Incidence Of Chronic Heart Failure Research Articles

Impact of High-Voltage Device Implantation in Elderly Japanese Patients With Heart Failure as Primary Prevention - Post Hoc Analysis of HINODE.

Despite an increased incidence of chronic heart failure (HF) and sudden cardiac death (SCD), the use of implantable cardioverter-defibrillators (ICDs) and cardiac resynchronization therapy (CRT) is much lower in Japan than in Western countries. The HF Indication and SCD Prevention Trial Japan (HINODE) prospectively assessed the mortality rate, appropriately treated ventricular arrhythmias (VA), and HF in Japanese patients with a higher risk of HF.Methods and Results: HINODE consisted of ICD, CRT-defibrillator (CRT-D), pacing, and non-device treatment cohorts. This subanalysis evaluated the impact of the implantation of high-voltage devices (HVD; ICD and CRT-D) in 171 Japanese patients. We compared all-cause mortality, VA, and HF events between elderly (age >70 years at study enrollment) and non-elderly HVD recipients. The estimated survival rate through 24 months in the HVD cohort was 85.8% (97.5% lower control limit 77.6%). The risk of all-cause mortality was increased for the elderly vs. non-elderly (hazard ratio [HR] 2.82; 95% confidence interval [CI] 1.01-7.91; P=0.039), but did not differ after excluding ICD patients with CRT-D indication (HR 2.32; 95% CI 0.79-6.78; P=0.11). There were no differences in VA and HF event-free rates between elderly and non-elderly HVD recipients (P=0.73 and P=0.55, respectively). Although elderly patients may have a higher risk of mortality in general, the benefit of HVD therapy in this group is comparable to that in non-elderly patients.

Optimizing the management of heart failure: structuring the care pathway

The incidence of chronic heart failure continues to rise in Western countries, justifying the implementation of an optimized multidisciplinary organization based on medical and nursing convergence. Around the main heart failure, assistance and transplantation unit at Toulouse University Hospital, several structures have been put in place to better manage heart failure patients and improve their care pathway.

PFKFB3 Inhibitor 3PO Reduces Cardiac Remodeling after Myocardial Infarction by Regulating the TGF-β1/SMAD2/3 Pathway.

Adverse cardiac remodeling, including cardiac fibrosis, after myocardial infarction (MI) is a major cause of long-term heart failure. 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), an enzyme that regulates glucose metabolism, also plays an important role in various fibrotic and cardiovascular diseases. However, its effects on MI remain unknown. Here, PFKFB3 inhibitor 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO) and a permanent left anterior descending ligation mouse model were used to explore the functional role of PFKFB3 in MI. We showed that PFKFB3 expression increased significantly in the area of cardiac infarction during the early phase after MI, peaking on day 3. 3PO treatment markedly improved cardiac function, accompanied by decreased infarction size and collagen density in the infarct area. Meanwhile, 3PO attenuated cardiac fibrosis after MI by reducing the expression of collagen and fibronectin in murine hearts. Notably, 3PO reduced PFKFB3 expression and inhibited the transforming growth factor-beta 1/mothers against the decapentaplegic homolog 2/3 (TGF-β1/SMAD2/3) signaling pathway to inhibit cardiac fibrosis after MI. Moreover, PFKFB3 expression in neonatal rat cardiac fibroblasts (NRCFs) increased significantly after MI and under hypoxia, whereas 3PO alleviated the migratory capacity and activation of NRCFs induced by TGF-β1. In conclusion, 3PO effectively reduced fibrosis and improved adverse cardiac remodeling after MI, suggesting PFKFB3 inhibition as a novel therapeutic strategy to reduce the incidence of chronic heart failure following MI.

Trends in Incidence of Chronic Heart Failure in Patients With Rheumatoid Arthritis: A Population-Based Study Validating Different Heart Failure Definitions.

To assess trends in the incidence of heart failure (HF) in patients with incident rheumatoid arthritis (RA) from 1980 to 2009 and to compare different HF definitions in RA. The study population comprised Olmsted County, Minnesota residents with incident RA (age ≥ 18 yrs, 1987 American College of Rheumatology criteria met in 1980-2009). All subjects were followed until death, migration, or April 30, 2019. Incident HF events were defined as follows: (1) meeting the Framingham criteria for HF, (2) diagnosis of HF (outpatient or inpatient) by a physician, or (3) International Classification of Diseases, 9th revision (ICD-9), or ICD, 10th revision (ICD-10), codes for HF. Patients with HF prior to the RA incidence/index date were excluded. Cox proportional hazards models were used to compare incident HF events by decade, adjusting for age, sex, and cardiovascular risk factors. HF definitions 2 and 3 were compared to the Framingham criteria. The study included 905 patients with RA (mean age 55.9 years; 68.6% female; median follow-up 13.4 years). The 10-year cumulative incidence of HF events by any chart-reviewed method in the RA cohort in the 1980s was 11.66% (95% CI 7.86-17.29), in the 1990s it was 12.64% (95% CI 9.31-17.17), and in the 2000s it was 7.67% (95% CI 5.36-10.97). The incidence of HF did not change across the decades of RA incidence using any of the HF definitions. Physician diagnosis of HF and ICD-9/10 code-based definitions of HF performed well compared to the Framingham criteria, showing moderate to high sensitivity and specificity. The incidence of HF in patients with incident RA in the 2000s vs the 1980s was not statistically significantly different. Physician diagnosis of HF and ICD-9/10 codes for HF performed well against the Framingham criteria.

Prognostic value of N-terminal Brain Natriuretic Peptide (NT-proBNP) in Risk Assessment of Adverse Cardiovascular Events in Patients with Atrial Fibrillation and Heart Failure with Reduced Left Ventricular Systolic Function

According to Russian epidemiological studies, the incidence of chronic heart failure (HF) in the general population is approximately 7%, increasing from 0.3% in the group aged 2029 years to 70% in patients aged 90 years [1]. In the general population, the incidence of atrial fibrillation (AF) ranges from 1% to 2%, which increases with age, that is, from 0.5% at the age of 4050 years to 5%15% at the age of 80 years [2]. HF and AF aggravate significantly each others course and mutually increase the risk of adverse outcomes [3, 4]. Moreover, the incidence of AF in patients with HF increases with increasing New York Heart Association (NYHA) grade; that is, among patients with HF of NYHA grade I, the incidence of AF is 5%, whereas among patients with HF NYHA grade IV, the AF incidence in 50% [5].
 Chronic HF is a syndrome with complex pathophysiology, which is characterized by the activation of neurohumoral systems, namely, the reninangiotensinaldosterone system (RAAS), sympathetic nervous system (SNS), and insufficient activity of the natriuretic peptide (NUP) system. In the early stage of HF, i.e. asymptomatic dysfunction of the left ventricle, the activation of the SNS and RAAS plays a compensatory role aimed at maintaining cardiac output and circulatory homeostasis [6]. Moreover, the NUP system has a counter-regulatory function in relation to the RAAS and SNS, and with prolonged and excessive activation of the SNS and RAAS or with insufficient NUP system activity, imbalance occurs and HF progresses [7].
 The brain natriuretic peptide (BNP) and biologically inactive N-terminal fragment of BNP (NT-proBNP) are the most studied and significant in clinical practice representatives of the NUP system. BNP and NT-proBNP are secreted by cardiomyocytes of the left ventricular (LV) myocardium in response to an increase in the mechanical load and stress of the LV myocardium. NT-proBNP is widely used as a test to rule out HF in patients with dyspnea. The NUP level also correlates with the severity and prognosis in patients with an established diagnosis of HF, and studies have reported that the NUP level acts as a criterion for treatment efficiency in patients with HF [8]. NT-proBNP is a biomarker not only for HF but also for several other conditions, such as acute coronary syndrome and myocardial infarction (MI), because it is associated with an increased risk of death from all causes, regardless of age, stable effort angina grade, myocardial infarction history, and LV ejection fraction (LVEF) [9].
 NT-proBNP levels can be influenced by several additional factors such as age, obesity, or glomerular filtration rate. The prognostic value of NT-proBNP is relevant in comorbid patients with AF associated HF because AF can increase NT-proBNP levels independently [10]. Given that NUP secretion depends on intracardiac hemodynamics, the NT-proBNP levels may also depend on the approach to managing AF. Tachycardia is associated with high NT-proBNP levels [11].
 The rhythm control approach has advantages over the heart rate control approach in patients with HF and LVEF 50% to reduce mortality and the number of unplanned hospitalizations due to HF progression [12].
 To date, the prognostic significance of NT-proBNP levels in relation to the risk of adverse events in patients with HF and reduced LV systolic function associated with AF, depending on the approach of AF management, remains unresolved.
 This study aimed to assess the predictive value of NT-proBNP in relation to the development of adverse cardiovascular events in patients with permanent or persistent AF associated with HF and LVEF 50%.

Risk Assessment of Adverse Outcomes in Symptomatic Patients With Arterial Hypertension and Chronic Heart Failure With Preserved Ejection Fraction Using THE HFA-PEFF Algorithm

Aim To study the incidence of heart failure (HF) in patients with arterial hypertension (AH), symptoms of HF, and left ventricular ejection fraction (LV EF) ≥50 % using a novel, modified HFA-PEFF diagnostic algorithm and to evaluate the liver hydration status and density depending on the established HF profiles and the prognostic significance of this algorithm.Material and methods This study included 180 patients (median age, 72 years) with AH, symptoms of HF, and LV EF ≥50 %. The incidence of chronic HF with preserved ejection fraction (CHFpEF) was studied with the stepwise, modified HFA-PEFF diagnostic algorithm, and long-term outcomes were assessed at 3, 6, and 12 months of follow-up. The hydration status was determined by a bioimpedance vector analysis, and the liver density was measured by indirect fibroelastometry. The following tests were performed for all patients: standard, general clinical and laboratory examination with evaluation of CH symptoms (including N-terminal pro-brain natriuretic peptide test); extended echocardiography with assessment of structural and functional parameters of the heart; a KCCQ questionnaire was used for evaluation of patients' condition and quality of life (QoL). Long-term outcomes were studied by phone calls at 3, 6, and 12 months following discharge from the hospital/visit (worsened QoL, repeated hospitalization for cardiovascular causes, cardiovascular death or all-cause death).Results The following profiles were determined by the HFA-PEFF algorithm: with CHFpEF, with intermediate probability of HF, and without HF (58.9, 31.1, and 10 %, respectively). The study showed that patients with CHFpEF compared to patients of the intermediate group and without HF, had higher levels of brain natriuretic peptide, more pronounced signs of congestion according to results of the bioimpedance vector analysis and a higher liver density according to results of indirect fibroelastometry of the liver, which allowed identification of a group of patients with a high probability of CHFpEF. The diagnosis of HF by HFA-PEFF had an adverse prognostic significance with respect of worsened QoL according to the KCCQ questionnaire, and of repeated admission for HF during a year.Conclusion In AH patients with symptoms of HF and LV EF ≥50 %, CHFpEF was detected with the HFA-PEFF algorithm in 58.9 % of cases. Patients with AH and verified CHFpEF had a high incidence of hyperhydration and increased liver density. A diagnosis of CHFpEF by the HFA-PEFF algorithm had an adverse prognostic significance with respect of long-term outcomes.

Association of serum N-terminal pro-brain natriuretic peptide levels with survival and renal outcomes among elderly patients with acute kidney injury in chronic heart failure.

Elderly patients exhibit a higher incidence of chronic heart failure (CHF). Patients with CHF can develop acute kidney injury (AKI) during follow-up, which can result in poor prognosis. This relationship between kidney dysfunction and levels of N-terminal pro-brain natriuretic peptides (NT-proBNP), with regard to prognosis, is complicated and has rarely been analyzed in elderly patients with CHF. We conducted a retrospective cohort study involving patients with a CHF history aged ≥ 65 years, who experienced an episode of AKI. Kaplan-Meier curves and Cox or logistic proportional hazards regression models were used to evaluate the association between serum NT-proBNP concentrations and mortality or renal recovery by day 90. A total of 1,160 eligible patients with AKI were available for the study. Of this sample, 41.5% of patients died within 90 days of the onset of AKI. Patients with a decreased change in NT-proBNP accompanying the episode of AKI had a lower risk (adjusted OR = 0.56, 95% CI = 0.34-0.91) of more severe AKI (stage 2 and 3 vs. stage 1). The more severe AKI were associated with higher mortality and non-recovery of renal function in elderly patients with CHF, independent of NT-proBNP levels. Elevated levels of baseline lnNT-proBNP (adjusted HR = 1.27, 95% CI = 1.17-1.38) predicted mortality in elderly patients with CHF within 90 days of AKI onset. Patients with a decrease in NT-proBNP accompanying AKI had a lower risk of mortality (adjusted HR = 0.62, 95% CI = 0.48-0.79). However, a decrease in NT-proBNP is a risk factor (adjusted OR = 1.59, 95% CI = 1.02-2.48) for the non-recovery of renal function following AKI-especially in elderly survivors with low baseline NT-proBNP levels. A decreased change in NT-proBNP maybe protective for elderly patients with CHF by improving survival outcomes and preventing severe AKI. However, an excessive decrease in NT-proBNP is a risk factor for the non-recovery of renal function following AKI. Avoiding excessive changes in NT-proBNP may be protective for survival and renal injury prognosis.

Abstract 10739: Impact of Cardiac Device Implantation in Elderly Japanese Patients With Heart Failure as Primary Prevention-A Post Hoc Analysis of the HINODE Trial

Introduction: Despite increase in the incidence of chronic heart failure (HF) and sudden cardia death (SCD), the current use of implantable cardioverter-defibrillator (ICD) and cardiac resynchronization therapy (CRT) in Japan is much lower than in Western countries. The HF Indication and SCD Prevention Trial Japan (HINODE) was designed to prospectively assess the rate of mortality, appropriately treated ventricular arrhythmias (VA) and heart failure (HF) for comparison with references from historical landmark trial MADIT-RIT in Japanese patients. Hypothesis: This sub analysis of HINODE evaluates the impact of ICD or CRT implantation in elderly Japanese patients concomitant with higher risk of heart failure. Methods: After treatment decisions following contemporary practice in Japan, patients were prospectively enrolled into four cohorts: (1) ICD (2) CRT with defibrillator (CRT-D) (3) standard medical therapy (‘non-device’) (4) pacing (indicated for CRT; received pacemaker or CRT pacing). We compared the all-cause mortality between elderly and non-elderly patients with elderly defined as age>70 at the time of study enrollment. Results: The HINODE study enrolled 354 patients (191 elderly) followed for 19.6 ± 6.5 months with a minimum of 12 months and an absolute death rate of 11.0%. The estimated survival rate for device recipients (n=239) through 24 months was 86.1% (97.5% LCL: 79.8%) with no significant difference for elderly vs non-elderly patients (HR 1.97, 95%CI: 0.86-4.54). Analysis within cohorts showed increased risk of all-cause mortality for elderly with an ICD compared to non-elderly with an ICD (HR 5.09 95% CI: 1.1-23.6). However, ICD cohort excluding those with CRT-D indication showed no significant difference (HR 3.70, 95% CI: 0.75-18.35). No significant difference showed in other cohorts: CRT-D (HR 1.53 95% CI: 0.34-6.84) or pacing (HR 0.84, 95%CI: 0.2-3.5). Ventricular event free rate in ICD and CRT-D patients also had no difference (HR 0.84 95% CI: 0.31-2.25) Conclusions: Although elderly patients might be associated with higher risk of mortality in general, benefit of device therapy is comparable to non-elderly patients. We might consider device therapy despite age as a standalone risk in contemporary Japanese clinical practice.

Dapagliflozin and euglycaemic diabetic ketoacidosis – ‘But doctor my sugars were normal!’

Dear Editor, A ‘Dear Doctor Letter’ was issued by the manufacturer of Forxiga (dapagliflozin) in November 2021; this followed reviews by the European Medicines Agency and the UK Medicines and Healthcare products Regulatory Agency. The letter stated that ‘The removal of the T1DM indication is not due to any safety concern for dapagliflozin in any indication, including T1DM’ but must be discontinued ‘in patients with T1DM by or in consultation with a physician specialised in diabetes care and be conducted as soon as clinically practical.’1 Dapagliflozin was previously approved in the treatment of diabetes for combination with insulin therapy in type 1 diabetes and with oral medications and insulin in type 2 patients. The pathogenesis of EuDKA occurs as a consequence of absolute insulin deficiency leading to reduced glucose utilisation and enhanced lipolysis; increased delivery of free fatty acids (FFAs) to the liver coupled with raised glucagon levels promotes FFA oxidation, and subsequent production of ketone bodies.2 Rosenstock and Ferrannini also reported that following a US FDA safety communication, the majority of reports of EuDKA between 2014 and 2015 in the US were actually in patients with type 2 diabetes.2 The UK Yellow Card report did not specify the type of diabetes. A review of the UK MHRA Yellow Card reporting system on dapagliflozin in October 20223 showed the following results: total number of adverse drug reactions (ADRs) reports, 2155; serious ADR reports, 1371; fatal ADR reports, 26 (cut-off 31 August 2022). Details of ADRs which could be related to EuDKA are shown in Table 1. The number of reports submitted had risen following the letter from the manufacturer. It is expected that a large number of these reports could be related to the concomitant use of dapagliflozin and insulin therapy in patients with type 2 diabetes. Appropriate monitoring and awareness on the part of health care professionals and patients are necessary to prevent potentially harmful and fatal consequences. The advice from both the manufacturer and the medicines regulatory agencies surrounding the actions required in patients with type 1 diabetes is clear and we may prevent problems by close monitoring of patients in diabetes specialist units. Such task is facilitated by the use of electronic medical records and access to the list of all medications used by these patients. Following the research findings on the occurrence of EuDKA in patients with type 2 diabetes, we may argue that these patients should also be included in a review for EuDKA. From personal and documented reports, patients with type 2 diabetes often react negatively to the introduction of insulin therapy to their medications.4 Part of the rationale to include insulin therapy usually includes improved glycaemic control. Following a period of improvement in their self-monitored blood glucose, some patients might react by stopping or reducing their use of insulin. The resulting ketonaemia in patients with insulin deficiency taking SGLT2 inhibitors is initially asymptomatic or clinically undetectable and could gradually lead to severe ketoacidosis. There are data which document the increased incidence of chronic heart failure, especially in people with type 2 diabetes;5 as this diagnosis is also included in the newer indications for dapagliflozin it will be important to communicate the association of EuDKA and dapagliflozin use to specialists who might not necessarily be expert in managing this complication of diabetes. Most patients with type 2 diabetes are managed in primary care and initiating a community-wide alert would take time to complete and require significant human resource, increased budget, and likely lead to increased patient anxiety. Blood tests to detect low endogenous insulin secretion would also take time and increased resources. A more rapid and simple approach is required. One option could be to request that all patients with long-standing type 2 diabetes who are treated with insulin in combination with dapagliflozin or any other SGLT2 inhibitors should be advised to use blood or urine ketone testing to detect EuDKA, particularly when insulin doses are being reduced or withdrawn. Awareness of these such parameters would help health professionals to quickly identify and treat patients at risk. The Association of British Clinical Diabetologists and Diabetes UK have produced joint guidance on communication and education requirements to be provided to patients who were prescribed an SGLT2 inhibitor for the first time.6 This provides useful and practical suggestions for minimising adverse reaction to the use of these medicines. Michael Stacey, MD, FRCP, Senior Lecturer, Royal Centre for Defence Medicine, UK There are no conflicts of interest declared.

LPS differentially affects expression of CD14 and CCR2 in monocyte subsets of Post-STEMI patients with hyperglycemia

AimsFollowing ST-segment elevation myocardial infarction (STEMI), recruitment and activation of monocytes [classical (CD14++CD16-CCR2++), intermediate (CD14++CD16+CCR2+), non-classical (CD14LowCD16++CCR2Low)] are needed for myocardial wound healing. Monocyte surface receptor CC chemokine receptor type 2 (CCR2) is responsible for monocyte chemotaxis to sites of inflammation and the lipopolysaccharide (LPS)-binding protein co-receptor, CD14, is involved in pro-inflammatory monocyte activation. The purpose of this investigation was to determine the effects of ex-vivo LPS activation on monocyte subset CD14 and CCR2 expression in post-STEMI individuals with normal and elevated random blood glucose. MethodsPost-STEMI subjects were identified as normal random glucose (NG, <98 mg/dL, n = 13) or impaired random glucose (IG, ≥98 mg/dL, n = 26) and monocytes were analyzed for non-activated and LPS-activated (1 µg/mL for 4 h) CCR2 and CD14 expression. ResultsNon-activated intermediate monocytes from IG showed decreased CD14 expression when compared to NG, which was maintained following LPS-activation. The NG group showed a larger absolute reduction in classical CCR2 expression, leading to a significant difference between NG and IG following LPS-activation. ConclusionResults suggest a heightened response to pro-inflammatory activation in IG following STEMI, which may impair or delay post-STEMI myocardial healing, and thus increase the incidence of chronic heart failure. NIH 1R34HL121402.

ПРОЯВЛЕНИЯ СЕРДЕЧНОЙ НЕДОСТАТОЧНОСТИ У МУЖЧИН МОЛОЖЕ 60 ЛЕТ С ИНФАРКТОМ МИОКАРДА, ОСЛОЖНЕННЫМ ОСТРЫМ ПОВРЕЖДЕНИЕМ ПОЧЕК

Relevance. Acute kidney injury in myocardial infarction worsens its prognosis, including due to the development of chronic heart failure. Moreover, most of the data was obtained for patients over 60 years old. Aim. To evaluate the features of the heart failure manifestations in men under 60 years old with myocardial infarction complicated by acute kidney injury to improve prevention and outcomes. Material and methods. The study included men 19-60 years old with type I myocardial infarction. The patients were divided into two age-comparable groups: I - study group, with acute kidney injury - 25 patients; II - control, without it - 486 patients. A comparative analysis of the heart failure main manifestations frequency in the first 48 hours (1) and at the end of the third week of the disease (2), their dynamics, analysis of their impact on the risk of chronic heart failure development in acute kidney injury (ANOVA) was performed. Results. The study group (4.0%) differed from the control (21.8%) in a lower frequency of acrocyanosis (p = 0.03) and liver enlargement (8.0 and 25.7%; respectively; p = 0.046) at the end of the eighth week diseases. The main risk markers of the chronic heart failure development in study group were: winter period of the year (absolute risk: 94.1%; relative - 3.76; p = 0.0003), respiratory infections 2-3 times a year (absolute risk: 81.8%; p = 0.003), left ventricular myocardial mass index1 ≥ 173.3 g/m2 (absolute risk: 100%; p = 0.008) and mean arterial pressure1 ≥ 120 mm Hg (absolute risk: 100%; relative - 1.88; p = 0.01). Conclusions. Men under 60 years old with acute kidney injury in myocardial infarction are characterized by a higher incidence of chronic heart failure. The listed above values of the different predictors should be used in the formation of the high-risk groups for the chronic heart failure in acute kidney injury development, as well as for prognostic modeling.

Regional Disparities in Adherence to Guidelines for the Treatment of Chronic Heart Failure.

Objective The incidence of chronic heart failure (CHF) is likely to keep increasing in Japan as the population ages, placing increased burdens on medical facilities, particularly on the limited numbers of rural hospitals. We explored the appropriateness of CHF treatment in rural areas in Japan. Methods We compared rates of adherence to therapeutic guidelines for CHF between residents with a left ventricular ejection fraction <35% living in urban areas (n = 207) and those in rural areas (n = 180). Treatments included pharmacological [beta-blockers, angiotensin-converting enzyme inhibitors (ACEi)/angiotensin II receptor blocker (ARB), mineralocorticoid receptor antagonist (MRA) and anticoagulants for atrial fibrillation] and non-pharmacological [implantable cardioverter defibrillator (ICD)/cardiac resynchronization therapy (CRT), cardiac rehabilitation and HF education] approaches. Patients This study included 387 patients with CHF, prior myocardial infarction or cardiomyopathy, and a left ventricular ejection fraction (LVEF) <35% as determined by echocardiography. Results The respective rates of treatments administered in urban and rural areas were as follows: beta-blockers, 91.3% vs. 61.7% (p<0.05); ACEi/ARB, 86.5% vs. 68.3% (p<0.05); MRA, 74.4% vs. 59.4% (p<0.01); anticoagulants, 100% vs. 86.5%, (p<0.05); ICD/CRT, 45.4% vs. 5.0% (p<0.05); cardiac rehabilitation, 32.4% vs. 13.3% (p<0.05) and HF education, 33.3% vs. 32.8% (p=0.75). Conclusion Regional disparities in treatment for CHF persist, even in Japan. Improvements in the use of guideline-directed treatment in rural areas might improve the outcomes for CHF patients.

Cardio-renal syndrome type 2: Therapeutic and prognostic impact

Chronic heart failure (CHF) is a serious disease, and its prevalence is steadily increasing. Among patients with CHF, 30-60% have chronic renal impairment, defining cardio-renal syndrome (CRS) type 2. Patients with CRS type 2 have a higher morbidity and mortality and have a therapeutic problem. The objective of our study was to evaluate the therapeutic and prognostic impact of CKD in CHF patients. This was a retrospective study involving 70 patients with CHF (LVEF ≤ 50%) divided into two groups: – Type 2 cardio-renal syndrome (SCR) group: patients with creatinine clearance <60 ml/min, – A control group: patients with creatinine clearance ≥ 60 ml/min. Patients with CRS type 2 were older (66 years versus 54 years, P = 0.001). The risk of developing CRS type 2 was correlated with the female genus and the presence of high blood pressure. The presence of a CRS type 2 worsens the clinical picture of the CHF, as dyspnea stage IV was more severe (68% versus 38%, P = 0.03) and blood pressure was higher for Systolic (141 versus 122, P = 0.002) and diastolic (86 versus 75 P = 0.01) in the CRS type 2 group. Biologically, patients with CRS type 2 had more anaemia with lower average haemoglobin. (12.9 versus 13.9, P = 0.01). Therapeutically, nitrates were used more often in patients with CRS type 2 (20% versus 5%, P = 0.05). As for the evolution of our patients, the occurrence of outbreaks of heart failure and mortality were significantly higher in the SCR group type 2. The occurrence of a SCR worsens the initial picture of heart failure, exposes it to more cardiovascular events, and aggravates the patient's prognosis. Management must be early and prevention of cardiovascular risk factors remains the most effective way to limit the incidence of CHF and CRS.

Артеріальна гіпертензія і серцева недостатність у загальнолікарській практиці

The Framingham study demonstrated that myocardial infarction (25% of cases) and arterial hypertension (AH) (75% of cases) caused the development of chronic heart failure (CHF). The most significant predictor of CHF development was an increase in systolic blood pressure (SBP) and pulse pressure and each increase in SBP by 20 mm Hg and pulse blood pressure by 16 mm Hg led to an increase in the incidence of CHF by 52% and 55%, respectively. The presented clinical case of a patient with CHF, developed due to long-term hypertension, considered the mechanisms of CHF development, as well as the issue of pharmacotherapy of AH in combination with chronic heart failure with systolic dysfunction. The key mechanisms that directly lead to the development of CHF in AH are hemodynamic overload, reduction of myocardial contractility, left ventricular hypertrophy (LVH). The likelihood of CHF development in patients with AH is by 4 times higher, whilst in patients with LVH it is by 15 times higher. Along with LVH, one of the early manifestations of LV remodeling in AH is the development of diastolic dysfunction, which precedes the development of systolic abnormalities in AH and LVH. Antihypertensive therapy resulted in reduction of the incidence of CHF by approximately 52% compared to patients who did not receive adequate therapy. The decrease in the incidence of CHF was linearly dependent on the decrease in SBP: each decrease of SBP by 10 mm Hg led to a 26% reduction in the relative risk in CHF development. It has been established that AH is not only one of the leading etiological factors in CHF development, but also have similar key links in pathogenesis. The strategy for the selection of pathogenetic pharmacotherapy should be determined taking into account the above circumstance. Currently, the European Society of Cardiology recommends prescribing beta-blockers to all patients with stable CHF Class II–IV as a standard treatment in combination with ACE inhibitors and diuretics in the absence of contraindications. In addition to RAAS blockers, medications for patients with AH in combination with systolic CHF can be supplemented with thiazide or loop diuretics, as well as mineralocorticoid receptor ant agonists (MRA).

Arterial Hypertension and Heart Failure in General Practice

The Framingham study demonstrated that myocardial infarction (25% of cases) and arterial hypertension (AH) (75% of cases) caused the development of chronic heart failure (CHF). The most significant predictor of CHF development was an increase in systolic blood pressure (SBP) and pulse pressure and each increase in SBP by 20 mm Hg and pulse blood pressure by 16 mm Hg led to an increase in the incidence of CHF by 52% and 55%, respectively. The presented clinical case of a patient with CHF, developed due to long-term hypertension, considered the mechanisms of CHF development, as well as the issue of pharmacotherapy of AH in combination with chronic heart failure with systolic dysfunction. The key mechanisms that directly lead to the development of CHF in AH are hemodynamic overload, reduction of myocardial contractility, left ventricular hypertrophy (LVH). The likelihood of CHF development in patients with AH is by 4 times higher, whilst in patients with LVH it is by 15 times higher. Along with LVH, one of the early manifestations of LV remodeling in AH is the development of diastolic dysfunction, which precedes the development of systolic abnormalities in AH and LVH. Antihypertensive therapy resulted in reduction of the incidence of CHF by approximately 52% compared to patients who did not receive adequate therapy. The decrease in the incidence of CHF was linearly dependent on the decrease in SBP: each decrease of SBP by 10 mm Hg led to a 26% reduction in the relative risk in CHF development. It has been established that AH is not only one of the leading etiological factors in CHF development, but also have similar key links in pathogenesis. The strategy for the selection of pathogenetic pharmacotherapy should be determined taking into account the above circumstance. Currently, the European Society of Cardiology recommends prescribing beta-blockers to all patients with stable CHF Class II–IV as a standard treatment in combination with ACE inhibitors and diuretics in the absence of contraindications. In addition to RAAS blockers, medications for patients with AH in combination with systolic CHF can be supplemented with thiazide or loop diuretics, as well as mineralocorticoid receptor antagonists (MRA).

Evidence-based drug therapy for heart failure-an update

Chronic heart failure affects millions of people worldwide and is associated with high morbidity and mortality. Because of steadily increasing ageing populations and improved survival rates after myocardial infarction, the incidence of chronic heart failure is rising. As acute decompensated heart failure is one of the leading causes for hospitalization in Germany, heart failure imposes ahuge economic burden on its health care system. Guideline directed therapy is important to improve prognosis. In the following, we give an overview about novel heart failure clinical trial results and point to important comorbidities.

Diagnosis and Treatment of Chronic Heart Failure in Diabetes of the 2nd Type

Chronic heart failure (CHF) is an acute medical and social problem relating to the priorities of the national health systems of most countries of the world due to the increasing spread of this syndrome, despite the continuous improvement of treatment. The near future promises only the worsening of the problem: the incidence and prevalence of CHF increases due to the increase in life expectancy.Thus, the need to clarify the features of the diagnosis of CHF in patients with diabetes mellitus and the improvement of their therapy is beyond doubt.The aim of this research is to clarify the frequency of chronic heart failure in patients with diabetes type 2 in the specialized | department of the hospital and the unorganized urban population, to assess the adequacy of its diagnosis and treatment.To achieve this goal, the following tasks:1. To identify the prevalence of chronic heart failure in patients with diabetes type 2.2. To assess the level of diagnosis of chronic heart failure in patients with diabetes type 2.3. To analyze the state of drug therapy in patients with diabetes type 2 in the presence of chronic heart failure.For the first time, the prevalence of CHF in patients with diabetes type 2 mellitus in an unorganized urban population studied.

Impact of renal dysfunction on the management and outcome of acute heart failure: results from the French prospective, multicentre, DeFSSICA survey

ObjectivesCardiorenal syndrome (CRS) is the combination of acute heart failure syndrome (AHF) and renal dysfunction (creatinine clearance (CrCl) ≤60 mL/min). Real-life data were used to compare the management and outcome...

Chronic Heart Failure in Rheumatoid Arthritis Patients (Part I): Prevalence, Etiology and Pathogenesis

Rheumatoid arthritis (RA) is a disease with a high cardiovascular risk, which is caused, in particular, by an increased incidence of chronic heart failure (CHF). Analysis of the results of the main studies on the prevalence of CHF, the features of the etiology and pathogenesis of myocardial dysfunction in RA was the purpose of the review. According to the registers, population and epidemiological studies, the risk of CHF and CHF-associated mortality in RA patients is 1.5-2.5 times higher than in the general population. In most of the studies only clinically manifested congestive heart failure (HF) was considered, so the actual prevalence of CHF may be significantly underestimated. An increase in the risk of CHF was noted immediately after the debut of RA, with the prevalence of HF with preserved systolic function of the left ventricle, which indicates the important role of diastole disturbance in the pathogenesis of myocardial dysfunction. Chronic systemic autoimmune inflammation contributes to the development of CHF in RA patients, in addition to coronary heart disease, traditional risk factors (TRFs) of cardiovascular diseases (CVD). Inflammation plays a leading role in the development of CHF through various mechanisms including direct damage to the myocardium and coronary arteries (myocarditis, coronary vasculitis, microcirculatory disorders), aggravation of the severity of TRFs of CVD, accelerated progression of ischemic heart disease, endothelial dysfunction, increased vascular wall stiffness, cardiac and vascular remodeling. Early diagnosis of CHF and timely measures that can slow its progression is needed due to the high risk of CHF and CHF-associated mortality in RA patients, especially in patients with risk factors for CHF.

Hyperlipidemia Impairs Autophagy in Chronic Heart Failure

Hyperlipidemia is a major risk factor contributing to myocardial infarction and ischemic cardiomyopathy. Despite the progress in revascularization, incidence of chronic heart failure and the need for ventricular assist device (VAD) implantation are increasing. It is important to decipher molecular mechanisms and effects of comorbidities to evaluate the myocardial response to VAD therapy.