1,721,186 research outputs found
Diabetes leading to heart failure and heart failure leading to diabetes: epidemiological and clinical evidence
No full textType 2 diabetes mellitus (T2DM) is a risk factor that plays a major role in the onset of heart failure (HF) both directly, by impairing cardiac function, and indirectly, through associated diseases such as hypertension, coronary disease, renal dysfunction, obesity, and other metabolic disorders. In a population of HF patients, the presence of T2DM ranged from 20 to 40%, according to the population studied, risk factor characteristics, geographic area, and age, and it is associated with a worse prognosis. Finally, patients with HF, when compared with those without HF, show an increased risk for the onset of T2DM due to several mechanisms that predispose the HF patient to insulin resistance. Despite the epidemiological data confirmed the relationship between T2DM and HF, the exact prevalence of HF in T2DM comes from interventional trials rather than from observational registries aimed to prospectively evaluate the risk of HF occurrence in T2DM population. This review is focused on the vicious cycle linking HF and T2DM, from epidemiological data to prognostic implications
Are HFpEF and HFmrEF So Different? The Need to Understand Distinct Phenotypes
Full text linkTraditionally, patients with heart failure (HF) are divided according to ejection fraction (EF) threshold more or <50%. In 2016, the ESC guidelines introduced a new subgroup of HF patients including those subjects with EF ranging between 40 and 49% called heart failure with midrange EF (HFmrEF). This group is poorly represented in clinical trials, and it includes both patients with previous HFrEF having a good response to therapy and subjects with initial preserved EF appearance in which systolic function has been impaired. The categorization according to EF has recently been questioned because this variable is not really a representative of the myocardial contractile function and it could vary in relation to different hemodynamic conditions. Therefore, EF could significantly change over a short-term period and its measurement depends on the scan time course. Finally, although EF is widely recognized and measured worldwide, it has significant interobserver variability even in the most accredited echo laboratories. These assumptions imply that the same patient evaluated in different periods or by different physicians could be classified as HFmrEF or HFpEF. Thus, the two HF subtypes probably subtend different responses to the underlying pathophysiological mechanisms. Similarly, the adaptation to hemodynamic stimuli and to metabolic alterations could be different for different HF stages and periods. In this review, we analyze similarities and dissimilarities and we hypothesize that clinical and morphological characteristics of the two syndromes are not so discordant
Acute Heart Failure Treatment: Traditional and New Drugs
No full textGoals of treatment in acute heart failure (AHF) are different with regard to the clinical presentation, etiology and hemodynamic profiles. Therefore AHF is a colorful picture that encompasses several syndromes with particular characteristics. Unfortunately the protocol treatments proposed until now regarding old and new drugs, showed neutral or negative results in most of trials.This could depend on patient population selection, syndrome heterogeneity, drugs used, administration and posology, study design and study target. Most of the trials showed positive results in the early period but any improvement in mortality and re-hospitalization at a later stage. In this review we summarize the drugs more commonly used in AHF syndromes on the basis of pressure values, organ perfusion, pulmonary and venous congestion. However, a significant improvement in outcome needs to consider not only the acute phase but the effect of each drug on cardiac damage, organ perfusion, neurohormonal activation and renal injury after a short period. The most important goal of treatment should be an outcome improvement at the post-discharge phase. This could be obtained in the future assuming an 'holistic' point of view looking for all the potential consequences and benefits at both cardiac and systemic levels. Copyright (C) 2010 S. Karger AG, Base
Acute COVID-19 Management in Heart Failure Patients: A Specific Setting Requiring Detailed Inpatient and Outpatient Hospital Care
Full text linkThe relationship existing between heart failure (HF) and COVID-19 remains questioned and poorly elucidated. Many reports suggest that HF events are reduced during pandemics, although other studies have demonstrated higher mortality and sudden death in patients affected by HF. Several vascular, thrombotic, and respiratory features may deteriorate stable HF patients; therefore, the infection may directly cause direct myocardial damage, leading to cardiac function deterioration. Another concern is related to the possibility that antiviral, anti-inflammatory, and corticosteroid agents commonly employed during acute COVID-19 infection may have potentially deleterious effects on the cardiovascular (CV) system. For these reasons, HF patients deserve specific management with a tailored approach in order to avoid arrhythmic complications and fluid retention events. In this review, we describe the complex interplay between COVID-19 and HF, the evolving trend of infection with related CV events, and the specific management strategy to adopt in this setting
Laboratory and Metabolomic Fingerprint in Heart Failure with Preserved Ejection Fraction: From Clinical Classification to Biomarker Signature
Full text linkHeart failure with preserved ejection fraction (HFpEF) remains a poorly characterized syndrome with many unknown aspects related to different patient profiles, various associated risk factors and a wide range of aetiologies. It comprises several pathophysiological pathways, such as endothelial dysfunction, myocardial fibrosis, extracellular matrix deposition and intense inflammatory system activation. Until now, HFpEF has only been described with regard to clinical features and its most commonly associated risk factors, disregarding all biological mechanisms responsible for cardiovascular deteriorations. Recently, innovations in laboratory and metabolomic findings have shown that HFpEF appears to be strictly related to specific cells and molecular mechanisms’ dysregulation. Indeed, some biomarkers are efficient in early identification of these processes, adding new insights into diagnosis and risk stratification. Moreover, recent advances in intermediate metabolites provide relevant information on intrinsic cellular and energetic substrate alterations. Therefore, a systematic combination of clinical imaging and laboratory findings may lead to a ‘precision medicine’ approach providing prognostic and therapeutic advantages. The current review reports traditional and emerging biomarkers in HFpEF and it purposes a new diagnostic approach based on integrative information achieved from risk factor burden, hemodynamic dysfunction and biomarkers’ signature partnership
Recent advances in pharmacological treatment of heart failure
Full text linkBackground: Over the last years, several trials offered new evidence on heart failure (HF) treatment. Design and results: For HF with reduced left ventricular ejection fraction, type 2 sodium—glucose cotransporter inhibitors, aside from sacubitril—valsartan, demonstrated extraordinary efficacy in ameliorating patients' prognosis. Some new molecules (eg vericiguat, omecamtiv mecarbil and ferric carboxymaltose) correct iron deficiency and have shown to be capable of furthering reducing the burden of HF hospitalisation. Finally, there is new evidence on the possible therapeutic approaches of HF patients with mid-range or preserved left ventricular ejection fraction. Conclusions: This review aimed to revise the main novelties in the field of HF therapy and focus on how the daily clinical approach to patient treatment is changing
Anemia in Cardio-Renal Syndrome: clinical impact and pathophysiologic mechanisms
Full text linkAnemia is a disease that is often associated with heart failure (HF) and renal insufficiency (RI). This unfavorable triad of conditions has been called Cardio-Renal-Anemia Syndrome (CRS). The association of HF, RI, and anemia is poorly reported in multicenter clinical trials, so the pathophysiologic mechanisms and treatment options need to be better defined. When CRS patients develop anemia, a "perfect storm" often occurs: HF and RI cause anemia which will worsen the first two conditions. Anemia appears to be the result of complex interactions between cardiac performance, bone marrow homeostasis, renal dysfunction, and various drug side effects. However, neurohormonal and inflammatory activities play a key role in the beginning and progression of the disease. As a consequence, endogenous erythropoietin activity dysfunction with inadequate production and tissue resistance occurs. Despite the advances of therapy in the neurohormonal activation blockade, mortality and hospitalization in HF still remain unacceptably high, suggesting that specific comorbidity treatments could have a significant positive prognostic impact. Anemia should be recognized as one of the novel targets in HF treatment. © 2011 Springer Science+Business Media, LLC
Cardio-renal syndrome: an entity cardiologists and nephrologists should be dealing with collegially
No full textHeart failure may lead to acute kidney injury and viceversa. Chronic kidney disease may affect the clinical outcome in terms of cardiovascular morbidity and mortality while chronic heart failure may cause CKD. All these disorders contribute to the composite definition of cardio-renal syndromes. Renal impairment in HF patients has been increasingly recognized as an independent risk factor for morbidity and mortality; however, the most important clinical trials in HF tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in HF are not known, and several pathways could contribute to the "vicious heart/kidney circle." Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin-aldosterone pathways and arginine-vasopressin release. All these mechanisms cause fluid and sodium retention, peripheral vasoconstriction and an increased congestion as well as cardiac workload. Therapy addressed to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardio-renal syndrome
Variations of peripheral markers of serotoninergic system in selected vascular patients
No full textBACKGROUND AND AIM: Serotonin (5-HT), a decarboxylated derivative of tryptophan, is synthesized in the enterochromaffin cells and released into blood stream to be incorporated into platelets. At the site of endothelial lesions, platelets aggregate and secrete 5-HT that presents several vascular actions involved in thrombosis and atherogenesis. In fact, 5-HT may induce vasoconstriction in the presence of endothelial injury, aggregation of platelets, and mitogenesis of arterial smooth muscle cells and endothelial cells. It may also contribute to the vascular inflammation associated with atherogenesis by increasing the synthesis of Interleukin-6 in vascular smooth muscle cells. We evaluated serotonin levels in plasma and platelets of patients with unstable angina and ischemic stroke, to identify an association between serotonin and atherosclerosis of coronary and cerebral arteries.
METHODS AND RESULTS: Twenty patients (14 men, 6 women, mean age 69 +/- 10 years) with unstable angina and 15 patients (7 men, 8 women, mean age 81 +/- 10 years) with ischemic stroke were included in the study. Twenty-four healthy subjects matched for age and sex constituted the control group. Blood samples were drawn in the morning to determine plasma and platelet concentrations of serotonin. In patients with unstable angina serotonin levels in platelets were significantly lower (p < 0.001) than those observed in controls, while serotonin concentrations in plasma did not significantly differ from those found in controls. In patients affected by stroke serotonin levels in plasma and in platelets did not significantly differ from those found in normal subjects.
CONCLUSIONS: Our findings may contribute to the knowledge to different mechanisms involved in the pathogenesis of cardiac and cerebral ischemia
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