I’ve just finished watching a documentary on Netflix called The Widowmaker which alternately had me fascinated, disgusted, bored, excited, and angry.
This movie is about the treatment of coronary artery disease and what we can do about the large number of people who drop dead from heart attacks, some 4 million in the last 30 years.
The documentary, as all medical documentaries tend to do, simplifies, dumbs down and hyperbolizes a very important medical condition. Despite that it makes some really important points and I’m going to recommend it to all my patients.
At the very least it gets people thinking about their risk of dying from heart disease which remains the #1 killer of men and women in the United States.
Perhaps it will have more patients question the value of stents outside the setting of an acute heart attack. This is a good thing.
Perhaps it will stimulate individuals to be more proactive about their risk of heart attack. This is a good thing.
Take a look. Think about it. If you decide you might benefit from a coronary calcium scan of your heart let me know.
I’ll dissect this movie in detail in subsequent posts. There are a lot of inaccuracies but some fundamental and important points are made that patients need to now.
Stents do not prevent heart attacks.
Standard risk factors do not do well at predicting who will have a heart attack.
It is a reasonable question. If statins are a treatment for abnormally high cholesterol levels why would we start them on a patient with normal or low levels.
The answer is that we are not concerned with cholesterol levels. What we are concerned with is atherosclerotic cardiovascular disease (ASCVD) and its downstream consequences including heart attack and stroke.
Thus, the new guidelines recommend calculating a patient’s 10 year risk of heart attack and stroke due to ASCVD ( see here for my discussion of smart phone app that makes this calculation) and if it is over 7.5% to consider starting a statin drug to reduce ASCVD risk.
Cholesterol is just one of many factors that effect the risk but we know that irrespective of cholesterol level, starting a statin will substantially lower the risk.
A patient who has smoked cigarettes lifelong asked me this question recently.
When I plugged the patient’s excellent cholesterol values into the ASCVD app, the 10 year risk of heart attack or stroke was quite high, 14.9%. Bad cholesterol (LDL) was 90, well below what is considered optimal. Good cholesterol (HDL) was 60, well above what is considered optimal.
Studies have demonstrated that even patients with cholesterol numbers this good benefit from statin therapy. Their risk of heart attack and stroke will be substantially reduced over time.
My patient has not yet had a heart attack or stroke and it is likely that despite engaging in the extremely damaging behavior of cigarette smoking , the genetically programmed excellent cholesterol values have somewhat protected from ASCVD.
However, a vascular screening study has demonstrated that early atherosclerotic plaque in both the patients carotids. The patient has ASCVD and it is only a matter of time if the patient keeps smoking before the patient has a clinical event related to it.
I told my patient that if he/she stopped smoking cigarettes his/her estimated 10 year risk would drop to 9.7% and I would not recommend statin therapy.
We discussed methods to help quit and the patient indicated that the patient would start using a nicotine patch and try to quit in the next few months.
Unfortunately, at follow up smoking was ongoing.
Thus, my recommendation to start statin therapy despite her excellent cholesterol values.
Other groups of patients besides cigarette smokers can have advanced or premature ASCVD with excellent or “normal” cholesterol values. Diabetics often have low bad cholesterol values associated with low good cholesterol and high triglycerides.
Sometimes, ASCVD develops prematurely even in patients who have a low 10 year risk based on standard risk factors. This is usually in patients with a strong family history of ASCVD who have an inherited atherogenic abnormality of lipid metabolism that is not manifested in the standard cholesterol parameters (see Dealing With the Cardiovascular Cards You’ve Been Dealt).
To identify these patients a search for subclinical atherosclerosis by vascular screening or coronary calcium scan is necessary. When advanced plaque is identified statin therapy is often warranted even with a low estimated 10 year risk and normal cholesterol values.
So some patients can have very high cholesterol values and I don’t recommend any therapy, some have low and I do. I’m much more focused on the presence or absence of ASCVD in my treatment decisions.
Ultimately we are not treating “high cholesterol” when we start cholesterol lowering therapy we are working to prevent or slow the progression of ASCVD,
I can tell you exactly when the pain started. I was riding my bike in Forest Park, the great urban park of St. Louis. Ordinarily, I cycle from my house to the park, cutting across the ivy-covered semi-Ivy league campus of nearby Washington University and circling its beautiful acres on a recently refinished bike path.
As I started the slow incline that parallels Skinker Avenue just West of Forest Park, a cyclist flashed past me. I could swear he said “Oh dear, oh dear. I shall be late.”
Instead of continuing straight along the bike path, the late cyclist suddenly veered to the left, following a heretofore untraveled spur that led up into the dark, impenetrable forests of the park.
At this point, the sensible, sixty-something portion of my psyche should have taken over and had me continue on the relatively straight, flat and well-traveled road that I had grown accustomed to. Alas, it was the teenage boy who took control and insisted on us taking the road less traveled.
The spur of the bike path had not been regularly maintained and there were numerous rough spots: ridges and chasms emerged with disconcerting frequency as I progressed.
The lure of exploration pulled me on. I kept my speed up as I descended a hill with the path turning sharply to the right. Suddenly an even sharper right turn emerged with a particularly uneven section of path. I lost control of the bike and landed heavily on my left side.
I felt a sudden sharp pain just to the left of my breastbone about midway in my chest.
As a cardiologist I spend a lot of time talking to people about chest pain and thinking about what is causing it.
The heart is in the chest and it is natural to believe that pain that comes from this area could be a manifestation of the dreaded heart attack. Since heart attacks are the #1 killer of both men and women and they can very quickly lead to life-threatening arrhythmias it is wise to take seriously any pain in the chest.
Three Types of Chest Pain
I was trained to sort what patient’s described to me about their chest pain into three bins: Typical anginal pain, atypical anginal pain and non cardiac pain.
Angina is doctor-speak for chest pain that is due to the heart muscle not getting enough blood (usually due to a blocked coronary artery)
Cardiologists consider any discomfort from the lower ribs up to the bottom of the neck as chest pain although patients often don’t perceive it as a pain.
Heart attack pain often feels like a pressure, a heaviness or a burning and in addition to somewhere in the anterior chest region it can manifest in the neck or jaw or one or both of the upper arms.
My chest pain was worse when I took a deep breath (pleuritic) and this almost always indicates a lung cause or inflammation in the muscle/bones/joints that are related to breathing. Furthermore, pushing on the ribs made it worse making it virtually certain that it was musculoskeletal.
A brief (well done) history and physical exam therefore would assign my chest pain to the “non cardiac” bin.
Typical anginal pain is brought on by exertion, lasts 3-15 minutes and is relieved by nitroglycerin or rest.
The probability of a patient with non cardiac chest pain having significantly blocked coronary arteries is generally lower than that of a patient with typical anginal pain. However, as this chart demonstrates, patients (generally those with significant risk factors) can have severely blocked coronary arteries and have non cardiac chest pain.
For example, I have risk factors of age (>55 years), being male, hyperlipidemia and hypertension. A cardiac catheterization done on me at the time of my non cardiac chest pain might well show significantly blocked coronary arteries. Of course, these blocked arteries would have absolutely nothing to do with my pain.
This fundamental paradox is the source of a lot of the overtesting and over treatment that occurs in cardiology. Most of the time, chest pain that prompts a patient to come to the ER or doctor’s office does not fall easily into the non cardiac category or the typical anginal category: these are the atypical anginal patients.
Additional testing is required , progressing from EKGS and cardiac enzymes to stress testing to cardiac catheterization. If there are elevation of the cardiac enzymes or abnormalities of the EKG that indicate a recent or active heart attack then a cardiac catheterization is warranted because it is very highly likely that a tightly blocked coronary artery is the cause and opening that artery will be beneficial.
However, most patients have normal cardiac enzymes and unremarkable EKGS and can end up getting catheterizations (due to either inaccurate stress tests or cardiologist’s recommendation) that they don’t need.
Once a catheterization is done, patients may then get a stenting procedure on a blocked coronary artery that wasn’t causing any problems. Not uncommonly, multiple blocked coronary arteries are found and the patient is rushed off to have a bypass operation. If the blocked arteries weren’t the cause of the patient’s chest pain (i.e. the pain was non cardiac) these procedures are likely doing more harm than good.
When To Go To ER With Chest Pain
I’ve spent thirty years fielding after hours telephone calls from patients who are having chest pain.
It is not easy to make a reliable determination of who is likely having a heart attack or other potentially dangerous cardiac problem and who is not just based on the history.
If a patient called me describing what I described above I would likely advise him to go to the ER for evaluation (although I would be pretty sure it wasn’t a heart attack: sometimes rib fractures are associated with collapsed lungs or hemorrhage into the pleural space and sometimes trauma to the chest can cause heart damage). It’s always better to err on the side of caution when were’ dealing with potentially life-threatening problems.
After office hours, the only way to get an electrocardiogram and cardiac enzymes to be sure that the chest pain is or is not a heart attack is to go to an ER. Generally, if the patient has escalated the level of concern to calling the on call cardiologist, the symptoms are worrisome.
The bottom line for me is that you only get one chance to die (You only die once (YODO)
If you’re having a heart attack at any second your heart can go into ventricular tachycardia or ventricular fibrillation and you will die within minutes.
Thus, I have to have a very low threshold for advising trips to the ER. If I’m wrong, the patient could die.
I didn’t go to the ER because I was 100% certain that my chest pain was non cardiac. I’m also a doctor and therefore a very bad patient. I survived, however, and over several weeks the pain gradually subsided.
As a result of this fall (and several other bike falls I’ve had in the last few years) I’ve re-evaluated my cycling. I’m going to stay on very well-maintained paths and slow way down when the going gets rough.
Hopefully, this will allow me to continue the cycling which I’m convinced is helping to prevent me from visiting the ER with a true heart attack!
Since I’ve been utilizing coronary calcium CT scans to detect early atherosclerotic plaque (see here) in my patients, I have frequently been asked about the relationship between calcium supplements and heart attack risk.
For example, Mrs. Jones has just found out that she has a very high calcium score and that it reflects the amount of atherosclerotic plaque lining and potentially clogging the coronary arteries to her heart. She has also been taking calcium and Vitamin D supplements recommended to her to prevent bone thinning and fractures in the future.
Did all that extra calcium she was consuming end up depositing in her coronary arteries, thus increasing her risk of heart disease?
This is a complex and not fully settled issue, however, there is enough evidence to suggest that we be cautious about calcium supplements.
A recent meta-analysis (Bolland MJ, Avenell A, Baron JA, Grey A, MacLennan GS, Gamble GD, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ 2010;341:c3691) of cardiovascular events in randomized, placebo controlled trials of calcium supplements (without vitamin D co-administration) showed that calcium supplements significantly increased the risk of myocardial infarction by 31% in five trials involving 8151 participants.
A recent meta-analysis of trials involving calcium and Vitamin D supplements found a similar increased risk of cardiovascular disease in the subjects randomized to taking calcium and Vitamin D.
These authors concluded
“in our analysis, treating 1000 patients with calcium or calcium and vitamin D for five years would cause an additional six myocardial infarctions or strokes (number needed to harm of 178) and prevent only three fractures (number needed to treat of 302”
How Might Calcium Supplements Increase Cardiovascular Risks?
Calcium supplements acutely and chronically increase serum calcium concentration. Higher calcium levels are associated with more carotid artery plaque, aortic calcification, and a higher incidence of heart attack and death.
Just like atherosclerosis, the process of calcium deposition into the arteries is very complex. Higher calcium levels could alter certain regulators of the process, such as fetuin A, pyrophosphate and bone morphogenic protein-7 or bind to calcium receptors on vascular smooth muscle cells lining the arteries
Higher calcium levels may also promote clot formation.
Bone Fracture versus Heart Attack
The informed doctor would have to tell Mrs. Jones that her calcium supplements may have contributed to her advanced coronary calcium and raised her risk of heart attack and stroke.
As with all medications, she and her doctor are going to have to discuss the relative risks and benefits.
If she has great concerns about fractures and has very low bone mineral bone density (osteoporosis) along with no family history of premature heart disease then the calcium supplementation may be appropriate.
Conversely, if she has high risk factors for coronary heart disease and/or a strong family history of premature coronary heart disease and only slightly low bone mineral density, avoiding the calcium supplements would be appropriate.
Preventing Fractures and Heart Attacks
It’s best to get calcium from the foods we eat rather than a sudden concentrated load of a supplement. Full fat dairy products like yogurt and cheese are heart healthy (see here and here) and they are an excellent source of calcium.
Weight-bearing exercise (such as running/jogging/hiking) and strength-building exercise (lifting weights, resistance machines, etc.) are also important for strengthening bones.
Thus, eating full fat dairy and aerobic exercise will help prevent both a fracture and a heart attack.
Important findings from the IMPROVE-IT trial were presented at the American Heart Association meeting yesterday. They demonstrate for the first time that the cholesterol lowering drug ezetimibe (brand name Zetia) lowers the risk of heart attack and stroke when added to a statin drug in high risk patients (those who have sustained a heart attack or had unstable angina) over a statin drug plus placebo.
That study showed
The primary endpoint of CV death/MI/UA/coronary revascularization beyond 30 days/stroke was significantly lower in the ezetimibe/simvastatin arm compared with the simvastatin arm over the duration of follow-up (32.7% vs. 34.7%, hazard ratio [HR] 0.94, 95% confidence interval [CI] 0.89-0.99; p = 0.016).
Prior to this study, Zetia had been prescribed to millions of patients since 2002 garnering Merck, its maker, profits of 30 billion dollars despite there being no evidence that it reduced heart attack or stroke.
Dr. Melissa Walton-Shirley wrote an excellent article on the status of Zetia at the beginning of 2014, summarizing thusly:
Perhaps the lesson to be learned is that starting in 2014, let’s not put compounds on the market for human ingestion without knowing if they help or hurt. Let’s make it unacceptable for a company to make tens of billion dollars from the sale of a compound without knowing if it lowers mortality or improves quality of life
I have previously bashed Zetia on this site and I only prescribe it in very rare cases. These new data may change my approach.
Before embracing Zetia, though, I want to see the full paper in published form and examine the data in detail. Many questions need to be answered. For example, the addition of the drug to simvastatin lowered heart attack and stroke compared to simvastatin alone but there was no difference in overall death rates or cardiovascular death rates. That raises a red flag.
In addition, this study does not support the use of Zetia in patients who have not had heart attacks or near heart attacks (primary prevention).
Science moves slowly but inexorably toward the truth if done properly. It’s important that public policy and drug prescribing not get in front of the science as it did with this drug.
The other night I had the best cioppino I have ever had. I’ve had variations of this wonderful tomato-based seafood stew all over the world (including the legendary bouillabaisse in Marseilles) but I left my heart with the Dungeness crab cioppino served at Sotto Mare Oysteria and Seafood restaurant in North Beach, San Francisco. It makes sense, since cioppino was invented by Genoan fishermen from the SF Bay Area in the 19th century who threw together the freshest catch from their day at sea.
The recipe for Sotto Mare’s cioppino is actually available online as follows:
¼ cup olive oil
1 tsp. crushed red chile flakes
8 cloves garlic, finely chopped
3 cups fish stock
1 ½ cups whole peeled tomatoes in juice, crushed
10 leaves basil
1 lb. cod, cut into 2″ chunks
1 lb. cleaned calamari, bodies cut into ½″-wide rings
12 oz. medium shrimp, deveined
12 oz. bay scallops
16 clams, cleaned
16 mussels, cleaned
2 2-lb. Dungeness crabs or snow crab legs, halved
Kosher salt and freshly ground black pepper, to taste
It involves a lot of shellfish: calamari, shrimp, scallop, clams, mussels, crabs and I think a large part of what made it so good was the freshness of the shellfish obtained from the nearby Pacific Ocean.
Shellfish, Dietary Cholesterol and Cardiovascular Risk
Shellfish contain a lot of cholesterol and many of my patients have been told to minimize or avoid shellfish, especially shrimp, due to concerns they will exceed the (completely arbitrary) 300 mg daily limit suggested by the American Heart Association and the USDA nutritional guidelines.
There is no scientific basis for being concerned about the amount of cholesterol one consumes when eating shellfish (or for any food for that matter, as I previously wrote about with regard to eggs here)
But there are definitely warnings out there on the internet and traditional new media from seemingly responsible authorities.
“Since our bodies make plenty of cholesterol for our needs,we do not need to add any in our diet. Cholesterol is found in all foods that come from animals: red meat, poultry, fish, eggs, milk, cheese, yogurt, and every other meat and dairy product. Choosing lean cuts of meat is not enough; the cholesterol is mainly in the lean portion. Many people are surprised to learn that chicken contains as much cholesterol as beef. Every four-ounce serving of beef or chicken contains 100 milligrams of cholesterol. Also, most shellfish are very high in cholesterol. All animal products should be avoided for this reason. “
The Physician Committee for Responsible Medicine appears to be a front for vegan-promotion. They go on to state that every 100 mg of cholesterol you consume raises your cholesterol by 5 mg/dl and that
“Every time you reduce your cholesterol level by 1 percent, you reduce your risk of heart disease by 2 percent. For example, a reduction from 300 mg/dl to 200 mg/dl (i.e., a one-third reduction) will yield a two-thirds reduction in the risk of a heart attack”
A Fox News publication simultaneously extolls the virtues of shrimp consumption (noting that “three ounces of shrimp (or about seven medium-sized shrimp) has a mere 84 calories, 1g of fat, and an impressive 18g of lean protein” and that they are a great source of selenium, “an antioxidant that fights cancer-causing free radicals in your body”) and warns you against eating it (“If you are watching your cholesterol, it’s best to go easy on shrimp because four large shrimp have 42.5mg of cholesterol”)
Other publications advise those with high cholesterol or higher risk of heart disease to choose low-cholesterol varieties of shellfish over shrimp.
The Science Supporting Shrimp
Let’s look at what is actually known about consuming shrimp and shellfish.
A study of over 13,000 subjects (the ARIC study) found no increased risk of cardiovascular disease in the high shellfish consumers versus the low shellfish consumers.
A study in 1996 compared consuming a diet with 300 grams (about 10 oz.) of steamed shrimp/day (providing 590 mg of cholesterol daily) versus a baseline diet of 107 mg/ cholesterol in 18 individuals without cholesterol problems. The shrimp consumers compared to baseline had a 7% higher LDL or bad cholesterol but a 12% higher HDL or good cholesterol. Thus, the ratio of total to good cholesterol went down. We now know that this ratio is a much more important risk marker for cardiovascular disease than the total cholesterol. Triglycerides dropped significantly when subjects were consuming shrimp versus the baseline, low cholesterol diet.
A 1990 study looked at multiple different types of shellfish substituted for meat, cheese and eggs, and found that oyster, clam, crab and mussel diets (with lower cholesterol and higher omega-3 fatty acid profiles) lowered VLDL triglycerides and VLDL cholesterol. These shellfish diets, except for the mussel diet, also lowered LDL and total cholesterol. Shrimp and squid had no effect on the lipid profiles.
Benefits of Shrimp and Shellfish Consumption
I’ve focused on shrimp in this post because it has the highest cholesterol content of all shellfish and therefore is the most likely to be considered bad for heart patients or patients with high cholesterol. I’m presuming if I can convince you that shrimp are heart healthy, then you will believe that all shellfish are.
Take a look at this chart of the nutrient composition of shrimp and you can understand that, once you eliminate unsubstantiated fears of the cholesterol content, this a great food.
I am not a big advocate of examining the macronutrient composition of foods in order to predict their health benefits. This approach to nutritional science resulted in the development of highly processed low-fat monstrosities that currently sit in boxes and bags and line the most prominent parts of supermarket shelves. The overall effect of foods on the cardiovascular system depends on an incredibly complicated interaction of food components, bacteria in the gut and genetic predispositions: areas we are only beginning to understand. However, for those readers who are concerned about such things there is reassurance.
Start with the fact that there are no carbohydrates in shellfish: since carbs and added sugar are likely the biggest culprits in our obesity epidemic, shrimp and shellfish are great tools in helping to manage weight. Shrimp have a very high percentage and quality of protein content for muscle building.
Some avid shrimp promoters insist that shrimp should be consumed regularly to reduce the risk of both cancer and heart disease. The fat in shrimp is mostly polyunsaturated fat with a high ratio of omega-3 to omega-6 which is considered optimal . Eating 100 ounces of shrimp daily gives you 180 mg of EPA and DHA (considered the most important of the omega-3 fish oils for heart health) daily, close to the 250 mg daily the USDA recommends for most adults.
Astaxanthin has been found to be a potent natural antioxidant, exceeding ten times the antioxidant activity of β-carotene and 500 times that of α-tocopherol. The astaxanthin level of wild shrimps has been reported to vary between 740 and 1400 μg/100 g in edible meat portions.
If I were a vegan or vegetarian I would consider slipping shrimp into my dishes instead of tofu.
The cioppino recipe above doesn’t add a lot to the shellfish and fish: a little olive oil and tomatoes, basil and garlic-these things are not going to jack up the calories, sugar or fat content.
Depending on how you cook shrimp, the resulting dish will have markedly different nutrient composition compared to the raw nutrients listed above.
Breading and deep frying the shrimp takes 3 oz from 60 calories to 206 and the fat grams from 1 to 10. I suspect that you or your body will figure this out and eat less later. Given the fairly low fat and carbohydrate content of the Sotto Mare cioppino, I am ashamed to admit, I ate that whole bowl pictured above (which the menu said could be shared between two).
The SOSC doesn’t share my love of cioppino; she ordered the linguine with clam sauce. Three ounces of clams have only 26 mg of cholesterol but it seems to me the majority of calories in this dish are coming from the carbs in the pasta and whatever the composition of the sauce is. In any event, the SOSC pronounced it the best she has ever had.
Mercury in Shellfish
The level of mercury is a concern in all the fish that we consume. Fortunately a recent study from Maine University found that shrimp is very low in mercury. This included varieties from Thai shrimp farms, Maine shrimp farms and the Gulf of Mexico. In comparison to other types of fish, shellfish are universally on the low end of the mercury level graph as shown below.
Fear neither the cholesterol nor the mercury in shrimp and consume your cioppino with gusto and without guilt!
The skeptical cardiologist dislikes running. When I start running my whole body seems to be telling me I am making a serious mistake. After running, my knees hurt (worse than the normal level of pain) and if I do enough of it, my hips hurt too.
Despite this, I have incorporated running into my exercise routine over the last few years since I stopped playing tennis. I primarily get my aerobic exercise now by using elliptical type devices and I try to get at least 150 minutes of vigorous elliptical work per week. About once a week, I run a mile on a treadmill at 6 MPH.
My current patient exercise recommendation is for 150 minutes of moderate intensity aerobic exercise. I have advised patients in the past, that walking at a moderate pace was adequate exercise, and I’ve felt, based on prior studies, that running was not necessary to achieve the cardiovascular benefits of exercise.
Any Running Associated With Lower Risk of Dying
A new study published recently in JACC has made me reconsider this advice.
As part of a prospective longitudinal cohort study at the Cooper Clinic in Dallas, Texas, Lee, et al. looked at data from a group of 55,137 adults on whom they had information on running or jogging activity during the previous 3 months.
To reduce confounding bias in the association between running and mortality, the total amount of other physical activities except running was adjusted in all multivariable regression models.
They obtained information on death from The National Death Index and over 15 years found 3,413 all-cause death and 1,217 deaths from cardiovascular disease.
Those individuals who described themselves as having done any running in the last 3 months had a 30% lower risk of all-cause mortality and a 45% lower cardiovascular mortality.
As you might expect, the non-runners were older, smoked more and were fatter. The investigators ran analyses that controlled for the differences in these factors. The protective effect of running, even a small amount, persisted, regardless of age, gender, body mass index, smoking or alcohol consumption.
Amazingly, it didn’t matter how much you ran.
This finding is quite remarkable.
Those who ran <51 minutes per week did just as well as those who ran >176 minutes per week.
Of the 20,67 that had two examinations, those who were runners at both examinations had the best outcomes with a 50% lower risk of CVD mortality.
These findings are not definitive. We need more studies in this area but they are food for thought.
Why Would Running Be A Better Form of Exercise For Your Heart
Perhaps the person who doesn’t want to run has a fundamentally different mindset about his/her health than the person who is willing to run just a little bit. Does this inclination to run mirror the person’s overall approach to their health? We can assess factors like cigarette smoking, obesity, diabetes and cholesterol but there are likely (so far) intangible factors that contribute to our health that tend to cluster with a pro-active health attitude.
Why do I run? After all, I don’t like it, it hurts my knees and I didn’t think it was contributing to my overall health. I did the mile run for a few reasons:
Running a mile in 10 minutes served as a milestone, a fixed goal if you will, for my cardiovascular fitness. I can get a very good idea of where I’m at by measuring my heart rate. I’m 60 years old and my predicted maximal heart rate (220 minus age) is 160. When I’m out of shape, my heart rate will get as high as 155 BPM during the mile, when in shape it is 10 BPM lower. 145 BPM is 91% of my predicted maximal HR.
My sense is that a good goal for cardiovascular fitness is to get the heart rate up to 90% or so of your predicted maximal. It may be that running more reliably gets you to that threshold than other activities.
Also, as the significant other of the skeptical cardiologist points out, “you can’t cheat at running.” There’s a certain amount of effort you have to put into it and there’s no way to escape it as there is on a bicycle or an elliptical. With walking you could choose a speed ranging from the snail-like up to 4 MPH or so.
Those who don’t run may also have orthopedic limitations (plantar fasciitis, osteoarthritis, rheumatoid arthritis) or pulmonary problems (COPD, asthma) or undiagnosed heart problems (heart failure, valve defects, rhythm problems) that are not captured by the examinations the investigators performed.
These findings, the authors of the paper suggest, may make people more likely to run:
“Because time is one of the strongest barriers to participate in physical activity, this study may motivate more people to start running and continue to run as an attainable health goal for mortality benefits. Compared with moderate-intensity activity, vigorous-intensity activity, such as running, may be a better option for time efficiency, producing similar, if not greater, mortality benefits in 5 to 10 min/day in many healthy but sedentary individuals who may find 15 to 20 min/day of moderate-intensity activity too time consuming.”
Some Possible Mechanisms For The Benefits of Running
As I was putting the finishing touches on this post I notice that the Sept 23 issue of the Journal of the American College of Cardiology sitting in front of me has two articles that are directly relevant to this issue. I haven’t had time to analyze these in detail but the conclusions of the first study are that
“low doses of casual, lifelong exercise do not prevent the decreased compliance and distensibility observed with healthy, sedentary aging. In contrast, 4 to 5 exercise sessions/week throughout adulthood prevent most of these age-related changes”
Thus, the mechanism through which running or more “committed” exercising improves survival could be mediated through improving the diastolic properties of the heart.
I spent most of my academic cardiology career studying diastolic function and it is an incredibly complicated and poorly understood area. Simply put, the heart has to contract to pump out blood (we call this systole) then it has to fill back up with blood (we call this diastole). With aging, the heart’s ability to contract doesn’t change but its ability to fill changes dramatically. Thus, diastolic properties become impaired with aging and this study suggests that dedicated regular exercise prevents that.
The other study showed that regular exercise helps to slow age-related increase in blood pressure. Lower blood pressure with aging could be a mechanism for preventing the age-related decline in diastolic performance of the heart.
Changing Exercise Prescription
From now on when I talk to my patients about exercise, I will inquire about running specifically and I’ll mention these studies which suggest a little running may go along way toward forestalling the aging process of the heart and lowering their risk of dying.