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A male patient, 33 years old, smoker, with a 20-year history of SLE, consulted the ER for right hand fatigue. He didn't assume his medications constantly. Computed Tomography showed a fronto-parieto-occipital cerebral infarction, and the angio-CT showed a plaque in left internal carotid artery. The patient was admitted to the Stroke Unit for minor ischemic stroke. The ECG showed pathological Q waves in the anterior leads from V1 to V4 revealing a likely previous silent myocardial infarction. The echocardiogram demonstrated moderate left ventricular dysfunction with 40% EF and segmental wall motion abnormalities, namely ipoakinesia of anterior wall and apex. This findings were confirmed by cardiac MRI highliting subendocardial LGE in these areas suggesting an ischemic genesis. Due to the hemorrhagic risk related to recent cerebral ischemic event, coronary angiography was postponed a month later. The coronary angiography revealed a significant stenosis of the proximal left anterior descending artery (iFR < 0.65). Qualitative assessment of the lesion with IVUS showed a “mixed” plaque. The lesion was treated with PCI and the implant of two overlapped DES and the patient underwent dual antiplatelet therapy. Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder with heterogeneous presentation, characterised by alternating periods of flares and remission, and irreversible organ damage. The skin, joints, heart, kidneys, central nervous system and haematologic system are some of the most affected organs. Although recent data suggest that mortality decreased in patients with SLE over the last 30 years, mortality due to cardiovascular disease (CVD), usually defined as a combination of coronary, cerebrovascular and/or peripheral arterial disease, has remained high. Stroke and myocardial infarction (MI) are major CVD events that are potentially life-threatening. Lupus specific cardiovascular risk factors are believed to contribute to the high risk for MI, such as renal involvement, that has been associated with increased subclinical atherosclerosis and ischaemic heart disease, and antiphospholipid syndrome (APS), defined by venous, arterial or small vessel thrombosis and/or obstetric complications together with persistent positivity for antiphospholipid antibodies (aPL). Though several risk factors have been suggested, the exact mechanisms behind the high MI incidence in SLE remain essentially unknown. MIs in SLE are in most cases associated with coronary atherosclerosis. Subclinical atherosclerosis has been reported in many case–control studies, but a direct causal relationship between coronary artery disease (CAD) and MI in SLE has not yet been well documented. The pathogenesis of cardiovascular diseases in SLE is not fully understood. The inflammatory nature of SLE is believed to be an important factor in accelerating atherosclerosis. Systemic inflammation may lead to an abnormal lipid profile with elevated triglycerides, total cholesterol, and low-density lipoprotein cholesterol and dysfunctional high-density lipoprotein cholesterol. Additionally, promotes endothelial dysfunction and vascular injury. Our case showed the key role of an integrated imaging approach with echocardiography and cardiac MRI to confirm diagnosis of past myocardial infarction in a very young man affected by LES. IVUS played a great role to characterize the nature of the lesion, confirming the association between coronary atherosclerosis and MIs in SLE.

Introduction Clinically relevant pulmonary embolism (PE) related to pacemaker leads is reported in up to 3.5% of cases of implantations. We reported a particular case of acute massive PE in a patient bearer of a Cardiac Resynchronization Therapy-Defibrillator (CRT-D). Case presentation A 49-year-old man presented to our ER reporting dyspnea and localized pain to the left hemithorax. Past medical history included HFrEF due to idiopathic dilated cardiomyopathy complicated by apical thrombosis, CRT-D, Charcot-Marie-Tooth syndrome, dyslipidemia, and a hepatic nodule undergoing diagnosis. Recently, he reported COVID-19 and successive pleuropneumonia requiring hospitalization. At home, he was taking Acenocoumarin, Sacubitril/Valsartan 97/103mg bid, Carvedilol 6.25mg bid, Digoxin 0.0625mg, and Canrenon 50mg with questionable adherence. On physical examination, he was pyretic, mildly hypotensive and hypoxemic. An ECG showed atrio-guided biventricular stimulation at 110 bpm. A transthoracic echocardiogram (TTE) revealed biventricular disfunction and dilation, mitral and tricuspid regurgitation, PAPs 60 mmHg, and a thrombotic formation in the left ventricle apex. Blood tests found elevated D-Dimer and infection markers, INR 1.1. A CT angiography confirmed a bilateral acute massive PE associated with lung consolidations and left pleural effusion. We excluded deep vein thrombosis in the lower limbs. Patient was admitted to CCU and treated with intravenous heparin, antibiotics, and support therapy. After one week, we performed a transesophageal echocardiogram that confirmed the previous TTE except for a minor PAPs and unknown thrombotic formations on the atrial side of the tricuspid valve, adhering to CRT-D leads, pedunculated, highly mobile, the largest with an area of 1.9cm2. Cardiac surgery wasn't indicated; we excluded thrombophilia and thoracic cancer. Patient is still hospitalized, asymptomatic and with a precarious cardiovascular status. Discussion The incidence of asymptomatic clot adhering to cardiac device's leads found by echocardiography is 1.4%, and thromboembolic complications are even rarer, especially after years from the implant. In our patient, the right atrium thrombosis is probably the cause of PE, and possible precipitating factors were pneumonia or unknown hepatic neoplasm. In the diagnostic workup, TTE probably wasn't sensitive enough to detect those thrombi. Conclusions We presented a particular case of PE in a relatively young patient affected with HFrEF. Even if thrombosis related to pacemaker leads is rare, it should be considered as a possible cause of PE in a patient bearer of a cardiac stimulating device.

Aims Worsening of cardiac function with increased arrhythmic risk is common in cancer patients undergoing chemotherapy. Impaired LV global longitudinal strain (GLS) in these patients despite preserved ejection fraction is a common issue. Recently, myocardial work by speckle-tracking echocardiography has been used to overcome GLS limitations in various conditions, but little is known about its usefulness in the detection of cardiac toxicity. Moreover, left atrial (LA) toxicity may occur early in the course of cancer therapy. The main aim of the study was to assess the cardiotoxic effects of tyrosine kinase inhibitors (TKIs) on patients with Philadelphia chromosome-positive chronic myeloid leukaemia (Ph+ CML) by using novel echocardiographic tools as myocardial work and atrial strain analysis. Methods and results We retrospectively enrolled Ph+ CML patients treated with TKIs followed at the cardio-oncology outpatient clinic of our hospital from December 2018 to March 2019 who underwent clinical evaluation with ECG and echocardiogram (TTE) before and after 1 year of treatment with TKIs. Healthy subjects were enrolled in the control group matched for gender, age and cardiovascular risk factors. Myocardial work was derived from the strain-pressure relation, integrating in its calculation the non-invasive arterial pressure. LA longitudinal strain (reservoir, conduit, and booster) was obtained from an optimized apical 4-chamber view of the LA. The study recruited 32 patients in Ph+ CML group and 32 healthy controls. 39% of patients were treated with Imatinib, 29.3% with Nilotinib, 4.9% with Dasatinib and 4.9% with Ponatinib. Main results are detailed in Table 1. At 1-year follow-up there was a significant reduction compared to baseline in global constructive work (2555.22 ± 564.33 vs. 2119.31 ± 700.19; P = 0.0001), global work efficiency (96.13 ± 1.90 vs. 94.00 ± 2.96; P = 0.002), and global work index (2340.75 ± 579.57 vs. 1938.46 ± 680.23; P = 0.001), and a non-significant reduction in global wasted work (P = 0.393). Regarding left atrial strain analysis at the 1-year follow-up there was a statistically significant reduction in LA contractile strain (booster= 14.63 ± 1.408 vs. 12.38 ± 1.581; P = 0.018). LA contractile strain reduction was also observed in the comparison with controls (12.38 ± 2.99 vs. 14.91 ± 3.09; P = 0.009). Any other significant difference was detected between baseline and FU TTE data in the Ph+ CML group. Conclusions New imaging methods for the study of cardiotoxicity provide an additional tool for early prediction of potential adverse effects of antineoplastic drugs. TKIs therapy leads to an impairment of atrial contractility, which can be detected by atrial strain e myocardial work analysis.

Aims The myocardial work (MW) is a new echocardiographic method, based on the pressure–strain loop, which allows to quantify the cardiac performance. On the other hand, the pulse wave velocity (PWV) evaluates arterial stiffness, knowing that as the stiffness of an artery increases, the transmission velocity of the anterograde and the retrograde sphygmic wave increase. The aim of the study is to evaluate the correlation between MW and PWV parameters. Methods and results We enrolled 32 healthy patients (mean age: 39 ± 17 years), who underwent transthoracic Doppler echocardiography (TTE). The MW parameters was derived from the strain–pressure loop, including in its calculation the measurement non-invasive arterial pressure, according to standard speckle tracking echocardiography recommendations. The PWV measurement was obtained by tonometry at the level of the common carotid artery and the common femoral artery. None of the parameters measured was pathological according to the normality studies considered. It was found a linear correlation between PWV and global wasted work (GWW) (linear R2: 0.603; P = 0.001) and an inverse linear correlation between PWC and global work efficiency (GWE) (linear R2: −0.307; P = 0.032). Conclusions The study highlights the possibility of PWV to predict pre-clinical myocardial changes, given the correlation with GWW and the linear inverse correlation with GWE.

Aims Left ventricular function recovery (LV-REC) or left ventricular adverse remodelling (LV-REM) after acute myocardial infarction (AMI) play an important role for identifying patients at risk of heart failure. In this study we aim to evaluate the usefulness of non-invasive myocardial work (MW), a new index of global and regional myocardial performance, to predict LV-REC or LV-REM after AMI. Methods and results Fifty patients with AMI (mean age, 63.8 ± 13.4 years), treated by primary percutaneous coronary intervention (PCI), were prospectively enrolled. They underwent a baseline transthoracic Doppler echocardiography (TTE) within 48 h after PCI and a second TTE after a median of 31 days during the follow-up. MW was derived from the strain-pressure loops, integrating in its calculation the non-invasive arterial pressure, according to standard speckle tracking echocardiography recommendations. LV-REC was defined as an absolute improvement of left ventricular ejection fraction (LVEF) ≥ 5% from LVEF at baseline, whereas LV-REM was defined as an increase of ≥ 20% of the LV end diastolic volume (LVEDV) at 1 month follow-up. We overall found a significant improvement from baseline to one-month follow-up for values of LVEF (49.8 ± 9.5% vs. 52.8 ± 9.3%, P = 0.001), global longitudinal strain (GLS) (−13.4 ± 3.9% vs. −18.7 ± 5.4%, P = 0.016), global work index (GWI) (1368.6 ± 435.2 vs. 1788 ± 493 mmHg/%, P = 0.0001), global work efficiency (GWE) (89.96 ± 9.3% vs. 91.3 ± 6.4%, P = 0.001), global constructive work (GCW) (1619.16 ± 497.9 mmHg/% vs. 2008.6 ± 535.3 mmHg/%, P = 0.0001), global wasted work (GWW) (188.8 ± 19.8 mmHg/% vs. 149.2 ± 16.5 mmHg/%). However, LV-REC at 1 month of follow-up was observed only in 36% of the population enrolled, whereas LV-REM was described in 18% of cases. Using ROC curve analysis, we identified a cut off value of 202 mmHg/% for baseline GWW (sensitivity 75%, specificity 62%, AUC 0.6667, CI 95%: 0.51618–0.81715, P = 0.0001) to identify patients with LV-REM at 1 month. With regards to conventional echo parameters, patients with LV-REC showed lower baseline wall motion score index (WMSI) than those without LV-REC (1.73 vs. 1.38, P = 0.007). Conclusions Among standard and advanced TTE parameters, only baseline GWW is able to predict early LV-REM at 1 month after primary PCI. Therefore, it could be used during baseline evaluation of AMI patients for a more accurate stratification of those at higher risk of heart failure. However, further larger scale studies are needed to validate these findings.