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Importance: Sodium glucose cotransporter 2 inhibitors reduce morbidity and mortality in patients with heart failure and reduced ejection fraction (HFrEF). Clinicians may find estimates of the projected long-term benefits of sodium glucose cotransporter 2 inhibitors a helpful addition to clinical trial results when communicating the benefits of this class of drug to patients. Objective: To estimate the projected long-term treatment effects of dapagliflozin in patients with HFrEF over the duration of a patient’s lifetime. Design, Setting, and Participants: Exploratory analysis was performed of Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure (DAPA-HF), a phase 3 randomized, placebo-controlled clinical trial conducted at 410 sites in 20 countries. Patients with an ejection fraction less than or equal to 40% in New York Heart Association functional classification II to IV and elevated plasma levels of N-terminal pro B-type natriuretic peptide were enrolled between February 15, 2017, and August 17, 2018, with final follow-up on June 6, 2019. Mean (SD) duration of follow-up was 17.6 (5.2) months. Interventions: Dapagliflozin, 10 mg, once daily vs placebo in addition to standard therapy. Main Outcomes and Measures: The primary composite outcome was time to first hospitalization for heart failure, urgent heart failure visit requiring intravenous therapy, or cardiovascular death. The trial results were extrapolated to estimate the projected long-term treatment effects of dapagliflozin over the duration of a patient’s lifetime for the primary outcome and the secondary outcome of death from any cause. Results: A total of 4744 patients (1109 women [23.4%]; 3635 men [76.6%]) were randomized in DAPA-HF, with a mean (SD) age of 66.3 (10.9) years. The extrapolated mean event-free survival for an individual aged 65 years from a primary composite end point event was 6.2 years for placebo and 8.3 years for dapagliflozin, representing an event-free survival time gain of 2.1 years (95% CI, 0.8-3.3 years; P = .002). When considering death from any cause, mean extrapolated life expectancy for an individual aged 65 years was 9.1 years for placebo and 10.8 years for dapagliflozin, with a gain in survival of 1.7 years (95% CI, 0.1-3.3; P = .03) with dapagliflozin. Similar results were seen when extrapolated across the age range studied. In analyses of subgroups of patients in DAPA-HF, consistent benefits were seen with dapagliflozin on both event-free and overall survival. Conclusions and Relevance: These findings indicate that dapagliflozin provides clinically meaningful gains in extrapolated event-free and overall survival. These findings may be helpful in communicating the benefits of this treatment to patients with HFrEF. Trial registration: ClinicalTrials.gov Identifier: NCT03036124.

Background: Patients with chest pain are risk-stratified using serial high-sensitivity troponin (T) assays (hsTnT). Those with change in (Δ)hsTnT

Background: Sodium-glucose cotransporter 2 inhibitors reduce the risk of heart failure hospitalization and cardiovascular death in patients with heart failure and reduced ejection fraction (HFrEF). However, their effects on cardiac structure and function in HFrEF are uncertain. Methods: We designed a multicenter, randomized, double-blind, placebo-controlled trial (the SUGAR-DM-HF trial [Studies of Empagliflozin and Its Cardiovascular, Renal and Metabolic Effects in Patients With Diabetes Mellitus, or Prediabetes, and Heart Failure]) to investigate the cardiac effects of empagliflozin in patients in New York Heart Association functional class II to IV with a left ventricular (LV) ejection fraction ≤40% and type 2 diabetes or prediabetes. Patients were randomly assigned 1:1 to empagliflozin 10 mg once daily or placebo, stratified by age ( Results: From April 2018 to August 2019, 105 patients were randomly assigned: mean age 68.7 (SD, 11.1) years, 77 (73.3%) male, 82 (78.1%) diabetes and 23 (21.9%) prediabetes, mean LV ejection fraction 32.5% (9.8%), and 81 (77.1%) New York Heart Association II and 24 (22.9%) New York Heart Association III. Patients received standard treatment for HFrEF. In comparison with placebo, empagliflozin reduced LV end-systolic volume index by 6.0 (95% CI, –10.8 to –1.2) mL/m 2 ( P =0.015). There was no difference in LV global longitudinal strain. Empagliflozin reduced LV end-diastolic volume index by 8.2 (95% CI, –13.7 to –2.6) mL/m 2 ( P =0.0042) and reduced N-terminal pro-B-type natriuretic peptide by 28% (2%–47%), P =0.038. There were no between-group differences in other cardiovascular magnetic resonance measures, diuretic intensification, Kansas City Cardiomyopathy Questionnaire Total Symptom Score, 6-minute walk distance, or B-lines. Conclusions: The sodium-glucose cotransporter 2 inhibitor empagliflozin reduced LV volumes in patients with HFrEF and type 2 diabetes or prediabetes. Favorable reverse LV remodeling may be a mechanism by which sodium-glucose cotransporter 2 inhibitors reduce heart failure hospitalization and mortality in HFrEF. Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03485092.

Supplemental Digital Content is available in the text., Background: The resistive reserve ratio (RRR) expresses the ratio between basal and hyperemic microvascular resistance. RRR measures the vasodilatory capacity of the microcirculation. We compared RRR, index of microcirculatory resistance (IMR), and coronary flow reserve (CFR) for predicting microvascular obstruction (MVO), myocardial hemorrhage, infarct size, and clinical outcomes, after ST-segment–elevation myocardial infarction. Methods: In the T-TIME trial (Trial of Low-Dose Adjunctive Alteplase During Primary PCI), 440 patients with acute ST-segment–elevation myocardial infarction from 11 UK hospitals were prospectively enrolled. In a subset of 144 patients, IMR, CFR, and RRR were measured post-primary percutaneous coronary intervention. MVO extent (% left ventricular mass) was determined by cardiovascular magnetic resonance imaging at 2 to 7 days. Infarct size was determined at 3 months. One-year major adverse cardiac events, heart failure hospitalizations, and all-cause death/heart failure hospitalizations were assessed. Results: In these 144 patients (mean age, 59±11 years, 80% male), median IMR was 29.5 (interquartile range: 17.0–55.0), CFR was 1.4 (1.1–2.0), and RRR was 1.7 (1.3–2.3). MVO occurred in 41% of patients. IMR>40 was multivariably associated with more MVO (coefficient, 0.53 [95% CI, 0.05–1.02]; P=0.031), myocardial hemorrhage presence (odds ratio [OR], 3.20 [95% CI, 1.25–8.24]; P=0.016), and infarct size (coefficient, 5.05 [95% CI, 0.84–9.26]; P=0.019), independently of CFR≤2.0, RRR≤1.7, myocardial perfusion grade≤1, and Thrombolysis in Myocardial Infarction frame count. RRR was multivariably associated with MVO extent (coefficient, −0.60 [95% CI, −0.97 to −0.23]; P=0.002), myocardial hemorrhage presence (OR, 0.34 [95% CI, 0.15–0.75]; P=0.008), and infarct size (coefficient, −3.41 [95% CI, −6.76 to −0.06]; P=0.046). IMR>40 was associated with heart failure hospitalization (OR, 5.34 [95% CI, 1.80–15.81] P=0.002), major adverse cardiac events (OR, 4.46 [95% CI, 1.70–11.70] P=0.002), and all-cause death/heart failure hospitalization (OR, 4.08 [95% CI, 1.55–10.79] P=0.005). RRR was associated with heart failure hospitalization (OR, 0.44 [95% CI, 0.19–0.99] P=0.047). CFR was not associated with infarct characteristics or clinical outcomes. Conclusions: In acute ST-segment–elevationl infarction, IMR and RRR, but not CFR, were associated with MVO, myocardial hemorrhage, infarct size, and clinical outcomes. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02257294.

No abstract available.

Background— Galectin-3 is a biomarker associated with inflammation and fibrosis that predicts adverse outcome and relates to biomarkers of extracellular matrix turnover in patients with heart failure, particularly when left ventricular (LV) systolic function is preserved. Whether galectin-3 is related to LV remodeling after acute myocardial infarction is unknown. Methods and Results— Circulating galectin-3 and various extracellular matrix biomarkers were measured in 100 patients (age, 58.9±12.0 years; 77% men) admitted with acute myocardial infarction and LV dysfunction, at baseline (mean 46 hours) and at 24 weeks, with cardiac MRI at each time-point. LV remodeling was defined as change in LV end-systolic volume index. Relationships among galectin-3, biomarkers, and LV remodeling were analyzed across the entire cohort, then according to median baseline LV ejection fraction. Galectin-3 levels were elevated in 22 patients (22%) at baseline and increased significantly over time from 14.7±5.5 to 16.3±6.6 ng/mL ( P =0.007). Baseline galectin-3 did not correlate with any LV parameters at baseline or change in any parameter over time. Galectin-3 was positively associated with remodeling in patients with supramedian baseline LV ejection fraction (ie, >49.2%; r =0.40; P =0.01) but not when LV ejection fraction was ≤49.2%. Galectin-3 correlated significantly with matrix metalloproteinase-3 and monocyte chemoattractant protein-1 at baseline, biomarkers that have been shown to relate to LV remodeling in this cohort. Conclusions— Galectin-3 correlated significantly with certain biomarkers involved in extracellular matrix turnover, although no definite relationship was identified with LV remodeling. Whether galectin-3 plays a pathological role in remodeling remains unclear but merits further study. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00132093.

I read with interest the article by Bagai et al1 titled “Individualizing Duration of Dual Antiplatelet Therapy After Acute Coronary Syndrome or Percutaneous Coronary Intervention.” The authors suggest that after acute coronary syndrome for those deemed not at high risk of bleeding, “extended DAPT beyond 1 year is advised,” …

In patients with cardiovascular disease, a high pulse pressure is related to an increased risk of cardiovascular events but in patients with advanced heart failure, a low pulse pressure is predictive of adverse (cardiovascular) events.We studied the prognostic importance of pulse pressure in a group of post-myocardial infarction patients, with and without signs and symptoms of heart failure. Subjects had been randomised in the CAPRICORN clinical trial, and followed up for a mean of 1.3 years.Blood pressure was measured in 1,955 patients with a left ventricular ejection fraction a parts per thousand currency sign40%, between 3 and 21 days post myocardial infarction. Cox proportional survival models were reproduced for those with Killip Class I (n = 1342) versus classes II/III/IV heart failure (n = 613).Overall mean (SD) age was 63 (12) years, mean (SD) left ventricular ejection fraction 33(6)%, mean (SD) baseline blood pressure was 121 (17)/74 (10) mmHg and most (73%) were male. In patients with Killip Class 1, pulse pressure was not predictive for any outcome. However, in patients with Killip Class II-IV, a low pulse pressure independently predicted all cause mortality (HR 0.83 per 10 mmHg, CI 0.71-0.98, p = 0.025), cardiovascular mortality (HR 0.83 per 10 mmHg, CI 0.70-0.98, p = 0.025) and sudden death (HR 0.77 per 10 mmHg, CI 0.60-1.00, p = 0.047). A lower pulse pressure did not predict hospitalisation for worsening heart failure.A low pulse pressure is an independent predictor of mortality in subjects with depressed left ventricular ejection fraction after a recent myocardial infarction and evidence of Killip Class II-IV heart failure.

Aims Apelin, a novel peptide with a putative role in cardiovascular homeostasis, has gained interest as an endogenous inotrope, but has yet to be described following acute myocardial infarction (AMI) in man. We aimed to characterize plasma apelin concentrations following AMI and to examine its relationship with clinical and prognostic biomarkers. Methods and results Plasma concentrations of apelin, N-terminal probrain natriuretic peptide (NT-proBNP), norepinephrine, and arginine vasopressin were measured in 100 patients [mean age 58.9 ± 12 (SD) years, 77% male] admitted with AMI, with echocardiographic left ventricular (LV) ejection fraction

Objectives: All patients should undergo formal assessment of ventricular function following acute myocardial infarction (AMI). Cardiac magnetic resonance (CMR) is not widely used as a test before discharge in AMI patients. This study sought to determine the impact of contrast-enhanced CMR (ceCMR) scanning before discharge in addition to standard transthoracic echocardiography (TTE) on patient care following AMI. Methods: 100 patients admitted with AMI, all of whom had a left ventricular ejection fraction (LVEF) Results: Each patient (77% male, mean age 58.9 years, SD 12) underwent TTE and ceCMR at a mean 1.4 (range 0.8–3.2) and 4.2 days (range 2–11), respectively, following admission. ceCMR significantly influenced the management of 24/100 (24%) of the patient cohort, through detection of LV thrombus, right ventricular infarction, intracardiac neoplasia, and a variety of intrathoracic and intra-abdominal pathology. There were no issues regarding safety in this high-risk group of patients. Conclusion: In a cohort of AMI patients with reduced LVEF, ceCMR scanning before discharge improved the management of 24% of the cohort. ceCMR is a useful and safe adjunct to standard care after AMI.

Renal dysfunction is a frequent and progressive complication of chronic heart failure and is a powerful predictor of cardiovascular mortality. It is intimately associated with cardiovascular disease even in its earliest stages. Although cardiovascular and renal disease share many risk factors, the prognostic implications do not simply reflect widespread atherosclerotic vascular disease as this appears to be as important in those with heart failure secondary to idiopathic dilated cardiomyopathy as it is in those with coronary artery disease. There may be a role in the progression of heart failure, as the deleterious effects of even "mild" renal impairment seem to be borne out in predicting outcome, in a broad range of heart failure patients including those with heart failure and preserved systolic function. Renal dysfunction is both an indication for, as well as frequently limiting intervention with intensive disease modifying therapy. Although renal impairment is common in heart failure and these patients are at higher risk for adverse events including death, they are under represented in clinical trials.

Aims An increased pulse pressure (PP) has consistently predicted increased cardiovascular morbidity and mortality in cardiovascular risk patients and mild chronic heart failure (CHF). In contrast, a decreased PP was related to increased mortality in patients with acute decompensated heart failure. However, the predictive value of PP in patients with advanced CHF is not known.Methods and results PP was analysed for its effect on mortality, adjusting for other modifiers of risk, using Cox proportional hazards regression analysis of data collected from 1901 patients with New York Heart Association Class III or IV CHF (mean age 65 and mean ejection fraction 0.26). Natriuretic peptides were measured in a subgroup. Multivariable Cox-regression analysis demonstrated that lower PP was associated with an increased mortality [hazard ratio (HR) 0.91 per 10 mmHg; 0.93-0.99], independent of mean arterial pressure (MAP) and other well known prognostic markers. In patients with a PP below the median value of 45 mmHg, PP was a stronger predictor of mortality than MAP (HR for PP 0.80 per 10 mmHg; 0.64-0.99). In patients with a PP above the median value of 45 mmHg, MAP was a stronger predictor of mortality than PP (HR for MAP 0.83 per 10 mmHg increase; 0.72-0.95). In addition, lower PP was independently related to increased atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP).Conclusion In patients with advanced CHF, low PP is an independent predictor of mortality. In addition, low PP was related to increased levels of ANP and BNP.

Beygui et al. [(1)][1] deserve credit for demonstrating, through the ALBATROSS (Aldosterone Lethal Effects Blockade in Acute Myocardial Infarction Treated With or Without Reperfusion to Improve Outcome and Survival at Six Months Follow-up) study, that the beneficial effects on cardiovascular

Advances in the understanding of genetic aspects of cardiovascular diseases, together with an increase in the availability of genetic analysis, have resulted in not only increased diagnosis of known inherited conditions, but also the identification of novel syndromes. The combination of potassium-sensitive periodic paralysis, ventricular arrhythmias and dysmorphism, initially described by Andersen and Tawil, represents such a novel condition. We report a case in which genetic analysis led to the diagnosis of Andersen-Tawil syndrome after 15 years of protracted non-invasive and invasive investigations from initial presentation to ultimate diagnosis in a young female. In conclusion, we describe the clinical and genetic features of Andersen-Tawil syndrome and demonstrate the utility of genetic testing in the diagnosis of cardiovascular disease.

AimsA low pulse pressure (PP) may reflect poor cardiac output (CO), but has not been well characterized by invasive haemodynamic studies.MethodsWe investigated the relationship between PP and cardiac index (CI) in patients with cardiovascular disease including those with normal and impaired cardiac function. Cardiac catheterization data from 1897 patients was analysed.ResultsMean age was 59 years; 57% were men, mean (SD) PP was 65 (25) mmHg and mean (SD) CI was 2.9 (0.8) l/min/m(2). Correlation between CI and PP was absent if the CI was more than 3 l/min/m(2), with a weak correlation if CI was between 2 and 3 l/min/m(2) (r = 0.161; P ConclusionIn patients with a CI of less than 3 l/min/m(2), a low PP is a marker of a low CI. In patients with severe heart failure and a low CO, PP pressure might be useful as a 'poor-man's' surrogate of CO.

Atrial fibrillation increases the risk of systemic thromboembolism in general and stroke in particular. Not all patients who develop atrial fibrillation are at significantly heightened risk of thromboembolic complications, however, with the development of risk scoring systems aiding clinicians in determining whether formal anticoagulation is mandated. The most commonly used contemporary scoring systems—CHADS2and CHA2DS2-VASc—provide a reliable means of assessing stroke risk, but certain cardiac conditions are associated with an increased incidence of thromboembolism without impacting on these risk scores. Hypertrophic cardiomyopathy, with its apical variant, is such a condition. We present a case of a patient with apical hypertrophic cardiomyopathy and atrial fibrillation who suffered dire thromboembolic consequences despite a reassuringly low CHA2DS2-VASc score and suggest that this scoring system is modified to incorporate the thromboembolic risk inherent to certain cardiomyopathies irrespective of impairment of left ventricular systolic dysfunction or clinical heart failure.

We present a case of a 39-year-old man with Becker muscular dystrophy and severe congestive cardiac failure. Cardiac magnetic resonance imaging revealed subendocardial late gadolinium enhancement, similar to that seen in myocardial infarction. He had no risk factors for atherosclerotic coronary artery disease and coronary angiography was normal. We propose that regional subendocardial myocardial fibrosis which has been described histologically in the cardiomyopathy associated with Becker muscular dystrophy may resemble previous infarction at contrast enhanced cardiac magnetic resonance imaging.

Dr Januzzi raises several interesting points regarding galectin-3 levels after acute myocardial infarction. We found that galectin-3 increased modestly but significantly (by ≈12%) between baseline (≈day 2) and 24 weeks.1 Serial measurement of galectin-3 in healthy volunteers suggests a reference change value of the order of 61% for galectin-3.2 A recent analysis of serial galectin-3 levels in 2 chronic heart failure trials suggests, however, that a rise …

Background— Microvascular obstruction (MO) is associated with large acute myocardial infarction and lower left ventricular (LV) ejection fraction and predicts greater remodeling, but whether this effect is abolished by contemporary antiremodeling therapies is subject to debate. We examined the influence of several infarct characteristics, including MO, on LV remodeling in an optimally treated post–acute myocardial infarction cohort, using contrast-enhanced cardiac magnetic resonance. Methods and Results— One hundred patients (mean age, 58.9±12 years, 77%men) underwent contrast-enhanced cardiac magnetic resonance at baseline (≈4 days) and at 12 and 24 weeks. The effects on LV remodeling (ie, change in LV end-systolic volume index [ΔLVESVi]) of infarct site, transmurality, endocardial extent, and the presence of early and late MO were analyzed. Mean baseline infarct volume index decreased from 34.0 (21.2) mL/m 2 to 20.9 (12.9) mL/m 2 at 24 weeks ( P r =0.47, P r =0.26, P 2 , respectively, P =0.001); those with early MO only displayed an intermediate ΔLVESVi (−4.9 [13.0] mL/m 2 ). Importantly, late MO was seen frequently despite optimal coronary blood flow having been restored at angiography. Conclusions— Late MO on predischarge contrast-enhanced cardiac magnetic resonance remains an ominous predictor of adverse LV remodeling despite powerful antiremodeling therapy and may be useful in the risk stratification of survivors of acute myocardial infarction. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00132093.

The effects of several prescription and illicitly-used drugs on electrocardiographic repolarization are well documented, most frequently manifested as prolongation of the corrected QT (QTc) interval. The combination of multiple repolarization-modulating drugs taken in high dosage can occasionally lead to extreme abnormalities of the QTc interval and ST-segment on the surface ECG, which can lead to the erroneous diagnosis of underlying myocardial ischemia and inappropriate treatment. We report on one such case in which the acute management of a syncopal patient was detrimentally influenced by misinterpretation of a very unusual ECG. Copyright © 2010 Wiley Periodicals, Inc.

Left ventricular ejection fraction (LVEF) is a powerful prognostic marker after acute myocardial infarction and is dependent on infarct magnitude. Contrast-enhanced cardiac magnetic resonance (ceCMR) represents the current criterion standard means of LVEF and infarct size measurement. Infarct size and LVEF can be estimated from the 12-lead electrocardiogram (ECG) using the Selvester QRS score. We examined for the first time the relationship between serial measures of LVEF and infarct size by ceCMR and ECG in patients with reperfused anterior ST-elevation myocardial infarction (STEMI) and depressed LVEF.Thirty-four patients (mean +/- SD age, 59 +/- 11.8 years; 70.6% male) underwent ceCMR and simultaneous ECG at mean 93 hours after admission and at 12 and 24 weeks. The QRS score was calculated on each ECG, from which infarct size and LVEF were estimated and compared with the equivalent ceCMR measurements.Infarct size on ceCMR was higher than that by QRS score at each time-point (P.001) with modest correlation (r = 0.56-0.78, P.001). Left ventricular ejection fraction was consistently significantly higher on CMR than on ECG, with weak correlation (r = 0.37-0.51, P.05). We derived a novel equation relating QRS score to CMR-measured LVEF in the subacute phase of infarction: LVEF = 61 - (1.7 x QRS score) (%).In patients with reperfused anterior ST-elevation myocardial infarction and depressed LVEF, ceCMR is moderately correlated with the QRS in the serial measurement of infarct size and LVEF. Infarct size (measured by ceCMR) and LVEF are consistently higher than those calculated on the QRS score in the acute and subacute phases of infarction.

In patients with atherosclerotic disease, a high pulse pressure is an important predictor of cardiovascular events. However, in patients with chronic heart failure (CHF) a low pulse pressure is related to worse outcome, although no distinction was made between ischaemic and non ischaemic heart failure. We therefore aimed to compare the prognostic value of pulse pressure ( PP) between those with ischaemic and non ischaemic advanced heart failure.Method and results: Pulse pressure was analysed for its effect on mortality, adjusting for other modifiers of risk, using Cox proportional hazards regression analysis of data collected from 1901 patients with NYHA class III or IV heart failure ( mean age 65 years, mean ejection fraction 26%). In ischaemic heart failure ( n= 1118), low mean arterial pressure ( MAP) was an independent predictor of overall mortality ( Hazard Ratio ( HR) 0.88 per 10 mm Hg; p= 0.04), while pulse pressure was not. In contrast, in non ischaemic heart failure ( n= 783), a low pulse pressure was an independent predictor of overall mortality ( HR 0.84 per 10 mm Hg; p= 0.036), while mean arterial pressure was not. In addition, higher NYHA class and lower pulse pressure ( HR 0.87 per 10 mm Hg; p= 0.002) were the only independent predictors for first heart failure hospitalisation in both ischaemic and non ischaemic patients.Conclusion: Low pulse pressure is a readily obtainable risk marker of death in advanced non ischaemic heart failure. Mean arterial pressure remains an important component of blood pressure in predicting mortality, especially in those with heart failure of an ischaemic aetiology. It is postulated that pulse pressure may reflect a deleterious haemodynamic state, in non-atherosclerotic heart failure patients. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

Aims Aldosterone antagonism reduces cardiovascular morbidity and mortality in patients with left ventricular (LV) systolic dysfunction and heart failure or diabetes after acute myocardial infarction (AMI). The mechanism of this effect is unclear. We performed a contrast-enhanced cardiac magnetic resonance study to assess the effects of eplerenone on LV remodeling after AMI. Methods One hundred patients (mean age, 58.9 ± 12 years; 77% male) with LV systolic dysfunction but without heart failure or diabetes were randomized to 24 weeks' double-blind treatment with eplerenone or placebo started 1 to 14 days after AMI. Contrast-enhanced cardiac magnetic resonance was performed, and plasma concentrations of matrix metalloproteinase-2 (MMP-2) and MMP-9 were measured before randomization and at 12 and 24 weeks. Results Baseline LV ejection fraction was, by chance, significantly higher in eplerenone than in placebo-treated patients. Eplerenone had no effect on the primary end point (change in LV end-systolic volume index); after covariate adjustment, the primary end point fell by 6.1 ± 2.7 mL/m 2 with eplerenone compared to placebo ( P = .027), and LV end-diastolic volume index fell by 7.5 ± 3.4 mL/m 2 ( P = .031); eplerenone did not significantly influence LV ejection fraction. Eplerenone, after covariate adjustment, significantly decreased MMP-2 and increased MMP-9 over 24 weeks relative to placebo. Conclusions In a population of patients with AMI with high uptake of contemporary antiremodeling therapy, eplerenone provides modest incremental protection against LV remodeling, only after covariate adjustment.

A 63-year-old female received an implantable cardioverter defibrillator having been resuscitated from an out-of-hospital (ventricular fibrillation) cardiac arrest. She had pre-existent diagnoses of left ventricular dysfunction (ejection fraction 15%) and aortic valve and root replacement surgery; coronary angiography revealed modest, non-flow-limiting coronary artery disease only. She sustained significant hypoxic brain injury which improved during her admission to …

Introduction Microvascular obstruction (MVO) is associated with large acute myocardial infarction (AMI) and lower left ventricular (LV) ejection fraction, and predicts greater remodelling, but whether this effect is abolished by contemporary anti-remodelling therapies is subject to debate. We examined the influence of several infarct characteristics, including MVO, on LV remodelling in an optimally-treated post-AMI cohort enrolled in a clinical trial investigating the potential anti-remodelling effects of eplerenone, using contrast-enhanced cardiac magnetic resonance (ceCMR). Methods Hundred patients (mean age 58.9±12 years, 77% male) admitted with AMI in the previous 1-14 days underwent ceCMR at baseline (∼4 days), 12 and 24 weeks. The effects on LV remodelling (ie, change in LV end-systolic volume index (▵LVESVI)) of infarct site, transmurality, endocardial extent, and the presence of early and late MVO were analysed. Tests for interaction between MVO persistence and eplerenone therapy were also performed. Results Mean baseline infarct volume index decreased from 34.0 (21.2) ml/m2 to 20.9 (12.9) ml/m2 at 24 weeks (p Conclusions Late MVO on pre-discharge ceCMR remains an ominous predictor of adverse LV remodelling despite powerful anti-remodelling therapy, and may be useful in the risk-stratification of survivors of AMI. Eplerenone may attenuate remodelling more powerfully in patients at the highest risk of remodelling, that is, those with persistent MVO.