Vascular aging is recognized as one of the hallmarks of atherosclerosis. Currently, a growing body of evidence suggests that there exists a mutual crosstalk between telomere dysfunction and mitochondrial dysmetabolism during the process of vascular senescence. This underscores the importance of comprehensively studying the molecular mediators involved in this complex and intricate connection. In pursuit of this goal, the “VICTORIA” protocol entails a prospective single-center cohort study aimed at recruiting patients undergoing coronary angiography at Niguarda Hospital in Italy. The primary objective is to explore potential associations between peripheral markers of cell aging (telomere length and mtDNA content), dysregulation of non-coding RNA [specifically lncRNA TERRA and mitochondrial microRNA (MitomiR)], and the varied presentations of ischemic heart disease (stable angina, unstable angina, NSTEMI, and STEMI). Furthermore, we aim to investigate whether these markers correlate with vulnerable plaque characteristics, as assessed by optical coherence tomography findings. Additionally, systemic levels of pro-inflammatory biomarkers and novel indicators of senescence will be assessed. Patients will be followed up at 1 year to monitor primary outcomes including mortality, myocardial infarction, stroke, unplanned revascularization, and rehospitalization. The anticipated findings of this study hold promise for advancing our understanding of the telomere-mitochondria crosstalk, potentially paving the way for novel treatment modalities and refined risk stratification approaches for acute coronary syndrome.

Pulmonary embolism (PE) is the third leading cause of cardiovascular mortality worldwide. Percutaneous mechanical thrombectomy is indicated in patients with contraindications to thrombolysis. Complications include atrial or ventricular perforation causing tamponade. We describe one case of pericardial tamponade in an elderly woman who underwent thrombectomy for acute PE. An 88-year-old woman presented with acute shortness of breath. She was tachycardic, oxygen saturation of 80% and blood pressure of 95/57 mmHg. Bedside ultrasound showed a dilated right ventricle. Electrocardiogram showed large S wave in lead I, Q wave and inverted T wave in lead III. Computed tomography (CT) angiogram of the chest revealed an extensive saddle PE. Tissue plasminogen activator was deferred given patient’s age. Full dose anticoagulation was started and she underwent a successful percutaneous thrombectomy with FlowTriever device. Two hours later, she developed severe back pain and hypotension to 88/63 mmHg. Hemoglobin dropped from 13.7 g/dL to 8.8 g/dL. CT chest angiogram showed dense pericardial effusion, likely hemopericardium, with mass effect on the heart. Bedside pericardiocentesis was attempted and converted to pericardial window given sustained hypotension. She went into cardiac arrest. Emergent thoracotomy revealed significant hemothorax. The pericardium was opened yielding a blue, globally ischemic, and non-contracting heart. Cardiac massage and intra-cardiac epinephrine attempted unsuccessfully. Percutaneous thrombectomy using the large bore design FlowTriever system has shown promising results in reducing clot burden and improving hemodynamics. Attention must be paid to life threatening complications such as cardiac tamponade which can be precipitated by using these devices.