RESUMEN
SARS-CoV-2 has been circulating in population worldwide for the past year and a half, and thus a vast amount of scientific literature has been produced in order to study the biology of the virus and the pathophysiology of COVID-19, as well as to determine the best way to prevent infection, treat the patients and eliminate the virus. SARS-CoV-2 binding to the ACE2 receptor is the key initiator of COVID-19. The ability of SARS-CoV-2 to infect various types of cells requires special attention to be given to the cardiovascular system, as it is commonly affected. Thorough diagnostics and patient monitoring are beneficial in reducing the risk of cardiovascular morbidity and to ensure the most favorable outcomes for the infected patients, even after they are cured of the acute disease. The multidisciplinary nature of the fight against the COVID-19 pandemic requires careful consideration from the attending clinicians, in order to provide fast and reliable treatment to their patients in accordance with evidence-based medicine principles. In this narrative review, we reviewed the available literature on cardiovascular implications of COVID-19; both the acute and the chronic.
RESUMEN
Rheological abnormalities are well known in patients with peripheral arterial occlusive disease (PAOD). We wanted to determine whether rheological variables are related to restenosis after femoropopliteal percutaneous transluminal angioplasty (PTA). In 114 patients (62 men; median age 70 years) undergoing femoropopliteal PTA for symptomatic peripheral arterial occlusive disease (PAOD) plasma viscosity, red cell aggregation, whole blood viscosity, hematocrit, fibrinogen, platelet count, leukocytes and C-reactive protein were determined the day after the procedure and at 1, 3, and 12 months. The primary endpoint was restenosis >50% documented by duplexsonography up to 12 months. Cox proportional hazards analysis was used to assess the risk of restenosis for postinterventional values of rheological variables. Forty-eight patients (42%) developed restenosis at 12 months. Patients with restenosis had higher baseline plasma viscosity (PV) (medians, 1.71 vs. 1.65 millipascal seconds [mPa.s]; p = 0.04) and lower platelet count (224 vs. 240 x 10(3)/microl; p = 0.03) than patients without restenosis. The hazard ratio (HR; 95% CI) of incident restenosis was 9.2 (1.12-76; p = 0.03) for PV and 0.99 (0.99-1.0; p = 0.07) for PLT. When examining jointly both high PV and low platelet count (PLT), patients with PV > 1.66 mPa.s and PLT < 233 x 10(3)/microl (i.e. variables split at their respective median) had an increased risk of restenosis (log-rank test p = 0.01). Multivariate Cox proportional hazard analysis showed that plasma viscosity (p = 0.02), low platelet count (p = 0.01), lesion length (p = 0.0037) and lack of hypertension (p = 0.01) were associated with restenosis at 12 months. No associations were found between restenosis and the other rheological and inflammatory variables studied. Our data suggest that increased PV and low PLT contribute to restenosis after femoropopliteal PTA.
