Worse Left Ventricular Ejection Fraction Research Articles

Cardiac magnetic resonance assessment of acute rejection and cardiac allograft vasculopathy in pediatric heart transplant

In pediatric heart transplant (PHT), cardiac catheterization with endomyocardial biopsy (EMB) is standard for diagnosing acute rejection (AR) and cardiac allograft vasculopathy (CAV) but is costly and invasive. To evaluate the ability of cardiac magnetic resonance (CMR) to noninvasively identify differences in PHT patients with AR and CAV. Patients were enrolled at three children's hospitals. Data were collected from surveillance EMB or EMB for-cause AR. Patients were excluded if they had concurrent diagnoses of AR and CAV, CMR obtained >7days from AR diagnosis, they had EMB negative AR, or could not undergo contrasted, unsedated CMR. Kruskal-Wallis test was used to compare groups: (1) No AR or CAV (Healthy), (2) AR, (3) CAV. Wilcoxon rank-sum test was used for pairwise comparisons. Fifty-nine patients met inclusion criteria (median age 17years [IQR 15-19]) 10 (17%) with AR, and 11 (19%) with CAV. AR subjects had worse left ventricular ejection fraction compared to Healthy patients (p=0.001). Global circumferential strain (GCS) was worse in AR (p=0.054) and CAV (p=0.019), compared to Healthy patients. ECV, native T1, and T2 z-scores were elevated in patients with AR. CMR was able to identify differences between CAV and AR. CAV subjects had normal global function but abnormal GCS which may suggest subclinical dysfunction. AR patients have abnormal function and tissue characteristics consistent with edema (elevated ECV, native T1 and T2 z-scores). Characterization of CMR patterns is critical for the development of noninvasive biomarkers for PHT and may decrease dependence on EMB.

Aircraft noise exposure induces pro-inflammatory vascular conditioning and amplifies vascular dysfunction and impairment of cardiac function after myocardial infarction.

Traffic noise may play an important role in the development and deterioration of ischaemic heart disease. Thus, we sought to determine the mechanisms of cardiovascular dysfunction and inflammation induced by aircraft noise in a mouse model of myocardial infarction (MI) and in humans with incident MI. C57BL/6J mice were exposed to noise alone (average sound pressure level 72 dB; peak level 85 dB) for up to 4 days, resulting in pro-inflammatory aortic gene expression in the myeloid cell adhesion/diapedesis pathways. The noise alone promoted adhesion and infiltration of inflammatory myeloid cells in vascular/cardiac tissue, paralleled by an increased percentage of leucocytes with a pro-inflammatory, reactive oxygen species (ROS)-producing phenotype and augmented expression of nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase type 2 (Nox2)/phosphorylation of nuclear factor 'kappa light chain enhancer' of activated B-cells (phospho-NFκB) in peripheral blood. Ligation of the left anterior descending artery resulted in worsening of cardiac function, pronounced cardiac infiltration of CD11b+ myeloid cells and Ly6Chigh monocytes, and induction of interleukin (IL) 6, IL-1β, CCL-2, and Nox2, being aggravated by noise exposure prior to MI. MI induced stronger endothelial dysfunction and more pronounced increases in vascular ROS in animals preconditioned with noise. Participants of the population-based Gutenberg Health Cohort Study (median follow-up:11.4 years) with incident MI revealed elevated C-reactive protein at baseline and worse left ventricular ejection fraction (LVEF) after MI in case of a history of noise exposure and subsequent annoyance development. Aircraft noise exposure before MI substantially amplifies subsequent cardiovascular inflammation and aggravates ischaemic heart failure, facilitated by a pro-inflammatory vascular conditioning. Our translational results suggest that measures to reduce environmental noise exposure will be helpful in improving the clinical outcome of subjects with MI.Key questionKey finding Take-home-MessageAircraft noise exposure before MI substantially amplifies cardiovascular inflammation and aggravates cardiac impairment after MI.

Nothing to do does not mean any consequences.

Key Points Post‐TAVR new‐onset left bundle branch block (nLBBB) has clinical and echocardiographic prognostic implications, being associated with higher rates of permanent pacemaker (PPM) implantation and hospitalization for heart failure, and with worse left ventricular ejection fraction and remodeling. Close monitoring of patients who developed post‐TAVR nLBBB is needed, and predefined clinical, electrocardiographic and echocardiographic follow‐up should be scheduled at discharge Future studies aimed at identifying predictors of post‐TAVR nLBBB occurrence and regression, as well as the time windows in which it is likely will help in targeting patients at higher risk of PPM

66 MYOCARDIAL EDEMA CONTRIBUTES TO INTERSTITIAL EXPANSION AND ASSOCIATES WITH MECHANICAL AND ELECTROCARDIOGRAPHIC CHANGES IN TAKOTSUBO SYNDROME: A CMR T1 AND T2 MAPPING STUDY

Abstract Background myocardial edema has a central role in takotsubo syndrome (TTS). Relationships between edema, mechanical and electrical abnormalities in TTS are still elusive. Methods n=32 hospitalized TTS patients and n=23 controls were analyzed. We performed cardiac magnetic resonance (CMR) with tissue mapping for the assessment of edema and interstitial expansion, global longitudinal (GLS) and circumferential strain (GCS) were evaluated by CMR feature-tracking. Twelve-lead ECGs were recorded at the time of CMR in TTS patients, aVR voltage, negative T-wave voltage and QTc length were calculated. Results mean age of the TTS cohort was 72±12-year-old, 94% women, undergoing CMR at a median of 4 days (interquartile range 2, 6) after hospital admission. Compared with controls, patients had increased LV mass (55±11 g/m2 vs 46±8 g/m2, p<0.001), worse left ventricular ejection fraction (LVEF), GLS and GCS (all p<0.001), higher septal native T1 (1116±73 msec vs 970±23 msec, p<0.001), T2 (56±5 msec vs 46±2 msec, p<0.001) and extra-cellular volume (ECV) fraction (32±5% vs 24±1%, p<0.001). TTS patients had higher apicobasal gradient of T2 values (12±6 msec vs 2±6 msec, p<0.001), basal LV wall displayed higher native T1, T2 and ECV (all p<0.002) but similar circumferential strain against controls (-23±3% vs -24±4%, p=0.351). In the TTS cohort, septal T2 value showed significant correlations with native T1 (r=0.609, p<0.001), ECV (r=0.689, p<0.001), LVEF (r=-0.459, p=0.008) and aVR voltage (r=-0.437, p<0.05). Negative T waves voltage and QTc length significantly correlated with apicobasal T2 mapping gradient (r=0.499, p=0.007 and r=0.372, p=0.047 respectively) but not with other tissue mapping measurements. Conclusions CMR T1 and T2 mapping demonstrated increased myocardial water content conditioning interstitial expansion in acute TTS. Myocardial edema was detected even outside areas of abnormal wall motion, its burden and distribution associated with mechanical and electrocardiographic changes, making it a potential prognostic marker and therapeutic target in TTS.

Importance of cardiac imaging assessment of epicardial adipose tissue after a first episode of myocardial infarction.

Over the past years, information about the crosstalk between the epicardial adipose tissue (EAT) and the cardiovascular system has emerged. Notably, in the context of acute myocardial infarction (AMI), EAT might have a potential role in the pathophysiology of ventricular structural changes and function, and the clinical evolution of patients. This study aims to assess the impact of EAT on morpho-functional changes in the left ventricle (LV) and the outcome of patients after an AMI. We studied prospectively admitted patients to our hospital with a first episode of AMI. All patients underwent percutaneous coronary intervention (PCI) during admission. Transthoracic echocardiography (TTE) was performed within 24-48 h after PCI, as well as blood samples to assess levels of galectin-3 (Gal-3). Cardiac magnetic resonance (CMR) was performed 5-7 days after PCI. Clinical follow-up was performed at 1 and 5 years after MI. Mean age of our cohort (n = 41) was 57.5 ± 10 years, and 38 (93%) were male. Nine patients had normal BMI, 15 had overweight (BMI 25-30), and 17 were obese (BMI > 30). Twenty three patients (56%) had ≥ 4 mm thickness of EAT measured with echo. In these patients, baseline left ventricular ejection fraction (LVEF) after AMI was significantly lower, as well as global longitudinal strain. EAT thickness ≥ 4 m patients presented larger infarct size, higher extracellular volume, and higher T1 times than patients with EAT < 4 mm. As for Gal-3, the median was 16.5 ng/mL [12.7-25.2]. At five-year follow-up 5 patients had major cardiac events, and all of them had EAT ≥ 4 mm. Patients with EAT >4 mm have worse LVEF and GLS, larger infarct size and longer T1 values after a MI, and higher levels of Gal-3. EAT >4 mm was an independent predictor of MACE at 5-year follow-up. EAT thickness is a feasible, noninvasive, low-cost parameter that might provide important information regarding the chronic inflammatory process in the myocardium after an infarction.

The long-term clinical course of moderate tricuspid regurgitation

Abstract Background Moderate TR is a frequent condition, worsening mid and long-term survival, particularly in patients &amp;gt;75 years old, and in those suffering from left ventricular systolic dysfunction. As TR is often clinically unsuspected until an advanced stage of congestive heart failure (HF), there is a great need of early diagnosis and long-term appropriate follow-up. However, data focusing on the clinical and echocardiographic course of a cohort of patients with moderate TR is lacking, and the most appropriate type and time of management of these patients is still heavily debated. Purpose To evaluate the evolution and the long-term clinical outcome of a cohort of patients suffering from moderate and moderate to severe TR, regardless of its etiology. Methods Clinical outcome and echocardiographic follow-up were assessed in 212 patients diagnosed with moderate and moderate to severe TR in our centre between January 2014 and December 2019. TR progression at follow-up was defined as TR grade increase to at least severe. The primary endpoint was all-cause death; secondary endpoints were cardiovascular (CV) death and HF hospitalization. Results After a median follow-up of 4.2 years, TR progression occurred in 76 patients (36%): patients with TR progression presented with more history of coronary artery disease (p=0.042), atrial fibrillation (AF, p=0.007) and chronic kidney disease (CKD, p=0.007) and with baseline larger right ventricle end-diastolic diameter (RVEDD, p&amp;lt;0.001) and worse left ventricular ejection fraction (LVEF, p=0.048). After univariate and multivariate analyses, a history of AF (HR 2.3, CI 1.2–4.5, p=0.011) and RVEDD (HR 2.4, CI 1.3–4.4, p=0.003) were independent predictors of TR progression. The primary endpoint occurred in 57 patients (27%) and was significantly more frequent (p=0.015) in the group of patients with TR progression compared to those without TR progression; multivariate analyses showed TR grade progression (HR 4.3, CI 2.1–9.1, p&amp;lt;0.001), CKD (HR 3.2, CI 1.5–7.1, p=0.002) and LVEF (HR 0.9, CI 0.93–0.99, p=0.007) as being independently associated with the primary outcome. Moreover, both CV death (p=0.003) and HF hospitalization (p=0.0139) were significantly more frequent in patients with TR progression. Conclusions Our results showed that moderate TR, by progressing in a relevant proportion of patients over a long-term follow-up, significantly increases the risk of mortality and HF hospitalization. We identified specific risk factors associated with TR progression, which could help to identify patients at risk before an advanced stage of this disease. We believe that this cohort of patients should be appropriately managed and closely followed-up to avoid adverse clinical events related to the natural course of this valvulopathy. Funding Acknowledgement Type of funding sources: None.

Utility of the Age Shock Index in 27312 patients with an acute coronary syndrome

Abstract Introduction The Shock Index (SI), defined as the ratio of heart rate (HR) to systolic blood pressure (SBP), represents a bedside reflection of the integrated response from the cardiovascular and autonomic systems and has been reported to predict adverse prognosis in patients with acute coronary syndromes (ACS). Age Shock Index (ASI), the product of SI multiplied with age, could also be useful in this setting, but its prognostic value is yet to be determined in ACS patients. Methods Acute myocardial infarction patients included in a national registry between October 2010 and January 2022. Optimal shock index cutoff was determined according to ROC curve analysis. Patients were categorized into two groups based on their initial ASI. Baseline characteristics, management and outcomes were compared between the two groups. The primary outcome was in-hospital cardiovascular death. Results A total of 27312 patients were included with a mean age of 66±13 years, 72.3% male, 47.5% with ST-elevation myocardial infarction. Based on ROC analysis, which showed AUC=0.80, the optimal ASI cutoff was 44 (with a sensitivity of 73% and a specificity of 74%); 19997 patients (73.2%) had an ASI &amp;lt;44 and 26.8% had an ASI ≥44. The former group was older (mean age of 75±10.0 vs 63±13.0 years, p&amp;lt;0.001), and had more comorbidities: arterial hypertension (77.3% vs 66.3%, p&amp;lt;0.001), diabetes mellitus (39.8% vs 28.1%, p&amp;lt;0.001), peripheral artery disease (7.1% vs 4.4%, p&amp;lt;0.001) and previous history of heart failure (11.0% vs 4.3%, p&amp;lt;0.001). Patients with ASI ≥44 had higher Killip class at admission and worse left ventricular ejection fraction on discharge (46.0±13.0 vs 53.0±11.0, p&amp;lt;0.001). In a multivariate regression analysis, after adjusting for possible confounders, ASI ≥44 was an independent predictor of cardiovascular death (HR 3.09, 95% CI: 2.56–3.71, p&amp;lt;0.001). ASI was a significantly better predictor of cardiovascular death than Shock Index (AUCASI = 0,80 vs AUCSI = 0.72, p&amp;lt;0,0001), but not in comparison to GRACE score (AUCASI=0.80 vs AUCGRACE=0.85, p&amp;lt;0.001) and TIMI (score AUCASI=0.80 vs AUCGRACE=0.84, p&amp;lt;0.001). At one year, using a Kaplan Meyer survival analysis, mortality was higher in patients with ASI ≥44 (log rank p&amp;lt;0.001) Conclusion ASI can identify almost immediately ACS patients at high risk of cardiovascular death, and combined with its simple use, makes it a practical tool for early risk stratification in these patients. Funding Acknowledgement Type of funding sources: None.

Sacubitril/valsartan compared to ramipril in high risk post myocardial infarction patients stratified according use of mineralocorticoid receptor antagonists: insight from PARADISE MI trial

Abstract Background Mineralocorticoid receptor antagonists (MRAs) reduce the risk of cardiovascular death or heart failure admission in patients with myocardial infarction (MI) and left ventricular systolic dysfunction (LVSD) combined with either heart failure (HF) or diabetes. Whether use of MRA and initiation of sacubitril/valsartan are safe and whether MRAs modify the effect of sacubitril/valsartan initiation in high-risk MI patients is unknown. Purpose This analysis examined whether background treatment with a MRA modifies the treatment effect and safety of sacubitril/valsartan in patients with a MI and LVSD and/or pulmonary congestion. Methods In the PARADISE MI Trial (Prospective ARNI vs. ACE inhibitor trial to DetermIne Superiority in reducing heart failure Events after Myocardial Infarction) N=5661 patients were randomized to either sacubitril/valsartan (97/103 mg twice daily) or ramipril (5 mg twice daily) within 7 days of their MI. The primary outcome in this analysis was the composite of worsening HF (HF hospitalization or outpatient worsening) or cardiovascular death evaluated by the clinical endpoint committee (CEC-adjudicated) or the investigators. Safety was defined as symptomatic hypotension, hyperkalemia &amp;gt;5.5 mmol/L or permanent drug discontinuation. Results A total of 2338 patients (41%) were treated with an MRA and they were more often Caucasian (79% vs. 73%), had worse left ventricular ejection fraction (34±8 vs. 38±10%), a higher KILLIP Class (63% vs. 55% in class II or more) and a lower estimated Glomerular filtration rate (71 vs. 73 ml/min/1.73 m2), than patients not taking an MRA. Age (63 years), sex (24% females), and frequency of diabetes (42%) did not differ. The treatment effect of sacubitril/valsartan compared with ramipril was similar in patients taking or not taking an MRA: hazard ratio (MRA): (95% confidence interval [CI]): 0.96 (0.77, 1.19) versus (95% CI: 0.87 (0.71, 1.05), respectively, for the primary endpoint (p value for interaction = 0.51) (CEC adjudicated) (Figure 1); similar findings were observed if investigator reported endpoints were evaluated (P=0.61 for interaction). Safety of sacubitril/valsartan compared to ramipril initiation was not changed by +/−MRA use, but an increase in symptomatic hypotension was observed (HR(MRA): 1.37 and HR: 1.39, P&amp;lt;0.001) in both groups (P=0.968 for interaction), whereas an increased risk of hyperkalemia or permanent drug discontinuation was not observed in the sacubitril/valsartan group (P&amp;gt;0.05 for all comparisons). Conclusions As expected, patients taking MRAs had a higher risk. Use of a MRA did not modify the treatment effect and safety of initiation of sacubitril/valsartan compared to ramipril in the post MI setting in patients with LVSD and/or congestion. Our analyses support that sacubitril/valsartan and MRAs can be used simultaneously. Funding Acknowledgement Type of funding sources: Private company. Main funding source(s): Novartis sponsored Randomized clinical trial

Association of Growth Differentiation Factor 15 with Arterial Stiffness and Endothelial Function in Subpopulations of Patients with Coronary Artery Disease: A Proof-of-Concept Study.

Growth-differentiation factor-15 (GDF-15) is a biomarker belonging to the transforming growth factor-beta cytokine superfamily, which is linked to many pathological conditions, including inflammation and myocardial injury. Pulse wave velocity (cfPWV) and augmentation index (AIx) are indices of arterial stiffness, which are associated with the severity of coronary artery disease (CAD). Flow-mediated dilatation (FMD) is a well-studied surrogate marker of endothelial-dependent dysfunction and systemic inflammation. In this proof-of-concept study, we aimed to investigate the relationship between circulating GDF-15, endothelial dysfunction, and indices of arterial stiffness in different settings of coronary artery disease and myocardial injury. In this cross-sectional single-center study, we enrolled patients (n = 22) after interventional treatment for acute myocardial infarction (AMI), patients (n = 11) admitted with chest pain and elevated cardiac enzymes but without evidence of obstructing CAD (MI-NOCAD) in percutaneous coronary angiography (CAG), and patients (n = 20) who underwent CAG according to indications without evident obstructive CAD in CAG (NOCAD). FMD was assessed at the brachial artery. AIx of the central aortic pressure and cfPWV were estimated by applanation tonometry at the radial and carotid-femoral site, respectively, with a validated acquisition system (Sphygmo- Cor, AtCor Medical, Sydney (NSW), Australia). ELISA was used to determine circulating GDF- 15 serum levels (R&D Systems, Minneapolis, MN). Clinical and demographic data and values of routine biochemical biomarkers were obtained. The highest high-sensitive cardiac Troponin I (hsTpnI) value during hospitalization was also recorded. Left ventricular ejection fraction (LVEF) was assessed with a transthoracic echocardiogram. Patients with AMI were older, had worse LVEF, higher values of hsTpnI and increased circulating GDF-15 levels. Importantly, AMI patients had increased cfPWV values, deteriorated AIx values, blunted FMD and worse serum creatinine levels compared to MI-NOCAD and NOCAD patients, respectively, whereas MI-NOCAD and NOCAD did not differ from each other significantly on these biomarkers. Both AMI and MI-NOCAD patients presented a higher but comparable white blood cell count than NOCAD patients. A strong linear correlation between GDF-15 and cfPWV, hsTpnI, AIx, white blood cell count and creatinine but not with FMD was demonstrated in the general study population. This proof-of-concept study showed that higher circulating levels of GDF-15, an inflammatory biomarker, were associated significantly with increased arterial stiffness only in AMI patients, whereas elevated GDF-15 demonstrated a linear relationship with the severity of the myocardial injury.

Lung Ultrasound Patterns in Multisystem Inflammatory Syndrome in Children (MIS-C)-Characteristics and Prognostic Value.

Objective and design: Following COVID-19 infection, children can develop an hyperinflammatory state termed Multisystem Inflammatory Syndrome in Children (MIS-C). Lung Ultrasound (LUS) features of COVID-19 in children have been described, but data describing the LUS findings of MIS-C are limited. The aim of this retrospective observational study conducted between 1 March and 31 December 2020, at a tertiary pediatric hospital in Milano, is to describe LUS patterns in patients with MIS-C and to verify correlation with illness severity. The secondary objective is to evaluate concordance of LUS with Chest X-ray (CXR). Methodology: Clinical and laboratory data were collected for all patients (age 0–18 years) admitted with MIS-C, as well as LUS and CXR patterns at admission. PICU admission, needed for respiratory support and inotrope administration, hospital, and PICU length of stay, were considered as outcomes and evaluated in the different LUS patterns. An agreement between LUS and CXR evaluation was assessed with Cohen’ k. Results: 24 children, who had a LUS examination upon admission, were enrolled. LUS pattern of subpleural consolidations < or > 1 cm with or without pleural effusion were associated with worse Left Ventricular Ejection Fraction at admission and need for inotropes. Subpleural consolidations < 1 cm were also associated with PICU length of stay. Agreement of CXR with LUS for consolidations and effusion was slight. Conclusion: LUS pattern of subpleural consolidations and consolidations with or without pleural effusion are predictors of disease severity; under this aspect, LUS can be used at admission to stratify risk of severe disease.

Cardiac arrest in non-ST segment elevation myocardial infarction: what to expect

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Ischemic heart disease is the leading cause of cardiac arrest (CA). While in ST segment elevation myocardial infarction its approach is well defined, in non-ST segment elevation myocardial infarction (NSTEMI) it is still a matter of debate. This study aimed to characterize patients with NSTEMI and out-of-hospital CA and to evaluate its prognosis. Methods This was a national multicenter retrospective study of patients hospitalized for NSTEMI undergoing coronary angiography (ANG) between October 2010 and September 2019. Results Out of a total of 9544 patients, 96 were admitted after CA. The baseline characteristics of both groups were similar, with the exception of more past history of heart failure (10,5% vs 5,6%, p=0,038) and peripheral artery disease (11,5% vs 5,9%, p=0,023) in patients with CA. In the peri-arrest period, 64,6% of the patients reported chest pain. Patients with CA had worse left ventricular ejection fraction (49±13% vs 53±12%, p=0,006), ended up reaching higher Killip classes more often and needing more inotropic and mechanical support. The median time from admission to ANG was similar in both groups (0 (0;3) vs 1 (0;2) days, p=0,796). CA patients had more multivessel coronary disease (66% vs 55,5%, p=0,043) and left main artery involvement (25,3% vs 11,2%, p&amp;lt;0,001). The proportion of revascularization procedures was similar. During hospitalization, patients with CA were less treated with beta-blockers (77,9% vs 85,2%, p=0,046) and ACE inhibitors (77,7% vs 86,1%, p=0,018), a difference that disappeared at discharge. However, statin prescription at discharge was lower in CA patients (88,3% vs 94,4%, p=0,040). In a multivariate analysis for events occurred during hospitalization, CA was associated with a significant increase in myocardial reinfarction (adjusted OR 5,42 (95% CI 2,10-1,98)), stroke (adjusted OR 5,38 (95% CI 1,24-2,32)) and death (adjusted OR 13,86 (95% CI 5,98-32,17)). After excluding patients with indication for an immediate invasive strategy, we verified that mortality was higher in CA patients who underwent ANG in the first 24 hours. CA was not associated with a significant increase in the 1-year mortality rate (adjusted HR 0,67 (95% CI 0,10-4,90)). Conclusions In this study, NSTEMI patients surviving CA had more severe coronary events. CA was independently associated with a significant increase in in-hospital major adverse events. However, during the 1-year follow-up there was no significant increase in mortality.

Mitral valve-in-valve and valve-in-ring procedures: Midterm outcomes in a French nationwide registry.

Report contemporary outcomes in patients included in the Mitragister registry and treated with transcatheter mitral valve implantationfor failed surgical annuloplasty rings or deteriorated bioprosthesis. Midterm survival rates have been reported, but little is known about contemporary morbimortality endpoints. The primary safety outcome was the technical success rate. The primary efficacy composite endpoint was a composite of cardiovascular mortality and heart failure hospitalizations. From 2016 to 2021, 102 patients (median age: 81 [74;84] years, 61% female, Euroscore II 11.0% [7.8;16.0]) undergoing valve-in-valve (ViV; n = 89) or valve-in-ring (ViR; n = 13) procedures were consecutively included. At baseline, ViR group patients had worse left ventricular ejection fraction (50% vs. 60%; p = 0.004) and more frequently severe regurgitation (46% vs. 15%; p = 0.014). The primary safety outcome was 95%: 77% and 98% in the ViR and ViV populations, respectively, (p = 0.014). At intermediate follow-up (6-12 months) clinical improvement was notable, 88% of the patients were in NYHA class ≤ II (vs. 25% at baseline; p < 0.001). At a mean follow-up of 17.1 ± 11.0 months, the primary efficacy composite reached 27%. By multivariate analysis, paravalvular leak (PVL) was the only independent predictor (hazard ratio:2.39, 95% confidence interval: 1.08-5.29; p = 0.031) while ViR was not found statistically associated (p = 0.456). This study confirms the safety and efficacy of the mitral ViV procedure. ViR patients appear at higher risk of procedural complications. The presence of PVL could be associated with markedly worse midterm prognosis. Whatever the intervention, procedural strategies to reduce PVL incidence remain to be assessed to prevent latter adverse outcomes.

Early and late new-onset of atrial fibrillation in acute coronary syndromes: Their differences in mortality and cardiac event.

BackgroundIn a stressful situation like acute coronary syndrome (ACS), the occurrence of the first episode of atrial fibrillation is more frequent. The impact of the timing occurrence of AF new‐onset (nAF) in the setting of ACS is still debatable.MethodsMulticenter retrospective study based on the Acute Coronary Syndrome Portuguese National Registry, including 29 851 patients admitted for ACS between 1/10/2010 and 4/09/2019. The group with early nAF ‐ nAF in the first 48 h of hospitalization; and late nAF ‐ patients with nAF after the first 48 h of in‐hospital admission.ResultsNew‐onset AF was identified in 1067 patients, nonetheless, just 38.1% had late nAF. The group with late nAF presented more cardiovascular comorbidities and worse left ventricular ejection fraction. Late nAF patients received more anti‐arrhythmic therapy, and early nAF had a higher beta‐block prescription. Early nAF had higher rates of in‐hospital complications, on the other hand, late nAF group exhibited more mortality and readmission at one year follow‐up. Multiple logistic regression revealed that symptoms onset to the first medical contact time, admission hemoglobin <12 g/dl, right bundle branch block at admission, and diuretic therapy during the hospitalization for ACS were predictors of late nAF in ACS.ConclusionsThe ACS population could be divided by the timing of nAF occurrence into the two groups with different characteristics, therapeutic approaches, and outcomes. Late nAF patients had a worse prognosis at 1 year follow‐up, however, the early nAF group had more major adverse cardiac events during the hospitalization for ACS.

Variability in Reassessment of Left Ventricular Ejection Fraction After Myocardial Infarction in the Acute Myocardial Infarction Quality Assurance Canada Study

Persistently depressed left ventricular ejection fraction (LVEF) after myocardial infarction (MI) is associated with adverse prognosis and directs the use of evidence-based treatments to prevent sudden cardiac death and/or progressive heart failure. To assess adherence with guideline-recommended LVEF reassessment and to study the evolution of LVEF over 6 months of follow-up. This was a multicenter cohort study at Canadian academic and community hospitals with on-site cardiac catheterization services. Patients with type 1 acute MI and LVEF less than or equal to 45% during the index hospitalization were enrolled between January 2018 and August 2019 and were followed-up for 6 months. Data analysis was performed from May 2020 to September 2021. Baseline clinical factors, in-hospital care and LVEF, and site-specific features. The main outcomes were receipt of repeat LVEF assessment by 6 months and the presence of a persistent LVEF reduction at 2 thresholds: LVEF less than or equal to 40%, prompting consideration of additional medical therapy for heart failure, or LVEF less than or equal to 35%, prompting referral for implanted cardioverter defibrillator in addition to medical therapy. This study included 501 patients (mean [SD] age, 63.3 [13.0] years; 113 women [22.6%]). Overall, 370 patients (73.4%) presented with STEMI, and 454 (90.6%) had in-hospital revascularization. The median (IQR) baseline LVEF was 40% (34%-43%). Of 458 patients (91.4%) who completed the 6-month follow-up, 303 (66.2%; 95% CI, 61.7%-70.5%) had LVEF reassessment, with a range of 46.7% to 90.0% across sites (χ213 = 19.6; P = .11). Participants from community hospitals were more likely than those from academic hospitals to undergo LVEF reassessment (73.6% vs 63.2%; χ21 = 4.50; P = .03), as were those with worse LVEF at baseline. Follow-up LVEF improved by an absolute median (IQR) of 8% (3%-15%). However, 103 patients (34.1%) met the definitions of clinically relevant LVEF reduction, including 52 patients (17.2%) with LVEF less than or equal to 35% and 51 patients (16.9%) with LVEF of 35.1% to 40.0%. In this cohort study, approximately 1 in 3 patients with at least mild LVEF reduction after acute MI did not undergo indicated LVEF reassessment within 6 months, suggesting that programs to improve the quality of post-MI care should include measures to ensure that indicated repeat cardiac imaging is performed. In those with follow-up imaging, clinically relevant persistent LVEF reduction was identified in more than one-third of patients.

Elevated uric acid is related to the no-/slow-reflow phenomenon in STEMI undergoing primary PCI.

No-/slow-reflow phenomenon (NRP) is a severe complication in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). This study aimed to explore the relationship between elevated serum uric acid (SUA) and NRP in patients with STEMI undergoing pPCI, focusing on inflammation and angiographic findings. A total of 610 patients who received pPCI for STEMI were retrospectively enrolled. Patients were divided into a hyperuricaemia group and a non-hyperuricaemia group according to SUA levels. Clinical information and angiographic indicators were compared between the two groups. Thrombolysis in myocardial infarction (TIMI) flow and TIMI myocardial perfusion grade (TMPG) <3 after stent implantation were defined as TIMI-NRP and TMPG-NRP, respectively. A logistic model was used to analyse the relationship between hyperuricaemia and NRP. The hyperuricaemia group had a higher incidence of TIMI-NRP (24.9% vs 14.0%, p<.001) and TMPG-NRP (33.0% vs 24.9%, p=.03), higher levels of C-reactive protein (7.2 vs 4.1mg/L, p<.001) and worse left ventricular ejection fraction (51.5% vs 54.0%, p=.002) than the non-hyperuricaemia group. As for angiographic findings, there was no significant difference between the two groups in terms of lesion characteristics measured by quantitative coronary angiography. After multivariable adjustment, elevated SUA was significantly associated with TIMI-NRP (odds ratio: 1.94, 95% confidence interval: 1.24-3.01, p=.003). Subgroup analysis showed that the effect of hyperuricaemia in TIMI-NRP was more pronounced in patients with delayed perfusion as well as in patients with diabetes mellitus. Elevated SUA is associated with severe inflammation and has higher incidence of TIMI-NRP in patients with STEMI undergoing pPCI, especially in those with delayed perfusion or diabetes mellitus.

Mitral Regurgitation Following Acute Myocardial Infarction Treated by Percutaneous Coronary Intervention—Prevalence, Risk factors, and Predictors of Outcome

Mitral regurgitation (MR) following acute myocardial infarction (AMI) worsens prognosis and reports of prevalence vary significantly. The objective was to determine prevalence, risk factors, and outcomes related to MR following AMI. We identified 1000 consecutive patients admitted with AMI in 2016/17 treated by percutaneous coronary intervention with pre-discharge transthoracic echocardiography. MR was observed in 294 of 1000 (29%), graded as mild (n=224 [76%]), moderate (n=61 [21%]) and severe (n=9 [3%]). Compared with patients without MR, patients with MR were older (70 ± 12 vs 63 ± 13 years; p <0.001), with worse left ventricular ejection fraction (LVEF) (52 ± 15% vs 55 ± 11%; p <0.001) and creatinine clearance (69 ± 33 ml/min vs 90 ± 39 ml/min; p <0.001). They also had higher rates of hypertension (64% vs 55%; p=0.012), heart failure (3.4% vs 1.1%; p=0.014), previous MI (28% vs 20%; p=0.005) and severe flow-limitation in the circumflex (50% vs 33%; p <0.001) or right coronary artery (51% vs 42%; p=0.014). Prevalence and severity of MR were unaffected by AMI subtype. Revascularization later than 72 hours from symptom-onset was associated with increased likelihood of MR (33% vs 25%; p=0.036) in patients with non-ST elevation myocardial infarction (NSTEMI). After a mean of 3.2 years, 56 of 288 (19%) patients with untreated MR died. Age and LVEF independently predicted mortality. The presence of even mild MR was associated with increased mortality (p=0.029), despite accounting for confounders. In conclusion, MR is observed in over one-quarter of patients after AMI and associated with lower survival, even when mild. Prevalence and severity are independent of MI subtype, but MR was more common with delayed revascularization following NSTEMI.

Association of Left Ventricular Systolic Function With Incident Heart Failure in Late Life

Limited data exist regarding the association of subtle subclinical systolic dysfunction and incident heart failure (HF) in late life. To assess the independent associations of subclinical impairments in systolic performance with incident HF in late life. This study was a time-to-event analysis of participants without heart failure in the Atherosclerosis Risk in Communities (ARIC) study, a prospective, community-based cohort study, who underwent protocol echocardiography at the fifth study visit (January 1, 2011, to December 31, 2013). Findings were validated independently in participants in the Copenhagen City Heart Study (CCHS). Data analysis was performed from June 1, 2018, to February 28, 2020. Left ventricular ejection fraction (LVEF), longitudinal strain (LS), and circumferential strain (CS) measured by 2-dimensional and strain echocardiography. Main outcomes were incident adjudicated HF and HF with preserved and reduced LVEF at a median follow-up of 5.5 years (interquartile range, 5.0-5.8 years). Cox proportional hazards regression models adjusted for demographics, hypertension, diabetes, obesity, smoking, coronary disease, estimated glomerular filtration rate, LV mass index, e', E/e', and left atrial volume index. Lower 10th percentile limits were determined in 374 participants free of cardiovascular disease or risk factors. Among 4960 ARIC participants (mean [SD] age, 75 [5] years; 2933 [59.0%] female; 965 [19%] Black), LVEF was less than 50% in only 76 (1.5%). In the 3552 participants with complete assessment of LVEF, LS, and CS, 983 (27.7%) had 1 or more of the following findings: LVEF less than 60%, LS less than 16.0%, or CS less than 23.7%. Modeled continuously or dichotomized, worse LVEF, LS, and CS were each independently associated with incident HF. The adjusted hazard ratio (HR) per SD decrease in LVEF was 1.41 (95% CI, 1.29-1.55); the HR for LVEF less than 60% was 2.59 (95% CI, 1.99-3.37). Similar findings were observed for continuous LS (HR, 1.37; 95% CI, 1.22-1.53) and dichotomized LS (HR, 1.93; 95% CI, 1.46-2.55) and for continuous CS (HR, 1.39; 95% CI, 1.22-1.57) and dichotomized CS (HR, 2.30; 95% CI, 1.64-3.22). Although the magnitude of risk for incident HF or death associated with impaired LVEF was greater using guideline (HR, 2.99; 95% CI, 2.19-4.09) compared with ARIC-based limits (HR, 1.88; 95% CI, 1.58-2.25), the number of participants classified as impaired was less (104 [2.1%] based on guideline thresholds compared with 692 [13.9%] based on LVEF <60%). The population-attributable risk associated with LVEF less than 60% was 11% compared with 5% using guideline-based limits, a finding replicated in 908 participants in the CCHS. These findings suggest that relatively subtle impairments of systolic function (detected based on LVEF or strain) are independently associated with incident HF and HF with reduced LVEF in late life. Current recommended assessments of LV function may substantially underestimate the prevalence of prognostically important impairments in systolic function in this population.

Clinical value of soluble suppression of tumourigenicity 2 (sST2) in addition to NTproBNP measurements in a general cardiac outpatient population

BACKGROUND AND AIMS: The soluble form of suppression of tumourigenicity 2 (sST2), a recently introduced biomarker, is a strong and NTproBNP-independent predictor of outcome in heart failure patients. This study sought to evaluate the added clinical value of sST2 in addition to NTproBNP in a heterogeneous cardiac outpatient population. METHODS: A total of 297 all-comer patients visiting the outpatient clinic of Heart Clinic Zurich, Switzerland, from January to December 2018 were included. Patients were divided into four groups depending on their sST2 and NTproBNP levels: group 1 (n = 91, 30.6% of all patients) with normal levels of both biomarkers, group 2 (n = 41, 13.8%) with isolated elevation of sST2 but normal NTproBNP, group 3 (n = 97, 32.7%) with elevated NTproBNP but normal sST2 levels, and group 4 (n = 68, 22.9%) with elevation of both biomarkers. Differences between groups, Spearman’s correlations and linear and multiple regression analysis for sST2 were calculated. RESULTS: The median age was 74 ± 19 years and 41.8% were women. NTproBNP levels continuously increased across the groups (medians in pg/ml: group 1 123.0, group 2 152.0, group 3 990.0 and group 4 2610.0), whereas sST2 levels did not (medians in ng/ml: 28.7, 58.9, 28.4 and 63.7 for groups 1 to 4, respectively). In patients with normal NTproBNP (groups 1 and 2), elevation of sST2 (group 2) was associated with significantly higher rates of coronary artery disease, peripheral vascular disease and renal dysfunction. In patients with elevated NTproBNP (groups 3 and 4), the additional elevation of sST2 (group 4) was associated with clinical signs of heart failure, higher EuroScore II and worse left ventricular ejection fraction (LVEF group 3 58.0% vs group 4 53.3%, p = 0.022). Correlation of sST2 was overall weak and weaker than of NTproBNP with most clinical variables. Soluble ST2 significantly correlated with EuroScore II (R = 0.280), kidney function (R = −0.259), C-reactive protein (R = 0.248), right ventricular function (R = 0.213) and left atrial volume (R = 0.199), all p ≤0.001. In multiple regression analysis, left atrial volume was the strongest independent predictor of sST2 elevation (p = 0.002). CONCLUSION: In this all-comer cardiology population, the added clinical value of sST2 measurements in addition to NTproBNP was small. In patients with elevated NTproBNP, the simultaneous elevation of sST2 was associated with clinical signs of heart failure. Soluble ST2 measurements could thus be beneficial in patients with uncertain signs of heart failure and confounding factors for NTproBNP elevation. Surprisingly, this study found elevated sST2 levels in a substantial number of a patients with normal NTproBNP levels, pointing to an additional pathway of sST2 elevation independent of heart failure.

Using proximity extension proteomics assay to identify biomarkers associated with infarct size and ejection fraction after ST-elevation myocardial infarction

Plasma concentrations of many cardiovascular and inflammatory proteins are altered after ST-elevation myocardial infarction (STEMI) and may provide prognostic information. We conducted a large-scale proteomic analysis in patients with STEMI, correlating protein levels to infarct size and left ventricular ejection fraction (LVEF) determined with cardiac magnetic resonance imaging. We analysed 131 cardiovascular and inflammatory proteins using a multiplex proximity extension assay and blood samples obtained at baseline, 6, 24, and 96 h from the randomised clinical trial CHILL-MI. Cardiac magnetic resonance imaging data at 4 ± 2 days and 6 months were available as per trial protocol. Using a linear regression model with bootstrap resampling and false discovery rate adjustment we identified five proteins (ST2, interleukin-6, pentraxin-3, interleukin-10, renin, and myoglobin) with elevated values corresponding to larger infarct size or worse LVEF and four proteins (TNF-related apoptosis-inducing ligand, TNF-related activation induced cytokine, interleukin-16, and cystatin B) with values inversely related to LVEF and infarct size, concluding that among 131 circulating inflammatory and cardiovascular proteins in the acute and sub-acute phase of STEMI, nine showed a relationship with infarct size and LVEF post-STEMI, with IL-6 and ST2 exhibiting the strongest association.

Who Has Seen Patients With ST-Segment-Elevation Myocardial Infarction? First Results From Italian Real-World Coronavirus Disease 2019.

BackgroundAfter the coronavirus disease 2019 outbreak, social isolation measures were introduced to contain infection. Although there is currently a slowing down of the infection, a reduction of hospitalizations, especially for myocardial infarction, was observed. The aim of our study is to evaluate the impact of the infectious disease on ST‐segment–elevation myocardial infarction (STEMI) care during the coronavirus disease 2019 pandemic, through the analysis of recent cases of patients who underwent percutaneous coronary intervention.Methods and ResultsConsecutive patients affected by STEMI from March 1 to 31, 2020, during social restrictions of Italian government, were collected and compared with patients with STEMI treated during March 2019. During March 2020, we observed a 63% reduction of patients with STEMI who were admitted to our catheterization laboratory, when compared with the same period of 2019 (13 versus 35 patients). Changes in all time components of STEMI care were notably observed, particularly for longer median time in symptom‐to‐first medical contact, spoke‐to‐hub, and the cumulative symptom‐to‐wire delay. Procedural data and in‐hospital outcomes were similar between the 2 groups, whereas the length of hospitalization was longer in patients of 2020. In this group, we also observed higher levels of cardiac biomarkers and a worse left ventricular ejection fraction at baseline and discharge.ConclusionsThe coronavirus disease 2019 outbreak induced a reduction of hospital access for STEMI with an increase in treatment delay, longer hospitalization, higher levels of cardiac biomarkers, and worse left ventricular function.