Cocaine Use and Pulmonary Hypertension

Abstract

Evidence linking cocaine to the risk of pulmonary hypertension (PH) is limited and inconsistent. We examined whether cocaine use, in the absence of other known causes of PH, was associated with elevated systolic pulmonary artery pressure (sPAP) and increased probability of PH. We compared patients with documented cocaine use to a randomly selected age, sex, and race-matched control group without history of cocaine use. All participants had no known causes of PH and underwent echocardiography for noninvasive estimation of sPAP. We used routinely reported echocardiographic parameters and contemporary guidelines to grade the probability of PH. In 88 patients with documented cocaine use (mean age ± standard deviation 51.7 ± 9.5 years), 33% were women and 89% were of Black race. The commonest route of cocaine use was smoking (74%). Cocaine users compared with the control group had significantly higher sPAP (mean ± standard deviation, 30.1 ± 13.1 vs 22.0 ± 9.8 mm Hg, p <0.001) and greater likelihood of PH (25% vs 10%, p = 0.012). In multivariable analyses adjusted for potential confounders including left ventricular diastolic dysfunction, cocaine use conferred a fivefold greater odds of echocardiographic PH (p = 0.006). Additionally, a stepwise increase in the likelihood of PH was noted across cocaine users with negative or no drug screen on the day of echocardiography to cocaine users with a positive drug screen (multivariable p for trend = 0.008). In conclusion, cocaine use was associated with a higher sPAP and an increased likelihood of echocardiographic PH with a probable acute-on-chronic effect.

Figure 1.

Cocaine use and pulmonary hypertension. The diagram shows routes of cocaine use (smoking, snorting, ingesting, and intravenous) using proportional Venn diagram, distribution of systolic pulmonary artery pressure using histogram, normal Gaussian curve and Kernel density curve, and probability of pulmonary hypertension (low, intermediate, and high) using pie chart in the control group (upper panel) and the cocaine group (lower panel). N denotes number of participants.

Figure 2.

Distribution of systolic pulmonary artery pressure among cocaine users and control group participants. The diagram shows mean (diamond-shaped marker inside the box), median (line inside the box), interquartile range (bottom and top edges of the box), 1.5 times interquartile range (whiskers extending from each box), and outliers (circle-shaped markers outside the box). N denotes number of participants. *Adjusted p value was derived using multivariable linear regression analyses adjusted for age, body-mass index, current or past cigarette smoking, current or past marijuana use, left ventricular diastolic dysfunction, atrial fibrillation, and coronary artery disease.