Adenosine-Induced Coronary Steal Is Observed in Patients Presenting With ST-Segment-Elevation Myocardial Infarction.

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 <0.9), no change in flow (CFR=0.9-1.1), and hyperemic flow (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<0.001) and a higher collateral flow index by pressure (0.25±0.10 versus 0.15±0.10, 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.

Correction to: Clinical outcomes of patients undergoing primary percutaneous coronary intervention for acute myocardial infarction requiring the intensive care unit.

[This corrects the article DOI: 10.1186/s40560-018-0275-y.].

Clinical outcomes of patients undergoing primary percutaneous coronary intervention for acute myocardial infarction requiring the intensive care unit.

Background: Outcomes for patients with ST-segment elevation myocardial infarction continue to improve, largely due to timely provision of reperfusion by primary percutaneous coronary intervention (PPCI). However, despite prompt and successful PPCI, a small proportion of patients require ventilatory and hemodynamic support in an intensive care unit (ICU). The outcome of these patients remains poorly defined. Methods: A retrospective review of all consecutive admissions post-PPCI pathway to a single ICU between January 2009 and May 2014 was performed. Patients were analysed based on survival and indication for admission. Preadmission characteristics and ICU course were reviewed. Univariate and multivariable regression analysis was performed to determine predictors of outcome. Results: During the study period 2902 PPCI were performed and 101 patients were admitted to ICU following PPCI (incidence 3.5%). ICU mortality post-PPCI was 33.7%. Pre-ICU admission factors in a multivariable logistic regression analysis associated with increased mortality included requirement for an intra-aortic balloon pump and a high SOFA score. Conclusions: ICU admission post PPCI is associated with significant mortality. Mortality was related to high presenting SOFA score and need for IABP. These results provide important prognostic information and an acceptable method for risk-stratifying patients with acute myocardial infarction requiring intensive care.

Novel bioabsorbable polymer and polymer-free metallic drug-eluting stents.

The introduction of drug-eluting stents (DES) significantly reduced angiographic restenosis and the clinical need for revascularization following percutaneous coronary intervention. However, concerns remain regarding the long-term safety and efficacy of DES. The use of durable polymers for drug elution that have limited biocompatibility is thought to contribute toward DES failure, by promoting an adverse local inflammatory response and vascular toxicity. Biodegradable polymer and polymer-free metallic stents represent two novel technological solutions to this challenging clinical problem. This review summarizes the available clinical evidence supporting the use of either biodegradable polymer or polymer-free DES platforms.

Implantation of bioresorbable vascular scaffolds following acute coronary syndrome is associated with reduced early neointimal growth and strut coverage.

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<0.001) areas were observed at follow-up, with larger reductions in mean flow area in stable patients (-14.5±14.2 vs. -4.9±7.9%, p=0.03). ACS patients had reduced neointimal growth (0.51±0.18 vs. 0.87±0.37 mm2, p=0.002), and increased percentage of uncovered struts (2.68±1.67 vs. 1.43±0.87%, p=0.015). CONCLUSIONS: Early neointimal growth and strut coverage are reduced following ACS in patients receiving BVS. These results may, in part, explain the high rates of ST in registry data.

Optical coherence tomography imaging of coronary atherosclerosis is affected by intraobserver and interobserver variability.

AIMS: Optical coherence tomography (OCT) has emerged as a novel imaging modality that allows plaque classification through identification of features including lipid, calcification and fibrous cap. However, subtle changes in light attenuation as the optical beam traverses the plaque in vivo are challenging to interpret and data on strength of observer agreement are minimal. Thus, we sought to assess both the intra and interobserver variability for plaque composition/classification using OCT. METHODS: OCT imaging was performed in 50 patients prior to percutaneous coronary intervention. Analysis was performed offline by two independent, experienced OCT operators. Target lesion luminal dimensions and plaque composition were assessed at minimal luminal area (MLA) and at five 1-mm longitudinal intervals proximal and distal to the MLA. An OCT thin-capped fibroatheroma (OCT-TCFA) was defined as greater than 90 degree lipid arc with minimal fibrous cap thickness less than 0.85 µm. RESULTS: Overall, 540 frames of OCT were included and exceptional consistency was seen for all measures of luminal geometry [all intraclass correlation coefficients (ICC) >0.97, P < 0.001]. Intraobserver agreements for calcification and lipid arc were strong (both ICC >0.84, P < 0.001), whereas interobserver agreement was higher for calcium (ICC 0.76) than lipid (ICC 0.69). Interobserver agreement of minimal fibrous cap thickness was moderate (ICC 0.52, 95% confidence interval 0.45-0.58, P < 0.001], but improved as cap thickness decreased. Overall, intra and interobserver agreements for OCT-defined plaque classification were strong (K = 0.86 and 0.71, respectively). CONCLUSION: Luminal dimensions and plaque compositional features identified by OCT are minimally affected by observer variability, permitting dependable plaque classification.

Interpretation of fractional flow reserve in ST-elevation myocardial infarction culprit lesions.

BACKGROUND: Pressure wire assessment of the infarct-related artery (IRA) in ST-elevation myocardial infarction (STEMI) is not recommended until microcirculatory dysfunction recovers. OBJECTIVE: The objective of this study was to assess serial fractional flow reserve (FFR) and the index of microcirculatory resistance (IMR) in the IRA of STEMI patients to better understand and interpret FFR during primary percutaneous coronary intervention (PPCI). METHODS: Forty-one patients undergoing PPCI for STEMI were studied with a pressure wire at baseline after thrombectomy and after stenting. RESULTS: The majority of STEMI culprit lesions in the IRA were haemodynamically significant (mean FFR pre-PPCI: 0.54±0.20); only 4/41 culprit lesions had FFR greater than 0.80. The FFR of the culprit lesion and the initial IMR were correlated (r=0.45, P=0.004). Patients with a normal initial IMR of less than 25 exhibited lower culprit lesion FFR values (0.47±0.20 vs. 0.60±0.18, P=0.03) despite milder angiographic stenoses [angiographic stenoses (%): 80.4±10.4 vs. 86.6±8.0, P=0.03] but showed a reduction in the IMR during PPCI (pre-PPCI: 16.9±5.7 vs. post-PPCI: 32.2±22.6, P=0.009). CONCLUSION: STEMI culprit lesions are haemodynamically significant. A subset of STEMI IRAs has initially preserved microcirculatory function; thus, the culprit stenosis may feasibly be assessed through FFR.

Serial assessment of the index of microcirculatory resistance during primary percutaneous coronary intervention comparing manual aspiration catheter thrombectomy with balloon angioplasty (IMPACT study): a randomised controlled pilot study.

OBJECTIVE: Utilising a novel study design, we evaluated serial measurements of the index of microcirculatory resistance (IMR) in patients undergoing primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) to assess the impact of device therapy on microvascular function, and determine what proportion of microvascular injury is related to the PPCI procedure, and what is an inevitable consequence of STEMI. DESIGN: 41 patients undergoing PPCI for STEMI were randomised to balloon angioplasty (BA, n=20) or manual thrombectomy (MT, n=21) prior to stenting. Serial IMR measurements, corrected for collaterals, were recorded at baseline and at each stage of the procedure. Microvascular obstruction (MVO) and infarct size at 24 h and 3 months were measured by troponin and cardiac MRI (CMR). RESULTS: IMR did not change significantly following PPCI, but patients with lower IMR values (<32, n=30) at baseline had a significant increase in IMR following PPCI (baseline: 21.2±7.9 vs post-stent: 33.0±23.7, p=0.01) attributable to prestent IRA instrumentation (baseline: 21.7±8.0 vs post-BA or MT: 36.9±25.9, p=0.006). Post-stent IMR correlated with early MVO on CMR (p=0.01). There was no significant difference in post-stent IMR, presence of early MVO or final infarct size between patients with BA and patients treated with MT. CONCLUSIONS: Patients with STEMI and less microcirculatory dysfunction may be susceptible to acute iatrogenic microcirculatory injury from prestent coronary devices. MT did not appear to be superior to BA in maintaining microcirculatory integrity when the guide wire partially restores IRA flow during PPCI. TRIAL REGISTRATION NUMBER: ISRCTN31767278.

Cardiac complications of thoracic irradiation.

Adjuvant radiation therapy in the management of early stage breast cancer, Hodgkin's disease, and to a lesser extent other thoracic malignancies has led to a significant improvement in disease-specific survival. Cardiovascular disease is now the most common nonmalignancy cause of death in radiation-treated cancer survivors, most often occurring decades after treatment. The spectrum of radiation-induced cardiac disease is broad, potentially involving any component of the heart. The relative risk of coronary artery disease, congestive heart failure, valvular heart disease, pericardial disease, conduction abnormalities, and sudden cardiac death is particularly increased. Over the years contemporary techniques have been introduced to reduce cardiac morbidity and mortality in radiation-treated cancer survivors; however, the long-term effects on the heart still remain unclear, mandating longer follow-up. Awareness and early identification of potential cardiac complications is crucial in cancer survivors, with the management often being quite complex. This review examines the epidemiology of radiation-induced cardiac disease together with its pathophysiology and explores the available treatment strategies and the potential utility of various screening strategies for affected cancer survivors.