Smokers paradox
Fonarow et al. have explored the ‘smoker’s paradox’ in a novel inception cohort of hospitalized heart failure patients included in the OPTIMIZE-HF registry, by determining the impact of current or recent smoking on outcomes during hospitalization and in the first 60–90 day period following hospital discharge.
Adjustments for known important potential confounders were performed. Smokers were more likely to have left ventricular systolic dysfunction (59 vs. 51%), were more likely to be male (61 vs. 46%), and had higher B-type natriuretic peptide (BNP) levels (895 vs. 789 pg/mL). However, smokers were much younger (63 vs. 75 years of age), were less likely to have a previous history of heart failure admission (84 vs. 89%), and were less likely to have a diagnosis of diabetes requiring insulin therapy (14 vs. 17%). Despite this, when compared with non-smokers, the risk of in-hospital mortality was ∼30% lower for current or recent smokers, while the risk for re-hospitalization or post-discharge mortality was similar between the two groups.
How could this be? Assuming the authors appropriately assembled an inception cohort, correctly classified smokers, and appropriately adjusted for important potential confounders, only one of two conclusions can be drawn: either smoking is somehow ‘protective’ in heart failure patients; or a substantial component of the adverse effects of smoking in heart failure is reversible and has a short half-life (i.e. days) so that ‘enforced’ in-hospital smoking cessation led to an imbalance of beneficial therapies in the smokers (usual therapy plus smoking cessation) compared with their non-smoking cohorts (usual therapies only). The former hypothesis (that smoking is protective) can probably be refuted immediately. There is overwhelming evidence that smoking increases the incidence of heart failure, as well as heart failure morbidity and mortality (including sudden death) for those who have heart failure.
It can be argued that there is substantially more merit in the second argument. Constituents of inhaled tobacco damage the cardiovascular system in numerous ways: producing endothelial and platelet dysfunction; enhancing coagulation; increasing heart rate and blood pressure; increasing myocardial oxygen demand and consumption; and inducing vasoconstriction. Cigarette smoking also significantly increases carboxyhaemoglobin production, impairing oxygen carriage and release, which has a negative inotropic effect, increasing left ventricular end-diastolic pressure. Thus the abrupt removal of these deleterious effects of cigarette smoking following hospital admission and enforced smoking cessation, in addition to the provision of the usual heart failure therapies in smokers, might well be expected to ‘outstrip’ the impact of usual therapies alone in non-smokers.