Sex differences in long-term outcomes in older adults undergoing invasive treatment for non-ST elevation acute coronary syndrome : An ICON-1 sub-study

Background: Cardiovascular disease is the leading cause of mortality for females globally, yet females are underrepresented in studies of acute coronary syndrome (ACS). Studies investigating sex-related differences in clinical outcomes of patients with non-ST elevation ACS (NSTEACS) have reported divergent results, and it is unknown whether long-term outcomes for older people with NSTEACS differ between males and females. Methods: The multi-centre prospective cohort study, ICON-1, consisted of patients aged ≥75 years undergoing coronary angiography following NSTEACS. The primary composite endpoint was all-cause mortality, myocardial infarction, unplanned revascularisation, stroke, and bleeding. We report outcomes at five-years by sex. Results: Of 264 patients, 102 (38.6%) females and 162 (61.4%) males completed the five-year follow-up and were included in the analytic cohort. At admission, females were older than males (82 ± 4.3 years vs 80.0 ± 4.1 years p = 0.018). Co-morbidity profile and GRACE score were similar between the groups. There were no differences in the provision of invasive or pharmacological treatments between sexes. At five-years, there were no association between sex and the primary outcome. Conclusion: In older adults with invasive treatment of NSTEACS, provision of guideline-indicated care and long-term clinical outcomes were similar between males and females

CMR Native T1 Mapping Allows Differentiation of Reversible Versus Irreversible Myocardial Damage in ST-Segment–Elevation Myocardial Infarction

Background—CMR T1 mapping is a quantitative imaging technique allowing the assessment of myocardial injury early after ST-segment–elevation myocardial infarction. We sought to investigate the ability of acute native T1 mapping to differentiate reversible and irreversible myocardial injury and its predictive value for left ventricular remodeling. Methods and Results—Sixty ST-segment–elevation myocardial infarction patients underwent acute and 6-month 3T CMR, including cine, T2-weighted (T2W) imaging, native shortened modified look-locker inversion recovery T1 mapping, rest first pass perfusion, and late gadolinium enhancement. T1 cutoff values for oedematous versus necrotic myocardium were identified as 1251 ms and 1400 ms, respectively, with prediction accuracy of 96.7% (95% confidence interval, 82.8% to 99.9%). Using the proposed threshold of 1400 ms, the volume of irreversibly damaged tissue was in good agreement with the 6-month late gadolinium enhancement volume (r=0.99) and correlated strongly with the log area under the curve troponin (r=0.80) and strongly with 6-month ejection fraction (r=−0.73). Acute T1 values were a strong predictor of 6-month wall thickening compared with late gadolinium enhancement. Conclusions—Acute native shortened modified look-locker inversion recovery T1 mapping differentiates reversible and irreversible myocardial injury, and it is a strong predictor of left ventricular remodeling in ST-segment–elevation myocardial infarction. A single CMR acquisition of native T1 mapping could potentially represent a fast, safe, and accurate method for early stratification of acute patients in need of more aggressive treatment. Further confirmatory studies will be needed

Acute Microvascular Impairment Post-Reperfused STEMI Is Reversible and Has Additional Clinical Predictive Value: A CMR OxAMI Study

OBJECTIVES: This study sought to investigate the clinical utility and the predictive relevance of absolute rest myocardial blood flow (MBF) by cardiac magnetic resonance (CMR) in acute myocardial infarction. BACKGROUND: Microvascular obstruction (MVO) remains one of the worst prognostic factors in patients with reperfused ST-segment elevation myocardial infarction (STEMI). Clinical trials have focused on cardioprotective strategies to maintain microvascular functionality, but there is a need for a noninvasive test to determine their efficacy. METHODS: A total of 64 STEMI patients post-primary percutaneous coronary intervention underwent 3-T CMR scans acutely and at 6 months (6M). The protocol included cine function, T2-weighted edema imaging, pre-contrast T1 mapping, rest first-pass perfusion, and late gadolinium enhancement imaging. Segmental MBF, corrected for rate pressure product (MBFcor), was quantified in remote, edematous, and infarcted myocardium. RESULTS: Acute MBFcor was significantly reduced in infarcted myocardium compared with remote MBF (MBFinfarct 0.76 ± 0.20 ml/min/g vs. MBFremote 1.02 ± 0.21 ml/min/g, p 45% at 6M increased by 1.38:1 [p 2 or index of myocardial resistance <40, acute MBF was associated with long-term functional recovery and was an independent predictor of infarct size reduction. CONCLUSIONS: Acute MBF by CMR could represent a novel quantitative imaging biomarker of microvascular reversibility, and it could be used to identify patients who may benefit from more intensive or novel therapie

Vascular characterisation using multimodal imaging and relationship to functional lipid indices in blood

Reduction in LDL cholesterol (LDL-c) has been shown to be effective in decreasing cardiovascular events. However, 1 in 5 patients return with a second event within 5 years despite achieving very low LDL-c. New lipid-lowering drugs have been shown to be efficacious in reducing LDL-c, however, in unselected populations the numbers needed to treat with these agents were unmanageably high. Therefore, attention should be sharply focused on developing stratification tools that not only identify high risk patients but also incorporate a mechanistic understanding when applying targeted therapies. Matching a prominent disease feature (inflammation, lipid accumulation etc.) with a drug mechanism of action may offer an opportunity to achieve more precise intervention. Remarkably, however, it is still unclear how reducing LDL-c translates into improved cardiovascular outcomes. One prevalent theory is that LDL-c reduction leads to evacuation of lipid from atherosclerotic plaque, rendering plaque less prone to rupture. Tools to measure plaque lipid content in humans in vivo have been fundamentally insensitive and incapable of systematically quantify lipid in every individual. Thus limiting the applicability of using plaque lipid quantification as an approach to select individuals for new lipid-lowering drugs. Recently, a new quantitative magnetic resonance imaging (MRI) T2 mapping technique has been shown to be capable of accurate, reproducible quantification of carotid plaque lipid on a voxel-by-voxel basis. Accordingly, this thesis hypothesized that using this newly validated technique, plaque lipid content and distribution can be systematically evaluated in all patients with clinical evidence of atherosclerosis. In addition, lipid content quantified on T2 mapping is reduced following intensive LDL-c reduction which can be assessed on subjects with no pre-defined carotid disease. Furthermore, blood lipid biomarkers are dissociated from plaque lipid content and its change on therapy. Finally, plaque lipid content is not influenced by perivascular adipose tissue, marker of inflammation, via paracrine local effect. T2 mapping MRI technique was able to identify patients with propensity to develop lipid-rich plaques at multi-sites vascular territories in patients scheduled for carotid endarterectomy (CEA) or presenting with acute coronary syndrome (ACS). Plaque lipid content and distribution quantified on T2 mapping MRI technique were related to the symptomatic status of plaques in patients scheduled for CEA. Intensive LDL-c reduction using high intensity statin treatment was associated with significant changes in plaque composition which was detected on T2 mapping as early as three months. There was no significant predictor of changes in carotid plaque lipid content using baseline, attained or change in blood lipid biomarkers following statin treatment. There was no spatial relationship between carotid plaque lipid content and adjacent perivascular adipose tissue. These findings support the use of plaque imaging as a potential tool to identify suitable patients for intensive lipid-lowering treatments and to track patients’ response to these therapies.</p

Vascular characterisation using multimodal imaging and relationship to functional lipid indices in blood

Reduction in LDL cholesterol (LDL-c) has been shown to be effective in decreasing cardiovascular events. However, 1 in 5 patients return with a second event within 5 years despite achieving very low LDL-c. New lipid-lowering drugs have been shown to be efficacious in reducing LDL-c, however, in unselected populations the numbers needed to treat with these agents were unmanageably high. Therefore, attention should be sharply focused on developing stratification tools that not only identify high risk patients but also incorporate a mechanistic understanding when applying targeted therapies. Matching a prominent disease feature (inflammation, lipid accumulation etc.) with a drug mechanism of action may offer an opportunity to achieve more precise intervention. Remarkably, however, it is still unclear how reducing LDL-c translates into improved cardiovascular outcomes. One prevalent theory is that LDL-c reduction leads to evacuation of lipid from atherosclerotic plaque, rendering plaque less prone to rupture. Tools to measure plaque lipid content in humans in vivo have been fundamentally insensitive and incapable of systematically quantify lipid in every individual. Thus limiting the applicability of using plaque lipid quantification as an approach to select individuals for new lipid-lowering drugs. Recently, a new quantitative magnetic resonance imaging (MRI) T2 mapping technique has been shown to be capable of accurate, reproducible quantification of carotid plaque lipid on a voxel-by-voxel basis. Accordingly, this thesis hypothesized that using this newly validated technique, plaque lipid content and distribution can be systematically evaluated in all patients with clinical evidence of atherosclerosis. In addition, lipid content quantified on T2 mapping is reduced following intensive LDL-c reduction which can be assessed on subjects with no pre-defined carotid disease. Furthermore, blood lipid biomarkers are dissociated from plaque lipid content and its change on therapy. Finally, plaque lipid content is not influenced by perivascular adipose tissue, marker of inflammation, via paracrine local effect. T2 mapping MRI technique was able to identify patients with propensity to develop lipid-rich plaques at multi-sites vascular territories in patients scheduled for carotid endarterectomy (CEA) or presenting with acute coronary syndrome (ACS). Plaque lipid content and distribution quantified on T2 mapping MRI technique were related to the symptomatic status of plaques in patients scheduled for CEA. Intensive LDL-c reduction using high intensity statin treatment was associated with significant changes in plaque composition which was detected on T2 mapping as early as three months. There was no significant predictor of changes in carotid plaque lipid content using baseline, attained or change in blood lipid biomarkers following statin treatment. There was no spatial relationship between carotid plaque lipid content and adjacent perivascular adipose tissue. These findings support the use of plaque imaging as a potential tool to identify suitable patients for intensive lipid-lowering treatments and to track patientsâ response to these therapies.</p

Calcium Modifications Therapies in Contemporary Percutaneous Coronary Intervention

Coronary artery calcifications (CAC) has been known to be associated with worse Percutaneous Coronary Intervention (PCI) short- and long-term outcomes. Nowadays with the increased prevalence of the risk factors leading to CAC in the population and also more PCI procedures done in older patients and with the growing number of higher risk cases of chronic total occlusion (CTO) PCI and PCI after coronary artery bypass grafting(CABG), severe cases of CAC are now encountered on a daily basis in the catheterization lab and remain a big challenge to the interventional community, making it crucial to identify cases of severe CAC and plan a CAC PCI modification strategy upfront. Improved CAC detection with intravascular imaging helped identifying more of these severe CAC cases and predicting response to therapy and stent expansion based on CAC distribution in the vessel. Multiple available therapies for CAC modification has evolved over the years, familiarity with the specifics and special considerations and limitations of each of these tools is essential in the choice and application of these therapies when used in severe CAC treatment. In this review we discuss CAC pathophysiology, modes of detection, and different available therapies for CAC modification

Percutaneous coronary intervention versus coronary artery bypass grafting in complex coronary artery disease: Long-term clinical outcomes from a high-volume center

Background: Clinical equipoise between a percutaneous coronary intervention (PCI) and coronary artery bypass grafting surgery (CABG) in the treatment of complex coronary artery disease (CAD), including unprotected left main coronary artery (LMCA) and/or three-vessel disease (3VD), remains debatable. Methods: A retrospective analysis of an unselected cohort undergoing contemporary PCI versus CABG at a large center in 2015. Patients who received nonemergent treatment of unprotected LMCA and/or 3VD were included. The primary study endpoint was all-cause mortality at 5 years. Secondary endpoints included a composite of all-cause mortality, spontaneous myocardial infarction (MI), or ischemia-driven repeat revascularization at 30 days and 1 year. Results: Four hundred and thirty patients met the inclusion criteria, 225 had PCI, and 205 had CABG. PCI patients were older with frequent LMCA involvement and higher EuroSCORE yet they had a fourfold shorter in-hospital stay compared to CABG patients. At 5 years, there was no significant difference in the primary endpoint between CABG and PCI (adjusted Hazard ratios 0.68, 95% confidence interval: 0.38–1.22, P = 0.19). Likewise, there was no significant difference in the incidence of the secondary composite endpoint or its components at 30 days or 1 year. A propensity score-matched analysis in 220 patients revealed similar outcomes. Conclusions: In real-world long-term contemporary data, survival after PCI was comparable to CABG at 5 years in patients with unprotected LMCA and/or 3VD. At 1 year, the incidence of spontaneous MI and ischemia-driven repeat revascularization did not differ between the two cohorts. The mode of revascularization in these complex patients should be guided by the heart team