In 1999, I was asked by Pfizer to investigate the potential use of sildenafil, commonly known today as Viagra, for indications beyond its initial approval for erectile dysfunction. After conducting thorough research, I discovered studies published by the May and Baker pharmaceutical company that suggested a type 5 phosphodiesterase (PDE5) inhibitor could reduce pulmonary pressure in experimental animals [1-3].

My focus here is to tell the personal and historical story about the discovery and characterization of pulmonary hypertension caused by extreme cold, a condition now recognized as Northern Pulmonary Hypertension (NPH).

Platelets have emerged as immune-inflammatory cells that may contribute to the pathogenesis and prognosis of pulmonary arterial hypertension (PAH), although their clinical relevance remains uncertain.

Acute chest syndrome in sickle cell disease (SCD) carries high morbidity and mortality, with up to 15% of patients requiring invasive mechanical ventilation. However, the rates and mechanisms of ventilator-induced lung injury (VILI) in SCD remain poorly understood.

Access to infant cardiac surgery is inadequate in large parts of the globe. Consequently, there remains a persistent need for decision-making in children and adults with unoperated shunt lesions and varying pulmonary vascular resistance.

In the late 1940s, the US Air Force recorded an unacceptable number of crashes and emergency landings, prompting a formal enquiry. It was resolved that neither the engine nor the pilot was at fault. Attention turned instead to the design of the cockpit, which was based on the ‘average’ airman from 1926.

Pulmonary Hypertension (PH) is a critical disease characterized by increased pulmonary arterial pressure and the development of vascular resistance, which can lead to fatal outcomes if left untreated. Cardiovascular and Respiratory Nurses (CRNs) play a significant role in the management of PH; however, there is a lack of sufficient studies examining their role competence.

Using lung immunohistochemistry and stereology, platelets were found to accumulate and co-localize with leukocytes, particularly monocytes, within the mural and adventitial space of remodeled vessels of patients with pulmonary arterial hypertension. 

Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of pulmonary hypertension that is caused by persistent obstruction of the pulmonary arteries by organized thrombi and associated microvascular disease.

The natural history of late-onset pulmonary arterial hypertension (PAH) with features of venous/capillary involvement and the associations with rare variants in PAH genes are not well known.