Résumé
It is now widely known that COVID-19 can also cause various extrapulmonary manifestations. Possible mechanisms of cardiovascular damage include direct myocardial damage due to hypercoagulability caused by systemic inflammation, which may also lead to destabilisation of coronary plaques. We present a case of a 30-year-old young man following asymptomatic COVID-19 infection, who was admitted to the emergency room of the Grande Ospedale Metropolitano di Reggio Calabria, Italy, with typical chest pain. The patient had no cardiovascular disease, cardiovascular risk factors including no family history of cardiovascular disease. Urgent coronary angiography showed critical stenosis of the middle-proximal portion of the left anterior descending artery (80%) with ulcerated plaque appearance. Regardless of cardiovascular risk factors, our case report emphasises the need to determine COVID-19 status in all patients with acute myocardial infarction during this pandemic.Copyright © 2023, CKS.
Résumé
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 CTangiography confirmed a bilateral acute massive PE associated with lung consolidations and left pleural effusion. We excluded deep vein thrombosis in the lower limbs. Patientwas admitted to CCU and treatedwith intravenous heparin, antibiotics, and support therapy. After one week, we performed a transesophageal echocardiogramthat 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(s): 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. Conclusion(s): 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. (Figure Presented).