Perioperative beta blockers associated with more heart attacks

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The 30-day myocardial infarction and mortality rate was significantly higher (2.74% v. 0.7%) in patients who got beta blockers in conjunction with noncardiac surgery, according to an article in the October 2008 issue of Archives of Surgery (Kaafarani HMA. Arch Surg 2008;143:940-944).

This paper adds to the finding of the POISE study (Perioperative Ischemic Evaluation Trial) of more than 8,000 patients undergoing noncardiac surgery, which was published in the May issue of the Lancet. Although there were fewer MIs in the group receiving extended-release metoprolol, all-cause mortality and disabling strokes were significantly more likely in that group (MedScape 10/29/08).

The authors’ interpretation was: “Our results highlight the risk in assuming a perioperative beta-blocker regimen has benefit without substantial harm, and the importance and need for large randomised trials in the perioperative setting. Patients are unlikely to accept the risks associated with perioperative extended-release metoprolol” (Lancet 2008: 71:1839-1847).

AAPS President Mark Kellen, M.D., comments that these studies illustrate the danger of centralized control of medicine, with instant reporting to bureacurats through electronic records and pay for “performance” (meaning compliance with “guidelines”).

“In a system where physicians are independent clinicians paid by patients and not third parties, information is slowly incorporated into our practices, putting only a few patients at a time at risk of complications from new medicines and procedures,” he states.

In contrast, “national guidelines can easily be prone to overtreatment, given the bias for publishing favorable studies about a drug or treatment over negative studies or studies showing harm. Immense amounts of money can change hands with the recommendation to use a certain treatment.”

With centralized control, decisions about the “standard of care” could be implemented in a very short time, with potentially disastrous results for millions of patients.

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  • Joseph Boggi

    All this study says is that the heart rate should be controlled on this regimen for it to have it’s desired effect.

    You can conceive of the original purpose of beta blockers. That is to control the heart rate, and hence lower the double product, and hence lower the risk of heart attack. The folks who got into trouble were not beta blocked. Indeed, their heart rates were high.

    Back about 20 years, they noted that Carafate decreased stress ulcers in a small study. In that small study more people died in the treated arm, nevertheless carafate became popular. Further study was needed. If you went by this study, no carafate would be used. In another better example, they used to use a drug for clotting after surgery that wound up causing more heart attacks, because of it’s clotting properties. They had finally gotten around to properly studying a long time favorite drug.

    Use of beta blockers in general lowers cardiac mortality. Since these folks heart rate was high, they were not beta blocked. That is all this study says. If you are not beta blocked your risk of cardiac complications is higher.

    The arm of the study with the long term beta blocked patients did much better.

    To go on and say that this is a reason not to have general guidelines, is interesting. The take home point of this article is the heart rate. Vitals are vital, if the heart rate is already high, then you should start to wonder.

  • Joseph Boggi

    “What we found was really amazing and very similar to the POISE trial — those on beta blockers had higher mortality. Also, those who ended up dying were not necessarily in the highest-risk cardiac group, and what was very interesting was that their heart rate was not properly controlled as per ACC/AHA [American College of Cardiology/American Heart Association] guidelines. So the conclusion is that one, patients who are going to receive beta blockers should have cardiac risk factors or cardiac problems, and two, that heart rate should really be well controlled to achieve the desired effect.””

    More importantly, NO treatment changes should be made based on a retrospective cohort study. Period!!!

    Time for a prospective randomized study which documents proper heart rate control, and hence evidence of beta blockade.

  • Joseph Boggi

    The Lancet article is more convincing. It is a randomized study. While patients did have fewer MIs, more patients died and more had strokes.

    In that article the treatment was started just 2-4 hours before surgery. Given that interval, I am not at all sure that you can say much about the treatment arm of the study. Those comments can be found on the links noted.

    This reminds me of the lopressor for acute MI study. When evaluated in the field on real patients, there was little benefit from using lopressor on an acute MI.

    Instituting a powerful drug, along with surgery is probably not the thing to do.

    They need to do a large study which first beta blocks the patients and then takes them to surgery before throwing out the notion that beta blockade for elective surgery should stop.

  • Frank Timmins

    Joseph Boggi brings up varying approaches to the evaluation of perioperative beta blockers and their efficacy. His difference of opinion with the article underlines the intended point of the article. That is to say that bureaucratic “standards of care” will guarantee an unacceptable amount of “unintended consequences”.

  • Harry J. Rose, MD

    Everybody thought Swan-Ganz catheters were a great idea too.

  • Malcolm Findlater MD

    I haven’t had the opportunity to review the articles themselves. As I read this my first impulse was to think, well the ones on betablockers are at higher risk. But the absence of true betablockade is intuitive.

    I agree with the AAPS author that this is an example of guidelines gone awry. By pushing us, especially those of us who did better in anatomy than physiology, puts patients at risk because it is often clear why some of these guidelines are valuable if we understand the pathophysiology. But if we do things by rote, we can easily miss the forest for the trees.

    I recently heard of a study that was to be published by now, but hasn’t been, that suggested getting a glycated hemoglobin below 6% was associated with increased CV events. So maybe some were following guidelines so strictly that they were causing harm without knowing why.

    I’m an old guy and remember all the dangers of betablockers: Never use them in patients with diabetes——-oops that may be the group most benefitted by the cardioprotective effect. Never use them in patients with congestive heart failure——-oops they may the drug of choice in patients with diastolic dysfunction (not even recognized at that time) and are now being recommended in patients with systolic dysfunction.

  • Howard Long MD MPH

    “In the β-blocker group, patients who died perioperatively had significantly higher preoperative heart rate (86 vs 70 beats/min, P =.03). ”

    This affrims the point above of Boggi and Findlater: dead ones were NOT beta-blocked.

    Dictated care from retrospective studies so poorly controlled is just pretext for perpetuation of politician power.

    Howard Long

  • Dar Lostrom

    Real world experience with low dose Metoprolol (beta blocker to decrease adversity of elevated Adrenaline and Catecholamine toxicity) after life-threatening Stress-induced Cardiomyopathy (Tako Tsubo/Broken Heart Syndrome).

    As the spontaneous caretaker of my dad’s wife (91) who suffered sudden collapse from the above, I took copious notes while monitoring her recovery (33 days) after she returned from hospital and started on the single (only) drug (Toporal) at a 25 mg dose (wt: 81 lbs). The reason I felt thus compelled was because the pharmacist had cautioned how this medication can cause hypotension (w/typical starting dose of 50 mg)…and…because just two weeks before onset of this event such elderly woman was found by blood test at her PCP to have below range glucose (54) which (for several weeks earlier) had been causing a variety of symptoms including early morning dizziness/fatigue/headache and (undiagnosed) hypotension.

    Prior to this event, such spry/active/petite woman was on one pharmaceutical, Digoxin (250 mcg) and had been for years, but this was stopped in hospital. Since I have long advocated the supplementation of heart anti-oxidant CoQ10 (Ubiquinol) she had already been using 120 mg/day and once home, after my research revealed that beta blockers (including Metoprolol) will impede natural production of this essential antioxidant, I doubled her dose to 240 mg/day so as to counter any unintended/worsening effect of such added beta blocker.

    Yet, by the 4th day while on this supplement and Toporal, there were steadily evolving symptoms with (first-ever) edema in ankles/dry cough/restless-crying out sleep/unusual dreams/low stamina/strength/intolerance/severe hind/lower leg pain prompted me to call the doctor who agreed that I could stop such Rx “to see how she did” while I needed to be aware that “if we are going to treat your mother with chemical therapy, this is the only medication I can put her on.” And since I felt her symptoms were far too compromising to ignore as well as counter-intuitive for full recovery, I did stop giving her this Rx.

    By (even) the next day, each symptom was lessening, but at the same time what became noticeable was significant short term memory loss (I believe due to intermittent imbalance of glucose in such elderly brain since I have found recent (Dec 08) research that confirms how “low blood sugar can trigger Alzheimer’s plaque” (in as quickly as a 24 hr. period). Needless to say, this woman had likely dealt with much (biochemical) ‘stress’ of underlying/undiagnosed Hypoglycemia…and thus, after the Adrenaline/pro-inflammatory assault (almost flat-lined twice) and then as she was placed on the Metoprolol beta blocker (even with protective Co/Q10) this has, altogether, left her, now 3-12 mo. later with acute and evolving short term memory loss. And yet, physically, by end of one month (as we learned is common with Stress-induced Cardiomyopathy) she is back to her normal activity level and stamina.

    The major point I wish to leave the reader with is that, if I, as the vigilant and educated caregiver/daughter, had not decided to stay on in the folks’ home on a day-to-day basis to monitor, I believe that the continuance of such post beta blocker therapy, to an already aged and recently further weakened heart, “would” have killed this woman. And if official “guidelines” do not fully address the biochemistry of the patient AND the secondary effects of pharmaceutical intervention (why wasn’t CoQ10 prescribed at same time/did Cardiologist know from training?) clear through recovery, then this is an inherent and life-threatening flaw in the delivery of ‘system-ized’ medicine. Thank you kindly for your time, and this portal to offer feedback from the purview of such patient advocacy and real-life experience.

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