Purpose of Review The COVID-19 pandemic has infected over > 11 million as of today people worldwide and is associated with significant cardiovascular manifestations, particularly in subjects with preexisting comorbidities and cardiovascular risk factors. Recently, a predisposition for arterial and venous thromboses has been reported in COVID-19 infection. We hypothesize that besides conventional risk factors, subjects with elevated lipoprotein(a) (Lp(a)) may have a particularly high risk of developing cardiovascular complications. Recent Findings The Lp(a) molecule has the propensity for inhibiting endogenous fibrinolysis through its apolipoprotein(a) component and for enhancing proinflammatory effects such as through its content of oxidized phospholipids. The LPA gene contains an interleukin-6 (IL-6) response element that may induce an acute phase-type increase in Lp(a) levels following a cytokine storm from COVID-19. Summary Thus, subjects with either baseline elevated Lp(a) or those who have an increase following COVID-19 infection, or both, may be at very high risk of developing thromboses. Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. We propose studies to test the hypothesis that Lp(a) may contribute to cardiovascular complications of COVID-19.

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Introduction: Research is elucidating vascular impairment in the pathophysiology of Alzheimer’s disease (AD) and as a treatment target. NCP-5 is external counterpulsation (ECP) therapy approved for treating unstable angina and granted FDA Breakthrough Status for mild cognitive impairment (MCI) and AD. It increases cardiac output and improves endothelial function. A study was done to assess NCP-5 on cognitive function. Methods: Randomized, single-blind, sham-controlled; 10 US sites. Subjects 55-85 years (Montreal Cognitive Assessment score ≥11) were given NCP-5 (n=95) or active sham (n=95). Primary endpoint: mean change from baseline in Vascular Dementia Assessment Scale-cognitive subscale (VADAS-Cog) at 12, 18, and 24 weeks, powered for a 2-point change. Results: Primary endpoint met (change, -4.45 points); NCP-5 showed statistically significantly greater improvement from baseline vs active sham on VADAS-Cog. In subjects with type 2 diabetes (T2D; n=36), NCP-5 improved cognition from baseline (change, -17.01 points; p <0.005). NCP-5 was statistically significantly superior to active sham on Alzheimer’s Disease Cooperative Study-Clinical Global Impression of Change at weeks 12 (odds ratio [OR], 2.13; p =0.013) and 24 (OR, 2.56; p =0.002). NCP-5 had a statistically significant decrease on Neuropsychiatric Inventory Aggression Index vs active sham at week 24 ( p =0.041). Neuroimaging showed a decline in right hippocampal volume (HV) that was statistically significantly greater with NCP-5 at week 24 ( p =0.012) and at longitudinal assessment to 12 months ( p =0.008), possibly related to smaller HV seen at baseline with NCP-5. However, the decline in regional cerebral blood flow (rCBF) in the left hippocampus from baseline to month 12 and for the longitudinal assessment was statistically significantly less with NCP-5 than with active sham ( p =0.010 and 0.019, respectively). NCP-5 had a low-risk safety profile (10,644 exposures), and the most common AE was mild skin irritation/injury. Conclusions: Renew NCP-5 improved cognitive performance and global function, particularly in those with T2D. Findings support the role of targeting vascular dysfunction, specifically with NCP-5, for the treatment of MCI and mild dementia of the Alzheimer’s type.