Effect of atorvastatin on the lipid profile, markers of immune inflammation and symptomatic severity of heart failure in patients with myocarditis

2020 ◽  
Vol 22 (3) ◽  
pp. 76-81
Author(s):  
N. N. Ryzhman ◽  
S. L. Grishaev ◽  
D. V. Cherkashin ◽  
E. V. Gladysheva ◽  
V. Yu. Filippov ◽  
...  

Abstract. The effect of atorvastatin on the immune system and lipid metabolism after 24-week treatment of patients with chronic myocarditis is considered. Statins have been found to improve the clinical course of heart failure with a preserved ejection fraction in patients with myocarditis: they reduce the functional class of heart failure, improve the systolic function of the heart and its arrhythmogenic potential. Despite the large amount of conflicting data in the field of statin use in heart failure, one can think about the possible influence of molecular differences in statins on their pharmacological and pleiotropic effects. In particular, atorvastatin, which has lipophilic properties, is able to penetrate cardiomyocytes in contrast to hydrophilic rosuvastatin, which may partially explain the positive cardiac effects of atorvastatin in patients with heart failure with a preserved ejection fraction. The probable basis for the positive effect of atorvastatin on morphofunctional parameters in heart failure is its positive pleiotropic effects associated with a decrease in рro-inflammatory immune markers and subsequent leveling of negative neurohumoral activation. An additional mechanism that caused the positive effect of atorvastatin on the clinical course of heart failure can be considered a factor of preservation of systolic function of the left ventricle.

Author(s):  
Milton Packer ◽  
Javed Butler ◽  
Faiez Zannad ◽  
Gerasimos Filippatos ◽  
Joao Pedro Ferreira ◽  
...  

Background: Empagliflozin reduces the risk of cardiovascular death or hospitalization for heart failure in patients with heart failure and a preserved ejection fraction, but additional data are needed about its effect on inpatient and outpatient heart failure events. Methods: We randomly assigned 5988 patients with class II-IV heart failure with an ejection fraction of >40% to double-blind treatment with placebo or empagliflozin (10 mg once daily), in addition to usual therapy, for a median of 26 months. We prospectively collected information on inpatient and outpatient events reflecting worsening heart failure and prespecified their analysis in individual and composite endpoints. Results: Empagliflozin reduced the combined risk of cardiovascular death, hospitalization for heart failure or an emergent/urgent heart failure visit requiring intravenous treatment (432 vs 546 patients; empagliflozin vs placebo, respectively; hazard ratio 0.77, 95% CI: 0.67-0.87), P <0.0001. This benefit reached statistical significance at 18 days after randomization. Empagliflozin reduced the total number of heart failure hospitalizations that required intensive care (hazard ratio 0.71, 95% CI 0.52-0.96, P=0.028) and the total number of all hospitalizations that required a vasopressor or positive inotropic drug (hazard ratio 0.73, 95% CI: 0.55-0.97,P=0.033). As compared with placebo, fewer patients in the empagliflozin group reported outpatient intensification of diuretics (482 vs 610, hazard ratio 0.76, 95% CI: 0.67-0.86, P<0.0001), and patients assigned to empagliflozin were 20-50% more likely to have a better NYHA functional class, with significant effects at 12 weeks that were maintained for at least 2 years. The benefit on total heart failure hospitalizations was similar in patients with an ejection fraction of >40-<50% and 50-<60%, but was attenuated at higher ejection fractions. Conclusions: In patients with heart failure and a preserved ejection fraction, empagliflozin produced a meaningful, early and sustained reduction in the risk and severity of a broad range of inpatient and outpatient worsening heart failure events. Clinical Trial Registration: The registration identifier at ClinicalTrials.gov is NCT03057977


2021 ◽  
Vol 12 (2) ◽  
pp. 81-91
Author(s):  
A. N. Shevelok

Purpose: to investigate the prognostic value of secondary hyperaldosteronism patients with heart failure with preserved ejection fraction. Materials and methods: prospective cohort study included 158 patients with hyperaldosteronism and heart failure with preserved ejection fraction. Baseline blood aldosterone levels were determined in all patients. Hyperaldosteronemia was diagnosed when the plasma aldosterone level was > 160 pg/ml. The primary endpoint was all-cause mortality. Results: at baseline, hyperaldosteronemia was detected in 59 of 158 patients (37.3%). Hyperaldosteronemic patients were younger, had higher functional class and NT-proBNP level, and a higher rate of comorbidity (all Ps <0.05). Over a median follow‐up of 32 (28-38) months, a total of 50 (37.6%) patients died. Cardiovascular death occurred in 32 (20.3%) cases, non-cardiovascular – in 18 (11.4%) cases. A total of 65 (41.1%) patients were hospitalized for HF. High aldosterone levels were associated with a significant (p <0.05) increase in the risk of hospitalization for HF (adjusted odds ratio (OR) 2.14, 95% confidence interval (CI) 1.34-9.68), all-cause death (OR 1.64; 95% CI 1.23-7.65, P = 0.033) and HF death (OR 1.56; 95 % CI 1.14-11.3, P = 0.021). Conclusion: Hyperaldosteronism in patients with heart failure with preserved ejection fraction secondary hyperaldosteronism is an independent predictor of hospitalization for heart failure, all-cause, and cardiovascular mortality. The inclusion of plasma aldosterone level in the existing prognosis models of heart failure with preserved ejection fraction will help improve their predictive value and optimize the management of high-risk patients.


2021 ◽  
Vol 27 (2) ◽  
pp. 17-36
Author(s):  
Branimir Kanazirev

During these more than 20 years of evolution in understandings of the mechanisms of heart failure (HF) with preserved fractional ejection, there has been a rich variety of terminology, including „diastolic heart failure“, „heart failure with preserved systolic function“ and „heart failure with preserved fraction“. By defi nition, the latter term “ejection fraction-induced heart failure” proved to be the most appropriate and was accepted as the most correct, as the presence of diastolic dysfunction is not unique only to this group and exists in these patients, albeit subclinically and discrete disturbance in the longitudinal systolic function of the left ventricle against the background of the preserved ejection fraction. The problem, however, is not in the value of the ejection fraction or in the paradox of the combination of a well-functioning left ventricle and classic symptoms of heart failure, but in the non-infl uence of the prognosis of these patients in the way it is in patients with suppressed EF. Unlike patients with heart failure with a reduced ejection fraction, the prognosis and results in patients with HF with preserved EF do not mark the expected results and so far there are not enough effective and promising therapies.


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