SARS-CoV-2 is a rapidly evolving pandemic causing great morbimortality. Medical therapy with hydroxicloroquine, azitromycin and protease inhibitors is being empirically used, with reported data of ...QTc interval prolongation. Our aim is to assess QT interval behaviour in a not critically ill and not monitored cohort of patients. We evaluated admitted and ambulatory patients with COVID-19 patients with 12 lead electrocardiogram at 48 h after treatment initiation. Other clinical and analytical variables were collected. Statistical analysis was performed to assess the magnitude of the QT interval prolongation under treatment and to identify clinical, analytical and electrocardiographic risk markers of QT prolongation independent predictors. We included 219 patients (mean age of 63.6 ± 17.4 years, 48.9% were women and 16.4% were outpatients. The median baseline QTc was 416 ms (IQR 404-433), and after treatment QTc was prolonged to 423 ms (405-438) (P < 0.001), with an average increase of 1.8%. Most of the patients presented a normal QTc under treatment, with only 31 cases (14.1%) showing a QTc interval > 460 ms, and just one case with QTc > 500 ms. Advanced age, longer QTc basal at the basal ECG and lower potassium levels were independent predictors of QTc interval prolongation. Ambulatory and not critically ill patients with COVID-19 treated with hydroxychloroquine, azithromycin and/or antiretrovirals develop a significant, but not relevant, QT interval prolongation.
Statins are among the most commonly prescribed medications worldwide. Statin-associated muscle symptoms (SAMS) represent a frequent statin-related adverse effect associated with statin ...discontinuation and increased cardiovascular disease (CVD) events. Emerging evidence indicate that the majority of SAMS might not be actually caused by statins, and the nocebo/drucebo effect (i.e. adverse effects caused by negative expectations) might also explain SAMS. Lifestyle advice in including physical activity (PA) is a cornerstone in the management of CVD risk. Despite its widely known benefits for CVD protection, evidence of increased creatine-kinase levels in statin-treated athletes exposed to a marathon has been generalized, at least to some extent, to the general population and other types of PA. This generalization is likely inappropriate and might induce fear around PA in statin users. In addition, the guidelines for lipid management focus on aerobic PA while the potential of reducing sedentary behavior and undertaking resistance training have been overlooked and might need to be considered in future guidelines. The aim of this report is to provide a novel proposal for the concurrent prescription of statin therapy and PA addressing the most common and clinically relevant scenarios by simultaneously considering the different stages of statin therapy and the history of PA. These scenarios include i) statin therapy initiation in physically inactive patients, ii) PA/exercise initiation in statin-treated patients, iii) statin therapy initiation in physically active patients, and iv) statin therapy in athletes and very active individuals performing SAMS-risky activities.
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Despite elevated low-density lipoprotein (LDL) cholesterol levels, some older subjects with heterozygous familial hypercholesterolemia (HeFH) do not develop atherosclerotic cardiovascular disease ...(ACVD) during their lifetime. The factors related to this resilient state have not been fully established. The aim of this study was to evaluate differential characteristics between older HeFH subjects with and without ACVD and factors associated with the presence of ACVD. Subjects were part of the Spanish Atherosclerosis Society Dyslipidemia Registry, and those ≥ 70 years old and with HeFH were included. Baseline characteristics of these subjects with and without ACVD were compared. A multivariate analysis was performed to assess factors associated with the presence of ACVD. A total of 2148 subjects with HeFH were included. Resilient subjects were mostly female, younger and presented fewer comorbidities with respect to the ACVD group. Subjects without ACVD had higher baseline high-density lipoprotein (HDL) cholesterol (55.8 ± 17.1 vs. 47.9 ± 15.4 mg/dL;
< 0.001) and lower lipoprotein(a) Lp(a) (53.4 ± 67.9 vs. 66.6 ± 85.6 mg/dL;
< 0.001) levels with respect to those in the ACVD group. Lp(a) and the presence of ≥3 risk factors were associated with the presence of ACVD.
Dyslipidemia is a frequent side effect associated with nilotinib treatment. Patients with chronic myeloid leukemia (CML) under treatment with nilotinib who develop dyslipidemia have been shown to ...have a higher risk of presenting atherosclerotic cardiovascular disease (ACVD). Therapeutic discontinuation in selected individuals could be a strategy in order to prevent the development of ACVD. Observational study of patients with CML under nilotinib treatment. The lipid values were gathered before starting with nilotinib and after 3 months. Such values were also measured before discontinuation in patients who suspended nilotinib treatment, as well as 3 and 12 months later. 32 patients were included, 19 of them treated in monotherapy with nilotinib. The concentrations of total cholesterol and low-density lipoproteins (LDL) increased significantly after 3 months of treatment (27.29 mg/dL ± 22.88, p < 0.01). Of the total number of patients treated, 12 discontinued the treatment. LDL concentration was significantly reduced after 3 months of the nilotinib discontinuation (- 27.58 mg/dL ± 38.30, p = 0.030), remaining substantially lower after 12 months, compared to the time previous to discontinuation (- 24.58 mg/dL ± 37.31, p = 0.043). Nilotinib suspension reduces significantly LDL concentrations. These data support the strategy of therapeutic discontinuation in order to prevent future cardiovascular complications, especially in patients with prior cardiovascular risk factors.
Aortic pulse wave velocity (PWV) is an independent predictor of risk for atherosclerotic cardiovascular disease. Metabolic syndrome (MetS) is more prevalent in patients with systemic lupus ...erythematosus (SLE) compared with matched healthy subjects. Aortic PWV is increased in MetS. The purpose of this cross-sectional study was to determine the association between MetS and aortic PWV and other surrogate biomarkers of subclinical atherosclerosis in SLE.
One hundred twenty-eight patients with SLE were studied. We established the presence of MetS according to the National Cholesterol Education Program Adult Treatment Panel III definition and we measured PWV, glucose, insulin, glycosylated hemoglobin (HbA(1c)), insulin sensitivity (HOMA index), lipid levels, uric acid, homocysteine, fibrinogen, D-dimer, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), interleukin 6 (IL-6), IL-8, IL-10, C3, C4, autoantibodies, SLE Disease Activity Index (SLEDAI), and Systemic Lupus International Collaborating Clinics/ACR Damage Index. Duration of SLE and treatment was also recorded. Multivariate logistic regression analysis was used to identify independent determinants of increased PWV.
SLE patients with MetS had higher aortic PWV (9.8 +/- 2.4 vs 8.5 +/- 1.7 m/s; p = 0.002) and increased biomarkers of subclinical atherosclerosis such as CRP, IL-6, C3, uric acid, homocysteine, fibrinogen and D-dimer, compared to those without MetS. HOMA index and insulin and HbA(1c) levels were also higher in this group. No differences were found in variables related to lupus activity (ESR, C4, SLEDAI, IL-8, IL-10, and treatment for SLE). In the multivariate model, increased PWV was associated with age, male sex, MetS, duration of SLE, and CRP.
MetS may contribute to the development of accelerated atherosclerosis in SLE.
Hypertension (HT) is more prevalent in patients with systemic lupus erythematosus (SLE) than among the general population and it has been associated with atherosclerotic cardiovascular diseases in ...these patients. We examined the proportion of HT and factors associated with it in young and old women with SLE.
Participants (112 women with SLE and 223 healthy age-matched women) were categorized as young (age ≤ 40 years) or old (age > 40 years). We compared cardiovascular and specific SLE-related variables and inflammatory markers in hypertensive and normotensive women with SLE for each age range. We also assessed the factors independently associated with HT in the entire cohort and in each age range by means of a multivariate regression analysis.
The prevalence of HT was higher in women with SLE than in controls (56% vs 29%; p < 0.001), and was proportionally higher in younger women with SLE (40% vs 11%; p < 0.001) than in older women with SLE (74% vs 47%; p = 0.001). After adjustment for potential confounders, HT was associated with renal involvement and higher nonobesity-related insulin levels in younger women with SLE. In older patients, HT was associated with age, renal involvement, and obesity. Finally, in the entire cohort, HT was associated with age, insulin, renal involvement, and the Systemic Lupus Erythematosus Disease Activity Index score.
An association between HT and insulin has been identified in women with SLE, particularly younger ones. Factors associated with HT in women with SLE differed depending on their age. HT was more prevalent in women with SLE than in control subjects, being proportionally higher in young women with SLE.
Reactivation of human parvovirus B19 is exceptional and characteristic of immunosuppression, with anaemia being the predominant manifestation although pancytopenia and thrombotic microangiopathy may ...also occur. We describe a patient with a history of diffuse large B-cell lymphoma with pure erythrocyte aplasia due to reactivation of parvovirus B19, who was treated with corticosteroids and immunoglobulins.
Infection with human parvovirus B19 is identified by polymerase chain reaction (PCR) testing of blood and the presence of typical giant proerythroblasts in the bone marrow.Cytomegalovirus infection should be considered in immunosuppressed patients with fever and non-specific symptoms with haematological changes.The treatment of persistent infection in immunosuppressed patients is based on the administration of IV immunoglobulins at high doses.
Recently, an inverse relationship between the blood concentration of lipoprotein(a) (Lp(a)) and triglycerides (TG) has been demonstrated. The larger the VLDL particle size, the greater the presence ...of VLDL rich in apoliprotein E and in subjects with the apoE2/E2 genotype, the lower Lp(a) concentration. The mechanism of this inverse association is unknown. The objective of this analysis was to evaluate the Lp(a)-TG association in patients treated at the lipid units included in the registry of the Spanish Society of Atherosclerosis (SEA) by comparing the different dyslipidemias.
Five thousand two hundred and seventy-five subjects ≥18 years of age registered in the registry before March 31, 2023, with Lp(a) concentration data and complete lipid profile information without treatment were included.
The mean age was 53.0 ± 14.0 years, with 48% women. The 9.5% of subjects (n = 502) had diabetes and the 22.4% (n = 1184) were obese. The median TG level was 130 mg/dL (IQR 88.0-210) and Lp(a) 55.0 nmol/L (IQR 17.9-156). Lp(a) concentration showed a negative association with TG concentration when TG values exceeded 300 mg/dL. Subjects with TG > 1000 mg/dL showed the lowest level of Lp(a), 17.9 nmol/L, and subjects with TG < 300 mg/dL had a mean Lp(a) concentration of 60.1 nmol/L. In subjects without diabetes or obesity, the inverse association of Lp(a)-TG was especially important (p < 0.001). The median Lp(a) was 58.3 nmol/L in those with TG < 300 mg/dL and 22.0 nmol/L if TG > 1000 mg/dL. No association was found between TG and Lp(a) in subjects with diabetes and obesity, nor in subjects with familial hypercholesterolemia. In subjects with multifactorial combined hyperlipemia with TG < 300 mg/dL, Lp(a) was 64.6 nmol/L; in the range of 300-399 mg/dL of TG, Lp(a) decreased to 38. 8 nmol/L, and up to 22.3 nmol/L when TG > 1000 mg/dL.
Our results show an inverse Lp(a)-TG relationship in TG concentrations > 300 mg/dL in subjects without diabetes, obesity and without familial hypercholesterolemia. Our results suggest that, in those hypertriglyceridemias due to hepatic overproduction of VLDL, the formation of Lp(a) is reduced, unlike those in which the peripheral catabolism of TG-rich lipoproteins is reduced.
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