As a cardiologist focused on prevention my goal is to see patients before they have a heart attack (myocardial infarction or MI). If I can assess risk and start appropriate lifestyle and pharmacologic treatments early in their life, even the highest risk patients can live their entire lives free of MI and without cardiac interventions like stents and bypass operations.
But what about those patients who have already had an MI at a young age. Although I’ve seen a fair number of patients have their first MI in their 40s, and a lot in their fifties it is rare to have it at age 37 as one reader (who we will call Arthur) described in an email to me.
Patients like Arthur are rightfully quite anxious about their heart health and typically have lots of really good questions about the cause of their early disease, the best treatments and lifestyle changes, and their long-term prognosis. There is often a sense that drastic or draconian diet changes are needed.
In preventing future cardiac problems for Arthur, we are engaged in “secondary prevention.” But what of pre-MI Arthur? Pre-MI Arthur had silently developed atherosclerotic plaques in his coronary arteries that were at high risk for rupturing or fissuring and causing his MI. With his first MI, he could have dropped dead.
Thus, pre-MI Arthur, who is totally free of any symptoms of significance would benefit equally from the diet, lifestyle changes, and medications we recommend for post-MI Arthur.
What follows are selections from my reader’s email with my accompanying comments.
Dear Dr Pearson, first off a big thanks to you for your efforts in providing up-to-date and scientifically grounded musings on cardiovascular-related topics in your blog, which is accessible while shying away from oversimplifying or being condescending towards the reader.
Thank you! It is encouraging words like this that motivate me to continue this pro bono project.
I’m writing to you because a couple of years ago, right around my 37th birthday, I had the dubious pleasure of being surprised by a massive heart attack from a 99% blockage in the LAD artery. After several days of struggles in the hospital (most of which I fortunately was not conscious for) I pulled through thanks to a stent, with perhaps surprisingly not too much apparent damage to the muscle, and a normal ejection fraction.
Readers may have gotten the impression that I am philosophically opposed to stents in patients with coronary artery disease but the this young man’s history exemplifies the precise presentation for which stents work wonderfully-an acute heart attack.
The heart muscle supplied by the LAD (left anterior descending) coronary artery (aka the widow maker) begins to die within minutes of a 100% blockage but if the LAD is opened with a stenting procedure within 90 minutes of the onset of the blockage the death of muscle is interrupted. Thus, one can emerge from this process without damage to the main pumping chamber of the heart (left ventricle), typically measured by the percentage of blood ejected from the left ventricle (aka the ejection fraction.)
Arthur goes on to reveal some background information on his case
I don’t want this email to devolve into a lengthy dissertation on the background of this incident, let’s suffice it to say that while I had suffered some odd symptoms in the form of sustained palpitations during the days before this happened, and while my labs/vitals were not necessarily “perfect”, I didn’t suffer from hypertension, hyperlipidemia, diabetes (non-smoker) and I exercised regularly. But of course non of this offers a “guarantee” as you’ve certainly touched upon in posts on your blog.
It is not uncommon for patients to recall symptoms in the days or weeks leading up to their first heart attack. If the symptom is a briefer, less intense version of the main symptom that prompted them to call EMS for their MI it is likely these were true warning symptoms.
But palpitations are so common and typically benign that they are not a useful harbinger of an MI.
As I discussed here , absence of the standard risk factors despite an exemplary lifestyle and diet does not protect you from our reader’s fate.
The High Fat Diet? Safe or Not
Now my question: I mentioned that quick background to note some things that are encouraging: a high level dose of atorvastatin has helped get my LDL down to 40-50. Metropolol has helped keep my systolic blood pressure controlled, and during the catheterization (or in conjunction), my cardiologist didn’t really notice much more build up than in the area mentioned above (I’m aware though that this “might” also be typical in very premature cases). The only area where I feel I somewhat deviate from the guidance I have received, is in terms of my diet. Before, I wasn’t necessarily splurging on red meat, but I was certainly more relaxed about consuming saturated fat than I am today. For a long time, I have been eating in a way that perhaps most closely resembles the Mediterranean diet, but perhaps with more emphasis on foods high in unsaturated fats. These days, I might consume a diet of around 7% of total calories from saturated fat (mostly dairy) and as much as 45% of total calories from fat stemming from (mainly) a variety of nuts, but also meat alternatives like avocado.
The diet you are describing is excellent for a patient with premature coronary artery disease as long as 1) you are maintaining a good body weight 2) getting lots of fruit and vegetables and 3) you enjoy it and find it sustainable for the rest of your life.
Unfortunately, there is no evidence that changing to a vegan or vegetarian diet will lower your risk of repeat MI. Those who promote the Esselstyn, Pritikin or Ornish type diets claim to “reverse heart disease” and to be science-based but, as I’ve pointed out (see here) the science behind these studies is really bad.
Some individuals just inherit the risk and must learn to deal with the cardiovascular cards they’ve been dealt. Although proponents of very low fat consumption (both saturated and unsaturated fats or oils) like Esselstyn ( see my debunking of the incredibly bad science behind his dietary recommendation here) claim their diets reverse coronary atherosclerosis this is a false claim.
The PREDIMED study published in 2013 in the New England Journal of Medicine was a landmark primary prevention study that demonstrated that a higher fat diet,with a lot of that fat unsaturated, is superior to a low-fat diet in reducing cardiac events.
Participants were randomized to one of three diets: a MED supplemented with extra-virgin olive oil, MED supplemented with mixed nuts or a control diet (advice to reduce dietary fat). Participants received quarterly individual and group educational sessions and either free provision of olive oil, mixed nuts or small nonfood gifts.
The high extra virgin olive oil group ingested an average of 3.6 tablespoons/day (51 grams/day equal to 459 calories/day) of olive oil with 98% of it being extra virgin olive oil.
The high nut group ate 8.2% of their total daily calories in the form of nuts, including an additional approximately one-ounce packet of nuts (15g of walnuts, 7.5 g of almonds, and 7.5g of hazelnuts) provided by the study coordinators.
7447 persons were enrolled (ages 55 to 80 years) for an average 4.8 years.
Those persons following the MED diet (either supplemented with olive oil or nuts) were 30% less likely to have a major cardiovascular event (heart attack, stroke or death from cardiovascular causes.) There was a statistically significant reduction in stroke rate (≈39%) when considered as an isolated endpoint.
We don’t know exactly what components of the MED are the most beneficial. This trial suggests that olive oil and nuts are at least two of the key ingredient so it makes sense to increase your consumption of these foods.
As I’ve discussed (?ad nauseam) in other posts, full-fat dairy and eggs, although banned by most “heart-healthy diets”, have not been shown to increase heart disease risk. Fermented dairy consumption, in particular, in the form of plain full-fat yogurt (not adulterated with sugar) and full-fat cheese is consistently associated with a lower risk of coronary heart disease. Plain full-fat yogurt and full-fat cheese (from goat milk) were consumed by the inhabitants of Crete, the Greek Island on which the original MED was based.
It has to be emphasized that within this pattern of eating you want to be consuming real foods, not processed products of the industrial food industry which have been manipulated to appear healthy due to being “low-fat” or “low cholesterol.”
The Mediterranean diet is a pattern of eating which is varied, interesting and sustainable. It is a diet that can last a lifetime.
This Table summarizes dietary recommendations for those on the Mediterranean diet versus those on the Low-Fat diet.
The vast majority of evidence in cardiac nutrition shows that unsaturated fat consumption when replacing carbohydrates, especially refined carbohydrates, is beneficial.
Secondary Prevention: the CORDIOPREV trial
PREDIMED was a primary prevention trial; patients had not experienced MIs, stents, bypasses, or strokes. Arthur is now considered a case of secondary prevention.
There is a similar ongoing trial of secondary prevention, The CORDIOPREV study (Coronary Diet Intervention With Olive Oil and Cardiovascular Prevention) with the primary objective of comparing the effect of 2 healthy dietary patterns (low-fat rich in complex carbohydrates versus a Mediterranean diet rich in extra virgin olive oil) on the incidence of cardiovascular events.
Last November, the results of one secondary outcome of the CORDIOPREV study were published. At baseline, subjects underwent ultrasonic evaluation of their carotid arteries to assess the intima-media thickness of both common carotid arteries (IMT-CC.) In addition, researchers measured carotid plaques (number and height), at the beginning of the study and after 5 and 7 years of dietary intervention. I’ve utilized IMT-CC (aka vascular age) and early carotid plaque to identify subclinical atherosclerosis in the youngish.
IMT-CC significantly decreased at 5 and 7 years compared to baseline in the Med diet group but did not decrease in the control, low-fat group.
The maximal height of carotid plaques significantly decreased in the Med diet group whereas it increased in the control group.
We are awaiting the long-term outcome data from CORDIOPREV but these data showing regression of carotid plaque height and decline in IMT are very encouraging that the higher fat Med diet can cause regression of atherosclerosis (in conjunction with modern pharmacologic CAD therapy).
Mediterranean-style Ketogenic Diets
A randomized controlled trial published in the journal Obesity a year ago demonstrated superior weight reduction with a high-fat Mediterranean diet compared to a low-fat diet with similar levels of LDL-C at the end. The high-fat dieters utilized the Keyto device and app which I’ve written about (I Am A Keto-Friendly Cardiologist And I Love Keyto) and as described below focuses on unsaturated fats from plants.
The Mediterranean-style ketogenic diet app, paired with a breath acetone biofeedback device, uses a traffic light system to recommend consumption of foods (ad libitum, cautiously, avoid) according to the amount of net carbohydrates based on nutritional information gathered from the United States Department of Agriculture food database. The app emphasizes avoidance of refined carbohydrates, and priority is placed on fats from plant- (e.g., olive oil, avocado, nuts) and fish-based (e.g., salmon) sources that fit the Mediterranean guidelines
Arthur is not eating a ketogenic diet but my point is that even if you upped your fat consumption to ketogenic levels with mostly unsaturated fats you would not be increasing your cardiovascular risk.
I would also be fine with Arthur liberalizing his saturated fat content. For those who choose the ketogenic diet under my care, we carefully watch biomarkers including the LDL-C and advanced biomarkers I mention below.
I am happy with how this diet makes me feel during the day, and it seems to help me with weight management. But I’m of course aware of how my relaxed attitude towards total fats (as % of calories) deviates from most of the standard advice for my situation. Here I take some comfort in that my cholesterol (and triglycerides) seems to fall within a good range. But my question is if this is a naive way to view my dietary choice? Are there other mechanisms/channels suggested by the research whereby a high-fat (even if not heavy in saturated fat) diet might contribute to continued atherosclerosis?
It is wonderful that you have found a diet you are so happy with.
The major thing right now that is putting your LDL-C in such a low range (and lowering your risk of future cardiac problems) is the high-dose statin that you are taking. There is no evidence that lowering your unsaturated fat intake would further lower that. More importantly, there is nothing to suggest that changing the macronutrient composition of your current diet will lower your risk of further events.
With the LDL-C in its current range (assuming no smoking or uncontrolled diabetes) you will have regression of any plaque and minimal cardiac events. Your prognosis is excellent.
Thoughts on Patients with very Premature CAD
Just to note, I’m also aware that the isolated focus on macronutrients may be misplaced as well. But of course I can’t help but notice areas that I have control over where I might deviate somewhat.
Finally, of course I’m curious what your thoughts might be around premature cases. Even though my understanding is that the prognosis is typically not “great”, are there some things the research has pointed to in terms of contributing to (relatively) successful outcomes for very premature CAD? Or perhaps the opposite – mistakes often made in treatment of premature cases (for any number of reasons) that might exacerbate the risks?
I talk about premature CAD a lot on this blog. I’m a big proponent of the early detection of advanced or premature asymptomatic CAD. About a year ago I summarized the optimal approach.
Depending age we utilize either coronary artery calcium screening or vascular screening to detect subclinical atherosclerosis for primary prevention.
For those with advanced subclinical atherosclerosis, a strong family history or a history like my reader of early heart attack, stent, bypass or stroke I check three key biomarkers that are not in the standard lip panel
- Lipoprotein (a) (a highly atherogenic, inherited marker that is not measured in standard lipid panels)
- Apolipoprotein B (apoB, now recognized as our single best measure of atherogenic dyslipidemia)
- High-sensitivity CRP (the most studied and useful measure of inflammation)
You didn’t mention lipoprotein (a) but this has to be checked. In patients like you with such early onset of symptomatic CAD with fairly unremarkable standard risk factors , I find the majority have elevated lipoprotein (a).
Once risk markers are identified we are going to have very aggressive goals for lowering apo B, LDL-C and CRP. These will be accomplished by statins as tolerated with help of other lipid-lower agents known to reduce cardiovascular risk including ezetimibe and PCSK9inhibitors.
N.B. Since I started writing this and shortly before I published this the final results of the CORDIOPREV trial were published (https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)00122-2/fulltext).
This did show a reduction in major cardiac events with the high fat Med diet compared to the low fat diet! I will examine this in more detail and report back.
h/t Marilyn Mann