For the sake of argument, let us assume that researchers at the CDC are correct and that a brief exposure to secondhand smoke, such as that experienced in a restaurant, can trigger a heart attack in someone who has severe, pre-existing coronary artery disease. Without even getting into the issue of how the CDC’s and Surgeon General’s statements (as well as those of hundreds of anti-smoking groups) fail to qualify their claims by making it clear that they apply only to those who severe coronary artery stenosis to begin with, let’s give them the benefit of the doubt for now and analyze the significance of the stipulated fact: a brief encounter with secondhand smoke can cause someone with severe coronary disease to suffer a heart attack by increasing the coagulation (clotting) potential of the blood platelets and causing endothelial dysfunction.
Anti-smoking researchers are touting studies like those in Helena, Pueblo and elsewhere – which they claim demonstrate a dramatic and immediate reduction in heart attacks caused by workplace/restaurant/bar smoking bans – as supporting the scientific claim that brief secondhand smoke exposure triggers a substantial number of heart attacks. The thinking is that if brief secondhand smoke exposure is triggering lots of heart attacks and that exposure is eliminated, then those heart attacks will be prevented.
The Rest of the Story
I think it is important to point out the flaw in this logic. First, readers should understand that in order for a brief tobacco smoke exposure to cause a heart attack, an individual must already have severe, pre-existing coronary artery stenosis. The coronary arteries do not go from completely patent (open) to closed off in a matter of minutes. However, if they are already severely compromised (say, more than 90% blocked), then it is possible that a small decrease in the artery diameter – such as that induced by formation of a clot on an existing plaque – could trigger a heart attack.
Second, readers should understand that there are a large number of acute “exposures” that can increase the coagulability of the blood and compromise endothelial function, thus potentially triggering a heart attack in someone with severe coronary artery narrowing. For example, eating a high-fat meal has been shown to cause endothelial dysfunction and to increase the stickiness of platelets to the same extent as secondhand smoke.
Importantly, even “exposures” such as stress can have the same effect. Researchers shows that stress – even the kind of mental stress induced by having an individual solve a difficult math problem – can cause the same kind of changes to the coronary circulation and the aggregation potential of platelets that acute exposure to secondhand smoke causes.
Third, it is important to note that the body does not know what is causing increased stickiness of blood platelets or endothelial dysfunction when it is occurring. In other words, there is nothing qualitatively different between changes induced by tobacco smoke exposure versus the same type of changes induced by stress or by eating a high-fat meal. There is nothing unique about the tobacco smoke exposure that distinguishes its effects from those precipitated by these other exposures.
Putting all of this together, the critical point is that someone who is at risk of having a heart attack triggered by a brief exposure to secondhand smoke has such brittle coronary artery disease that they are basically a heart attack waiting to happen. It is only a matter of time before some exposure puts them over the edge and triggers an inability of the coronary arteries to keep up with the oxygen demands of the heart and for a heart attack to therefore occur.
If the person is not exposed to tobacco smoke in a restaurant on Tuesday, who is to say that he or she will not eat a high-fat meal and have the final step of the heart attack pathway take place on Wednesday? Someone in such a brittle situation can simply not go around for a long time without experiencing cardiac ischemia. If they are so close to a heart attack that a 20-minute exposure to secondhand smoke could trigger such an attack by causing an increase in platelet aggregation, then the same degree of platelet aggregation caused by an acute stressful event is also going to trigger that heart attack.
The point is this: in such an individual, you cannot prevent a heart attack by eliminating all exposures that might increase the clotting ability of the blood or hamper endothelial function. Clinically, that would be be a crazy approach (and in fact would represent medical malpractice).
In such a situation, there are only two approaches that work. One is to prevent exposures from increasing the blood's clotting ability through medications such as aspirin (there are some other pharmaceutical approaches as well). The second is to repair the coronary artery stenosis through angioplasty or bypass surgery.
Any patient who has coronary artery stenosis so severe that a single acute exposure to secondhand smoke will trigger a heart attack needs to have a definitive procedure - such as angioplasty or coronary artery bypass surgery - immediately. You are simply not going to prevent a heart attack in that person by having them avoid secondhand smoke exposure. Something else is going to trigger that heart attack, and probably in short order. After all, the person cannot stop eating. She cannot eliminate all mental stress.
For this reason, it is implausible that reducing secondhand smoke exposure could result in a rapid 41% decline in heart attacks by eliminating cases of heart attacks triggered by acute secondhand smoke exposure in restaurants.
Let me say, also, that even if tobacco smoke were the sole trigger for heart attacks, the effects of eliminating exposure in restaurants alone is just not significant enough to explain a 41% reduction in heart attacks. But the reality is that tobacco smoke is just one of many potential triggers and even if occasionally tobacco smoke serves as a trigger, it is just not plausible that banning smoking in restaurants will substantially decrease heart attacks by putting an end to a common trigger for such attacks. They will simply be triggered by some other exposure.
I don't think the researchers who are using the studies of the Helena ilk to support the claim that brief exposures to secondhand smoke trigger heart attacks have thought this out to any extent.
By the way, if what these researchers are claiming is true, then it would actually be reasonable for a physician to tell a patient with severe coronary artery stenosis that he should simply avoid going to restaurants or other settings where there is smoking taking place. But such advice, we know, would be malpractice. If the patient's disease is that brittle, he is a heart attack waiting to happen and he needs definitive surgical intervention, probably with pharmaceutical intervention as well.
So even if we accept the claim that brief exposure to secondhand smoke is a common trigger for heart attacks among people with severe coronary artery stenosis, this would still not result in restaurant smoking bans causing any substantial decline in heart attacks in the short-term.
Note that smoking bans would still be expected to reduce heart attacks in the long-term, because over many years, the incidence of coronary artery disease would be reduced. But to posit that a heart attack decline on the order of 20% in one year or 40% in three years will occur in response to banning smoking in restaurants is simply implausible.
Finally, I would add that if it were true that exposure to tobacco smoke in restaurants was a common cause of heart attacks, would we not expect to occasionally observe someone in a restaurant keeling over from a heart attack? I've stipulated here, for the sake of argument, that the anti-smoking researchers' claim is true, but let's remember that it is merely a hypothetical or theoretical concern. There's no actual evidence that this is the case.