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New echocardiographic techniques in the evaluation of left ventricular function in obesity - Di Bello - 2. Obesity. Review. Authors. Vitantonio Di Bello,Corresponding author. Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Department of Cardiac Thoracic and Vascular, University of Pisa, Pisa, Italy. Search for more papers by this author. Iacopo Fabiani,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Lorenzo Conte,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Valentina Barletta,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Maria Grazia Delle Donne,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Cucco Cuono,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Laura Anna Leo,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Frank Lloyd Dini,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Mario Marzilli,Cardiac,Thoracic and Vascular Department, University of Pisa, Pisa, Italy. Search for more papers by this author. Aldo Pinchera,Department of Endocrinology, University of Pisa, Pisa, Italy. Search for more papers by this author. Ferruccio Santini. Department of Endocrinology, University of Pisa, Pisa, Italy. Search for more papers by this author. Full financial disclosures and author notes may be found in the online version of this article. Abstract. Objective: Obesity has reached global epidemic proportions and is associated with numerous comorbidities, including major cardiovascular (CV) diseases. Design and Methods: It has many adverse effects on hemodynamics and CV structure and function: it increases total blood volume and cardiac output, and the cardiac workload is greater. Typically, obese patients have a higher cardiac output but a lower level of total peripheral resistance at any given level of arterial pressure. Most of the increase in cardiac output in obesity is caused by stroke volume, although heart rate typically mildly increases also due to enhanced sympathetic activation. Results: Over the last few years, experimental investigations have unraveled some important pathogenetic mechanisms that may underlie a specific form of “obesity cardiomyopathy.” Bariatric surgery represents an effective alternative to treat obesity when nonsurgical weight loss programs (diet + behavior modifications + regular exercise) have failed. A great numbers of questions are still open in the global comprehension of the pathophysiological interactions between obesity and heart. Conclusion: Conventional two- dimensional Doppler echocardiography, integrated by relative new technological ultrasonic approaches, represents the reference technique to study and possibly clarify both the very complex hemodynamic changes induced by obesity and those relative to obesity treatment. Introduction. Obesity is one of the most prevalent diseases today to be considered almost an epidemic problem among industrialized countries and those undergoing technological change. The incidence rates are in fact growing rapidly and reach even 7. Severe obesity . Recent evidence indicates that obesity is associated with more morbidity than smoking, alcoholism and poverty, and, according to currents trends, will account for over 3. U. S (4- 6). Overweight and obese in Italy are about 3. International Obesity Task Force (7, 8). Obesity is associated to hypertension and also it adversely effects plasma lipids, increasing triglycerides, and decreasing the high- density lipoprotein cholesterol, and is the major contributor to adult- onset diabetes mellitus and insulin resistance syndrome (so called metabolic syndrome) (9). Pathogenesis of Left Ventricular Dysfunction in Obesity. Obesity has been linked to a spectrum of cardiovascular (CV) changes ranging from a hyper dynamic circulation, through subclinical cardiac structural changes, to overt heart failure (1. Obesity induces several modifications in cardiac structure and function because of hemodynamic overload and represents a risk factor for heart failure (1. Adipose tissue is a metabolically active compartment, which requires 2- 3 m. L/min/1. 00 g of blood and constitutes an important blood reserve. There is indeed a correlation between metabolism of adipocytes and blood flow. With the accumulation of adipose tissue, blood flow at that level also increases (in patients with severe obesity it can reach half the cardiac output at rest) and blood volume expands in order to compensate the increased oxygen demand. The expansion of blood volume results in a dilation of left ventricle (LV) and is accompanied by an eccentric hypertrophy of the myocardium even in normotensive subjects (ventricular cavity/ventricular diameter ratio remains almost unchanged). Both eccentric and concentric patterns of left ventricular hypertrophy (LVH) have been described in overweight people, even if the former is more common. This mechanism represents a form of initial adjustment, which cannot compensate the hemodynamic overload for a long period of time. This is the reason why atrial and ventricular remodeling is common in obese patients, such as a result of atrial and ventricular dysfunction. The larger atrial size is related both to an expanded intravascular volume and to the altered left filling properties. In addition to the increased preload, LV afterload is elevated because of higher vascular resistances caused by excess adipose tissue and greater conduit artery stiffness. BMI is related to impaired diastolic functional indices. Diastolic dysfunction, combined with the systolic dysfunction, may progress resulting in congestive heart failure (CHF). In humans and animal models, the development of obesity leads not only to increased deposits of fat in the adipose tissue, but also to the accumulation of significant quantities of lipids in other organs and districts. Fatty deposits can damage the function of organs and tissue with different mechanisms (1. Lipid accumulation in “non- fat” cells, resulting in dysfunction at cellular level with consequent lipotoxicity (low mitochondrial oxidative capacity, increased lipolysis) (1. Over the last few years, experimental investigations have unraveled some important pathogenetic mechanisms, such as cardiac steatosis, lipoapoptosis, and the activation of specific cardiac genes that may underlie a specific form of “obesity cardiomyopathy.” It should be emphasized that previously endocrine mechanisms have been mainly demonstrated in experimental studies, so their applicability in humans needs further appropriate studies. All the complex structural and functional alterations that were found in severely obese patients (increased left ventricular mass (LVM), increased interstitial collagen content, LV, and left atrium (LA) dilatation, alterations of systolic and diastolic intramyocardial function), confirmed by different studies (1. Furthermore, insulin resistance is an independent risk factor for CV disease and type 2 diabetes mellitus; hypertension, dyslipidemia, and obesity are often found in association with insulin resistance (1. A recent epidemiological study has demonstrated that insulin resistance could be a link between obesity and CHF. Insulin resistance, by an increase of circulating insulin, is capable of stimulating IGF- 1 receptors, which are probably implicated also in the pathogenesis of myocardial hypertrophy observed in patients with obesity. Insulin may act as a growth factor in the myocardium and hyperinsulinemia leads to increased LVM in rats. Hyperinsulinemia may lead to sodium retention that could cause a subclinical myocardial dysfunction as a result of volume expansion. Hyperinsulinemia may lead to sympathetic nervous system activation. Insulin resistance is related to an increased pressure response to angiotensin- II, which stimulates LVH and interstitial fibrosis (2. II levels that favors myocardial tissue proliferation and stimulates cardiac fibrosis interacting with aldosterone). As described above, in these recent years, the physiopathological models of heart remodeling in obesity have been changing, according to progressive knowledge. In particular, from the traditional hemodynamic model (2. Ultimately, the explanation of cardiac remodeling in obesity as the result of stroke volume enhancement given by increased preload condition determining left ventricular dilation and hypertrophy (eccentric type) (hemodynamic model) has progressed toward the consideration of the complex local action of epicardial fat and the interaction of hypertension, impaired glucose metabolism, and diabetes (local and systemic metabolic effects) (2. The integration between hemodynamic and metabolic models explains in part some different geometric patterns (see concentric hypertrophy) due to the action of leptin on myocardial hypertrophy (2. In this field of research, MRI has been useful for a better definition of left and right volumes and masses and then for a better comprehension of heart remodeling in obese patients (2. In fact, MRI as well as having a high degree of precision in the measure of heart LV and right ventricular (RV) chambers volumes, mass and function, is practically the unique methodological approach for analyzing the new mechanisms, in obesity physiopathology, interfering with heart function (such as aortic stiffness, fatty infiltration of the heart (epicardial), and fat diffusion in whole body (2. Echocardiographic Techniques. To study the physiopathological hemodynamic changes linked to obesity, through the years, different ultrasonic techniques have been used and those relatively new have supported conventional ones. Conventional two- dimensional (2.
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