In recent years, atrial fibrillation (AF) has increasingly become a focus of attention because it represents the most encountered arrhythmia in clinical practice and a major cause of morbidity and mortality. Issues underlying AF have long been debated; nevertheless, electrical, contractile, and structural remodeling is demonstrated to be the pivotal contributor to arrhythmic substrate. Fibrosis is a hallmark of arrhythmogenic structural remodeling, resulting from an accumulation of fibrillar collagen deposits, as a reparative process to replace degenerating myocardium with concomitant reactive fibrosis, which causes interstitial expansion. Although the precise role of fibrosis in AF initiation and maintenance remains to be fully elucidated, a better definition of its extent and distribution may assist in designing individually tailored ablation approaches and improving procedure outcomes by targeting the fibrotic substrates with an organized strategy employing imaging resources. A deep comprehension of the mechanisms underlying atrial fibrosis could be crucial to setting up improved strategies for preventing AF-promoting structural remodeling. Imaging modalities such as echocardiography, cardiac computed tomography, and cardiac magnetic resonance, combined sometimes with invasive electroanatomical mapping, could provide valuable information for the optimal patients' management if their use is not limited to cardiac anatomy study but extended to characterize abnormal left atrial substrate. Although pulmonary vein isolation is usually efficacious in treating paroxysmal AF, it is not sufficient for many patients with nonparoxysmal arrhythmias, particularly those with longstanding persistent AF. Noninvasive imaging techniques play a pivotal role in the planning of arrhythmic substrates ablation and show a strong correlation with electro-anatomic mapping, whose novel multipolar mapping catheters allow nowadays a more precise comprehension of atrial substrate. This review aims to explore the impact of the various imaging modalities for the detection of atrial fibrosis and their role in the management of AF.

Cardiac resynchronization therapy (CRT) in heart failure patients has been shown to improve patient outcomes in some but not all patients. A few studies have identified that septal flash on imaging is associated with response to CRT, but there has yet to be systematic review to evaluate the consistency of the finding across the literature. A search of MEDLINE and EMBASE was conducted to identify studies, which evaluate septal flash and its association with CRT response. Studies that met the inclusion criteria were statistically pooled with random-effects meta-analysis and heterogeneity was assessed using the I² statistic. A total of nine studies were included with 2307 participants (mean age 76 years, 67% male). Septal flash on imaging before CRT implantation was seen in 53% of patients and the proportion of CRT responders from the included studies varied from 52% to 77%. In patients who were CRT responders, septal flash was seen in 40% of patients compared to 10% in those deemed to be CRT nonresponders. Meta-analysis of eight of the nine included studies suggests that the presence of septal flash at preimplant was associated with an increased likelihood of CRT response (relative risk 2.55 95% confidence interval 2.04–3.19, P < 0.001, I² = 51%). Septal flash was also reported to be associated with left ventricular reverse remodeling, but the association with survival and symptomatic improvement was less clear. Septal flash is a well-defined and distinctive contraction pattern that is easily recognizable on cardiac imaging. Septal flash may be associated with CRT response and should be evaluated in the patients that are considered for CRT devices.

Objectives: To evaluate short- and long-term outcome in a single prospective cohort of Takotsubo syndrome (TTS) patients, trying to early identify those with better prognosis and to assess the prevalence of left ventricular ejection fraction (LVEF) recovery over time. Methods: Forty-nine patients prospectively enrolled underwent to assessment of demographic, clinical, and echocardiographic characteristics, and later were followed to identify the outcomes during a mean follow-up (FU) of 93 months. At the end of the FU phase, a subgroup of patients underwent to a clinical and echocardiographic re-evaluation. As major adverse cardiac events (MACE) were considered: Intra and extra-hospital death, re-hospitalizations for acute heart failure or atrial fibrillation (AF) or acute myocardial infarction (AMI) and TTS recurrence; minor events were considered minor symptoms of heart failure and angina not requiring hospitalization. Results: The prevalence of re-hospitalizations (MACE) over time was: 41% (n = 12) for HF; 6.8% (n = 2) for AMI; 3.4% (n = 1) for TTS relapse and 20% (n = 6) for AF. Minor events were the symptoms of chest pain and dyspnea not requiring hospitalization in 6 (20.7%) and 12 (34.4%) patients, respectively. LVEF at the time of admission was predictor for MACE. Stratifying patients on the LVEF admission median value (40%). Patients with LVEF <40% at admission had a significantly lower survival free from adverse cardiac events compared to patients with LVEF ≥40%. Twenty-seven (93%) patients underwent to a clinical reassessment with electrocardiogram and echocardiographic examination. LVEF value showed a statistically significant increase (P = 0.004) at the end of FU. Conclusions: At admission, “high-risk” patients (LVEF <40%) can be easily detected, allowing an appropriate pharmacological and/or mechanical support strategy and a more “careful” FU.

Background: Congenital myopathies (CMs) are a group of rare genetic muscle disorders. Cardiac involvement can be seen in these patients. We aimed to evaluate the myocardial strain parameters by 2D speckle-tracking echocardiography (STE) in patients with CM. Materials and Methods: Twenty-four patients with CM whose diagnosis was confirmed by genetic analysis or muscle biopsy were included in the study, and 48 patients were involved as a control group. Left ventricular ejection fraction (LVEF%) was calculated by biplane Simpson method, and myocardial strain analysis was performed by 2D STE. Results: The median age of the study population was 26 (19–35 interquartile range [IQR]) and 43 (60%) were women. In the analysis performed after the exclusion of two patients with multiminicore disease (MMD) who developed heart failure, although mild, LVEF% (62 [60–65 IQR] vs. 64 [63–66 IQR], P = 0.008) and right ventricular global longitudinal strain (RVGLS) were significantly lower in the CM group (−21.8 [−19.7, −24.9 IQR] vs. −23.9 [−22.4, −25.6 IQR], P = 0.0017). Left ventricular global longitudinal strain (LVGLS) was observed similarly in both groups (−19.9 [−18.7, −20.7 IQR] vs. −20.5 [−19.3, −21.9 IQR], P = 0.069). LVEF% (33 and 46), LVGLS (−7.5 and −10.7), and RVGLS (−14.9 and −16.1) values were low in two siblings with MMD. Conclusion: Although LVEF% and RVGLS were significantly lower in the CM group, LVGLS was similar. The decrease in RVGLS and LVEF% was mild, and heart failure was not observed in any patient except MMD patients who were not included in the analysis.

Background: Type 2 diabetes mellitus (T2DM) insidiously affects the myocardium with subsequent cardiomyopathy and induces microvascular damage in the kidneys reflected by albuminuria. We aimed to investigate the relationship between albuminuria and subclinical left ventricular (LV) systolic dysfunction in asymptomatic normotensive patients with T2DM assessed by two-dimensional speckle-tracking echocardiography. Materials and Methods and Results: Sixty normotensive patients with T2DM were included and subdivided into two subgroups, each including thirty patients according to the presence of albuminuria, together with thirty control subjects. All underwent echocardiographic examination, including LV regional and global longitudinal strain (GLS) measurements. Laboratory tests were withdrawn, including serum glycated hemoglobin (HbA1C) and albumin–creatinine ratio (ACR). When compared to the control group, patients with T2DM had a significantly lower average peak systolic LV GLS (−16.18% ± 2.78% vs. −18.13% ± 2.86%, P < 0.001), however, there was no significant difference in average peak systolic LV GLS between both diabetic subgroups (−15.57% ± 2.77% in the albuminuric subgroup vs. −16.79% ± 2.70% in the nonalbuminuric subgroup, P = 0.077). Moreover, there was a significant correlation between ACR and reduction of GLS in patients with T2DM and albuminuria (r = 0.55, P = 0.002). However, this correlation was absent in patients with T2DM without albuminuria (r = 0.107, P = 0.573). Conclusions: Patients with T2DM have subclinical LV systolic dysfunction with a reduction of average LV GLS that correlates with ACR in patients with T2DM and albuminuria.

Objective: It is crucial to determine the high-risk group in ST-elevated myocardial infarction (STEMI). Left ventricle ejection fraction (LVEF) and left atrial volume index (LAVI) are the well-established parameters for risk prediction. However, major adverse cardiovascular events (MACEs) may be predicted less than actual when LVEF or LAVI are in the normal range. It was investigated LAVI to LVEF ratio (LAVI/LVEFr) for more accurate MACE prediction. Methods: Patients with STEMI were included in the study. LAVI and LVEF were obtained at admission. The LAVI/LVEFr was calculated as LAVI dividing by LVEF. The composite primary endpoint of the study was all-cause mortality and new-onset heart failure for 8 years follow-up. Results: A total of 176 patients were divided into two groups according to the presence of MACE. MACE (+) group consisted of 70 (39.7%) patients who were older and more likely to be male. While LVEF (P < 0.001) was lower, LAVI (P < 0.001) and LAVI/LVEFr (P < 0.001) were higher in MACE (+) group. Age (P = 0.003), serum creatinine (P < 0.001), and LAVI/LVEFr (P < 0.001) were independent predictors of MACE. Conclusion: Combined usage of LAVI and LVEF (LAVI/LVEFr), increased age, and serum creatinine level were the independent predictors of MACE during 8 years of follow-up in STEMI patients.

Background: Aortic elastic properties have been related to coronary artery disease (CAD) morbidity and mortality. We aimed to assess the relation of aortic elasticity indices to the severity and complexity of CAD assessed using the SYNTAX Score (SS), evaluating which of these indices have better predictivity for CAD severity. Materials and Methods: We prospectively enrolled 150 individuals who underwent elective coronary angiography for suspected CAD, out of them 29 (19.3%) had normal or nonsignificant angiographic findings (Group I), whereas 121 (80.7%) had significant CAD (Group II) for whom the SS was calculated. Echo-derived aortic elasticity indices were performed for all patients. Results: Logistic regression analyses showed that each of aortic distensibility, stiffness index, elastic modulus, aortic strain, and aortic peak early diastolic velocity were predictors for significant CAD and further for more complex CAD as indicated by intermediate-high SS. Receiver operator characteristic curves-derived cutoff points were performed for each of the aortic elasticity indices. Along with diabetes, decreased aortic strain ≤10.2% was the only independent predictor of intermediate-high SS (odds ratio = 4.31, 95% confidence interval = 1.38–13.50, P = 0.01). Conclusion: Simple M-mode derived aortic elasticity indices, particularly aortic strain ≤10.2%, might predict patients with more severe and complex CAD.

We present the case of a patient with recurrent episodes of ventricular fibrillation without evidence of structural cardiac diseases on imaging techniques and negative genetic testing for the most common primary arrhythmia syndromes. A new variant c.6023C>T p.Pro2008Leu of the SCN5A protein, responsible for the sodium inward current (I_Na) through the cardiomyocytes, was found. A likely pathogenic effect of this gene variant was hypothesized.

A 55-year-old male with a history of severe organic mitral regurgitation treated with surgical mitral valve (MV) repair was referred for a transcatheter MV replacement due to recurrent regurgitation. After the release of the first transcatheter MV, a severe paravalvular leak coming from the lateral side was observed. To promptly tackle this issue, a second valve with further postdilation was successfully implanted and the paravalvular leak disappeared. This case highlights the feasibility of implanting a second valve in case of severe paravalvular leaks after MV-in-ring procedures due to device malapposition.

We have recently published in the journal the case of a 66-year-old female affected by typical Takotsubo syndrome (TTS) with apical ballooning, who presented important novel apical wall thickening despite normalization of left ventricular ejection fraction at a follow-up cardiac magnetic resonance (CMR) 1 month after the acute event. In the absence of significant elevated edema-sensitive T2 values at CMR, this constellation was interpreted as apical hypertrophic cardiomyopathy, initially mimicked by TTS. However, a routine late follow-up echocardiography and CMR after 6 months showed complete resolution of apical wall thickening. “Pseudohypertrophy” caused by transient significant myocardial edema seems to be a more frequent phenotype in the subacute phase of TTS than is yet known, which may cause diagnostic confusion.

A 60-year-old female presented with dyspnea and chest pressure. Clinical presentation, laboratory data, echocardiography, and cardiac magnetic resonance (CMR) imaging findings confirmed diagnosis of eosinophilic myocarditis and obviated unnecessary invasive endomyocardial biopsy. She was treated with oral steroid and oral anticoagulation. Follow-up CMR imaging showed resolution of the left ventricle thrombus with improvement in endomyocardial inflammation.