Stroke Risk during TAVR: Is Prevention Better than Cure?

Periprocedural stroke is an uncommon but feared complication in patients undergoing transcatheter aortic valve replacement (TAVR). Typically embolic, it occurs more frequent in the first days (within seven days) after the procedure and it is secondary to procedural factors. It has a wide clinical spectrum and it is associated with increased mortality and a controversial worse impact on cognitive functions. Capture of the debris by different cerebral embolic protection devices (CEPDs) during the TAVR were thought to be a safe and effective preventive strategy to reduce the risk of stroke. A lot of trials were conducted to demonstrate a benefit of CEPDs, but the current evidence is not conclusive on their impact on periprocedural strokes

Myocardial infarction with non-obstructive coronary arteries (MINOCA. focus on coronary microvascular dysfunction and genetic susceptibility

Among the most common causes of death worldwide, ischemic heart disease (IHD) is recognized to rank first. Even if atherosclerotic disease of the epicardial arteries is known as the leading cause of IHD, the presence of myocardial infarction with non-obstructive coronary artery disease (MINOCA) is increasingly recognized. Notwithstanding the increasing interest, MINOCA remains a puzzling clinical entity that can be classified by distinguishing different underlying mechanisms, which can be divided into atherosclerotic and non-atherosclerotic. In particular, coronary microvascular dysfunction (CMD), classifiable in non-atherosclerotic mechanisms, is a leading factor for the pathophysiology and prognosis of patients with MINOCA. Genetic susceptibility may have a role in primum movens in CMD. However, few results have been obtained for understanding the genetic mechanisms underlying CMD. Future studies are essential in order to find a deeper understanding of the role of multiple genetic variants in the genesis of microcirculation dysfunction. Progress in research would allow early identification of high-risk patients and the development of pharmacological, patient-tailored strategies. The aim of this review is to revise the pathophysiology and underlying mechanisms of MINOCA, focusing on CMD and actual knowledge about genetic predisposition to it

Structural and myocardial dysfunction in heart failure beyond ejection fraction

Heart failure is a multifaceted syndrome addressing for a high rate of death among the general population. The common approach to this disease has been always based on the evaluation of the left ventricular ejection fraction by two-dimensional echocardiography with Simpson’s method. Mounting evidences have demonstrated the pitfalls of this method and have suggested that the management of heart failure requires a deep knowledge of the pathophysiological insights of the disease and cannot rely only on the evaluation of the left ventricular ejection fraction. Several advanced imaging technologies overwhelm the evaluation of ejection fraction and could provide a better understanding of the myocardial abnormalities underlying heart failure. Considering the limitation of left ventricular ejection fraction and the systemic involvement of heart failure, classifications of heart failure based on ejection fraction should be substituted with a comprehensive “staging” of multiorgan damage, not only considering the heart but also the lungs, kidneys, and liver, such as the HLM staging system. Such a holistic approach based on the HLM staging system and multimodality imaging can provide a global assessment of patient features allowing for targeted therapies and better heart failure management

The evolving role of echocardiography in the assessment of patent foramen ovale in patients with left-side thromboembolism

Patent foramen ovale (PFO) is the most common congenital cardiac abnormality found approximately in 25% of the adult population The pathophysiological role of paradoxical embolization through the PFO in ischemic stroke is well established. "Self-expanding double disk" and, more recently, suture-based "deviceless" systems are used for PFO closure in the setting of secondary prevention after ischemic stroke likely related to paradoxical embolization. Ultrasound plays a significant role in PFO assessment, indication to treatment, intra-procedural guidance, and follow-up for those undergoing PFO closure. Three different techniques are frequently used for these purposes: transesophageal echocardiography, transthoracic echocardiogram, and transcranial Doppler. In this review, advantages and limits of these techniques are discussed in detail to improve our skills in detection and treatment of this important condition by using ultrasound

Ischemic Heart Disease and Heart Failure: Role of Coronary Ion Channels

Heart failure is a complex syndrome responsible for high rates of death and hospitalization. Ischemic heart disease is one of the most frequent causes of heart failure and it is normally attributed to coronary artery disease, defined by the presence of one or more obstructive plaques, which determine a reduced coronary blood flow, causing myocardial ischemia and consequent heart failure. However, coronary obstruction is only an element of a complex pathophysiological process that leads to myocardial ischemia. In the literature, attention paid to the role of microcirculation, in the pathophysiology of ischemic heart disease and heart failure, is growing. Coronary microvascular dysfunction determines an inability of coronary circulation to satisfy myocardial metabolic demands, due to the imbalance of coronary blood flow regulatory mechanisms, including ion channels, leading to the development of hypoxia, fibrosis and tissue death, which may determine a loss of myocardial function, even beyond the presence of atherosclerotic epicardial plaques. For this reason, ion channels may represent the link among coronary microvascular dysfunction, ischemic heart disease and consequent heart failure

Multimodality imaging in ICD implantation decision making: 123-iodine metaiodobenzylguanidine imaging and cardiac magnetic resonance imaging

Introduction: According to guidelines, implantable cardioverter defibrillator (ICD) is recommended in prevention of sudden cardiac death (SCD) in heart failure (HF) patients (pts). Guidelines have several limitations because ICD indication is based mainly on left ventricular ejection fraction (EF). Recently, 123-iodine metaiodobenzylguanidine imaging (123-I MIBG) seems to identify, independently from EF, pts at high risk of SCD (heart/mediastinum (H/M) ratio < 1.6 and a summed score (SS)> 26). Hypothesis: Our aim is to assess the role of 123-I MIBG combined with cardiac MRI to predict malignant ventricular tachyarrhythmia in HF pts. Methods: we enrolled 69 pts, consecutively admitted to our hospital with diagnosis of HF and EF<35%, NYHA class II and III, who underwent 123-I MIBG imaging and cardiac MRI. Summed score (SS) of 26 was used as cut-off to identify high risk (group 1) versus low risk (group 2) pts. Late gadolinium enhancement (LGE) and number of segments with scars were evaluated in the 2 groups. All pts underwent to ICD implantation. We assessed ventricular arrhythmic (VA) events at 18 months follow-up. Results: 21 pts were included in group 1 and 48 pts in group 2. All baseline characteristics were similar in 2 groups. In group 1, H/M ratio was 1.47± 0.24 and in group 2 21.63 ± 0.27 (p=0.015). The percentage of the pts with LGE was 70.9 % in group 1 vs 39.1 % in group 2 (p=0.023). At 18 months follow-up VA events in group 1 were 19.05% vs 4.17% in group 2 (p < 0.037). Moreover VA events were statistically recorded greater in pts with both SS > 26 and LGE compared to pts with only SS >26 (46.7% vs 19.6%, p= 0.046). Conclusions: Our results seem to confirm that reduced 123-I MIBG uptake (H/M and SS) and presence of LGE are associated with the occurrence of life-threatening ventricular arrhythmias in HF patients independently from EF. The use of integrated imaging could be a useful tool in the future to increase the specificity of the selection of pts for ICD therapy

Cardiac and Vascular Remodeling After 6 Months of Therapy With Sacubitril/Valsartan: Mechanistic Insights From Advanced Echocardiographic Analysis

14Background: Effects of Sacubitril/Valsartan (S/V) on left ventricular (LV) mechanics and ventricular-arterial coupling in patients with heart failure with reduced ejection fraction (HFrEF) are not completely understood. The aim of this study was to evaluate both cardiac and vascular remodeling in a group of HFrEF patients undergoing S/V therapy. Methods: Fifty HFrEF patients eligible to start a therapy with S/V were enrolled. Echocardiographic evaluation was performed at baseline and after 6 months of followup (FU). Beside standard evaluation, including global longitudinal strain (GLS), estimated hemodynamic forces (HDFs) and non-invasive pressure-volume curves (PV loop) were assessed using dedicated softwares. HDFs were evaluated over the entire cardiac cycle, in systole and diastole, both in apex to base (A-B) and latero-septal (L-S) directions. The distribution of LV HDFs was evaluated by L-S over A-B HDFs ratio (L-S/A-B HDFs ratio). Parameters derived from estimated PV loop curves were left ventricular end-systolic elastance (Ees), arterial elastance (Ea), and ventricular-arterial coupling (VAC). Results: At 6 months of FU indexed left ventricular end-diastolic and end-systolic volumes decreased (EDVi: 101 ± 28mL vs. 86 ± 30mL, p < 0.001; ESVi: 72 ± 23mL vs. 55 ± 24mL, p < 0.001), ejection fraction and GLS significantly improved (EF: 29 ± 6% vs. 37 ± 7%, p < 0.001; GLS: −9 ± 3% vs. −13 ± 4%, p < 0.001). A reduction of Ea (2.11 ± 0.91 mmHg/mL vs. 1.72 ± 0.44 mmHg/mL, p = 0.008) and an improvement of Ees (1.01 ± 0.37 mmHg/mL vs. 1.35 ± 0.6 mmHg/mL, p < 0.001) and VAC (2.3 ± 1.1 vs. 1.5 ± 0.7, p < 0.001) were observed. Re-alignment of HDFs occurred, with a reduction of diastolic L-S/A-B HDFs ratio [23 (20–35)% vs. 20 (11–28) %, p < 0.001]. Conclusion: S/V therapy leads to a complex phenomenon of reverse remodeling involving increased myocardial contractility, HDFs distribution improvement, and afterload reduction.openopenMonosilio, Sara; Filomena, Domenico; Luongo, Federico; Sannino, Michele; Cimino, Sara; Neccia, Matteo; Mariani, Marco Valerio; Birtolo, Lucia Ilaria; Benedetti, Giulia; Tonti, Giovanni; Pedrizzetti, Gianni; Vizza, Carmine Dario; Maestrini, Viviana; Agati, LucianoMonosilio, Sara; Filomena, Domenico; Luongo, Federico; Sannino, Michele; Cimino, Sara; Neccia, Matteo; Mariani, Marco Valerio; Birtolo, Lucia Ilaria; Benedetti, Giulia; Tonti, Giovanni; Pedrizzetti, Gianni; Vizza, Carmine Dario; Maestrini, Viviana; Agati, Lucian

3D Echo Characterization of Proportionate and Disproportionate Functional Mitral Regurgitation before and after Percutaneous Mitral Valve Repair

Background: The impact of percutaneous mitral valve repair (PMVr) on long-term prognosis in patients with functional mitral regurgitation (FMR) is still unclear. Recently, a new conceptual framework classifying FMR as proportionate (P-MR) and disproportionate (D-MR) was proposed, according to the effective regurgitant orifice area/left ventricular end-diastolic volume (EROA/LVEDV) ratio. The aim was to assess its possible influence on PMVr efficacy. Methods: A total of 56 patients were enrolled. MV annulus, LV volumes and function were assessed. Global longitudinal strain (GLS) was also calculated. Patients were divided into two groups, according to the EROA/LVEDV ratio. Echocardiographic follow-up was performed after 6 months, and adverse events were collected after 12 months. Results: D-MR patients (n = 28, 50%) had a significantly more elliptical MV annulus (p = 0.048), lower tenting volume (p = 0.01), higher LV ejection fraction (LVEF: 32 &plusmn; 7 vs. 26 &plusmn; 5%, p = 0.003), lower LVEDV, LV end-systolic volume (LVESV) and mass (LVEDV/i: 80 &plusmn; 20 vs. 126 &plusmn; 27 mL, p = 0.001; LVESV/i: 60 &plusmn; 20 vs. 94 &plusmn; 23 mL, p &lt; 0.001; LV mass: 249 &plusmn; 63 vs. 301 &plusmn; 69 gr, p = 0.035). GLS was more impaired in P-MR (p = 0.048). After 6 months, P-MR patients showed a higher rate of MR recurrence. After 12 months, the rate of CV death and rehospitalization due to HF was significantly higher in P-MR patients (46% vs. 7%, p &lt; 0.001). P-MR status was strongly associated with CV death/rehospitalization (HR = 3.4, CI 95% = 1.3&ndash;8.6, p = 0.009). Conclusions: Patients with P-MR seem to have worse outcomes after PVMr than D-MR patients. Our study confirms the importance of the EROA/LVEDV ratio in defining different subsets of FMR based on the anatomical characteristic of MV and LV

T2-mapping increase is the prevalent imaging biomarker of myocardial involvement in active COVID-19: a Cardiovascular Magnetic Resonance study

Abstract Background Early detection of myocardial involvement can be relevant in coronavirus disease 2019 (COVID-19) patients to timely target symptomatic treatment and decrease the occurrence of the cardiac sequelae of the infection. The aim of the present study was to assess the clinical value of cardiovascular magnetic resonance (CMR) in characterizing myocardial damage in active COVID-19 patients, through the correlation between qualitative and quantitative imaging biomarkers with clinical and laboratory evidence of myocardial injury. Methods In this retrospective observational cohort study, we enrolled 27 patients with diagnosis of active COVID-19 and suspected cardiac involvement, referred to our institution for CMR between March 2020 and January 2021. Clinical and laboratory characteristics, including high sensitivity troponin T (hs-cTnT), and CMR imaging data were obtained. Relationships between CMR parameters, clinical and laboratory findings were explored. Comparisons were made with age-, sex- and risk factor–matched control group of 27 individuals, including healthy controls and patients without other signs or history of myocardial disease, who underwent CMR examination between January 2020 and January 2021. Results The median (IQR) time interval between COVID-19 diagnosis and CMR examination was 20 (13.5–31.5) days. Hs-cTnT values were collected within 24 h prior to CMR and resulted abnormally increased in 18 patients (66.6%). A total of 20 cases (74%) presented tissue signal abnormalities, including increased myocardial native T1 (n = 11), myocardial T2 (n = 14) and extracellular volume fraction (ECV) (n = 10), late gadolinium enhancement (LGE) (n = 12) or pericardial enhancement (n = 2). A CMR diagnosis of myocarditis was established in 9 (33.3%), pericarditis in 2 (7.4%) and myocardial infarction with non-obstructive coronary arteries in 3 (11.11%) patients. T2 mapping values showed a moderate positive linear correlation with Hs-cTnT (r = 0.58; p = 0.002). A high degree positive linear correlation between ECV and Hs-cTnT was also found (r 0.77; p < 0.001). Conclusions CMR allows in vivo recognition and characterization of myocardial damage in a cohort of selected COVID-19 individuals by means of a multiparametric scanning protocol including conventional imaging and T1–T2 mapping sequences. Abnormal T2 mapping was the most commonly abnormality observed in our cohort and positively correlated with hs-cTnT values, reflecting the predominant edematous changes characterizing the active phase of disease

Myocardial tissue characterization in heart failure with preserved ejection fraction. from histopathology and cardiac magnetic resonance findings to therapeutic targets

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical syndrome responsible for high mortality and morbidity rates. It has an ever growing social and economic impact and a deeper knowledge of molecular and pathophysiological basis is essential for the ideal management of HFpEF patients. The association between HFpEF and traditional cardiovascular risk factors is known. However, myocardial alterations, as well as pathophysiological mechanisms involved are not completely defined. Under the definition of HFpEF there is a wide spectrum of different myocardial structural alterations. Myocardial hypertrophy and fibrosis, coronary microvascular dysfunction, oxidative stress and inflammation are only some of the main pathological detectable processes. Furthermore, there is a lack of effective pharmacological targets to improve HFpEF patients' outcomes and risk factors control is the primary and unique approach to treat those patients. Myocardial tissue characterization, through invasive and non-invasive techniques, such as endomyocardial biopsy and cardiac magnetic resonance respectively, may represent the starting point to understand the genetic, molecular and pathophysiological mechanisms underlying this complex syndrome. The correlation between histopathological findings and imaging aspects may be the future challenge for the earlier and large-scale HFpEF diagnosis, in order to plan a specific and effective treatment able to modify the disease's natural course