Search Results (266)

Background: Sex-related differences in left ventricular (LV) reverse remodeling following ST-segment elevation myocardial infarction (STEMI) remain underexplored. We aimed to investigate predictors of reverse remodeling and its association with clinical outcomes, with a focus on sex-specific differences. Methods: We enrolled 253 STEMI patients (91 women, 28%) and assessed echocardiographic parameters at baseline and six months. LV reverse remodeling was defined as a ≥15% reduction in LV end-diastolic volume (LVEDV). Multivariate logistic regression identified independent predictors of remodeling. Clinical outcomes were evaluated over a median follow-up of 17 months (IQR 14–22 months), including major adverse cardiac events (MACEs). Kaplan–Meier and Cox regression analyses were performed. Results: Reverse remodeling occurred in 43% of patients and was more frequent in men than women (47% vs. 37%, p = 0.04). Male sex (OR 0.30; 95% CI: 0.14–0.65; p < 0.0001) and baseline global work efficiency (GWE) (OR 1.64; 95% CI: 1.45–1.85; p < 0.0001) were independent predictors. Men exhibited greater reductions in LVEDV, greater improvements in LV ejection fraction, and superior myocardial work indices. Over the follow-up, patients with reverse remodeling had significantly lower MACE rates compared to those without (10% vs. 24%, p < 0.01). Cox regression demonstrated that reverse remodeling was associated with a reduced risk of MACEs (HR 0.318; 95% CI: 0.181–0.557; p < 0.0001). Conclusions: LV reverse remodeling after STEMI is associated with improved clinical outcomes and is influenced by sex-specific differences. Baseline myocardial work indices, particularly GWE, are strong predictors of reverse remodeling. Men demonstrated a more favorable remodeling profile and myocardial recovery compared to women. Full article

Background/Objectives: Anatomical and functional damage of the mitral valve (MV) apparatus in patients with dilated cardiomyopathy (DCM) is secondary to left ventricular (LV) injury, leading to functional mitral regurgitation (FMR). Real-time four-dimensional echocardiography (RT 4DE) is a useful imaging technique in different pathologies, including DCM. Left atrial (LA) strain, as measured by left atrium quantification software, is an accurate technique for evaluating increased filling pressure. The MV has a complex three-dimensional morphology and motion. Four-dimensional echocardiography (4DE) has revolutionized clinical imaging of the mitral valve apparatus. This study aims (1) to characterize the mitral annulus (MA) parameters in patients with DCM and advanced-stage heart failure (HF) according to etiology and (2) to find correlations between left atrial function and MA remodeling in this group of patients, using 4DE quantification software. Methods: A total of 82 patients with DCM and an LV ejection fraction ≤ 40% were recruited. Conventional 2DE and RT 4DE were conducted in DCM patients with a compensated phase of HF before discharge. The measured parameters were left atrial reservoir strain (LASr), annular area (AA), annular perimeter (AP), anteroposterior diameter (A-Pd), posteromedial to anterolateral diameter (PM-ALd), commissural distance (CD), interregional distance (ITD), annular height (AH), nonplanar angle (NPA), tenting height (TH), tenting area (TA), and tenting volume (TV). Results: Measured parameters revealed more advanced damage of LA and MA parameters in ischemic compared to nonischemic etiology. Univariate analysis identified AA, AP, A-Pd, PM-ALd, CD, ITD, TH, TA, and TV (p < 0.0001) as determinants of LASr. Including these parameters in a stepwise multivariate logistic regression, PM-ALd (p = 0.03), TH (p = 0.043), and TV (p = 0.0001) were the best predictors of LAsr in these patients. Conclusions: The results of this study revealed the correlation between LA function depression and MA remodeling in patients with DCM. Full article

Cardiac remodeling in feline hypertrophic cardiomyopathy (HCM) is poorly understood. To investigate underlying molecular mechanisms, we determined microRNA–mRNA interactions, regulatory networks, and upstream regulators using left ventricle (LV) and left atrium (LA) mRNA and microRNA sequencing datasets from cats with HCM and controls. Upstream regulators, molecules, and pathways associated with ischemia, inflammation, fibrosis, and cellular changes were observed in the HCM heart. In both the HCM LV and LA, TNFα, IL1β, and TGFβ were identified as upstream regulators, along with FGF23, THBS4, and FAMB177 as the top increased molecules. Relevant microRNAs included upstream regulator miR-132, enriched miR-124-3p, miR-122b-3p, miR-146-5p (HCM LV and LA), miR-370, miR-1185-5p, miR-12194-3p (HCM LV), miR-153-3p, miR-185-5p, and miR-185-3p (HCM LA). Macrophage pathways were activated, and granulocyte and agranulocyte adhesion and diapedesis were the most connected pathways. The HIF1α signaling pathway in the HCM LV, upstream regulators miR-1-3p and miR-204, and reduced miR-29 and miR-122-5p suggest cardioprotective mechanisms. Observed in the healthy heart and suspected to be involved in cardiac homeostasis were upstream regulators miR-96, inhibited WNT3A and miR-145, as well as miR-140-5p, miR-141-3p, miR-208b-3p, and miR-885-3p. This study provides further insights into the pathogenesis of HCM, and identifies the factors involved in the maintenance of a healthy LV and LA. Full article

Background: Transthoracic echocardiography (TTE) is the primary imaging modality to assess cardiac morphology and function. In athletes, distinguishing physiological adaptations from pathological changes is essential. This study aimed to evaluate long-term cardiac structural and functional changes in professional soccer players. Methods: This retrospective study included 20 healthy male professional soccer players (mean age 21.2 ± 3.4 years) from the German first division, examined annually from 2016 to 2024 (mean follow-up 5.6 ± 2.0 years). TTE parameters associated with the “athlete’s heart” were assessed, including left ventricular end-diastolic diameter (LVEDD), interventricular septal thickness (IVSD), relative wall thickness (RWT), indexed LV mass (LVMi), and left atrial volume index (LAVi), along with 3D-derived LV and RV volumes. Advanced deformation imaging included global longitudinal strain (GLS), right ventricular strain (RVS), and left/right atrial reservoir strain (LASr and RASr, respectively). Baseline and final follow-up values were compared. Results: No significant changes were observed over time in conventional or advanced echocardiographic parameters (e.g., LVEDD: 54.5 ± 3.1 mm vs. 54.6 ± 3.9 mm; p = 0.868; GLS: −18.7% ± 2.2% vs. −18.4% ± 1.9%; p = 0.670). Ventricular volumes and strain values also remained stable throughout follow-up. Conclusions: Over a mean follow-up of more than five years, professional soccer players showed stable cardiac morphology and function without evidence of pathological remodeling. These findings support the concept that long-term high-level training in mixed-discipline sports leads to balanced, physiological cardiac adaptation. Full article

Loop diuretics like furosemide are commonly used in heart failure (HF) treatment, but their effects on disease progression are still unclear. Furosemide treatment accelerates HF deterioration in a swine model, but the mechanism of acceleration is poorly understood. We hypothesized that furosemide activates inflammatory signaling in the failing left ventricular (LV) myocardium, leading to adverse remodeling of the extracellular matrix (ECM). A total of 14 Yorkshire pigs underwent permanent transvenous pacemaker implantation and were paced at 200 beats per minute; 9 non-instrumented pigs provided controls. Seven paced animals received normal saline, and seven received furosemide at a dose of 1 mg/kg intramuscularly. Weekly echocardiograms were performed. Furosemide-treated animals reached the HF endpoint a mean of 3.2 days sooner than saline-treated controls (mean 28.9 ± 3.8 SEM for furosemide and 32.1 ± 2.5 SEM for saline). The inflammatory signaling protein transforming growth factor-beta (TGF-β) and its downstream proteins were significantly (p ≤ 0.05) elevated in the LV after furosemide treatment. The regulatory factors in cell proliferation, mitogen-activated protein kinase signaling pathway proteins, and matrix metalloproteinases were elevated in the furosemide-treated animals (p ≤ 0.05). Our data showed that furosemide treatment increased ECM remodeling and myocardial fibrosis, reflecting increased TGF-β signaling factors, supporting prior results showing worsened HF. Full article

Sodium–glucose cotransporter 2 inhibitors (iSGLT2) have become the fourth pillar of the medical treatment for heart failure with reduced ejection fraction (HFrEF). However, the mechanisms of action of iSGLT2 remain poorly understood. The effectiveness of combined ARNI and iSGLT2 therapy in left ventricular (LV) remodeling is still under study. We aim to investigate the effects of ARNI + iSGLT2 combination therapy in patients affected by HFrEF in terms of ventricular remodeling using speckle tracking echocardiography (STE). In this observational study, 136 patients with HFrEF taking ARNI were enrolled. All patients were evaluated at baseline (before iSGLT2), at 3 months and at 12 months from the beginning of iSGLT2 therapy. Echocardiographic parameters, including STE analysis and volumetric and LV contractile function indices, were collected at the three timepoints. The objectives were (1) to evaluate the effects of ARNI + iSGLT2 combination therapy on ultrasound (US) measurements; (2) to evaluate the effects on the variation of laboratory data indicative of HF (NT-pro-BNP); and (3) to evaluate the medium-long term impact of the ARNI + iSGLT2 combination therapy in terms of major cardiovascular events (MACVE). After only three months of combined ARNI + iSGLT2 therapy, we reported a significant improvement in ventricular and atrial volumetric indices, systolic function indices and myocardial deformation parameters assessed by STE. We also reported a significant decrease in NTproBNP levels. This trend was confirmed at 12 months follow-up. Furthermore, narrowing down the analysis to patients who were already treated with ARNI when they started taking iSGLT2, we reported similar results in the improvement of US parameters and NTproBNP levels. Our study has shown that the ARNI + iSGLT2 combination therapy leads to a clinical improvement and positive ventricular remodeling. Even the single introduction of additional iSGLT-2 in HFrEF patients on an otherwise optimized therapy resulted in a significant improvement in US and laboratory variables. The results of our study suggest implementing iSGLT-2 therapy as soon as possible, as the structural and functional cardiac improvements achieved by these drugs are achieved in the short term and maintained in the long term. Full article

Background: Aging and the female sex are considered risk factors for the development of heart failure with preserved ejection fraction (HFpEF). Unlike other risk factors, such as hypertension, obesity, or diabetes, they do not represent therapeutic targets. Methods: In a recently developed two-hit murine HFpEF model (angiotensin II + high-fat diet; MHS), we studied the relative contributions of the biological sex, aging, and gonadal hormones to cardiac remodeling and function. We aimed to reproduce a frequent HFpEF phenotype in mice characterized by aging, hypertension, the female sex, menopause, and metabolic alterations. Using the MHS mouse model, we studied cardiac remodeling and function in C57Bl6/J mice of both sexes, young (12 weeks) and old (20 months), that were gonadectomized (Gx) or not. Results: We observed that in mice, aging was associated with body weight gain, cardiac hypertrophy (CH), left ventricle (LV) concentric remodeling, and left atrial (LA) enlargement. Diastolic parameters such as E and A wave velocities were modulated by aging but only in females. Submitting young and old mice to MHS for 28 days induced the expected HFpEF phenotype consisting of CH, LV wall thickening, LA enlargement, and diastolic dysfunction with a preserved EF except for old males, in which it was significantly reduced. Young mice were Gx at five weeks, and old mice at six months (over a year before MHS). Gx increased myocardial fibrosis in MHS females and helped preserve the EF in males. Conclusions: Our results suggest that MHS has sex-specific effects on old mice, and the loss of gonadal hormones significantly impacts the observed heart failure phenotype. Full article

Objectives: We compared changes in hepatic and cardiac iron levels, left ventricular (LV) and right ventricular (RV) dimensions and function, and bi-atrial areas, all assessed through magnetic resonance imaging (MRI), between patients with non-transfusion-dependent thalassemia (NTDT) and those with neo-transfusion-dependent thalassemia (neo-TDT) over an 18-month follow-up period. Methods: We included 32 NTDT patients (42.78 ± 12.62 years, 53.1% females) and 58 neo-TDT (>4 transfusions per year) patients (44.08 ± 14.13 years, 46.6% females), consecutively enrolled in the Extension-Myocardial Iron Overload in Thalassemia project. Iron overload was quantified by T2* technique, biventricular function and atrial areas by cine images. Macroscopic myocardial fibrosis was detected by the late gadolinium enhancement technique. Results: Changes in cardiac and hepatic iron levels, in biventricular ejection fractions, in LV mass index, and bi-atrial areas were comparable between the two groups. A trend of worsening biventricular dimensions was observed in the NTDT group, while the neo-TDT group showed an improvement (decrease) in biventricular size (LV stroke volume index: p = 0.036; LV cardiac index: p = 0.031; RV end-diastolic volume index: p = 0.034; RV stroke volume index: p = 0.033). The inter-group comparison showed significant differences in the changes of biventricular end-diastolic volume indexes (LV: p = 0.011 and RV: p = 0.034) and stroke volume indexes (LV: p = 0.036 and RV: p = 0.033) and in the cardiac index (p < 0.0001). At both MRI scans, the frequency of replacement myocardial fibrosis was comparable between the two groups. Conclusions: Our 18-month longitudinal data revealed distinct patterns of cardiac remodeling in NTDT and neo-TDT patients. The progressive ventricular dilation observed in NTDT patients highlights the need for careful MRI monitoring and potential interventions to address the long-term cardiac consequences of anemia. Full article

Background/Objectives: This study aims to investigate the potential etiopathogenesis of HFpEF development and identify possible different phenotypes of HFpEF in patients with chronic obstructive pulmonary disease (COPD) and systemic sclerosis-associated interstitial lung diseases (SS-ILDs). It could help clinicians improve early HFpEF personalized detection and management. Methods: This study included 150 patients with chronic lung diseases (CLDs), such as COPD and SS-ILD, who were outside of exacerbation, had no history of chronic heart failure (CHF), and had a left ventricular ejection fraction (LV EF) of ≥50%. The functional status of the lungs, heart, endothelial dysfunction, and acid–base balance was assessed. The results obtained were compared in groups of patients with CLD depending on the presence or absence of HF with preserved ejection fraction (HFpEF). The diagnosis of HFpEF was established based on the HFA-PEFF Score classification. Nonparametric statistical methods were used. Results: In patients with CLD, indicators such as age, longitudinal size of the right atrium, mid-regional pro-atrial natriuretic peptide (MR-proANP), and highly sensitive cardiac troponin T (hsTnT) were higher than in the group of patients without HFpEF. In patients with COPD and HFpEF, statistically significant changes were found in the volume of the left atrium. In patients with SS-ILD and HFpEF, statistically significant differenceswere found in SBP before and after the 6 min walk test (6MWT), the Borg scale before 6MWT, MR-proANP, and the longitudinal dimension of the right atrium. Conclusions: The results of our study allow us to identify two different mechanisms of HFpEF development: In patients with COPD, the predominant factor in the development of HFpEF was hypoxia, while in patients with SS-ILD, myocardial dysfunction with remodeling developed against the background of secondary pulmonary hypertension, highlighting the importance of phenotype-specific evaluation. These findings suggest potential approaches for personalized risk stratification and the development of targeted management strategies for patients with HFpEF. Full article

Background/Objectives: Cardiovascular diseases are the most prevalent comorbidities in patients with acromegaly (APs). Acromegalic cardiomyopathy is the leading cause of mortality in APs. This study aimed to assess changes in morphology and function of the left heart in naïve APs 12 months after the beginning of acromegaly treatment and to explore the effects of disease activity and body composition parameters on changes in the left heart. Methods: This prospective study involved 34 APs and 34 healthy controls (CON) matched for age, gender, and BMI. DXA and 2D echocardiography were performed at diagnosis and 12 months after the beginning of the treatment. Results: In APs, the prevalence of left ventricular (LV) hypertrophy was 70%. LV mass index (LVMI) was greater in APs compared to CON (124 vs. 86 ± g/m², p < 0.001), but with no difference in size and systolic function of the LV. APs presented with increased left atrium volume (LAVI) and with diastolic dysfunction of the LV. Twelve months after the beginning of acromegaly treatment, IGF-1 levels decreased significantly (p < 0.001), and biochemical control of disease was achieved in 73.52% of APs. We found that in all APs, LAVI and LVMI decreased (all p < 0.05), and diastolic function of the LV improved without changes in systolic function. In multiple analyses, the changes in body surface area (β = −0.444, p < 0.001) and in lean body mass (β = −0.298, p = 0.027) were independent predictors of reverse remodelling of LVMI after the treatment. Conclusions: This study confirmed remodelling reversal of the left heart structure, followed by an improvement in diastolic function in naïve APs 12 months after the beginning of acromegaly treatment. Full article

Background/Objectives: Left ventricular (LV) pseudoaneurysm is a rare but life-threatening complication after acute myocardial infarction, often resulting from inadequate excision of damaged myocardium and use of only a xenopericardial patch during primary LV free wall rupture repair. Methods: A 62-year-old female developed a giant LV pseudoaneurysm one year after initial surgical repair of a free wall rupture with a xenopericardial patch. Imaging confirmed a large pseudoaneurysm with a broad neck and mural thrombus. She underwent pseudoaneurysmectomy, LV reconstruction with a Dacron patch overlaid by a xenopericardial patch, and concomitant mitral and tricuspid valve repair. Results: Surgical exploration revealed a broad-necked pseudoaneurysm and dehisced patch material. The aneurysm was resected, and the LV was reconstructed, resulting in the exclusion of the pseudoaneurysm and improvement of the shape and function. The patient recovered uneventfully and was discharged in good clinical condition with restored LV function. Conclusions: Pseudoaneurysm formation after LV free wall rupture repair is often due to insufficient resection and the use of only a xenopericardial patch. Surgical management with complete excision, Dacron patch reconstruction, and xenopericardial reinforcement facilitates the favorable remodeling of LV geometry and function, and reduces the risk of recurrence. Full article

Accurate prognostic stratification in patients with chronic heart failure and reduced ejection fraction (HFrEF) remains a significant clinical challenge. Many different parameters, including left ventricular (LV) and right ventricular (RV) function and cardiopulmonary exercise testing (CPET) parameters, are available in the literature. LV ejection fraction (LVEF) is the most used parameter in clinical practice. This study aimed to analyze CPET and echocardiographic data in patients under evaluation for heart transplantation (HTx) to identify the parameter that best correlates with cardiac events. Methods and Results. Echocardiography and CPET were performed in patients with HFrEF under evaluation for HTx. The population comprised 170 patients (mean age: 55 ± 9 years; 88% male; non-ischemic etiology: 63%). LVEF was 30.4 ± 7.6%, peak oxygen uptake (Vo_2peak) was 17.08 ± 4.6 mL/Kg/min; minute ventilation (VE)/carbon dioxide production (Vco₂) slope was 34.8 ± 8.7. During a follow-up of 4 ± 1 years, 37 hospitalizations, 4 deaths, 14 HTx, and 5 LV assist device implantation occurred. Patients who experienced major events had a lower Vo_2peak (p < 0.005), higher VE/Vco₂ slope (p < 0.005), greater LV end-systolic diameter (p < 0.005), and RV end-diastolic diameter (p < 0.005) than patients without events. Conversely, LVEF did not differ between these two groups. VE/Vco₂ slope and RV dimensions significantly correlated with hard cardiac events (p = 0.019 and p = 0.008, respectively). Conclusions. In patients with HFrEF, parameters quantifying the system reserve (i.e., Vo_2peak and VE/Vco₂ slope) and those demonstrating advanced biventricular remodeling may help stratify the risk of cardiac events. Conversely, LVEF showed a limited prognostic value in this setting. Full article

Background: Myocardial fibrosis in aortic stenosis (AS) is associated with a significant risk of poor clinical outcomes. Myocardial fibrosis can be evaluated using cardiovascular magnetic resonance (CMR) imaging and may be useful for risk-stratifying patients at high risk for poorer outcomes. A circulating biomarker of fibrosis may be a cheaper, more accessible alternative to CMR in lower-to-middle-income countries. This study evaluated the correlation between serum biomarkers of myocardial fibrosis (TGF-β1, PICP, and PIIINP) with CMR markers of myocardial fibrosis (T1 mapping, extracellular volume fraction (ECV), and late gadolinium enhancement (LGE)). Methods: Twenty-one high-gradient (mean gradient ≥ 40 mmHg) severe AS (aortic valve area < 1.0 cm²) participants underwent T1 mapping and LGE imaging using CMR. Blood serum was collected for enzyme-linked immunosorbent assays of the listed biomarkers. Results: Serum TGF-β1 was associated significantly with the global T1 relaxation time on CMR (r = 0.46 with 95% CI 0.03 to 0.74, p = 0.04). In the high T1 time group (1056 vs. 1023 ms), trends toward elevated serum TGF-β1 concentration (13,044 vs. 10,341 pg/mL, p = 0.08) and ECV (26% vs. 24%, p = 0.07) were observed. The high T1 and trend towards elevated TGF-β1 concentration in this group tracked adverse LV remodeling and systolic dysfunction. There were no significant associations between PICP/PIIINP and T1 mapping or between the biomarkers and LGE quantity. Conclusions: Serum TGF-β1 is a potential surrogate for diffuse interstitial fibrosis measured by T1 mapping and ECV on CMR. Serum PICP and PIIINP may be less appropriate as surrogate markers of fibrosis in view of their temporal trends over the course of AS. Larger studies are needed to validate the utility of TGF-β1 as a marker of diffuse fibrosis and to evaluate the utility of serial PICP/PIIINP measurements to predict decompensation. Full article

Background/Objectives: Cardiac resynchronization therapy (CRT) with fusion pacing (“LV only”), also known as fusion-CRT (f-CRT), represents a feasible alternative to cardiac resynchronization therapy (CRT) with biventricular pacing (BiVP), not only in cases of BiVP failure, but also as a primary therapy option due to its potential benefits over traditional CRT. Fusion pacing may be particularly beneficial in selected patients and understanding the structural and functional differences between responders could guide future optimization strategies. This study provides a descriptive comparison between super-responders (SRs) and non-super-responders (NSRs) undergoing fusion-CRT. Methods: Patients with RA/LV-only pacing systems or biventricular CRT systems operating predominantly in LV-only pacing mode due to intrinsic RV conduction were included. A follow-up protocol was conducted for all patients at 6 months and then annually. Data from the most recent follow-up were used for statistical analysis. Super-responders (SRs) were those with substantial reverse remodeling, quantified by a ≥30% reduction in LVESV and a stable LVEF of ≥45% at follow-up. Although SRs were defined based on these reverse remodeling criteria, separate analyses of additional echocardiographic parameters (e.g., left atrial dimensions) were performed to independently assess the broader impact of fusion-CRT on cardiac structure and function. Results: Among 71 patients, 55 were non-super-responders (NSRs) and 16 were super-responders (SRs), with a mean follow-up of 43.2 months. SRs were predominantly female and had smaller left ventricular (LV) dimensions: LVEDd (6.30 cm vs. 6.80 cm, p = 0.02), LVEDV (185 mL vs. 240 mL, p = 0.03), LVESV (132.5 mL vs. 175 mL, p = 0.03), and a higher LVEF (p = 0.03). The follow-up LVEF was positively correlated with changes in LVESV (ρ = 0.557, p < 0.001), but not with NYHA class changes (ρ = 0.184, p = 0.125). Larger baseline LV and left atrial (LA) volumes were associated with a reduced follow-up LVEF (LVESV: ρ = −0.426, p < 0.001; LVEDV: ρ = −0.394, p < 0.001; LAv: ρ = −0.374, p = 0.001). Both groups showed improvement in the NYHA class (p < 0.001, p = 0.007). MR improved significantly in SRs (p = 0.02) and worsened slightly in NSRs (p = 0.13), while TR worsened significantly in the NSRs group (p = 0.03). Conclusions: Our findings highlight key differences in clinical and echocardiographic parameters between SRs and NSRs following fusion-CRT. These observations may contribute to a better understanding of response patterns and inform future prospective studies aiming to optimize patient selection and timing of therapy. Full article

Acute myocardial necrosis activates the immune response and inflammatory processes. Although the initial response is helpful in restoring tissue injury, dysregulated and exacerbated inflammation contributes to the progression of cardiac remodeling. Inflammasomes play important roles in post-infarction inflammation. NALP1/NLRP1, NLRP 3, and NLRC4 are the best-known inflammasomes. NLRP3, which has received the most study in cardiovascular disease, has been linked to increased IL-1β (IL1B) production and caspase-1 activity, as well as impaired cardiac function. The role of NLRP1 and NLRC4 inflammasomes after acute myocardial infarction (MI) is poorly understood. We evaluated the expression of myocardial inflammasomes and inflammatory markers 72 h after MI in rats. Male Wistar rats were divided into Sham (n = 15) and MI (n = 16) groups. MI was induced by ligating the left anterior descending coronary artery. Infarct size was assessed by histology. Myocardial protein and gene expression was analyzed by Western blot and RT-qPCR, respectively. IL-1β (Il1b) concentrations in serum and heart macerate supernatant were evaluated by ELISA. Statistical analysis was performed using Student’s t test. Rats with an MI size less than 30% of the total left ventricle (LV) area were excluded; infarct size was 46 ± 11% of the total LV area in MI. The interstitial collagen fraction was higher in MI. Nlrc4, caspase-1 (Casp1), and IL-1β (Il1b) protein expressions were higher in MI. Nlrp3, Nlrp1, ASC (Pycard), pro-caspase-1, and pro-IL-1β (Il1b) expressions did not differ between groups. Expression of the Nlrp3 and ASC (Pycard) genes, as well as myocardial and serum IL-1β (Il1b) concentrations, was higher in MI. Acute post-myocardial infarction inflammation is characterized by increased protein expression of Nlrc4, caspase-1, and interleukin-1β; increased gene expression of Nlrp3 and ASC (Pycard); and elevated serum and myocardial concentrations of interleukin-1β in combination with an increased myocardial collagen interstitial fraction. Full article