Does Cigarette Use Modify Blood Pressure Measurement or the Effectiveness of Blood Pressure Medications?

Smoking is the most common cause of avoidable cardiovascular disease worldwide. ¹ The incidence of hypertension is increased in people who smoke 15 or more cigarettes per day. ² The acute and chronic effects of cigarette smoking are worth reviewing, as this may impact the choice of drugs and dosing considerations in the hypertensive population.

The acute effects of smoking on blood pressure (BP) are related to overactivity in the sympathetic nervous system, which results in an increase in myocardial oxygen consumption due to an acute increase in BP, heart rate, and myocardial contractility. ³ Acutely, BP rises transiently within minutes and starts to decrease back to baseline by 15 minutes after smoking a cigarette. ⁴ This transient increase in BP may be most prominent after the first cigarette of the day even in habitual smokers. One study showed an average 20‐mm Hg increase in systolic BP after the first cigarette. ⁴ This effect may be amplified with caffeine use. ⁵

Interestingly, habitual smokers have been shown in some studies to have lower BP than nonsmokers, ⁶ , ⁷ and this appears to be related to decreased body weight. ⁸ A major contributor to the lower BP is likely from cotinine, the major metabolite of nicotine, ⁹ which has some vasodilatory effects. Despite this observation, smoking should be avoided in any hypertensive patient because it can markedly increase the risk of cardiovascular disease and result in the progression of chronic kidney disease. ¹⁰ , ¹¹ Chronic smoking also induces arterial stiffness, which can persist for a decade after smoking cessation, ¹² and this alone is an increased cardiovascular risk factor. Smoking has also been shown to cause a decrease in left ventricular function in asymptomatic individuals. ¹³

A recent prospective study examined factors associated with renal function decline in 53 hypertensive patients whose serum creatinine increased from 1.5 mg/dL to 1.9 mg/dL despite a significant decrease in mean arterial pressure (127–97 mmHg). ¹⁰ Smoking was the most significant independent factor underlying the progression of chronic kidney disease in smokers vs nonsmokers. The mechanism is unclear but may be due to an acute increase in systemic hypertension from smoking resulting in glomerular hypertension.

Cigarette smoking can also affect metabolism of antihypertensive drugs and their efficacy. β‐Blockers in particular have been implicated in being less efficacious when taken by smokers. β‐Blockers have been shown to be less effective for BP and heart rate reductions in smokers compared with nonsmokers in 2 large hypertension trials, as well as being less effective in preventing end‐organ damage in smokers on β‐blockade. ¹⁴ , ¹⁵ To the contrary, however, another trial of primary myocardial infarction prevention in patients with hypertension found no difference in benefit derived from β‐blockers between smokers and nonsmokers. ¹⁶ This interaction may have a pharmacodynamic basis since nicotine causes catecholamine release and an increase in BP and heart rate. There may also be a pharmacokinetic basis for this interaction. The area under the curve of propranolol after a single dose was 50% lower in smokers vs nonsmokers, and its oral clearance was increased by 77% in smokers. ¹⁷ More recent studies have shown that the newer β‐blocker nebivolol, which has vasodilating effects, may have a positive effect on smoking‐induced endothelial dysfunction in smokers as evidenced by an increase in forearm blood flow. ¹⁸

Smoking should be actively discouraged by physicians especially in their hypertensive patients who are already at increased risk for cardiovascular disease. It is important to get an accurate history about smoking in your hypertensive patient, as this may also influence your choice in β‐blocker if prescribed.