Pulmonary arterial hypertension (PAH) is a progressive and life-threatening disease characterized by irreversible pulmonary vascular remodeling, ultimately leading to right heart failure, hemodynamic instability, and death. Although numerous risk factors for the development of PAH have been described, methamphetamine-associated PAH (MA-PAH) has gained increasing recognition in recent years. Emerging data suggest significant differences in functional class, morbidity, and mortality in patients with MA-PAH compared to other forms of the disease, necessitating a reconsideration of risk stratification approaches in this cohort [1].

Methamphetamine is a highly addictive psychostimulant whose prevalence in the United States has increased dramatically, with an overall increase of 43% from 2015 to 2019, while non-drug (non-injection) use increased by 105% over the same period [2]. Only recently has methamphetamine been recognized as an independent risk factor for the development of PAH. Studies have shown that stimulant use is ten times more common among patients with idiopathic PAH (I-PAH) compared to patients with other established risk factors [3,4]. The pathophysiological mechanisms by which methamphetamine induces PAH remain incompletely understood. Proposed mechanisms include direct toxic injury to the pulmonary vascular wall, oxidative stress, dysregulation of the pulmonary vasodilator-to-vasoconstrictor ratio, and decreased activity of carboxylesterase 1 (CES1), an enzyme involved in drug and xenobiotic metabolism [5-7].

Retrospective analyses convincingly demonstrate that patients with I-PAH have a more severe functional class and a worse prognosis compared to other types of precapillary pulmonary hypertension. In a study by Charoenpong et al. involving 1830 patients from the PAH Biobank, mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) were higher in individuals with MA-PAH than in patients with PAH associated with connective tissue diseases (although no significant differences were observed from I-PAH) [8]. Data from the Pulmonary Hypertension Association Registry revealed that patients with MA-PAH have a lower cardiac index and a higher hospitalization rate than patients with I-PAH, while their functional status is generally worse [9]. A prospective cohort study conducted at the Stanford University Pulmonary Hypertension Program showed that patients with MA-PAH suffer from more severe heart failure symptoms compared to patients with I-PAH [1]. Moreover, Ramirez et al. presented evidence that, despite ongoing therapy, patients with MA-PAH have a lower 5-year survival rate, as well as worse functional status and exercise tolerance [10].

Echocardiography is an integral non-invasive screening method for pulmonary hypertension and is widely used to assess prognosis and monitor the effectiveness of therapy in PAH [11]. Numerous studies have confirmed the prognostic significance of right atrial (RA) mechanics, including RA ejection fraction, RA emptying fraction, RA size, and right ventricular outflow tract velocity integral, in determining the prognosis of pulmonary hypertension [12-14]. In recent years, the role of right atrial and right ventricular strain has been actively studied using speckle-tracking echocardiography for risk stratification and disease prognosis [15,16]. Echocardiographic gating allows one to assess the degree of myocardial deformation during contraction and provides unique information about subclinical myocardial dysfunction, which is not detected by standard