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Purpose Remote ischemic periconditioning (RIPC) has demonstrated cardioprotective effects and improved clinical outcomes as an adjunct to emergent percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). However, whether RIPC affects the cardiac sympathetic nerve activity in patients with STEMI remains unclear. This study investigated the effects of RIPC on cardiac sympathetic nerve activity in patients with STEMI. Methods We prospectively assigned patients with STEMI who underwent emergent PCI to receive RIPC or no procedure (control group) upon arrival at the cardiac catheterization laboratory. The primary endpoint was cardiac sympathetic nerve activity assessed through the washout rate (WR) in cardiac 123 I-metaiodobenzylguanidine ( 123 I-MIBG) imaging. Results Patients in the RIPC (n = 62) and control (n = 60) groups had similar demographic and clinical characteristics at baseline. Multivariable linear regression models revealed that the culprit lesion of the left anterior descending artery and hemoglobin level were significantly and independently associated with WR at discharge. WRs of the groups differed insignificantly at discharge. However, the RIPC group (n = 49) showed significantly lower WR than the control group (n = 47) at 1 year after discharge (p = 0.027). In the single-photon emission computed tomography analysis at 1 year after discharge, the RIPC group demonstrated significantly higher late uptake (p = 0.021) and lower WR (p = 0.013) in the nonculprit lesion, with a non-significant decrease in WR for the culprit lesion. Conclusion RIPC can suppress augmented cardiac sympathetic nerve activity in patients with STEMI, particularly in nonculprit lesions.

Background We aimed to evaluate the effect of early intravenous metoprolol treatment, microvascular obstruction (MVO), intramyocardial hemorrhage (IMH) and adverse left ventricular (LV) remodeling on the evolution of infarct and remote zone circumferential strain after acute anterior ST-segment elevation myocardial infarction (STEMI) with feature-tracking cardiovascular magnetic resonance (CMR). Methods A total of 191 patients with acute anterior STEMI enrolled in the METOCARD-CNIC randomized clinical trial were evaluated. LV infarct zone and remote zone circumferential strain were measured with feature-tracking CMR at 1 week and 6 months after STEMI. Results In the overall population, the infarct zone circumferential strain significantly improved from 1 week to 6 months after STEMI (− 8.6 ± 9.0% to − 14.5 ± 8.0%; P  < 0.001), while no changes in the remote zone strain were observed (− 19.5 ± 5.9% to − 19.2 ± 3.9%; P  = 0.466). Patients who received early intravenous metoprolol had significantly more preserved infarct zone circumferential strain compared to the controls at 1 week ( P  = 0.038) and at 6 months ( P  = 0.033) after STEMI, while no differences in remote zone strain were observed. The infarct zone circumferential strain was significantly impaired in patients with MVO and IMH compared to those without ( P  < 0.001 at 1 week and 6 months), however it improved between both time points regardless of the presence of MVO or IMH ( P  < 0.001). In patients who developed adverse LV remodeling (defined as ≥ 20% increase in LV end-diastolic volume) remote zone circumferential strain worsened between 1 week and 6 months after STEMI ( P  = 0.036), while in the absence of adverse LV remodeling no significant changes in remote zone strain were observed. Conclusions Regional LV circumferential strain with feature-tracking CMR allowed comprehensive evaluation of the sequelae of an acute STEMI treated with primary percutaneous coronary intervention and demonstrated long-lasting cardioprotective effects of early intravenous metoprolol. Trial registration ClinicalTrials.gov, NCT01311700 . Registered 8 March 2011 - Retrospectively registered.

BackgroundPrognosis in acute myocardial infarction (AMI) depends on the amount of infarct-related artery (IRA)-subtended myocardium and associated damage but has not been described in great detail. Consequently, we sought to describe IRA-associated pathophysiological consequences using cardiac magnetic resonance (CMR).Methods1235 AMI patients (n = 795 ST-elevation (STEMI) and 440 non-STEMI) underwent CMR following percutaneous coronary intervention. Blinded core-laboratory data were compared according to left anterior descending (LAD), left circumflex (LCx) and right coronary artery (RCA) regarding major adverse clinical events (MACE) within 12 months. Left ventricular (LV) global longitudinal/circumferential/radial (GLS/GCS/GRS) as well as left atrial (LA) total (εs), passive (εe) and active (εa) strains were determined using CMR-feature tracking. Tissue characterisation included infarct size (IS) and microvascular obstruction.ResultsLAD and LCx were associated with higher mortality compared to RCA lesions (4.6% and 4.4% vs 1.6%). LAD lesions showed largest IS (16.8%), largest ventricular [LV ejection fraction (EF) 47.4%, GLS − 13.2%, GCS − 20.8%] and atrial (εs 20.2%) impairment. There was less impairment in LCx (IS 11.8%, LVEF 50.8%, GLS − 17.4%, GCS − 25.0%, εs 20.7%) followed by RCA lesions (IS 11.3%, LVEF 50.8%, GLS − 19.1%, GCS − 26.6%, εs 21.7%). In AUC analyses, εs (LAD, RCA) and GLS (LCx) best predicted MACE (AUC > 0.69). Multivariate analyses identified εs (p = 0.017) in LAD and GLS (p = 0.034) in LCx infarcts as independent predictors of MACE.ConclusionsCMR allows IRA-specific phenotyping and characterisation of morphologic and functional changes. These alterations carry infarct-specific prognostic implications, and may represent novel diagnostic and therapeutic targets following AMI.Trial registrationClinicalTrials.gov: NCT00712101 and NCT01612312Graphic abstract

Background and aimsCurrent ESC guidelines on the management of patients after acute myocardial infarction only include the evaluation of left ventricular (LV) function by assessment of the ejection fraction in addition to clinical risk scores to estimate the patient’s prognosis. We aimed to determine, whether comprehensive evaluation of cardiac function using LV and right ventricular (RV) global longitudinal strain (GLS) and left atrial (LA) reservoir strain improves the prediction of survival in patients with acute myocardial infarction.MethodsIn patients with non-ST segment elevation or ST segment elevation myocardial infarction receiving echocardiography within 1 year after revascularisation, LV-GLS, RV-GLS and LA reservoir strain were quantified. In multivariable Cox regression analysis, HRs and 95% CIs were calculated per 1 SD increase in strain measure, adjusting for age, sex, systolic blood pressure, low-density lipoprotein cholesterol, smoking, diabetes and family history of premature coronary artery disease.ResultsDuring a median follow-up of 1.5 (0.5–4.2) years, 157 (11.1%) out of 1409 patients (64.4±13.5 years, 24.7% female) died. LV-GLS (1.68 (1.37–2.06), p<0.001), RV-GLS (1.39 (1.16–1.67), p<0.001) and LA reservoir strain (0.57 (0.47–0.69), p<0.001) were associated with mortality. Adding LV ejection fraction, tricuspid annular plane systolic excursion (TAPSE) or LA volume index to these models did not alter the association of strain measures of the LV (1.41 (1.06–1.89), p=0.02), RV (1.48 (1.03–2.13), p=0.04) or LA (0.61 (0.49–0.76), p<0.001). In receiver operating characteristics, combining the three strain measures improved the prediction of mortality above risk factors (AUC: 0.67 (0.63–0.71) to 0.75 (0.70–0.80)), while further addition of LV ejection fraction, TAPSE and LA volume index did not (0.75 (0.70–0.81)).ConclusionThe comprehensive evaluation of contractility of various cardiac chambers via transthoracic echocardiography using myocardial strain analysis, when routinely performed after acute myocardial infarction, may help to detect patients at increased mortality risk.

Cardiac rupture (CR) is a fatal complication of ST-elevation myocardial infarction (STEMI) with poor prognosis. The aim of this study was to develop and validate practical risk score to predict the CR after STEMI. A total of 11,234 STEMI patients from 7 centers in China were enrolled in our study, we firstly developed a simplified fast-track CR risk model from 7455 STEMI patients, and then prospectively validated the CR risk model using receiver-operating characteristic (ROC) curves by the other 3779 consecutive STEMI patients. This trial is registered with ClinicalTrials.gov, number NCT02484326. The incidence of CR was 2.12% (238/11,234), and the thirty-day mortality in CR patients was 86%. We developed a risk model which had 7 independent baseline clinical predictors (female sex, advanced age, anterior myocardial infarction, delayed admission, heart rate, elevated white blood cell count and anemia). The CR risk score system differentiated STEMI patients with incidence of CR ranging from 0.2% to 13%. The risk score system demonstrated good predictive value with area under the ROC of 0.78 (95% CI 0.73–0.84) in validation cohort. Primary percutaneous coronary intervention decreased the incidence of CR in high risk group (3.9% vs. 6.2%, p<0.05) and very high risk group (8.0% vs. 15.2%, p<0.05). A simple risk score system based on 7 baseline clinical variables could identify patients with high risk of CR, for whom appropriate treatment strategies can be implemented.

Left ventricular (LV) remodeling after myocardial infarction (MI) is a strong predictor of heart failure and mortality. The predictors of long-term remodeling after MI have been incompletely studied. We therefore examined the correlates of LV remodeling in patients with large ST-segment elevation myocardial infarction and a patent infarct artery after percutaneous 2coronary intervention (PCI) from the randomized Post-Myocardial Infarction Remodeling Prevention Therapy trial. Peri-infarct pacing had a neutral effect on long-term remodeling in patients with large first MI. The present analysis includes 109 patients in whom an open artery was restored after PCI, and in whom LV end-diastolic volume (LVEDV) at baseline and 18 months was assessed by transthoracic echocardiography. Multivariable models were fit to identify the independent predictors of LVEDV at baseline and 18 months. By multivariable analysis, male sex (p = 0.004) and anterior MI location (p = 0.03) were independently associated with baseline LVEDV. The following variables were independent predictors of increased LVEDV at 18 months: younger age (p = 0.01), male sex (p = 0.03), peak creatine phosphokinase (p = 0.03), shorter time from MI to baseline transthoracic echocardiography (p = 0.04), baseline LVEDV (p < 0.0001), and lack of statin use (p = 0.03). In conclusion, patients with large MI and an open infarct artery after PCI, anterior MI location, and male sex were associated with greater baseline LVEDV, but MI location was not associated with 18-month LVEDV. In contrast, younger age, peak creatine phosphokinase, male sex, baseline LVEDV, and lack of statin use were associated with long-term LV remodeling.

Objective To quantify the shape and strength of the association between heart rate (HR) recorded during the first 30 min of intensive-care admission and in-hospital death in contemporary acute myocardial infarction (AMI), after adjustment for modern reperfusion, pharmacotherapy, and haemodynamic variables. Methods We extracted 1,510 adults with a primary International Classification of Diseases, Ninth Revision (ICD-9) diagnosis of AMI (410.xx) from MIMIC-III (2008–2012). HR was defined as the mean of the first three electrocardiographic readings obtained within 30 min of ICU triage, before administration of rate-modifying drugs. We modelled HR both as clinically meaningful categories (< 60, 60–99, ≥ 100 bpm) and as a continuous exposure using restricted cubic splines (RCS). Multivariable logistic regression adjusted for age, sex, Killip class, systolic blood pressure, coronary revascularisation, β-blocker use, atrial fibrillation/flutter, hypertension, diabetes, chronic obstructive pulmonary disease, serum creatinine, haemoglobin, white blood cell count, sodium, potassium, glucose, platelet count and anion gap. Pre-specified subgroup analyses compared ST-elevation MI (STEMI) with non-ST-elevation ACS (NSTE-ACS). Results Mean age was 66.7 ± 13.9 years; 33.6% were women; STEMI accounted for 42%. Overall in-hospital mortality was 10.9%. HR ≥ 100 bpm (23% of patients) was associated with higher death risk (adjusted OR 2.45, 95% CI 1.56–3.85) versus 60–99 bpm. Bradycardia < 60 bpm (15%) was also associated with excess risk (adjusted OR 1.58, 95% CI 1.02–2.45), yielding a U-shaped RCS curve (non-linearity p  = 0.01). The HR–mortality gradient was steeper in STEMI than in NSTE-ACS (interaction p  = 0.04). Findings were robust after including the 46 patients who died within 24 h of admission. Conclusion Admission HR exhibits a U-shaped, independent relation with early mortality in modern AMI care; values outside 60–99 bpm identify high-risk patients despite urgent reperfusion and optimal medical therapy.

ObjectiveWe hypothesised that, compared with culprit-only primary percutaneous coronary intervention (PCI), additional preventive PCI in selected patients with ST-elevation myocardial infarction with multivessel disease would not be associated with iatrogenic myocardial infarction, and would be associated with reductions in left ventricular (LV) volumes in the longer term.MethodsIn the preventive angioplasty in myocardial infarction trial (PRAMI; ISRCTN73028481), cardiac magnetic resonance (CMR) was prespecified in two centres and performed (median, IQR) 3 (1, 5) and 209 (189, 957) days after primary PCI.ResultsFrom 219 enrolled patients in two sites, 84% underwent CMR. 42 (50%) were randomised to culprit-artery-only PCI and 42 (50%) were randomised to preventive PCI. Follow-up CMR scans were available in 72 (86%) patients. There were two (4.8%) cases of procedure-related myocardial infarction in the preventive PCI group. The culprit-artery-only group had a higher proportion of anterior myocardial infarctions (MIs) (55% vs 24%). Infarct sizes (% LV mass) at baseline and follow-up were similar. At follow-up, there was no difference in LV ejection fraction (%, median (IQR), (culprit-artery-only PCI vs preventive PCI) 51.7 (42.9, 60.2) vs 54.4 (49.3, 62.8), p=0.23), LV end-diastolic volume (mL/m2, 69.3 (59.4, 79.9) vs 66.1 (54.7, 73.7), p=0.48) and LV end-systolic volume (mL/m2, 31.8 (24.4, 43.0) vs 30.7 (23.0, 36.3), p=0.20). Non-culprit angiographic lesions had low-risk Syntax scores and 47% had non-complex characteristics.ConclusionsCompared with culprit-only PCI, non-infarct-artery MI in the preventive PCI strategy was uncommon and LV volumes and ejection fraction were similar.

In a registry-based trial, FFR-guided PCI of nonculprit lesions did not result in a lower risk of a composite of death from any cause, myocardial infarction, or unplanned revascularization than culprit-lesion-only PCI.

BackgroundSmall studies suggest that postconditioning reperfusion interrupted by brief repetitive cycles of reocclusions, may protect the myocardium in the clinical setting.ObjectiveTo test the hypothesis that postconditioning limits infarct size in relation to the area at risk in patients with ST elevation myocardial infarction (STEMI).Methods76 patients (aged 37–87 years) eligible for primary percutaneous coronary intervention due to STEMI were randomised to standard percutaneous coronary intervention (n=38) or postconditioning, consisting of four cycles of 60 s reperfusion and 60 s of reocclusion before permanent reperfusion (n=38).ResultsThe area at risk was determined from angiographic abnormally contracting segments. Infarct size was quantified from delayed enhancement MRI on days 6–9. Infarct size, expressed in relation to the area at risk, did not differ between the control group (44%; 30, 56) (median and quartiles) and the post-conditioned group (47%; 23, 63). The slope of the regression lines relating infarct size to the area at risk differed between the two groups. Infarct size was significantly (p=0.001) reduced by postconditioning in patients with large areas at risk. The area under the curve and peak troponin T release and CKMB during 48 h did not differ between patients in the control and postconditioning groups.ConclusionsThis prospective, randomised trial suggests that postconditioning does not reduce infarct size in patients with STEMI in the overall study group. The data indicate that postconditioning may be of value in patients with large areas at risk.Clinical trial registration informationKarolinska Clinical Trial Registration (http://www.kctr.se). Unique identifier: CT20080014.