Speckle tracking echocardiography is an advanced imaging technique that allows for a more detailed assessment of cardiac global and regional function. Reference values for segmental longitudinal layered strain (subendocardial, mid-myocardial, and subepicardial) are scarce, limiting the clinical use of these measurements in clinical practice. Two hundred consecutive Caucasian healthy subjects (mean age = 37 ± 11 years) were enrolled in the study. The mean values of global longitudinal strain (GLS) for endocardial (Endo), mid-myocardial (Myo) and epicardial (Epi) layers were −22.9 ± 2.7, −20.0 ± 2.4 and −17.5 ± 2.1, respectively. The GLSEndo/GLSMyo ratio was 1.1 ± 0.05, while the GLSEndo/GLSEpi ratio was 1.3 ± 0.05. The apical strain-sparing ratio was >1 in 10% of the subjects (endocardium) and 7% (mid-myocardium). The lower limits for segmental LS were as follows: for endocardial LS, −10% (basal), −12% (mid), −14% (apical); for mid-myocardial LS, −10% −10% (basal), −10% (mid), −10% (apical); and for epicardial LS, −7% (basal), −8% (mid), −8% (apical). The findings of this study provide data regarding the lower limit of normality of LS for each LV segment and suggest, for practical considerations, that an LS value below 10% should be considered abnormal in any segment. Further larger studies are warranted to confirm these findings.

Background: Left ventricular noncompaction is a rare cardiomyopathy characterized by a thin, compacted epicardial layer and a noncompacted endocardial layer, with trabeculations and recesses that communicate with the left ventricular cavity. In the advanced stage of the disease, the classical triad of heart failure, ventricular arrhythmia, and systemic embolization is common. Segments involved are the apex and mid inferior and lateral walls. The right ventricular apex may be affected as well. Case presentation: A 29-year-old Caucasian male was hospitalized with dyspnea and fatigue at minimal exertion during the last months before admission. He also described a history of edema of the legs and abdominal pain in the last weeks. Physical examination revealed dyspnea, pulmonary rales, cardiomegaly, hepatomegaly, and splenomegaly. Electrocardiography showed sinus rhythm with nonspecific repolarization changes. Twenty-four-hour Holter monitoring identified ventricular tachycardia episodes with right bundle branch block morphology. Transthoracic echocardiography at admission revealed dilated left ventricle with trabeculations located predominantly at the apex but also in the apical and mid portion of lateral and inferior wall; end-systolic ratio of noncompacted to compacted layers > 2; moderate mitral regurgitation; and reduced left ventricular ejection fraction. Between apical trabeculations, multiple thrombi were found. The right ventricle had normal morphology and function. Speckle-tracking echocardiography also revealed systolic left ventricle dysfunction and solid body rotation. Abdominal echocardiography showed hepatomegaly and splenomegaly. Abdominal computed tomography was suggestive for hepatic and renal infarctions. Laboratory tests revealed high levels of N-terminal pro-brain natriuretic peptide and liver enzymes. Cardiac magnetic resonance evaluation at 1 month after discharge confirmed the diagnosis. The patient received anticoagulants, antiarrhythmics, and heart failure treatment. After 2 months, before device implantation, he presented clinical improvement, and echocardiographic evaluation did not detect thrombi in the left ventricle. Coronary angiography was within normal range. A cardioverter defibrillator was implanted for prevention of sudden cardiac death. Conclusions: Left ventricular noncompaction is rare cardiomyopathy, but it should always be considered as a possible diagnosis in a patient hospitalized with heart failure, ventricular arrhythmias, and systemic embolic events. Echocardiography and cardiac magnetic resonance are essential imaging tools for diagnosis and follow-up.

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.

Background and Objectives: This is a retrospective study conducted at the Clinical County Hospital of Craiova, Romania, providing valuable insights into hemorrhagic transformation (HT) in thrombolyzed patients with acute ischemic stroke (AIS). Hemorrhagic complications remain a significant concern after intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA). This study aims to analyze clinical and biological factors associated with HT following thrombolysis. Materials and Methods: A retrospective analysis was conducted on 356 patients who received rt-PA at the Clinical County Hospital of Craiova between January 2020 and December 2024. Patients were divided into three groups based on CT findings at 24 h post-thrombolysis: no HT, minimal HT, and massive HT. Baseline characteristics were analyzed, including demographics, medical history, NIHSS scores, imaging findings, and laboratory parameters. Statistical analysis was performed using ANOVA and chi-square tests, with a significance threshold of p < 0.05. Results: HT occurred in 12.08% of patients (minimal HT: 8.15%, massive HT: 3.93%). Mortality was significantly higher in the massive HT group (71.43%) compared to minimal HT (41.38%) and non-HT (13.42%) (p < 0.001). Lower platelet count (p = 0.003), elevated blood glucose (p = 0.004), prolonged QT interval (p = 0.004), and reduced fibrinogen levels (p = 0.005) were significantly associated with HT. Other risk factors included atrial fibrillation (p = 0.001), hypertension (p = 0.005), delayed door-to-needle time (p < 0.001), diabetes mellitus (p = 0.007), dense ACM sign on CT (p = 0.003), older age (p < 0.001), obesity (p = 0.001), early neurological deterioration at 2 h/24 h (p < 0.001), elevated GOT (p < 0.001), elevated GPT (p = 0.002), lower LDL cholesterol (p < 0.001), lower total cholesterol (p = 0.001), and lower triglycerides (p < 0.001). Conclusions: Patients with HT had worse clinical outcomes, with massive HT associated with the highest mortality. Risk factors include age, nutritional status, hyperglycemia, and low platelet and fibrinogen levels, among others.

Background/Objectives: This study aimed to evaluate layer-specific strain according to etiology and assess whether subtle changes in longitudinal and circumferential layer strain are involved in predicting cardiac mortality during a two-year follow-up in patients with dilated cardiomyopathy admitted with heart failure decompensation. Methods: 97 patients with dilated cardiomyopathy and a left ventricle ejection fraction ≤ 40% were recruited, 51 with ischemic and 46 with nonischemic etiologies. Conventional and two-dimensional speckle-tracking echocardiography (2D-STE) were conducted in dilated cardiomyopathy patients with a compensated phase of heart failure before discharge. Layer-specific longitudinal and circumferential strain was assessed from the endocardium, mid-myocardium, and epicardium by two-dimensional (2D) speckle-tracking echocardiography. The gradient between the endocardium and epicardium was calculated. Results: Patients with nonischemic etiology of dilated cardiomyopathy presented smaller values of global and layer strain than patients in the ischemic group. GLS, GLSend, GLSend-GLSepi, CSPMend, CSPMend-CSPMepi, CSAP, CSAPend, and CSAPend-CSAPepi were the parameters with statistically significant decreased values in non-survivors compared with survivors. In multivariate analysis, only CSPMend showed an independent value in predicting mortality at two-year follow-up. Receiver operator curve analysis provided CSPMend of −10.8% as a cut-off value with a sensitivity of 80% and specificity of 61.05% in identifying the dilated cardiomyopathy and heart failure patients with a risk of death at two-year follow-up. Conclusions: GLS, GCS, and layer-specific strain analysis showed decreased values in nonischemic compared with ischemic dilated cardiomyopathy and also in non-survivors compared with survivors. CSPMend was the most sensitive strain parameter to identify patients with increased mortality risk at two-year follow-up.

Mitral regurgitation is among the most common valvular heart diseases. Mitral regurgitation in patients with dilated cardiomyopathy is a complex pathology involving annular dilatation, papillary muscle displacement, systolic leaflet tethering, and left ventricular remodeling. Quantification of mitral apparatus damage in these patients is essential for successful interventional and surgical therapy. Mitral regurgitation in the presence of dilated cardiomyopathy is classified as Carpentier type IIIB, with restricted leaflet mobility as a standard feature. Echocardiography allows accurate evaluation of the complex anatomy and function of the mitral apparatus. Updated guidelines recommend two-dimensional followed by systematic three-dimensional echocardiographic evaluation in patients with mitral regurgitation. New three-dimensional echocardiographic software packages provide many parameters that help identify the precise morphology and function of the various components of the mitral apparatus, helping to determine the etiology of mitral regurgitation and evaluate disease severity. This review provides the first point-by-point approach to the assessment of all old and new echocardiographic methods, from the simplest to the most complex, used to examine the components of the mitral valve apparatus in patients with dilated cardiomyopathy. Although these parameters are still under research, this information will be helpful for establishing therapeutic procedures in a disease with a poor prognosis.