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Acute coronary vasoconstrictive effects of cigarette smoking in coronary heart disease
Insights
Cigarette smoking acutely impairs the coronary vasculature's ability to increase blood flow when the heart needs more oxygen, even in patients with coronary artery disease. This reduces myocardial oxygen delivery.
Area of Science:
- Cardiology
- Vascular Physiology
Background:
- Coronary artery disease (CAD) affects blood flow to the heart muscle.
- The impact of acute cigarette smoking on coronary vascular regulation in CAD patients is not fully understood.
Purpose of the Study:
- To investigate the acute effects of cigarette smoking on coronary sinus flow and myocardial oxygen delivery in patients with CAD.
Main Methods:
- Measurements of coronary sinus flow and myocardial oxygen delivery were taken at rest and during atrial pacing.
- These measurements were repeated after patients smoked two high-nicotine cigarettes.
Main Results:
- Smoking increased heart rate and double product but did not significantly alter coronary sinus flow at rest.
- During pacing, smoking reduced coronary sinus flow and increased coronary vascular resistance at comparable double products.
- Myocardial oxygen delivery decreased proportionally to the reduction in coronary sinus flow.
Conclusions:
- Acute cigarette smoking impairs the coronary vasculature's ability to regulate blood flow in response to increased myocardial oxygen demand.
- This suggests a detrimental effect of smoking on oxygen supply to the heart muscle in CAD patients.
Abstract:
To investigate the effect of cigarette smoking on the coronary vasculature, coronary sinus flow and myocardial oxygen delivery were measured at rest and during incremental atrial pacing in 10 patients with coronary artery disease. Measurements were then repeated while the patients smoked 2 unfiltered, high-nicotine cigarettes. Although smoking significantly increased the heart rate at rest and double product, coronary sinus flow did not change significantly (141 +/- 32 vs 146 +/- 28 ml/min). At the lowest equivalent pacing rate before and during smoking, the double products were comparable. However, coronary sinus flow was reduced by smoking (146 +/- 28 vs 159 +/- 28 ml/min, p less than 0.01) and coronary vascular resistance was increased (0.96 +/- 0.15 vs 0.83 +/- 0.13 mm Hg ml-1 min, p less than 0.02). The double products were also comparable at the peak pacing rate before and during smoking. Nonetheless, the coronary sinus flow was again lower (167 +/- 23 vs 227 +/- 41 ml/min, p = 0.02) and the coronary vascular resistance was higher (0.77 +/- 0.10 vs 0.63 +/- 0.09 mm Hg ml-1 min, p less than 0.01) during smoking. The transmyocardial arteriovenous oxygen difference was unchanged by smoking; therefore, myocardial oxygen delivery was reduced in proportion to the reductions in coronary sinus flow. Thus, cigarette smoking appears to acutely alter the ability of the coronary vasculature to regulate flow in accordance with the oxygen requirements of the myocardium.