ASSA14-10-02 Treatment Effect of Trimetazidin on Cardiac Function in Mild-Moderate Systolic Heart Failure Patients with Coronary Heart Disease

Abstract: As a cardiovascular disease, heart failure is one of prime mortality cause in the world. Coronary heart disease has a role in development of heart failure so that it becomes one of heart failure’s major clinical risk factor. This study aimed to calculate the prevalence of and identify the factors that influence coronary heart disease status of heart failure patients at Alamanda ward of RSUD Ulin Banjarmasin in 2016. Factors that were studied consisted of age, sex, family history of heart disease, smoking, diabetes mellitus, and hypertension. This study used analytical observation with cross-sectional approach on medical records that were obtained by purposive sampling method. The result showed 46.4% of 263 heart failure patients had coronary heart disease status. Multivariate analysis inferred hypertension as the factor that influences the coronary heart disease status of heart failure patients (OR = 1.98, 95% CI = 1.06 – 3.71, P = 0.033). Keywords: cardiovascular disease, heart failure, coronary heart disease, hypertension

Download Full-text

Heart Failure And Diabetes: Perspective Of A Dangerous Association

Current Hypertension Reviews ◽

10.2174/1573402117666210406111927 ◽

2021 ◽

Vol 17 ◽

Author(s):

Liliana Ehtel Favaloro ◽

Roxana Daniela Ratto ◽

Carla Musso

Keyword(s):

Risk Factors ◽

Heart Failure ◽

Coronary Heart Disease ◽

Heart Disease ◽

Mechanisms Of Action ◽

Sglt2 Inhibitors ◽

Diabetic Patients ◽

Heart Failure Patients ◽

The Relationship

: The relationship between diabetes and risk of heart failure has been described in previous trials, releasing the importance of the hyperglycemic state that added to other risk factors, favors the development of coronary heart disease. The mechanism by which in the absence of hypertension, obesity and/or dyslipidemia, diabetic patients develop cardiomyopathyhas been less studied. Recently, the Sodium Glucose Co-transporter type 2 inhibitors (SGLT2 inhibitors) used for the treatment of heart failure patients with or without diabetes has been a breakthrough in the field of medicine. This review describes the established pathophysiology of diabetic cardiomyopathy and SGLT2 inhibitors, their mechanisms of action, and benefits in this group of patients.

Download Full-text

Matricellular Protein Cilp1 Promotes Myocardial Fibrosis in Response to Myocardial Infarction

Circulation Research ◽

10.1161/circresaha.121.319482 ◽

2021 ◽

Author(s):

Qing-Jun Zhang ◽

Yu He ◽

Yongnan Li ◽

Huali Shen ◽

Ling Lin ◽

...

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Heart Disease ◽

Cardiac Function ◽

Mechanism Of Action ◽

Cardiac Remodeling ◽

Cardiac Fibroblasts ◽

Neonatal Rat ◽

Heart Failure Patients ◽

Mtorc1 Signaling

Rationale: Cartilage intermediate layer protein 1 (Cilp1) is a secreted extracellular matrix (ECM) protein normally associated with bone and cartilage development. Its function and mechanism of action in adult heart disease remain elusive. Objective: To establish the function and mechanism of action of Cilp1 in post-myocardial infarction (MI) cardiac remodeling. Methods and Results: We investigated the expression of Cilp1 in mouse models of pathological cardiac remodeling and human heart failure patients. Cilp1 was expressed predominantly in cardiac fibroblasts and upregulated in response to cardiac injury and in the heart and blood of heart failure patients. We generated Cilp1 knock out (KO) and transgenic (Tg) mice with N-terminal half of the protein (NCilp1) overexpressed in myofibroblasts. Cilp1 KO mice had better cardiac function, reduced number of immune cells and myofibroblasts, and enhanced microvascular survival after MI compared to wild-type (WT) littermates. Conversely, NCilp1-Tg mice had augmented loss of cardiac function, increased number of myofibroblasts and infarct size after the MI injury. RNA-seq and gene ontology analysis indicated that cell proliferation and mTORC1 signaling were downregulated in KO hearts compared to WT hearts. In vivo BrdU labeling and immunofluorescence staining showed that myofibroblast proliferation in the Cilp1 KO heart was downregulated. Biaxial mechanical testing and ECM gene expression analysis indicated that while MI caused significant stiffness in WT hearts it had little effect on KO hearts. Upregulation of collagen expression after MI injury was attenuated in KO hearts. Recombinant CILP1 protein or NCilp1-conditioned medium promoted proliferation of neonatal rat ventricular cardiac fibroblasts via the mTORC1 signaling pathway. Conclusions: Our studies established a pathological role of Cilp1 in promoting post-MI remodeling, identified a novel function of Cilp1 in promoting myofibroblast proliferation, and suggested that Cilp1 may serve as a potential biomarker for pathological cardiac remodeling and target for fibrotic heart disease.

Download Full-text