By Dr. Joseph Mercola (Mercola.com)
Story at-a-glance
- Recent research shows stents do not improve angina, thereby negating the sole remaining medical indication for angioplasty or the placement of a stent to unblock a blocked artery
- Earlier research showed angioplasty does not reduce mortality, nonfatal myocardial infarction or hospitalization rates for acute coronary syndrome
- Coronary artery disease is not a disease per se. It’s a symptom of “a diffuse systemic disease,” caused primarily by poor diet, inactivity, insulin resistance and stress
- The largest study done on heart attack incidence revealed only 41 percent of people who have a heart attack actually have a blocked artery. Of those, 50 percent of the blockages occurred after the heart attack. This means at least 80 percent of heart attacks are not associated with blocked arteries at all
- Three primary causes of heart attacks are decreased parasympathetic tone followed by sympathetic nervous system activation, lack of microcirculation and lactic acid buildup in the heart muscle
Heart disease is one of the most common chronic health problems in the United States, and we're wasting tens of billions of dollars on ineffective treatments and surgical procedures. In this interview, Dr. Thomas Cowan, a practicing physician and founding board member of the Weston A. Price Foundation, shares recently published data1,2 showing the ineffectiveness of stents — a commonly performed surgical procedure used to remediate damage from coronary artery disease.
Stents Were Never Indicated for Anything but Angina Relief
There are a number of parameters that are crucial for evaluating the efficacy of a treatment for heart disease. For instance, will the patient actually live longer as a result of that intervention? Mortality is one parameter of assessment. Another parameter is the risk of heart attack as a result of the intervention. Alleviation of angina (chest pain) is a third. “There's probably more, but those are the three big ones,” Cowan says.
Earlier research had already dismissed the use of percutaneous interventions (PCI) for most of these parameters, showing the use of stents had no impact on long-term rates of death, nonfatal myocardial infarctions (MI) or hospitalization rates for acute coronary syndrome. The sole indication for the use of stents was angina, as some of the findings showed it helped reduce prevalence of chest pain.
“What [that] means is the state of the literature, before this current Lancet study, was that doing stents or other interventions … has never been shown to help people live longer or to prevent further heart attacks. They have been shown to be of aid in people who are having an acute MI, but in anything but that indication, the state of the science was that they don't help people live longer, and they don't prevent further heart attacks.
As this study says, the indication was for relieving angina … It was actually not appropriate, and possibly even not allowed, to tell somebody we were doing a bypass or stent so that you would live longer or not have a heart attack. You could tell them that you could do it because you're having chest pain, and this will relieve your chest pain,” Cowan notes.
Do Stents Actually Relieve Angina?
Interestingly, there had never been a double-blind study assessing whether, in fact, stent placement relieves angina. The reason for this lack of data was because doing such a study was considered unethical. In a nutshell, it was assumed that stents were beneficial, and therefore denying patients of this benefit would place them at risk.
Eventually, though, a group of interventional cardiologists in England got approval from the review board to perform a comparative study in which half the patients with stable angina received a stent, while the other half received sham surgery. The sham surgery consisted of inserting and removing a catheter in the artery without actually placing a stent. The level of chest pain and exercise tolerance was then assessed and compared between the two groups.
Lo and behold, there was no difference in chest pain (angina) between the treatment group and the sham group. This means that the one and only indication for doing a stent, which is to relieve angina, is also invalid. “It's hard to come up with what the indication is at this point, except in the rare instance of an acute MI,” Cowan says.
Blocked Arteries Are but One Symptom of a Diffuse Systemic Disease
The ultimate tragedy here, aside from the exorbitant cost, is that patients continue receiving this useless intervention even though there are several simple strategies that are known to be effective, are far less expensive, and pose no risk to the patient.
“The Atlantic … [had] one of the most … provocative, quotes I've ever heard from a standard cardiologist,” Cowan says. “This was from Dr. Mandrola ... [H]er quote … summarizes exactly what we're talking about … [Q]uote: ‘This study will begin to change the mindset of cardiologists and patients that focal blockages need to be fixed.’
Focal blockages are these blocked arteries that they put the stents in. Quote: ‘Instead, these findings help doctors and patients understand that coronary artery disease is a diffuse systemic disease. A focal blockage is just one manifestation of a larger disease’ …
Now, the thing that was so shocking to me about that is... this is literally the first time I've ever heard a cardiologist admit that there is a diffuse focal disease here, of which blocked arteries is only one of the manifestations. That is such a heretical position. I've never heard a cardiologist say that. They say, ‘You have blocked arteries. That's your problem. We're going to unblock your arteries.’
To suggest that what they have is a systemic disease changes everything. I can't emphasize that enough. This is not a blocked artery disease. A blocked artery may or may not be significant symptom in this disease. The question that I would ask every listener [to pose to their cardiologist is] … ‘I wonder what diffuse systemic disease this [blocked artery] is a manifestation of?’
I mean, that's the question. ‘I've heard there's a cardiologist who's saying that this blocked artery is only one manifestation,’ which then, of course, is a perfect explanation for why stents don't work. [Blocked arteries are] not the disease. They're just one of the symptoms of the disease. ‘If that's the case, then what's my disease?’ I would be very interested to hear the answer.”
High Cholesterol Does Not Cause Heart Attacks
As noted by Cowan, many cardiologists would probably answer that question saying the underlying problem is high cholesterol. Alas, the evidence does not support this position either. “I actually looked up four papers, [one] in JAMA, three in The Lancet, showing that life expectancy tends to increase as cholesterol goes up, and that there is no relationship between high cholesterol and death,” Cowan says.
Many other studies have also come to this conclusion. In short, the “diffuse systemic disease” behind blocked arteries is NOT high cholesterol. So, what is? The answer to this question is detailed in Cowan’s book, “Human Heart, Cosmic Heart,” which we reviewed in an earlier interview. The book explores and tries to answer the question of why people have heart attacks if it’s not blocked arteries.
In his 2004 book, “The Etiopathogenesis of Coronary Heart Disease,”3 the late Dr. Giorgio Baroldi wrote that the largest study done on heart attack incidence revealed only 41 percent of people who have a heart attack actually have a blocked artery, and of those, 50 percent of the blockages occur after the heart attack, not prior to it. This means at least 80 percent of heart attacks are not associated with blocked arteries at all. So, what’s really the cause of a heart attack? Cowan explains:
“It's obviously complex, and there's a number of manifestations, but the three most important things that I point out in my book is, No. 1 ... at least 90 percent of people who have a heart attack have an autonomic nervous system imbalance. Specifically, they have a suppressed parasympathetic nervous system tone, which is caused by a number of things, including chronic stress, poor sleep, high blood pressure, diabetes, i.e. a high-sugar, low-fat type of diet [and] smoking …
Conventional cardiologists are certainly aware of the role of the autonomic nervous system, which is why standard cardiology care includes beta blockers, which block the sympathetic nervous system, but again, the actual research on this does not show chronic high sympathetic activity. It shows chronic low parasympathetic activity. I would admit they're similar, but they're not the same.
What's dangerous to people's health is chronic stress, chronic sleep deprivation, high carbohydrate diet, low mitochondrial function. All the things that you talk about in your book [‘Fat for Fuel’] that leads to low sympathetic tone. Then, in the face of a sympathetic stressor, you have a heart attack. It's not the same to say it's a sympathetic overactivity, which is why I think we could do a lot better than blocking the sympathetic nervous system.”
The Riddle’s Solution
The second reason for heart attacks, Cowan explains, is lack of microcirculation to the heart. To understand how the blood flows to and through your heart, check out the Riddle’s Solution section on heartattacknew.com’s FAQ page.4 There, you’ll find detailed images of what the actual blood flow looks like. Contrary to popular belief, blood flow is not restricted to just two, three or four coronary arteries (opinions differ on the actual number).
Rather, you have a multitude of smaller blood vessels, capillaries, feeding blood into your heart, and if one or more of your main arteries get blocked, your body will automatically sprout new blood vessels to make up for the reduced flow. In other words, your body performs its own bypass. According to Cowan, your body is “perfectly capable of bringing the blood to whatever area of the heart it needs, and as long as your capillary network is intact, you will be protected from having a heart attack.”
Naturally, this raises the question of what might cause an individual to not have a robust network of capillaries. Not surprisingly, the same factors that cause low sympathetic tone also lead to loss of microcirculation. For example, smoking has a corrosive effect on microcirculation, not just in your extremities but also your heart. A high-sugar, low-fat diet, prediabetes and diabetes, and chronic inflammation also reduce microcirculation.
“We know that overt diabetes actually corrodes and destroys your microcirculation, your capillary network,” Cowan says. “That's a predominant reason. We have millions of people living on high-carbohydrate diets, low-fat diets, which has an inflammatory effect on their microcirculation. There are other reasons, too, but those are probably the big ones.”
Naturally, one of the most effective ways to encourage and improve microcirculation is physical movement, so chronic inactivity will also deteriorate your body’s ability to maintain healthy microcirculation. “Again, conventional cardiology is aware of this issue. That's why they use Plavix and aspirin, to keep the microcirculation intact,” Cowan notes.
The Role of Mitochondria in Heart Attacks
Another area of concern is your mitochondria. Unfortunately, this is an area that conventional cardiology is still largely unfamiliar with. In essence, angina is a symptom of poor mitochondrial function, causing a buildup of lactic acid that triggers cramps and pain. When this pain and cramping occurs in your heart, it’s called angina. The lactic acid buildup also restricts blood flow and makes the tissue more toxic.
When a cramp occurs in your leg, you stop moving it, which allows some of the lactic acid to drain off. But your heart cannot stop, so the glycolytic fermentation continues, and the lactic acid continues to build up, eventually interfering with the ability of calcium to get into the muscle. This in turn renders the muscle — in this case your heart — unable to contract, which is exactly what you see on a stress echo or a nuclear thallium scan.
“You see a dyskinetic or an akinetic muscle, which means it doesn't move, because the calcium can't get into the cells because the tissue has become too acidic,” Cowan explains. “Eventually, the acidosis continues, and that becomes the cause of necrosis of the tissue, which is what we call a heart attack …
By the way … [the] dyskinetic area … the part of the heart that's not moving, creates pressure … in the artery embedded in that part of the heart, which causes clots to break off. That explains why you get clots forming after the heart attack, not before. This lactic acidosis buildup is one of the key events, without which you won't have angina, and you won't have the progression to necrosis.
Those are the three [primary causes of heart attacks]: The autonomic nervous system, the microcirculation and lactic acid buildup. Luckily, there are safe, nontoxic, effective ways to address each of those, either individually or together.”
Enhanced External Counterpulsation — A Noninvasive Treatment Alternative
One highly effective and noninvasive treatment option that will help improve microcirculation to your heart — which, again, is a common factor responsible for heart attacks — is enhanced external counterpulsation (EECP). It’s a Medicare insurance-approved therapy, and studies show EECP alone can relieve about 80 percent of angina.
As explained earlier, the reason you don’t experience a heart attack due to blockage is because you’re protected by collateral circulation. However, if you have diabetes or chronic inflammation, that will eventually deteriorate your capillaries, reducing this built-in protection. EECP works by inflating compression cuffs on your thighs and calves that are synchronized with your EKG.
When your heart is in diastole (relaxed), the balloons inflate, forcing blood toward your heart, thereby forcing the growth of new capillaries. It’s a really powerful and safe alternative to coronary bypass surgery for most people. Rather than bypassing one or two large arteries, you create thousands of new capillary beds that supply even more blood than the bypassed vessels. As noted by Cowan:
“New blood vessels mean more blood flow, and the blockage becomes irrelevant. This has been shown to be curative, meaning it will stop people with angina for at least five to seven years with one course of treatment … sometimes longer. It's Medicare approved.
It's paid for by insurance. It's been studied in the literature. Again, at least 80 percent effective for getting rid of patients' angina, which, by the way, was the last [indication] for stents, which is now no longer [a valid indication].”
The sessions are about one hour long, and most patients will need about 35 sessions to receive benefit. Aside from angina, it’s also effective for heart failure and diastolic dysfunction. Many elite athletes also use it as an aid to maintain cardiac fitness when they are injured and unable to actively exercise, as EECP basically works as a passive form of exercise. To find a provider, visit EECP.com.5
Interestingly, EECP also appears to have hormonal benefits. There are studies showing it results in decreased insulin resistance. Many patients also tend to lose weight, and experience improved blood sugar control. There’s cause to believe these beneficial side effects are related to the fact that it mimics exercise.
I was so intrigued with EECP’s benefits that I actually purchased one. They aren’t cheap; the traditional ones are close to $50,000, but I found a bright young entrepreneur, Louis Manera, who was well connected in the EECP community and is actually in the process of providing great new units at a significant discount. If you are a clinician, or even a patient with heart disease, this is something you might want to consider.
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