Heartfelt with Dr Melissa Walton-Shirley

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No mortality benefit with stents in stable angina: Not news, not the point, and what's "stable"?

Feb 29, 2012 09:21 EST


Patient A: Bill has a known 80% LAD lesion, 70% circ, and 40% RCA and declined a PCI at the time of a cath a few months back, opting to try medical therapy. The cath was performed because of a nine-minute Bruce protocol with mild LAD ischemia on a nuclear. He just couldn't live without knowing if his arteries were blocked or not. Bill likes to walk, play golf, and loves to try to have sex with his wife. His medications include aspirin, a statin, and a beta blocker. His bisoprolol was recently increased to 7.5 mg bid because of recent angina when his golf cart broke down and he had to walk back to the clubhouse. He's complained of moderate erectile dysfunction (ED) and fatigue since his initial diagnosis. His cardiologist just wrote a referral to a genitourinary test for a testosterone level and an ED workup, as he explains to him that he's likely out of shape and needs to condition more. He is scheduled for an eight-week follow-up. "Let me know if you have any more difficulties," the cardiologist says, "and I can see you sooner." The patient thinks as he's putting on his coat, "I thought that's what I just did." One year later, he feels about the same, still having trouble occasionally with chest pain and in the bedroom. Five years later, he is cardiac-event free, but he is now seeing his family doctor for depression. He retired early because he just doesn't feel well and no longer goes out with his friends.

Patient B: Tom has a 90% LAD lesion, 50% circ, and a 50% RCA. He initially saw a cardiologist because he can't play tennis without moderate substernal chest pain but has very good exercise tolerance, completing 10 minutes on a Bruce protocol and a "less-than-hyperdynamic response in the anterior wall." He opts to undergo a PCI to the LAD. Three weeks later, he comes back and says, "I'm having no chest pain, but I'm short of breath a little when I play tennis, and I'm having some difficulty with fatigue." The cardiologist looks at his medication regimen and says, "You know, you had no demonstrable ischemia in anything but the LAD distribution, you are having no angina, so let's taper off your beta blocker and see how you feel. Be sure to stay on your aspirin, statin, and carry some nitro. By the way, let's go over the Mediterranean diet and then see me in a few weeks." A month later, he reports he won his tennis match yesterday, he and his wife are scheduled for a cruise in eight weeks, and he's never felt better. Five years later, he's cardiac-event free and feels great. 

Point 1: Patients don't just see cardiologists because they don't want to die. They actually see us because they want to "live" and live well. Medication side effects, the cost of medications, the ability to do activities without having to consider a stopping point that may produce chest pain are all part of the formula of what it takes to be a "heart patient." Whether or not a PCI is the appropriate course of action for our patient will have to be decided in the exam room on a case-by-case basis. It cannot and will not ever be legislated. As for reimbursement, we are obligated to do what is right for the patient, no matter the reimbursement issues that we may face. We swore an oath to do that despite any economic reimbursement or medical-legal issue. When the issues of patient comfort and safety are our first consideration, there is no other argument that counts.

Point 2: What exactly is "stable" angina? It is generally defined as predictable cardiovascular symptoms of shortness of breath or discomfort located somewhere between the belly button and the ear lobes, chest, arms, or upper back when one exerts oneself. Despite this fairly classic definition, the diagnoses of stable angina and, more concerning, the diagnosis of unstable angina are often missed. How is one to approach large territories of silent ischemia? What about those patients who have their gallbladder out for severe rest pain only to discover they had a 90% LAD lesion now completely relieved with a PCI? What about the young patient I saw once with excellent exercise tolerance who had an esophagogastroduodenoscopy with a diagnosis of an ulcer but called me one night after we accidentally met at a meeting. He just wanted to talk to me about his ongoing pain of six months' duration. When I cathed him, his LAD was hanging on by a hair with haziness and what appeared to be an ulcerated plaque. He was obese, and his glucose challenge in the hospital registered a blood sugar of around 300. He had no clue that he was literally a ticking time bomb, and neither did the other two physicians that saw him. You couldn't hold a gun to my head and make me say he had a stable situation. His symptoms were moderate, but in nondiabetics, the same pain might have been severe enough to warrant the "acceptable label" of "unstable," which would have generated a referral for cath a few months earlier.

Randomized prospective trials, adequately powered have given us great insight into the question "to cath or not to cath," but when it comes down to it, the variables in our patients are so highly complex, so thoroughly affected by genetics, environment, diet, undiagnosed diabetes, first- or secondhand smoke exposure, activity levels, and job expectations that every patient should be labeled as "guilty" of having progressive angina until proven otherwise. Add to this the great danger that lies in the patient's interpretation of their symptoms and then their physician's interpretation of their symptom complex, it is no wonder that patients can still get into trouble. Despite all the data, we can still rely only upon common sense and a high index of suspicion to help us navigate a course for our patients. Whether we discuss old news, new news, or no news, and whether or not our actions lower our patient's mortality, isn't all we owe them in the long run.

Living well is important, not just living.

See also:

No mortality or MI benefit in stable CAD patients treated with PCI: New meta-analysis





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Your comments
No mortality benefit with stents in stable angina: Not news, not the point, and what's "stable"?
# 1 of 25
February 29, 2012 01:19 (EST)
W.E. Feeman, Jr, MD
An ounce of prevention is still worth a pound of cure.  And cigarette smoking still pushes ATD events to earlier times compared to ex-smokers and never smokers.  Treat lipids to plaque regression levels, lower the blood pressure to below 140/90, bring the 2 hr pp Blood glucose to below 200 mg/dl, and MOST importantly, get the patient to stop smoking--and you don't need to worry about stents in the first place.  The same is true in stable ATHD patients--I've been treating patients that way for years.
# 2 of 25
February 29, 2012 10:02 (EST)
Andrey Espinoza

Shirely, this is the first time I agree with you 100%. Spot on and great examples.....god knows we have seen them more times than one can shake a stick at!

Thanks for making me feel like "I am not alone" lol.
# 3 of 25
February 29, 2012 10:23 (EST)
Melissa

Dr. Feeman, agree with your stance on smoking! Truth be known, I've treated very few patients who didn't smoke and required a PCI below the age of 50. In Kentucky, believe you me, we have legions of folks in their thirties and forties who experience ACS--the perks of living in tobacco country. 

Andrey,

So glad we could agree!!! Hope it won't be the last!  :)

 

Melissa

# 4 of 25
March 1, 2012 09:17 (EST)
Vivek Chaturvedi

Beautifuly put. I am in a unique position to say this, having practised prevetive cardiology  and clinical trials earlier and now interventional cardiology and EP

I think quality of life is as bit important, if not more than mortlaity. I love to se the smile on my patients faces after they are pain free. Having said that, it is true that PCI is often used inappropriately and that can cause real trouble. 

I think we should talk to ouir patients more often. What he/she wants and how active he is is worth far more than all guidelines and books put together

Vivek Chaturvedi

# 5 of 25
March 1, 2012 10:20 (EST)
becky c

HEAR HEAR!  Coomon sense is dead!!!!!  I about fell over when I read Pt 1' doctor's response to his ED problem!!!!!   Gee----wonder why he's got a problem in bed??? 

All these "new-fangled" drugs that will target this, that, or the other thing.......try listening to your patient then start with the tried and true and go from there.  Both our professions start off with "do no harm" and "treat your patient".  Too bad revenue has gotten in the way.  Melissa, I'd rather be poor and know I did my best than to have all the money in the world because some company got me to use their brand new treatment and knew it wouldn't work as well as something else, or DIDN'T do something because "the insurance company" wouldn't pay for it!
# 6 of 25
March 2, 2012 07:53 (EST)
Melissa

Thanks Becky,

great to hear from you!! I fight daily for the opportunity to do a stress exam with wall motion analysis post exercise. Anthem wants me to do a resting echo and a plain tread mill, or use a hoola hoop for 15 minutes or hop scotch or something and guess at whether or not the patient is ischemic, or in what territory they are ischemic. They always quote "the guidelines" to which I answer, "but the guidelines writers are about 10 years behind the data", etc. and then after threats, I finally get an approval number.

 
# 7 of 25
March 2, 2012 12:01 (EST)
stephen pollock

thank you.. I have been saying that stents are and remain a very effective and credible treatment for angina.. stable or unstable.  I have cad, and i do not want angina when i play golf, work out, etc.  As physicians we need to guard against limiting therapies that are effective at more than just preventing mortality.
# 8 of 25
March 2, 2012 12:47 (EST)
tom s
Where is Leadership of ACC? Intead of self pomoting each other how are they themselves handling the continued regulations which impossible in a real practice settig
# 9 of 25
March 3, 2012 09:23 (EST)
DVF
Dr Walton-Shirley's post raises the call for a re-introduction of common sense into the clinical encounter. Unfortunately this is a difficult task. It seems to be in increasingly short supply and is actively legislated against.  The concept of a guideline has been morphed into rule or law and is increasingly applied in a black or white fashion.  I must have an unusual practice as only about 20% have issues that are black or white.  Our exam room conversations frequently cover smoking, diet, exercise, medication costs and side effects, and symptoms but rarely bump into death.  We seem to be missing the fact that while we continue to mentally masterbate the Stent v Med v Surgery issues there is a clinic full of patients who just want to feel better.
# 10 of 25
March 4, 2012 07:30 (EST)
Dr. John Vyselaar
Excellent post! Right on the money. True stenting may not always improve mortality but symptoms and quality of life are very important.  I am a noninvasive cardiologist but have referred PLENTY of patients for PCI after medical management has not worked.  The majority of patients with anything beyond class I angina have had significantly better symptom control with PCI than with high-dose beta blockers and nitrates.  I work in Canada where we do not face the same oversight for "appropriateness" that you can have in the USA with HMOs.  I think that there is no way for a nonphysician to be able to oversee this decision-making process.  As Dr. Walton-Shirley points out, patient care is very complicated with many interrelated variables.  I think insurers and third parties, and legislators should get out of the oversight business altogether.  They can sponsor CME events on decision-making, or something like that, if they feel the need.
# 11 of 25
March 5, 2012 01:29 (EST)
Dr Subhrajit Das
For stable angina choice  of drug is more important.Nitrate,beta locker,statin and ecospirin and clopidogrel have good combination.I gave these to several  patients.When patient complains of headache due to nitrate then you can add ace inhibitor.
# 12 of 25
March 5, 2012 10:32 (EST)
Colin Rose

The plural of anecdote is not data.

What is the point of doing RCTs is we don`t intend to abide by their results?

The COURAGE trial showed that what was accepted "common sense" is treating stable or stabilized CAD was wrong. Optimal medical management even without significant lifestyle change was as good as immediate PCI for symptom management as well as preventing MI. So until further notice, if one prides oneself on practicing "evidence based medicine", that is what one should do.
# 13 of 25
March 5, 2012 12:50 (EST)
john ashcroft

Courage not only showed that PCI doesnt save lives, but that relieve from angina compared to medical therapy is so small, and short lasting.

If all you use for your patients is bisoprolol in large doses and you dont pickup on the fact that they are having side effects ... I dont call that "optimal medical therapy". There are a few other treatment options that can be tried rather than PCI.

And the most powerful option is actually taking to your patient so they actually understand what is going on when they get angina as they walk back from the club house, and are not scared s....less that they are going to die.

 
# 14 of 25
March 6, 2012 09:13 (EST)
Colin Rose

John, I agree. It is is important to explain that reversible ischemia of any degree caused by large old plaques never killed anyone. MIs are caused by plaque rupture mostly of early unstable plaques not even seen on angiography. So, there is really no point in doing angiography for symptoms that are not intractable.

By far the most important treatment for regressing plaques and for treating and preventing DM2 and hypertension is significant lifestyle change which was not part of the OMT in COURAGE. The COURAGE investigators only made a  feable attempt to raise HDL with exercise. No data was presented showing that patients lost weight or made any significant dietary change. 
# 15 of 25
March 11, 2012 12:06 (EST)
Anand

Dr Walton-Shirley,

Very nice persepctive. I would love to have you as my cardiologist.

My situation iwas very similar to your patient B. i have always had a healthy lifestyle, BMI < 24 but very bad lipid profile without statin therapy. My LDL was 200 with total cholesterol around 290. Another complicating factor was excessive Lpa of 190 mg/dL. Still is. 

Despite regular and vigorous exercise, decent diet, non-smoker, my exercise tolerance started to deteriorate and at 47, started having chest pain during exercise. Went in a for stress scho and couldn't finish 2 minutes on Bruce because of ST elevation. I felt no pain during the stress protocol but the attending cardiologist was alarmed and hospitalized me immediately. Cath showed 90% stenosis mid LAD, 70% stenosis in OBM1 and 50% stenosis in RCA. I was terribly disappointed that  all my supposedly healthy lifestyle had not prevented coronary artery disease. The LAD was stented with a DES.

I am on a statin and niacin now, and my life is much improved. I can exercise, go hiking, ride my bike and do all the things i used to do.  But if i interpret some of the comments by some of the cardiologisyts who post on this website, i should have been sent home with a recommendation to improve my 'lifestyle'. 

 

 

Anand 
# 16 of 25
March 11, 2012 02:36 (EDT)
Melissa

Anand,

You are very kind. Wish you the best of luck!

Melissa

# 17 of 25
March 12, 2012 11:45 (EDT)
J. Jodkowski
We, as physicians have been brought into forgetting altogether, that every single patient we're seeing at our offices is an "anecdote" by itself. Not a 1/30000 of some  huge RCT. (BTW, Courage had roughly 2500 pts out of 35000 with CAD screened, of which about 1/3 switched from OMT to invasive during the trial. Where's the everyday patient in that?) The statistical approach is very convenient to regulators, MHO's etc. Please read the dictionary definition of the word "guideline". It  is definitely not the "Holy Book".
# 18 of 25
March 12, 2012 12:17 (EDT)
oldie

after a dobutamine stress test 'suggesting three damaged areas of the heart wall and blockage probaby trivascular' five cardiologists urged me take a cath. ALL of them said the entry point was in 'the groin'. To me this is the crease between the thigh and genitals. I couldn't take a needle there and held off for eightmonths until discovering the entry point was in the femortal artery which is IN THE MIDDLE OF THE THIGH. I could take a bayonet there without much fuss.I took the cath and a stent in RCA 95% block. I had never had angina of any sort but years of serious dizzies, gut anxiety, nausea, tachy, pre-syncope, body malaise ('tingling' is the daft word they use) diagnosed as high stress burnout. I'm 83, do 4km interval training on a bike or run/walk) no problem, but still get those symptoms (minus the tachy)when least expected. So I quite understand the dificulties of diagnosis. My interventionist cardiiologist sees me every three months. 'Still exercising?'  Yes. 'Any pain?'  No. ' Good, come back in June'. But my quality of life?. Sick as dog five or six times a month. Family stressed out. Where is common sense?
# 19 of 25
March 12, 2012 09:18 (EDT)
Melissa

Hate to call you "Oldie" because you certainly don't seem to have an "Oldie's" schedule. Of course, we cannot advise you in this capacity, but I would encourage you to write a note to your cardiologist that previews your visit,  outlining your symptoms and your concerns. Sometimes if one preps their practitioner with a little information, the daily distractions and time constraints of an office schedule can be side stepped and your questions might be more thoroughly addressed.  I am sorry you have had this difficult experience.  You might ask your cardiologist if intermittant tachycardia monitoring is available to patients in his office that have symptoms  that come and go. He can explain whether or not that might be an appropriate next step. Good luck!!!

Melissa

# 20 of 25
March 13, 2012 02:45 (EDT)
oldie

why, thank you so much for replying, Melissa. I will press harder next visit to the card. I can't complain. Icalculate he's done  4000 (four thousand) caths in 20 years in the heart hospital so I count myself lucky I was allotted to him
bless 
# 21 of 25
March 19, 2012 07:52 (EDT)
Maria Ies Azambuja

It may be time to think "out of the box" of the classic risk factors

Seasonality and secular variations of CHD mortality trends need to be incorporated to the reasoning on CHD (or CHDs?) causality (ies).

Infection and particularly a role for influenza not only as a trigger but also as an early life  determinant of vulnerability to disease and death need to be properly considered.

 

See:

 The Inflammation Paradigm: towards a consensus to explain coronary heart disease mortality in the 20th century

http://www.sciencedirect.com/science/article/pii/S1875457008000041  

 

and

 

Influenza recycling and secular trends in mortality and natality

http://www.actuaries.org.uk/research-and-resources/documents/influenza-recycling-and-secular-trends-mortality-and-natality

 
# 22 of 25
March 19, 2012 08:56 (EDT)
Gary Mezo
Shouldering the Risk Burden: Infection as the Reversible Cause of Arteriosclerosis 
 
Read this article in CIRCULATION:
http://circ.ahajournals.org/content/107/11/e74.full.pdf

Then read the outcome of the study mentioned here:
http://www.nanobiotech.us/storage/57%20Maniscalco.%202004.%20Pathophys%20with%20US%20lipid%20table.pdf
 
Since the time of these articles, it has been scientifically determined that CNPs (Calcifying Nanoparticles aka Nanobacteria) are indeed not a living infectious agent by current microbiological definitions of life. But nontheless CNPs do self-propagate, cause infection, LPS biofilm, mediate long-term endovascular inflammatory cascades and are responsible for the deposition of pathological calcification in the intimal-medial space of coronary arteries and arteries throughout the vascular tree. Like Prions & Viruses (which are not "alive" either), they cause pathology that effects disease and leads to vascular health decline. CNPs utilize & oxidize VLDL & LDL from the host bloodstream. Amyloid plaque deposition from our immune response eventually walls-off the intimal-medial CNP infection, depriving the CNPs of their lipid foodstuff causing them to form calcific igloos in the plaque and become semi-dormant. The waxing-waning inflammatory cascades that occur in CAD are directly caused by our immune response to CNP pathology....ultimately, when our immune system attempts to "normalize" the area of infection through neovascularization, new bloodflow enters the area....giving the CNPs their lipids again....causing the CNP to leave their semidormant state and become active again...making their LPS Biofilm....restarting the inflammatory cascade and our immune system to isolate and wall-off the area with amyloid plaque deposition....this process of waxing & waning inflammatory cascades continues until the plaque is large, swollen & "vulnerable"....bursting plaque contents into the lumen like the popping of a pimple....causing a raging clotting cascade, vessel occlusion.....possibly MI or Death. I am available for correspondence at gmezo@nanobiotech.us
 
I am the inventor of NanobacTX and was Director of Research at the Nanobac when cardiologist, Benedict Maniscalco, MD, FACC conducted his study. I am Director of Research & CEO at NanoBiotech.
# 23 of 25
March 23, 2012 11:46 (EDT)
Anecdote disliker
Hear, hear!  It's easy to persuade oneself to maximize benefits the patient supposedly got, and to minimize side effects/discomfort caused by procedures.  Sounds like special pleading to me.
# 24 of 25
March 23, 2012 02:46 (EDT)
Mauro Montevecchi, MD
Great points which are very reasonable and ultimately get concerns across.  But I think it is easy to use two specific examples, which could both have been handled differently.  On top of this the point of the articles is that OMT is reasonable to try first, but not the only therapy.  Patient 1 obviously could have been tried on OMT like they were and then ultimately gone for PCI, and patient 2 may have benefited from OMT prior to PCI.  The fact is you don't know until you try, but the good news is that you are NOT killing people by trying OMT first, which I think is the take home point that many people are missing. 
# 25 of 25
April 1, 2012 08:38 (EDT)
Melissa

Mauro,

I agree completely, the only issues are that we are not certain who has a vulnerable plaque and who does not 100% of the time. We are cultured such that we feel if we "tack the plaque" we have "done something" . We have to (1) get over that  (2) find a way to tag vulnerable plaque, then we can truly know we are comparing apples to apples. 

Melissa


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About Dr Melissa Walton-Shirley
Dr Walton-Shirley performs invasive cardiology, nuclear cardiology, and stress echocardiography in a private practice in Glasgow, KY.

Her chief medical interests are CHF/hypertrophic obstructive cardiomyopathy and the promotion of primary PCI for acute MI. Recently she played a significant role in helping to launch an ambitious pilot study of primary PCI in Kentucky, the Kentucky Primary Angioplasty Pilot Project. She has also participated in the TIMI 19, Duke-HF, NRMI, and CRUSADE trials and is proud to have been an advocate of the first smoke-free initiative in Kentucky (2011). She champions a smoke-free America.

Dr Walton-Shirley received her undergraduate degree at the University of Kentucky and went to medical school and did her residency and fellowship at the University of Louisville. She is married with two daughters. Her interests include singing, writing poetry and songs, fitness, and, of course, theheart.org.