Atrial fibrillation in heart failure. Obesity, diabetes with HF

Atrial fibrillation is a common cause of acute decompensation in patients with CNNFV. Potential mechanisms responsible for AF are discussed in more detail below. AF can lead to decompensation of heart failure in patients with diastolic dysfunction, but this dysfunction itself (in the absence of heart failure) is also a risk factor for the appearance of AF.   

Thus, diastolic dysfunction , AF and SNFV are independent and interrelated states that in elderly people probably have common pathogenetic mechanisms. The prevalence of ventricular arrhythmias in patients with CNFV is poorly understood. Tachycardia caused by atrial arrhythmias is recognized by the FR for acute decompensation of CNNFV. Bradycardia and an adverse slowdown in atrioventricular conduction caused by first-degree heart block can also negatively affect LV filling in some patients. 
 

Obesity is associated with an increased risk of heart failure. In general, patients with SNFV are more likely to be obese than patients with SNFV; the prevalence of diastolic dysfunction in obese patients is increasing. Obesity not only leads to an unfavorable hemodynamic load on the heart, but also is a source of a large number of biologically active protein and non-protein mediators, many of which are associated with various mechanisms of chronic inflammation. 

An increase in body mass index is the RF of development of hypertension, diabetes, coronary heart disease, and AF, each of which is associated with SNF. Studies using tissue Doppler imaging or invasive LV pressure measurements have revealed a link between diastolic dysfunction, increased LV filling pressure, and obesity. 

Diabetes mellitus is a powerful RF HF. The prevalence of diabetes among patients with SNFV and patients with SNFV is similar, which indicates the involvement of diabetes in the pathogenesis of both forms of heart failure. Diabetes mellitus predisposes to IHD, impaired renal function and hypertension. Numerous direct effects of diabetes and hyperglycemia on myocardial structure and function have been described. 

Morphological changes in a diabetic heart : CMC hypertrophy, an increase in extracellular matrix (fibrosis) and intramyocardial microangiopathy. Functional changes representing the continuum: endothelium-dependent and endothelium-independent microvascular dysfunction, impaired relaxation and increased passive diastolic stiffness and contractile dysfunction. 

The mechanisms contributing to the structural and functional changes in the CA and myocardium are diverse and include metabolic disturbances, activation of proinflammatory and profibrotic mediators, autonomic cardiac neuropathy, as well as an increase in the number of glycosylation end products that contribute to increased accumulation of collagen and an increase in its stiffness. The accumulation of glycosylation end products may also play a role in the development of age-related cardiovascular rigidity.

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