ABSTRACT
We present the case of a 72-year-old woman diagnosed with rheumatic fever at the age of 6. In 1972, she was diagnosed with mitral valve insufficiency and mitral valve stenosis, then in 1974, a decision was made to perform mitral valve replacement surgery with a 32-mm Braunwald-Cutter ball cage prosthesis. An echocardiogram performed in 2014 revealed normal biventricular systolic function, mechanical prosthesis in mitral position with maximum speed of 1.9 m/s, maximum gradient of 15 mmHg, mean gradient of 6 mmHg, severe tricuspid valve insufficiency, inferior vena cava measuring 15 mm with more than 50% collapse and pulmonary artery systolic pressure of 40 mmHg. We report the use of the 32-mm Braunwald-Cutter ball cage prosthesis with the longest longevity that remains functional after more than 43 years of implantation.
ABSTRACT
BACKGROUND: Systemic inflammation is characterised by high circulating levels of inflammatory cytokines and increased macrophage infiltration in peripheral tissues. Most importantly, this inflammatory state does not involve damage or loss of function of the infiltrated tissue, which is a distinctive feature of the low-grade systemic inflammation. The term "meta-inflammation" has also been used to refer to the low-grade systemic inflammation due to its strong relationship with the development of cardio-metabolic diseases in obesity. OBJECTIVE: A review is presented on the recent clinical and experimental evidence concerning the role of adipose tissue inflammation as a key mediator of low-grade systemic inflammation. Furthermore, the main molecular mechanisms involved in the inflammatory polarization of macrophages with the ability to infiltrate both the adipose tissue and the vascular endothelium via activation of toll-like receptors by metabolic damage-associated molecular patterns, such as advanced glycation-end products and oxidized lipoproteins, is discussed. Finally, a review is made of the pathogenic mechanisms through which the low-grade systemic inflammation contributes to develop insulin resistance, dyslipidaemia, atherogenesis, type 2 diabetes, and hypertension in obese individuals. CONCLUSIONS: A better understanding of the molecular mechanisms of low-grade systemic inflammation in promoting cardio-metabolic diseases is necessary, in order to further design novel anti-inflammatory therapies that take into consideration clinical data, as well as the circulating levels of cytokines, immune cells, and metabolic damage-associated molecular patterns in each patient.
