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Male Speaker: An interesting topic that I’ve become a lot more aware of, over the last few years, and as the title says, “What your feet say about your heart?” and the answer is, a lot.

As far as this talk is concerned, I have no specific disclosures to make and it all starts at what we observe. When we look at feet, we look at – we see them, we look at the color and we look at deformities. You touch them. When you touch them, you’re feeling for a tactile sense, you’re feeling for temperature, you’re feeling for pulses. You put a Doppler to it, so you hear sounds that are emanating out of it and you perform various tests that help you evaluate what’s going on in.

Also, you can be fooled and you can be like the old Indian photograph of the blind man and the elephant. When you’re blinded and you’re feeling something, you know, the one blind man is feeling the trunk– so this is a rope and one is feeling the leg and saying this is a tree trunk and someone else is feeling the ear in saying this is a big giant leave. So when you’re blinded, what’s put in front of you, isn’t always what the reality of the situation is.

Now, there are many cardiac pathologies, I'm hardly qualify as anywhere near as an internist let alone the cardiologist, but there are certain cardiac pathologies which we’re all aware of, that manifest in the foot.

We may be the first to identify it and make the appropriate referrals. I am a big believer that indeed the foot is a mirror of systemic disease. I like to tell people, particularly new students when they come in and said, “I hope you never take care of feet.” And they look at me like I'm crazy. I'm taking leave of my senses, and then the second thing is, you take care of patients with foot problems.

There’s a big difference when you think about it. You know, a patient with a foot problem is very different than just taking care of a foot. If you could disarticulate the foot at the ankle and, you know, we hear all sorts of wonderful talks about bunionectomies and what’s – and I always tell a patient, “Look, I could unscrew this foot at the ankle and take this foot to my work bench and this is what I would do to correct that deformity. And you pick it up on Monday, and we screw it back in. But that’s not the way the life works.” What the procedure that may be right for the foot may not be right for the patient. And sometimes we have to modify and do things even though that’s not what you would do precisely for that foot problem but as to what that patient needs at that particular time in their life.

So ischemic heart disease, valvular heart disease, that which is infected and non-infected, dysrhythmias, congestive heart failure, cardiomyopathies and neoplasms, all can have manifestations in the foot. And like it or not, we’re all going to die someday and chances are, statistically, that the largest chance you have is you’re going to die from some kind of heart disease, whether heart failure or cardiac shock or ischemic heart disease or myocardial infarction. Heart disease and cancer are the largest killers in the United States and for the foreseeable future will remain it.

Now, in conducting our history and physical, we need to again look for things that are indicative of systemic disease as well as podiatric disease. Questions that you ask vis-a-vis looking for atherosclerotic disease or looking for – in the cardiovascular system. We’re not talking about other systems here. That’s for another talk another time.

Claudication, important question. But remember, you have to understand the activity level. It’s not sufficient to say to a patient, “How many blocks can you walk? Can you walk five blocks without your calf?” If the patient is in a wheelchair and you’re asking him, “How many blocks can you walk?” or if the patient is sedentary in activity levels, they’re not going to be claudicated because they’re not doing enough activity to claudicate. The difference would be in performing a static resting EKG, which most cardiologists for the most part will say is – they’re not going to say it’s worthless but next to worthless as opposed to doing a stress EKG, okay, to see what happens when you stress that hard. What’s happening? Things that show up on a stress EKG are very different than what show up on a resting EKG.

Same thing with claudication. And when we get to ABIs we’ll talk about that in a few minutes.

[05:03]

Clearly, presence of rest pain, asking patients about chest pain. I have uncovered over career many, many patients who have atypical chest pain. And some of it is GI, some of it could be costochondritis and sometimes it’s been angina, stable or unstable, and making a referral to the cardiologist more than one time. I’ve gotten a call back from cardiologist saying, you know, “Thank you for sending John. He had a pretty nasty occlusion that was getting ready to thrombose.” And in that particular case, we’re truly, truly, truly life savers.

So recognize that chest pain is different in males than females. Males typically report ischemic chest pain or cardiac pain as a crushing substernal, sometimes reported as indigestion. Females are very different. They may complain of a pain in the neck, jaw, back, sometimes the flu-like symptoms, muscular aches and pains, which is why cardiac disease in females, particularly post-menopausal female, is a pretty serious thing and that picked up a sudden death or sudden cardiac events in females are more common than we’d like to admit, history of shortness of breath, history of palpitations.

In electronic medical records now, they’re all pre-populated in the review of systems. And if you read the various models that are out there, every one of them is going to say the same, review of systems, they just press the repeat button and it just gets followed through time and time again. No shortness of breath, no chest pain, but are you really asking the patient these things.

Now, I’m not saying you have to do that in an 18-year old who comes in with a paronychia that you have to do an in-depth, do you get chest pain when you run, are you getting shortness of breath. But if you have a 55-year old hypertensive or diabetic or smoker or someone who have hyperlipidemia, darn right, these are important questions to ask them. And if you do it and you do it properly, you’re going to pick up disease that may have been previously undiagnosed.

As a part of the physical examination, the cardiovascular, blood pressures, pulse rate, respiratory rate and also looking at the BMI. I mean, these are all things that we’re writing down because Medicare says, “We’re going to pay extra if you do that.” But are we really doing it and are we doing ourselves… or not ourselves, are what we doing all patients a real service by not doing it. And none of these things are more complex than a first year medical student or a nursing student could do.

Now, ischemic heart disease, the prevalence of this is decreasing slightly but statistically significantly over the years is probably because of a greater control of risk factors. Fewer people are smoking, more people are taking care of their weight, cholesterol levels are routinely checked and patients are put on statins and anti-hyperlipidemic therapies earlier on. Patients who are pre-diabetic, the range of that are put on metformin early on.

There’s a whole class of pre-diabetics are being identified in people with A1c's as low as 6.2, 6.3 are now actively treated. You don’t have to come in with a sugar, an FPS of 300 and and A1c of 11 just to start therapy on this. So there’s greater awareness of risk factors and greater intervention.

Certain parts of the country aren’t doing as well as others who are still down in the Deep South. Peripheral arterial disease and ischemic heart disease is much higher. Here you go then. And these are the people who have six pancakes, bacon and turkey grease and everything rolled into a deep fryer and put whipped cream on top of it for breakfast. So it’s still… we’ve got a lot, as a country, to go.

Now, the relationship between CAD and PAD is the same disease, narrowing and hardening of the arteries, plaque deposition within the arteries. We don’t have a lot of time here to spend upon the derivation of it. Remember that this is -- the calcium and the plaque deposition or later down the stages, this all starts much earlier with foam cells that’s picking lipids within the arteries. Systemic inflammation, inflammatory disease is definitely linked to this. So there’s lots of host factors that apply it. But just recognize that it’s the same disease wherever be it in the LAD or wherever it be in the anterior tibial artery. It’s the same pathologic process that is causing that atherosclerotic plaque build-up and then narrowing of the lumen.

The danger is in the heart, obviously, is when that plaque ruptures and thrombosis that you have an acute coronary event. That happens although to a lesser extent in the leg, but usually there is enough collateralization in the leg that no one is going to keel over and have a sudden death from a thrombosis in the anterior tibial artery. But certainly, if that happens in the major coronary artery, it could be devastating results. A lot of these are undiagnosed. About 6% of US adults over 40 have a low ABI, that’s a lot of patients that come in. Mostly, it’s going to be in the older ages, as we get older that is a greater prevalence of unknown peripheral arterial disease in patients with coronary artery disease.

We see patient all the time who come in and give a history that they have had a stent, that they have had a CABG, that they have had angina. These are the patients that sometimes slip through the cracks in terms of diagnosing the peripheral arterial disease and they may be at risk for critical ischemic events in the lower extremity as well. The cardiologist for the most part are pretty good in screening for PAD in patients who have known CAD, but not always. You will see it. Start asking patients who have known cardiac patients, “Have you ever had peripheral arterial testing on it?” And not in frequently, they will say, “What’s that?” Or, “No, I have never had it.”

PAD and CAD risk factors are the same, the traditional ones, age, male, sex, smoking, hypercholesterolemia, hypertension, diabetes. There are emerging risk factors which we now elevated CRP as a marker of systemic inflammatory conditions, coronary artery calcium screening for that, increased levels of homocysteine, apolipoprotein, apolipoprotein A, apolipoprotein B are risk factors for the development of CAD and PAD. And as we keep saying more and more on knowing that systemic inflammation is bad. It is bad in terms of what it does to your arteries and it is also believed to be now quite accurately prooncogenic. Patients with systemic inflammation seemed to have also increase risk of development of malignancies.

Our life culture has changed significantly to sedentary lifestyles. I mean, this is the classic meal for many as even hit Europe where you have seen -- but it is not everyone just follows the Mediterranean, even David, they didn’t follow the Mediterranean diet.

Our role as podiatric physicians also has to be as a part of the medical team to co-manage comorbidities. Smoking cessation, again, Medicare recognized that. If you are going to write it down on your chart that you’re doing this, you damn well better be doing it as well, encouraging patients to control their lipids, blood pressure, diabetic, glycemic control, making sure patients who are on anti-platelet therapy with aspirin or clopidogrel are following that and taking care of them. These are all things that you do when you work in conjunction with the patient internist. And if you talk to the internist in this language, internist could care less that the patient has a forefoot varus of 3 degrees. You are going to start writing letters and saying that this patient pronates past the perpendicular, that’s important to us and I’m not minimizing it. The internist could care less on it. And if you write a letter saying "Dear Doctor, our mutual patient, I noticed that today his blood pressure was 170/98 and he tells me he has not been taking his Plavix and I noticed an irregular pulse,” they are going to say, “Well, this guy, he is not just cutting toenails. This doctor really knows what he or she is doing.” And you’re doing good for your patients.

Now in terms of recognizing PAD, okay, we need to risk assess, I’m not doing a significant vascular exam, as I said before, on an 18-year old.

[0:15:03]

But we’re looking for the classic signs and symptoms that we all look at, okay, pulses, temperature gradient, digital hair, capillary filton, capillary return, these are all things that we know as good as anyone.

Any podiatrist where it – any podiatrist can identify peripheral arterial disease by clinically. Now, how severe it is and what extent of it is and where it’s located, different story.

I hate when someone and the vascular people hate it as well when a podiatrist refers a patients as rule out peripheral arterial disease, rule out PVD.

And the vascular people hate it, and you should too, you should say, "I’m referring you this patient with diminished pulses, with a decreased ABI, with coolness, with symptoms of claudication, with rest pain. Please evaluate for degree and extent of vascular disease."

Tests we can do in the office, okay, ABI, real easy, all you need is a blood pressure cuff, and a hand-held Doppler and ABIs can be done very easily.

You can get you know, sending out, depending upon your skill set, and your relationship with other people in the vascular team, you know, we’re usually not ordering the angiograms and we’re not ordering the – you can do PVRs in the office if you’re adept at doing it, and not just doing it for billing purpose, if you really can understand those waveforms and make some sense out of it, also.

This is a patient from just the other day, who had an issue, had a stent in his LAD, came in to me, very sedentary-type guy, no particular complaints, not claudication, but again, very sedentary guy, didn’t do much walking, or anything else around, no complaint of rest pain, but because of a cardiac history, I did an ABI, and got a – I think it was about 0.7 on one side and maybe a 0.74 on the other side.

And given the fact that he has significant – he’s a player, he’s got cardiac disease, and a low ABI, I sent him for a vascular consultation. Now whether you’re sent to a vascular surgeon or an interventionalists, depends upon your relationship in your hospital, recognized as a turf war in that between the vascular surgeons and the vascular interventionalists.

And we want to throw in there, sometimes, a radiology interventionalist, that’s a third cog in the wheel there and that there’s certainly a turf war going on there. I found referring to an institution that has their interventionalists and their surgeons in a good cooperative relationship, they work closely together, that’s where your patients are going to get the best care.

In any event, here is a –sent of an exercise – ABI was done, the exercise ABI even confirmed that there was significant ischemic disease, and the patient was often agreed to an angiogram and you see right over here, had almost a 95% stenosis in the external iliac artery here, these point stenotic areas are very adept for doing angioplasty and stenting. The patient had an angioplasty and a Zilver stent put in there and you can see a complete much greater flow and profusion in the iliac.

Also, if you look at in the SFA, the profunda looks pretty good, but if you look diffuse disease throughout the SFA, these also in smaller lesions can do well with stenting, but usually diffuse disease is some form of atherectomy is going to be done, even orbital or a directional atherectomy will be done as well.

So example, just by looking at the ABI, which I did in my office, based upon a history of coronary artery disease, I found a patient who has significant peripheral vascular disease.

Now, this is not an insignificant thing. If you look at the survival of patients with peripheral arterial disease, it’s not a good picture. If you’re someone who has a critical limb ischemia – 50% of them are dead in five years, usually from some form of cardiovascular disease.

[20:09]

If you look at claudicants, intermittent claudicants, again at five years, about 30% of those, one of three will meet their demise. So the mortality associated with this is quite severe, and it is something that you can do your patients tremendous, tremendous benefit by picking up early and making the appropriate referral.

ABI is, again, an easy test to do. It is shown to be an indicator of vascular disease at other sites as well as the peripherals. Again, if you identify it in a lower limb, chances are the patient also has disease in their carotids and in their coronaries.

The effectiveness of ABI as a common screening test is up there with Pap smear, fecal blood occult test, mammography. In fact, it exceeds the first screening test. So this is a test that is very inexpensive to administer and you get a high return in terms of identifying disease for it. Now, most people do this test wrong. The patient should be lying flat. You don’t want the patient sitting in there. You want to have the patient at rest to get a baseline. The cuff width should be at least 40% of the limb’s circumference. And I gave you the reference here, this was in Circulation of December of 2012, so this was a whole protocol of doing the ABI and you can look at that and this is an article you probably should have in your personal libraries. Doppler is the most reliable. Measure the systolic blood pressure on each arm and ankle. First arm, first PT, first DP, other PT, other DP on other arm, so you’re doing a clockwise approach on it. And then the ABI of each leg is calculated by dividing the higher of the PT or the DP pressure by the higher of the right or the left arm systolic blood pressure.

Coronary artery disease and PAD correlate. There is a very potent and clinically significant correlation here. If you identify the PAD, pretty good shot that there’s going to be coronary artery disease as well.

Now, the other side is just the same. A high ABI also correlates with increased cardiovascular disease. If you come up with an ABI of 1.2 or 1.3 certainly, that shows that there is inelasticity in the arteries that is calcification within there. So too high and too low are both predictors of cardiac disease.

ABI is now part of the Framingham Risk Score to predict cardiovascular events and mortality. You’ve all heard the Framingham study, which was a very potent and robust study identifying risk factors for the development of cardiac disease. ABI is now a part of that.

And in terms of the American Heart Association and the American College of Cardiology, class 2-A evidence, measurement of ABI is reasonable for cardiovascular risk assessment in asymptomatic adults.

So I think I made my case for doing ABIs, particularly in at-risk populations. Other non-invasive testings, segmental pressures and PVIs, you don’t need this to tell you that someone has PAD. This will be helpful in determining the level where it exists. Is it above the knee? Is it below the knee? And also quantifying it a little bit better.

Again, many docs do these tests in their office. The reimbursement is fairly robust for it. But if you’re not really adept at reading these waveforms and you’re just doing it as a test and not looking at it, you’re not doing what you really should be doing for the patients.

Now, in terms of acute ischemia, when someone comes in for sudden onset pain, sudden onset discoloration of the limb, usually this is going to be a thrombotic episode. Usually, they’re not associated with arrhythmias. They could be a history of claudication. They have risk factors for atherosclerosis. The abnormal contralateral pulse may be present as opposed to embolic phenomena, which means there is embolism coming off from someplace else. The embolic ischemia usually, there’s going to be an arrhythmia present, okay.

[25:02]

Also will be sudden onset, usually, no history of claudication. And normally, there will be a normal contralateral pulse.

So the first case is a thrombotic, just like a thrombosis in coronary artery, it’s a thrombosis in the lower extremity artery and they got all the signs and symptoms of preexisting vascular disease.

Embolism, a different story, that’s coming from someplace else lodging in an artery and cutting all circulation acutely. Usually, an ideology of an arterial emboli is going to come somewhere higher up in the aorta or the arterial tree. It may be associated with livedo reticularis, which is a swelling of the veins due to obstruction of the capillaries. This is where you have microemboli that obstruct down to the capillary level. Just don’t be confused, this can also occur in autoimmune disease, certain malignancies, acute pancreatitis or infections, but again livedo reticularis is a swelling or a dilatation of small capillaries in the vascularly comprised patients. Usually, these are cholesterol emboli that flowoff from a plaque somewhere higher up in the arterial tree.

Arterial emboli can also come from the heart, usually in patients with AFib. AFib is common. You can’t go one night. You can’t watch one football game. You can’t open up one magazine where you don’t see an ad for the various anticoagulant medications aimed at patients with AFib. Recognize, AFib can be chronic and AFib can be paroxysmal. It’s the paroxysmal that’s the most dangerous. Because these patients, when they go into AFib and come out is when they develop the clots that can flow.

Symptoms, irregular rapid pulse, they can have weakness, they can have shortness of breath, they may or may not have chest pain. Usually, they’d be hypertensive to some degree. Looking at the EKG, you can see the classic atrial fib patent or atrial flutter, in some cases. And this is where the clot generates from.

Now, if it goes north, it ends up in the brain and they have an acute stroke, which can be life threatening. And if it goes south, it goes down on to the lower extremity where they can manifest as an acute ischemic event.

So AFib also doesn’t have to be a large clot, it can throw off microemboli, which will manifest as we see. If it goes on the upper side here, we see microemboli going to the brain, it can result in TIAs and mental impairment. If it goes south, it ends up in the feet.

And you can see again the livedo reticularis. This is a patient who came to me a number of years ago who was running through the airport but suddenly felt a pain in his toe. He came to me. I saw that. It was a callus that had a little hemorrhage under it. He wasn’t diabetic. You have to find what was going on here. And when I felt his pulses, they were irregular pulse. And this was a classic case of AFib that manifested by a little embolic phenomena or necrosis in the foot. And when you send this patient to the cardiologist and say, “I think this patient has AFib.” And the response is, “You’re know, what? You’re a podiatrist and you picked this up?” And I said, “Yeah, we pick it up and we do this stuff routinely.”

Other forms of bacterial of the arterial emboli can come from endocarditis. Again, these patients generally are sick. Also, the small little emboli that can form splinter hemorrhages under the nail. And as we saw here that we saw adept at recognizing. Janeway lesions are again small foci resulting from localized necrosis from embolic phenomena. They can last days to week. They’re usually associated with acute bacterial endocarditis. Again, septic emboli lodging in the small vessels of the extremities.

So be differentiated from Osler's nodes, which are red, purple cutaneous nodules, again caused by septic microemboli. Usually these are seen in the tip of the toes and these are more common in subacute bacterial endocarditis than they are in the acute variant of it. Again, Janeway from Osler’s nodes, again recognize even one result of an arterial emboli usually coming from the heart valve.

You can have a non-bacterial endocarditis as well. These are patients who have rheumatoid valvular disease or direct trauma to the heart, immune complex, or in patients with malignancies that have tumor necrosis factor.

[0:30:05]

This is a patient with metastatic pancreatic adenocarcinoma that ended up because of the tumor necrosis factor flowing off these microemboli. Cardiac neoplasm myxomas occur. Myxomas can be that the loci for emboli as well as Raynaud’s disease.

Okay. Quincke’s pulse would be in patients with aortic insufficiency, aortic valvular disease. These are common. Aortic insufficiency, as we grow older, as people live longer, the aortic ring around the valve tends to calcify. So these are people who are usually advanced. And aortic insufficiency if left, the mortality rate at two years once it become symptomatic is about 100%. This was the reason but these are usually sick patients that developed and now in the last few years of the TAVR procedure which you hear for all the time, which is an endoscopic approach to replace the aortic valve. But these patients will see what’s referred to as Quincke’s pulse.

When you have an aortic insufficiency, you get regurgitated blood flow and this affects the diastolic pressure component which will increase in stroke volume and you will you see alternating. You look at these toenails and you will see actually the pulsations of the blood. And that’s a pretty good sign particularly in an older individual that they may be suffering from an aortic insufficiency. There are whole host of cardiac dysrhythmias from heart blocks, atrial fibs that can be picked up just by putting your fingers and feeling the pulse. This is not something that’s uncommon.

Congestive heart failure, usually these patients are pre-diagnosed. We know congestive heart failure results in pitting edema. Venous leg ulcerations that’s there. Patients with CHF, it also affects their gait pattern. They have much shorter stride and step lengths.

Ulcers. We see a whole host of foot ulcers in different ideologies. We can talk work hours just on the differential diagnosis of foot ulcers. Recognize, some of them are ischemic, okay, which the PAD, CAD, some of them are embolic we’ve talked about. Some of them are neoplastic, neurotrophic, vascular, this whole host of causes of this. Our job is to determine when presented with a patient with a distal ulcer as to what the cause is.

DFUs, 78% of patients with DFUs have signs of left ventricular dysfunction. Wow, that’s a big number. All right. So if you see these and these patients are not – you don’t feel that being properly managed by their internist or cardiologist, you might want to make a suggestion that they see.

Again the home stretch, clubbing of the nails. You can see, this is the angle that the nail plate makes with the proximal nail fold. This should be more acute in the normal. Clubbing of the nails is associated with lung disease and cardiac disease usually hypoxia, SBE, atrial myxomas also as well.

So as you can see that there are lots of systemic disease, both cardiac and non-cardiac, that can be manifested in the foot. I implore you when you’re looking at patients again, just don’t look at feet, look at patients with foot problems. What you see here most importantly can be a wonderful service that you can provide for your patients. It also ups your esteem and your prestige within the medical community. You’re not just a guy who cuts toenails and takes care of fungal nails. You’re a true physician and that’s what you’re trained to be, that’s what I know you can do and that’s what you will continue to do.

So thank you for staying late at the end of the day and enjoy what’s rest of the day. And I want to really thank you, present people for putting together a fabulous program for the rest of us.

Thank you.

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