Denise Braganza

Expansion and malapposition characteristics after bioresorbable vascular scaffold implantation

This study sought to investigate the postdeployment expansion and malapposition characteristics of the bioresorbable vascular scaffold (BVS) in real‐world practice.

Mid-term clinical outcomes of ABSORB bioresorbable vascular scaffold implantation in a real-world population: A single-center experience.

BACKGROUND Available data on the use of the ABSORB bioresorbable vascular scaffold (BVS) (Abbott Vascular, Santa Clara, CA) in real-world patients is limited. The aim of this study was to assess the mid-term clinical outcomes in a real-world population treated with ABSORB BVS. METHODS AND MATERIALS We retrospectively evaluated all patients treated with ABSORB at Papworth Hospital, Papworth Everard, UK between July 2012 and July 2014. A total of 108 patients (126 lesions) were identified. Clinical follow-up was performed on all subjects by clinic visit or telephone interview. RESULTS Most patients were male (91.7%) with a relative high incidence of previous myocardial infarction (MI) (40.7%). Clinical presentation was equally divided between stable angina and acute coronary syndrome (ACS) (51.8% vs. 48.2%, p=0.59). Of the ACS patients, 26.9% presented with ST-elevation myocardial MI. Intravascular imaging was used in all cases. Predilatation (92.9%) and postdilatation (82.5%) were frequently performed. Major adverse cardiac event (MACE) rates defined as the composite of all-cause death, follow-up MI and target vessel revascularization were 2.5% at 6-month and 4.5% at 1-year. The 1-year target lesion failure rate, defined as the composite of cardiac death, target-vessel MI and target lesion revascularization was 1.9%. There was 1 case of subacute stent thrombosis. CONCLUSIONS The use of ABSORB BVS in real-world patients appears to be associated with good mid-term clinical outcomes when guided by intravascular imaging. Larger studies are required to evaluate further the role of BVS in routine clinical practice and examine how this compares to metallic devices. SUMMARY Available data on the use of the ABSORB BVS in real-world patients is limited. We retrospectively evaluated all patients treated with ABSORB BVS between July 2012 and July 2014. A total of 108 patients (126 lesions) were identified. Clinical presentation was equally divided between stable angina and acute coronary syndrome (51.8% vs. 48.2%, p=0.59). Predilatation (92.9%) and postdilatation (82.5%) were frequently performed. Estimated MACE rates at 6-month and 1-year were 2.5% and 4.5% respectively, with a 1-year TLF rate of 1.9%. These results suggest that the use of ABSORB BVS use in the real-world is associated with good mid-term clinical outcomes when guided by intravascular imaging.

B VH-IVUS findings predict major adverse cardiovascular events. The Viva Study (virtual histology intravascular ultrasound in vulnerable atherosclerosis)

Background Identification of high-risk atherosclerotic plaques offers opportunities for risk stratification and targeted intensive treatment of patients with coronary artery disease. Virtual Histology intravascular ultrasound (VH-IVUS) has been validated in human atherectomy and post-mortem studies and can classify plaques into presumed high- and low-risk groups. However, VH-IVUS-defined plaques have not been shown to be associated with major adverse cardiovascular events (MACE), or biomarkers that confer increased cardiovascular risk, such as serum cytokines or shortened leukocyte telomere length (LTL). Methods 170 patients with stable angina or troponin-positive acute coronary syndrome (ACS), referred for percutaneous coronary intervention (PCI) were prospectively enrolled and underwent full 3-vessel VH-IVUS pre-PCI. Troponin-I (cTnI), IL-6, IL-18, hsCRP, neopterin, MCP-1 and sICAM-1 were measured pre-PCI and 24-h post-PCI. LTL was determined by qPCR. The combined primary endpoint (MACE) included unplanned revascularisation, myocardial infarction (MI) and death, with a secondary endpoint of post-PCI MI (MI 4a). Results 18 MACE occurred in 16 patients (median follow-up: 625 (463–990) days). 30 372 mm of VH-IVUS were analysed and 1106 plaques classified (Abstract B Figure 1) locally and via a core-lab. After multivariable regression:Abstract B Figure 1 Total number of non-calcified VH-IVUS-identified thin capped fibroatheromata (VHTCFA) was the only factor independently associated with MACE (HR=3.16, (95%CI=1.16 to 8.64), p=0.025). Total VHTCFA number (OR=1.26 (1.03 to 1.53) p=0.021) and total stent length (OR=1.04 (1.01 to 1.08), p=0.01) were the only factors independently associated with MI 4a. A novel 3-vessel vulnerability index (necrotic core: fibrous tissue ratio) and side branch loss were independently associated with stenting-related cTnI rise (standardised beta coefficient (sβ)=0.29, p=0.004 and sβ=0.23, p=0.019 respectively). Necrotic core area at the minimum luminal area frame was the only factor independently associated with ACS presentation (OR=1.59, p=0.030). Stented vessel VHTCFA number (OR=1.75 (1.22 to 2.51), p=0.002) was independently associated with the lower LTL tertile (DNA-based cardiovascular risk predictor). Stenting-related IL-6 rise was the only biomarker independently associated with MACE (HR=1.03 (1.01–1.05), p=0.007). Conclusion We present the first report of an association between VHTCFA and MACE. This provides novel evidence that VHTCFA definitions are important in their own right (rather than as analogues of histological TFCA definitions). We also present the first report of associations between VHTCFA and MI 4a as well as a novel vulnerability index that is association with stenting-related troponin rise. Finally, we report a novel association between VHTCFA and DNA-based cardiovascular risk prediction (LTL).

Stunning and Right Ventricular Dysfunction Is Induced by Coronary Balloon Occlusion and Rapid Pacing in Humans: Insights From Right Ventricular Conductance Catheter Studies

Background We sought to determine whether right ventricular stunning could be detected after supply (during coronary balloon occlusion [BO]) and supply/demand ischemia (induced by rapid pacing [RP] during transcatheter aortic valve replacement) in humans. Methods and Results Ten subjects with single‐vessel right coronary artery disease undergoing percutaneous coronary intervention with normal ventricular function were studied in the BO group. Ten subjects undergoing transfemoral transcatheter aortic valve replacement were studied in the RP group. In both, a conductance catheter was placed into the right ventricle, and pressure volume loops were recorded at baseline and for intervals over 15 minutes after a low‐pressure BO for 1 minute or a cumulative duration of RP for up to 1 minute. Ischemia‐induced diastolic dysfunction was seen 1 minute after RP (end‐diastolic pressure [mm Hg]: 8.1±4.2 versus 12.1±4.1, P<0.001) and BO (end‐diastolic pressure [mm Hg]: 8.1±4.0 versus 8.7±4.0, P=0.03). Impairment of systolic and diastolic function after BO remained at 15‐minutes recovery (ejection fraction [%]: 55.7±9.0 versus 47.8±6.3, P<0.01; end‐diastolic pressure [mm Hg]: 8.1±4.0 versus 9.2±3.9, P<0.01). Persistent diastolic dysfunction was also evident in the RP group at 15‐minutes recovery (end‐diastolic pressure [mm Hg]: 8.1±4.1 versus 9.9±4.4, P=0.03) and there was also sustained impairment of load‐independent indices of systolic function at 15 minutes after RP (end‐systolic elastance and ventriculo‐arterial coupling [mm Hg/mL]: 1.25±0.31 versus 0.85±0.43, P<0.01). Conclusions RP and right coronary artery balloon occlusion both cause ischemic right ventricular dysfunction with stunning observed later during the procedure. This may have intraoperative implications in patients without right ventricular functional reserve.

12 Out-of-hospital cardiac arrest: evaluation of patient outcomes and impact on icu resources

Background Recent European Society of Cardiology guidelines recommend that Primary Percutaneous Coronary Intervention (PPCI) be considered in all patients resuscitated from out-of-hospital cardiac arrest (OHCA). Methods We evaluated the impact of expanding PPCI provision on patient outcomes and ICU resources. Data on all patients admitted to a tertiary PPCI centre from 2010 to 2015 were analysed. Results 301 patients were admitted via the PPCI pathway following OHCA. The number of OHCA patients increased from 5.5% (n=38) of total admissions in 2010 to 8.4% (n=67) in 2015 (p=0.03). Mean number of comorbidities increased from 0.97 to 1.63 (p=0.03). 92% were diagnosed with myocardial infarction in 2010, compared to 60% in 2015 (p<0.001). More patients required ICU admission (13% in 2010 to 58% in 2015, p<0.001) and support for at least two organ systems (11% in 2010 to 48% in 2015, p<0.001). Rate of survival to discharge decreased from 100% to 81% (p=0.004) and proportion discharged home also decreased from 95% to 58% (p<0.001). Conclusions Over the study period, the number of OHCA patients admitted to our PPCI centre climbed yearly. They were increasingly likely to have more comorbidity and require more intense organ support. Despite this, outcomes were less favourable. Our findings highlight the need for careful expansion of indications for PPCI admission following OHCA to avoid unsuccessful demand on ICU resources. Abstract 12 Figure 1 Organ support and survival to hospital discharge

053 LONGTERM NATURAL HISTORY OF RADIOFREQUENCY INTRAVASCULAR ULTRASOUND IDENTIFIED CORONARY PLAQUES

Introduction Prior studies have shown that virtual-histology intravascular ultrasound (VH-IVUS) identified thin-capped fibroatheroma (VHTCFA) (figure 1) and plaque burden (PB) >70% are associated with major adverse cardiovascular events (MACE). This study examined non-culprit lesion features that predict MACE in long-term follow up and culprit lesion features responsible for myocardial infarction (MI). Table 1 Plaque characteristics Univariate analysis HR (95% CI) Univariate analysis p value Multivariate analysis HR (95% CI) Multivariate analysis p value VHThCFA 1.17 (0.23 to 6.24) 0.86 Total VHTFCA 6.37 (1.45 to 27.94) 0.014 2.18 (0.41 to 11.71) 0.36 Non-calcified VHTCFA 4.01 (0.87 to 18.68) 0.077 2.91 (0.57 to 15.00) 0.20 Calcified VHTCFA 1.51 (0.40 to 5.75) 0.55 Remodelling index 26.82 (0.36 to 1975) 0.13 MLA<4 mm2 3.61 (1.15 to 11.32) 0.028 1.23 (0.24 to 6.22) 0.80 Plaque burden>70% 7.77 (2.06 to 29.28) 0.002 7.77 (2.06 to 29.28) 0.002 Plaque volume (mm3) 1.00 (1.00 to 1.00) 0.34 Necrotic core volume (mm3) 1.00 (0.99 to 1.01) 0.57 NC percentage 1.01 (0.93 to 1.10) 0.79 Methods 170 patients with stable angina (n=100) or MI (n=70) underwent three-vessel VH-IVUS prior to percutaneous coronary intervention (PCI). Patients were followed for MACE which consisted of death, MI, cerebrovascular event, hospitalisation with unstable angina or unplanned revascularisation. Non-culprit lesion features were tested for association with future MACE, and culprit lesion features were assessed for initial presentation with MI, using univariate and multivariate analysis. Results 30 372 mm of VH-IVUS were analysed and 1096 plaques classified. 45 MACE occurred in 30 patients over a median follow up of 1115 (968–1537) days. These included 3 deaths, 6 MIs, 3 cerebrovascular events, 15 hospitalisations due to unstable angina, 3 unplanned coronary bypass operations and 15 unplanned PCI. By univariate analysis, non-culprit VHTCFA (HR=7.37, p=0.014), MLA<4 mm2 (HR=3.61, p=0.028) and PB>70% (HR=7.77, p<0.001) were associated with future non-restenotic MACE on long-term follow up (table 1). By multivariate analysis PB>70% (HR=7.77, p<0.001) remained independently associated with MACE. On univariate analysis, multiple culprit lesion features were associated with initial presentation with MI (table 2), including total and calcified VHTCFA, remodelling index, PB>70%, MLA <4 mm2, plaque rupture and thrombus. By multivariate analysis, PB>70% (OR (OR)=6.32, p<0.001), thrombus (OR=9.03, p<0.001) and MLA<4 mm2 (OR=3.01, p=0.02) were independently associated with MI. Interestingly, culprit lesion calcified VHTCFA were associated with initial MI (OR=2.59 (1.61–4.16), p<0.001), whereas non-calcified VHTCFA were more likely to be associated with future MACE HR=4.01 (0.87–18.68), p=0.077. Conclusion Despite the dynamic nature of coronary plaques, non-culprit VHTCFA, MLA<4 mm2 and PB>70% were associated with future MACE on long-term follow up, with PB>70% being independently associated. These same features in culprit lesions (amongst others) were associated with MI presentation, emphasising their biological importance. Interestingly, non-calcified VHTCFA are more likely to be associated with future MACE, whereas it is the calcified variant that is associated with MI presentation. This may represent a phenotypic transformation in the VHTCFA from non-calcified to calcified which could reflect multiple healed plaque rupture events (figure 2). This theory requires further investigation. Table 1 Non-culprit lesion features associated with future MACE VHThCFA (VH-IVUS thick-capped fibroatheroma), VHTCFA (VH-IVUS thin-capped fibroatheroma), MLA (minimum luminal area), NC (necrotic core), HR, CI Table 2 Plaque characteristics Univariate analysis OR (95% CI) Univariate analysis p value Multivariate analysis OR (95% CI) Multivariate analysis p value VHThCFA 0.84 (0.44 to 1.60) 0.59 Total VHTFCA 3.05 (1.78 to 5.23) <0.001 Non-calcified VHTCFA 1.18 (0.66 to 2.10) 0.58 Calcified VHTCFA 2.59 (1.61 to 4.16) <0.001 Remodelling index 28.05 (5.53 to 142.25) <0.001 MLA<4 mm2 8.86 (5.18 to 15.14) <0.001 3.01 (1.52 to 5.96) 0.002 Plaque burden>70% 15.41 (8.80 to 27.01) <0.001 6.32 (3.23 to 12.37) <0.001 Plaque volume (mm3) 1.004 (1.002 to 1.005) <0.001 Thrombus 20.29 (5.58 to 73.76) <0.001 9.03 (1.60 to 50.98) 0.013 Ruptured plaque 6.77 (2.09 to 21.92) 0.001 Table 2 Culprit lesion features associated with MI presentation OR Figure 1 VH-IVUS thin-capped fibroatheroma (VHTCFA). Figure 2 VH-IVUS thick-capped fibroatheroma (VHThCFA). Note that this fibroatheroma has two distinct layers (arrows) of necrotic core (red) and dense calcium (white), perhaps representing two temporally distinct plaque rupture events that have now healed.

060 CORONARY ROTATIONAL ATHERECTOMY USING BURR-TO-ARTERY RATIOS OF LESS THAN 0.5 IS ASSOCIATED WITH LOW LEVELS OF COMPLICATIONS, HIGH PROCEDURAL SUCCESS RATES AND FAVOURABLE 12-MONTH OUTCOMES

Background Rotational atherectomy (RA) is an established treatment of heavily-calcified coronary stenoses. Previous data suggest higher procedural complication rates when Burr-to-Artery (BTA) ratios exceed 0.7; the manufacturer-recommended BTA being 0.6. Little contemporary data exists regarding safe and optimal burr sizing, which may be important when considering RA via the radial approach with lower-caliber guiding catheters. Methods Single-centre retrospective review of patients undergoing elective RA between 2004 and 2011. Procedural success was defined as successful stent deployment with residual stenosis <30%, and complications defined as death, pericardial effusion/tamponade, coronary dissection/perforation and emergent CABG. Demographic and outcome data were obtained from local/national databases and casenote review. Quantitative coronary angiographic analysis was performed on archived films. Results Elective RA was successful in 197/220 cases (89.5%) with 72% of cases male and 22% diabetic (mean age 71.1±8.9 years). Target vessel was LAD (50.9%), RCA (35.0%), LCx (10.9%) and LMS (3.2%). Mean reference diameter was 3.45±0.6 mm and mean diameter stenosis (DS) 71.9±12.9%. Maximum burr size/case ranged from 1.25–2 mm (mode 1.5 mm) with mean BTA 0.43±0.08. 10 procedural complications occurred (4.5%); one wire fracture, two dissections, three perforations, two emergency CABG, one unretractable burr and one death. No difference in mean BTA was observed between procedures with/without complications (0.38±0.03 vs 0.43±0.08; p=0.33), but residual DS was higher in those with complications (12.3±21.2 vs 58.8±31.2; p<0.01). No correlation was observed between maximum burr size and age, sex, DS or minimum luminal diameter. At 36-month follow-up mortality was 11.7% and target vessel revascularisation (TVR) 22.8%. Conclusions Elective RA with low BTA is associated with high procedural success and low complication rates. These data imply that elective RA with a lower BTA than recommended is both safe and effective and need not preclude a transradial approach.

Oral amiodarone provoking inferior ST elevation and unmasking Brugada-like electrocardiogram feature.

A woman presented with broad complex tachycardia. She was converted to sinus rhythm with intravenous amiodarone and continued on oral amiodarone. The amiodarone was stopped 3 weeks later as she was pregnant. Electrocardiogram (ECG) then revealed coved-type ST elevation in C1, suggestive of Brugada syndrome, and widespread inferior ST elevation. Electrocardiogram several months later showed resolution of inferior ST elevation.

107 Plaque composition and plaque volume in non-stented vessels determines serum biomarker levels after stenting in stable angina: a VH-IVUS study

Introduction Previous work has shown that plaque composition in stented vessels determined by virtual histology intravascular ultrasound (VH-IVUS) predicts myocardial necrosis after percutaneous coronary intervention (PCI). However, disease in non-stented vessels may also determine myocardial necrosis, for example, reduced collateral blood flow may increase the area of myocardial necrosis after PCI. We examined whether plaque composition or volume (determined by VH-IVUS) in non-stented vessels or the whole coronary tree contributed to stenting-related rises in serum biomarkers. Methods Hundred patients with stable angina, referred for elective PCI underwent full 3-vessel VH-IVUS. Serum Troponin-I, interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hsCRP) were measured before and 24 h after PCI. Troponin-I and hsCRP results were logarithmically transformed (log10) to a normal distribution to permit calculation of Pearsons correlation coefficient. Results In stable angina patients, there was no significant difference in total plaque volume (563±60 mm3 vs 632±62 mm3 respectively, mean±SEM p=0.42), nor in necrotic core volume (NC) (73±13 mm3 vs 61±10 mm3 respectively, p=0.48) between stented and non-stented vessels. After PCI for stable angina the biomarker levels were: troponin-I: 0.27 ng/ml (0.06–0.94 ng/ml), IL-6: 8.0 pg/ml (5.5–11.4 pg/ml) and hsCRP: 5.7 mg/l (3.4–10.0 mg/l) (median (IQR)). Troponin-I levels correlated with total NC and total plaque volume on 3-vessel VH-IVUS (r=0.45, p=0.003; r=0.417, p=0.006 respectively), and in non-stented vessels (NC vs troponin-I: r=0.423, p=0.006; plaque volume vs troponin-I: r=0.37, p=0.018). However there was no correlation between troponin-I and either NC or plaque volume in the stented vessels (p=0.2 and p=0.45 respectively). Similarly, serum IL-6 correlated with both NC and plaque volume on 3-vessel VH-IVUS (r=0.414, p=0.009; r=0.412, p=0.009 respectively) and in non-stented vessels (r=0.47, p=0.003; r=0.376, p=0.003 respectively). However, there was no correlation between IL-6 and NC or plaque volume in stented vessels (p=0.33 and p=0.47 respectively). There were no significant correlations between VH-IVUS parameters and hsCRP. Adjusting for plaque volume the correlation between the 3-vessel NC/total plaque volume ratio and IL-6 remained (r=0.329, p=0.044) but not between 3-vessel NC/plaque volume ratio and troponin-I (p=0.23). Although Troponin-I rise correlated with total length of stents implanted (r=0.36, p=0.002), IL-6 and hsCRP did not (p=0.41 and p=0.94 respectively). Conclusion Three-vessel and non-stented vessel plaque composition and plaque volume determined by VH-IVUS correlate with troponin-I and IL-6 levels after PCI for stable angina, whereas plaque composition or plaque volume of the stented vessel do not. This difference highlights the importance of disease in non-stented vessels in PCI-related myocardial necrosis.