Influence of Pathophysiologic Patterns of Coronary Artery Disease on Immediate Percutaneous Coronary Intervention Outcomes.

BACKGROUND: Diffuse coronary artery disease affects the safety and efficacy of percutaneous coronary intervention (PCI). Pathophysiologic coronary artery disease patterns can be quantified using fractional flow reserve (FFR) pullbacks incorporating the pullback pressure gradient (PPG) calculation. This study aimed to establish the capacity of PPG to predict optimal revascularization and procedural outcomes. METHODS: This prospective, investigator-initiated, single-arm, multicenter study enrolled patients with at least one epicardial lesion with an FFR ≤0.80 scheduled for PCI. Manual FFR pullbacks were used to calculate PPG. The primary outcome of optimal revascularization was defined as an FFR ≥0.88 after PCI. RESULTS: A total of 993 patients with 1044 vessels were included. The mean FFR was 0.68±0.12, PPG 0.62±0.17, and the post-PCI FFR was 0.87±0.07. PPG was significantly correlated with the change in FFR after PCI (r=0.65 [95% CI, 0.61-0.69]; P<0.001) and demonstrated excellent predictive capacity for optimal revascularization (area under the receiver operating characteristic curve, 0.82 [95% CI, 0.79-0.84]; P<0.001). FFR alone did not predict revascularization outcomes (area under the receiver operating characteristic curve, 0.54 [95% CI, 0.50-0.57]). PPG influenced treatment decisions in 14% of patients, redirecting them from PCI to alternative treatment modalities. Periprocedural myocardial infarction occurred more frequently in patients with low PPG (<0.62) compared with those with focal disease (odds ratio, 1.71 [95% CI, 1.00-2.97]). CONCLUSIONS: Pathophysiologic coronary artery disease patterns distinctly affect the safety and effectiveness of PCI. PPG showed an excellent predictive capacity for optimal revascularization and demonstrated added value compared with an FFR measurement. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04789317.

Rationale and design of the pullback pressure gradient (PPG) global registry.

INTRODUCTION: Diffuse disease has been identified as one of the main reasons leading to low post-PCI fractional flow reserve (FFR) and residual angina after PCI. Coronary pressure pullbacks allow for the evaluation of hemodynamic coronary artery disease (CAD) patterns. The pullback pressure gradient (PPG) is a novel metric that quantifies the distribution and magnitude of pressure losses along the coronary artery in a focal-to-diffuse continuum. AIM: The primary objective is to determine the predictive capacity of the PPG for post-PCI FFR. METHODS: This prospective, large-scale, controlled, investigator-initiated, multicenter study is enrolling patients with at least 1 lesion in a major epicardial vessel with a distal FFR ≤ 0.80 intended to be treated by PCI. The study will include 982 subjects. A standardized physiological assessment will be performed pre-PCI, including the online calculation of PPG from FFR pullbacks performed manually. PPG quantifies the CAD pattern by combining several parameters from the FFR pullback curve. Post-PCI physiology will be recorded using a standardized protocol with FFR pullbacks. We hypothesize that PPG will predict optimal PCI results (post-PCI FFR ≥ 0.88) with an area under the ROC curve (AUC) ≥ 0.80. Secondary objectives include patient-reported and clinical outcomes in patients with focal vs. diffuse CAD defined by the PPG. Clinical follow-up will be collected for up to 36 months, and an independent clinical event committee will adjudicate events. RESULTS: Recruitment is ongoing and is expected to be completed in the second half of 2023. CONCLUSION: This international, large-scale, prospective study with pre-specified powered hypotheses will determine the ability of the preprocedural PPG index to predict optimal revascularization assessed by post-PCI FFR. In addition, it will evaluate the impact of PPG on treatment decisions and the predictive performance of PPG for angina relief and clinical outcomes.

Statin Treatment Intensity, Discontinuation, and Long-Term Outcome in Patients With Acute Myocardial Infarction and Impaired Kidney Function.

ABSTRACT: Statin dosage in patients with acute myocardial infarction (AMI) and concomitant kidney dysfunction is a clinical dilemma. We studied discontinuation during the first year after an AMI and long-term outcome in patients receiving high versus low-moderate intensity statin treatment, in relation to kidney function. For the intention-to-treat analysis (ITT-A), we included all patients admitted to Swedish coronary care units for a first AMI between 2005 and 2016 that survived in-hospital, had known creatinine, and initiated statin therapy (N = 112,727). High intensity was initiated in 38.7% and low-moderate in 61.3%. In patients with estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m 2 , 25% discontinued treatment the first year; however, the discontinuation rate was similar regardless of the statin intensity. After excluding patients who died, changed therapy, or were nonadherent during the first year, 84,705 remained for the on-treatment analysis (OT-A). Patients were followed for 12.6 (median 5.6) years. In patients with eGFR 30-59 mL/min, high-intensity statin was associated with lower risk for the composite death, reinfarction, or stroke both in ITT-A (hazard ratio [HR] 0.93; 95% confidence interval, 0.87-0.99) and OT-A (HR 0.90; 0.83-0.99); the interaction test for OT-A indicated no heterogeneity for the eGFR < 60 mL/min group ( P = 0.46). Similar associations were seen for all-cause mortality. We confirm that high-intensity statin treatment is associated with improved long-term outcome after AMI in patients with reduced kidney function. Most patients with reduced kidney function initiated on high-intensity statins are persistent after 1 year and equally persistent as patients initiated on low-moderate intensity.

Aortic stiffness and aortic-brachial stiffness mismatch as markers of renal dysfunction in hypertension.

PURPOSE: The dismal combination of hypertension and chronic kidney disease potentiates both cardiovascular disease and loss of renal function. Research points to the importance of arterial and left ventricular stiffening in this process but few studies have compared aspects of central and peripheral hemodynamics in relation to renal function in hypertension. MATERIALS AND METHODS: We investigated 107 hypertensive individuals with renal function ranging from normal to severe dysfunction with pulse wave analysis to obtain central blood pressures (BP), augmentation index, carotid-femoral and carotid-radial pulse wave velocity (cfPWV, crPWV), aortic-to-brachial stiffness mismatch (cfPWV/crPWV), endothelial function by forearm flow-mediated vasodilation and myocardial microvascular function by subendocardial viability ratio, and indices of left ventricular structure (left ventricular mass index and relative wall thickness, RWT) and diastolic function (left atrial volume index, E/A, and E/é). RESULTS: Mean age was 58 years, BP 149/87 mm Hg, 9% had cardiovascular disease, and 31% were on antihypertensive treatment. Mean estimated glomerular filtration rate (eGFR) was 74 (range 130-21) ml/min × 1.73 m2. Whereas cfPWV and cfPWV/crPWV were independently related to eGFR (r = -0.20, p = 0.002, r = -0.16, p = 0.01), central diastolic BP (r = 0.21, p = 0.04), RWT (r = -0.34, p = 0.001), E/é (r = -0.39, p < 0.001) and E/A (r = 0.27, p = 0.01) were related to eGFR in bivariate correlations, but these findings were not retained in multivariate analyses. Remaining markers of hypertensive heart disease and measures of microvascular function were not related to eGFR. CONCLUSION: Increased aortic stiffness and aortic-to-brachial stiffness mismatch are independently related to reduced eGFR in hypertensive patients, suggesting an important role for aortic stiffness in the evolution of hypertension-mediated renal dysfunction. Aortic stiffness and aortic-brachial stiffness mismatch may be useful early markers to find hypertensive patients at risk for decline in renal function.

Effectiveness of Enhanced External Counterpulsation Treatment on Symptom Burden, Medication Profile, Physical Capacity, Cardiac Anxiety, and Health-Related Quality of Life in Patients With Refractory Angina Pectoris.

BACKGROUND: Patients with refractory angina pectoris experience recurrent symptoms that limit their functional capacity, including psychological distress and impaired health-related quality of life (HRQoL), despite optimized medical therapy. Enhanced external counterpulsation (EECP) is an evidence-based alternative noninvasive treatment. Although physical well-being and mental well-being are equally important components of health, few studies have investigated the psychological effects of EECP in patients with refractory angina pectoris. OBJECTIVE: The aim of this study was to evaluate the effects of EECP treatment in patients with refractory angina pectoris regarding medication profile, physical capacity, cardiac anxiety, and HRQoL. METHODS: This quasi-experimental study with 1-group pretest-posttest design includes a 6-month follow-up of 50 patients (men, n = 37; mean age, 65.8 years) who had undergone 1 EECP course. The following pretreatment and posttreatment data were collected: medication use, 6-minute walk test results, functional class according to the Canadian Cardiovascular Society, and self-reported (ie, questionnaire data) cardiac anxiety and HRQoL. In addition, the questionnaires were also completed at a 6-month follow-up. RESULTS: After EECP treatment, patients used significantly less nitrates (P < .001), walking distance increased on average by 46 m (P < .001), and Canadian Cardiovascular Society class improved (P < .001). In addition, all but 1 subscale of cardiac anxiety and all HRQoL components improved significantly (P < .05). The positive effects for cardiac anxiety and HRQoL were maintained at the 6-month follow-up. CONCLUSIONS: Enhanced external counterpulsation treatment resulted in reduced symptom burden, improved physical capacity, and less cardiac anxiety, leading to increased physical activity and enhanced life satisfaction for patients with refractory angina pectoris. Enhanced external counterpulsation treatment should be considered to improve the life situation for these patients.

Post-acute COVID-19 syndrome: prevalence of peripheral microvascular endothelial dysfunction and associations with NT-proBNP dynamics.

BACKGROUND: Post-acute COVID-19 syndrome (PACS) has been linked to microvascular endothelial dysfunction as a potential underlying pathomechanism and can manifest even following a mild course of the initial infection. Prevalence of microvascular endothelial dysfunction and circulating natriuretic peptides in such PACS patients remains unknown. METHODS AND RESULTS: This prospective, cross-sectional cohort study enrolled 92 patients (82% females, median age 48 years) with PACS. Reactive hyperemia index (RHI) was evaluated with peripheral arterial tonometry where <1.67 was defined as microvascular endothelial dysfunction, 1.67-2.0 impaired- and >2 normal endothelial function, on average 31 months after the acute infection. N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were collected at two different time points within over 1-year span. In total, 41% of PACS subjects had microvascular endothelial dysfunction and 20% had impaired RHI. No major differences in clinical characteristics, routine chemistry laboratory testing or symptom burden were observed across the groups. Only subjects with microvascular endothelial dysfunction and impaired endothelial function had a significant increase in NT-proBNP levels over time and those with larger increase in NT-proBNP had significantly lower RHI. There was a significant correlation between relative or absolute increase in NT-proBNP and RHI, which remained significant in a multivariable adjusted linear regression. CONCLUSIONS: Peripheral microvascular endothelial dysfunction was prevalent in a symptomatic PACS population long after recovery from a mild acute infection. Increases in NT-proBNP levels were associated with microvascular endothelial dysfunction, suggesting a link between and providing a foundation for future studies on post viral microvascular endothelial dysfunction in PACS.

Enhanced External Counterpulsation for Management of Postacute Sequelae of SARS-CoV-2 Associated Microvascular Angina and Fatigue: An Interventional Pilot Study.

Background: Postacute sequelae of SARS-CoV-2 infection (PASC) are a novel clinical syndrome characterized in part by endothelial dysfunction. Enhanced external counterpulsation (EECP) produces pulsatile shear stress, which has been associated with improvements in systemic endothelial function. Objective: To explore the effects of EECP on symptom burden, physical capacity, mental health, and health-related quality of life (HRQoL) in patients with PASC-associated angina and microvascular dysfunction (MVD). Methods: An interventional pilot study was performed, including 10 patients (male = 5, mean age 50.3 years) recruited from a tertiary specialized PASC clinic. Patients with angina and MVD, defined as index of microcirculatory resistance (IMR) ≥25 and/or diagnosed through stress perfusion cardiac magnetic resonance imaging, were included. Patients underwent one modified EECP course (15 one-hour sessions over five weeks). Symptom burden, six-minute walk test, and validated generic self-reported instruments for measuring psychological distress and HRQoL were assessed before and one month after treatment. Results: At baseline, most commonly reported PASC symptoms were angina (100%), fatigue (80%), and dyspnea (80%). Other symptoms included palpitations (50%), concentration impairment (50%), muscle pain (30%), and brain fog (30%). Mean IMR was 63.6. After EECP, 6MWD increased (mean 29.5 m, median 21 m) and angina and fatigue improved. Mean depression scores showed reduced symptoms (-0.8). Mean HRQoL scores improved in seven out of eight subscales (+0.2 to 10.5). Conclusions: Patients with PASC-associated angina and evidence of MVD experienced subjective and objective benefits from EECP. The treatment was well-tolerated. These findings warrant controlled studies in a larger cohort.

Prevalence and prognostic impact of left ventricular systolic dysfunction or pulmonary congestion after acute myocardial infarction.

AIMS: The aim was to describe the prevalence, characteristics, and outcome of patients with acute myocardial infarction (MI) developing left ventricular (LV) systolic dysfunction or pulmonary congestion by applying different criteria to define the population. METHODS AND RESULTS: In patients with MI included in the Swedish web-system for enhancement and development of evidence-based care in heart disease (SWEDEHEART) registry, four different sets of criteria were applied, creating four not mutually exclusive subsets of patients: patients with MI and ejection fraction (EF) < 50% and/or pulmonary congestion (subset 1); EF < 40% and/or pulmonary congestion (subset 2); EF < 40% and/or pulmonary congestion and at least one high-risk feature (subset 3, PARADISE-MI like); and EF < 50% and no diabetes mellitus (subset 4, DAPA-MI like). Subsets 1, 2, 3, and 4 constituted 31.6%, 15.0%, 12.8%, and 22.8% of all patients with MI (n = 87 177), respectively. The age and prevalence of different co-morbidities varied between subsets. For median age, 70 to 77, for diabetes mellitus, 22 to 33%; for chronic kidney disease, 22 to 38%, for prior MI, 17 to 21%, for atrial fibrillation, 7 to 14%, and for ST-elevations, 38 to 50%. The cumulative incidence of death or heart failure hospitalization at 3 years was 17.4% (95% CI: 17.1-17.7%) in all MIs; 26.9% (26.3-27.4%) in subset 1; 37.6% (36.7-38.5%) in subset 2; 41.8% (40.7-42.8%) in subset 3; and 22.6% (22.0-23.2%) in subset 4. CONCLUSIONS: Depending on the definition, LV systolic dysfunction or pulmonary congestion is present in 13-32% of all patients with MI and is associated with a two to three times higher risk of subsequent death or HF admission. There is a need to optimize management and improve outcomes for this high-risk population.

Dysregulations in hemostasis, metabolism, immune response, and angiogenesis in post-acute COVID-19 syndrome with and without postural orthostatic tachycardia syndrome: a multi-omic profiling study.

Post-acute COVID-19 (PACS) are associated with cardiovascular dysfunction, especially postural orthostatic tachycardia syndrome (POTS). Patients with PACS, both in the absence or presence of POTS, exhibit a wide range of persisting symptoms long after the acute infection. Some of these symptoms may stem from alterations in cardiovascular homeostasis, but the exact mechanisms are poorly understood. The aim of this study was to provide a broad molecular characterization of patients with PACS with (PACS + POTS) and without (PACS-POTS) POTS compared to healthy subjects, including a broad proteomic characterization with a focus on plasma cardiometabolic proteins, quantification of cytokines/chemokines and determination of plasma sphingolipid levels. Twenty-one healthy subjects without a prior COVID-19 infection (mean age 43 years, 95% females), 20 non-hospitalized patients with PACS + POTS (mean age 39 years, 95% females) and 22 non-hospitalized patients with PACS-POTS (mean age 44 years, 100% females) were studied. PACS patients were non-hospitalized and recruited ≈18 months after the acute infection. Cardiometabolic proteomic analyses revealed a dysregulation of ≈200 out of 700 analyzed proteins in both PACS groups vs. healthy subjects with the majority (> 90%) being upregulated. There was a large overlap (> 90%) with no major differences between the PACS groups. Gene ontology enrichment analysis revealed alterations in hemostasis/coagulation, metabolism, immune responses, and angiogenesis in PACS vs. healthy controls. Furthermore, 11 out of 33 cytokines/chemokines were significantly upregulated both in PACS + POTS and PACS-POTS vs. healthy controls and none of the cytokines were downregulated. There were no differences in between the PACS groups in the cytokine levels. Lastly, 16 and 19 out of 88 sphingolipids were significantly dysregulated in PACS + POTS and PACS-POTS, respectively, compared to controls with no differences between the groups. Collectively, these observations suggest a clear and distinct dysregulation in the proteome, cytokines/chemokines, and sphingolipid levels in PACS patients compared to healthy subjects without any clear signature associated with POTS. This enhances our understanding and might pave the way for future experimental and clinical investigations to elucidate and/or target resolution of inflammation and micro-clots and restore the hemostasis and immunity in PACS.

Adverse events and their management during enhanced external counterpulsation treatment in patients with refractory angina pectoris: observations from a routine clinical practice.

AIMS: Enhanced external counterpulsation (EECP) is a non-invasive treatment (35 one-hour sessions) for patients with refractory angina pectoris (RAP). To avoid interruption of treatment, more knowledge is needed about potential adverse events (AE) of EECP and their appropriate management. To describe occurrence of AE and clinical actions related to EECP treatment in patients with RAP and compare the distribution of AE between responders and non-responders to treatment. METHODS AND RESULTS: A retrospective study was conducted by reviewing medical records of 119 patients with RAP who had undergone one EECP treatment and a 6-min-walk test pre- and post-treatment. Sociodemographic, medical, and clinical data related to EECP were collected from patients' medical records. An increased walking distance by 10% post-treatment, measured by 6-min-walk test, was considered a responder. The treatment completion rate was high, and the occurrence of AE was low. Adverse events occurred more often in the beginning and gradually decreased towards the end of EECP treatment. The AE were either device related (e.g. muscle pain/soreness) or non-device related (e.g. bradycardia). Medical (e.g. medication adjustments) and/or nursing (e.g. extra padding around the calves, wound dressing) actions were used. The AE distribution did not differ between responders (n = 49, 41.2%) and non-responders. Skin lesion/blister occurred mostly in responders and paraesthesia occurred mostly in non-responders. CONCLUSION: Enhanced external counterpulsation appears to be a safe and well-tolerated treatment option in patients with RAP. However, nurses should be attentive and flexible to meet their patients' needs to prevent AE and early termination of treatment.

Transradial versus trans-femoral access site in high-speed rotational atherectomy in Sweden.

BACKGROUND: Radial artery is the preferred access site in contemporary percutaneous coronary intervention (PCI). However, limited data exist regarding utilization pattern, safety, and long-term efficacy of transradial artery access (TRA) PCI in heavily calcified lesions using high-speed rotational atherectomy (HSRA). METHODS: All patients who underwent HSRA-PCI in Sweden between 2005 and 2016 were included. Outcomes were major adverse cardiac events (MACE, including death, myocardial infarction (MI) or target vessel revascularisation (TVR)), in-hospital bleeding and restenosis. Inverse probability of treatment weighting was used to adjust for the non-randomized access site selection. RESULTS: We included 1479 patients of whom 649 had TRA and 782 transfemoral artery access (TFA) HSRA-PCI. The rate of TRA increased significantly by 18% per year but remained lower in HSRA-PCI (60%) than in the overall PCI population (85%) in 2016. TRA was associated with comparable angiographic success but significantly lower risk for major (adjusted OR 0.16; 95% CI 0.05-0.47) or any in-hospital bleeding (adjusted OR 0.32; 95% CI 0.13-0.78). At one year, the adjusted risk for MACE (HR 0.87; 95% CI 0.67-1.13) and its individual components did not differ between TRA and TFA patients. The risk for restenosis did not significantly differ between TRA and TFA HSRA-PCI treated lesions (adjusted HR 0.92; 95% CI 0.46-1.81). CONCLUSION: HSRA-PCI by TRA was associated with significantly lower risk for in-hospital bleeding and equivalent long-term efficacy when compared with TFA. Our data support the feasibility and superior safety profile of TRA in HSRA-PCI.

Predictors of treatment benefits after enhanced external counterpulsation in patients with refractory angina pectoris.

BACKGROUND: Enhanced external counterpulsation (EECP) is a noninvasive treatment that can decrease limiting symptoms in patients with refractory angina pectoris (RAP). Identifying responders to EECP is important as EECP is not widely available and relatively time intensive. HYPOTHESIS: The effect of EECP treatment on physical capacity in patients with RAP can be predicted from baseline patient characteristics and clinical factors. METHODS: This explorative study includes all patients from a cardiology clinic who had finished one EECP treatment and a 6 min walk test pre and post EECP. Clinical data, including Canadian Cardiovascular Society (CCS) classification and left ventricular ejection fraction (LVEF), were assessed before treatment. If patients increased their 6 min walking distance (6MWD) by 10% post EECP, they were considered responders. RESULTS: Of the 119 patients (men = 97, 40-91 years), 49 (41.2%) were responders. Multinomial regression analysis showed that functional status (i.e., CCS class ≥3) (OR 3.10, 95% CI 1.12-8.57), LVEF <50% (OR 2.82, 95% CI 1.02-7.80), and prior performed revascularization (i.e., ≤ 1 type of intervention) (OR 2.77, 95% CI 1.06-7.20) were predictors of response to EECP (p < .05, Accuracy 63.6%). Traditional risk factors (e.g., gender, smoking, and comorbidities) did not predict response. CONCLUSIONS: EECP treatment should be considered preferentially for patients that have a greater functional impairment, evidence of systolic left ventricular dysfunction, and exposure to fewer types of revascularization, either PCI or CABG. Improvement in 6MWD post EECP could imply improvement in physical capacity, which is a likely contributor to improved well-being among patients with RAP.

Adherence to beta-blockers and long-term risk of heart failure and mortality after a myocardial infarction.

AIMS: The aim of this study is to investigate the association between adherence to beta-blocker treatment after a first acute myocardial infarction (AMI) and long-term risk of heart failure (HF) and death. METHODS AND RESULTS: All patients admitted for a first AMI included in the nationwide Swedish web-system for enhancement and development of evidence-based care in heart disease evaluated according to recommended therapies register between 2005 and 2010 were eligible (n = 71 638). After exclusion of patients who died in-hospital, patients with previous HF, patients with unknown left ventricular ejection fraction (EF), and patients who died during the first year after the index event, 38 608 patients remained in the final analysis. Adherence to prescribed beta-blockers was determined for 1 year after the index event using the national registry for prescribed drugs and was measured as proportion of days covered, the ratio between the numbers of days covered by the dispensed prescriptions and number of days in the period. As customary, a threshold level for proportion of days covered ≥80% was used to classify patients as adherent or non-adherent. At discharge 90.6% (n = 36 869) of all patients were prescribed a beta-blocker. Among 38 608 1 year survivors, 31.1% (n = 12 013) were non-adherent to beta-blockers. Patients with reduced EF with and without HF were more likely to remain adherent to beta-blockers at 1-year compared with patients with normal EF without HF (NEF). Being married/cohabiting and having higher income level, hypertension, ST-elevation MI, and percutaneous coronary intervention were associated with better adherence. Adherence was independently associated with lower all-cause mortality [hazard ratio (HR) 0.77, 95% confidence interval [CI] 0.71-0.84] and a lower risk for the composite of HF readmission/death, (HR 0.83, 95% CI 0.78-0.89, P value <0.001) during the subsequent 4 years of follow up. These associations were favourable but less apparent in patients with HFNEF and NEF. CONCLUSIONS: Nearly one in three AMI patients was non-adherent to beta-blockers within the first year. Adherence was independently associated with improved long-term outcomes; however, uncertainty remains for patients with HFNEF and NEF.

Prasugrel versus ticagrelor in patients with myocardial infarction undergoing percutaneous coronary intervention.

OBJECTIVE: The comparative efficacy and safety of prasugrel and ticagrelor in patients with myocardial infarction (MI) treated with percutaneous coronary intervention (PCI) remain unclear. We aimed to investigate the association of treatment with clinical outcomes. METHODS: In the SWEDEHEART (Swedish Web-system for enhancement and development of evidence-based care in heart disease evaluated according to recommended therapies) registry, all patients with MI treated with PCI and discharged on prasugrel or ticagrelor from 2010 to 2016 were included. Outcomes were 1-year major adverse cardiac and cerebrovascular events (MACCE, death, MI or stroke), individual components and bleeding. Multivariable adjustment, inverse probability of treatment weighting (IPTW) and propensity score matching (PSM) were used to adjust for confounders. RESULTS: We included 37 990 patients, 2073 in the prasugrel group and 35 917 in the ticagrelor group. Patients in the prasugrel group were younger, more often admitted with ST elevation MI and more likely to have diabetes. Six to twelve months after discharge, 20% of patients in each group discontinued the P2Y12 receptor inhibitor they received at discharge. The risk for MACCE did not significantly differ between prasugrel-treated and ticagrelor-treated patients (adjusted HR 1.03, 95% CI 0.86 to 1.24). We found no significant difference in the adjusted risk for death, recurrent MI or stroke alone between the two treatments. There was no significant difference in the risk for bleeding with prasugrel versus ticagrelor (2.5% vs 3.2%, adjusted HR 0.92, 95% CI 0.69 to 1.22). IPTW and PSM analyses confirmed the results. CONCLUSION: In patients with MI treated with PCI, prasugrel and ticagrelor were associated with similar efficacy and safety during 1-year follow-up.

Acute versus chronic myocardial injury and long-term outcomes.

OBJECTIVE: There is a paucity of data regarding prognosis in patients with acute versus chronic myocardial injury for long-term outcomes. We hypothesised that patients with chronic myocardial injury have a similar long-term prognosis as patients with acute myocardial injury. METHODS: In an observational cohort study of 22 589 patients who had high-sensitivity cardiac troponin T (hs-cTnT) measured in the emergency department during 2011-2014, we identified all patients with level >14 ng/L and categorised them as acute myocardial injury, type 1 myocardial infarction (T1MI), type 2 myocardial infarction (T2MI) or chronic myocardial injury through adjudication. We estimated adjusted HRs with 95% CIs for the primary outcome all-cause mortality and secondary outcomes MI, and heart failure in patients with acute myocardial injury, T1MI and T2MI compared with chronic myocardial injury. RESULTS: In total, 3853 patients were included. During 3.9 (±2) years of follow-up, 48%, 24%, 44% and 49% of patients with acute myocardial injury, T1MI, T2MI and chronic myocardial injury died, respectively. Patients with acute myocardial injury had higher adjusted risks of death (1.21, 95% CI 1.08 to 1.36) and heart failure (1.24, 95% CI 1.07 to 1.43), but a similar risk for myocardial infarction (MI) compared with the reference group. Patients with T1MI had a lower adjusted risk of death (0.86, 95% CI 0.74 to 1.00) and higher risk of MI (2.09, 95% CI 1.62 to 2.68), but a similar risk of heart failure. Patients with T2MI had a higher adjusted risk of death (1.46, 95% CI 1.18 to 1.80) and heart failure (1.30, 95% CI 1.00 to 1.69) compared with patients with chronic myocardial injury. CONCLUSIONS: Absolute long-term risks for death are similar, and adjusted risks are slightly higher, among patients with acute myocardial injury and T2MI, respectively, compared with chronic myocardial injury. The lowest risk of long-term mortality was found in patients with T1MI. Both acute and chronic myocardial injury are associated with very high risks of adverse outcomes.

Risk and predictors of readmission for heart failure following a myocardial infarction between 2004 and 2013: A Swedish nationwide observational study.

BACKGROUND: Data are scarce regarding the risk, temporal trends and predictors of late-onset heart failure (LOHF) after acute myocardial infarction (AMI). We aimed at studying the risk and predictors of LOHF and the composite event of LOHF or death after AMI. METHODS: AMI patients first entered in the nationwide SWEDEHEART registry between 2004 and 2013 were included. Patients with a prior history of heart failure (HF) and those who died in-hospital were excluded. Dates and ICD-codes for LOHF in the national patient and death registries were used to determine time to first readmission due to LOHF and/or death. RESULTS: A total of 150,566 AMI patients were included in the analysis. The 1-year, 2-year and 5-year cumulative risk of developing LOHF were 11.4%, 14.6% and 21.8% respectively. The risk of LOHF within 2years decreased from 15.5% to 14.4% (2004-2005 vs 2010-2011), p<0.001. Calendar year was protective of LOHF/death after adjustment (HR 0.96, 95% CI 0.94-0.98, p<0.001). In-hospital HF, age, diabetes mellitus, chronic kidney disease, peripheral arterial disease, chronic obstructive pulmonary disease and atrial fibrillation, were strong predictors of LOHF. Risk profile improved and use of evidence based therapies increased during the time period. CONCLUSIONS: Survivors of AMI remain at a continued risk of LOHF. However, the overall risk of LOHF shows a decreasing trend after an index AMI over time. Lower risk of LOHF may relate to decreasing burden of comorbidities and increasing use of evidence based treatments.

Intravenous beta-blocker therapy in ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention is not associated with benefit regarding short-term mortality: a Swedish nationwide observational study.

AIMS: Our aim was to investigate the impact of intravenous (IV) beta-blocker therapy on short-term mortality and other in-hospital events in patients with ST-segment elevation myocardial infarction (STEMI) treated with dual antiplatelet therapy (DAPT) and primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: Using the nationwide Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies (SWEDEHEART) registry, we identified all patients with STEMI undergoing PCI between 2006 and 2013. Patients with cardiogenic shock and cardiac arrest at presentation were excluded. The primary endpoint was mortality within 30 days. Secondary endpoints were in-hospital events (mortality, cardiogenic shock and left ventricular ejection fraction [LVEF] <40% at discharge). We adjusted for confounders with a multivariable model and propensity score matching. Out of 16,909 patients, 2,876 (17.0%) were treated with an IV beta-blocker. After adjusting for confounders, the IV beta-blocker group had higher 30-day all-cause mortality (HR: 1.44, 95% CI: 1.14-1.83), more in-hospital cardiogenic shock (OR: 1.53, 95% CI: 1.09-2.16) and were more often discharged with an LVEF <40% (OR: 1.70, 95% CI: 1.51-1.92). CONCLUSIONS: In this large nationwide observational study, the use of IV beta-blockers in patients with STEMI treated with primary PCI was associated with higher short-term mortality, lower LVEF at discharge, as well as a higher risk of in-hospital cardiogenic shock.

Heart failure with normal ejection fraction is uncommon in acute myocardial infarction settings but associated with poor outcomes: a study of 91,360 patients admitted with index myocardial infarction between 1998 and 2010.

AIM: Data are scant on the incidence and prognosis of heart failure (HF) with normal ejection fraction (HFNEF, EF >49%) in an acute myocardial infarction (AMI) setting. The aim of this study was to examine incidence and predictors of HFNEF during an index acute myocardial infarction (AMI) and its subsequent associations with patient outcomes. METHODS AND RESULTS: This study analysed 91 360 patients with LVEF data from the SWEDEHEART registry on consecutive AMI patients between 1998 and 2010. Echocardiography or LV angiography was used to assess LVEF. In-hospital HF diagnoses required presence of crackles, and use of i.v. diuretics or inotropic drugs during admission. Among HF patients, the proportion of HFNEF patients increased (from 18% to 31%) during the period. Incidence of HFNEF in the AMI population remained fairly unchanged (from 7.7% to 8.1%). In contrast, the proportion of HF patients with reduced EF (HFREF, EF ≤49%) declined (from 47% to 26%), as did the proportion of REF patients without HF (from 20% to 16%). AMI patients with NEF without HF increased (from 25% to 50%). HFREF and HFNEF patients showed considerably higher long-term mortality compared with patients with no HF, irrespective of EF [the HFREF and HFNEF hazard ratio, compared with NEF, was 4.5 (4.4-4-6) and 3.3 (3.1-3.4), respectively, and 1.6 (1.5-1.65) for REF]. The adjusted HFNEF hazard ratio, compared with NEF, was 1.9 (1.8-2.0). Age, female gender, diabetes mellitus, hypertension, AF, and chronic kidney disease were strong predictors of HFNEF (P < 0.001). CONCLUSION: The proportion of AMI patients with HFNEF is constant over time. HFNEF patients have a considerably worse long-term prognosis compared with patients without clinical HF, irrespective of EF.