A 59-year-old man was diagnosed with pulmonary arterial hypertension (PAH) after presenting with progressive dyspnoea on exertion and a history of anorexigen use. Right heart catheterization confirmed a mean pulmonary arterial pressure (mPAP) of 35 mmHg, a pulmonary capillary wedge pressure (PCWP) of 6 mmHg, a cardiac output of 6.27 L/min, and a pulmonary vascular resistance (PVR) of 4.9 Wood units. Ventilation–perfusion scanning demonstrated bilateral segmental perfusion defects; however, pulmonary angiography excluded chronic thromboembolic pulmonary hypertension and was consistent with small-vessel PAH. Vasoreactivity testing with inhaled nitric oxide was negative. At diagnosis, he was classified as New York Heart Association (NYHA) Functional Class III. He was initiated on combination therapy with bosentan 125 mg twice daily and sildenafil 40 mg three times daily. Following treatment, the patient demonstrated sustained clinical and hemodynamic improvement, with mPAP decreasing to 22 mmHg, PVR to 3.1 Wood units, and improvement to NYHA Functional Class II. At routine follow-up, he remained clinically stable, with a six-minute walk distance (6MWD) of 547 m. However, a change in insurance coverage prevented continued access to high-dose sildenafil while bosentan therapy was maintained. As concomitant use of phosphodiesterase-5 inhibitors (PDE-5is) and soluble guanylate cyclase (sGC) stimulators is contraindicated, an alternative treatment strategy was required to maintain nitric oxide pathway modulation.