Constantin Militaru

Background: Left ventricular remodeling after myocardial infarction is heterogeneous, and conventional baseline measures of systolic function only partly anticipate its course. Left ventricular ejection fraction (LVEF) and myocardial work reflect different aspects of systolic performance. We examined whether deviation of global work index (GWI) from the value expected for LVEF is associated with reverse remodeling after reperfused ST-elevation myocardial infarction (STEMI). Methods: In 101 prospectively enrolled patients with single-vessel STEMI, echocardiography was performed 12–24 h after reperfusion and at 12 ± 2 months. Residual GWI (GWIr) was calculated as observed GWI minus regression-predicted GWI for the corresponding LVEF. The primary outcome was follow-up 3D end-systolic volume (3D-ESV), adjusted for baseline. Results: Of 60 patients with paired imaging, 58 had baseline GWI; 18 showed reverse remodeling (≥15% 3D-ESV reduction). Each 1-SD higher GWIr was associated with 3.74 mL lower follow-up 3D-ESV (95% CI −6.70 to −0.77; p = 0.015) and higher odds of reverse remodeling (odds ratio 2.38, 95% CI 1.28–5.01; p = 0.005). For the continuous outcome, absolute GWI had a comparable point estimate with a wider confidence interval. Conclusions: Higher GWIr, indicating myocardial work higher than expected for LVEF, was associated with lower follow-up 3D-ESV and higher odds of reverse remodeling after adjustment for baseline 3D-ESV. These exploratory findings require external validation.

Background/Objectives: Ventricular recovery after ST-segment elevation myocardial infarction (STEMI) is commonly assessed using either structural (volumetric) or functional (ejection-fraction) criteria, although these may capture different aspects of recovery. We examined whether their cross-classification identifies distinct recovery patterns and whether myocardial mechanics and left atrial function provide additional information. Methods: We prospectively followed 101 patients with first STEMI and single-vessel coronary artery disease treated with PCI. Echocardiography was performed 12–24 h after reperfusion and at 12 ± 2 months. Structural recovery (≥15% reduction in 3D LV end-systolic volume) and functional recovery (≥5-point absolute LVEF increase) were cross-classified into four recovery patterns. Results: Among 53 patients with complete paired measurements, 10 (18.9%) showed concordant recovery, 7 (13.2%) isolated structural recovery, 9 (17.0%) isolated functional recovery, and 27 (50.9%) no recovery; 30.2% therefore showed discordant recovery. The no-recovery group was heterogeneous, including both volumetric deterioration and stable or improving volumes below the recovery threshold. Continuous changes in 3D-ESV and LVEF were only moderately correlated (ρ = 0.353, p = 0.0095), and discordance persisted in sensitivity analyses. Myocardial mechanics and LASR did not differentiate recovery patterns, but several of these baseline markers showed exploratory associations with clinical outcomes after false-discovery-rate correction. Conclusions: Structural and functional recovery after STEMI are complementary rather than interchangeable, and this discordance persisted across extensive sensitivity analyses; however, assignment of individual patients to specific recovery categories remained sensitive to the chosen thresholds and LVEF measurement method. Myocardial mechanics and LASR may provide additional information about clinical expression.

Background: Rapid, disproportionate expansion of post-infarction left ventricular (LV) aneurysms represents a high-risk remodeling phenotype characterized by progressive mechanical deterioration and severe geometric distortion. Methods: A 54-year-old male presented with late anterior myocardial infarction complicated by a partially thrombosed apical LV aneurysm with an initial left ventricular ejection fraction (LVEF) of 35%. Despite clinical stability under optimal guideline-directed medical therapy, serial multimodality imaging at 7 weeks revealed an aggressive, disproportionate expansion of the aneurysmal component to 120 mL, inducing severe ventricular geometric distortion and secondary functional degradation (LVEF 20%). Multimodality imaging demonstrated a favorable geometry of the functional ventricle with preserved contractile function. Results: The patient underwent prompt surgical ventricular restoration using a double-patch Dor technique, effectively excluding the large aneurysm and restoring physiological ventricular geometry. The postoperative course was uneventful. At 6-month follow-up, cardiovascular magnetic resonance confirmed sustained reverse remodeling and significant recovery of systolic LV function (LVEF 47%). Conclusions: This case illustrates that rapid post-infarction aneurysmal expansion may occur despite apparent clinical stability. Comprehensive multimodality imaging may help identify selected patients in whom a reconstructible myocardial substrate supports surgical ventricular restoration despite severely reduced LVEF, even when conventional clinical indications for aneurysmectomy are absent.

Background: Hypertrophic cardiomyopathy (HCM) is a genetic disorder marked by myocardial hypertrophy, leading to diastolic and systolic dysfunction and heart failure. Traditionally, the burn-out stage is defined by systolic dysfunction, but we propose expanding its definition to include advanced diastolic dysfunction. Methods: We retrospectively analyzed HCM patients (2004–2023) with either systolic dysfunction (left ventricular ejection fraction [LVEF] < 50%) or advanced diastolic dysfunction (preserved LVEF with left atrial enlargement and elevated filling pressures: E/A ≥ 2 or E/e′ ≥ 14). Both subgroups were included under the term “end-stage HCM” and compared to HCM controls with preserved LVEF and impaired relaxation. Results: Of 696 HCM patients, 94 had end-stage HCM (23 with systolic dysfunction, 71 with advanced diastolic dysfunction). Median age was 56.5 years, and 55.3% were male. End-stage HCM patients were more symptomatic at follow-up than controls (91.5% vs. 75.0%, p-value = 0.006), with higher rates of dyspnea and advanced heart failure (38.3% vs. 6.3%, p-value < 0.001). Advanced diastolic dysfunction was associated with a more symptomatic profile (p-value = 0.013) and a high annual mortality rate (2.34%, p = 0.014). Male sex, older age, lower LVEF, and higher E/A predicted systolic dysfunction. Conclusions: Advanced diastolic dysfunction represents an alternative progression pathway in burn-out HCM, requiring distinct management strategies alongside systolic dysfunction.

Background and Objectives: This observational study investigates the relationship between Lipoprotein (a) (Lp(a)) levels and the risk of acute myocardial infarction (AMI). This study aims to highlight the association of elevated Lipoprotein (a) levels with an increased atherogenic profile and the potential risk of AMI. Materials and Methods: We conducted a case–control study involving 106 individuals, including 64 AMI patients (both STEMI and NSTEMI) and 42 healthy controls. Comprehensive clinical and biochemical assessments, including Lp(a) measurements, were conducted. Results: Patients with Lp(a) levels ≥ 30 mg/dL had a threefold increased risk of AMI compared to those with lower levels, independent of traditional risk factors such as cholesterol, smoking, and body weight. Elevated Lp(a) was observed in 50% of AMI patients compared to 28.57% in controls (p = 0.028). Notably, a multivariate analysis identified high Lp(a) levels, low HDL-C levels, and obesity as significant independent predictors of AMI, indicating these factors may contribute to AMI risk more prominently than other conventional risk factors in patients with elevated Lp(a). Moreover, the association between Lp(a) and AMI risk was consistent across various patient subgroups, with low HDL-C further compounding the risk. Conclusions: Lp(a) is a significant independent risk factor for acute myocardial infarction; therefore, screening for Lp(a) levels can help identify high-risk individuals beyond traditional markers. Therapeutic approaches targeting Lp(a) may reduce AMI incidence. Future research should explore how Lp(a) promotes atherosclerosis and assess Lp(a)-lowering therapies to improve patient outcomes.

Introduction: Cardiovascular diseases are the leading cause of mortality worldwide, with a significant impact on socioeconomic aspects. Various biomarkers have been studied in relation to the diagnosis, progression, and prognosis of atherosclerotic disease, with lipoprotein (a) [Lp (a)] standing out as an important predictor of cardiovascular risk. This observational study aimed to clarify the association between Lp (a) levels and the severity of significant multivessel coronary lesions in acute myocardial infarction (AMI) patients. Materials and Methods: Conducted at the Clinical Emergency County Hospital of Craiova, Romania, the study involved 256 young patients divided into two groups based on Lp (a) levels: Group A (Lp (a) < 30 mg/dL) and Group B (Lp (a) ≥ 30 mg/dL). Patients included young adults up to 55 years for males and 60 years for females, excluding those with familial hypercholesterolemia. Results: The study revealed a significant association between elevated Lp (a) levels and the presence of multivessel coronary lesions. Patients with Lp (a) concentrations ≥ 30 mg/dL exhibited a higher prevalence of multivessel disease compared to those with lower levels. Discussion: The findings suggest that elevated Lp (a) levels are a crucial biomarker for the risk of coronary artery disease, particularly in young patients with AMI. The study emphasizes the need for aggressive lipid management strategies and personalized treatment approaches, considering the significant role of Lp (a) in atherosclerosis and AMI. Conclusions: Lipoprotein A levels above 30 mg/dL are associated with a higher prevalence of multivessel coronary lesions. Multivariate analysis revealed that higher Lp (a) levels and lower HDL levels are linked to an increased risk of multivessel coronary lesions.

Atrial fibrillation is frequently seen in patients with dilated cardiomyopathy (DCM), and its presence impacts the function of the heart, with clinical and prognostic consequences. In this prospective single-center study, we aimed to assess the impact of atrial fibrillation on cardiac structure and function, using comprehensive two- and three-dimensional echocardiography. We included 41 patients with DCM and persistent or permanent atrial fibrillation (38 male, age 58.8 ± 11 years), as well as 47 patients with DCM and in sinus rhythm (35 male, age 58 ± 12.5 years). Cardiac chambers and mitral and tricuspid valves’ structure and function were assessed via standard two-dimensional, speckle-tracking, and three-dimensional echocardiography (3DE). Patients with DCM and atrial fibrillation had a more impaired left ventricular global longitudinal strain, higher 3DE left atrial volumes, and reduced function compared to patients in sinus rhythm in the presence of similar left ventricle volumes. Mitral annulus configuration was altered in atrial fibrillation DCM patients. Also, right heart volumes were larger, with more severe atrial and ventricular dysfunction, despite similar estimated pulmonary artery pressures and severity of tricuspid regurgitation. Using advanced echocardiography techniques, we demonstrated that atrial fibrillation induces significant remodeling in all heart chambers.

Cardiomyopathies are structural and functional myocardial disorders that are not caused by other specific conditions such as coronary artery disease, arterial hypertension, valvular disease or congenital heart diseases. They are grouped into specific morphological and functional phenotypes, and sub-classified into familial and non-familial forms, with the dilated phenotype being the most frequent. However, there are many overlapping features between these phenotypes, complicating the diagnosis and management of patients. We report here the case of three related patients with different types of cardiomyopathies, emphasizing the importance of a multimodal approach to diagnosis.

Dilated cardiomyopathies (DCMs) are a heterogenous group of primary myocardial diseases, representing one of the leading causes of heart failure, and the main indication for heart transplantation. While the degree of left ventricular dilation and dysfunction are two key determinants of adverse outcomes in DCM patients, right ventricular (RV) remodeling and dysfunction further negatively influence patient prognosis. Consequently, RV functional assessment and diagnosing RV involvement by using an integrative approach based on multimodality imaging is of paramount importance in the evaluation of DCM patients and provides incremental prognostic and therapeutic information. Transthoracic echocardiography remains the first-line imaging modality used for the assessment of the RV, and newer techniques such as speckle-tracking and three-dimensional echocardiography significantly improve its diagnostic and prognostic accuracy. Nonetheless, cardiac magnetic resonance (CMR) is considered the gold standard imaging modality for the evaluation of RV size and function, and all DCM patients should be evaluated by CMR at least once. Accordingly, this review provides a comprehensive overview of the anatomy and function of the RV, and the pathophysiology, diagnosis, and prognostic value of RV dysfunction in DCM patients, based on traditional and novel imaging techniques.

Adults living with HIV (human immunodeficiency virus) infection (ALHIV) have high rates of cardiovascular events. New approaches are needed to detect subclinical cardiac dysfunction. We used conventional and speckle tracking echocardiography to investigate whether ALHIV display latent cardiac dysfunction. We analyzed 85 young subjects with HIV infection and free from cardiovascular risk factors (31 ± 4 years) and 80 matched healthy volunteers. We measured left ventricular (LV) layered global longitudinal strain, circumferential strain, peak longitudinal strain in the reservoir and contraction phases of the left atrium (LASr respectively LASct). In the HIV group, LV ejection fraction and s’ TDI (tissue doppler imaging) were slightly lower but still in the normal ranges. Layered longitudinal strain showed no significant difference, whereas circumferential global strain was significantly lower in the HIV group (−20.3 ± 3.9 vs. −22.3 ± 3.0, p < 0.001). LASr (34.3% ± 7.3% vs. 38.0% ± 6.9%, p < 0.001) was also lower in ALHIV and multivariate analysis showed that age (β = −0.737, p = 0.01) and infection duration (β = −0.221, p = 0.02) were independently associated with LASr. In the absence of cardiovascular risk factors, adults living with HIV display normal LV systolic function. Left atrial reservoir strain, is, however, decreased and suggests early diastolic dysfunction.