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Background Intravascular imaging has defined various vulnerable plaque (VP) phenotypes that predict future clinical events. Atherosclerosis is an inflammatory process and inflammation, measured by systemic biomarkers can also predict events and anti-inflammatory therapy is beneficial. We were interested to assess the relationship between plaque phenotypes and key inflammatory biomarkers, measured close to the coronary. Methods Ninety-two patients scheduled for elective percutaneous coronary intervention (PCI) underwent virtual histology intravascular ultrasound, optical coherence tomography, pressure wire and blood sampling from the guide catheter (GC), coronary sinus (CS) to determine trans-myocardial gradient (TMG = CS-GC) and from peripheral blood. Procedure related troponin release was assessed at 6-hours post-PCI from peripheral venous blood. Biomarker data were analysed and compared with coronary data. Results Interleukin (IL)-6 was associated with increased levels of tumour necrosis factor (TNF)-α and C-reactive protein (CRP) and the pre-PCI IL-6 TMG correlated with plaque features of vulnerability: plaque burden - PB (r = 0.253, p = 0.04) and minimal lumen area - MLA (r = −0.438, p = 0.007), although no relationship existed for thin-capped fibroatheroma defined by either imaging modality. Peripheral IL-6 levels had no correlation with post PCI troponin, although the pre-PCI IL-6 TMG was related (r = 0.334, p = 0.006), as was PB (r = 0.27, p = 0.029). Conclusion IL-6 TMG pre-PCI correlates with plaque burden and MLA that have been shown to predict future clinical events and is correlated with post-PCI troponin release. These associations were not apparent from peripheral blood and suggest that local coronary biomarker signatures may help further define vulnerability and risk.

Aims Post-infarction ventricular septal defect (PIVSD) is a mechanical complication of acute myocardial infarction (AMI) with a poor prognosis. Surgical repair is the mainstay of treatment, although percutaneous closure is increasingly undertaken. Methods and resuts Patients treated with surgical or percutaneous repair of PIVSD (2010–2021) were identified at 16 UK centres. Case note review was undertaken. The primary outcome was long-term mortality. Patient groups were allocated based upon initial management (percutaneous or surgical). Three-hundred sixty-two patients received 416 procedures (131 percutaneous, 231 surgery). 16.1% of percutaneous patients subsequently had surgery. 7.8% of surgical patients subsequently had percutaneous treatment. Times from AMI to treatment were similar [percutaneous 9 (6–14) vs. surgical 9 (4–22) days, P = 0.18]. Surgical patients were more likely to have cardiogenic shock (62.8% vs. 51.9%, P = 0.044). Percutaneous patients were substantially older [72 (64–77) vs. 67 (61–73) years, P < 0.001] and more likely to be discussed in a heart team setting. There was no difference in long-term mortality between patients (61.1% vs. 53.7%, P = 0.17). In-hospital mortality was lower in the surgical group (55.0% vs. 44.2%, P = 0.048) with no difference in mortality after hospital discharge (P = 0.65). Cardiogenic shock [adjusted hazard ratio (aHR) 1.97 (95% confidence interval 1.37–2.84), P < 0.001), percutaneous approach [aHR 1.44 (1.01–2.05), P = 0.042], and number of vessels with coronary artery disease [aHR 1.22 (1.01–1.47), P = 0.043] were independently associated with long-term mortality. Conclusion Surgical and percutaneous repair are viable options for management of PIVSD. There was no difference in post-discharge long-term mortality between patients, although in-hospital mortality was lower for surgery.

Introduction Observational studies have shown that migraine has been associated with patent foramen ovale (PFO). Whilst studies investigating PFO closure for the treatment of migraine have been neutral, there is some evidence that symptoms of migraine may improve if the PFO was closed after ischemic stroke. Aim To establish whether closure of PFO in patients with stroke or transient ischemic attack (TIA) is associated with reduction in the severity of co-existent migraine headaches. Material and methods Patients with ischemic stroke or TIA, PFO suitable for percutaneous closure and migraine, were given migraine severity questionnaires prior to PFO closure. These were followed up at 6 and 12 months after closure with the same questionnaire. The primary endpoint was change in migraine severity using the Migraine Severity Scale (MIGSEV). Migraine episode frequency, disability (using the MIDAS scale), and pain intensity were also assessed. Results Sixty-two patients were included in the analysis. MIGSEV scores reduced from 7 (7–8) at baseline to 4 (3.25–6) at 6-month follow-up, and 3 (0–4) at 12-month follow-up (p < 0.001). Other measures of migraine headache were also improved at both 6- and 12-month follow-up. Twenty-four (38%) patients were rendered migraine free at 12 months. Conclusions PFO closure for stroke or TIA prevention in patients with migraine was associated with a reduction in markers of migraine headache severity.

A patient with a history of coronary artery bypass graft presented with breathlessness and was found to have an 11 × 6 cm aneurysm in a distally occluded saphenous vein graft. This case describes the investigation, heart team discussion, and percutaneous closure of the aneurysm. (Level of Difficulty: Beginner.), Graphical abstract, A patient with a history of coronary artery bypass graft presented with breathlessness and was found to have an 11- × 6-cm aneurysm in a distally…

Background Adenosine is used to treat no‐reflow in the infarct‐related artery (IRA) during ST‐segment–elevation myocardial infarction intervention. However, the physiological effect of adenosine in the IRA is variable. Coronary steal—a reduction of blood flow to the distal coronary bed—can occur in response to adenosine and this is facilitated by collaterals. We investigated the effects of adenosine on coronary flow reserve (CFR) in patients presenting with ST‐segment–elevation myocardial infarction to better understand the physiological mechanism underpinning the variable response to adenosine. Methods and Results Pressure‐wire assessment of the IRA after percutaneous coronary intervention was performed in 93 patients presenting with ST‐segment–elevation myocardial infarction to calculate index of microvascular resistance, CFR, and collateral flow index by pressure. Modified collateral Rentrop grade to the IRA was recorded, as was microvascular obstruction by cardiac magnetic resonance imaging. Coronary steal (CFR 1.1) after adenosine occurred in 19 (20%), 15 (16%), and 59 (63%) patients, respectively. Patients with coronary steal had higher modified Rentrop score to the IRA (1 [0, 1.75] versus 0 [0, 1], P P =0.004) than the hyperemic group. The coronary steal group also had significantly higher index of microvascular resistance (61.68 [28.13, 87.04] versus 23.93 [14.67, 37.00], P =0.006) and had more disease (stenosis >50%) in the donor arteries (52.63% versus 22.03%, P =0.02) than the hyperemic group. Conclusions Adenosine‐induced coronary steal may be responsible for a reduction in coronary flow reserve in a proportion of patients presenting with ST‐segment–elevation myocardial infarction. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03145194. URL: https://www.isrctn.com ; Unique identifier: ISRCTN3176727.

Paravalvular leak (PVL) is a challenging complication of valve replacement surgery that can cause heart failure and haemolysis. Surgical repair is the traditional treatment for severe, symptomatic PVL, but many patients with PVL fall into high-risk categories for redo surgery. Percutaneous techniques for closure of PVL have been increasingly refined over the last decade with availability of approved purpose-specific devices for closure. Percutaneous closure requires a heart team approach, with attention paid to appropriate preprocedural and periprocedural imaging to ensure a successful closure with minimal residual leak or complication. There are limited studies addressing the selection of a percutaneous approach to PVL. No randomised trials comparing surgical and percutaneous repair have been conducted. Large national registries from the UK and Ireland and from Spain have demonstrated that high rates of technical success can be achieved, with mortality comparable with surgical repair. Six retrospective studies comparing surgical and percutaneous approaches have been published. These broadly show comparable technical success between the interventions, with reduced short-term mortality among patients treated percutaneously. Long-term outcomes were similar between both treatment options. Percutaneous repair is an attractive treatment option in many patients due to its reduced invasiveness and quicker recovery period. However, more prospective studies are needed to validate its place in the armamentarium of the heart team.

Background The incretin hormone glucagon-like peptide 1 (GLP-1) has been shown to protect against lethal ischemia-reperfusion injury in animal models and against nonlethal ischemia reperfusion injury in humans. Furthermore, GLP-1 receptor agonists have been shown to reduce major adverse cardiovascular and cerebrovascular events (MACCE) in large-scale studies. We sought to investigate whether GLP-1 reduced percutaneous coronary intervention (PCI)–associated myocardial infarction (PMI) during elective PCI. Methods The study was a randomized, double-blind controlled trial in which patients undergoing elective PCI received an intravenous infusion of either GLP-1 at 1.2 pmol/kg/min or matched 0.9% saline placebo before and during the procedure. Randomization was performed in 1:1 fashion, with stratification for diabetes mellitus. Six-hour cardiac troponin I (cTnI) was measured with a primary end point of PMI defined as rise ≫×5 upper limit of normal (280 ng/L). Secondary end points included cTnI rise and MACCE at 12 months. Results A total of 192 patients were randomized with 152 (79%) male and a mean age of 68.1 ± 8.9 years. No significant differences in patient demographics were noted between the groups. There was no difference in the rate of PMI between GLP-1 and placebo (9 [9.8%] vs 8 [8.3%], P = 1.0) or in the secondary end points of difference in median cTnI between groups (9.5 [0-88.5] vs 20 [0-58.5] ng/L, P = .25) and MACCE at 12 months (7 [7.3%] vs 9 [9.4%], P = .61). Conclusions In this randomized, placebo-controlled trial, GLP-1 did not reduce the low incidence of PMI or abrogate biomarker rise during elective PCI, nor did it influence the 12-month MACCE rate which also remained low. Clinical trial registration Clinicaltrials.gov Number: NCT02127996 https://clinicaltrials.gov/ct2/show/NCT02127996

The role of glycoprotein IIb/IIIa inhibitors (GPI) in primary percutaneous coronary intervention (PPCI) remains uncertain. Previous analyses compare PPCI outcomes with clopidogrel plus GPI, versus without GPI. This does not reflect modern contemporary PPCI practice with ticagrelor or prasugrel. Nor does it answer the important question faced daily by PPCI operators: should GPI be used routinely or selectively? We aim to determine whether a strategy of routine use of GPI in contemporary PPCI practice is superior to selective GPI use. A total of 110,327 consecutive PPCIs performed in England were prospectively recorded in the British Cardiovascular Intervention Society Database (2009 to 2015). The cohort was divided into routine and selective GPI usage groups based on the PPCI operator's strategy, defined as GPI used in75% and25% PPCIs, respectively. Overall, GPI use declined from 73.1% to 43.3% of PPCIs. Routine compared with selective GPI usage was associated with lower all-cause 1-year mortality: 9.7% versus 11.0%, p 0.001. There was a consistent survival benefit for routine GPI usage as compared with selective GPI usage: univariable analysis (hazard ratio = 0.88 [95% confidence interval 0.83 to 0.93], p 0.001), multivariable analysis (hazard ratio = 0.82 [0.77 to 0.88], p 0.001). For survival, there was no interaction between GPI usage and the type of P2Y12-inhibitor used. In conclusion, a strategy of routine GPI usage in patients who underwent PPCI was associated with lower all-cause mortality as compared with selective GPI usage. This benefit was maintained despite 44.3% of patients receiving prasugrel or ticagrelor.

Aims We aimed to investigate the effects of an initial learning period with mandatory optical coherence tomography (OCT) guidance for the implantation of everolimus-eluting bioresorbable vascular scaffolds (BVS). Methods and results We analysed procedural and clinical outcomes of all BVS implantations at a single centre where OCT guidance was mandatory in the initial rollout (OCT-mandatory) phase. We compared these data with the later phase where use of OCT was at operator discretion (OCT-selective or angiography). We implanted 406 BVS in 306 vessels (201 OCT, 105 angiography) in 272 patients. Follow-up duration was 38±10 months. Annualised rates of device-oriented cardiac events (DOCE) and scaffold thrombosis (ScT) were 1.4% and 0.4%, respectively. The risks of DOCE (HR 1.06, 95% CI: 0.33-3.34; p=0.71) and ScT (HR 0.48, 95% CI: 0.07-3.85; p=0.49) were not significantly different when comparing the OCT and angiography groups. Conclusions Routine use of OCT to guide and optimise BVS implants results in very acceptable outcomes. Further, the benefits of such an early OCT-mandatory "learning" period persist after cessation of routine OCT usage when imaging is not routinely used. A period of mandatory OCT usage for BVS implants may therefore be beneficial in improving patient outcomes with these devices.

Paravalvular leak (PVL) is a complication that occurs in 5-17% of patients after surgical prosthetic valve implantation. Whereas PVLs can be benign, some PVLs are associated with substantial morbidity and mortality. Percutaneous closure using occluders specifically designed to improve closure and reduce procedural complications has now become the first-line treatment for PVL. In this Review, we first detail the frequency and clinical consequences of PVL closure. The role of cardiac imaging in the assessment and management of PVL, including echocardiographic imaging and adjunctive techniques such as CT, is then discussed, together with important considerations for the percutaneous closure of PVL, such as access site and device selection. Finally, we summarize the clinical evidence for percutaneous closure of PVL, including large national registries from Ireland, Spain and the UK, as well as head-to-head data comparing this procedure with surgical closure.

Patent foramen ovale (PFO) is a common abnormality affecting between 20% and 34% of the adult population. For most people it is a benign finding; however, in some the PFO can open widely, enabling a paradoxical embolus to transit from the venous to arterial circulation, which is associated with stroke and systemic embolisation. Percutaneous closure of PFO in patients with cryptogenic stroke has been undertaken for a number of years, and a number of purpose-specific septal occluders have been marketed. Recent randomised controlled trials have demonstrated that closure of PFO in patients with cryptogenic stroke is associated with reduced rates of recurrent stroke. After a brief overview of the anatomy of a PFO, this review considers the evidence for PFO closure in cryptogenic stroke. The review also addresses other potential indications for closure, including systemic embolisation, decompression sickness, platypnoea–orthodeoxia syndrome and migraine with aura. It lays out the pre-procedural investigations and preparation for the procedure. Finally, it gives an overview of the procedure itself, including discussion of closure devices.

Patent foramen ovale (PFO) is a common abnormality affecting between 20% and 34% of the adult population. For most people, it is a benign finding; however, in some people, the PFO can open widely to enable paradoxical embolus to transit from the venous to arterial circulation, which is associated with stroke and systemic embolisation. Percutaneous closure of the PFO in patients with cryptogenic stroke has been undertaken for a number of years, and a number of purpose-specific septal occluders have been marketed. Recent randomised control trials have demonstrated that closure of PFO in patients with cryptogenic stroke is associated with reduced rates of recurrent stroke. After a brief overview of the anatomy of a PFO, this article considers the evidence for PFO closure in cryptogenic stroke. The article also addresses other potential indications for closure, including systemic arterial embolisation, decompression sickness, platypnoea–orthodeoxia syndrome and migraine with aura. The article lays out the pre-procedural investigations and preparation for the procedure. Finally, the article gives an overview of the procedure itself, including discussion of closure devices.

Background Incretin therapies appear to provide cardioprotection and improve cardiovascular outcomes in patients with diabetes, but the mechanism of this effect remains elusive. We have previously shown that glucagon-like peptide (GLP)-1 is a coronary vasodilator and we sought to investigate if this is an adenosine-mediated effect. Methods We recruited 41 patients having percutaneous coronary intervention (PCI) for stable angina and allocated them into four groups administering a specific study-related infusion following successful PCI: GLP-1 infusion (Group G) (n = 10); Placebo, normal saline infusion (Group P) (n = 11); GLP-1 + Theophylline infusion (Group GT) (n = 10); and Theophylline infusion (Group T) (n = 10). A pressure wire assessment of coronary distal pressure and flow velocity (thermodilution transit time—Tmn) at rest and hyperaemia was performed after PCI and repeated following the study infusion to derive basal and index of microvascular resistance (BMR and IMR). Results There were no significant differences in the demographics of patients recruited to our study. Most of the patients were not diabetic. GLP-1 caused significant reduction of resting Tmn that was not attenuated by theophylline: mean delta Tmn (SD) group G − 0.23 s (0.27) versus group GT − 0.18 s (0.37), p = 0.65. Theophylline alone (group T) did not significantly alter resting flow velocity compared to group GT: delta Tmn in group T 0.04 s (0.15), p = 0.30. The resulting decrease in BMR observed in group G persisted in group GT: − 20.83 mmHg s (24.54 vs. − 21.20 mmHg s (30.41), p = 0.97. GLP-1 did not increase circulating adenosine levels in group GT more than group T: delta median adenosine − 2.0 ng/ml (− 117.1, 14.8) versus − 0.5 ng/ml (− 19.6, 9.4); p = 0.60. Conclusion The vasodilatory effect of GLP-1 is not abolished by theophylline and GLP-1 does not increase adenosine levels, indicating an adenosine-independent mechanism of GLP-1 coronary vasodilatation. Trial registration: The local research ethics committee approved the study (National Research Ethics Service-NRES Committee, East of England): REC reference 14/EE/0018. The study was performed according to institutional guidelines, was registered on http://www.clinicaltrials.gov (unique identifier: NCT03502083) and the study conformed to the principles outlined in the Declaration of Helsinki.

Postinfarct ventricular septal defects (VSDs) are a mechanical complication of acute myocardial infarction (AMI) with a very poor prognosis. They are estimated to occur in 0.2% of patients presenting with AMI, with 1-month survival of 6% without intervention. Guidelines recommend surgical repair, but recent advances in transcatheter technology, and bespoke device development, mean it is increasingly viable as a closure option. Surgical mortality is between 30% and 50% for all-comers, while in series of transcatheter closure, mortality was 32%. Transcatheter closure appears durable, with no evidence of late leaks and low long-term mortality in series with up to 5-year follow-up. Guidelines recommend early closure, which is likely to provide most benefit for patients regardless of the closure method. Multimodality cardiac imaging including echocardiography, CT and cardiac MRI can define size, shape, location of defects and their relationship to other cardiac structures, assisting with treatment decisions. Brief delay to allow stabilisation of the patient is appropriate, but untreated patients risk rapid deterioration. Mechanical circulatory support may be helpful, although the preferred modality is unclear. Transcatheter closure involves large bore venous access and the formation of an arteriovenous loop (under fluoroscopic and trans-oesophageal echocardiographic guidance) in order to facilitate deployment of the device in the defect and close the postinfarct VSD. Guidelines suggest transcatheter closure as an alternative to surgical repair in centres where appropriate expertise exists, but decisions for all patients with postinfarct VSD should be led by the multidisciplinary heart team.

AIMS Registry data have suggested higher than anticipated rates of scaffold thrombosis following bioresorbable vascular scaffold (BVS) implantation. We examined early neointimal growth and strut coverage in BVS to ascertain whether this was affected by clinical presentation. METHODS AND RESULTS Patients undergoing optical coherence tomography (OCT)-guided BVS implantation, either for stable angina (SA) or acute coronary syndrome (ACS), were recruited to this observational study. Repeat OCT was performed at follow-up (median 74 days), and scaffolds analysed at 1 mm longitudinal intervals for scaffold/flow area, scaffold apposition, neointimal growth and strut coverage. Twenty-nine BVS were included in the analysis (62% implanted following ACS). There were no differences in baseline patient/lesion characteristics. All BVS achieved >90% predicted scaffold area with only 1.64% of struts classified as incompletely apposed, compared with 0.47% at follow-up (p=0.006). Reductions in mean scaffold (-4.0%, p=0.01) and flow (-8.4%, p

Summary Glucagon-like peptide-1-(7-36) amide (GLP-1) is a human incretin hormone responsible for the release of insulin in response to food. Pre-clinical and human physiological studies have demonstrated cardioprotection from ischemia-reperfusion injury. It can reduce infarct size, ischemic left ventricular dysfunction, and myocardial stunning. GLP-1 receptor agonists have also been shown to reduce infarct size in myocardial infarction. The mechanism through which this protection occurs is uncertain but may include hijacking the subcellular pathways of ischemic preconditioning, modulation of myocardial metabolism, and hemodynamic effects including peripheral, pulmonary, and coronary vasodilatation. This review will assess the evidence for each of these mechanisms in turn. Challenges remain in successfully translating cardioprotective interventions from bench-to-bedside. The window of cardioprotection is short and timing of cardioprotection in the appropriate clinical setting is critically important. We will emphasize the need for high-quality, well-designed research to evaluate GLP-1 as a cardioprotective agent for use in real-world practice.

Background The mechanism underlying the beneficial cardiovascular effects of the incretin GLP‐1 (glucagon‐like peptide 1) and its analogues in humans is elusive. We hypothesized that activating receptors located on vascular smooth muscle cells to induce either peripheral or coronary vasodilatation mediates the cardiovascular effect of GLP ‐1. Methods and Results Ten stable patients with angina awaiting left anterior descending artery stenting underwent forearm blood flow measurement using forearm plethysmography and post–percutaneous coronary intervention coronary blood flow measurement using a pressure‐flow wire before and after peripheral GLP ‐1 administration. Coronary sinus and artery bloods were sampled for GLP ‐1 levels. A further 11 control patients received saline rather than GLP ‐1 in the coronary blood flow protocol. GLP ‐1 receptor (GLP‐1R) expression was assessed by immunohistochemistry using a specific GLP ‐1R monoclonal antibody in human tissue to inform the physiological studies. There was no effect of GLP ‐1 on absolute forearm blood flow or forearm blood flow ratio after GLP ‐1, systemic hemodynamics were not affected, and no binding of GLP ‐1R monoclonal antibody was detected in vascular tissue. GLP ‐1 reduced resting coronary transit time (mean [ SD ], 0.87 [0.39] versus 0.63 [0.27] seconds; P =0.02) and basal microcirculatory resistance (mean [ SD ], 76.3 [37.9] versus 55.4 [30.4] mm Hg/s; P =0.02), whereas in controls, there was an increase in transit time (mean [SD], 0.48 [0.24] versus 0.83 [0.41] seconds; P P =0.02). GLP ‐1R monoclonal antibody binding was confirmed in ventricular tissue but not in vascular tissue, and transmyocardial GLP ‐1 extraction was observed. Conclusions GLP ‐1 causes coronary microvascular dilation and increased flow but does not influence peripheral tone. GLP ‐1R immunohistochemistry suggests that GLP ‐1 coronary vasodilatation is indirectly mediated by ventricular‐coronary cross talk.

Cardiovascular-safety studies assessing glucagon-like peptide (GLP)-1 receptor agonists and dipeptidyl peptidase 4 inhibitors have provided inconsistent data on the risk for developing heart failure. Animal studies have shown that GLP-1 is a vasodilator; if confirmed in humans, this may ameliorate heart failure symptoms.In a single-center, observational pilot study, we recruited 10 patients with advanced heart failure undergoing right heart catheterization, and we recorded pulmonary hemodynamic measures, including cardiac output calculated by thermodilution and the indirect Fick method before and after a 15-minute continuous infusion of native GLP-1 (7-36) NHThere was a neutral effect of GLP-1 on all pressure and hemodynamics indices as derived by cardiac output calculated by thermodilution. However, there was a small but consistent reduction in cardiac output as calculated by the indirect Fick method after GLP-1 infusion (baseline, 4.0 [1.1] L/min vs GLP-1, 3.6 [0.9] L/min; P = 0.003), driven by a consistent reduction in mixed venous oxygen saturation after GLP-1 infusion (baseline, 62.2% [7.0%] vs GLP-1, 59.3% [6.8%]; P 0.001), whereas arterial saturation remained constant (baseline, 96.8% [3.3%] vs GLP-1, 97.0% [3.2%]; P = 0.34). This resulted in an increase in systemic vascular resistance by Fick (baseline, 1285 [228] dyn · s/cmAcute infusion of GLP-1 has a neutral hemodynamic effect, when assessed by thermodilution, in patients with heart failure. However, GLP-1 reduces mixed venous oxygen saturation. ClinicalTrials.gov identifier: NCT02129179.

Introduction Glucagon-like peptide 1 (7–36) amide (GLP-1) is an incretin hormone, shown to protect against non-lethal cardiac ischemia-reperfusion injury. We investigated whether GLP-1 protected against PCI-induced myocardial infarction (PMI), attenuating cardiac troponin I (cTnI) release after elective PCI. Methods A double-blind, randomised, placebo-control trial, conducted in a single UK centre, administered an iv infusion of GLP-1 (1.2 pmol/Kg/min) or saline to patients approximately 30 min before elective PCI. The primary endpoint was PMI defined as a cTnI elevation >5 xURL at 6 hours post-PCI. Secondary endpoints include TIMI flow and blush grade after PCI, rise in cTnI elevation and creatinine at 6 hours post-PCI and major adverse cardiovascular and cerebrovascular events (MACCE) at 6 months. Results Of the 192 patients randomised (figure 1), 152 (79%) were male. Patient demographics were similar between the groups. There was no inter-group difference in the incidence of PMI: GLP-1 9 (9.8%) vs saline 8 (8.3%), p=0.28. Median cTnI elevation between the groups was also similar: GLP-1 20 [0–88.5] vs saline 10 [0–58.5] ng/L, p=0.28. Change in creatinine was no different between the groups (GLP-1–2.78±9.04 vs saline −1.75±8.74 μmol/L, p=0.73). Conclusion GLP-1 did not confer cardioprotection against PMI after elective PCI, although the incidence of PMI in contemporary PCI is low.

Introduction: Glucagon-like peptide 1 (7-36) amide (GLP-1) is an incretin hormone, which has been shown to protect against non-lethal cardiac ischemia-reperfusion injury. We sought to investigate whether GLP-1 protected against PCI-induced myocardial infarction (PMI) and attenuate cardiac troponin I (cTnI) release after elective PCI. Methods: A double-blind, randomised, placebo-control trial, stratified for diabetes mellitus, conducted in a single UK centre, administered an intravenous infusion of GLP-1 (1.2pmol/Kg/min) or saline to patients approximately 30-minutes before elective PCI. The primary endpoint was PMI defined as a cTnI elevation > 5xURL at 6-hours post-PCI. Secondary endpoints include, intra-procedural chest pain, TIMI flow and blush grade after PCI, rise in cTnI elevation and creatinine at 6-hours post-PCI and major adverse cardiovascular and cerebrovascular events (MACCE) at six months. Results: A CONSORT diagram for the study is shown in Figure 1. Of the 192 patients randomized, 152 (79%) were male, mean age 68.1±8.9 years. Patient demographics were similar between the groups. There was no inter-group difference in the incidence of PMI: GLP-1 9 (9.8%) vs. saline 8 (8.3%), p=0.28. Median [IQR] cTnI elevation between the groups was also similar: GLP-1 20 [0-88.5] vs. saline 10 [0-58.5] ng/L, p=0.28. Renal function was not impaired at 6 hours. Δ Creatinine was not significantly different. (GLP-1 -2.78±9.04 vs. saline -1.75±8.74 μmol/L, p=0.73). Other secondary end-point data will be available at time of presentation. Conclusion: GLP-1 did not confer cardioprotection against PMI after elective PCI, although the incidence of PMI in contemporary PCI is low.

Percutaneous coronary intervention-induced myocardial infarction (PMI) has prognostic significance. Identifying patients at high risk for PMI is desirable as it may alter strategy and facilitate early preventative therapy. We therefore sought to establish whether preprocedural demographic, interventional (plaque characteristics and coronary microcirculatory function), and inflammatory, endothelial damage, and platelet-derived biomarker data could predict the risk of PMI.We performed target vessel pressure wire to assess fractional flow reserve, index of microcirculatory resistance (IMR) and coronary flow reserve, plaque characterization by virtual histology intravascular ultrasound, and assayed peripheral biomarkers before uncomplicated PCI in 88 patients. We then analyzed post-PCI cardiac troponin level to adjudicate PMI based on the third universal definition of myocardial infarction.Overall incidence of PMI was 27%. Women [10/15 (66%) vs. 14/73 (19%), P0.001] and those with low body mass (27.1±3.9 vs. 29.7±5.5 kg/m; P=0.02) were at significantly higher risk of PMI. Preprocedural coronary flow reserve was lower in individuals with a subsequent PMI (1.8±1.2 vs. 2.1±1.3. P=0.03), and patients with higher pre-PCI IMR were more likely to sustain PMI [IMR22: 10/23 (44%) vs. ≤22: 14/65 (22%), P=0.04], although neither was predictive after multivariate analysis. Plaque characterization by virtual histology intravascular ultrasound did not discriminate those at risk of PMI. However, peripheral venous interleukin (IL)-18 and IL-8 levels were independently negatively and positively associated with PMI, respectively.Women and those with low BMI, particularly when associated with high IL-8 and low IL-18 levels, appear to be at increased risk of PMI.

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 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 P 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 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.

This review examines the rationale for using remote ischemic conditioning (RIC) in elective percutaneous coronary intervention (PCI) to prevent procedure-related ischemia–reperfusion injury and justifies the importance of periprocedural biomarker elevation following elective PCI as a valid target for RIC. We review the evidence for the use of RIC as a treatment in this setting and document the salutary rules that must be followed to successfully translate RIC for clinical benefit.

Objectives To assess the relationship between anatomical form and physiological function in atherosclerotic coronary arteries. Background Although adverse cardiovascular events are predicted by plaque morphology or invasively-derived hemodynamic indices, the link between these important prognostic measures remains unexplored. Methods Patients with stable angina underwent fractional flow reserve (FFR), coronary flow reserve (CFR), pressure-derived collateral flow index (CFIp), trans-myocardial biomarker sampling and radiofrequency intravascular ultrasound (IVUS) imaging prior to intervention. Physiological ischemia was defined as either FFR≤0.8 or CFR Results Mean FFR was 0.70±0.15 and CFR was 2.1±1.3, with 68/92 lesions having FFR≤0.8 and 61/92 having CFR 2 , PB≥70% and thin-cap fibroatheroma, respectively. Multivariate regression demonstrated FFR≤0.8 was independently predicted by MLA (odds ratio (OR) 0.53, 95% CI 0.29–0.97, p=0.04) and PB (OR 1.10, 95% CI 1.01–1.21, p=0.03). There were no identifiable relationships between plaque structure and CFR or CFIp. CFR Conclusions Measures of plaque structure including PB and MLA are independently associated with FFR, but not with CFR or CFIp. Instead, vessels with low CFR have increased lipid accumulation and a higher transmyocardial hsCRP gradient. These results may explain similarities in clinical outcomes between physiologically and anatomically orientated trials.

Optical coherence tomography (OCT) is an increasingly available intracoronary imaging modality that provides high-resolution imaging of coronary arteries. Its fundamental reliance on the emission and reflection of light enables rapid data acquisition without compromise of image resolution. As such, OCT can inform operators planning percutaneous coronary intervention (PCI) by accurately defining luminal geometry and detailing plaque composition. Following PCI, OCT imaging delivers a thorough assessment of the treated arterial segment and can identify specific features not always visible on alternate imaging modalities, including stent edge-related dissection, plaque tissue prolapse, incomplete stent apposition and the presence of intra-coronary thrombus. Clinical trials highlight that procedural strategy is frequently altered based on OCT findings, while concerns over final stent dimensions have been mitigated through use of a sizing protocol based on external elastic lamina dimensions in the reference arterial segment. Randomised trials are now warranted to definitively ascertain whether OCT-guidance improves clinical outcomes when utilised during PCI.

We read with interest the study by Basalay et al 1 recently published in Cardiovascular Research investigating the mechanism of remote ischaemic conditioning (RIc) signalling. Whilst the results are intriguing, a number of unresolved issues remain when considering RIc in humans. First, the authors state that Glucagon-like Peptide 1 (GLP-1) had a protective effect against ischaemia-reperfusion injury in humans. It is noteworthy that the cardioprotective effect of GLP-1 in humans is …

Electronic supplementary material The online version of this article (doi:10.1007/s12928-017-0464-y) contains supplementary material, which is available to authorized users.

In the version of this article initially published online, the Paravalvular Leak Device (PLD; Occlutech) was incorrectly described as having a “proximal disc that is slightly larger than the distal disc”, whereas the distal disc is actually slightly larger than the proximal disc. This error has been corrected for the HTML, PDF and print versions of the article.

We describe the coronary steal phenomenon in patients with profound fixed microvascular dysfunction in an infarct related artery (IRA) after primary percutaneous coronary intervention (PPCI). Following primary PCI we used pressure wire X to assess baseline and hyperemic (adenosine 140mcg/kg/min)

Background Glucagon-like peptide-1 (7–36) amide (GLP-1) protects against stunning and cumulative left ventricular dysfunction in humans. The mechanism remains uncertain but GLP-1 may act by opening mitochondrial K-ATP channels in a similar fashion to ischemic conditioning. We investigated whether blockade of K-ATP channels with glibenclamide abrogated the protective effect of GLP-1 in humans. Methods Thirty-two non-diabetic patients awaiting stenting of the left anterior descending artery (LAD) were allocated into 4 groups (control, glibenclamide, GLP-1, and GLP-1 + glibenclamide). Glibenclamide was given orally prior to the procedure. A left ventricular conductance catheter recorded pressure–volume loops during a 1-min low-pressure balloon occlusion (BO1) of the LAD. GLP-1 or saline was then infused for 30-min followed by a further 1-min balloon occlusion (BO2). In a non-invasive study, 10 non-diabetic patients were randomized to receive two dobutamine stress echocardiograms (DSE) during GLP-1 infusion with or without oral glibenclamide pretreatment. Results GLP-1 prevented stunning even with glibenclamide pretreatment; the Δ % dP/dtmax 30-min post-BO1 normalized to baseline after GLP-1: 0.3 ± 6.8 % (p = 0.02) and GLP-1 + glibenclamide: −0.8 ± 9.0 % (p = 0.04) compared to control: −11.5 ± 10.0 %. GLP-1 also reduced cumulative stunning after BO2: −12.8 ± 10.5 % (p = 0.02) as did GLP-1 + glibenclamide: −14.9 ± 9.2 % (p = 0.02) compared to control: −25.7 ± 9.6 %. Glibenclamide alone was no different to control. Glibenclamide pretreatment did not affect global or regional systolic function after GLP-1 at peak DSE stress (EF 74.6 ± 6.4 vs. 74.0 ± 8.0, p = 0.76) or recovery (EF 61.9 ± 5.7 vs. 61.4 ± 5.6, p = 0.74). Conclusions Glibenclamide pretreatment does not abrogate the protective effect of GLP-1 in human models of non-lethal myocardial ischemia. Trial registration Clinicaltrials.gov Unique Identifier: NCT02128022 Electronic supplementary material The online version of this article (doi:10.1186/s12933-016-0416-3) contains supplementary material, which is available to authorized users.

Transcatheter aortic valve replacement (TAVR) is an established therapy for patients with aortic stenosis [(1)][1]. Rapid pacing (RP), to ablate left ventricular (LV) ejection, stabilizes deployment and is necessary for balloon-expandable TAVR although it is less important for repositionable, self