Why don't stents prevent heart attack?



No study has ever documented that stents prevent future heart attack. But, in day-to-day practice, stents are frequently implanted for just this reason.

A little clarification. Stents do prevent heart attack--if the heart attack is already underway, either as an "acute myocardial infarction" or "unstable angina."

In other words, a plaque in a coronary artery can rupture just like a little volcano. Rather than spewing lava, the underlying plaque contents--fibrous tissue, inflammatory cells, cholesterol crystals, fatty material, debris--are exposed to flowing blood and trigger spasm of the artery and blood clot formation. A ruptured plaque is typically found in people who go to the emergency room with severe chest pain or have difficulty breathing.

A heart catheterization is performed, a severe (e.g., 90-100%--completely closed) is found. A stent in this situation is of clear-cut benefit.

What is not clearly beneficial is someone with no symptoms, symptoms only with physical activity that has been present for at least several months, or someone with a high heart scan score and no symptoms. In these circumstances, stent implantation does not reduce risk for future heart attack.

Why?



Take a look at this angiogram of a right coronary artery. You can seen plaque all along the artery (represented by areas that appear pinched off. There are at least 4 visible.)

Putting one 15 millimeter stent in the artery will only affect the area of artery stented. (Stents vary in length, but typically are 12-18 millimeters in length.) The right coronary artery is about 10 times or more this length. There are also two other arteries of similar length. A stent at one location will do nothing to affect the potential for rupture in any of the other plaque-laden areas.

Say a stent is implanted in the "worst" blockage in this right coronary artery, the plaque located at around 9 o'clock. What about all the other plaques? They can still rupture.

Why not put in many stents, say, 4 or 5, and stent all the visible plaques?

Two reasons: 1) Plaque you can't even see on an angiogram can still rupture, and 2) it is very costly (easily $30,000 at the very least), 3) incurs greater procedural risk, and 4) messes up the artery for future procedures, since a steel-lined artery that develops more disease in future will be more difficult to re-implant stents, bypass, or perform other procedural manipulations.

The point: Putting in stents does not reduce potential for plaque rupture in the entire artery.

What can prevent plaque rupture? That's the whole point of following an effective prevention program: prevent plaque rupture.

(Of course, this discussion cannot encompass the wide variety of potential situations that may cause your doctor to individualize your approach. Nonetheless, when advised to have an elective heart procedure, a healthy dose of skepticism and is clearly a good practice.)

Top image courtesy National Heart, Lung, and Blood Institute.

Comments (11) -

  • Get Primal

    2/13/2009 2:17:00 AM |

    Great post, it's too bad more effort and resources don't go into the initial prevention.  I'm a sales rep that works in the cath lab (peripheral vascular and vessel closure products), love the blog!

  • vin

    2/13/2009 9:57:00 AM |

    I don't ever remember my doctor ever talking about the chance of a plaque rupturing at one of the almost blocked points. His reason for putting in a stent at the worst point is to protect the patient from a total blockage at that point. So argument for a stent is to give the patient a few more years prior to a follow up bypass surgery.

  • Kiwi

    2/13/2009 10:07:00 AM |

    Hi Dr. Davis,
    What other procedures are likely in the future regarding blocked arteries? I understand dissolvable stents are being trialed. Are we likely to see any other developments?
    Thanks.

  • Lynn

    2/17/2009 3:45:00 AM |

    I am an otherwise very active and healthy 57 year old female who has already had 4 stents placed in my RCA following 2 separate MI's.  Each event was 5 years apart. Needless to say I feel like a time bomb.  I have visited several cardiologists and have finally found one who is looking at my CAD from a more aggressive standpoint and that is prevention. Following a recent cath procedure I have slightly 40% at the site of the last stenting.  This will no doubt need to be addressed but when?  I would prefer before I have another event!  However...I've yet to hear about what supplements (Vitamin D3 ) that could perhaps slow the progression of my disease of perhaps elminate/reduce the placque already there.
    Any suggestions?  If indeed you could answer, I'd prefer an email. Thanks for educating us!

  • Anonymous

    2/20/2009 2:32:00 AM |

    I am 45 year old (from India) have
    VERY strong history ( Father-3 Mi's)
    of Coronary disease and diabetes.
      My annual checkup showed
    TC- 282
    TG- 442
    LDL- 173
    HDL- 39
    Had slightly elevated #s before(10yr)
    My Internist sent me for a heart scan and MY SCORE is ZERO / ZERO /
    and ZERO, ANY comments Dr.

  • selahV

    2/27/2009 9:38:00 PM |

    I am scheduled for an angiogram next Friday.  My stress test showed what appears to be a blockage in a front artery of my heart, the doctor says.  What he didn't say was what would happen if I have a blockage when they get inside.  Should I be asking more questions?  what should I ask?

  • Anonymous

    6/29/2009 9:08:16 AM |

    I am a 47 year male from India and have undergone angiogram recently and the report shows there is 80% block in the main artery. Advice and guide whether  stent is adviceable if the patient is diabetic.

  • buy jeans

    11/3/2010 9:22:00 PM |

    (Of course, this discussion cannot encompass the wide variety of potential situations that may cause your doctor to individualize your approach. Nonetheless, when advised to have an elective heart procedure, a healthy dose of skepticism and is clearly a good practice.)

  • ultrasonic liposuction guide

    1/26/2011 5:42:45 AM |

    Medications are the best way to prevent this from happening.there is no reason to think stents would prevent heart attack. "What happens when you put a stent in is you're attacking one narrowing in the artery, but it's not the narrowing that's going to cause the next heart attack,"

  • how to

    2/3/2011 7:11:50 PM |

    I recently came across this article and have been reading along. I thought I would leave my first comment. I don't know what to say except that I have enjoyed reading. Really a nice post here!

  • ABBEY

    3/5/2011 6:01:21 AM |

    I am scheduled for an angiogram on Friday. My stress test showed what appears to be a blockage in an artery in front of my heart, says doctor. He did not say was what would happen if I have a crash when they are inside. Should I ask more questions? What should I do?

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Lethal lipids

Lethal lipids

There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself



This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).


If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does
not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.




Comments (15) -

  • Jenny

    5/8/2009 12:22:00 PM |

    Isn't it time we stopped talking about "risk factors" which is a flaky idea invented by drug companies and often means "associations" and start talking about causes?

    In this case, a CAUSE of heart problems is probably glycosylation [permanent binding of glucose to the protein] of receptors used in lipid removal. That's why cutting back on carbs which lowers glycosylation helps.  

    The CAUSE explanation for why  wheat is an issue for many people is most likely that they have genes for mild gluten intolerance which leads to systemic inflammation. New genes have been discovered recently which are making many more people test positive for gluten intolerance, usually people with other autoimmune markers.

    Without those genes wheat behaves just like another glucose-source in the diet. I do eat wheat, just not much of it, but I keep all my carbs low and have very low Apo-A and very high HDL.

    I do occasionally hear from people with diabetes who are fat sensitive and whose insulin requirements and blood sugar go up not down on a high fat/low carb diet. That's probably another genetic error at work. It's rarer, but it does exist. For such people the cause profile may be different.

    It would be nice to know what's the cause behind the positive effects of the fish oil on heart disease. Any clue?

    As long as we stick with "risk factors" we can end up thinking that yacht ownership is a "risk factor" for wealth since studies have repeatedly shown that people who own yachts are more wealthy than those who don't.

  • prophets

    5/8/2009 1:23:00 PM |

    i have this pathology.  the causes are pretty clear, imo.  i take nicotinic acid, fish oil, etc.  unfortunately, i had to self-diagnose my condition because every cardiologist i saw was so fixated on low-ldl/lipitor-is-everything analysis.

    thx for the note.

  • Steve

    5/8/2009 2:13:00 PM |

    high fat intake is a surprise! are you saying high saturated fat or unsaturated fat from oily fish for example?  
    Does elimination of sugar mean not eating fruit?

  • Anonymous

    5/8/2009 2:31:00 PM |

    After reading your post about the use if niacin to improve low HDL, I started niacin.
    I just got my test results:In 6 months, I've gone from 42 to 79!
    I'm still waiting for the results from my vitamin d level and CRP, but I bet I'm not disappointed.
    Thanks again for great information.
    Jeanne

  • Anonymous

    5/8/2009 2:33:00 PM |

    Oh, and my total cholesterol went up a little, to 211, but my tryglycerides are still very low (38), so I'm guessing my small dense LDL particles are very few.
    Jeanne

  • Kurt

    5/8/2009 2:51:00 PM |

    I've been reading this blog with interest for the past week. I'm a 44 year old male who had my first coronary artery calcium scan. My doctor wanted to prescribe statins for my cholesterol (LDL 155, HDL 65, Triglycerides 78) so I decided to have a scan first. I was hoping my high HDL had kept my arteries healthy. My score was 42 (LAD 42, the rest were 0). I thought that was pretty good ("mild plaque burden," the test result said), but the doctor told me I was in the 85th percentile - only 15% of men in my age group have a higher score. I'm wondering, do you see any good news in my results? Thanks.

  • waxjob

    5/8/2009 10:29:00 PM |

    I've just read a Norwegian study that was recently cited in a cardiology journal that has found high HDL readings can be dangerous.
    I'm a 57 yr old male and this is my lipid profile:
    185 (TC)
    76 HDL
    103 LDL
    29 Triglycerides (TRG)
    My HDL is nearly as high as my LDL and my triglycerides are almost non-existant. Nobody in my family has ever had heart problems but my profile doesn't look like any of the other ones I see and I'm wondering if I should go back and ask to see a cardiologist for a follow up?

  • billye

    5/9/2009 1:32:00 AM |

    I am already taking 7000mg fish oil providing a little more than 2400mg EPA and DHA on a daily basis. What is your reference of north of 3000mg talking about, total fish oil or just EPA and DHA?.  You say high fat intake like niacin.  Did you also mean to infer that high fat animal protean and cheese could be helpful? My doctor stopped me from taking all Staten's and I already stopped sugar, wheat and high carbohydrates.

    Billy E.

  • Rick

    5/9/2009 3:06:00 AM |

    Dr Davis,
    Could you qualify the high-fat intake treatment a bit? Is any kind of fat effective? And presumably there are conditions for what the fat can be combined with, too?

  • David

    5/9/2009 4:00:00 AM |

    Saturated fat in particular is the most effective for increasing HDL, decreasing Lp(a) (by nearly 12% in one study), and decreasing sdLDL. One should note that saturated fat may cause an increase in calculated LDL, but this is inconsequential, as the LDL particles will be of the larger, fluffier, more benign type. Also, if triglycerides are decreased (as they would be -- oftentimes dramatically -- on a lower carb, higher saturated fat diet), of course calculated LDL will go up. According to the Friedewald calculation: LDL cholesterol = Total cholesterol – HDL cholesterol – Triglycerides/5. Therefore, if all you do is decrease triglycerides (a good thing, to be sure!), your LDL could go up! This is why the NMR is a much better way to track changes. It measures particle number and size instead of making a mere "calculation."

  • Anonymous

    5/9/2009 2:09:00 PM |

    Dr Davis:

    Would you comment or send a link to a comment about when you would do a calcium scan vs a full CTA for stratification of cardiac risk?

    DoctorSH

  • Anonymous

    5/9/2009 11:13:00 PM |

    David -  I would love to read more about this.  Can you point me to any studies where they have gotten these results.

    Thanks,

    Bonnie

  • David

    5/11/2009 4:02:00 AM |

    Bonnie,

    Certainly. Here's a study with all of the things I mentioned: Increased HDL, decrease in small LDL (increase in LDL particle size, which is good), and ~12% reduction in Lp(a) -- and all with a low-carb/high-fat (60%) diet.

    http://www.nutritionandmetabolism.com/content/3/1/19

  • Ricardo

    5/21/2009 3:03:51 PM |

    Dear Dr. Davis, I believe these recent studies tell us that LDL is not as bad as we were thinking. When shall we expect to see small LDL as a standard medical test/marker, and LDL discarded?

    1- http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0002870308007175/
    2- http://astute.cardiosource.com/2007/vposters/pdf/275_Fonarow.pdf
    3- http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109706004797/
    4- http://www.ncbi.nlm.nih.gov/pubmed/17134630

  • mongander

    8/17/2009 9:16:53 PM |

    My HDL just doubled from under 40 to 80.  Have been on niacin and also use 1 oz of 190 proof Everclear to dissolve supplement powders which I then add to hot cocoa.  My doc thinks the increased HDL was due to the alcohol.

    Coincidentally, at the same time my HDL doubled, so did my PSA.  Now I'm scheduled for a prostate biopsy.  I'm 70.

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