The Source for Neurovascular News and Education

October 18, 2019

 

Although cigarette smokers tend to have SAH at a younger age and to be sicker overall than nonsmokers, they conversely show superior outcomes after their events.

 

Data from the Nationwide Inpatient Sample lend support to the idea of a “smoker’s paradox” among patients who experience aneurysmal subarachnoid hemorrhage (SAH), researchers recently reported online in the Journal of Neurosurgery.

Among a nearly 6,000-patient cohort treated with endovascular or microsurgical repair for ruptured cerebral aneurysm, smokers held an advantage over nonsmokers for a number of measures, including the likelihood of being discharged home and the odds of needing tracheostomy or gastrostomy placement. Yet the numbers also showed the harms of tobacco, in that smokers who developed SAH were younger and had more comorbidities compared with nonsmokers.

“While smoking is a potent risk factor for SAH, the impact of smoking on the outcomes following rupture of cerebral aneurysms is poorly understood,” write Hormuzdiyar H. Dasenbrock, MD, MPH (Brigham and Women’s Hospital, Boston, MA), and colleagues. Some studies have even hinted that nicotine replacement therapy can boost outcomes among smokers who experience SAH, suggesting a neuroprotective effect.

Dasenbrock, along with senior author Rose Du, MD, PhD (Brigham and Women’s Hospital), and colleagues had initially hypothesized that since smoking is linked to higher odds of delayed cerebral ischemia it would lead to higher mortality and worse outcomes.

To test that idea, they looked at 5,784 patients admitted for the treatment of ruptured cerebral aneurysm between 2009 and 2011. Around one-third (37.1%) were tobacco users, with most being current users. Compared with nonsmokers, smokers were younger on average (mean age 51.4 vs 56.2 years) and had more comorbidities, including hypertension, diabetes, chronic pulmonary disease, and others.

Mortality, total complications, and neurological complications did not differ by smoking status. Yet smokers were less likely to need tracheostomy or gastrostomy placement, to be discharged to institutional care, or to have a poor outcome (NIS SOM; a composite measure that accounted for the previous two factors as well as in-hospital mortality). Notably, these associations remained present even after adjustment for treatment modality.

Smokers vs Nonsmokers Treated for Aneurysmal SAH

 

Adjusted OR

95% CI

Tracheostomy or Gastrostomy Placement

0.63

0.51-0.78

Discharge to Institutional Care

0.71

0.57-0.89

Poor Outcome

0.65

0.55-0.77

 

“Because cigarette smoke is a mixture of more than 4,000 chemicals, the exact mechanisms by which smoking promotes cerebral aneurysm formation remain largely unknown,” the researchers acknowledge, also conceding that the reason for a smoker’s paradox is not clear.

“These data, along with two recent studies showing that nicotine replacement therapy among smokers who sustain SAH was associated with superior outcomes, suggests that further research, including prospective studies, are needed to confirm these findings and further elucidate the underlying pathophysiology,” they conclude.

 

Not Yet Enough to Spur Action

In an editorial accompanying the paper, Kevin M. Cockroft, MD, MSc (Penn State Hershey Medical Center, Hershey, PA), praises the researchers for making a strong effort to overcome the inherent limitations of an analysis based on administrative data.

“The result is a robust, well-made case for a better outcome among smokers with aneurysmal SAH compared with nonsmokers,” he writes. “This is certainly a provocative and some might say paradoxical finding, but before we start encouraging all of our patients with aneurysms to take up smoking, there are some additional issues worth considering.”

Among the factors clouding interpretation is the fact that the smokers included here are a diverse group with varying lengths and types of tobacco and/or nicotine use. Moreover, Cockroft adds, though extensive adjustments were made, other potential biases might stem from alcohol use, nicotine replacement, body mass index, and physical activity level.

There also is no information on long-term outcome, he notes, asking, “Will smoking hamper long-term brain recovery or will the comorbidities associated with smoking lead to other complications that impact long-term functional status?”

Thus, the message for clinicians is uncertain, Cockcroft concludes. Nor, he adds, are the findings sufficient at this point to justify a randomized controlled trial, though confirmatory data from other studies may “help better frame the questions and design requirements” for such a project.

 


 

Sources:

  • Dashnbrock HH, Rudy RF, Lai PMR, et al. Cigarette smoking and outcomes after aneurysmal subarachnoid hemorrhage: a nationwide analysis. J Neurosurg. 2017;Epub ahead of print.
  • Cockroft KM. A smoker’s paradox: does being a smoker really lead to a better outcome after aneurysmal SAH? J Neurosurg. 2017;Epub ahead of print.

 

Disclosures:

Dasenbrock, Du, and Cockroft report no relevant conflicts of interest.