Heart failure is a complex clinical syndrome that results from any functional or structural heart disorder, impairing ventricular filling or ejection of blood to the systemic circulation to meet the systemic needs. Heart failure can be caused by diseases of the endocardium, myocardium, pericardium, heart valves, vessels or metabolic disorders. Most patients with Heart failure have symptoms due to impaired left ventricular myocardial function. Patients usually present with symptoms of dyspnea, decreased exercise tolerance and fluid retention, characterized by pulmonary and peripheral edema. Heart failure due to left ventricular dysfunction is categorized according to left ventricular ejection fraction (LVEF) into heart failure with reduced ejection fraction (usually considered LVEF 40% or less), known as HFrEF and heart failure with preserved ejection fraction; known as HFpEF. The definition of HFrEF has varied among different studies and guidelines with different left ventricular ejection fraction (LVEF) cut-offs of ≤35%, < 40%, and ≤40%. Randomized controlled trials in patients with HF have mainly enrolled patients with HFrEF with an EF ≤35% or ≤40%, and it is only in these patients that efficacious therapies have been demonstrated to date. According to the most recent ACC/AHA guidelines on heart failure, HFrEF is defined as the clinical diagnosis of HF with EF ≤40%. In routine clinical practice, many clinicians would consider EF < 45% as significant systolic dysfunction and would consider it as HFrEF. Heart failure with preserved ejection fraction (HFpEF) on the other hand has also been variably classified as EF >40%, >45%, >50%, and/or ≥55%. The term HFpEF has been used since some of these patients do not have entirely normal EF but also do not have a major reduction in the systolic function. Patients with an EF between the range of 40% to 50% have been considered to represent an intermediate group of patients due to a variable cut off used for systolic dysfunction by the different studies. These patients should be routinely treated for underlying risk factors and comorbidities and with optimal guideline-directed therapy, similar to that of HFrEF. When heart failure develops, compensatory mechanisms attempt to increase the cardiac filling pressure, muscle mass and heart rate. However, in many cases, there is usually a progressive decline in heart function.