쉐도잉 연습: Why Even Fit People Are At Risk of a Heart Attack - 영상으로 영어 말하기 배우기

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One of my favorite things to do with students is to show them how the organs actually sit within the human body.

And I especially love opening up the pericardium to show students the real human heart.

Now the heart has actually been on my mind a bit more lately

because about a month ago I was running a half marathon race with my brother

and he had a heart attack during the race.

Often we think heart attacks only happen to people who are older, unhealthy, or those that don't exercise, but that isn't necessarily true. So today,

we're gonna use the story of what happened to my brother

as a backdrop to help us learn about what actually happens during a heart attack, what causes it, and what everyone, regardless of current health status or fitness level,

can specifically do to reduce the risk of a heart attack and other cardiovascular diseases.

Plus, we'll talk about what was unique about my brother's heart attack and the physiological adaptations that can make one's heart

more resilient to these types of cardiac events.

It's going to be a myocardial one, so let's do this.

The fancy pants medical term for a heart attack is myocardial infarction.

Myo refers to muscle, cardial refers to the heart.

An infarction means tissue death due to a lack of blood supply.

So basically a heart attack or myocardial infarction happens when blood flow to a part of the heart muscle is blocked, starving it of oxygen and nutrients,

which causes that muscle tissue to eventually die if this blood flow isn't restored.

But what is actually causing this blockage in blood flow?

Well, if you take a look at these two arteries, you can see a right coronary artery here, and the left coronary artery here.

And the word coronary means crown.

The early anatomists thought these arteries looked like they were encircling the top of the heart, kind of like a crown.

But these are the main arteries that supply blood to the myocardium of the heart.

And you can also see that they will continue to branch into smaller arteries

that will deliver blood to specific areas of the heart.

Like this is a big one called the left anterior descending artery.

And I mention this one because of the story we'll get into a little bit later on about my brother.

And because it is often nicknamed the widow maker.

Because if a significant blockage forms in this artery, it can result in death

because It supplies such a large area of the heart as opposed to say

if a blockage formed in one of these smaller branches which would cause more of a mild heart attack.

But what is actually causing these blockages?

Well, the most common culprit is coronary artery disease.

Coronary artery disease is when the coronary arteries develop something called atherosclerosis.

Atherosclerosis is the buildup of plaques within the wall of the artery.

Plaques are essentially fatty deposits made of cholesterol, calcium, and other substances that get built into the wall of the artery.

And in this case, we're talking about plaques forming in the coronary arteries, or any of the branches of the coronary arteries.

But atherosclerosis can technically affect any artery in the body.

Like you could get these plaques built up in the carotid arteries that supply the brain, eventually leading to a stroke.

But over time, and we're talking years here, these plaques can continue to grow,

further occluding or blocking the artery and therefore reducing blood flow downstream from the blockage.

But you might be thinking, okay Jonathan, so what?

Eventually this blockage just gets big enough that you suddenly just have a heart attack?

Well not exactly, because here's the crazy thing,

people often do not develop any symptoms until a coronary artery or one of its branches is occluded by about 70%.

Now

that percentage can vary a little bit based on exactly where

the clot is in the coronary vasculature as well as individual differences, but the point is there is a significant amount of blockage before symptoms develop.

This is also why this can be so unnerving, because it's occurring silently without your knowledge.

However, there are some screening tools

that you can utilize to get an idea of your risk and if you have plaque buildup, and we'll talk about those screening tools a little bit later on in the video.

But even a 70% occluded coronary vessel still isn't usually enough to cause a heart attack all by itself.

And here's what I mean by that.

It's not like when it hits 71% you just have a sudden heart attack.

If the plaque is stable, people will often first develop chest pain on exertion.

So someone might start hiking up the stairs or exert themselves in some way and feel chest pain.

But when they stop exerting themselves and rest, the pain goes away.

And this is referred to as stable angina.

Angina sometimes pronounced angina, but if you look at pronunciation guys, it's like American English is angina, British English is angina.

So take your pick.

But it's called stable because it's predictable with exertion and goes away with rest.

And angina just refers to strangling to refer to this type of chest pain that people experience during stable angina.

Now technically the plaque could continue to get larger

and larger until eventually the The person is even experiencing chest pain at rest and eventually resulting in a heart attack.

However, most commonly people will have a heart attack when the plaque suddenly ruptures.

When the plaque ruptures or breaks apart, the body responds by forming a clot, kind of as an attempt to heal the rupture.

But this actually isn't that great of a response

because this clot will form relatively quickly and can then completely block the artery, resulting in what a person would perceive as a sudden heart attack,

with symptoms such as chest pain or pressure that might radiate to the arm, neck or jaw, shortness of breath, nausea, sweating, or even lightheadedness.

And something else that's important to note is that symptoms can be more subtle in women, like fatigue or a feeling of indigestion, which is why heart attacks can sometimes be missed.

But if someone does have a heart attack, time is very important.

The myocardium of the heart is resilient, but it can only go for so long with diminished blood flow.

Often you'll hear 30 to 60 minutes, but irreversible damage can start in as little as 20 to 40 minutes with total blockage,

extending to that 30 to 60 minutes if there's still some partial flow.

But it again depends on exactly where the blockage is, like is it in that left anterior descending artery, the Widowmaker, or is it in a smaller branch?

It also depends on some very interesting individual variations

that a person could potentially have in their heart that might make them more resilient to heart attacks, and we'll We'll talk about those variations in just a minute.

But regardless of those factors, the sooner you can get to the hospital for intervention, the better.

Some of those interventions will include clot busting drugs to potentially break up the clot

and possibly even an angioblasty where they take a catheter in through the radial

or femoral artery and thread it up to the coronary arteries.

A guide wire crosses the blockage, then a balloon is inflated to compress the plaque and widen the vessel, restoring blood flow.

a stent, which is a metal mesh tube, is deployed to keep the artery open.

The balloon deflates, catheter is removed, and this percutaneous coronary intervention is done in as little as 20 to 30 minutes for the core procedure,

which is pretty remarkable.

But let's quickly talk about what puts you at an increased risk for developing plaque in the coronary arteries.

And a lot of this comes down to the inside lining of your arteries called the tunica intima.

Anything that damages or irritates the tunica intima can lead to plaque formation.

This could be through high blood pressure, as high blood pressure puts a mechanical stress on the intima.

Heartful chemicals from smoking can also damage and inflame the tunica intima,

and even chronic elevations in blood glucose levels from unmanaged diabetes can damage and inflame this inside lining.

Combine these factors with elevations in certain types of cholesterol plus certain genetics

that make one more predisposed to higher cholesterol and clotting issues, and you start to create a recipe for plaque formation.

And what is eye-opening is how this can happen to seemingly healthy people, like athletes or those that exercise.

Even with good fitness, underlying factors like undiagnosed high cholesterol or family history can lead to plaque buildup.

Which brings us to the heart attack with my brother.

So last month I was in San Luis Obispo, California with my brother Jeff, my brother-in-law Jeremy, who also happens to be my business partner here at the lab, and one of my best friends,

Greg, who by the way, just finished chemotherapy for testicular cancer.

And he was there to run, you know, just a 31 mile ultra with 60 obstacles, because apparently that's what you do when you're finishing up cancer treatment.

But, us other three mere mortals, we were there for the Spartan Beast.

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This is a trail half marathon with 30 obstacles.

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Now for some additional context, the four of us had just run a marathon four weeks earlier.

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So my brother had been training prior to the marathon and had run the marathon without any problems.

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Well, except for the problems that everyone experiences during a marathon, like the pain train

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that everyone feels during the last few miles where you start to question every life decision that you've ever had.

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But again, no heart or other major issues during the marathon.

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And he continued to train for the Spartan Beast.

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Now usually what happens at these Spartan events is that my brother and I will race in different age groups, because he's 10 years older than me.

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Sorry to age you, Jeff, but this means that we'll often start at different times.

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And so we've kind of developed this tradition where Jeremy

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and I will finish first and then we'll walk back a mile or so, so that we can watch Jeff go through the most painful part of the event

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because it's fun to watch people in discomfort when you're no longer experiencing it yourself.

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But usually the most painful part of the event is the last mile

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because they tend to stack obstacles back to back to back.

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And, just as a side note, if any of you ever go to a Spartan event, go back and watch the spear throw.

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Because if you want to see some entertaining temper tantrums, you're in for a treat at the Spartan spear throw.

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The spear throw is one of those obstacles that you can train for, but it's so skill-based that it's kind of the X-factor obstacle for a lot of people.

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And when people miss it, all the emotions built up from the previous hard 12 miles come out in quite the colorful fashion.

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Because that person who just missed the spear knows that they have to do 30 burpees as a penalty.

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Which no one wants to do at mile 12.

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And as one other side note, sorry everyone, bear with me on this, but if anyone from Spartan ownership or management is watching this video,

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Spartans have kind of gotten a little soft as of late.

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Because for those of you who don't know, it used to be 30 burpees for every obstacle that you failed.

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Not just for the spear throw.

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Now instead of making people do 30 burpees for failing any of the other obstacles, they have you run this dainty little penalty loop.

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Which, no one is afraid of that.

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I literally have watched people come up and just touch the obstacle as their attempt, and then just run one of these dainty little penalty loops.

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But if you still made the racers do 30 burpees for each failed obstacle, They don't do that little bypass thing.

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I mean, at this rate, you might as well just call it a trail race with optional obstacles.

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Burpees are what made Spartans Spartans.

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They actually instilled fear in people while running these races, not these stupid, dainty, little penalty loops.

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Okay, rant is over.

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So we go back to this area to look for my brother, and it seems to be taking a little bit longer than normal.

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So of course, we start joking around about how he might just be taking his sweet time, taking in the wonderful view of the landscape.

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But as time goes on, we do start to get a little bit concerned, and we try to send him a text.

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Now, at most races, we've actually had pretty good cell phone service, but at this one, it was horrible, so none of our texts were getting through.

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But then Jeremy was like, oh, I might be able to send him a text through the satellite service

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that I have on my new fancy pants iPhone.

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I don't actually have that feature on my iPhone

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because I'm a little bit cheap and I've had the same phone for the last six or seven years.

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And now it's just becoming a badge of honor and we can talk about that later.

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But Jeremy gets one text to go through, and gets one text back from Jeff that says, I'm at the hospital, not a joke, AFib.

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Now, there are three things that we need to discuss about this text.

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One, is the fact that he had to clarify that he wasn't joking, which shows that

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when the three of us get together we tend to revert back to our teenage selves and not take things very seriously.

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Two, we did actually have an emergency situation on our hands that we knew very little about at this point.

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And three, he said, AFib, not a heart attack.

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And this is where the physiology of this story gets interesting.

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When my brother was a few miles in, he was doing the monkey bar obstacle.

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And when he jumped off of this obstacle, he noticed his heart racing and he was having shortness of breath.

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But no chest pain or anything that he would consider major discomfort.

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He noticed that the symptoms would improve when he would walk and rest, but when he would start another obstacle or increase his effort, the symptoms again became more noticeable.

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And on some of the obstacles, he started to get lightheaded and have tunnel vision like he might pass out.

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Eventually the symptoms seemed to be more persistent, and he actually got down on his knees and a woman noticed this.

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And she came up and asked him if he needed help.

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He said yes, and she went and got some of the Spartan staff, and they loaded him in the truck and took him to the medical tent.

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The paramedics came up from the ambulance and they did an EKG on him.

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Once they got the results of the EKG, the paramedic said to him, You're coming with me!

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And the reason for this was that the paramedic saw atrial fibrillation on the EKG

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and was going to take him to the hospital.

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Now atrial fibrillation or AFib is the most common cardiac arrhythmia, and an arrhythmia is in irregular heartbeat.

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And specifically with AFib, the heart's upper chambers, called the atria, beat chaotically and irregularly.

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The atrial chambers beat out of sync with the lower ventricular chambers

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and this can cause a fast pounding heartbeat with shortness of breath or lightheadedness, symptoms that my brother was experiencing.

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Now one of the biggest concerns for AFib is clot formation

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and this is because the atrial chambers are fluttering rather than fully contracting.

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So some blood can pool or stagnate within the atrial chambers and start to form clots, and if a clot forms in one of the atrial chambers,

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it could eventually move from the heart to the lungs if the clot forms in the right atrium, or it could even go up to the brain if the clot forms in the left atrium,

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which is the more common side that clots form on during AFib.

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Plus, the rapid heart rate can overwork the heart, so obviously you don't want people to remain in atrial fibrillation for an extended period of time.

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So while in the ambulance, they attempted to use rate controlling medications as well performed a cardioversion, which is trying to shock the heart back into normal sinus rhythm.

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They were unable to keep him in normal sinus rhythm in the ambulance, but when he got to the hospital they performed a stronger cardioversion or a stronger shock.

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They sedated him for this one and they did get him back into normal sinus rhythm.

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But they also looked at his troponin levels.

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Troponin is an enzyme that you hear a lot about with heart attacks, because this is an enzyme that is released by the cardiac muscle fibers when they're stressed or damaged,

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which definitely happens during a heart attack.

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And he did have elevated troponin levels.

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So what was going on here?

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Was it AFib, a heart attack, or something else?

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Well AFib can technically increase your troponin levels a little bit because the heart is getting overworked with that rapid heart rate.

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Plus, shocking the heart can be a little bit hard on the heart as well

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and so this can also elevate your troponin levels.

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So there was a discussion with his care team of, is this troponin just a result of the afib and the shocking of the heart, or is it something else?

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And at this point my brother is completely stable and not in any discomfort, so the plan was to monitor him overnight and do repeat troponin levels every few hours.

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And if the troponin went down significantly over the next few blood draws, the team was thinking that this was more likely due to the afib and the cardioversion.

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However, if the troponin remained elevated or even went up, that would be more concerning and might mean something else had occurred

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and then they would want to perform an angiogram to look at his coronary arteries.

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Turns out, the troponin levels went up.

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So the next morning they performed an angiogram and the cardiologist found

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that he had a 50 to 60% occlusion or blockage in his left anterior descending artery.

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Remember that artery that's nicknamed the widow maker.

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And this is where we can have a very important discussion about why monitoring your heart

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and cardiovascular health is important for everyone, even those that exercise,

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because what the final diagnosis was for my brother was a type 2 myocardial infarction secondary to atrial fibrillation.

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So he did technically have a heart attack, but not the typical heart attack, hence the classification of type 2 myocardial infarction.

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Remember, most heart attacks happen when the plaque ruptures, which then stimulates clot formation,

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and this more typical heart attack is a type 1 myocardial infarction.

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But this did not happen to my brother.

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Even with the 50-60% occlusion, training for a marathon, running a marathon,

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training for a spartan, was not enough strain on his heart to induce symptoms or cause a heart attack.

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And had he not had AFib, nothing would have happened.

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he would have likely just finished the race like he'd finished every other race.

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And there's a big reason as to why people can exercise quite intensely and still not have any symptoms, even if they have plaque buildup.

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In anatomy, you often will learn about collateral circuits, or sometimes just simply referred to as collaterals.

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Collaterals are arteries from two different sources that can supply blood to a similar area, and these are found throughout the body, including the heart.

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So if the main blood supply to a certain area was blocked or compromised, the collateral can potentially take up the slack and supply enough blood to that area.

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But here's what is very interesting.

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When you develop plaques in your coronary arteries, your heart will develop new collaterals.

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So let's say there was a plaque that was developing in this artery reducing the blood flow to this area.

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This blood vessel nearby could create more collaterals

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or in other words grow more blood vessels in order to compensate and supply this area with enough blood.

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Now you're not going to grow an artery like this size.

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that you grow are very small vessels like arterioles which are tiny arteries and also capillaries which are even smaller than arterioles.

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But the growth of these smaller blood vessels does make a significant difference in blood flow

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and makes people more resilient to myocardial infarctions.

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Now I do want to be clear here, I'm not saying, hey, we should all develop plaques so that we can stimulate the coronary vasculature to grow more collaterals.

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This is just something the body does to protect itself.

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But, you know what else stimulates the development of new collateral blood vessels?

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Consistent cardiovascular exercise.

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And that is definitely the kind of stimulus that we want driving the development of new collateral blood vessels to our heart.

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And so, coming back to my brother, he had likely developed collaterals, yes due to the plaque, but also due to his training.

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His heart was getting enough blood flow even

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when there was an increased cardiac demand during training and racing but during this last Spartan,

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it was the AFib on top of the exercise that pushed things over the limit.

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The AFib pushed the demand on his heart to the point where that 50-60% blockage was now a problem, and even his collaterals couldn't keep up,

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which caused the heart attack and the elevated troponin levels.

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But what was the cause of the AFib?

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Well, we are not entirely certain.

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We think it may have been a perfect storm of the travel, some dehydration, lack of sleep prior to the race, and he did have a higher amount of caffeine that day with some pre-workout.

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Now, I don't want to freak everyone out with caffeine use, but arrhythmias are a potential side effect when taking higher doses of caffeine than one is used to, especially if you're caffeine naive,

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meaning that you don't take a lot of caffeine throughout the week.

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So, if you are going to try something new like a pre-workout supplement, it's usually best to start on the lower end to see how your body responds before moving to higher doses.

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But today, my brother is doing fine.

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He's working with a cardiologist to decide the best plan moving forward.

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If his blockage had been 70% or more, they likely would have put a stent in during the procedure in California.

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That is still a potential option that they are discussing with lifestyle modifications and the potential use of medications.

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What some of you might be wondering is, should someone still exercise in this situation?

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And with very few exceptions, the answer is yes.

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What I don't want people to do with this video is freak out about exercising

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because you might have unknown plaque build up in your coronary arteries.

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Because exercise still absolutely reduces your risk of cardiovascular disease.

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Remember, it also helps develop new collateral blood vessels.

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And my brother's situation may have been worse had he not done any training.

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What I do hope people take from this, besides learning some really cool anatomy and physiology, is staying on top of your cardiovascular health maintenance.

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regardless of your fitness level.

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This is done through your annual physicals where your blood pressure is checked, you get blood work that checks your blood glucose levels, cholesterol levels, so things like CBCs,

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CMPs, and lipid panels, and other potential tests depending on your current health status, age, and risk factors.

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And based on those results, this can give you and your healthcare provider an idea of your risk of developing plaques.

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And if you're at higher risk, your medical provider may order additional screening tests like a coronary artery calcium scan,

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which essentially detects and quantifies calcified plaque in the coronary arteries.

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And if that shows any results that are concerning, then a provider may even step up to a CT angiogram

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where they take images of the coronary arteries with contrast and

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that can give an even more definitive idea of the amount of plaque and calcium build up in those coronary arteries.

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And then of course, you do everything that you can from a lifestyle perspective to reduce your risk.

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and less otherwise specified by your health care provider, you continue to exercise because that will help with blood pressure, cholesterol and reduces your risk of metabolic dysfunction like diabetes.

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Diet obviously is also an important part of this and of course avoid smoking.

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Poor sleep and stress are also linked to increased risk of cardiovascular disease, so don't forget about your sleep or your mental health.

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이 레슨의 어휘와 말하기 포인트

이 C1 수준 말하기 레슨은 영상 “Why Even Fit People Are At Risk of a Heart Attack”을(를) 바탕으로 합니다. 가장 자주 반복되는 단어는 다음과 같습니다: blood, attack, plaque, coronary, artery. 이 영상에는 섀도잉할 문장 271개와 단어 4517개가 있습니다. 말하는 구간의 길이는 24:14입니다. 화자는 분당 약 186단어로 빠르게 말하므로 연음과 약하게 발음되는 소리가 많습니다. 영어에서 가장 많이 쓰이는 3,000단어에 속하는 단어가 80%뿐이라 어휘가 어려운 편입니다.

이 영상의 핵심 어휘

영상에서 가장 어려운 단어 15개를 발음, 뜻과 함께 정리했습니다.

단어	발음	뜻
artery 명사	/ˈɑɹ.təɹ.i/	동맥
obstacle 명사	/ˈɑbstəkəl/	장애, 장애물
collateral 명사	/kəˈlætəɹəl/	담보물
symptom 명사	/ˈsɪm(p)təm/	증상, 증후
infarction 명사	/ɪnˈfɑɹk.ʃən/	경색 형성
cholesterol 명사	/kəˈlɛstəɹɒl/	콜레스테롤, 콜레스테린
caffeine 명사	/ˈkæfiːn/	카페인
spear 명사	/spɪə̯(ɹ)/	창
atherosclerosis 명사	/ˌæθɚoʊskləˈɹoʊsəs/	죽상동맥경화증
rupture 명사	/ˈɹʌpt͡ʃɚ/	터짐
shortness 명사		짧음
calcium 명사	/ˈkælsi.əm/	칼슘
rhythm 명사	/ˈɹɪð.əm/	리듬
ambulance 명사	/ˈæmbjᵿl(ə)n(t)s/	앰뷸런스, 구급차
arrhythmia 명사	/eɪˈɹɪð.mɪ.ə/	부정맥

영상에 나오는 구동사

단어	뜻
come up 동사	올라오다
go up 동사	올라가다
get together 동사	만나다
go away 동사	떠나다, 떠나가다
go back 동사	돌아가다
go down 동사	내려가다

이 영상의 문법

화자가 가장 많이 쓰는 문형을 영상 속 실제 표현과 함께 정리했습니다.

문형	영상 속 표현
현재완료진행 have/has been + -ing — 전에 시작해 지금도 계속되는 동작	I've personally been using · I've been getting
조건문 if + 절, will/would + 동사 — 조건과 그 결과	if you have plaque buildup, and we'll talk · If the plaque is stable, people will often
“used to” used to + 동사 — 지금은 아닌 과거의 습관이나 상태	used to be · used to trip
수동태 be + 과거분사 — 누가 하는지보다 무슨 일이 일어나는지에 초점	is blocked · isn't restored · is often nicknamed

주의할 발음

화자는 don't, we'll, you're 같은 축약형과 약화된 형태를 50번 사용합니다. 들리는 대로 짧게 발음하세요.

“th” 소리: atherosclerosis /ˌæθɚoʊskləˈɹoʊsəs/, rhythm /ˈɹɪð.əm/, arrhythmia /eɪˈɹɪð.mɪ.ə/, catheter /ˈkæθɪtɚ/
“sh”와 “zh” 소리: infarction /ɪnˈfɑɹk.ʃən/, fibrillation /ˌfɪbɹɪˈleɪʃən/, exertion /ɪɡˈzɝʃən/, occlusion /əˈkluː.ʒən/, elevation /ˌɛlɪˈveɪʃn̩/
긴 단어 — 강세 위치에 주의: coronary /ˈkɔɹənɛɹi/, collateral /kəˈlætəɹəl/, myocardial /maɪoʊˈkɑɹdi.əl/, cardiovascular /ˌkɑːdi.əʊˈvæskjʊlə(ɹ)/, cholesterol /kəˈlɛstəɹɒl/

한국어 화자가 어려워하는 소리:

/f/ — ㅍ(/p/)으로 바꾸지 말고 윗니를 아랫입술에 대기: infarction /ɪnˈfɑɹk.ʃən/, caffeine /ˈkæfiːn/, fibrillation /ˌfɪbɹɪˈleɪʃən/, discomfort /dɪsˈkʌmfɚt/, inflame /ɪnˈfleɪm/
/v/ — ㅂ(/b/)과 구별하기: cardiovascular /ˌkɑːdi.əʊˈvæskjʊlə(ɹ)/, elevate /ˈɛləveɪt/, vasculature /ˈvæskjʊlət͡ʃə(ɹ)/, elevation /ˌɛlɪˈveɪʃn̩/, variation /ˌvɛəɹiˈeɪʃn̩/
/z/ — ㅈ이 아니라 성대를 울리는 /s/: resilient /ɹɪˈzɪl.jənt/, exertion /ɪɡˈzɝʃən/, personalize /ˈpɜː.sə.nə.laɪz/, physiology /ˌfɪziˈɑ.lə.d͡ʒi/, glucose /ˈɡluː.kəʊz/

이 영상으로 연습하는 방법

먼저 말하지 않고 영상을 끝까지 듣고 모르는 단어를 적어 둡니다.
0.75배속으로 한 문장씩 섀도잉을 시작하고, 익숙해지면 보통 속도로 돌아갑니다.
자신의 목소리를 녹음해 원본과 비교하고, artery, obstacle, collateral 같은 단어에 특히 주의합니다.

쉐도잉이란? 영어 실력을 빠르게 키우는 과학적 방법

쉐도잉(Shadowing)은 원래 전문 통역사 훈련을 위해 개발된 언어 학습 기법으로, 다언어 학자인 Dr. Alexander Arguelles에 의해 대중화된 방법입니다. 핵심 원리는 간단하지만 매우 강력합니다: 원어민의 영어를 들으면서 1~2초의 짧은 지연으로 즉시 소리 내어 따라 말하는 것——마치 '그림자(shadow)'처럼 화자를 따라가는 것입니다. 문법 공부나 수동적인 청취와 달리, 쉐도잉은 뇌와 입 근육이 동시에 실시간으로 영어를 처리하고 재현하도록 훈련합니다. 연구에 따르면 이 방법은 발음 정확도, 억양, 리듬, 연음, 청취력, 말하기 유창성을 크게 향상시킵니다. IELTS 스피킹 준비와 자연스러운 영어 소통을 원하는 분들에게 특히 효과적입니다.

섀도잉 방법: 단계별 전체 가이드 읽기 →

쉐도잉 연습: Why Even Fit People Are At Risk of a Heart Attack - 영상으로 영어 말하기 배우기

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