolimus-eluting stents, and three with paclitaxel-eluting stents (DES group). The control group was composed of 40 AOLs treated by BMS. The incidence of the primary composite end point of all-cause mortality, Q-wave myocardial infarction and target vessel revascularization (TVR) as TVR-major adverse cardiac event (TVR-MACE) was evaluated during a 1-year follow-up. Clinical and IVUS parameters were compared between the DES and BMS groups, and Cox hazards model was used to calculate hazard ratios of several factors for the 1-year TVR-MACE. RESULTS: Although the vessel, plaque, and stent volumes were significantly larger after the procedures in the DES group owing to longer lesions (18.3 ± 5.1 vs. 13.2 ± 5.9 mm, P<.001), the stent volume index (10.8 ± 2.6 vs. 12.4 ± 3.3, P=.024) was much smaller than that in the BMS group. During the 1-year follow-up, there were 13 TVR-MACEs in all patients (13% in DES vs. 20% in BMS, P=.4 by Kaplan-Meier analysis). The Cox hazards model did not indicate any specific unfavorable factor for the 1-year TVR-MACE. CONCLUSIONS: The present study showed equality between DES and BMS on de novo and native AOLs about the 1-year TVR-MACE rate, even though a DES was used in longer and bulkier lesions as compared to BMS.

Accuracy of computed tomographic angiography for stenosis quantification using quantitative coronary angiography or intravascular ultrasound as the gold standard.

Computed tomographic angiography (CTA) is considered to have limited accuracy for quantifying exact percent diameter stenosis in coronary arteries. However, most studies evaluating CTA use quantitative coronary angiography (QCA) as the gold standard, a technique with its own limitations. We sought to determine whether CTA measurements of stenosis severity correlate better with intravascular ultrasound (IVUS) than with QCA. Luminal dimensions of 67 de novo coronary lesions were measured by CTA, IVUS, and QCA. IVUS was performed when lesion severity by angiography was equivocal. Mean percent diameter stenosis by QCA was 51 +/- 9.8% and mean IVUS minimal luminal area was 3.8 +/- 1.8 mm(2). There was a moderate correlation between CTA minimal luminal area and IVUS minimal luminal area (r(2) = 0.41, p <0.001), but no relation between CTA and QCA measurements of minimal luminal diameter (r(2) = 0.01, p = 0.57) or diameter stenosis (r(2) = 0.02, p = 0.31). There was also no relation between IVUS minimal luminal area and QCA diameter stenosis (r(2) = 0.01, p = 0.50). When lesions with moderate or severe calcification were excluded, the correlation between CTA minimal luminal area and IVUS minimal luminal area was good (r(2) = 0.68, p <0.001). In conclusion, in this cohort of patients with intermediate-grade lesions on cardiac catheterization, absolute measurements of stenosis severity on CTA correlated with IVUS but not with QCA. Our findings suggest that limitations of quantitative coronary angiography as a gold standard need to be considered in studies evaluating the accuracy of coronary CTA.

Impact of plaque composition on cardiac troponin elevation after percutaneous coronary intervention: an ultrasound analysis.

OBJECTIVES: We used virtual histology-intravascular ultrasound (VH-IVUS) to study the relationship between pre-percutaneous coronary intervention (PCI) coronary plaque characteristics and post-PCI cardiac troponin I (cTnI) elevation. BACKGROUND: Percutaneous coronary intervention is often complicated by post-procedural myocardial necrosis as manifested by elevated cardiac markers. METHODS: Eighty consecutive patients (29 stable and 51 unstable angina) with normal pre-PCI cTnI levels were imaged before PCI using VH-IVUS. Patients were divided into 2 groups according to the presence (Group I, n = 38) or absence (Group II, n = 42) of post-PCI cTnI elevation > or =3x the upper limit of normal (0.08 ng/ml). RESULTS: The absolute and percent necrotic core volumes were significantly greater in Group I than in Group II (13.6 +/- 6.4 mm(3) vs. 7.9 +/- 4.4 mm(3), p < 0.001, and 19.8 +/- 10.4% vs. 12.8 +/- 8.4%, p = 0.015, respectively). The absolute and percent necrotic core areas were significantly greater in Group I than in Group II at the minimum lumen site (1.70 +/- 0.91 mm(2) vs. 0.61 +/- 0.39 mm(2), p < 0.001, and 22.9 +/- 11.7% vs. 10.4 +/- 6.6%, p < 0.001, respectively) and at the largest necrotic core site (2.00 +/- 0.86 mm(2) vs. 0.81 +/- 0.78 mm(2), p < 0.001, and 24.0 +/- 11.7% vs. 12.9 +/- 6.6%, p < 0.001, respectively). The DeltacTnI correlated with: 1) absolute and percent necrotic core area at the minimum lumen site and at the largest necrotic core site; 2) absolute necrotic core volume; 3) percent fibrofatty area at the minimum lumen site; and 4) lesion site plaque burden. In the multivariate analysis, absolute necrotic core area at the minimum lumen site was the only independent predictor of post-PCI cTnI elevation > or =3x the upper limit of normal (odds ratio: 1.318; 95% confidence interval: 1.090 to 1.594, p = 0.004). CONCLUSIONS: The VH-IVUS analysis shows that post-PCI cTnI elevation occurs in lesions with a large necrotic core area. The VH-IVUS may play an important role in detecting which lesions are high risks for myocardial necrosis after PCI.

Relation of drug-eluting stent strut distribution to stent thrombosis in coronary arteries.

The distribution of stent struts is critical to drug deposition and, therefore, may affect the amount of neointima and the risk of thrombosis after drug-eluting stent (DES) implantation. The aim of our study was to evaluate stent strut distribution in the setting of a drug-eluting stent thrombosis (ST). We retrospectively analyzed postprocedural intravascular ultrasound (IVUS) images of 13 patients who subsequently developed ST (14 DES thrombotic lesions) and a control group of 27 patients (30 DES lesions) matched for stent type and presence of chronic renal failure. In addition to standard IVUS measurements, visible struts were counted and maximum interstrut angle was measured at 1-mm intervals. Early ST was defined as < or =30 days after DES deployment and late ST as >30 days after DES deployment. Compared with DES controls, the ST group had a larger maximum interstrut angle (60.8 +/- 8.3 degrees vs 55.7 +/- 4.8 degrees , p = 0.014) and a similar number of stent struts (8.4 +/- 0.6 vs 8.7 +/- 0.6, p = NS). Maximum interstrut angle tended to be larger in late ST than in early ST (66.1 +/- 10.8 degrees vs 57.8 +/- 5.0 degrees , p = 0.071). The incidence of maximum interstrut angles > or =90 degrees and > or =120 degrees observed continuously for > or =2 mm of stent length was higher in the ST group (p = 0.009 and p = 0.096, respectively). In conclusion, DES-treated lesions leading to ST had larger maximum interstrut gaps distributed circumferentially and longitudinally, but a similar number of struts at the time of DES implantation compared with DES controls.

Attenuated plaque detected by intravascular ultrasound: clinical, angiographic, and morphologic features and post-percutaneous coronary intervention complications in patients with acute coronary syndromes.

OBJECTIVES: We evaluated the clinical significance of attenuated plaque (hypoechoic plaque with deep ultrasound attenuation). BACKGROUND: Attenuated plaques are unusual intravascular ultrasound (IVUS) findings in patients with acute coronary syndrome (ACS). METHODS: We reviewed clinical presentations and angiographic and pre-intervention IVUS findings in 293 ACS patients undergoing percutaneous coronary intervention (PCI) without a distal protection device: 187 with non-ST-segment elevation myocardial infarction (NSTEMI) and 106 with ST-segment elevation myocardial infarction (STEMI). RESULTS: Attenuated plaque was observed in 75 patients (25.6%): 39.6% of STEMI versus 17.6% of NSTEMI (p < 0.001). (We also reviewed 100 randomly selected patients with stable angina and pre-intervention IVUS; none had attenuated plaque.) Overall, in ACS patients with attenuated plaques: 1) the level of C-reactive protein was higher; 2) angiographic thrombus and initial coronary flow Thrombolysis In Myocardial Infarction flow grade <2 were more common; and 3) IVUS lesion site plaque burden and remodeling index were significantly greater, lesion site luminal dimensions significantly smaller, and thrombus, positive remodeling, and plaque rupture were more common. No-reflow (26.7% vs. 4.6%, p < 0.001) and deteriorated post-PCI coronary blood flow (8.0% vs. 2.8%, p = 0.001) were higher. In ACS patients with normal coronary blood flow at baseline, deterioration in the coronary blood flow post-PCI was more common in lesions with attenuated plaque. CONCLUSIONS: Attenuated plaque was more common in ACS patients with STEMI than NSTEMI. Attenuated plaque in ACS patients was associated with a higher C-reactive protein level, more severe and complex lesion morphology, reduced coronary blood flow before PCI, and especially no-reflow after PCI.

Disease progression in nonintervened saphenous vein graft segments a serial intravascular ultrasound analysis.

OBJECTIVES: We used serial intravascular ultrasound (IVUS) to assess disease progression in nonintervened saphenous vein graft (SVG) segments to determine the natural rate of disease progression in SVG. BACKGROUND: There are no serial IVUS studies of disease progression or luminal compromise in SVGs. METHODS: We assessed serial (baseline and follow-up at 16.2 +/- 7.4 months) IVUS findings in 50 nonintervened SVG segments in 44 patients. The SVG age was 13.5 +/- 3.6 years. RESULTS: Overall, from baseline to follow-up, plaque area increased (Delta = +0.58 +/- 1.25 mm(2), p = 0.003), and SVG and minimum lumen area (MLA) decreased (Delta = -0.50 +/- 1.14 mm(2), p = 0.002, and Delta = -1.08 +/- 1.28 mm(2), p < 0.001, respectively). The MLA decreased in 34 lesions (Delta = -1.67 +/- 1.08 mm(2)), and MLA increased in 16 lesions (Delta = +0.19 +/- 0.47 mm(2)). Compared with lesions with an increase in MLA, lesions with a decrease in MLA were associated with: 1) larger baseline SVG and plaque areas and plaque burden (15.57 +/- 3.90 mm(2) vs. 11.55 +/- 2.30 mm(2), p < 0.001; 7.97 +/- 3.77 mm(2) vs. 4.27 +/- 1.92 mm(2), p < 0.001; and 48.7 +/- 14.2% vs. 36.0 +/- 13.4%, p = 0.004, respectively); and 2) a greater decrease in SVG area (Delta = -0.96 +/- 1.05 mm(2) vs. +0.48 +/- 0.58 mm(2), p < 0.001) and greater increase in plaque area (Delta = +0.71 +/- 1.47 mm(2) vs. +0.29 +/- 0.45 mm(2), p < 0.001). The DeltaMLA correlated with both Deltaplaque area (r = -0.589, p < 0.001) and DeltaSVG area (r = 0.470, p = 0.001), and Deltaplaque area correlated with DeltaSVG area (r = 0.436, p = 0.002). There were linear relations between both the Deltaplaque area (r = 0.519, p < 0.001) and Deltalumen area (r = -0.500, p < 0.001) versus follow-up low-density lipoprotein (LDL) cholesterol; a follow-up LDL cholesterol of 100 mg/dl predicted no plaque increase. CONCLUSIONS: Lumen loss in nonintervened SVG segments correlated with an increase in plaque area and a decrease in SVG area (plaque growth and negative remodeling) with a linear relationship between plaque growth versus follow-up LDL cholesterol leading to long-term lumen loss.

Temporal relation between Clopidogrel cessation and stent thrombosis after drug-eluting stent implantation.

The risk of late thrombotic events and the need for prolonged dual antiplatelet therapy detract from the clinical advantage offered by drug-eluting stents (DESs). Short-term studies have shown premature clopidogrel cessation to be a strong predictor of stent thrombosis (ST) after DES implantation. Data pertaining to the utility of clopidogrel therapy and its optimal duration to prevent late ST remain limited. The study population consisted of 2,889 patients who underwent unrestricted intracoronary DES implantation from April 2003 to January 2007 for whom clopidogrel compliance data were available. Definite ST proved by angiography or autopsy within 12 months of the index procedure occurred in 61 patients. Comparisons of clinical and procedural characteristics in addition to outcomes (death and Q-wave myocardial infarction) were made between the ST and no-ST (2,828 patients) groups. Clopidogrel compliance was assessed at all follow-up time points. For patients in the ST group, clopidogrel compliance status for the remaining study period was defined as that at the time of ST. Logistic regression analysis was performed at 30 days, 6 months, and 12 months to identify independent predictors of cumulative ST. Patients with ST were more likely to have previous congestive heart failure and worse left ventricular ejection fraction. ST was associated with significantly higher mortality at 12 months (23.5% vs 3.2%, p <0.001). Clopidogrel compliance was 80.2% in the overall population and 73.8% in patients presenting with ST (82.6% in patients presenting with early ST and 43.8% in those with late ST). By logistic regression analysis, clopidogrel cessation was an independent predictor of cumulative ST at 30 days and 6 months but not at 12 months. In conclusion, high rates of clopidogrel compliance can be achieved in contemporary practice. Clopidogrel cessation by 12 months is no longer predictive of ST, thus suggesting the optimal duration of therapy for the prevention of ST to be 6 to 12 months.

Requirement for emergent coronary artery bypass surgery following percutaneous coronary intervention in the stent era.

Performance of percutaneous coronary intervention (PCI) at centers without cardiothoracic surgery is a contentious issue. Although this practice allows greater access to care, there are safety concerns. The aim was to assess the requirement for emergent coronary artery bypass grafting (CABG) after PCI and characterize patients at highest risk using independent predictors. The study population consisted of 21,957 unselected patients who underwent PCI from August 1994 (Food and Drug Administration stent approval) to January 2008 at a single medical center. Patients requiring emergent CABG (defined as within 24 hours of the index procedure) were identified. Logistic regression analysis was performed to assess for independent correlates of emergent CABG. Emergent CABG was required in 90 patients (cumulative incidence 0.41%). Indications for CABG included triple-vessel disease, dissection, acute closure, perforation, and failure to cross. These patients had significantly higher in-hospital cardiac death rates (7.8% vs 0.7%; p <0.01) and higher rates of Q-wave myocardial infarction, neurologic events, and renal insufficiency. Independent correlates of emergent CABG after PCI were acute ST-segment elevation myocardial infarction presentation, cardiogenic shock, triple-vessel disease, and type C lesion. Risk assessment based on these predictors identified 0.3% of the patient population to have a 9.3% cumulative incidence of emergent CABG. In conclusion, the need for emergent CABG after PCI in the stent era was low and was associated with poor in-hospital outcomes. Risk was nonuniform, with 0.3% of the study population, characterized by acute presentation and complex coronary disease, at heightened risk of emergent surgery.

Racial disparities in outcomes following percutaneous coronary intervention with drug-eluting stents.

Previous research has documented that African-Americans compared with non-African-Americans have higher rates of adverse cardiac outcomes and are less likely to be referred for an invasive cardiac procedure. These differences persist even after controlling for co-morbidities and socioeconomic status. We sought to compare 1-year outcomes between African-American and non-African-American patients in a clinical registry of patients after percutaneous coronary intervention receiving drug-eluting stents. We compared 1,221 African-American patients with 4,335 non-African-American patients referred for percutaneous coronary intervention. Patients were followed for 1 year with regard to major adverse cardiac events, including death, Q-wave myocardial infarction, and target vessel revascularization. We performed multivariable Cox proportional hazards regression to adjust for confounding variables, including median household income by zip code, to assess the contribution of African-American race to 1-year outcomes. At 1 year, African-American patients had significantly higher rates of overall major adverse cardiac events (17.7% African-American vs 12.4% non-African-American, p <0.001) and each component of death (7.8% African-American vs 5.4% non-African-American, p = 0.001), Q-wave myocardial infarction (1.2% African-American vs 0.2% non-African-American, p <0.001), and target vessel revascularization (10.7% African-American vs 7.5% non-African-American, p <0.001). Stent thrombosis was also higher in the African-American population at 1 year (2.5% African-American vs 0.7% non-African-American, p <0.001). After multivariable analysis and adjustment for socioeconomic status, however, African-American race was not a significant predictor of major adverse cardiac events. In conclusion, in this referral population, traditional risk factors and socioeconomic status accounted for the disparity between African-American and non-African-American patients.

The predictive value of computed tomography calcium scores: a comparison with quantitative volumetric intravascular ultrasound.

OBJECTIVE: To evaluate the relationship between coronary artery calcium scoring (CACS) and intravascular ultrasound (IVUS) calcification and disease severity. METHODS: Forty-five angina patients who underwent CACS 18+/-23 days before IVUS were studied. The CACS was recorded for each lesion matched to a specific IVUS lesion. Cross-sectional area measurements of the external elastic membrane, lumen area, plaque and media, and plaque burden were performed. The arc and length of calcification were measured. RESULTS: There were 106 calcified lesions detected by IVUS. Eighty-five of those lesions (80%) were detected by CACS, but 21 calcified lesions (20%) were missed. Fourteen (50%) out of 28 of the lesions with an IVUS-calcium arc below the 25th percentile (51.4 degrees ) were detected by CACS vs. 91% of lesions with an IVUS-calcium arc >51.4 degrees (P<.05). Similarly, 21 (58%) of 36 lesions 3 mm (P<.05). We divided IVUS-calcified lesions into CACS 10. Mean plaque burden, calcified length, and arc of calcium increased significantly, while minimum lumen area decreased with increasing CACS. There was the same tendency in culprit and nonculprit calcified lesions, respectively. Multivariate analysis showed a calcified length (regression coefficient=8.718, 95% CI 4.668-12.77, P<.001) and an arc of calcium (regression coefficient=2.789, 95% CI 1.419-4.119, P<.001) were significant predictors for CACS. CONCLUSIONS: This study suggests that a CACS could evaluate coronary calcium burden noninvasively through the accurate estimation of calcium-arc and length.

Five-year outcomes of moderate or ambiguous left main coronary artery disease and the intravascular ultrasound predictors of events.

The long-term outcome of a moderately diseased left main coronary artery (LMCA) remains unknown. One hundred and fourteen patients who underwent angiographic and intravascular ultrasound (IVUS) evaluation for moderate LMCA disease (< 50% diameter stenosis) without intervention were followed for 5 years. There were 11 patients who underwent coronary artery bypass graft surgery (CABG) within 30 days of IVUS analysis based on IVUS findings and 3 patients who died of noncardiac diseases during the follow-up period. These 14 patients were excluded from the cohort, and 100 patients comprised the study group. Six patients (6%) died (1 of cardiac causes and 5 of unknown causes) at a follow up of 31.5 +/- 17.0 months post-IVUS assessment. Two patients (2%) underwent CABG at a follow up of 19.0 +/- 7.1 months. There were no percutaneous LMCA interventions and no myocardial infarctions. Univariate predictors for events were age, mean plaque and media (P&M) area and plaque burden over the entire length of the LMCA lesion, and minimum luminal area (MLA), P&M area, plaque burden, and arc of calcium > 90 degrees at the MLA site. By multiple logistic regression analysis, plaque burden at the MLA (odds ratio = 1.34, 95% confidence interval 1.04-1.73; p = 0.025) was the only independent predictor of events. In conclusion, moderately diseased LMCAs had a 5- year event rate of 8%. The occurrence of future events in moderate diseased LMCAs is dependent on the amount of disease at the MLA site.

Can direct stenting in selected saphenous vein graft lesions be considered an alternative to percutaneous intervention with a distal protection device?

BACKGROUND: Distal embolization during percutaneous coronary intervention (PCI) of saphenous vein graft (SVG) lesions is associated with a high rate of myonecrosis. Although direct stenting (DS) is feasible with less catheter manipulations, its ability to prevent distal embolization in SVG lesions compared with distal protection devices (DPD) is unknown. METHODS: The study included 188 SVG lesions subjected to PCI, 101 patients with 101 lesions treated with DPD, and 87 patients with 87 lesions by DS without DPD. Major adverse cardiovascular events (MACE) in-hospital and at 30 days were compared. RESULTS: Baseline characteristics were comparable, except for higher frequencies of unstable angina (53% vs. 67%, P = 0.045) and prior myocardial infarction (38% vs. 53%, P = 0.07) in the DS group. There was no difference in lesion type aside from more restenotic lesions in the DS group (7% vs. 16%, P = 0.047). Drug-eluting stent deployment was similar. Stent length in the DPD group (22.8 +/- 7.2 mm) was significantly longer than that in the DS group (17.6 +/- 8.0 mm, P < 0.001). Although maximum creatine kinase (CK)-MB value in the DPD group (2.5 +/- 5.8 ng/ml) was significantly larger than in the DS group (1.3 +/- 1.5 ng/ml, P = 0.039), the frequency of CK-MB rise >2 times the upper limit of normal did not differ (11% vs. 6%, P = 0.2). There were no differences in MACE rates in-hospital and at 30 days. By multivariate analysis, neither DPD nor DS was a significant predictor for maximum CK-MB value. CONCLUSION: DS should be considered an alternative treatment to PCI with DPD for selected SVG lesions.