Polycythemia vera (PV) and heterozygous beta-thalassemia (HBT) have opposing effects on the hematocrit (Hct) and may mask the presence of each other. Missing the diagnosis of PV may have serious consequences, mainly by exposing the patient to the risk of thromboses. We present a case where the diagnosis of PV was delayed due to the coexistence of HBT, and review the relevant literature. It can be postulated that "stress erythropoiesis", known to occur in patients with thalassemic syndromes, increases the probability of somatic JAK2 mutations leading to development of PV.

Background Myocardial and vascular alterations among post-COVID-19 patients are observed. The coupling between arterial stiffness with left ventricular (LV) myocardial function (ventricular-arterial coupling, VAC) is an important determinant of cardiovascular performance and cardiac energetics. The aim of the study was to investigate the spectrum of cardiac and vascular abnormalities at mid-term follow-up in post-COVID-19 patients. Methods We enrolled 25 hospitalized patients for COVID-19, at one and six months after hospital discharge. The ratio (PWV/GLS) of carotid-femoral pulse wave velocity (cf-PWV), as a marker of arterial stiffness, to global longitudinal strain (LV-GLS), as a marker of left ventricular performance, was estimated as a marker of arterial elastance/left ventricular elastance index the long-term. The comparison was conducted with age and sex-matched non-COVID-19 controls. Results There was no difference in age (56.8±11.6 y vs. 57.4±9.5 y; p=0.85) and male sex (64% vs. 68%; P=0.76) between post-COVID-19 and control subjects respectively. At one-month follow-up, significant impairment was noted between post-COVID-19 and control subjects regarding: VAC (−0.71±0.24 m/s% vs. −0.44±0.11 m/sec%; p<0.001), LV-GLS (−17.9±3.1% vs. −21.9±2.7%; p<0.001), cf-PWV (12.3±3.5 m/s vs. 9.6±1.9; p<0.001). At six-month follow-up, an improvement was observed but there still was significant difference between post-COVID-19 and control subjects in: VAC (−0.62±0.19 m/sec% vs. −0.44±0.11 m/sec%; p<0.001), LV-GLS (−19.3±2.9% vs. −21.9±2.7%; p=0.001), cf-PWV (11.7±2.7 m/s vs. 9.6±1.9 m/s; p=0.001). Moreover, it was observed at 1-month: VAC adverse correlation with the levels of IL-6 (r=−0.54; p<0.001), CRP (−0.71; p=0.011) and at 6-months: IL-6 (r=−0.47; p=0.003), CRP (−0.56; p=0.007). Conclusion Ventricular-arterial coupling is impaired 6 months following COVID-19 highlighting the possible effects of SARS-CoV-2 infection in left ventricular mechanics and performance. Funding Acknowledgement Type of funding sources: None.

Background: Several studies have linked high Lipoprotein (a) [Lp(a)] concentrations to cardiovascular events, including the formation of Abdominal Aortic Aneurysms (AAA). We review and meta-analyze existing evidence on the association of Lp(a) levels with AAA. Methods: Studies evaluating the link of Lp(a) with AAA, up to December 27th 2021, were identified by a systematic search of PubMed, SCOPUS, and Web of Science databases. The results were qualitatively and quantitatively synthesized according to PRISMA guidelines. Results are presented as standardized mean differences (SMD) with 95% confidence intervals (CI). Results: A total of 5,078 subjects (1,637 patients with AAA vs. 3,441 controls) from 11 studies were included in the meta-analysis, with a mean age of 69.9 years and a male sex prevalence of 85.8%. Based on the qualitative synthesis, high Lp(a) concentrations are linked to abdominal aortic wall degradation and extracellular matrix disarrangement. Moreover, despite the considerable variability among races, high Lp(a) levels are related to increased AAA risk, independently of race differences. Accordingly, patients with AAA displayed significantly higher Lp(a) levels compared to controls (SMD: 0.86, 95% CI: 0.55-1.17, p<0.001). The outcome was not affected in a sensitivity analysis excluding three outlying studies (SMD: 0.40, 95% CI: 0.22-0.58, p<0.001). Conclusion: This meta-analysis indicates the association between high Lp(a) levels and the presence of AAA, although existing literature presents high heterogeneity. Further studies are needed to standardize Lp(a) measurements and to conclude whether Lp(a) can be used as a sensitive biomarker of early presymptomatic AAA diagnosis.