Burden of lipoprotein(a) for patients with atherosclerotic cardiovascular disease: A retrospective analysis from the United States.

BACKGROUND: Lipoprotein(a) (Lp(a)) is an inherited, independent, and causal risk factor for atherosclerotic cardiovascular disease (ASCVD). OBJECTIVE: To assess the burden of elevated Lp(a) for patients with ASCVD in a real-world setting in the United States. METHODS: This retrospective cohort study assessed US patients with available Lp(a) measurement and established ASCVD using Optum's Clinformatics Data Mart database (2007-2020). Index date was defined as the first diagnosis of an ASCVD event. Patient demographics, medications, health care resource utilization (HCRU), and occurrence of cardiovascular events were assessed for patients with elevated (≥150 nmol/L) vs normal (≥65 nmol/L) Lp(a) levels, within the first year of index date. HCRU was characterized by inpatient hospitalization, inpatient length of stay (LOS), outpatient visits, and emergency department (ED) visits. All comparative analyses of patients with elevated (≥150 nmol/L) vs normal (≥65 nmol/L) Lp(a) levels within the first year of index date were adjusted for age, sex, baseline statin use, and diabetes. RESULTS: 8,372 patients with ASCVD and Lp(a) measurement in nmol/L were included in this study. Patient demographics and baseline clinical characteristics were similar among those with normal and elevated Lp(a). However, the proportion of patients receiving statins and ß-blockers at baseline were significantly higher in the elevated vs normal Lp(a) group (54.76% vs 42.91%, P < 0.0001, and 30.92% vs 27.32%, P = 0.0183, respectively). At 1 year of follow-up, the rates per 100 person-years for ASCVD-related inpatient hospitalizations, outpatient hospitalizations, and ED visits were higher among patients with elevated Lp(a) compared with normal Lp(a) (13.33 vs 9.46, 89.08 vs 85.10, and 2.89 vs 2.29, respectively). The mean LOS per ASCVD-related hospitalization was 7.21 days in the elevated and 6.26 days in the normal Lp(a) group (P = 0.3462). During the 1-year post-index follow-up period, 15% of patients in the elevated Lp(a) group required revascularization compared with 10% of patients in the normal Lp(a) group (P = 0.0002). The odds of composite myocardial infarction, ischemic stroke, and revascularization occurrence of events within the first year of index was significantly higher in the elevated Lp(a) group compared with the normal Lp(a) group (1.46; 95% CI = 1.20-1.77; P < 0.05). CONCLUSIONS: HCRU within the first year of ASCVD diagnosis is substantial among patients with ASCVD and elevated Lp(a). Relatively higher rates of inpatient hospitalizations, increased LOS per hospitalization, and requirement of revascularization procedures within the first year of ASCVD index diagnosis were observed in patients with elevated Lp(a) compared with normal Lp(a) levels. Lp(a) testing in routine clinical practice could help in identification of high-risk patients with ASCVD and play an important role in the overall cardiovascular risk management, aiming to reduce the HCRU associated with ASCVD. DISCLOSURES: Ms Fonseca, Dr Laguna, Dr Itani, Dr Rachel Studer, and Dr Ferber are employees of Novartis Pharma AG, Basel, Switzerland. Ms Byrne is an employee of Novartis AG, Dublin, Ireland. Dr Costa-Scharplatz is an employee of Novartis Sweden AB, Stockholm, Sweden. Dr Heo and Ms Dillon are employees of Genesis Research. Genesis Research was commissioned to conduct the study (data extraction and analysis) on behalf of Novartis Pharma AG.

Manifestaciones trombóticas en la neumonía viral por SARS-CoV-2 pacientes hospitalizados en el Hospital «Irma de Lourdes Tzanetatos¼, Panamá, Panamá. De marzo de 2020 a septiembre de 2020 / Thrombotic manifestations in viral neumonia by CoV-2-SARS hospitalized patients at «Irma Lourdes Tzanetatos¼ Hospital, Panama, Panama. March 2020 to September 2020

La respuesta a la infección viral produce un estado de trombosis o hipercoagulabilidad que, unido a la inflamación de las células endoteliales, puede generar disfunción plaquetaria y predisposición a la formación de trombos que, aunque con frecuencia son más venosos, también pueden aparecer en el sistema arterial y producir infartos a cualquier nivel así como tromboembolia e hipertensión pulmonar. Estas manifestaciones han sido captadas hospitalariamente y al egreso de los pacientes detectados por SARS-CoV-2 habiendo ya cumplido el tiempo establecido de virulencia. Los criterios diagnósticos de respuesta inmunológica trombótica asociada a COVID-19 (RITAC) ayudan a seleccionar al paciente que está predispuesto a esta condición; a esto se añade que el paciente ya tiene un diagnóstico de infección por SARS-CoV-2 (AU)

The response to viral infection produces a prothrombotic state of hypercoagulability , united with an inflammation of endothelial cells, It can generate platelet dysfunction and predisposition to the formation of thrombus, that, although, are more frequently venous, Also, it can appear in the arterial system and cause heart attacks at any level; thromboembolism and pulmonary hypertension, as well. These manifestations have been captured hospitably and with the egress of patients detected by SARS-CoV-2. The diagnostic criteria of RITAC (abbreviation in Spanish of Thrombotic Immune Response Associated to COVID-19), help to select the patient who is predisposed to this condition; adding that the patient already has a diagnosis of SARS-CoV-2 infection (AU)

Transdermal estradiol reduces F2alpha-isoprostane levels in postmenopausal women.

OBJECTIVE: F2alpha-isoprostanes are considered the most reliable index of in vivo oxidative stress. Given the implication of oxidative stress in the pathogenesis of atherosclerosis, we investigated the effects of hormone therapy on the plasma levels of F2alpha-isoprostanes. DESIGN: Sixty-one healthy postmenopausal women were treated in a randomized trial with estradiol either orally (2 mg/day, 28 women) or transdermally (50 mug/day, 33 women) for 4 weeks. Then women in each group were randomly assigned to oral progestogen, either micronized progesterone (300 mg/day) or medroxyprogesterone acetate (5 mg/day) for 2 additional weeks. Plasma samples were collected before and at the end of each treatment period, either estradiol alone or estradiol plus progestogen. F2alpha-isoprostanes were measured by a commercial enzyme immunoassay. RESULTS: A significant reduction in the levels of F2alpha-isoprostanes was detected only in women receiving transdermal estradiol, alone or in combination with medroxyprogesterone acetate. CONCLUSIONS: Transdermal estradiol alone or associated with medroxyprogesterone acetate decreased plasma levels of F2alpha-isoprostanes. These data elucidate additional details of the beneficial effect of estradiol on oxidative stress, a relevant mechanism in atherogenesis.