The Bale/Doneen method of heart attack and stroke prevention: So you have a better idea?

Dr Melissa Walton-Shirley


March 03, 2011

Las Vegas was the perfect setting for a two-day boot camp on heart attack and stroke prevention. The Sin City venue, the site of the largest of four annual Bale/Doneen method courses, epitomizes the veritable crap-shoot-of-a-journey that every patient embarks on after a heart attack or stroke. The indictment of "usual care" is that any number of brand-new stents or freshly plumbed bypass grafts will do nothing to prevent a second heart attack in two-thirds of patients. "The recidivism for this illness is deplorable," said Dr Bradley F Bale, explaining why he as a family practitioner joined Amy Doneen, RNP, to make up a dynamic duo whose mission in life is to combat vascular disease. Over 60 participants, a mix of interventionalists, general cardiologists, endocrinologists, primary-care physicians, CV surgeons, RNPs, and dentists journeyed to Nevada in pursuit of the missing pieces in the prevention and "aftercare" of ACS and other vascular syndromes. Bale and Doneen are dynamic evangelists of their approach, and it appears their number of followers is growing.

The "paradigm" for event prevention is based upon a simple cartoon. The "cat in a gutter," crouched below ground level, ready to leap out and attack unsuspecting birds, is frequently referred to throughout the course. The "cat" is representative of atheroma, deemed stable unless it becomes "inflamed." The "gutter" is the blood vessel endothelium. As long as the gutter is "cool," the cat doesn't "leap out," but if the gutter heats up due to "inflammation," then the patient develops ACS or stroke. Evidence of atheroma in any branch of the vascular tree--ie, an abnormal calcium score, peripheral vascular disease, erectile dysfunction, an abnormal stress exam, vascular calcification on chest X-ray or on a mammogram--is considered an indication of a "cat in the gutter." The "fire" in the gutter floor is fueled by glucose intolerance and insulin resistance in 70% of victims of vascular events, a fact rarely explored by patients or acknowledged by practitioners. Other maladies, such as psoriasis, rheumatoid arthritis, gum disease, or smoke exposure, are also triggers that can make a vessel "come in hot," a phrase often used by Bale to describe vulnerable plaque. The paradigm suggests that 75 g of glucola with a one-hour and a two-hour finger-stick test during the course of a hospital admission would direct traffic to the right path toward cooling off the vessel in the majority of patients. 

The most remarkable aspect of the Bale-Doneen program is that Amy and Brad guarantee their work, something I've never seen cardiologists do. If the patient experiences a heart attack or stroke while being compliant with their plan, the patient will get their money back for any out-of-pocket costs. They assert that they have had only two patients to experience "an event" in nine years in over 500 cohorts. What is more amazing is that they claim to understand why their two patients did poorly. One of them was referred back to her primary-care physician with her biomarkers in good stead. A year later, she experienced a heart attack. When Bale called to follow up, she confessed that her family doctor, citing her excellent lipid profile and apparent good health, stopped all of her medications. The other patient developed a severe tooth abscess, which was enough to fuel the archenemy of any vascular prevention plan: inflammation.

The Bale/Doneen method relies upon abnormal Berkeley panels, myeloperoxidase (MPO) levels, PLAC tests, carotid intima media thickness (IMT), and abnormal triglyceride/HDL ratios of >5 to guide treatment strategies, among other indicators. Most of these are uncommon entities found in the everyday grind of general cardiology practice but are mainstays of this paradigm. They micromanage their patients' biomarkers based on major trial outcomes and subset analyses. They also refer patients for more conventional testing such as echo and risk stratification. Their method does not ignore the benefit of percutaneous intervention or bypass grafting when necessary. One of Bale's patients developed "new ischemia" on a stress exam recently and underwent an elective PCI but instead of just bolstering up plaque with metal, they investigated why the patient's status changed. They are on the hunt for smoldering inflammation and once it is identified, appropriate treatments will be implemented, secondary-prevention cocktails adjusted, and the "cooling" of his vessels documented by waning inflammatory markers.

For those who criticize the Bale-Doneen method as "undocumented and unproven," they cite "evidence" from a major trial for every single recommendation. The ever-popular "just get them on a statin--any statin" approach, they believe, is largely incorrect. They do not use atorvastatin, especially in women and insulin resistant patients, citing subset analyses from ASCOT, WOSCOPS, CARE and PROVE-IT to support their penchant for pravastatin--that it "prevents diabetes." They favor carvedilol over metoprolol and other beta blockers because of COMET, stating, "The science is there," and their concerns that metoprolol increases NT-proBNP and promotes insulin resistance. They utilize ramipril because "you really can't beat the HOPE trial." They throw tons of sustained-release niacin at folks because of HATS, with Bale pointing out, "It's hard to prove statistical significance in 160 patients, but they did it!" They monitor their patients every three months for changes in inflammatory milieu in order to champion the opportunity for their patients to live well even in the face of severe vascular disease, and they insist it works.

On my return flight to Nashville, I saw the magnificent Grand Canyon unfold beneath me. Large furrows and breaks punctuated the earth's topography. Shades of pale yellow, gray, and red told the story of billions of years of daily assaults on its architecture, in much the same way our patients' endothelium is being etched on a minute-by-minute basis. A picture of a freshly ruptured plaque, black and shiny like caviar sitting within a freshly sectioned postmortem vessel, came to mind. It occurred to me that to simply lay a scaffolding over the vessel wall or build a bridge across it does nothing to stop the ongoing destruction any more than it would have affected the creation of this huge elongate crater in our earth's mantle . . . but to understand it, find the fire or the entities that are creating the furrows in our vessels . . . ah . . . that's the key. This paradigm has taken up the challenge of doing just that, and I think I should utilize this new information as a navigation tool for primary and secondary prevention. I will need to reexamine the thousands of slides presented during this course; otherwise, that small diploma tucked in my overhead compartment proudly declaring I completed the Bale/Doneen course will be worth no more than the paper it's written on. Perhaps it could help nearly all of my patients who have a two in three chance of having a second heart attack or stroke. At this point, I don't really have a better idea. Do you?

Disclosure: Melissa’s fees for the Bale/Doneen course were waived by the course organizers.


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