Background: in patients undergoing percutaneous coronary interventions (PCI), radial access should be favoured over femoral access as it reduces the risk of vascular complications and bleeding. Furthermore, a preventive role of radial access in the occurrence of acute kidney injury (AKI), mainly mediated by the reduction of bleeding and cholesterol crystal embolization into renal circulation, has been investigated in several studies, yielding conflicting results. Methods: we designed a retrospective study to appraise the effect of the use of a vascular access site on the occurrence of AKI in a cohort of 633 patients with acute myocardial infarction treated by PCI at our centre from 2018 to 2020. Results: after propensity score adjustment, radial access was associated with a reduced, albeit statistically not significant, incidence of AKI (14.7% vs. 21.0%; p = 0.06) and major bleeding (12.5% vs. 18.7%; p = 0.04) as compared to femoral access. At multivariate analysis, femoral access was an independent predictor of AKI, together with in-hospital occurrence of BARC 3–5 bleeding, Killip class >1 at presentation, female gender, baseline eGFR <60 mL/min, and baseline haemoglobin <12 g/dL. Conclusions: although limited by the observational design, our study supports the hypothesis that radial access may exert a protective role on the occurrence of AKI in patients with acute myocardial infarction undergoing PCI.

A young man of 29 years presented to the Emergency Room reporting worsening dyspnea for about 2 weeks. He had never had previous cardiovascular disease nor had risk factors for them. Hemodynamics were stable, but arterial blood gases showed hypocapnic hypoxia. The ECG revealed a S1Q3T3 pattern, incomplete right bundle branch block and signs of right ventricular overload. D–dimer was 4493 ng/ml. CT pulmonary angiogram (CTPA) showed massive bilateral embolism with thrombotic material in the right ventricle (RV) and almost complete obliteration of pulmonary trunk and main pulmonary arteries; moreover, there were subpleural nodularities in upper pulmonary lobes. Echocardiogram showed a dilated and hypokinetic RV, moderate tricuspid regurgitation with a sPAP of 80 mmHg, thrombotic pulmonary trunk obliteration and floating thrombi adhered to the tricuspid valve. UFH therapy was started. After ten days, there was no improvement in clinical status, echocardiography and CTPA. So, we decided to perform mechanical thrombectomy. In addition to thrombotic material, fibrous tissue was extracted and histologically analyzed. At the end of the procedure, the patient became hemodynamically unstable (BP 80/40 mmHg and HR 130 bpm) with dyspnea and tachypnea. ABG showed mixed acidosis. Right ventricular function worsened due to high afterload for the persistence of thrombotic material in the pulmonary trunk, defining a picture of obstructive shock. We started fibrinolysis (with rtPA), enoximone and norepinephrine, but asystole occurred and the patient eventually died. The histological examination revealed that the mass was a pleomorphic rhabdomyosarcoma of the pulmonary artery. Primary pulmonary artery sarcoma is an extremely rare and histologically heterogeneous disease. It develops mainly from great pulmonary arteries and then it grows up in the lumen of vessels. It may involve pulmonary valve and RV and invade pulmonary parenchyma and loco–regional lymph nodes. Diagnosis is challenging, because it simulates pulmonary embolism in clinical, echocardiographic and radiological presentation. Suspicion may arise from lack of benefit from anticoagulant therapy. Nodular pulmonary infiltrates are typical. There are two surgical approaches: pneumectomy or endarterectomy (as palliation). Prognosis is poor: mean survival of 1,5 month without therapy and 10 months with pneumectomy. In addition to the progression of the disease, death can occur for obstructive shock, as in our patient.

Background: a wider left main bifurcation angle (LMBA) has been linked to severe plaque development in the proximal left anterior descending artery (LAD). This study aimed to identify predictors of severe proximal LAD stenosis and major adverse cardiovascular events (MACE) using coronary computed tomography angiography (CCTA). Methods: from an initial cohort of 650 consecutive patients, we analyzed 499 patients who met the inclusion criteria after exclusions. Plaque morphology and characteristics were assessed by CCTA, and MACE occurrences were recorded at follow-up. A predictive score for LAD disease progression (CLAP score) was developed and validated. Results: severe proximal LAD stenosis was detected in 32% (160/499) of patients by CCTA. MACE occurred in 12.5% of patients at follow-up. Significant predictors of MACE were LMBA > 80° (HR: 4.47; 95% CI: 3.80–6.70; p < 0.001), diabetes (HR: 2.94; 95% CI: 1.54–4.63; p = 0.031), chronic kidney disease (HR: 1.71; 95% CI: 1.31–6.72; p = 0.041), high-risk plaques (HR: 2.30; 95% CI: 1.45–3.64; p < 0.01), obstructive CAD (HR: 2.50; 95% CI: 1.50 to 4.10, p = 0.01), and calcium score (CAC) (HR: 1.05; 95% CI: 1.02–1.08, p = 0.004). The CLAP score demonstrated good discriminatory power in both the development (AUC 0.91; 95% CI: 0.86–0.96) and validation cohorts (AUC 0.85; 95% CI: 0.79–0.91); Conclusions: LMBA > 80°, diabetes, chronic kidney disease, obstructive CAD, CAC score >180 and high-risk plaques were significant predictors of MACE in CCTA patients. The CLAP score effectively predicted LAD disease progression, aiding in risk stratification and optimization of intervention strategies for suspected coronary artery disease.