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"textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Heart failure (HF) has become one of the main public health problems for countries in the European Union and one of the diseases with the greatest morbidity and mortality in the general population. Prevalence studies such as Prevalence of Heart Failure in Spain (<span class="elsevierStyleItalic">Prevalencia de Insuficiencia Cardiaca en España</span>, PRICE)<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> and Heart Failure in Outpatient Clinics (EPISERVE)<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> have shown prevalence rates of 16% among patients older than 75 years. Inevitably, the consumption of healthcare resources attributable to this disease has been overwhelming. HF causes 5% of hospital admissions in our community and is the leading cause of hospitalization for patients older than 65 years. It is estimated that 2% of healthcare expenditures in developed countries are destined to HF, and there appears to be no trend towards a reduction in these figures.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The increasing incidence and prevalence of HF is due to several factors, such as the progressive increase in the age of the population, where HF constitutes the final stage of numerous heart conditions for which survival has increased and to the improved treatment of various chronic diseases that contribute to the onset of HF such as type 2 diabetes mellitus (DM2).</p><p id="par0010" class="elsevierStylePara elsevierViewall">In addition to the problem of high prevalence, there is the difficulty in correctly diagnosing HF, which is a real challenge.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Although diagnosing HF might seem relatively simple from a theoretical standpoint, given that it requires “simply” confirming that the patient meets a number of criteria, the diagnosis of HF in daily clinical practice usually entails significant difficulties. The most common symptom of HF is dyspnea. However, “shortness of breath”, as our patients would call it, can be due to numerous conditions, such as physical withdrawal, bronchopulmonary disease, obesity and other comorbidities in addition to HF. In addition, several of these conditions often coexist in patients with diastolic HF. Biochemical markers, which include B-type natriuretic peptide and N-terminal pro B-type natriuretic peptide, have high sensitivity but very low specificity.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Once again, patients with diastolic HF frequently have high levels of these markers due to extracardiac disorders, making the use of the markers difficult, in contrast to the situation with, for example, young patients with dilated cardiomyopathy and no other disease. Lastly, unlike systolic HF in which there is one parameter (left ventricular ejection fraction) that helps define the presence of the disease (despite the parameter’s limitations), “structural abnormalities” that require the diagnosis of HF with preserved ejection fraction (HFpEF) are a poorly defined and heterogeneous group that complicate the diagnosis.</p><p id="par0015" class="elsevierStylePara elsevierViewall">With all these data, it is easy to see that the diagnosis of HFpEF is a real challenge. Nevertheless, this is not the only difficulty: the few clinical trials that have addressed the treatment of this disease have failed to demonstrate some benefit for the evaluated drugs. This lack of success might be due to the fact that numerous disorders are included within the diagnosis of HFpEF. The option of grouping into clusters those patients who share this syndrome could be the first approach to achieve therapeutic success.</p><p id="par0020" class="elsevierStylePara elsevierViewall">DM2 is one of the most present comorbidities in HF and one that most affects the prognosis of HF. As highlighted by the authors, DM2 can be found in almost half of those with HF and increases the risk of morbidity and mortality in patients with HFpEF.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> These data on the prognoses of patients with diabetes and established HF come from large trials on HF, such as the Survival and Ventricular Enlargement (SAVE) trial,<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> the Valsartan in Acute Myocardial Infarction (VALIANT) trial<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> and the Candesartan in HF (CHARM) trial.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> All of these trials showed a greater mortality risk in men and women with diabetes. For example, the CHARM study showed that both men and women with diabetes presented a greater risk of cardiovascular death and hospitalization for HF compared with patients without diabetes, with a cumulative incidence of approximately 40% for 3 years. This high prevalence and association of the 2 entities can be observed in the opposite direction, and HF can be said to be an important contributor to cardiovascular morbidity and mortality in patients with diabetes, with myocardial dysfunction even being present in the absence of epicardial coronary artery disease. In fact, the term “diabetic cardiomyopathy”<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> has been coined to group these patients.</p><p id="par0025" class="elsevierStylePara elsevierViewall">HF is the final expression of numerous diseases that entail cardiac function impairment, many of which do not have a common pathophysiological nexus, as is the case with chronic obstructive pulmonary disease and DM2 itself, both of which are present in the genesis of HF in many patients. We therefore need to make an effort in the diagnosis and treatment of patients with HF, given the heterogeneity of the patients and the diseases that lead to HF. We also need to make adjusting the treatment to the comorbidities a priority in the approach strategy for HF. The classification of patients with HF according to the underlying diseases and the pathophysiological profiles comes from the need to improve the care for these patients. Classifying patients to improve their management is a logical step, which is why subgroups and profiles within HF have been created to improve the management. For example, Shah et al.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> proposed a classification of patients according to various profiles, including those that go beyond specific diseases, by proposing groups by pathophysiological mechanisms underlying HF (e.g., according to endothelial dysfunction and inflammation), all of which is aimed at adjusting the treatment of the mechanisms that lead to a loss of cardiac function.</p><p id="par0030" class="elsevierStylePara elsevierViewall">The study by Arévalo Lorido et al. proposes a classification of patients with HFpEF into profiles whose nexus is DM2. Implementing these profiles of patients with DM2 offers a better approach for these patients and provides a major opportunity to improve the treatment of HF, given that DM2 is the main comorbidity of HF. The time to advance the treatment of DM2 and HF is more than pertinent; the publication of the results from various trials on the use of SGLT2i and GLP-1 for HF open a new horizon for treatment, changes that have already been included in clinical practice guidelines. The data come from one of the few HF registries currently underway in Spain: the national HF registry RICA, which could also provide the results of changes in treatment for the patients. Many of these changes or adjustments could be performed according to the various proposed profiles.</p></span>"
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