Long-term effects of angiotensin receptor neprilysin inhibitor therapy in heart failure patients with reduced ejection fraction: A retrospective cohort study.

Heart failure is an increasing public health issue with substantial morbidity and mortality rates. This study aimed to evaluate the efficacy, safety, and long-term outcomes of angiotensin receptor neprilysin inhibitor (ARNi) in the treatment of heart failure with reduced ejection fraction (HFrEF) 5 years after treatment initiation. This retrospective study analyzed a cohort of 75 patients diagnosed with HFrEF over a period of 5 years after the initiation of ARNi therapy. The initial clinical condition, laboratory and echocardiographic measurements including left ventricular ejection fraction (LVEF), New York Heart Association functional classes (NYHA-FC) and the prognostic nutritional index were compared to the corresponding values obtained after a 5-year period of ARNi therapy. In addition, the number of annual hospitalizations, mortality rates and any history of adverse effects during the follow-up period were recorded. The N-terminal pro-brain natriuretic peptide (NT-proBNP) level, LVEF, and NYHA-FC values demonstrated significant improvement at the end of the 5-year follow-up period (all parameters, P < .001). Although the observed increase in the prognostic nutritional index was not statistically significant (P = .077), it is worth noting. A significant reduction in daily diuretic doses and hospitalizations due to heart failure was observed following the use of ARNi (all comparisons, P < .001). The prevalence of hypotension was around 16% (being symptomatic in 4%), making it the most frequently observed adverse event. The 5-year cardiovascular mortality rate was 17.3%. The use of ARNi in HFrEF patients was associated with a notable improvement in NYHA-FC, LVEF, and NT-proBNP levels in the long-term, while also leading to a better nutritional status and reduced need for diuretics and annual hospitalization. Additionally, ARNi usage has been associated with improved nutritional status, decreased reliance on diuretics, and reduced frequency of annual hospitalizations. These effects were associated with a lack of significant increase in adverse effects. These results may contribute to a better understanding of ARNi's long-term effects on patient outcomes.

Factors Affecting Smoking Cessation After Acute Myocardial Infarction.

OBJECTIVE: Persistent smoking after acute myocardial infarction is associated with an increased risk of recurrent cardiovascular events. Our aim was to determine the changes in smoking habits in patients after acute myocardial infarction and evaluate the factors affecting smoking cessation. MATERIAL AND METHODS: A total of 322 patients who had an acute myocardial infarction while smoking were included in the study. Participants were asked to fill out a 30-question survey. According to smoking status, 2 groups were identified, those who quit smoking (n = 155) and those who continued smoking (n = 167). RESULTS: The rate of smoking cessation among study participants was 48.2% (n = 155). Most of smoker participants had the intention to quit smoking (n = 124, 74.2%). The most common barriers for smoking cessation were nicotine withdrawal symptoms and the cessation rate was over 3 times higher in those with low nicotine dependence (P < .01). Weight gain was another common problem seen in 163 (50.6%) participants; among which the cessation rate was relatively low (43.6%). A total of 231 (71.7%) participants got an advice from their doctor to quit smoking and the probability of quitting was around 5 times higher in this group (P < .01). A total of 174 (54%) participants stated that they were considering quitting whenever they see the pictorial health warnings on cigarette packs and the probability of quitting was doubled in this group (P < .01). CONCLUSION: High number of patients continue on smoking after acute myocardial infarction. The most common barriers for smoking cessation are nicotine withdrawal symptoms. Doctors should play an active role in helping the patient quit smoking. Strict regulations of tobacco control can be very helpful in this regard.

The evaluation of the metabolic and autonomic predictors of cardiovascular diseases in relation to prostatic hyperplasia symptoms.

OBJECTIVES: High prevalence of cardiovascular diseases is present in benign prostatic hyperplasia patients. Risk prediction models were developed for early identification of these cardiovascular risks. We aimed to evaluate cardiovascular metabolic and autonomic predictors in relation to lower urinary tract symptoms' severity evaluated by the IPSS score. METHODS: This study included 318 healthy individuals recently diagnosed with BPH. Laboratory tests including metabolic, hormonal and inflammatory markers were recorded. The cardiovascular risk indices like the atherogenic index of plasma and the triglyceride glucose index were calculated. The heart rate recovery after graded exercise was calculated. RESULTS: There was a significant positive correlation between the IPSS score and both the atherogenic and the triglyceride glucose indices (r = 0.388, p < 0.01 and r = 0.109, p = 0.032, respectively). IPSS score was also significantly negatively correlated with heart rate recovery specially at the 3rd minute after exercise (r = -0.547, p < 0.01). On the other hand, the IPSS score had a significant positive correlation with the inflammatory markers and a significant negative correlation with serum testosterone levels. CONCLUSIONS: Our study results suggest the presence of a combination of hormonal and inflammatory changes in BPH patients affecting the severity of LUTS which is correlated with metabolic and autonomic parameters that can predict an increased risk of CVD (Tab. 3, Ref. 47).

The Role of Interferons in Cardiac Remodeling after Acute Myocardial Infarction.

OBJECTIVE: To determine the relationship of serial interferon (IFN) measurements and adverse cardiac remodeling (AR) after myocardial infarction (MI). STUDY DESIGN: Observational multi-centre study. PLACE AND DURATION OF STUDY: Departments of Cardiology of Diskapi Yildirim Beyazit Training and Research Hospital, Ataturk Training and Research Hospital, Numune Training and Research Hospital, and Dr. Nafiz Sincan Korez State Hospital, Turkey, from June 2015 to June 2020. METHODOLOGY: Forty-seven patients with acute MI were included. IFN levels were measured on the first day and at 14 days and 45 days post-MI. Reverse cardiac remodeling (RR) and AR were defined as the reduction of left ventricular end-diastolic volume by ≥12% and increases of ≥12% by cardiac magnetic resonance imaging at the 6-month follow-up. Statistical significance was accepted as p<0.05. RESULTS: Median IFN-α (50.1 vs. 34.8 pg/mL, p=0.035), IFN-ß (39.1 vs. 23.0 pg/mL, p=0.013), and IFN-γ (26.7 vs. 18.5 pg/mL, p=0.023) levels on the first day post-MI were higher in the AR group compared to the RR group. At 14 days post-MI, IFN levels had decreased in the AR group, while they had not changed in the RR group. At 45 days post-MI, IFN levels were similar between the AR and RR groups. High IFN-α level on the first-day post-MI was an independent predictor of AR (OR: 1.23, 95% CI: 1.06-1.43, p=0.008). CONCLUSION: High IFN levels in the acute phase post-MI are associated with AR. Among IFNs, IFN-α is an important predictor of AR. Stable IFN levels appear to be associated with cardiac healing. KEY WORDS: Cardiac remodeling, Interferons, Inflammation, Myocardial infarction.

Is there a relationship between heart rate recovery and blood pressure in white coat hypertension?

Aim    Increasing evidence suggests that autonomic dysfunction may be involved in the etiology of white coat hypertension (WCH). The aim of this study was to evaluate cardiac autonomic function by using heart rate recovery (HRR) indices in patients with WCH classified according to their circadian rhythm type of blood pressure (BP).Material and methods    This cross-sectional study included 120 participants over the age of 18 yrs, including 50 patients diagnosed with WCH and 70 healthy controls with normal in- and out-of-office BP and without any known disease. Circadian rhythm types, i.e., dippers and non-dippers, were identified using ambulatory BP monitoring. The HRR indices were calculated by subtracting the 1st-minute (HRR1), 2nd-minute (HRR2), and 3rd-minute (HRR3) heart rates from the maximal heart rate recorded during stress testing.Results    The lesser decline in nighttime BP (6.4±2.14 and 13.3±2.2 mmHg, respectively; p<0.001) and the smaller mean HRR1 (25.5±3.0 and 30.3±3.1 beats / min, respectively; p<0.001) were evident in WCH non-dippers compared to WCH dippers. Linear regression analysis showed that HRR1 (ß±SE=0.43±0.11; p<0.001) and diastolic BP at maximum exercise (ß±SE=0.14±0.07; p=0.040) are independent risk factors for the blunted decline in nighttime BP.Conclusion    Delayed recovery of heart rate after an exercise stress test is associated with non-dipper type of circadian rhythm of BP. This was more pronounced in WCH patients, and these patients are at risk of autonomic dysfunction.

The relationship of benign prostatic hyperplasia's symptoms severity with the risk of developing atrial fibrillation.

Background: Attention is drawn to the increased incidence of atrial fibrillation (AF) in benign prostatic hyperplasia (BPH) patients recently. Early predicting of AF in these patients can help in decreasing its clinical consequences. The aim of our study is to determine the association between BPH symptoms and AF predictors atrial electromechanical delay (AEMD) and the P-wave dispersion (PWD). Methods: 218 healthy individuals recently diagnosed with BPH were assigned into three groups according to symptoms severity using the International prostate symptom score (IPSS) questionnaire. The first group with mild symptoms (IPSS score between 0 and 7, n = 78), the second group with moderate symptoms (IPSS score between 8 and 19, n = 86), and the third group with severe symptoms (IPSS score between 20 and 35, n = 54). PWD and AEMD calculations were performed for all participants. Results: There were statistically significant differences between the three groups in terms of AEMD and PWD (p < .01 and p < .01, respectively). In all three study groups, a significant positive correlation was observed between IPSS questionnaire scores and both AEMD and PWD (for AEMD r = .29, p = .013 and for PWD r = .27, p = .017). On the other hand, there were significant differences between the three groups in terms of the inflammatory markers C-reactive protein (CRP) and fibrinogen (p < .01 and p < .01, respectively) and in terms of serum testosterone levels (p < .01). Conclusions: We concluded that periodic evaluation of patients with BPH in terms of symptoms severity can be helpful not only from urological aspect, but also in the early prediction of possible serious cardiovascular morbidity and mortality.

Determination of microRNAs associated with adverse left ventricular remodeling after myocardial infarction.

Increasing evidence indicates that microRNA (miRNA) regulated mechanisms in myocardial healing and ventricular remodeling following acute myocardial infarction (AMI). We aim to comprehensively investigate changes of exosomal miRNA profile during the post-MI period and determine potential miRNAs associated to adverse left ventricular remodeling (ALVR). We prospectively evaluated ST-elevated MI patients with cardiac magnetic resonance imaging at the 2 weeks and 6 months after AMI (n = 10). ALVR was defined as an increase in LV end-diastolic and end-systolic volume > 13%. The blood samples were taken for miRNA measurements at the baseline, 2 and 6 weeks after AMI. In the miRNA profile assessment, 8 miRNAs were identified that were associated ALVR (miR-199a-5p, miR-23b-3p, miR-26b-5p, miR-301a-3p, miR-374a-5p, miR-423-5p, miR-483-5p and miR-652-3p). Three of them (miR-301a-3p, miR-374a-5p and miR-423-5p) differed significantly between patients with and without ALVR during follow-up period and the rest of them during the acute phase of AMI. The detection of these miRNAs, which have different role in various pathways, necessitate future mechanistic studies unravel the complex remodeling process after AMI.

The relationship between long-term statin usage and myocardial injury related to percutaneous coronary interventions evaluated by high-sensitivity troponins.

OBJECTIVE: Myocardial injury related to percutaneous coronary interventions (PCI) might adversely affect the prognosis of patients with coronary artery disease. Our study aimed to investigate the effects of long-term statin usage on myocardial injury related to elective PCI. METHODS: In our study, total 102 patients were included and evaluated in 3 groups based on the statin usage before PCI, "potent statin" group (n=26), "weak statin" group (n=23), and "statin free" group (n=53). The occurrence of the procedural complications was identified (n=31). The myocardial injury was determined by serial high-sensitivity troponin T (hsTnT) testing at 0th, 2nd, 4th, and 12th hour of the procedure. RESULTS: The increase in hsTnT values in the 2nd and 4th hour was significantly lower in the potent statin group than in the other 2 groups (p=0.008 and p=0.009, respectively). In patients with procedural complications, the increase in hsTnT levels at the 2nd, 4th, and 12th hour were also lower in the potent statin group (p=0.032, p=0.019, and p=0.006, respectively). Also, in patients with procedural complications, hsTnT levels exceeding the myocardial infarction limit at the 4th and 12th hour were lower in the potent statin group (p=0.039 and p=0.006, respectively). CONCLUSION: These results show that elective PCI related myocardial injury was less frequent in patients who were using high-dose statins. This result was more pronounced in patients who developed complications during the procedure.

Higher levels of TWEAK and matrix metalloproteinase-3 during the acute phase of myocardial infarction are associated with adverse left ventricular remodeling.

INTRODUCTION: It is known that the levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK/TNFSF12) increase after myocardial infarction (MI) and that it interacts with sCD163. It has also been argued that TWEAK can induce matrix metalloproteinases (MMPs) in macrophages. AIM: To investigate the roles of TWEAK, sCD163, and MMPs in left ventricular (LV) adverse remodeling (AR) in the early post-MI period. MATERIAL AND METHODS: Forty-six patients with ST-elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention were enrolled in the study. Post-MI LV functions and volumes were assessed by cardiac magnetic resonance imaging at 2 weeks and 6 months. Cytokines and MMPs were measured using a bead-based multiplex immunoassay system at 1 day (baseline) and 2 weeks post-MI. AR was defined as an increase in LV end-diastolic volume of ≥ 10% at the 6-month follow up. RESULTS: The TWEAK, MMP-2, and MMP-3 baseline levels were higher in the patients with AR than those without AR. At 2 weeks post-MI, these expression levels were similar in patients with and without AR, but sCD163 expression was increased in patients without AR. The TWEAK and MMP levels were positively correlated in the early period post-MI. At first day post-MI, higher levels of TWEAK and MMP-3 were predictors of AR (OR = 1.03, p = 0.006; OR = 1.08, p = 0.015; respectively). CONCLUSIONS: TWEAK can induce MMPs in the early period post-MI, and these higher levels contribute to development of AR. Increased sCD163 levels at 2 weeks post-MI seem to be associated with the healing process through neutralizing the excessive inflammatory effects of TWEAK.