Chapters authored
Genetic Polymorphisms and Ischemic Heart Disease
Although the progression in diagnostic tools, prevention strategies, and therapies, ischemic heart disease still represents the major cause of mortality and morbidity worldwide that globally represents an important problem for individuals and healthcare resources. By convention, ischemic heart disease is associated with the presence of an atherosclerotic plaque that is able to limit the flow in large-medium-sized coronary arteries. Nevertheless, several findings suggest a more complex pathophysiology of ischemic heart disease. At this time, there is no well-defined assessment of myocardial ischemia pathophysiology. Moreover, several data have identified genetic variations at different loci that are linked with ischemic heart disease susceptibility. This chapter aims to examine this complicated disease and to review the evidence on the genetic heritability acting with other factors in determining the presence of ischemic heart disease, due to either an obstruction in epicardial vessels or a dysfunction of coronary microcirculation.
Part of the book: Genetic Polymorphisms
Heart Failure and Iron Deficiency
Heart failure (HF) is a major public health problem because it is one of the most common causes of morbidity and mortality in Western countries, with a prevalence of 1–2% in the adult population, rising to ≥10% in those age >70 years. In addition to the “classic” co-morbidities, such as COPD, arterial hypertension, diabetes, renal failure, etc., there are other conditions frequently found in patients with heart failure that many times are underestimated. One example are anemia and iron deficiency (ID). ID, regardless of anemia impair exercise tolerance, symptoms and quality of life, with a strong negative prognostic impact on hospitalization and mortality rate. Despite strong evidence of high prevalence of ID in these patients and current guidelines recommendations, the diagnosis of ID and its monitoring over time still have low priority for physicians in clinical practice. Consequently ID is under-treated; furthermore current therapies, in particular i.v. iron as ferric carboxymaltose, though effective, turn out to be poorly managed by clinicians. ID should be considered more in real world HF healthcare settings to improve patients’ quality of life and outcome.
Part of the book: Iron Deficiency Anemia