Recently the skeptical cardiologist was asked by Ilene, a reader with an HDL almost as high as her LDL and a history of branch retinal vein occlusion (BRVO) whether she should take the statin her cardiologist had prescribed.
I enjoy reading your articles and would appreciate your opinion on my situation. I recently took a lipid panel blood test: total cholesterol: 244 HDL:112 LDL:121 VLDL:11 CRP: 1.77 Triglycerides: 57. Also my Cardiac Agatston score is 21.
I had a Branch Retinol Vein Occlusion a year ago in my left eye (it’s healing beautifully) and as a precaution am now taking Amlodipine 5mg daily (my blood pressure was never too high to begin with) along with a daily baby aspirin.
I am otherwise a healthy 72 year old woman, exercise and eat healthy.
My regular doctor (Integrative MD) says my cholesterol ratio is wonderful….my cardiologist wants me to take a statin (Atorvastatin) in a low dose. The ONLY med I take is Amlodipine and I am not one to be taking a plethora of meds for the rest of my life (unless “absolutely” necessary. What is your suggestion…take a statin or not.
While I can’t provide medical advice to Ilene specifically it is worthwhile to ponder the general aspects of her case and how I would approach it as it likely applies to thousands of other patients including many of my own.
In my mind there are two questions here: 1) Should Ilene and patients like her take a statin to prevent future heart attacks and strokes and 2) Do statins effect the Branch Retinal Vein Occlusion (BRVO)?
Although I’m not a fan of integrative or functional medicine Ilene’s integrative MD is correct in saying that her ratio of total cholesterol to HDL cholesterol is wonderful. Perhaps that high HDL is protecting her from a build-up of atherosclerotic plaque.
On the other hand, Ilene tells me that “My father did have a heart attack in his 60’s”. Perhaps she inherited something from him that puts her in a higher than average risk category.
With the information from the CAC we don’t have to guess about the influence of the high HDL and the family history of CAD. Her score is at the 48th percentile, slightly below average for white women her age, thus it would appear she is not destined for her father’s fate.
In this case, the CAC score does not significantly alter our risk estimate as it is so close to the average for her age
Even if we count her as having hypertension because she is on the amlodipine her 10 year risk of heart attack and stroke is low at 3.2%.
Guidelines don’t recommend statin treatment unless risk is >7.5%.
Also, note that I answered yes to “Family history heart disease” but most studies generally only consider this a risk factor if father had heart attack prior to age 55 years. If we make that a no the risk drops to <3%.
Now that we’ve answered Ilene’s real question let’s see if the BRVO warrants statin therapy.
Branch Retinal Vein Occlusion
BRVO is the blockage of a vein from the retina and the second most
common cause of vision loss from retinal vascular disease, following diabetic retinopathy. It typically results in the painless loss of vision in one portion of one eye due to hemorrhage and edema in the retina.
A reasonable summary of BRVO provided by the American Academy of Ophthalmology can be found here.
BRVO is not clearly related to atherosclerosis or hyperlipidemia and there is no evidence that taking a statin would prevent recurrence or help the condition.
The leading theory for what causes BRVO is that the more delicate and distensible retinal veins are squished or compressed at points where the stiffer and thicker retinal arteries cross them. Up to Date notes:
Whereas branch retinal vein occlusion (BRVO) appears to be related to compression of the branch vein by retinal arterioles at the arteriovenous crossing points, central retinal vein occlusion (CRVO) is usually associated with primary thrombus formation.
Although BRVO is more common in patients with hypertension and atherosclerosis it is not clear that one causes the other or that treatment of hypertension or atherosclerosis diminishes the risk of BRVO. So statins are not recommended.
Every patient case for me leads to more questions, more investigations and more knowledge. Here are some questions that occurred to me from ilene’s case.
-Why would someone with no symptoms and no heart problems be seeing a cardiologist?
(“I started seeing a cardiologist just to make sure all systems were “go” and stayed that way!… we take care of our cars so why not my body. )
I kind of like this answer and I definitely see lots of patients with that philosophy but if we extrapolate the car analogy: going to a cardiologist would be like taking your car to a mechanic who only works on engines or perhaps one specific part of the engine (help me out here people who know about cars.)
-Why was Ilene unwilling to take a statin? (I pretty much know the answer to this (see here) for most patients.
‘m just afraid of the horrible muscle related side effects of statin drugs…and that’s why I’m taking Berberine 500mg twice a day.
Yep. I feel a post abut Berberine may be in the works!
-Finally, should a 72 year old with a CAC score of 21 and BRVO be taking a baby aspirin?
The skeptical cardiologist primarily makes decisions on blood pressure treatment these days based on patient self-monitoring. If high readings are obtained in the office I instruct patients to use an automatic BP cuff at home and make a measurement when they first get up and again 12 hours later. After two weeks they report the values to me.
Although I’ve been recommending self-monitoring to my patients for decades it is only recently that guidelines have endorsed the approach and good scientific studies verified its superiority. I was pleased when the 2017 ACC/AHA guidelines for High Blood Pressure made home self-monitoring of BP a IA recommendation.
And last year a very good study, the TASMNH4 was published which demonstrated the superiority of self-monitoring compared to usual care.
TASMINH4 was a parallel randomised controlled trial done in 142 general practices in the UK, and included hypertensive patients older than 35 years, with blood pressure higher than 140/90 mm Hg, who were willing to self-monitor their blood pressure. Patients were randomly assigned (1:1:1) to self-monitoring blood pressure (self-montoring group), to self-monitoring blood pressure with telemonitoring (telemonitoring group), or to usual care (clinic blood pressure; usual care group).
The home BP goal was 135/85 mm Hg, 5 mm Hg lower than the office BP goal. At one year both home self-monitoring groups had significantly lower systolic blood pressure than the usual care group.
This trial was not powered to detect cardiovascular outcomes, but the differences between the interventions and control in systolic blood pressure would be expected to result in around a 20% reduction in stroke risk and 10% reduction in coronary heart disease risk. Although not significantly different from each other at 12 months, blood pressure in the group using telemonitoring for medication titration became lower more quickly (at 6 months) than those self-monitoring alone, an effect which is likely to further reduce cardiovascular events and might improve longer term control.
Advantages of Home Self-Monitored Blood Pressure-Limitations of Office BPs
Every patient I see in my office gets a BP check. This is typically done by one of the office assistants who is “rooming” the patient using the classic method with , listening with stethoscope for Korotkov sounds. If the BP seems unexpectedly high or low I will recheck it myself.
Often the BP we record is significantly higher than what the patient has been getting at home or at other physician offices.
There are multiple factors that could be raising the office BP: mental stress from driving to the doctor or being hurried or physical stress from walking from the parking lot.
In addition, I feel that multiple assessments of out of office BP over the course of the day and different days are more likely representative of the BP that we are consistently exposed to rather than one reading in the doctor’s office.
Accuracy and technique in the doctor’s office is also an issue.
Interestingly, we have assumed that manual office BP measurement is superior to automatic but this recent paper found the opposite:
Automated office blood pressure readings, only when recorded properly with the patient sitting alone in a quiet place, are more accurate than office BP readings in routine clinical practice and are similar to awake ambulatory BP readings, with mean AOBP being devoid of any white coat effect.
A patient left a comment to that paper which is quite insightful:
I had a high blood pressure event several years ago. Since then I have monitored my BP at home, sitting with both feet flat on the floor, not eating or drinking, not speaking or moving around, on a chair with a back, and without clothes on the arm being used for the measure. My BP remains normal.
I have never had my BP taken correctly in a doctor’s office. They will do it while I am speaking with the doctor, sitting on an exam table with my legs swinging, with the monitor band over my heavy winter sweater, right after I have sat down. They do not ensure that my arm is supported or at the right height. If I recommend that I take off my sweater, or move to a chair with a back, they tell me that is not needed. I have decided to refuse such measurements. How can they possibly be monitoring my health this way?
This patient’s observations are not unique and I suspect the majority of office BPs have most if not all of the limitations she describes.
Self Monitoring Improves Patient Engagement In BP Control
I have found self-monitoring of patient’s BP to substantially enhance patient engagement in the process. Self-monitoring patients are more empowered to understand the lifestyle factors which influence their BP and make positive changes.
Blood pressures are amazingly dynamic and as patient’s gain understanding of what influences their BP they are going to be able to take control of it.
I take my BP almost daily and adjust my BP medications based on the readings. After prolonged work or exercise in heat, for example, BPs will decline to a point where I’m light headed or fatigued. Less BP med at this time is indicated. Conversely, if I’ve been overly stressed BPs increase and upward titration of medication is warranted.
With some of my most engaged and enlightened patients we perform similar titrations depending on their circumstances. Sometimes patients perform these titrations on their own and tell me about them at the next office visit.
What’s The Best Way To Communicate Home BPs?
Many of my patients provide me with a hand-written record of their BPs over two weeks. Some mail them to me, others bring them in to the office. We scan these into the EMR. I look at these and make an estimate of the average systolic blood pressure, the variation over time and the variation during the day. It’s not feasible for me or my staff to enter the numbers or precisely obtain an average.
Some patients send us the numbers through the internet-based patient portal into the EMR. This is preferable as I can view these and respond quickly and directly back to the patient with recommendations.
More and more patients are utilizing their smart phones to record and aggregate their health data and will bring them in for me to look at during an office visit. I’ve described one stylish and slick BP cuff, the QardioArm which has neither tubes nor wires and works through a smartphone app. Omron , also has multiple cuffs which communicate via BlueTooth to store data in a smartphone app.
Ideally, we would have a way for me to view those digitally recorded BPs with nicely calculated averages online and within the EMR. Unfortunately, such connectivity is not routinely available.
However, for my patients who are already monitoring their heart rhythms with a Kardia mobile ECG and are connected with me online through KardiaPro Remote I can view their BP recordings online.
I’ll discuss in detail in a subsequent post the Omron Evolv home automatic BP cuff (my current favorite) which is wireless and tubeless and connects seamlessly to KardiaPro allowing me to view both BP and heart rhythm (and weight) recordings in my patients
To me, this empowerment of patients to record, monitor and respond to their own physiologic parameters is the future of medicine.
From the 2017 ACC/AHA BP guidelines
and the proper technique for office BP measurement
Old habits die hard in medicine. For decades the skeptical cardiologist and his cardiology brethren and sistren have prescribed aspirin to prevent stroke in patients with atrial fibrillation.
For those patients with atrial fibrillation (AF) who were considered low risk it was felt that aspirin provided some benefit in preventing the clots that fly out of the heart (and land in arteries elsewhere in the body) at an acceptably low risk of bleeding. For higher risk patients more powerful and effective agents (oral anticoagulants) are usually recommended.
The American guidelines on AF (2014) gave a IIB recommendation to aspirin. IIB is not a ringing endorsement having been described as “this is our suggestion, but you may want to think about it.”
For patients with nonvalvular AF and a CHA2DS2-VASc score of 1, no antithrombotic therapy or treatment with an oral anticoagulant (OAC) or aspirin may be considered. (Level of Evidence: C)*
Thus, in the 2016 European guidelines on the management of AF the authors state that “the evidence supporting antiplatelet mono therapy (e.g. aspirin or clopidogrel) for stroke prevention in AF is very limited” and the bleeding rate” is similar to OAC”:
Aspirin and other antiplatelets have no role in stroke prevention (III A). The combination of anticoagulation with antiplatelets increases bleeding risk and is only justified in selected patients for a short period of time; for example, in patients with an acute coronary syndrome or stent, balancing the risk of bleeding, stroke and myocardial ischaemia (IIa B/C).
Stroke risk evaluation is based on the CHADS-VASc score. With a score ≥2 in male and ≥3 in female patients, anticoagulation for stroke prevention is clearly recommended, while in a score of 1 in males and 2 in females, anticoagulation should be considered. No antithrombotic therapy of any kind should be prescribed in patients with a CHADS-VASc score of 0 (males) or 1 (females).
Antiplatelet therapy increases bleeding risk, especially dual antiplatelet therapy (2.0% vs. 1.3% with antiplatelet monotherapy; P < 0.001), with bleeding rates that are similar to those on OAC. Thus, antiplatelet therapy cannot be recommended for stroke prevention in AF patients.
“The European guidelines have done away with aspirin for stroke prevention in atrial fibrillation. It barely made it into our current US guidelines. I don’t think aspirin should be in there and I don’t think it will be there in the next guidelines. The role of aspirin will fall away,” said Bernard J. Gersh, MB, ChB, DPhil, Professor of Medicine at the Mayo Clinic in Rochester, Minnesota. “It’s not that aspirin is less effective than the oral anticoagulants, it’s that there’s no role for it. There are no good data to support aspirin in the prevention of stroke in atrial fibrillation.”
“The use of aspirin has probably been misguided, based upon a single trial which showed a profound effect and was probably just an anomaly,” said N.A. Mark Estes III, MD, Professor of Medicine and Director of the New England Cardiac Arrhythmia Center at Tufts University in Boston, and a past president of the Heart Rhythm Society
I would just take it off of your clinical armamentarium because the best available data indicate that it doesn’t prevent strokes. I’m certainly not using it in my patients. Increasingly in my patients with a CHA2DS2-VASc of 1, I’m discussing the risks and benefits of a novel oral anticoagulant,” said Dr. Estes.
Those are amazingly definitive statements. But, as I’ve learned we can’t just except what the “experts” and the guidelines tell us we have to look at the original studies informing these decisions.
It compared warfarin (measured by PT ratio) to placebo and aspirin 325 mg to placebo in preventing stroke in AF patients. Warfarin reduced stroke by 67% and aspirin by 42%. The risk of significant bleeding was similar at around 1.5% per year for all three arms.
Based on this and other AF trials (AFASAK, CAFA, SPINAF, EAFT, et al. ) when I gave talks or taught cardiology fellows in the 1990s my message (similar to this presentation) emphasized the superior benefits of warfarin compared to aspirin (especially when monitored by INR in a 2.0 to 3.0 range) in higher risk AF patients. Overall it was felt that aspirin (dosing varying from 100 to 325 mg) reduced stroke/embolism by 20-30% compared to placebo and would offer benefit to those patients at low risk or who could not tolerate warfarin.
Based on the 2014 American guidelines (and a focused update in 2019 which did not address this issue) I had not been actively taking my low risk patients off baby aspirin.
I was prompted to re-research this question and write this post because a 58 year old woman with paroxysmal AF and hypertension called the office today asking if I wanted her to take a baby aspirin daily. She has a CHADS2VASC score of 2 (woman and hypertension) and falls into the category where we should have an in depth conversation about the risks and benefits of anticoagulant therapy.
I have that discussion with her each visit and thus far we’ve decided to hold off on starting an anticoagulant drug like Eliquis. She has promised to record her ECG daily (using her Kardia Mobile ECG device) and report any onset of AF. If AF recurs we will have another discussion about Eliquis.
I spent several hours pouring over the original studies and more recent studies, reviews and meta-analyses and reached the following conclusions:
With the advent of the newer oral anticoagulants (NOACs) in the last decade which offer better stroke reduction and less bleeding than warfarin patient-physician discussions should be about taking a NOAC or not. Aspirin should not be considered as a lower risk/effective alternative as its benefits are minimal and bleeding risks similar to NOACs.
I told my patient no on the daily baby aspirin and from now on I will recommend stopping aspirin (assuming no other reason to be on it) to all my low risk AF patients.
The components of the stroke risk score- CHA2DS2-VASc = Congestive Heart failure, hypertension, Age ≥75 (doubled), Diabetes, Stroke (doubled), Vascular disease, Age 65–74, and Sex (female);
For those interested in a discussion on why females get a point in the risk score but a different cut-off for OAC therapy this is from the ESC guidelines:
Many risk factors contribute to the increased risk of stroke in patients with AF as expressed in the CHA2DS2-VASc score. The evidence for female sex as a risk factor has been assessed in many studies. Most studies support the finding that females with AF are at increased risk of stroke. One meta-analysis found a 1.31-fold (95% CI: 1.18–1.46) elevated risk of stroke in females with AF, with the risk appearing greatest for females ≥75 years of age (S4.1.1-35). Recent studies have suggested that female sex, in the absence of other AF risk factors (CHA2DS2-VASc score of 0 in males and 1 in females), carries a low stroke risk that is similar to males. The excess risk for females was especially evident among those with ≥2 non–sex-related stroke risk factors; thus, female sex is a risk modifier and is age dependent (S4.1.1-49). Adding female sex to the CHA2DS2-VASc score matters for age >65 years or ≥2 non–sex-related stroke risk factors
If you’re curious what constitutes a IIB recommendation it is described in the yellow box below My best summary is still “not a ringing endorsement”.
If you want to see the ESC guideline recommendations in detail
This being July 4, the skeptical cardiologist is reminded of how much he owes the United States for allowing him to become a legal citizen and resident. I asked my sister, Vickie, who emigrated with me from England in 1959 what she was thankful for in the United States and she texted back:
The opportunities this country gives so many refugees. I am friends with so many that love the USA for the freedom we have and wonderful people who have supported them! Thanks for asking!
The US has been kind to refugees in the past, especially around the time my family immigrated to the US in the late 1950s.
In 1956, President Eisenhower used “parole powers” to let in Hungarian refugees fleeing Soviet retribution after their failed revolt. By 1960 there were more than 200,000 Hungarian refugees in the US.
In January of 1959, Fidel Castro overthrew Batista in Cuba and, thousands of Cubans were admitted to the US as political refugees. Eventually, all these Cubans were made US citizens.
The United States eventually enacted the 1966 Cuban Adjustment Act to allow permanent resident status to Cuban refugees who arrivee after 1959. About one million Cubans emigratee to the United States between 1959 and 1990.
Immigration Policy in 1959
Given recent turmoil surrounding immigrants and immigration I felt compelled to look back on what the immigration process looked like when I entered the US.
The process of my gaining citizenship began in 1959 when my dad and mom decided to emigrate from England and come to the United States.
The Immigration and Nationality Act of 1952 made it easy for us to come here because it “(1) reaffirmed the national origins quota system, (2) limited immigration from the Eastern Hemisphere while leaving the Western Hemisphere unrestricted, (3) established preferences for skilled workers and relatives of U.S. citizens and permanent resident aliens; and (4) tightened security and screening standards and procedures.”
Decisions on who to allow into the country it seems have long been a source of controversy as this summary of post-world war II US immigration policy makes clear. The 1952 Immigration Act under which we entered ended policies dating from the 1890s that excluded Asian immigrants. However, only 100 immigrants from each country in Asia were allowed.
The bill upheld the ethnicity-based quota system for new immigrants that favored white Europeans, revising limitations to admit one-sixth of 1 percent of each group already in the United States.
Under the 1952 act my family was welcomed into the US. When my dad visited the American consulate in Liverpool he was told he was a shoe-in since he was a white European who was trained as a chemist. In addition, my mother’s sister resided in the U.S.A. (Coffeyville, Kansas to be exact).
I Become A Citizen
In 1968, after 9 years in America, my parents were sworn in as United States Citizens.
It was at that time that I became naturalized under section 341 of that 1952 Immigration Act which allowed children under the age of 18 to become citizens when their parents had passed all the citizenship requirements and were sworn in.
There is so much that I take for granted in the US. I feel like even the poorest Americans are better off than 99.9% of the people who have ever lived. The framers of the US constitution were really brave, insightful men and that first amendment is something I am profoundly grateful for.
Amendment I. Congress shall make no law respecting an establishment of religion, or prohibiting the free exercise thereof; or abridging the freedom of speech, or of the press; or the right of the people peaceably to assemble, and to petition the government for a redress of grievances.
I won’t bore you with a long list of other great things about the US (like free public bathrooms and high doctor salaries) but will end with a paean to the great National Park System which has preserved the beauty and the wildness of vast swaths of unique areas across the continent.
I have taken my family hiking in as many of these wonders as time allowed: Zion, Rocky Mountain, Bryce, Yosemite, Great Smoky Mountains, Grand Canyon, Yellowstone, Grand Tetons, US Virgin Islands and Saguaro.
My first paean to the national park system was at the end of my Saguaro post:
Since my kids became old enough to appreciate hiking and nature I have tried to focus family vacations on visits to National parks. I can’t think of any more valuable experience for them than hiking in some of the most beautiful places on earth and experiencing diverse and fascinating flora and fauna. And all of this comes at a ridiculously low price for the user.
For example, because I’m 62 years old I qualify for a Lifetime senior pass to all National parks and monuments. Cost? 10$!!!! I’m finally seeing the perquisites of becoming a senior citizen.
Since the National Park Service was created in 1916 it has grown to protect 88 million acres, 43,000 miles of shoreline, 85,000 miles of rivers and streams, 12,000 miles of trail and 8,500 miles of road in more than 400 national parks, sites and monuments.
I sure hope the vision of prior Presidents, Congressman and ardent conservationists (all praise be to Teddy Roosevelt!) who established the federal system that protects these national treasures continues.
This post still serves as a good introduction to the test (rationale, procedure, risks) but in the 5 years since it was published there has been a substantial body of data published on CAC and in 2018 it was embraced by major organizations.
Overall, I’ve written 20 posts in which CAC plays a predominant role since then and I feels it’s time to put the most important changes and concepts in one spot.
Detection Of Subclinical Atherosclerosis: What’s Your Risk of Dropping Dead?
We have the tools available to look for atherosclerotic plaques before they rupture and cause heart attacks or stroke. Ultrasound screening of the carotid artery, as I discussed here, is one such tool: vascular screening is an accurate, harmless and painless way to assess for subclinical atherosclerosis.
In my practice, the answer to the question of who should or should not take aspirin is based on whether my patient has or does not have significant atherosclerosis. If they have had a clinical event due to atherosclerotic cardiovascular disease (stroke, heart attack, coronary stent, coronary bypass surgery, documented blocked arteries to the legs) I recommend they take one 81 milligram (baby) uncoated aspirin daily. If they have not had a clinical event but I have documented by either
vascular screening (significant carotid plaque)
coronary calcium score (high score (cut-off is debatable, more on this in a subsequent post)
Incidentally discovered plaque in the aorta or peripheral arteries (found by CT or ultrasound done for other reasons)
then I recommend a daily baby aspirin (assuming no high risk of bleeding).
Help In Deciding Who Needs Aggressive Treatment
Second, CAC is an outstanding tool for further refining risk of heart attack and stroke and helping better determine who needs to take statins or undergo aggressive lifestyle reduction, something I described in detail in my post “Should All Men Over Sixty Take a Statin Drug”.
After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.
As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.
By identifying subclinical atherosclerosis, CAC scoring identifies those who do or don’t need statins.
This is particularly important for patients who have many reservations about statins or who are “on the fence” about taking them when standard risk factor calculations suggest they would benefit.
In 2015 I wrote about a documentary entitled “The Widowmaker” (see here and here) which is about the treatment and prevention 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.
Although CAC has some similarities to mammography (both utilize low dose radiation, 0.5 mSV) I concluded that CAC was not “the mammography of the heart” as the documentary proclaims.
In October, 2016 the skeptical cardiologist predicted that Donald Trump’s coronary calcium score, if remeasured, would be >100 . At that time I pointed out that this score is consistent with moderate coronary plaque build up and implies a moderate risk of heart attack and stroke.
Trumps’ score gave him a seven-fold increase risk of a cardiovascular event in comparison to Hilary Clinton (who had a zero coronary calcium score) .
I was able to predict this score because we knew that Trump’s coronary calcium was 98 in 2013 and that on average calcium scores increase by about 10% per year.
What is most notable about the Trump CAC incident is that Trump, like all recent presidents and all astronauts underwent the screening. If the test is routine for presidents why is it not routine for Mr and Mrs Joe Q Public?
A three-phased approach to coronary artery disease (CAD) risk assessment is recommended, beginning with initial risk-stratification using a population-appropriate risk calculator and resting ECG. For aircrew identified as being at increased risk, enhanced screening is recommended by means of Coronary Artery Calcium Score alone or combined with a CT coronary angiography investigation.
I was very pleased to read that the newly updated AHA/ACC lipid guidelines (full PDF available here) emphasize the use of CAC for decision-making in intermediate risk patients.
For those patients aged 40-75 without known ASCVD whose 10 year risk of stroke and heart attack is between 7.5% and 20% (intermediate, see here on using risk estimator) the guidelines recommend “consider measuring CAC”.
If the score is zero, for most consider no statin. If score >100 and/or >75th percentile, statin therapy should be started.
A Few Final Points On CAC
First, it’s never too early to start thinking about your risk of cardiovascular disease. I have been using CAC more frequently in the last few years in individuals <40 years with a strong family of early sudden death or heart attack and often we find very abnormal values (see here for my discussion on CAC in the youngish.)
If heart disease runs in your family or you have any of the “risk-enhancing” factors listed above, consider a CAC, nontraditional lipid/biomarkers, or vascular screening to better determine were you stand and what you can do about it.
Included in my discussions with my patients with premature ASCVD is a strong recommendation to encourage their brothers, sisters and children to undergo a thoughtful assessment for ASCVD risk. With these new studies and the new ACC/AHA guideline recommendations if they are age 40-75 years there is ample support for making CAC a part of such assessment.
Hopefully very soon, CMS and the health insurance companies will begin reimbursement for CAC. As it currently stands, however, the 125$ you will spend for the test at my hospital is money well spent.
If you want to be proactive about the cardiovascular health of yourself or a loved one, download the MESA app and evaluate your risk. Ask your doctor if a CACS will help refine that risk further.
There are many other questions to answer with regard to CAC-should they be repeated?, how do statins influence the score?, is there information in the scan beyond just the score that is important? Is a scan helpful after a normal stress test?
Like most things in cardiology we have a lot to learn about CAC. There are many more studies to perform. Many questions yet to be answered.
A study showing improved outcomes using CAC guided therapy versus non CAC guided therapy would be nice. However, due to the long time and thousands of patients necessary it is unlikely we will have results within a decade.
I don’t want to wait a decade to start aggressively identifying who of my patients is at high risk for sudden death. You only get one chance to stop a death.
For some time the skeptical cardiologist has been seeking information about the practice of medicine and cardiology during the Victorian era.
Why the Victorian era? Because my favorite writer, Charles Dickens, consistently portrays doctors of that era as incompetent.
And, sadly to say, as I have explored what doctors had to offer in the real world of the nineteenth century it was, in point of fact, very little.
From time to time as I gather this information on my medical forebears I will share it with my gentle readers:
To begin with, however, I present to you one of my favorite examples which is taken from The Old Curiosity Shop.
“The doctor, who was a red-nosed gentleman with a great bunch of seals dangling below a waistcoat of ribbed black satin, arrived with all speed, and taking his seat by the bedside of poor Nell, drew out his watch, and felt her pulse. Then he looked at her tongue, then he felt her pulse again, and while he did so, he eyed the half-emptied wine-glass as if in profound abstraction.
‘I should give her,’ said the doctor at length, ‘a tea-spoonful, every now and then, of hot brandy and water.’
‘Why, that’s exactly what we’ve done, sir!’ said the delighted landlady.
‘I should also,’ observed the doctor, who had passed the foot-bath on the stairs, ‘I should also,’ said the doctor, in the voice of an oracle, ‘put her feet in hot water, and wrap them up in flannel. I should likewise,’ said the doctor with increased solemnity, ‘give her something light for supper—the wing of a roasted fowl now—’
‘Why, goodness gracious me, sir, it’s cooking at the kitchen fire this instant!’ cried the landlady. And so indeed it was, for the schoolmaster had ordered it to be put down, and it was getting on so well that the doctor might have smelt it if he had tried; perhaps he did.
‘You may then,’ said the doctor, rising gravely, ‘give her a glass of hot mulled port wine, if she likes wine—’
‘And a toast, Sir?’ suggested the landlady. ‘Ay,’ said the doctor, in the tone of a man who makes a dignified concession. ‘And a toast—of bread. But be very particular to make it of bread, if you please, ma’am.’
With which parting injunction, slowly and portentously delivered, the doctor departed, leaving the whole house in admiration of that wisdom which tallied so closely with their own. Everybody said he was a very shrewd doctor indeed, and knew perfectly what people’s constitutions were; which there appears some reason to suppose he did.”
Since reading this I have endeavored to make all my medical pronouncements with solemnity and gravity and as slowly and portentously as possible.
N.B. The Old Curiosity Shop was the fourth novel of Charles Dickens. The novel was published in installments in the periodical Master Humphrey’s Clock. The first installment was printed in April of 1840 and the last was printed in February of 1841.
Supporters of vegetarian/ultra low fat diets like to claim that there is solid scientific evidence of the cardiovascular benefits of their chosen diets.
To buttress these claims they will cite the studies of Esseslystn, Pritikin and Ornish.
I’ve previously discussed the bad science underlying the programs of Esselsystn and Pritikin but have only briefly touched on the inadequacy of Dean Ornish’s studies.
The Ornish website proclaims that their program is the first program “scientifically proven to undo (reverse) heart disease.” That’s a huge claim. If it were true, wouldn’t the Dietary Guidelines for Americans, the American Heart Association, and most cardiologists and nutrition experts be recommending it?
Who Is Dean Ornish?
Dean Ornish has an MD degree from Baylor University and trained in internal medicine but has no formal cardiology or nutrition training (although many internet sites including Wikipedia describe him as a cardiologist.)
Ornish, according to the Encyclopedia of World Biographies became depressed and suicidal in college and underwent psychotherapy “but it was only when he met the man who had helped his older sister overcome her debilitating migraine headaches that his own outlook vastly improved. Under the watch of his new mentor, Swami Satchidananda, Ornish began yoga, meditation, and a vegetarian diet, and even spent time at the Swami’s Virginia center.”
Dr. Ornish’s Program for Reversing Heart Disease® is the first program scientifically proven to “undo” (reverse) heart disease by making comprehensive lifestyle changes.
The Ornish claims are based on a study he performed between 1986 and 1992 which originally had 28 patients with coronary artery disease in an experimental arm and 20 in a control group. You can read the details of the one year results here.and the five year results here.
There are so many limitations to this study that the mind boggles that it was published in a reputable journal.
-Recruitment of patients.
193 patients with significant coronary lesions from coronary angiography were “identified” but only 93 “remained eligible.” These were “randomly” assigned to the experimental or control groups. Somehow , this randomization process assigned 53 to the experimental group and 40 to the usual-care control group.
If this were truly a 1:1 randomization the numbers would be equal and the baseline characteristics equal.
Only 23 of the 53 assigned to the experimental group agreed to participate and only 20 of the control group.
The control group was older, less likely to be employed and less educated.
“The primary reason for refusal in the experimental group was not wanting to undergo intensive lifestyle changes and/or not wanting a second coronary angiogram; control patients refused primarily because they did not want to undergo a second angiogram.”
In other words, all of the slackers were weeded out of the experimental group and all of the patients who were intensely motivated to change their lifestyle were weeded out of the control group. Gee, I wonder which group will do better?
The experimental patients received “intensive lifestyle changes (<10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support). The control group had none of the above.
Needless to say this was not blinded and the researchers definitely knew which patients were in which group.
Control-group patients were “not asked to make lifestyle changes, although they were free to do so.”
There is very little known about the 20 slackers in the control group. I can’t find basic information about them-crucial things like how many smoked or quit smoking or how many were on statin drugs.
Progression or regression of coronary artery lesions was assessed in both groups by quantitative coronary angiography (QCA) at baseline and after about a year.
QCA as a test for assessing coronary artery disease has a number of limitations and as a result is no longer utilized for this purpose in clinical trials. When investigators want to know if an intervention is improving CAD they use techniques such as intravascular ultraound or coronary CT angiography (see here) which allow measurement of total atherosclerotic plaque burden.
Rather than burden the reader with the details at this point I’ve included a discussion of this as an addendum.
Ornish has widely promoted this heavily flawed study as showing “reversal of heart disease” because at one year the average percent coronary artery stenosis by angiogram had dropped from 40% to 37.8% in the intensive lifestyle group and increased from 42.7% to 46.1% in the control patients.
The minimal diameter (meaning the tightest stenosis) changed from 1.64 mm at baseline in the experimental to 1.65 at one year. At 5 years the minimal diameter had increased another whopping .001 mm to 1.651.
In other words even if we overlook the huge methodologic flaws in the study the so-called “reversal” was minuscule.
Utlimately, dropping coronary artery blockages by <5 % doesn’t really matter unless that is also helping to prevent heart attacks or death or strokes or some outcome that really matters.
There were no significant differences between the groups at 5 years in hard events such as heart attack or death. In fact 2 of the experimental group died versus 1 of the control group by 5 years.
There were less stents and bypasses performed in the Ornish group but the decision to proceed to stent or bypass is notoriously capricious when performed outside the setting of acute MI. The patients in the experimental group under the guidance of Ornish and their Ornish counselors would be strongly motivated to do everything possible to avoid intervention.
I’ve gotten a lot of flack for humorously suggesting that Nathan Pritikin killed himself as a result of the austere no fat diet he consumed but the bottom line on any lifestyle change is both quality and quantity of life.
If you are miserable most days due to your rigid diet you might consider that life is no longer worth living
Ornish’s Lifestyle Intervention Is Not A Trial Of Diet …And Other Points
Although often cited as justification of ultralow fat diet, the Ornish Lifestyle trial doesn’t test diet alone.
It is a trial of multiple different interventions with frequent counseling and meetings to reinforce and guide patients.
The interventions included things that we know are really important for long term health-regular exercise, smoking cessation, and weight management. These factors alone could account for any differences in the outcome but they are easily adopted without becoming a vegetarian.
The patients who agreed to the experimental arm were a clearly highly motivated bunch who agreed to this really strict regimen. Even in this population there was a 25% drop out rate.
Since investigators clearly knew who the “experimental patients” were and they were clearly interested in good outcomes in these patients there is a high possibility of bias in reporting outcomes and referring for interventions.
Despite all the limitations the study does raise an interesting hypothesis. Should we all be eating vegan diets?
if Ornish really wanted to scientifically prove his approach he should have repeated it with much better methodology and much larger numbers.
Finally, this tiny study has never been reproduced at any other center.
Because of the small numbers, lack of true blinding, lack of hard outcomes and use of multiple modalities for lifestyle intervention, this study cannot be used to support the Ornish/Esselstyn/Pritikin dietary approach.
It most certainly doesn’t show that the Ornish Lifestyle Program “reverses heart disease.” Consequently, you will not find any evidence-based source of nutritional information or guideline (unless it has a vegan/vegetarian philosophy or is being funded by the Ornish/Pritikin lifestyle money-making machines) recommending these diets.
N.B.1 A recent paper on noninvasive assessment of atherosclerotic plaque has a great infographic which shows how coronary artery disease progresses and how and when in the progression various imaging modalities are able to detect plaque:
I’ve inserted a vertical red arrow which shows how IVUS detects very early atheroma whereas angiography (ICA, green line) only detects later plaque when it has started protruding into the lumen of the artery.
The paper notes that “Intravascular ultrasound (IVUS) constitutes the current gold standard for plaque quantification. Multiple studies using IVUS and other techniques have revealed a robust relation between statin therapy and plaque regression. In the ASTEROID trial coronary atheroma volume regressed by 6.8% during 24 months of high-intensity lipid therapy. A meta-analysis of IVUS trials including 7864 patients showed an association between plaque regression and decreased cardiovascular events.”
While I believe Ornish started off as a legitimate scientist several authors have pointed out that he has joined the ranks of pseudoscientific practiioners.
In the end, the problem is that Dr. Ornish has yoked his science to advocates of pseudoscience, such as Deepak Chopra and Rustum Roy. Why he’s done this, I don’t know. The reason could be common philosophy. It could be expedience. It could be any number of things. By doing so, however, Dr. Ornish has made a Faustian deal with the devil that may give him short-term notoriety now but virtually guarantees serious problems with his ultimately being taken seriously scientifically, as he is tainted by this association. Let me yet again reemphasize that this relabeling of diet, exercise, and lifestyle as somehow being “alternative” is nothing more than a Trojan Horse. Inside the horse is a whole lot of woo, pseudoscience and quackery such as homepathy, reiki, Hoxsey therapy, acid-base pseudoscience, Hulda Clark’s “zapper,” and many others,
In less than a month AliveCor plans to release its KardiaMobile 6L which will provide 6 ECG leads using a smartphone based mobile ECG system that is similar to the Kardia single lead system.
AliveCor’s website proclaims “This is your heart x 6.”
I was fortunate enough to obtain a demo version of the 6L and have been evaluating it.
My first impressions are that this is a remarkable step forward in the technology of personal ECG monitoring. I’m not sure if I would call it “your heart x 6” but I feel the ability to view six high quality leads compared to one is definitely going to add to the diagnostic capabilities of the Kardia device.
Kardia 6L Setup And Hardware
The 6L is similar in design and function to the single lead device.
I’m including this cool spinning video (from the AliveCor website) which makes it appear, slick, stylish and futuristic
Once paired to the Kardia smartphone app (available for iOS or Android smartphones for free) it communicates with the smartphone using BLE to create ECG tracings.
Like the single lead Kardia the 6L has two sensors on top for left and right hand contact. But in addition, there is a third on the bottom which can be put on a left knee or ankle.
The combination of these sensors and contact points yield the 6 classic frontal leads of a full 12 lead ECG: leads I, II, III, aVL, aVR, and aVF. This is accomplished, AliveCor points out “without messy gels and wires.
I found that using the device was simple and strait-forward and we were able to get high quality tracings with minimal difficulty within a minute of starting the process in all the patients we tried it on.
The Diagnostic Power Of Six Leads
Below is a tracing on a patient with known atrial fibrillation. The algorithm correctly diagnoses it. With 6 different views of the electrical activity of the atrium I (and the Kardia algorithm) have a better chance of determining if p waves are present, thereby presumably increasing the accuracy of rhythm determination
Depending on the electrical vector of the left and right atria, the best lead to visualize p waves varies from patient to patient, thus having 6 to choose from should improve our ability to differentiate sinus rhythm from afib.
In the example below, the Kardia 6L very accurately registered the left axis deviation and left anterior fascicular block that we also noted on this patient’s 12 lead ECG. This 6L capability, determining the axis of the heart in the frontal plane, will further add to the useful information Kardia provides.
For a good summary of axis determination and what abnormal axes tells us see here.
The History of ECG Leads
When I began my cardiology training the 12-lead ECG was standard but it has not always been that way. I took this timeline figure from a nice review of the history of the ECG
Einthoven’s first 3 lead EKG in 1901 was enormous.
It is mind-boggling to consider that we can now record 6 ECG leads with a smartphone and a device the size of a stick of gum
For the first 30 years of the ECG era cardiologists only had 3 ECG leads to provide information on cardiac pathology. Here’s a figure from a state of the art paper in 1924 on “coronary thrombosis” (which we now term a myocardial infarction) showing changes diagnostic of an “attack” and subsequent atrial fibrillation
In the 1930s the 6 precordial leads were developed providing more information on electrical activity in the horizontal axis of the heart. The development of the augmented leads (aVr, aVL, aVF) in 1942 filled in the gaps of the frontal plane and the combination of all of these 12 leads was sanctified by the AHA in 1954.
I’ll write a more detailed analysis of the Kardia 6L after spending more time using it in patient care.
Specifically I’ll be analyzing (and looking for published data relative to):
-the relative accuracy of the 6L versus the single lead Kardia for afib determination (which, at this point would be the major reason for current Kardia users to upgrade.)
-the utility of the 6L for determination of cardiac axis and electrical intervals in comparison to the standard 12 lead ECG, especially in patients on anti-arrhythmic drugs
For now, this latest output from the meticulous and thoughtful folks at AliveCor has knocked my socks off!
N.B. If one uses the single lead kardia device in the traditional manner (left hand and right hand on the sensors) one is recording ECG lead I. However, if you put your right hand on the right sensor and touch the left sensor to your left leg you are now recording ECG lead II and if to the right leg, ECG lead III.
I describe this in detail here. For certain individuals the lead II recordings are much better than lead I and reduce the prevalence of “unclassified” recordings.
My feeling is that by automatically including the leg (and leads II and III) the 6L will intrinsically provide high voltage leads for review and analysis, thereby improving the ability to accurately classify rhythm.
And (totally unrelated to the 6L discussion) one can also record precordial ECG leads by putting the device on the chest thus theoretically completing the full 12 leads of the standard ECG.
Please also note that I have no financial or consulting ties to AliveCor. I’m just a big fan of their products.
The wide-spread public conception that catheter ablation cures atrial fibrillation and reduces one’s risk of stroke or dying has fueled a $4.5 billion industry. Until very recently there were no published randomized trials supporting this expensive and risky procedure.
The recently published landmark CABANA trial found that in patients with afib “the strategy of catheter ablation, compared with medical therapy, did not significantly reduce the primary composite end point of death, disabling stroke, serious bleeding, or cardiac arrest. ”
So there is no proven benefit of ablation on death, stroke, bleeding or cardiac arrest. This means that a medical management approach to management of afib is always an acceptable approach. Especially an enlightened medical approach.
In CABANA, women and those patients >75 years of age did worse with ablation as this chart shows.
What about complications? I mentioned that ablation was risky and this is because any time you put a catheter in someone’s heart you can create life-threatening problems. When you then heat up the tip of that catheter it is possible to burn/damage/destroy things that are not your target.
A reassuring finding of CABANA was that ablation did not do worse than drugs. But one of the messages I heard from HRS was that CABANA showed that AF ablation is safe. This is a problem.
The complications in the ablation arm were more serious and more numerous than those in the drug arm. We will have to wait for the published paper for formal comparisons. CABANA likely represents a best-case scenario because it allowed only experienced operators and centers to be part of the trial. Many people undergo ablation by less experienced operators.
Another important safety issue is the asymmetry of procedural complications. When you talk privately with ablation doctors, many, perhaps most, relay the story of a tragic death of an otherwise healthy middle-aged adult from an atrial-esophageal fistula.
Yes. A well-recognized and highly feared complication of ablation , atrial-esophageal fistula, causes rapid death due to exsanguination through a channel between the left atrium and the esophagus which develop due to destruction/burning of the normal esophageal/atrial tissue.
In this chart taken from the CABANA abstract presentation you can see the complications which do not include a highly feared atrial-esophageal fistula.
Can Catheter Ablation Improve Quality of Life?
Basically, after the CABANA trial we have no evidence that ablation will improve hard outcomes in afib patients. However, there are numerous patients who feel they have greatly benefited from the procedure, experiencing years of afib free existence.
This benefit of ablation, of improving quality of life and making patients feel better is important.
The CABANA trial also looked at quality of life and in part II of this article I’ll examine that in detail.
Update 6/12/2019 357 PM.
Twitter follower @mrice5025 was kind of enough to read the above closely enough to realize that the number of atrial esophageal fistulae was actually zero in the CABANA trial and I have corrected the text accordingly.
I have seen a case of this mostly fatal complication in a patient who had an ablation done at an outside hospital 5 weeks earlier and who rapidly died from it and I try to be very aware of its possibility as early diagnosis and surgery is the key to survival.
AF ablation carries a small risk of complications with the most serious being atrioesophageal fistula (AEF). Although the incidence is less than 0.1%, it is usually fatal Esophageal perforation or fistula was reported in 31 patients (0.016%) in the Global Survey of Esophageal and Gastric Injury in Atrial Fibrillation study. Symptom onset for esophageal perforation or fistula was reported on average 19.3 days after the ablation procedure but could appear as short as 6 days and as long as 59 days post ablation.Esophageal injury has been observed most frequently with percutaneous radiofrequency ablation, although it has also been reported with other energy sources including cryoablation,high-intensity focused ultrasound and even surgical ablation.
The featured image comes from this Cleveland Clinic video which has some great graphics and reasonable information (once you get by the annoying lady at the beginning who describes ablation as “an excellent minimally invasive” procedure.)
At my hospital, St. Luke’s, I have three outstanding electrophysiologists who do excellent ablations,, Jonas Cooper, Cary Fredman, and Mauricio Sanchez.