Biomarkers in heart failure

Abstract

Nowadays, heart failure (HF) has an increasing prevalence, particularly in the elderly, and is becoming a clinical problem of epidemic proportion in terms of morbidity and mortality. Developing biological markers, that can aid in the diagnosis of HF and in the differentiation of congestive heart failure (CHF) from other causes of dyspnoea, will reduce the cost of health care. However, an ideal biomarker has not yet been identified. Potential markers of HF include neuro-hormonal mediators, markers of myocyte injury, and indicators of systemic inflammation. Among these, the BNP and NT-pro-BNP are the most widely studied and appear to be useful in patients with dyspnoea of unknown aetiology, and for risk assessment of patients with established HF. However these markers should be used as an addition tool, and not as a substitute of clinical assessment.

The Role of Statins in Preventing the Progression of Congestive Heart Failure in Patients with Metabolic Syndrome

“…It's caused primarily by coronary or ischemic heart disease and it is characterized by a specific echocardiographic criterion that is the reduction of ejection fraction lower than 30% [5,6]. Less frequent causes, but not less important, are arterial hypertension, valve diseases, and cardiomyopathies (hypertrophic, dilated and restrictive forms) [2][3][4][5][6][7]. Diastolic dysfunction is an abnormality in the left ventricular (LV) myocardial relaxation and/or compliance thanks to which blood flows into the left ventricle during diastole [8][9][10][11][12][13][14][15]; it's seen in one third of patients, it is commonly caused by hypertension, hypertrophic or infiltrative diseases and possibly diabetes.…”

“…Systolic ventricular dysfunction is the most frequent form of loss of compliance because it is diagnosed in two thirds of patients. It's caused primarily by coronary or ischemic heart disease and it is characterized by a specific echocardiographic criterion that is the reduction of ejection fraction lower than 30% [5,6]. Less frequent causes, but not less important, are arterial hypertension, valve diseases, and cardiomyopathies (hypertrophic, dilated and restrictive forms) [2][3][4][5][6][7].…”

“…Which types of mechanisms could explain the link existing between these two diseases is not clear despite many trials, creates interesting hypothesis and provides several interpretations, but very little clinical evidence exists even if it is true that their physiopathology is too complex to relate them without discussions. Throughout the ages, MetS was proposed as an "emerging factor" of different pathological conditions related with left ventricular systolic and diastolic dysfunctions and it is also possible to assert that its determinants, referring to NCEP ATP III [3][4][5][6][7] definition, are more frequent in patients with HF and can be considered as HF independent predictors even in patients without a history of ischemic disease. Several important definitions of the metabolic syndrome have been proposed.…”

“…Current data suggests that the coexistence of the main pathogenetic HF determinants in the same individual considerably increases the possibility of developing the disease. Several scientific trials have demonstrated an important relation between HF and Metabolic Syndrome diagnosis and moreover it has been proved that single risk factors of ventricular dysfunction like hypertension, obesity or diabetes mellitus are independently associated with an increased risk of heart failure, regardless of coronary heart disease [3][4][5][6]. Which types of mechanisms could explain the link existing between these two diseases is not clear despite many trials, creates interesting hypothesis and provides several interpretations, but very little clinical evidence exists even if it is true that their physiopathology is too complex to relate them without discussions.…”

“…Compensatory mechanisms are both a mechanical phenomenon and neurohormonal processes activation. The transformation of ventricular geometry resulting from an increased end-diastolic pressure is subsequent to impaired systolic or diastolic function (loss of myocytes, extracellular matrix alterations, spherical morphology, vessel wall remodeling, mitral valve insufficiency) while the major neurohormonal systems that are activated are the renin-angiotensin system, the sympathetic nervous system, endothelin pathway, natriuretic peptides, and tissue necrosis factor [4][5][6][7][8][9][10][11][12][13][14][15].…”