Manejo y tratamiento actual de la insuficiencia cardiaca en unidades acreditadas de cardiología y medicina interna en España / Current heart failure disease management and treatment in accredited units from cardiology and internal medicine in Spain

Antecedentes y objetivos La insuficiencia cardiaca (IC) es una patología compleja con una alta prevalencia, incidencia y mortalidad que conlleva un importante coste sanitario. En España existen unidades de IC (UIC) multidisciplinares, lideradas por cardiología y medicina interna. Nuestro objetivo era conocer su organización actual y adherencia a las últimas recomendaciones científicas. Materiales y métodos Un comité científico formado por cardiólogos e internistas elaboró una encuesta a finales de 2021, que fue enviada a 110 UIC. Setenta y tres de cardiología, acreditadas por SEC-Excelente, y 37 de medicina interna, integradas en el programa UMIPIC. Resultados Se recibieron 83 encuestas cumplimentadas (75,5%); 49 de cardiología y 34 de medicina interna. Los resultados mostraron que las UIC están integradas mayoritariamente por un cardiólogo, internista y enfermería especializada (34,9%). El perfil de paciente atendido en las UIC cardiológicas es muy diferente al paciente de las UMIPIC, siendo estos últimos mayores, con fracción de eyección ventricular izquierda conservada y más carga de comorbilidad. La mayoría de UIC actualmente realizan seguimiento mixto, presencial y telemático (73,5%). Los péptidos natriuréticos son los biomarcadores más utilizados (90%). Se titulan los cuatro grupos farmacológicos fundamentales de tratamiento de la IC a la vez mayoritariamente (85%). Solo 24% de las unidades mantienen una comunicación fluida con atención primaria. Conclusiones Los dos modelos de UIC liderados por cardiología y medicina interna son complementarios, disponen de enfermería especializada, y siguen al paciente de forma mixta, con una adherencia farmacológica muy alta a las últimas recomendaciones científicas. El principal punto de mejora es la coordinación con atención primaria (AU)

Background and objectives Heart failure (HF) is a complex disease with high prevalence, incidence and mortality rates leading to high healthcare burden. In Spain, there are multidisciplinary HF units coordinated by cardiology and internal medicine. Our objective was to describe its current organizational model and their adherence to the latest scientific recommendations. Materials and methods In late 2021, a scientific committee (with cardiology and internal medicine specialists) developed a questionnaire that was sent as an online survey to 110 HF units [73 from cardiology (accredited by SEC-Excelente) and 37 from internal medicine (integrated in UMIPIC program)]. Results We received 83 answers (75.5% total: 49 from cardiology and 34 from internal medicine). The results showed that HF units are mostly integrated by specialists from cardiology, internal medicine and specialized nurse practitioners (34.9%). Patient characteristics from HF units are widely different when comparing those in cardiology to UMIPIC, being the latter older, more frequently with preserved ejection fraction and higher comorbidity burden. Most HF units (73.5%) currently use a hybrid face-to-face/virtual model to perform patient follow-up. Natriuretic peptides are the biomarkers most commonly used (90%). All four disease-modifying drug classes are mainly implemented at the same time (85%). Only 24% of HF units hold fluent communication with primary care. Conclusions Both models from cardiology and internal medicine HF units are complementary, they include specialized nursing, they use hybrid approach for patient follow-up and they display a high adherence to the latest guideline recommendations. Coordination with primary care remains as the major improvement area (AU)

Genetic predisposition to albuminuria is associated with increased arterial stiffness: role of elastin.

BACKGROUND AND PURPOSE: The Munich Wistar Frömter (MWF) rat strain represents an experimental model to study cardiovascular alterations under conditions of progressive albuminuria. The aim of this study was to evaluate the association between genetic predisposition to albuminuria and the development of arterial stiffness and/or vascular remodelling. EXPERIMENTAL APPROACH: Experiments were performed in mesenteric arteries from 12-week-old MWF, Wistar Kyoto (WKY) and consomic MWF-6(SHR) and MWF-8(SHR) rats in which chromosomes 6 or 8 associated with albuminuria from MWF were replaced by the respective chromosome from spontaneously hypertensive rats (SHR). KEY RESULTS: Incremental distensibility, wall stress and strain were reduced, and arterial stiffness was significantly increased in albuminuric MWF compared with WKY. Albuminuria suppression in both consomic strains was associated with lower ß-values in MWF-8(SHR) and MWF-6(SHR) compared with MWF. Moreover, elastin content was significantly lower in MWF external elastic lamina compared with WKY and both consomic strains. In addition, a reduction in arterial external and internal diameter and cross-sectional area was detected in MWF compared with WKY, thus exhibiting an inward hypotrophic remodelling. However, these alterations remained unchanged in both consomic strains. CONCLUSION AND IMPLICATIONS: These data demonstrate that albuminuria in MWF is associated with increased arterial stiffness due to a reduction of elastin content in the external elastic lamina. Moreover, inward hypotrophic remodelling in MWF is not directly associated with albuminuria. In contrast, we demonstrated that two major genetic loci affect both the development of albuminuria and arterial stiffness, thus linking albuminuria and impairment of mechanical properties of resistance arteries.

Vascular AMPK as an attractive target in the treatment of vascular complications of obesity.

The key for the survival of all organisms is the regulation and control of energy metabolism. Thus, several strategies have evolved in each tissue in order to balance nutrient supply with energy demand. Adenosine monophosphate-activated protein kinase (AMPK) is now recognized as a key participant in energy metabolism. It ensures an appropriate energetic supply by promoting energy conserving pathways in detriment of anabolic processes not essential for cell survival. Vascular AMPK plays a critical role in the regulation of blood flow and vascular tone through several mechanisms, including vasodilation by stimulating nitric oxide release in endothelial cells. Since obesity leads to endothelial damage and AMPK dysregulation, AMPK activation might be an important strategy to restore vascular function in cardiometabolic alterations. In the present review we focus on the role of vascular AMPK in both endothelial and smooth muscle cells, paying special attention to its dysregulation in obesity- and high-fat diet-related complications, as well as to the mechanisms and benefits of vascular AMPK activation.

Mild caloric restriction reduces blood pressure and activates endothelial AMPK-PI3K-Akt-eNOS pathway in obese Zucker rats.

Genetic obesity models exhibit endothelial dysfunction associated to adenosine monophosphate-activated protein kinase (AMPK) dysregulation. This study aims to assess if mild short-term caloric restriction (CR) restores endothelial AMPK activity leading to an improvement in endothelial function. Twelve-week old Zucker lean and obese (fa/fa) male rats had access to standard chow either ad libitum (AL, n=8) or 80% of AL (CR, n=8) for two weeks. Systolic blood pressure was significantly higher in fa/fa AL rats versus lean AL animals, but was normalized by CR. Endothelium-dependent relaxation to acetylcholine (ACh, 10(-9) to 10(-4) M) was reduced in fa/fa AL compared to control lean AL rats (p<0.001), and restored by CR. The AMPK activator AICAR (10(-5) to 8·10(-3) M) elicited a lower relaxation in fa/fa AL rings that was normalized by CR (p<0.001). Inhibition of PI3K (wortmannin, 10(-7) M), Akt (triciribine, 10(-5) M), or eNOS (L-NAME, 10(-4) M) markedly reduced AICAR-induced relaxation in lean AL, but not in fa/fa AL rats. These inhibitions were restored by CR in Zucker fa/fa rings. These data show that mild short-term CR improves endothelial function and lowers blood pressure in obesity due to the activation of the AMPK-PI3K-Akt-eNOS pathway.