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Low-density lipoprotein cholesterol (LDL-C) is a proven causative factor for developing atherosclerotic cardiovascular disease. Individuals with genetic conditions associated with lifelong very low LDL-C levels can be healthy. We now possess the pharmacological armamentarium (statins, ezetimibe, PCSK9 inhibitors) to reduce LDL-C to an unprecedented extent. Increasing numbers of patients are expected to achieve very low (

Introduction Aortic insufficiency (AI) following left ventricular assist device (LVAD) placement is a serious, well established complication. Transcatheter aortic valve replacement (TAVR) has been successfully used in LVAD patients developing AI. However, femoral/iliac arterial access required for TAVR is not always possible due to arterial calcifications and small arterial size. Transcaval approach is a novel alternative percutaneous catheter route from the IVC, through the retroperitoneal space, into the abdominal aorta. Transcaval TAVR in LVAD patients with severe AI has not been described. CASE Patient is a 28 year old female with history of postpartum STEMI secondary to spontaneous LAD/LCX dissection requiring CABG with subsequent cardiogenic shock requiring emergent LVAD (HeartMate 3) placement. One month following LVAD implantation, she presents with intractable nausea and vomiting. Physical exam illustrates a cachectic female who was hypotensive, tachycardic, with cool extremities. Laboratory evaluation reveals elevated lactate, transaminases and creatinine. Abdominal CTA shows a prior dissection in the infrarenal abdominal aorta, occlusion of the right external iliac artery and stenosis in the left external iliac artery. On echocardiography, there is severe, continuous, aortic regurgitation increased in severity compared to baseline. Right heart catheterization illustrates right atrial pressure 18 mmHg, pulmonary artery pressure 53/25 mmHg, pulmonary wedge pressure 24 mmHg, and cardiac index 1.3 L/min/m2. Patient is referred for urgent TAVR via transcaval access due to her stenotic and small sized iliac arteries. A pigtail was inserted in the left femoral artery and advanced to the abdominal aorta and another pigtail was inserted in the right femoral vein and advanced to the IVC to align with the aorta one. From the IVC, an astato wire was crossed into the aorta using wats to electrify the wire. A Sapien 3 valve was deployed. The caval aortic fistula was closed with a covered aortic stent. Final angiography showed complete occlusion of the fistula. Post intervention, patient experienced immediate improvement with resolution of cardiogenic shock. At three months, she remained asymptomatic and echocardiogram showed a well seated valve with no AI. DISCUSSION We present an urgent transcaval TAVR performed for a LVAD patient presenting with cardiogenic shock due to AI. Transcaval TAVR is a promising intervention that can be successfully used in LVAD patients developing AI with challenging iliofemoral arterial access.

Clinical trials with PCSK9 inhibitors have shown a robust decrease in plasma LDL levels and a significant reduction in the incidence of cardiovascular atherosclerotic events. However, the role of PCSK9 in atherosclerosis is not well investigated and it remains unclear whether PCSK9 inhibition has direct, LDL-independent, anti-atherosclerotic effects. This review outlines the molecular pathways and targets of PCSK9 in atherosclerosis and summarizes the experimental and clinical data supporting the anti-atherosclerotic (pleiotropic) actions of PCSK9 inhibitors. PCSK9 is expressed by various cell types that are involved in atherosclerosis (e.g., endothelial cell, smooth muscle cell, and macrophage) and is detected inside human atherosclerotic plaque. Preclinical studies have shown that inhibition of PCSK9 can attenuate atherogenesis and plaque inflammation. Besides increasing plasma LDL, PCSK9 appears to promote the initiation and progression of atherosclerosis. Inhibition of PCSK9 may confer atheroprotection that extends beyond its lipid-lowering effects.