What's the mechanism by which smoking contributes to heart disease?

Remembering this thread on “safe” cigarettes, and having just seen a broadside at my health club that mentioned smoking as a controllable heart-disease risk factor, I’m curious. How does smoking endanger heart health? Of course I can see how the lung damage might discourage one from physical activity, and that would indirectly lead to heart problems. But I gather there are direct effects too.

Is it the pharmacological action of the nicotine itself, or does it have more to do with the tar or adjunct chemicals?

Smoking increases blood pressure, decreases exercise tolerance and increases the tendency for blood to clot.

Okay, but I think we’re looking for more specific details. Which part or parts of cigarette smoke, for instance, increase blood pressure and how? Which ones have an anti-coagulant effect?

As far as exercise tolerance, I think that might have twigged something in the old noggin. Cigarette smoke has a fairly high concentration of carbon monoxide, IIRC. Monoxide binds to hemoglobin in red blood cells with something like 30 times a stronger bond than oxygen does, and thus reduces the blood’s ability to carry oxygen throughout the body. Without as much oxygen, muscles, and indeed everything in the body, can’t work as well.

I would think this might be a possible link for a habitual smoker to be getting less exercise on a regular basis, which could lead to heart disease. Seems a pretty tenuous connection though, now that I’ve typed it all up. I wonder how long carbon monoxide remains bonded to red blood cells after having a cigarette, compared to a typical smoker’s regular smoking routine?

Smoking has so many effects on the circulation system, has so many chemicals involved and takes years for damage to occur that many of the exact mechanisms are still to be drawn out. It thickens the blood (bad) and constricts vessels (bad). It has large effects on the number of radicals and oxidation levels in cells (bad )
here is one doctors hypothesis

“How can the recognized role of tobacco smoking in the pathogenesis of CAD be explained by the hypothesis of AA oxidopathy? Smoking has well-established procoagulant and coronary vasoconstrictive effects. As discussed earlier, factors directly fan the oxidative coagulative fires within the circulating blood. Cigarette smoke generates an enormous number of free radicals and markedly increases plasma oxidizability. As indicated earlier, both active and passive smoking impair endothelium-dependent arterial dilatation in healthy adults. There is a dose-related inverse relationship between the intensity of passive tobacco smoking and flow-mediated dilatation, indicating direct early arterial damage. Penn et at. reported a dose-dependent size increases of aortic lesions following exposure to 7,12 dimethylbenzene.278
We anticipated, and verified by direct microscopic observations, the ability of tobacco smoke to inflict direct plasma and cell membrane injury. To this purpose, we examined the immediate effects of free radical cascades generated by cigarette smoking on circulating blood in a volunteer who abstained from smoking for a period of 16 hours and then smoked three cigarettes in five minutes…”

lots more at http://www.garynull.com/Documents/AgingHealthfully/AAOxidopathyPart05.htm