Features and Outcomes of Methamphetamine-associated Pulmonary Arterial Hypertension

Zamanian, Roham T.; Hedlin, Haley; Greuenwald, Paul; Wilson, David M.; Segal, Joshua I.; Jorden, Michelle; Kudelko, Kristina; Liu, Juliana; Hsi, Andrew; Rupp, Allyson; Sweatt, Andrew J.; Tuder, Rubin M.; Berry, Gerald J.; Rabinovitch, Marlene; Doyle, Ramona L.; Perez, Vinicio de Jesus; Kawut, Steven M.

doi:10.1164/rccm.201705-0943oc

Cited by 91 publications

(85 citation statements)

References 35 publications

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“…Another significant unanswered question is whether stimulants may serve as secondary insults in at‐risk children and young adults with attention deficit disorder, especially given the increased use and growing recognition of amphetamines as a cause of pulmonary hypertension (Zamanian et al . ), though this remains largely untested. The decreased vascular density, vascular remodelling and epigenetic modifications that follow perinatal pulmonary vascular insults likely make these individuals uniquely susceptible to stressors later in life, and future studies should address this potential synergy.…”

Section: Increased Susceptibility To Late Pulmonary Vascular Insultsmentioning

confidence: 99%

Long‐term pulmonary vascular consequences of perinatal insults

Goss

2018

The Journal of Physiology

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Development of the pulmonary circulation is a critical component of fetal lung development, and continues throughout infancy and childhood, marking an extended window of susceptibility to vascular maldevelopment and maladaptation. Perinatal vascular insults may result in abnormal vascular structure or function, including decreased angiogenic signaling and vascular endowment, impaired vasoreactivity through increased pulmonary artery endothelial dysfunction and remodeling, or enhanced genetic susceptibility to pulmonary vascular disease through epigenetic modifications or germline mutations. Although some infants develop early onset pulmonary hypertension, due to the unique adaptive capabilities of the immature host many do not have clinically evident early pulmonary vascular dysfunction. These individuals remain at increased risk for development of late-onset pulmonary hypertension, and may be particularly susceptible to secondary insults. This review will address the role of perinatal vascular insults in the development of late pulmonary vascular dysfunction with an effort to highlight areas of critical research need.

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Section: Increased Susceptibility To Late Pulmonary Vascular Insultsmentioning

confidence: 99%

Long‐term pulmonary vascular consequences of perinatal insults

Goss

2018

The Journal of Physiology

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“…2 A 2017 90-patient prospective cohort study from Stanford University also found a strong association and characterized presentations and prognosis of meth-APAH. 3 The mechanism of meth-APAH is not known, but is presumed due to the similarities in chemical structure between methamphetamine and anorexigens, with both having activity at serotonin receptors. 4 Patients with PH and RV failure have been postulated to have a survival benefit if they have a coexisting PFO.…”

Section: Discussionmentioning

confidence: 99%

PH Grand Rounds: A Successful Case of Extracorporeal Membrane Oxygenation As a Bridge to Recovery

Levine¹,

Jernigan

Mankad

et al. 2018

Advances in Pulmonary Hypertension

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Presentation:A 50-year-old male with no known medical history presented to clinic for one year of progressive dyspnea on exertion. His family later confirmed patient was actively using methamphetamines. He was found to be in respiratory distress and was admitted to a community hospital, where he was intubated for acute hypoxic respiratory failure. Following intubation, he became hemodynamically unstable, required 3 vasopressor infusions, and had ongoing hypoxia with an oxygenation saturation of 88% on maximum ventilator support. Labs were notable for serum drug screen positivity for amphetamines and alcohol. Transthoracic echocardiogram (TTE) was performed and showed dilatation of the right ventricle (RV ), an intra-atrial shunt, and elevated estimated pulmonary arterial (PA) systolic pressures. Our tertiary care center was contacted for extracorporeal membrane oxygenation (ECMO) and transfer for management of pulmonary hypertension (PH) with right heart failure and refractory hypoxia.

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“…The first prospective cohort study conducted to examine the relationship between Meth and PAH was conducted by our group in 2017 (37). We compared the clinical presentation, disease characteristics, and outcomes of patients with Meth-APAH.…”

Section: Methamphetaminementioning

confidence: 99%

“…Two of these patients had RA, one had PA and one had an undiagnosed arthritis. Of the reported cases, pre-capillary PH was confirmed in all patients (mPAP [35][36][37][38][39][40][41][42][43][44][45][46][47][48] and the pulmonary pressures improved in all patients at 2-4 month follow up after discontinuation of drug. Three of the four were found to have improvement in their PA pressures with addition of PAH therapies while one of the RA cases improved with discontinuation of leflunomide and washout with cholestyramine alone (136).…”

Section: Leflunomidementioning

confidence: 99%

Drug- and toxin-induced pulmonary arterial hypertension: Current state of the literature

Ramírez

Thomas

Anderson

et al. 2020

gcsp

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Drug- and toxin-induced pulmonary arterial hypertension (PAH) is an increasingly important sub-group of group 1 pulmonary hypertension (PH). In the last 60 years, we have seen the rise and fall of numerous prescription and illicit agents that have caused severe and deadly outbreaks of PAH. Currently, drugs and toxins are classified into “possible” and “definite” risk factors for PAH. While the exact mechanisms and pathogenesis of drug- and toxin-induced PAH are currently unknown, novel clinical and basic science studies are beginning to unravel the biologic factors and genetic underpinnings responsible for disease development. The clinical management of affected patients can be challenging as it is often difficult to identify patients early and demonstrate causality between drugs and PAH. Given the recent trends in drug utilization and development, it is highly likely that we will continue to identify new agents capable of causing pulmonary vascular disease. We must keep a high index of suspicion in order to identify patients and new compounds deemed definite or likely risk factors for PAH. Practicing pharmacovigilance, raising awareness, and working in tandem with PH patient associations and drug regulatory agencies may ultimately be our most effective strategy in preventing the next deadly outbreak of drug- and toxin-induced PAH.

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Features and Outcomes of Methamphetamine-associated Pulmonary Arterial Hypertension

Abstract: Meth-APAH is a severe and progressive form of PAH with poor outcomes. Future studies should focus on mechanisms of disease and potential therapeutic considerations.

Cited by 91 publications

References 35 publications

Long‐term pulmonary vascular consequences of perinatal insults

Long‐term pulmonary vascular consequences of perinatal insults

PH Grand Rounds: A Successful Case of Extracorporeal Membrane Oxygenation As a Bridge to Recovery

Drug- and toxin-induced pulmonary arterial hypertension: Current state of the literature

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