Introduction The incidence, characteristics, and prognosis of pulmonary embolism (PE) in Coronavirus disease 2019 (COVID-19) have been poorly investigated. We aimed to investigate the prevalence and the correlates with the occurrence of PE as well as the association between PE and the risk of mortality in COVID-19. Methods Retrospective multicenter study on consecutive COVID-19 patients hospitalized at 7 Italian Hospitals. At admission, all patients underwent medical history, laboratory and echocardiographic evaluation. Results The study population consisted of 224 patients (mean age 69 ± 14, male sex 62%); PE was diagnosed in 32 cases (14%). Patients with PE were hospitalized after a longer time since symptoms onset (7 IQR 3–11 days, 3 IQR 1–6 days; p = 0.001) and showed higher D-dimers level (1819 IQR 568–5017 ng/ml vs 555 IQR 13–1530 ng/ml; p < 0.001) and higher prevalence of myocardial injury(47% vs 28%, p = 0.033). At multivariable analysis, tricuspid annular plane systolic excursion (TAPSE; HR = 0.84; 95% CI 0.66–0.98; p = 0.046) and systolic pulmonary arterial pressure (sPAP; HR = 1.12; 95% CI 1.03–1.23; p = 0.008) resulted the only parameters independently associated with PE occurrence. Mortality rates (50% vs 27%; p = 0.010) and cardiogenic shock (37% vs 14%; p = 0.001) were significantly higher in PE as compared with non-PE patients. At multivariate analysis PE was significant associated with mortality. Conclusion PE is relatively common complication in COVID-19 and is associated with increased mortality risk. TAPSE and sPAP resulted the only parameters independently associated with PE occurrence in COVID-19 patients.

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Objective The aim of the study is to describe the real-world use of the P2Y12 inhibitor cangrelor as a bridging strategy in patients at high thrombotic risk after percutaneous coronary intervention (PCI) and referred to surgery requiring perioperative withdrawal of dual antiplatelet therapy (DAPT). Materials and Methods We collected data from nine Italian centers on patients with previous PCI who were still on DAPT and undergoing nondeferrable surgery requiring DAPT discontinuation. A perioperative standardized bridging protocol with cangrelor was used. Results Between December 2017 and April 2019, 24 patients (mean age 72 years; male 79%) were enrolled. All patients were at high thrombotic risk after PCI and required nondeferrable intermediate to high bleeding risk surgery requiring DAPT discontinuation (4.6 ± 1.7 days). Cangrelor infusion was started at a bridging dose (0.75 µg/kg/min) 3 days before planned surgery and was discontinued 6.6 ± 1.5 hours prior to surgical incision. In 55% of patients, cangrelor was resumed at 9 ± 6 hours following surgery for a mean of 39 ± 38 hours. One cardiac death was reported after 3 hours of cangrelor discontinuation prior to surgery. No ischemic outcomes occurred after surgery and up to 30-days follow-up. The mean hemoglobin drop was <2 g/dL; nine patients received blood transfusions consistent with the type of surgery, but no life-threatening or fatal bleeding occurred. Conclusion Perioperative bridging therapy with cangrelor is a feasible approach for stented patients at high thrombotic risk and referred to surgery requiring DAPT discontinuation. Larger studies are warranted to support the safety of this strategy.

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Acute thrombotic events can unveil occult cancer, as they are its first manifestation in about 20 to 30% of all cases. Malignancy interacts in an intricate way with the hemostatic system, promoting both thrombosis and bleeding. The main pathway involved in these reactions involves the activation of tumor-associated procoagulant factors, which eventually results in clot formation. The clinical manifestation of cancer-related thrombotic events mainly involves the venous side, and manifests in a broad spectrum of conditions, including unusual sites of venous thrombosis. The selection of patients who have a balanced risk–benefit profile for management of anticoagulation is complex, given individual patient goals and preferences, different prognosis of specific cancers, common comorbidities, potential drug–drug interactions, underweight states, and the competing risks of morbidity and mortality. Anticoagulant treatment in cancer settings is broadly debated, considering the potential application of direct oral anticoagulants in both thromboprophylaxis and secondary prevention, having demonstrated its efficacy and safety compared to conventional treatment. This review aims to provide a brief overview of the pathophysiology and management of cancer-related thrombosis, summarizing the results obtained in recent clinical trials.

Immune checkpoint inhibitors (ICIs) are monoclonal antibodies that activate the immune system, aiming at enhancing antitumor immunity. ICIs have shown great promise in the treatment of several advanced malignancies. However, therapy with these immunomodulatory antibodies may lead to a wide spectrum of immune-related adverse events in any organ and any tissue. Cardiologic immune-related events include pericarditis, pericardial effusion, various types of arrhythmias including the occurrence of complete atrioventricular block, myocardial infarction, heart failure, and myocarditis. Although relatively rare, myocarditis is associated with a very high reported mortality in comparison to other adverse events. Myocarditis often presents significant diagnostic complexity and may be under-recognized. When confronted with an unexpected change in the clinical picture, the physician must differentiate between immune-related adverse events, cancer worsening, or other causes unrelated to the cancer or its therapy. However, this is not always easy. Therefore, with the increasing use of checkpoint inhibitors in cancer, all providers who care for patients with cancer should be made aware of this rare, but potentially fatal, cardiologic immune-related adverse event, and able to recognize when prompt consultation with a cardiologist specialist is indicated. In this review, we evaluate currently available scientific evidence and discuss clinical manifestations and new potential approaches to the diagnosis and therapy of acute myocarditis induced by ICIs. Temporary or permanent discontinuation of the ICIs and high-dose steroids have been administered to treat myocarditis, but symptoms may worsen in some patients despite therapy.

Background: In hypertensive patients, an impairment of midwall myocardial mechanics was described in presence of left ventricular (LV) concentric geometry. Under these circumstances, also LV longitudinal dysfunction was found. Purpose: Our aim was to evaluate longitudinal and circumferential systolic function and correlations between these two functional components in newly diagnosed hypertensive patients without clinically defined LV hypertrophy (LVH). One hundred and thirty-eight newly diagnosed, never-treated hypertensive patients without LVH and a control group of 105 healthy normotensive individuals underwent two-dimensional and speckle tracking echocardiography. Global longitudinal strain (GLS) was derived (in absolute value) and midwall fractional shortening (MFS) computed. In addition, the hypertensive population was divided into two groups according to GLS: normal GLS (≥20%, n = 94) and reduced GLS (<20%, n = 44). Results: Hypertensive patients had lower MFS (P < 0.001) and GLS (P < 0.0001) than healthy controls. By dividing hypertensive patients according to GLS thresholds of normalcy, MFS was lower in patients with GLS less than 20% (P < 0.0001) while no significant difference was found in LV geometry, ejection fraction and diastolic parameters in comparison with patients with GLS at least 20%. In the pooled hypertensive population, GLS resulted positively related to MFS (r = 0.33, P < 0.0001). By a multiple linear regression analysis, after adjusting for female sex, age, BMI, circumferential end-systolic stress, average e′, ejection fraction and relative wall thickness, MFS remained independently associated with GLS (β = 0.222, P < 0.005). Conclusion: In newly diagnosed and never-treated hypertensive patients without LVH, an early LV systolic dysfunction is testified by the reduction of both MFS and GLS. These two parameters resulted independently associated after adjusting for several confounders.

Background Coronary artery disease (CAD) has been recognized as a serious and potentially life‐threatening complication of Hepatitis C Virus (HCV) infection. High on‐treatment platelet reactivity has been associated with high risk of ischemic events in patients with CAD, but data regarding the association with HCV infection are still lacking. This post hoc analysis aims to assess high on‐treatment platelet reactivity, severity of CAD, and long‐term outcomes of patients with acute coronary syndrome (ACS) who were infected with HCV. Methods and Results Patients with ACS who were infected with HCV (n=47) were matched to patients with ACS and without HCV (n=137) for age, sex, diabetes mellitus, hypertension, and renal function. HCV‐infected patients with ACS had higher levels of platelet reactivity (ADP 10 –light transmittance aggregometry, 56±18% versus 44±22% [ P =0.002]; arachidonic acid–light transmittance aggregometry, 25±21% versus 16±15% [ P =0.011]) and higher rates of high on‐treatment platelet reactivity on clopidogrel and aspirin compared with patients without HCV. Moreover, HCV‐infected patients with ACS had higher rates of multivessel disease (53% versus 30%; P =0.004) and 3‐vessel disease (32% versus 7%; P <0.001) compared with patients without HCV. At long‐term follow‐up, estimated rates of major adverse cardiovascular events (cardiac death, nonfatal myocardial infarction, and ischemia‐driven revascularization) were 57% versus 34% ( P =0.005) in HCV‐ and non–HCV‐infected patients with ACS, respectively. In addition, thrombolysis In Myocardial Infarction (TIMI) major bleeding rates were higher in HCV‐infected patients (11% versus 3%; P =0.043) compared with noninfected patients. Multivariable analysis demonstrated that HCV infection was an independent predictor of high on‐treatment platelet reactivity, severity of CAD, and long‐term outcome. Conclusions In this hypothesis‐generating study, patients with ACS and HCV infection showed increased on‐treatment platelet reactivity, more severe CAD, and worse prognosis compared with patients without HCV.