Search

Standard therapy for venous thromboembolism (VTE) includes the use of heparins and vitamin K antagonists. Randomized clinical trials have shown that non-vitamin K oral anticoagulants are as effective and safe as standard therapy in VTE treatment, with an improved pharmacological profile. Edoxaban, a direct inhibitor of factor Xa, has demonstrated noninferiority to standard therapy for the treatment of VTE, preserving a high safety profile even in long-term therapy, in frail patients and in severe clinical presentations. The present paper focuses on the role of edoxaban in VTE treatment, from general population to cancer patients, presenting the available data from randomized clinical trials and real world, to discuss edoxaban use in clinical practice.Lay abstractAnticoagulants are the main treatment for venous thromboembolism (VTE), a condition in which a blood clot forms in the deep veins of the body, in areas such as the leg. Currently, direct oral anticoagulants are available as an alternative to warfarin, a drug that is sensitive to changes in the diet and requires constant monitoring. Direct-oral anticoagulants have been shown in large-scale studies to be as effective and safe as warfarin in the treatment of this disease, with the advantage of not being affected by the food the patient eats. Among these, edoxaban only needs to be taken once a day and has obtained many favorable results in high-risk populations (such as the elderly, patients with cancer, those receiving prolonged treatment or those with severe VTE). In this review we discuss the role of edoxaban for the treatment of VTE in several scenarios and review its role in clinical practice.Tweetable abstractEdoxaban is effective and safe for the treatment of venous thromboembolism (VTE) even in special population. Caution is needed in some patients to avoid major bleeding events. Favorable results are also shown in the ETNA VTE study, a real-world data prospective registry. #edoxaban #VTE #efficacy #safety

The antithrombotic management of patients after surgical or transcatheter bioprosthetic heart valves (BHVs) replacement is still challenging. Our review aims to describe the current evidence on the best antithrombotic strategy among patients undergoing BHVs replacement (surgical or transcatheter) and/or valve repair, with particular attention to those with atrial fibrillation.

Coronavirus 2019 (COVID-19) disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can lead to cardiac impairment, with increased troponin levels, left ventricular (LV) dysfunction and myocarditis ([1][1],[2][2]). Information for right ventricular (RV) involvement and

Mitral valve prolapse is generally a benign condition characterized by fibromyxomatous changes of the mitral leaflet with displacement into the left atrium and late-systolic regurgitation. Although it is an old clinical entity, it still arouses perplexity in diagnosis and clinical management. Complications, such as mitral regurgitation (MR), atrial fibrillation, congestive heart failure, endocarditis, ventricular arrhythmias, and sudden cardiac death (SCD), have been reported. A large proportion of the overall causes of SCD in young competitive athletes is explained by mitral valve prolapse. Recent studies have shown the fibrosis of the papillary muscles and inferobasal left ventricular wall in mitral valve prolapse, suggesting a possible origin of ventricular fatal arrhythmias. Athletes with mitral valve prolapse and MR should undergo annual evaluations including physical examination, echocardiogram, and exercise stress testing to evaluate the cardiovascular risks of competitive sports and obtain the eligibility. In this setting, multimodality imaging techniques - echocardiography, cardiac magnetic resonance, and cardiac computed tomography - should provide a broad spectrum of information, from diagnosis to clinical management of the major clinical profiles of the disease.

Background In patients with obstructive sleep apnea syndrome (OSAS), repetitive hypoxia due to sleep-induced apnea adversely affects the interaction between myocardial oxygen demand and supply, resulting in the development of subclinical cardiac dysfunction. The purpose of the study was to analyze the different involvement of left and right heart myocardial function in patients with OSAS treated with noninvasive ventilation (NIV). Methods Conventional Doppler echocardiography, Doppler myocardial imaging (DMI), and two-dimensional speckle tracking echocardiography (2DSTE) of left (LV) and right ventricular (RV) longitudinal and right atrial (RA) deformation were performed in 55 patients with OSAS undergoing NIV (M/F 38/17; mean age 67.8 ± 11.2 years). LV and RV global longitudinal strain (GLS) was calculated by averaging local strain along the entire right and left ventricle, before and during NIV, and after 6 months of nocturnal NIV therapy. Results LV morphology was comparable before and during NIV, whereas LV ejection fraction and LV DMI early diastolic peak velocity were significantly improved in patients with OSAS during NIV, as was LV regional peak myocardial strain (P < 0.001). RV diameters were slightly increased in patients with OSAS during ventilation, whereas pulmonary artery systolic pressure (PASP), RV GLS, and regional peak myocardial RV strain were significantly reduced during ventilation (P < 0.0001). RA transverse diameters and RA area were also slightly increased during NIV, whereas RA lateral wall strain was reduced (P < 0.001). Acute RV myocardial impairment completely reversed at follow-up, with a decrease in PASP and subsequent increase in both RV and RA myocardial performance. Conclusions Conventional 2DSTE is a useful tool for assessing left and right heart morphology and myocardial deformation in patients with OSAS and for monitoring both acute and chronic effects of NIV.

To test whether two-dimensional longitudinal strain (2DSE) performed after revascularization by percutaneous coronary intervention (PCI) could predict left ventricular (LV) remodeling in patients with recent non-ST elevation myocardial infarction (NSTEMI).In 70 patients (62.7 ± 8.7 years) with recent NSTEMI (between 72 hours and 14 days), undergoing coronary angiography for recurrent angina, myocardial deformation parameters were measured by 2DSE before and 24 hours after reperfusion therapy. Strain in all LV segments was averaged to obtain a global value (Global longitudinal Strain--GLS). Infarct size was estimated by clinical parameters and cardiac markers. After 6 months from intervention, LV negative remodeling was defined as lack of improvement of LV function, with increase in LV end-diastolic volume of greater than or equal than 15%.At follow-up, patients were subdivided into remodeled (n=32) and non-remodeled (n = 38) groups. Patients with negative LV remodeling had significantly lower baseline LV ejection fraction (44.8±6.9 vs. 48.7 ± 5.5 %; p0.05), higher peak troponin I (p0.001) and reduced GLS (- 10.6±6.1 vs - 17.6 ± 6.7 % p0.001) than those without LV remodeling. GLS showed a close correlation with peak troponin I after PCI (r = 0.64, P0.0001) and LV WMSI (r = 0.42, p0.01). By multivariable analysis, diabetes mellitus (P0.005), peak of Troponin I after PCI (P0.0005), GLS at baseline (OR: 4.3; p0.0001), and lack of improvement of GLS soon after PCI (OR: 1.45, P0.01) were powerful independent predictors of negative LV remodelling at follow-up. In particular, a GLS ≤ 12 % showed a sensitivity and a specificity respectively of 84.8% and 87.8% to predict negative LV remodelling at follow-up.in patients with recent NSTEMI, longitudinal LV global and regional speckle-tracking strain measurements are powerful independent predictors of LV remodeling after reperfusion therapy.

Objective: The aim of this study was to analyze right ventricular (RV) myocardial function in competitive athletes with left ventricular (LV) hypertrophy induced by either endurance or strength training. Methods: Standard Doppler echo, maximal electrocardiogram (ECG) ergometric test, and pulsed tissue Doppler (TD) of LV mitral annulus and of RV tricuspid annulus were performed in 32 competitive endurance athletes (long-distance swimmers; ATE) and in 26 strength-trained athletes (short-distance swimmers; ATS), all males. By use of TD, the following parameters of myocardial function were assessed: systolic peak velocities (Sm), precontraction time, contraction time, early (Em) and late (Am) diastolic velocities, Em/Am ratio, and relaxation time. Results: The two groups were comparable for age, but ATS at rest exhibited higher heart rate, systolic blood pressure, and body surface area. LV mass index did not significantly differ between the two groups. However, ATS characterized increased wall thickness and relative wall thickness, whereas LV stroke volume and both LV and RV end-diastolic diameters were greater in ATE. All transmitral and transtricuspid Doppler indexes were higher in ATE, with increased E/A ratios. TD analysis demonstrated in ATE higher Em and Em/Am ratio as well as longer relaxation time both at mitral and at tricuspid annulus level. In the overall population, distinct multiple linear regression models evidenced independent positive association between RV peak Em velocity and LV end-diastolic diameter (P < 0.001) as well as independent direct correlation of the same RV peak Em velocity with both LV stroke volume and maximal workload achieved by bicycle ergometer (both P < 0.001). Conclusions: Right ventricular early diastolic myocardial function is positively influenced by preload increase in athletes, and represents an independent determinant of cardiac performance during physical effort. Therefore, pulsed TD may be taken into account to distinguish different cardiac adaptation to either endurance or strength sport activities, and eventually to quantify RV adaptation degree to long-term training. (ECHOCARDIOGRAPHY, Volume 20, May 2003)

The aim of this study was to assess the effects of endurance training on myocardial regional systolic and diastolic function by pulsed Doppler tissue imaging (DTI). Twenty male water polo players and 20 male control subjects underwent standard Doppler echocardiography and pulsed DTI, performed in apical views by placing a sample volume on left ventricular (LV) basal septal and inferior walls. Age, body surface area, and blood pressure were comparable between the 2 groups, with lower heart rate in athletes (p

Objective: Atrial fibrillation (AF) is the most frequently encountered arrhythmic complication associated with coronary surgery. The aim of this paper was then to identify the clinical predictors of post-CABG AF occurrence. Methods: 150 consecutive patients were included in this study and divided into two groups according to the absence (SR group, 104 male and 22 female, age 58.4 ^ 8.8 years) or presence (AF group, 23 male and 1 female, age 65.4 ^ 6.3 years) of post-CABG AF. Forty-seven perioperative variables were considered. Results: After univariate analysis, advanced age (SR vs. AF: 58.4 ^ 8.8 vs. 65.4 ^ 6.3, P , 0:001), an increased BMI (SR vs. AF: 26.1 ^ 2.7 vs. 27.4 ^ 2.5, Pa 0:026), a prior history of paroxysmal AF (SR vs. AF: 3.2% vs. 16.7%, Pa 0:028), left atrial enlargement (SR vs. AF: 21.1% vs. 70.8%, P , 0:001) and a more severe coronary artery disease (CAD) (SR vs. AF: no. of diseased vessels: 2.42 ^ 0.7 vs. 2.91 ^ 0.3, Pa 0:001; three-vessel CAD (54.1% vs. 91.3%, Pa 0:002) were the only factors that statistically differed between the groups. Multivariate logistic regression analysis identified left atrial enlargement (P , 0:0001), a prior history of paroxysmal AF (Pa 0:007) and a more severe CAD (Pa 0:0047) to be independent correlates for AF. Conclusions: Post-CABG AF seems to require a well definite anatomical and electrical substrate that is generated by increased left atrial dimensions, a greater extension of coronary lesions and a possible electrical remodeling consequent to prior repetitive episodes of paroxysmal AF. q 1999 Published by Elsevier Science B.V. All rights reserved.

Our study was undertaken to assess the prognostic significance of pharmacological stress echocardiography in 325 diabetic patients. Pharmacological stress echocardiography was performed for diagnosis of coronary artery disease in 128 patients, and for risk stratification in 197 patients. Follow-up was 34 months. Cardiac-related death and non-fatal myocardial infarction were considered hard events. During the follow-up period, there were 38 deaths and 23 acute non-fatal myocardial infarctions. By univariate analysis, a pharmacological stress echocardiography positive response for ischaemia indicated an increased risk of cardiovascular death. However, by multivariate analysis, advanced age and peak ejection fraction

The aim of the study was to evaluate by Doppler tissue imaging (DTI) the combined effects of atrio-ventricular (AV) delay and heart rate (HR) changes on global and segmental right (RV) and left (LV) ventricular diastolic function in 15 patients with dual-chamber pacemakers paced in the DDD mode. RV and LV inflow velocities and regional systolic and diastolic pulsed-wave (PW) DTI parameters were analyzed at four different pacing modes: (1) HR 70 beats/min, AV delay 125 ms; (2) HR 70 beats/min, AV delay 188 ms; (3) HR 89 beats/min, AV delay 125 ms; (4) HR 89 beats/min, AV delay 188 ms. For each pacing mode selected, RV diastolic filling velocities always prevailed over LV ones. As for RV and LV adaptation to the four different stimulation protocols, a higher paced rate and a prolonged AV delay caused across both the AV valves a decrease of E wave and of E/A ratios. The intersegmental comparison of PW-DTI parameters outlined that RV free wall exhibited significantly higher peak systolic (Sm) and early-diastolic (Em) wall velocities, and longer systolic ejection time. Considering separately RV and LV segmental physiology at the four programmed pacing modes, an increase in HR determined a progressive shortening of systolic ejection times in all the segments analyzed. Moreover, in each region the Em/Am ratio decreased with higher HR and longer AV delay. Conversely, Em encountered a progressive reduction in RV free wall, while remaining quite unchanged in all the LV regions. Both ventricles shared a similar pattern of global and regional adaptation to programmed HR and AV delay modifications, consisting in a progressive greater contribution of late diastole to ventricular filling at higher HR and more prolonged AV delay. However, at a regional level the right ventricle exhibited higher systolic and diastolic wall velocities than all left ventricular regions.

The perioperative factors potentially associated with post-coronary artery bypass grafting (CABG) ventricular tachyarrhythmias (VT) onset have not been deeply investigated. Monomorphic or polymorphic ventricular tachycardia and ventricular fibrillation represent the most dreadful arrhythmic events that can complicate the postoperative course of CABG. As a consequence, the aim of our paper was to identify which perioperative variables might predict post-CABG VT occurrence. One hundred and fifty-two consecutive patients who underwent CABG surgery at our Institution were included in the study. Post-CABG VT occurred in 13 out of 152 patients (8.5%, six cases of monomorphic ventricular tachycardia and seven cases of ventricular fibrillation). At univariate analysis, VT patients were significantly younger (54.8±6.6 vs. 60.1±8.8, P=0.038), exhibited a more severe coronary artery disease (CAD) (number of diseased vessels 2.92±0.3 vs. 2.45±0.7, P=0.023, and percentage of patients with three-vessel CAD 91.7% vs. 57.3%, P=0.043) and received a greater number of CABGs than those remaining in sinus rhythm (SR) (percentage of patients receiving three or more CABGs 76.9% vs. 38.8%, P=0.018) Moreover, VT patients more frequently developed intra- or postoperative myocardial infarction (total CK>1000 76.9% vs. 38%, P=0.016 and MB-CK>normal range 72.7% vs. 30.7%, P=0.014), electrolyte derangement (84.6% vs. 45.6%, P=0.017) and a severe haemodynamic impairment (need for IABP 23% vs. 2.9%, P=0.009). At multivariate analysis, total CK>1000, postoperative electrolyte imbalance, the need for three or more CABGs and of IABP all were independent correlates for VT. In conclusion, post-CABG VT seem to be related to the preexistence of a severe underlying coronary artery disease along with perioperative triggering factors such as acute ischemia, electrolytic disorders and a sudden haemodynamic impairment.

Sustained ventricular tachyarrhythmias (VT), such as monomorphic or polymorphic ventricular tachycardia, and ventricular fibrillation, represent the most serious arrhythmic events that can complicate the postoperative course of coronary artery bypass grafting (CABG). The perioperative factors potentially associated with post-CABG sustained VT onset have not been thoroughly investigated. As a consequence, the aim of our study was to identify which perioperative variables might predict post-CABG VT occurrence. One hundred and fifty-two consecutive patients who underwent CABG surgery at our Institute were included in the study. Post-CABG VT occurred in 13 out of 152 patients (8.5%, six cases of monomorphic ventricular tachycardia and seven cases of ventricular fibrillation). Univariate analysis revealed that VT patients were significantly younger (54.8 +/- 6.6 vs 60.1 +/- 8.8, P = 0.038), exhibited more severe coronary artery disease (CAD) (no. of diseased vessels, 2.92 +/- 0.3 vs 2.45 +/- 0.7, P = 0.023; and percentage of patients with three-vessel CAD, 91.7 vs 57.3%, P = 0.043), and received a greater number of CABGs than those remaining in sinus rhythm (SR) (percentage of patients receiving three or more CABGs, 76.9 vs 38.8%, P = 0.018) Moreover, VT patients more frequently developed intra- or postoperative myocardial infarction (total CK > 1,000, 76.9 vs 38%, P = 0.016; and MB-CK > normal range, 72.7 vs 30.7%, P = 0.014), electrolyte derangement (84.6 vs 45.6%, P = 0.017), and a severe hemodynamic impairment (need for intra-aortic balloon pump (IABP), 23 vs 2.9%, P = 0.009). On multivariate analysis, total CK > 1,000, postoperative electrolyte imbalance, the need for three or more CABGs, and for IABP all were independent correlates for VT. In conclusion, post-CABG VT seem to be related to the preexistence of a severe underlying coronary artery disease along with perioperative triggering factors, such as acute ischemia, electrolytic disorders, and sudden hemodynamic impairment.

Background: Intraventricular conduction disturbances determine complete impairment of impulse propagation along the right or left bundle branch or the two left fascicles. Hypothesis: This study was undertaken to investigate the electrophysiologic significance of QRS axis (QRSA) orientation in bifascicular and trifascicular blocks. Methods: A group of 76 subjects, 43 with right bundle‐branch block (RBBB) and left anterior hemiblock (LAH) (Group A), and 33 with left bundle‐branch block (LBBB) (Group B) was submitted to electrophysiologic evaluation. Results: In Group A, QRSA was inversely related only to intraventricular conduction, while in Group B, QRSA inversely related to infrahisal conduction times. A value of ‐60°. Of the 9 Group B patients with a QRSA 60°, in only 8.3% were both infrahisal (HV1 and HV2) intervals dangerously prolonged, and 23.8% encountered an infrahisal second‐degree AV block during IAS. In Group A, atrioventricular conduction time >200 ms exhibited a better predictive accuracy than QRSA 80 ms. Conclusion: The degree of leftward QRSA deviation seems to reflect the entity of intraventricular conduction delay in patients with RBBB + LAH, while it appears to be directly related to infrahisal conduction prolongation in those with LBBB.

The aim of our study was to analyze the ventricular repolarization phase in patients with isolated aortic stenosis (AS) in order to search for possible abnormalities that might contribute to an explanation of the electrical instability peculiar to this valve disease. We selected a population of 39 patients with isolated AS (25 M and 14 F, mean age 60+/-16 yrs). As controls we considered a group of 31 age-matched healthy subjects 20 M and 11 F, mean age 55+/-14 yrs, P=NS. Disease severity was assessed by echocardiography, calculating the maximum and mean pressure gradients max and mean PG) and the functional valve orifice area. Various electrocardiographic intervals (QT, QT'c, JT, JTc) and indices (QT and QTc dispersion were adopted for a detailed non-invasive evaluation of the ventricular repolarization. In patients with AS, M-QT (391+/-45 ms vs 362+/-25 ms, P=0.002), M=QTc (431+/-29 ms vs 412+/-19 ms, P=0.003), M-JT (290+/-41 ms vs 265+/-26 ms, P=0.003, M-JTc 331+/-29 ms vs 302+/-19 ms, P0.001, QTD (67+/-34 ms vs 40+/-15 ms, P0.001), QTcD (77+/-36 ms vs 52+/-23 ms, P0.001) all resulted significantly greater than in controls. QTD and QTcD both resulted linearly related either to max PCi (r=0.388, P=0.018 and r=0.357, P=0.03) or to mean PG (r=0.513, P=0.004 and r=0.438, P=0.015), while M-JT and M-JTc turned out to be directly related only to mean PG (r=0.436, P=0.016 and r=0.483, P=0.007). Our findings suggest a prolonged duration of ventricular recovery and a greater dispersion of ventricular repolarization in patients with AS and might account for the electrical instability proper to this valve dysfunction. Besides, the existence of a linear direct relation between the severity of AS and the degree of inhomogeneity of left ventricular recovery, together with the correlation found among mean PCr and the total duration of the repolarization phase, expressed by the intervals JT and JTc, strongly suggest the hypothesis that in AS arrhythmogenic substrates development parallels the worsening of the valve defect.