The worsening heart failure (HF) epidemic and the associated healthcare costs pose a major burden to public health and the healthcare system.1 Despite significant therapeutic advances, outcomes for patients with HF remain suboptimal.2–4 Importantly, most clinical trials with novel agents in HF during the past decade have yielded neutral or modest results.5 The reasons for these unfavorable trends are complex.6 One issue gaining wide acceptance is that the one-size-fits-all approach to HF therapies is unlikely to be beneficial, especially when new therapies are given on top of comprehensive neurohormonal blockade. Thus, it is crucial for the development of novel therapies to better understand the various HF phenotypes and their pathophysiology and subsequently target relevant pathways in such subgroups of patients. Pulmonary hypertension (PH) is a heterogeneous entity with different causes leading to increased pressures in the pulmonary circulation. PH is a major and frequent consequence of left-sided HF, irrespective of left ventricular ejection fraction (LVEF) or presence of valvular disease.7–9 The presence of PH is associated with worse HF outcomes, regardless of LVEF and stage of HF,7,8 and prognosis is further aggravated when right ventricular (RV) dysfunction ensues, posing a number of diagnostic and therapeutic dilemmas that influence decision making.10,11 A combination of elevated LV filling pressures, reactive pulmonary arterial vasoconstriction, and pulmonary vascular remodeling results in PH secondary to left heart disease.12 Abnormal hemodynamic parameters indicative of PH in HF patients receiving optimal therapy may represent a potential therapeutic target. In this 2-part review, we summarize the current opinions and evidence related to PH in HF. In the first part, we describe the definitions and classification, cause, and epidemiology of PH in HF. In the second part, we discuss its prognostic impact, the …