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Inferior sinus venosus atrial septal defect (SVASD) is the rarest form of the atrial septal defect (ASD) and can sometimes go unnoticed. Although this defect can be associated with other congenital anomalies, its association with hypoplasia of the posterior mitral leaflet is extremely rare. In this case, we present a woman with a history of surgery for an ostium secundum ASD who exhibited persistent right heart chamber dilation. Echocardiography revealed hypoplasia of the posterior mitral leaflet, and cardiac magnetic resonance (CMR) imaging confirmed the presence of a previously undetected inferior sinus venosus ASD. [ABSTRACT FROM AUTHOR]

Following myocardial infarction (MI), adverse remodeling depends on the proper formation of fibrotic scars, composed of type I and III collagen. Our objective was to pinpoint the participation of previously unreported collagens in post-infarction cardiac fibrosis. Gene (qRT-PCR) and protein (immunohistochemistry followed by morphometric analysis) expression of fibrillar (types II and XI) and non-fibrillar (types VIII and XII) collagens were determined in RNA-sequencing data from 92 mice undergoing myocardial ischemia; mice submitted to permanent (non-reperfused MI, n = 8) or transient (reperfused MI, n = 8) coronary occlusion; and eight autopsies from chronic MI patients. In the RNA-sequencing analysis of mice undergoing myocardial ischemia, increased transcriptomic expression of collagen types II, VIII, XI, and XII was reported within the first week, a tendency that persisted 21 days afterwards. In reperfused and non-reperfused experimental MI models, their gene expression was heightened 21 days post-MI induction and positively correlated with infarct size. In chronic MI patients, immunohistochemistry analysis demonstrated their presence in fibrotic scars. Functional analysis indicated that these subunits probably confer tensile strength and ensure the cohesion of interstitial components. Our data reveal that novel collagens are present in the infarcted myocardium. These data could lay the groundwork for unraveling post-MI fibrotic scar composition, which could ultimately influence patient survivorship. [ABSTRACT FROM AUTHOR]

We hypothesized that a short-course high-intensity statin treatment during admission for myocardial infarction (MI) could rapidly reduce LDL-C and thus impact the choice of lipid-lowering therapy (LLT) at discharge. Our cohort comprised 133 MI patients (62.71 ± 11.3 years, 82% male) treated with atorvastatin 80 mg o.d. during admission. Basal LDL-C levels before admission were analyzed. We compared lipid profile variables before and during admission, and LLT at discharge was registered. Achieved theoretical LDL-C levels were estimated using LDL-C during admission and basal LDL-C as references and compared to LDL-C on first blood sample 4–6 weeks after discharge. A significant reduction in cholesterol from basal levels was noted during admission, including total cholesterol, triglycerides, HDL-C, non-HDL-C, and LDL-C (−39.23 ± 34.89 mg/dL, p < 0.001). LDL-C levels were reduced by 30% in days 1–2 and 40–45% in subsequent days (R2 0.766, p < 0.001). Using LDL-C during admission as a reference, most patients (88.7%) would theoretically achieve an LDL-C < 55 mg/dL with discharge LLT. However, if basal LDL-C levels were considered as a reference, only a small proportion of patients (30.1%) would achieve this lipid target, aligned with the proportion of patients with LDL-C < 55 mg/dL 4–6 weeks after discharge (36.8%). We conclude that statin treatment during admission for MI can induce a significant reduction in LDL-C and LLT at discharge is usually prescribed using LDL-C during admission as the reference, which leads to insufficient LDL-C reduction after discharge. Basal LDL-C before admission should be considered as the reference value for tailored LLT prescription. [ABSTRACT FROM AUTHOR]

Background: Patients with ST‐segment elevation myocardial infarction (STEMI), especially elderly individuals, have an increased risk of readmission for acute heart failure (AHF). Purpose: To study the impact of left ventricular ejection fraction (LVEF) by MRI to predict AHF in elderly (>70 years) and nonelderly patients after STEMI. Study Type: Prospective. Population: Multicenter registry of 759 reperfused STEMI patients (23.3% elderly). Field Strength/Sequence: 1.5‐T. Balanced steady‐state free precession (cine imaging) and segmented inversion recovery steady‐state free precession (late gadolinium enhancement) sequences. Assessment: One‐week MRI‐derived LVEF (%) was quantified. Sequential MRI data were recorded in 579 patients. Patients were categorized according to their MRI‐derived LVEF as preserved (p‐LVEF, ≥50%), mildly reduced (mr‐LVEF, 41%–49%), or reduced (r‐LVEF, ≤40%). Median follow‐up was 5 [2.33–7.54] years. Statistical Tests: Univariable (Student's t, Mann–Whitney U, chi‐square, and Fisher's exact tests) and multivariable (Cox proportional hazard regression) comparisons and continuous‐time multistate Markov model to analyze transitions between LVEF categories and to AHF. Hazard ratios (HR) with 95% confidence intervals (CIs) were computed. P < 0.05 was considered statistically significant. Results: Over the follow‐up period, 79 (10.4%) patients presented AHF. MRI‐LVEF was the most robust predictor in nonelderly (HR 0.94 [0.91–0.98]) and elderly patients (HR 0.94 [0.91–0.97]). Elderly patients had an increased AHF risk across the LVEF spectrum. An excess of risk (compared to p‐LVEF) was noted in patients with r‐LVEF both in nonelderly (HR 11.25 [5.67–22.32]) and elderly patients (HR 7.55 [3.29–17.34]). However, the mr‐LVEF category was associated with increased AHF risk only in elderly patients (HR 3.66 [1.54–8.68]). Less transitions to higher LVEF states (n = 19, 30.2% vs. n = 98, 53%) and more transitions to AHF state (n = 34, 53.9% vs. n = 45, 24.3%) were observed in elderly than nonelderly patients. Data Conclusion: MRI‐derived p‐LVEF confers a favorable prognosis and r‐LVEF identifies individuals at the highest risk of AHF in both elderly and nonelderly patients. Nevertheless, an excess of risk was also found in the mr‐LVEF category in the elderly group. Evidence Level: 2. Technical Efficacy: Stage 2. [ABSTRACT FROM AUTHOR]

Aims: Traditional adverse events in chronic coronary syndrome (CCS) include atherothrombotic events but usually exclude heart failure (HF). Data are scarce about how new‐onset HF modifies mortality risk. We aimed to determine the incidence of HF and compare its long‐term mortality risk with myocardial infarction (MI) and stroke in patients with known or suspected CCS. Methods: We prospectively evaluated 5811 consecutive HF‐free patients submitted to vasodilator stress cardiac magnetic resonance (CMR) for known or suspected CCS. Ischaemic burden and left ventricular ejection fraction were assessed by CMR. HF included outpatient diagnosis or acute HF hospitalization. The mortality risk for the incident events and their cross‐comparisons were evaluated using a Markov illness–death model with transition‐specific survival models. Results: The mean age was 55 ± 11 years, and 38.9% were female. At a median follow‐up of 5.44 (IQR = 2.53–8.55) years, 591 deaths were registered (1.79 per 100 P‐Y). The rates of new‐onset HF were higher compared with MI and stroke [1.02, 0.62, and 0.51, respectively (P < 0.05)]. The adjusted association between new‐onset HF, MI, and stroke, and subsequent mortality was time dependent. The risk increased almost linearly for HF and became significant by the third year. By Year 10, the mortality risk attributable to new‐onset HF was more than 2.5‐fold (HR: 2.68, 95% CI = 1.74–4.12). For MI, there was a significant increase in mortality risk up to the second year, followed by a monotonic decrease. For stroke, the mortality risk increased for the entire follow‐up but became significant by the third year. A cross‐comparison among incident endpoints HF outnumbers risk for those with MI by the sixth year (HRyear6.3: 1.88, 95% CI = 1.03–3.43). There was no difference in mortality risk between incident HF and stroke. Conclusions: In patients with CCS, long‐term rates of incident HF were higher than MI and stroke. Patients with new‐onset HF showed a higher risk of long‐term mortality. [ABSTRACT FROM AUTHOR]

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Hypoplasia of the posterior mitral valve leaflet (PMVL) is a very rare finding in adulthood and can coexist with other congenital heart defects. In this image, a transesophageal echocardiography (TOE) carried out on a 59‐year‐old woman with a 2‐month history of dyspnea revealed a hypoplastic PMVL causing severe mitral regurgitation associated with a secundum‐type atrial septal defect (ASD) with left‐to‐right shunting. This case demonstrates how essential 3‐dimensional TOE is for a comprehensive assessment of the mitral valve and to improve the diagnostic accuracy of concomitant congenital heart abnormalities. [ABSTRACT FROM AUTHOR]

Background: Left ventricular thrombus (LVTh) is a severe complication after ST-segment elevation myocardial infarction (STEMI)., Objectives: We aim to predict LVTh occurrence by cardiac magnetic resonance (CMR) using clinical, echocardiographic, and electrocardiographic (ECG) variables readily available at admission., Methods: We included 590 reperfused STEMI patients who underwent early (1-week) and/or late (6-month) CMR in our institution. Baseline clinical, echocardiographic (left ventricular ejection fraction -LVEF-) and ECG data (summatory of ST-segment elevation -sum-STE- and Q-wave and residual ST-elevation >1 mm -Q-STE-) during admission were registered. Multivariate binary logistic regression models and receiver operating characteristic curves were computed for LVTh prediction., Results: LVTh was detected by CMR in 43 (7.3 %) patients and was predicted by previous chronic coronary syndrome (CCS, HR 4.74 [1.82-12.35], p = 0.001), anterior STEMI (HR 10.93 [2.47-48.31], p = 0.002), LVEF (HR 0.96 [0.93-0.99] per %, p = 0.008), maximum sum-STE (HR 1.04 [1.01-1.07] per mm, p = 0.04), and Q-STE (HR 1.31 [1.08-1.6] per lead, p = 0.008). High-risk patients with both major (anterior STEMI and Q-STE in ≥1 leads) and 1-3 minor (CCS, maximum sum-STE >10 mm, LVEF <50%) factors showed the highest LVTh risk (19.6 % within 6 months). The model showed excellent discrimination ability (area under the curve=0.85 [0.81-0.9], p < 0.001). Simplified 4-variable (excluding sum-STE) and 3-variable (also excluding CCS) risk scores showed similar discrimination ability and were externally validated., Conclusions: LVTh within 6 months post-STEMI can be predicted using pre-discharge clinical (anterior infarction and CCS), echocardiographic (LVEF), and ECG (sum-STE and Q-STE) data. Our results can help select patients who should undergo CMR after STEMI for LVTh detection., Competing Interests: Conflict of interest disclosures Julio Núñez reports personal fees from Alleviant, Bayer, Astra Zeneca, Novartis, Boehringer-Ingelheim, Rovi, and Novo Nordisk, not related to the contents of this paper. The other authors report no conflicts of interest., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Introduction and Objectives: Angiogenesis helps to reestablish microcirculation after myocardial infarction (MI). In this study, we aimed to further understand the role of the antiangiogenic isoform vascular endothelial growth factor (VEGF)-A 165 b after MI and to explore its potential as a coadjuvant therapy to coronary reperfusion., Methods: Two mice MI models were formed: a) permanent coronary ligation (nonreperfused MI); b) transient 45-minute coronary occlusion followed by reperfusion (reperfused MI); in both models, animals underwent echocardiography before euthanasia at day 21 after MI induction. We determined serum and myocardial VEGF-A 165 b levels. In both experimental MI models, we assessed the functional and structural role of VEGF-A 165 b blockade. In a cohort of 104 ST-segment elevation MI patients, circulating VEGF-A 165 b levels were correlated with cardiovascular magnetic resonance-derived left ventricular ejection fraction at 6 months and with the occurrence of adverse events (death, heart failure, and/or reinfarction)., Results: In both models, circulating and myocardial VEGF-A 165 b levels were increased 21 days after MI induction. Serum VEGF-A 165 b levels inversely correlated with systolic function evaluated by echocardiography. VEGF-A 165 b blockade increased capillary density, reduced infarct size, and enhanced left ventricular function in reperfused, but not in nonreperfused, MI experiments. In patients, higher VEGF-A 165 b levels correlated with depressed ejection fraction and worse outcomes., Conclusions: In experimental and clinical studies, higher serum VEGF-A 165 b levels are associated with worse systolic function. Their blockade enhances neoangiogenesis, reduces infarct size, and increases ejection fraction in reperfused, but not in nonreperfused, MI experiments. Therefore, VEGF-A 165 b neutralization represents a potential coadjuvant therapy to coronary reperfusion., (Copyright © 2020 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.)