18 research outputs found
Estudo multicĂŞntrico comparativo de quatro diferentes tipos de sensores: atividade, acelerĂ´metro, temperatura e perĂodo de prĂ©-ejeçao
Recentemente diferentes princĂpios tĂŞm sido utilizados para estimular o coraçao na tentativa de recuperar o dĂ©bito cardĂaco. Neste estudo multicĂŞntrico, foram comparadas as respostas Ă estimulaçao por 4 tipos de sensores, sendo 3 tipos de resposta de alça aberta (atividade fĂsica, acelerĂ´metro e temperatura venosa central) implantados em 30 (SSIR-8 e DDDR-22), 9 (SSIR-5 -e DDDR-4) e 12 (SSIR) pacientes respectivamente. Um outro sensor do tipo alça fechada, sensĂvel Ă s variaçoes do sistema nervoso autĂ´nomo, foi implantado em 57 pacientes, todos no modo DDDR. Os resultados obtidos durante a realizaçao de atividade fĂsica diária, de teste ergomĂ©trico e de Holter de 24 horas foram comparados, sendo possĂvel observar uma maior fidelidade na curva de resposta de freqĂĽĂŞncia frente a atividade fĂsica, nos pacientes submetidos Ă estimulaçao de alça fechada
Estudo multicĂŞntrico comparativo de quatro diferentes tipos de sensores: atividade, acelerĂ´metro, temperatura e perĂodo de prĂ©-ejeçao
Recentemente diferentes princĂpios tĂŞm sido utilizados para estimular o coraçao na tentativa de recuperar o dĂ©bito cardĂaco. Neste estudo multicĂŞntrico, foram comparadas as respostas Ă estimulaçao por 4 tipos de sensores, sendo 3 tipos de resposta de alça aberta (atividade fĂsica, acelerĂ´metro e temperatura venosa central) implantados em 30 (SSIR-8 e DDDR-22), 9 (SSIR-5 -e DDDR-4) e 12 (SSIR) pacientes respectivamente. Um outro sensor do tipo alça fechada, sensĂvel Ă s variaçoes do sistema nervoso autĂ´nomo, foi implantado em 57 pacientes, todos no modo DDDR. Os resultados obtidos durante a realizaçao de atividade fĂsica diária, de teste ergomĂ©trico e de Holter de 24 horas foram comparados, sendo possĂvel observar uma maior fidelidade na curva de resposta de freqĂĽĂŞncia frente a atividade fĂsica, nos pacientes submetidos Ă estimulaçao de alça fechada
Effect of SGLT2 inhibitors on stroke and atrial fibrillation in diabetic kidney disease: Results from the CREDENCE trial and meta-analysis
BACKGROUND AND PURPOSE: Chronic kidney disease with reduced estimated glomerular filtration rate or elevated albuminuria increases risk for ischemic and hemorrhagic stroke. This study assessed the effects of sodium glucose cotransporter 2 inhibitors (SGLT2i) on stroke and atrial fibrillation/flutter (AF/AFL) from CREDENCE (Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation) and a meta-Analysis of large cardiovascular outcome trials (CVOTs) of SGLT2i in type 2 diabetes mellitus. METHODS: CREDENCE randomized 4401 participants with type 2 diabetes mellitus and chronic kidney disease to canagliflozin or placebo. Post hoc, we estimated effects on fatal or nonfatal stroke, stroke subtypes, and intermediate markers of stroke risk including AF/AFL. Stroke and AF/AFL data from 3 other completed large CVOTs and CREDENCE were pooled using random-effects meta-Analysis. RESULTS: In CREDENCE, 142 participants experienced a stroke during follow-up (10.9/1000 patient-years with canagliflozin, 14.2/1000 patient-years with placebo; hazard ratio [HR], 0.77 [95% CI, 0.55-1.08]). Effects by stroke subtypes were: ischemic (HR, 0.88 [95% CI, 0.61-1.28]; n=111), hemorrhagic (HR, 0.50 [95% CI, 0.19-1.32]; n=18), and undetermined (HR, 0.54 [95% CI, 0.20-1.46]; n=17). There was no clear effect on AF/AFL (HR, 0.76 [95% CI, 0.53-1.10]; n=115). The overall effects in the 4 CVOTs combined were: Total stroke (HRpooled, 0.96 [95% CI, 0.82-1.12]), ischemic stroke (HRpooled, 1.01 [95% CI, 0.89-1.14]), hemorrhagic stroke (HRpooled, 0.50 [95% CI, 0.30-0.83]), undetermined stroke (HRpooled, 0.86 [95% CI, 0.49-1.51]), and AF/AFL (HRpooled, 0.81 [95% CI, 0.71-0.93]). There was evidence that SGLT2i effects on total stroke varied by baseline estimated glomerular filtration rate (P=0.01), with protection in the lowest estimated glomerular filtration rate (45 mL/min/1.73 m2]) subgroup (HRpooled, 0.50 [95% CI, 0.31-0.79]). CONCLUSIONS: Although we found no clear effect of SGLT2i on total stroke in CREDENCE or across trials combined, there was some evidence of benefit in preventing hemorrhagic stroke and AF/AFL, as well as total stroke for those with lowest estimated glomerular filtration rate. Future research should focus on confirming these data and exploring potential mechanisms
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy
BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to 300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m 2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years
INHIBITION OF THE FACTOR XA (WITH RIVAROXABAN) SLOW DOWN PROGRESSION, PREVENTS COMPLICATION AND DECREASE MORTALITY IN CORONARY HEART DISEASE
A review presented, of the novel scientific data, mostly the results of large clinical trials, witnessing on clinical efficacy and safety of rivaroxaban — the anticoagulant, selective blocker of Xa factor — in treatment of acute and chronic coronary heart disease. The mechanisms explained, of the drug influence on atherothrombosis, especially the specifics of dosages and its combination with other antithrombotic drugs in various clinical situations
Syncope etiology and prognosis in patients aged over 35 years
Aim. To explore the etiology and prognosis of newly-onset syncope in patients aged over 35 years. Material and methods. The study included 502 patients aged 36-90 years. Clinical characteristics, laboratory and instrumental data, syncope recurrence, all-cause and cardiovascular mortality outcomes were analyzed retrospect-tively, in regard to syncope etiology. The association of syncope etiology with all-cause and cardiovascular mortality was examined by Kaplan-Meier method; Cox models were used to adjust for demographic characteristics and co-morbidities. Results. Major syncope etiology groups included: reflex-mediated syncope in 14% of the patients, cardiac – in 10%, neurogenic – in 6%, and orthostatic – in 12%. Syncope etiology remained unexplained in 45% of the cases. Total mortality was higher than that for general population of the same age and sex, but similar after co-morbidity adjustment. Syncope etiology was not associated with co-morbidity-adjusted all-cause mortality. Cardiovascular mortality was significantly higher in patients with cardiac syncope, compared to individuals with unexplained syncope: adjusted hazard ratio [95% confidence interval] 2.44 [1,02Â5,83] (p=0,044). Conclusion: The cause of newly-onset syncope can be identified in a half of the patients over 35 years. In this group, high mortality, irrespective of syncope etiology, is mainly explained by concomitant disease burden
HYPERURICEMIA CORRECTION IN MEN WITH METABOLIC SYNDROME: ACARBOSE POTENTIAL
The study was aimed at the investigation of “test” (6 days) and longer-term (8 weeks) acarbose treatment effects on plasma uric acid (UA) concentration in patients with metabolic syndrome (MS). Material and methods. In total, 33 men with MS and carbohydrate metabolism disturbances were administered 6-day “test” acarbose therapy. At baseline and 7 days later, saccharose tolerance test was performed, with the measurement of venous plasma levels of fasting UA, fasting fructose, glucose (fasting, 60 and 120 minutes after saccharose load), and insulin (fasting and 120 minutes after the load). 4 weeks later, 20 patients were administered 8-week acarbose therapy, with standard gradual dose increase. At baseline and after the treatment, venous plasma concentrations of UA and fructose were measured. Results. Hyperfructosemia was observed in 100% of the patients, with mean plasma fructose concentration of 0,82±0,97 mmol/l. Hyperuricemia was observed in 51,5% (n=17), with mean plasma UA concentration of 413,2±86,5 mmol/l. Six-week acarbose therapy resulted in a significant decrease of UA levels (p=0,0015) and fructose levels (p=0,049), as well as in postprandial levels of glucose (p=0,03) and insulin (p=0,013). Eight-week acarbose therapy was associated with mean decrease of plasma UA concentration by 5,8% (p=0,04), but no significant changes in fasting plasma levels of fructose (p>0,05)
Heart failure. The current state of the problem: achievements, frustrations, hopes and prospects
The article presents overview and statistical data on heart failure and cardiovascular diseases in Russia, world research data on various forms of heart failure in accordance with the modern classification, their clinical, anamnestic and prognostic differences, different approaches to the treatment of heart failure , discussion the prospects of this direction in cardiology, including the relevance of medical technology assessment