Current approaches to risk assessment of chronic heart failure after myocardial infarction

In the last decade, there has been an increase in the number of survivors of myocardial infarction (MI). However, the risk of developing chronic heart failure (CHF) remains high in this category of patients. Population aging and comorbidity further contribute to adverse outcomes. Optimization of approaches to identify predictors of postinfarction CHF is an important clinical task of modern medicine. The aim of the investigation is to develop a method to assess the risk of CHF development after MI. Material and Methods. The present analysis included 186 patients who underwent MI from January 2019 to January 2020: 86 patients with signs of CHF above functional class (FC) 2 (NYHA) (mean age 64.3 years) and 100 patients without signs of CHF or with CHF 1 (NYHA) (mean age 62.6 years) by day 30 of MI. A mathematical model of CHF risk after MI was built by factor and correlation analysis methods. Results. A method for assessing CHF risk after a previous MI was developed. The proposed formula is programmed in Excel table processor and includes 5 indicators: presence of atrial fibrillation, Killip class of acute heart failure, triglycerides level, ST-segment elevation of electrocardiogram, left ventricular ejection fraction less than 45 %. The authors’ approach allows long-term personalized monitoring, taking into account the ranked contribution of each factor in a particular patient; it is characterized by high sensitivity, specificity, and accuracy. Conclusion. The present study investigated the factors of formation of postinfarct chronic heart failure syndrome. An original mathematical formula for CHF risk estimation, including routine indices of MI patients, has been proposed. The approach allows personalized management of selected cohorts of patients – with increased and standard risk of postinfarction CHF

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.