A good friend (Lily Chen) sent me a YouTube, saying “myocardial
infarct is not caused by obstructing coronary artery after all” (原來心肌梗塞不是心臟血管太狹窄堵塞血不流通). This is the most important discovery in
cardiology the past 15-20 years. I have mentioned this
in my blog shortly after the TV journalist, Tim Russert, had a sudden death while recording voice-over in
2008.
But, the statement of “myocardial infarct is not caused by
obstructing coronary artery after all” (原來心肌梗塞不是心臟血管太狹窄堵塞血不流通) is not the whole truth; I
will elaborate since it is such an important, almost revolutionary concept.
The evolutionary
concepts of heart attack
Some of the material of this post comes from an article (with
a title of “Coronary Thrombosis”) in June 1, 1950 issue of Scientific
American, written by Dr. Paul White, a cardiologist at Massachusetts
General Hospital, a Harvard Medical School professor. Dr. White was most famous for being the
doctor for President Eisenhower when he was stricken by heart attack in 1955.
The sudden death of a seemingly healthy man/woman was
considered an act of gods over the age; he or she must have done something
terribly bad to evoke the wrath of gods.
Back in 1700 a French physician, Theophile Bonet, had proved complete
blockage of coronary artery in one person who died suddenly.
Lancisi, Pope Clement’s physician, also proved those who had
a sudden death all died of natural causes by doing post-mortem examinations in
1707. President Eisenhower had a first-rate
physician, so had Pope Clement.
The artery is more
animated and dynamic than a pipe
It is logical to think the cause of heart attack (myocardial
infarct) is caused by the progressive narrowing (stenosis) of coronary artery
until complete blockage, just like the clogging of the pipe under the sink.
Doctors had the second thought when it was discovered that most of the heart attacks occur
in the setting that there was less than 50% blockage. Subsequent studies learned that the plaque
builds up in the inner lining of the coronary artery over the years or decades,
and it is the rupture of the plaque, leading to formation of clot (thrombus)
that completely blocks the artery.
The cardiologists are dealing with a more animated and dynamic coronary artery, not a pipe; they would prefer leaving the "honor" of being called a "plumber" to urologists.
The blocked artery cuts off the blood supply to the heart
muscles (myocardium) distal to the point of blockage, leading to the necrosis/infarction/death
of the heart muscles; the ischemia (compromise of circulation) may trigger the
lethal ventricular arrhythmia.
Plaque, and the
plaque only, is the thing
Atherosclerosis (hardening of arteries) begins at the build-up
of the plaque in
the inner lining of coronary artery many years or decades before the heart
attack strikes.
(The above photo is taken from an article in New England Journal of Medicine)
The top panel shows most of the plaques initially
expand outwardly, causing little or no narrowing of the lumen of the
artery. But, given enough time it will
grow inward causing the stenosis (narrowing) of the lumen.
As a matter of fact, most of the plaques rupture when they cause some
degrees of narrowing, all be it less than 50% stenosis in most cases. The rupture leads to
clot (thrombus) formation that blocks the
artery.
The bottom panel shows a large inwardly grown plaque significantly
narrows the lumen of the artery and a tiny clot (thrombus) will completely blocks it. A disruption of the endothelial cells in the
inner lining is called “erosion” that produces the same effect of “rupture”.
The
middle panel shows if one survives the
rupture/erosion of the plague, a scar will be formed, constricting the artery,
causing narrowing of the lumen (stenosis).
A fibrotic (with deposition of calcium) plaque may be more stable, not
vulnerable to rupture. But one will be symptomatic with chest pain upon
exertion; for exercise will increase the demand of more oxygen for myocardium
that a narrowed artery cannot meet.
Why a non-obstructive
plaque is more dangerous than an obstructive one?
If a growing plaque pushes inward causing the narrowing of
the lumen of coronary artery, thus compromising the circulation, in which case
one may develop chest pain upon exertion (called angina) and seeks medical
attention.
If an outwardly expanding plaque ruptures before causing the
narrowing of the lumen, then one will never have any symptoms (chest pain/tightness/pressure
or shortness of breath) until the heart attack strikes.
Cholesterol, plaque
and statins (cholesterol-lowering drug)
Lipids
(cholesterol) are the major components of the plaque. The benefits of taking statins, the likes of
Lipitor, Pravachol, Crestor and Zocor, are not only lowering the LDL (bad
cholesterol) level, but “stabilizing”
the plaque as some theories suggest.
From 2003 to 2013, the death rate from heart attack fell
about 38% according a CDC data. One
cannot say doctors are not doing good jobs.
The reasons are multifactorial, but statins should get the most credits
in my view.
Mild disease of the
coronary artery may not be a good thing
So if a plaque is present (i.e. one has atherosclerosis or
hardening of artery), what
matters is not how much it blocks the artery, but how stable it is.
If one does cardiac catheterization (with injection of
contrast the coronary arteries can be visualized) it shows “mild” disease, say showing
15% or 30% or anything less than 50% stenosis, one needs to be treated as
aggressively as the more severe cases.
One school of thought is that a larger plaque that causes more narrowing
of the lumen may be more stable, thus less vulnerable to rupture. Unfortunately one cannot tell a plaque is a stable one or not on cardiac catheterization.
That is not to say the more narrowing of the artery the
better. If one has a large plaque that
causes severe stenosis, say greater than 75%, if it were to rupture, a small
clot (thrombus) will completely block the artery easily. Conversely a small stenosis, say less than
15% will take a relatively large clot to block the artery.
(The above photo is taken from Dr. Paul White’s article, “Coronary
thrombosis” in Scientific American)
This is to show prescient Dr. White was. There is a heart disease called Wolff
Parkinson White (WPW) syndrome, that “White” is Dr. Paul White. Keep in mind that Dr. White wrote this article in 1950.
Dr. White wrote,
“It is always in a diseased, badly
narrowed, atherosclerotic coronary artery that a thrombus, or clot, rather suddenly forms one day to
present the clinical picture which we call coronary thrombosis.”
What he wrote in 1950 is still
100% correct today. He knew the clot
forms rather suddenly on top of a “diseased, badly narrowed, atherosclerotic
coronary artery” that built up over the years or decades.
A disease free coronary artery is
one clean without plaque. A coronary
artery that has plaque is not disease free even though it has no narrowing/stenosis
of the lumen. Thus no plaque, no
narrowing, no rupture, no heart attack!
Dr. White wrote,
“. . . The stage is all set before the
thrombus is laid down in the diseased artery. Just how the blood is triggered to clot is not yet fully
clear. Most often, perhaps, a thrombus begins to form on a roughened bit of the
inner lining of the artery, or at a very much narrowed place in the vessel.
Within minutes or hours the thrombus grows large enough to block the blood flow
and to cause the various symptoms and signs that follow.”
What Dr. White described in 1950
was similar to what we call plaque rupture leading to clot.
How the blood clot (thrombus) forms after plaque rupture?
The mechanism of how clot was formed
that triggered heart attack was not fully elucidated in Dr. White’s time
(1950s), but it is well understood now.
We even had thrombolytic therapy (medicines to dissolve the clots). One
needs the full knowledge of coagulation cascades to fully understand the
mechanism; it is beyond the scope of this writing.
Suffice it to say that platelets
play a crucial role in clot formation; that is why anti-platelets aggregation
(preventing platelets to lump together) drugs, such as aspirin and Plavix (clopidogrel)
are so important in treating and preventing heart attack.
The following is the YouTube
that Lily Chen sent to me. Dr. 洪惠風 did a good job, telling the complicated story in less
than five minutes. This writing is to
further explain; less people would misunderstand and take “narrowing of
coronary artery” (心臟血管太狹窄) out of equation in
causing heart attack.
In fact, about 5 to 15% (depending on which
report one reads) of the heart attack are caused by steadily progressive
narrowing of the lumen to the point of complete occlusion by plaque that never
ruptured.
為什麼心臟病總是突然發作洪惠風主任
