IMPORTANT
FACTS TO KNOW BEFORE YOU SHOVEL SNOW!
1. If you suffer from hypertension or heart disease, do NOT shovel
snow or use a snow blower without first consulting your physician.
2. If you have a family history of heart disease, current smoker,
borderline hypertension, high cholesterol or obesity, you are at a
higher risk of heart attack and heart disease and need to take EXTREME
caution while shoveling snow.
Breathing in cold air and holding your breath while shoveling snow
can constrict blood vessels, raising heart rate and blood pressure
to dangerous levels. This can lead to heart attack. To avoid putting
extra strain on the heart, follow these snow shoveling tips:
. Push show. Do NOT lift snow unless absolutely necessary.
. Never hold your breath during exertion.
. Do NOT throw snow over your shoulder or to the side.
. Take frequent breaks and NEVER over exert yourself.
. Wear shoes with a sturdy tread.
. Lift with your legs and NOT your back.
. Avoid eating or smoking before shoveling.
. Do some warm up stretches before shoveling to loosen up tight muscles
and joints.
. Wear warm layered clothing and protect your eyes, face and extremities
from the cold.
If chest discomfort, shortness of breath, lightheadedness, or dizziness
occur during snow shoveling, STOP immediately and call your physician.
Be smart. Be safe. Your heart will thank you.
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SYMPTOMS
OF HEART ATTACK
(MYOCARDIAL INFARCTION, MI)
It is true that there has been a decline in the death rate of coronary
artery disease (CAD) in recent years in the United States. However,
CAD continues to be the leading cause of death. About one third of
all deaths in the U.S. are due to CAD, and of these about one half
are due to heart attack (myocardial infarction, MI).
About one half of all the people with heart attack will die within
one hour of the onset of symptoms. Most of the remaining people will
be admitted to a hospital. Of those admitted to the hospital, about
15% will die in the hospital; an additional 10% will die within the
first year of their heart attack. One of the major factors that will
determine a person’s outcome, both immediate and in the future,
is the timeliness in which he or she receives appropriate treatment.
Clearly, we can now appreciate the importance of recognizing the symptoms
of heart attack and then acting upon them, i.e. getting to a hospital’s
emergency room (E.R.) as quickly as possible.
Previously, we have described “angina”, that is chest
pain due to CAD: “The pain is the resultant of atheromatous
plaque buildup (cholesterol deposits) in the arteries on the surface
of the heart muscle. When the obstruction becomes significant enough
such that blood flow to the heart muscle is reduced, chest pain results.
The typical terms used to describe the character of angina are ”crushing”,
“pressure”, “vise-like”, “squeezing”,
“heavy”. The pain is most often located behind the breast
bone, but may spread across the whole front of the chest area. Often,
the pain will spread up into the neck or jaw area and down the inner
aspects of the arms (more often the left arm).
This character of chest pain also happens to be the same character
of chest pain related to myocardial infarction (MI) with some important
differences. Chest pain associated with MI is usually more INTENSE
and much more PROLONGED. It may last much beyond 10 minutes; usually
30 minutes to several hours.
Another important difference: chest pain of angina usually comes
on with exertion, i.e. when the heart has to work harder. Chest pain
of MI may often come on at REST; the person may actually awaken from
sleep with the chest pain. Statistically we know that most heart attacks
occur between 6 A.M. and noon.
Other important symptoms found with heart attack are nausea and vomiting,
profound weakness, dizziness, palpitations, cold perspiration, and
a sense of “impending doom”. There may be difficulty breathing
of various degrees, which at times may be quite severe.
When symptoms occur that suggest heart attack (myocardial infarction),
it is of the utmost importance that the person be evaluated in the
closest E.R. as QUICKLY as possible. Time should not be wasted in
trying to contact the primary care physician. The person should NOT
attempt to drive himself to the E.R. nor should the family attempt
to drive the person. “911” should be called with the request
of an ambulance for a possible heart attack victim. These professionals
can provide on-site life saving measures to the victim while transporting
him to the E.R.
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TREATMENT
OF MYOCARDIAL INFARCTION (MI) “CLOT BUSTERS” (THROMBOLYTICS)
Previously we described the major symptom of coronary artery disease(CAD)
as chest pain; for ANGINA it was usually exertional in nature and
of a short duration. In MYOCARDIAL INFARCTION it was more intense,
and of a longer duration. In both cases the pain was precipitated
by reduced blood flow in one of the coronary arteries. “The
pain is the result of atheromatous plaque buildup (cholesterol deposits)
in the arteries on the surface of the heart muscle. When the obstruction
becomes significant enough such that blood flow to the heart muscle
is reduced, chest pain results”. When arteries are blocked up
to 70%, deprived blood results. Usually this occurs when a person
exerts causing the heart to work more. But we know that many heart
attacks begin at rest, when the heart is actually working less. What’s
going on here? What's causing this process?
The process of heart attack is quite complex. The essence is that
a blocked artery of let’s say 70% can go to 100% (or nearly
so) in just a matter of minutes. Something happens to that atheromatous
plaque in the artery. It may crack or rupture. When this happens it
activates the clotting process. Clotting cells in the blood, called
platelets, arrive and start to clump. A complex process is activated
resulting in the growth of a clot (thrombus) that can partially or
totally block the blood flow in the artery. When this happens, the
heart muscle dependent on the flow of blood begins to suffer; it may
suffer a little, or it may suffer a lot. This outcome in turn is dependent
on how QUICKLY blood flow can be restored to the heart muscle. It
becomes obvious that if we could stop the formation of the clot or
dissolve the clot if it does form, we could minimize heart damage.
Enter the “clot busters” or “thrombolytics”.
The two most common clot busters in use are streptokinase and t-PA.
Both have the ability to dissolve the clots in a high percentage of
the times. However, whether benefit will result or not, i.e. will
heart muscle be “rescued” and damage from heart attack
be minimized, is directly related to the timeliness in which the clot
is dissolved - how QUICKLY the person receives the clot buster. The
SOONER the better. Clearly it has been shown that those who receive
this treatment within 6 hours of the onset of chest pain, stand to
gain the most. They will have the least amount of heart damage and
an ultimate better outcome or prognosis; there will be less chance
of a death and less chance of developing “heart failure”
both short term and long term. This has become known as the “open
artery hypothesis” which predicts that opening up an occluded
coronary artery will save heart muscle and improve survival rates.
At present, these thrombolytic agents, or “clot busters”
can only be administered in an emergency room (ER). They are not presently
being given by the paramedics. Consequently we stress that the key
here is TIMELINESS to treatment. When the symptoms are present that
suggest heart attack, 911 should be called requesting an ambulance
for a possible heart attack victim. This insures that the person will
be transported to the ER as quickly and safely as possible, and that
thrombolytic treatment (“clot busters”) will be started
if indicated. There are contraindications to this treatment, and only
the doctors can make that determination.
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TREATMENT
OF MYOCARDIAL INFARCTION (MI), PART 2
BEYOND "CLOT BUSTERS"
In a prior chapter we discussed the forefront of heart attack treatment
today, that is, the thrombolytic agents or “clot busters”.
We described what appears to be going on when a myocardial infarction
(MI, or heart attack) occurs. Usually, on a preexistent blockage in
a coronary artery (atheromatous plaque, or cholesterol deposit) there
is a rupture or a tear on this plaque. This event causes multiple
events to occur that set up clot (or thrombus) formation at this site.
Consequently, an artery that is blocked, let’s say 70%, can
go to 100% blocked in a matter of minutes because of the clot. Therein
lies the beauty of the thrombolytic agents, such as streptokinase
or t-PA, which can dissolve the clot and restore flow in the artery
and therefore to the heart muscle, reducing the amount of heart damage.
Previously, we mentioned that thrombolytics may be contraindicated
in some patients. Clearly these patients may certainly be candidates
for other medical treatments (as are the patients who also receive
the thrombolytics). Let’s review what medicines may be prescribed
and for what reason.
Aspirin (ASA): This blocks the effects of the platelets in the blood,
the cells used to start the clotting process which is important in
the heart attack process. Aspirin not only has benefit in the immediate
heart attack process but also has late effects. Statistically, taking
aspirin reduces the chance of a second heart attack.
Nitroglycerine (NTG): This can be given in tablet form or intravenously
(IV) to help control the pain of heart attack and perhaps help reduce
to the amount of heart damage.
Beta-blockers: Examples of this drug are Inderal (propanolol), Lopressor
(metoprolol), Tenormin (atenolol). This class of drug has multiple
beneficial effects. These includes controlling the pain of heart attack,
reducing the amount of damage to the heart muscle, and reducing the
possibility that the heart rhythm will become irregular (fibrillation,
a life threatening situation). In addition, taking a beta-blocker
after a heart attack may statistically reduce the chance of a second
heart attack.
Heparin: This in an intravenous blood thinner used after clot busters;
or, if the clot busters cannot be given, used in place of them. They
help keep the clot in the artery from growing, helping to keep the
artery open.
ACE inhibitors: Examples of this class of drug are Capoten and Vasotec.
These drugs have commonly been used to treat high blood pressure (hypertension)
and also congestive heart failure. There is now evidence to show that
these drugs may reduce the mortality rate after a heart attack. In
addition, they improve the “healing process” after a heart
attack, improving the chances that the heart will not enlarge and
therefore remain a more efficient pump.
It must be emphasized that not all patients will be able to be placed
on some of these drugs, for multiple reasons. We have to remember
that although each of these drugs has the possibility of a beneficial
outcome, they may also present serious consequences. It has to be
up to your primary care physician and cardiologist to determine what
treatment and medicines will be beneficial, and which may not.
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VIAGRA ("friend
or foe")
In recent weeks there has been quite a bit of press about
the drug VIAGRA. As you may or may not know, not all the news has
been favorable. Many of the most recent reports have sent a message
of caution and concern to those who are using or considering using
this drug. This report will try to clarify some of the concerns and
indications as well as the discuss the potential adverse reactions
of VIAGRA.
WHAT IS VIAGRA?
VIAGRA is a drug developed to treat impotence .
WHAT IS IMPOTENCE?
Impotence is the inability for a man to achieve and or sustain an
erection sufficient to engage in sexual intercourse. This affects
52% of men ages 40 - 70 yrs. old. The risk of developing impotence
increases with some health problems such as high blood pressure, coronary
artery disease, patients post heart bypass, diabetes, smokers and
some medications used to treat these and other conditions.
HOW DOES VIAGRA WORK?
VIAGRA works by allowing increased blood flow to certain areas of
the penile tissue and muscle required to cause an erection. Impotence,
from any of the causes noted above, occurs due to lack of blood flow
to the penile muscle and disruption of a certain chain of chemical
reactions within the tissue . VIAGRA does not automatically cause
an erection after the pill is taken. It allows the penis to respond
if sexual stimulation is instituted without of course!
HOW HAVE PEOPLE DIED FROM TAKING VIAGRA?
In speaking with the Representatives from Pfizer Pharmaceuticals who
make the drug and reading the available reports, it appears the deaths
that have occurred were due to underlying heart disease and not directly
due to VIAGRA itself. Sexual activity is exercise. If a person who
has not been able to have sexual relations for quite some time Due
to impotence now suddenly has the ability to have sex because Viagra
allows him to develop the erection, then he may be engaging in physical
Activity or exertion to a level that he may have not achieved for
quite some Time. This would be the same as someone who does not routinely
exercise Getting off the couch one day and running around the block.
Men who have known or unknown heart disease may be at risk for a heart
attack under these Circumstances. If you have not been exercising
routinely, if you have heart disease and have not had a recent physical
or stress test by your doctor or cardiologist, or if you have any
symptoms of heart disease (shortness of breath, chest discomfort or
pain, palpitations ) you should not take VIAGRA until advised by your
doctor.
UNDER NO CIRCUMSTANCES SHOULD ANY INDIVIDUAL TAKE OR USE ANY FORM
OF NITROGLYCERIN WHILE ON VIAGRA. THIS CAN CAUSE PROFOUND DROP IN
BLOOD PRESSURE AND POSSIBLY RESULT IN DEATH.
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ATRIAL FIBRILLATION
“ASK YOUR DOCTOR ABOUT COUMADIN”
Have you seen the commercial on TV which asks the
question, “Ask your doctor about Coumadin”? Well apparently
several people have, and they’re asking! And, consequently,
that has led to this little article.
Coumadin (which is the trade name for warfarin) is a “blood
thinner” , or technically an anticoagulant. Its effect is to
prevent thrombi or clots from forming. While there are many uses for
Coumadin, probably the two major uses in cardiology are for artificial
(mechanical) heart valves (prosthetic heart valves). In this instance,
because the mechanical valve is foreign to the body, blood tries to
clot on it. Obviously, this would be devastating. Clot would cause
the valve to malfunction. In addition, if clots did form and then
broke away they would end up in the arterial blood circulation causing
obstruction of smaller arteries at a distance. Probably the most devastating
manifestation of this would be if the clot ended up in a cerebral
(brain) artery; this would cause a stroke!
The second and probably the most common use for Coumadin is in atrial
fibrillation (AF). Atrial fibrillation (AF) is a disturbance of the
heart rhythm (arrhythmia). It is the most common sustained arrhythmia
encountered; it is estimated that in the U.S. alone there are probably
160,000 new cases a year, and that more than 2 million Americans are
affected with AF.
What happens in AF? Recall that the heart is composed of four chambers:
two upper chambers, the left and right atria; and two lower chambers,
the left and right ventricles. The upper and lower chambers (atria
and ventricles) beat in synchrony. First the atria beat sending blood
to the ventricles, then the ventricles beat sending blood out of the
heart to the rest of the body. It’s like a “one-two punch”.
The atria ensuring that the ventricles are filled to the maximum so
that they will be as efficient as possible. In atrial fibrillation
the atria loose their ability to beat, that is to contact meaningfully
sending blood to the ventricles. Instead, they fibrillate or quiver.
They do so very rapidly causing the heart to beat very rapidly. This
may have several effects. Obviously, two of these effects would be
(1) a heart beating fast and “out of control”. And, (2)
a heart pumping less efficiently because of the lose of the atria’s
help to fill the ventricles.
However, there is a third consequence. Because the atria no longer
beat or contract, but rather quiver, blood does not empty properly.
Blood ends up “stagnating” in the atria and thereby can
form thrombi (clots). Again, the devastating consequence exists that
these clots can dislodge and travel to the brain causing a stroke.
Depending on the person’s underlying heart condition causing
the AF, he may be at “high risk” or “low risk”
for developing clots. High risk patients should be treated with Coumadin;
low risk patient may be able to be treated with aspirin. Either modality,
if chosen properly can significantly reduce the risk of a stroke.
Only your doctor or Cardiologist can determine if you are in the “high”
or “low” risk category. Your medical history, physical
exam and an echocardiogram (ultrasound of the heart) all help in making
this determination.
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CORONARY
ARTERY DISEASE TREATMENT STRATEGIES: CORONARY ANGIOPLASTY - PART I
Coronary artery disease is the build up of plaques in the walls of
the blood vessels (arteries) which supply blood and oxygen to the
heart muscle. These plaques can be composed of cholesterol, fat, calcium
and sometimes blood clots which can ultimately obstruct blood flow
to the heart muscle point where the blood flow is significantly reduced
to the heart muscle , symptoms may develop such as chest pains, pressure,
tightness ,squeezing or shortness of breath, sweats, jaw or arm discomfort
etc. These symptoms are commonly referred to as ANGINA. If the flow
is cut off for a significant amount of time then damage to the heart
muscle may begin to occur and this is called a heart attack ( Myocardial
Infarction ). Heart attack severity may vary depending on the amount
of heart muscle damaged. Once the extent of the disease of the coronary
arteries has been established in patients with angina symptoms or
heart attack victims, then the treatment strategies can then be determined.
These strategies may include medications, Percutaneous intervention
(Angioplasty, Stents, etc. ) or coronary bypass surgery.
The vast majority of the cases the treatment decisions are fairly
straight forward. It is not at all uncommon, however, where the exact
treatment for a given situation is not clear or may have the option
to try any of one or two available treatments. Your physician will
usually review these with you and explain the risks and benefits and
rationale for these choices. Sometimes the physicians recommendations
are clear and directive and sometimes it is left up to the patient
to choose after the have received the appropriate information to help
them decide. At times the decisions are easy and at times very difficult.
No one treatment is the cure-all for all coronary artery disease and
this must be understood. In addition, the risks and benefits of the
treatments may vary from patient to patient, depending on their individual
situation.
Many patients are familiar with the procedure called " ANGIOPLASTY
" which is the procedure by which a catheter with a small balloon
mounted on it's tip is passed into the area where the plaque is obstructing
the artery, inflated and pushes the plaque to the side to make way
for the blood to flow more freely through the artery to the muscle.
The results obtained may vary depending on the extent of the disease
in the artery, the plaque composition, the vessel size or the location
of the plaque in the artery.
Angioplasty was first applied clinically in the 1970's. Great strides
Have been made, especially in the last 10 years. As we learned more
and More about the arteries, the disease process and the plaques,
newer devices have been developed to help handle and treat specific
coronary artery plaques.
We have seen the development of Stents, which are small stainless
steel mesh tubes to help bridge open the arteries. There has been
Athrectomy, devices which help by cutting and extracting out the plaque.
Rotoblators, which are small high speed drills which pulverize the
plaque into tiny particles. Each having it's place in the cardiologists
"Toolbox" to help treat the disease. All of these and other devices
have their place, their benefits and their drawbacks. None has proven
to be the "Magic Wand" to cure the disease.
In PART II we will talk more about stents, procedural risk and commonly
asked questions.
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CORONARY
ANGIOPLASTY TREATMENTS - PART II
Not every device to treat patients with coronary angioplasty is for
everyone as we described in part 1 of this series . Your clinical
situation may be very different from someone else's. For example,
one person may have had excellent results with a stent ,yet, another
may not be a candidate for a stent for various reasons. Vessel size,
extent of the disease within the vessel, location of the plaque or
proximity to other vessels could all determine which devices could
or could not be used.
All procedures carry a success and failure rate. Depending on the
Circumstances, success rates can range from less than 50% to greater
than 90%. The majority of the cases are probably in the 90% range
for procedural success. There does exist a risk of an unsuccessful
result. Complications that can occur are acute heart attack (3 - 5
% risk), need for emergency coronary bypass surgery (3 - 5 %), less
than 1 % risk of death in most cases. All of these risks may be higher
or lower depending on the nature of the individual patient's case.
These risks should all be discussed prior to going in to the procedure.
Discussing the individual's risks will help the patient to decide
between treatment strategies.
The development and evolution of the devices we use and the ongoing
Research to continuously improve the technology has clearly benefited
the physician performing the procedures and more importantly benefited
the patient.
Since the advent of angioplasty, the draw back has been and remains
the renarrowing (RESTENOSIS) which may occur and is highest in the
first 6 months following the procedure. The average restenosis rate
is approximately 30 - 40% in the first 6 months. In some situations
the rate can be slightly higher and in some somewhat lower (10- 20%).
The vessel size, lesion location and device used to treat the blockage
can all determine these potential results. The renarrowing is largely
due to the slow growth of muscle cells that heal the vessel's inner
lining after an intervention has occurred. It acts almost like scar
tissue to heal the vessel and sometimes grows back too much and cad
obstruct the blood flow in the artery. Poor diet, sedentary status,
high cholesterol and most of all smoking can help to accelerate the
renarrowing process. Generally you will undergo stress testing and
sometimes repeat angiograms to assess whether or not the vessel has
or is starting to renarrow. If renarrowing does occur, many times
the angioplasty can be done again.
In PART 3 we will discuss some of the commonly asked questions about
coronary intervention.
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CORONARY
ANGIOPLASTY TREATMENTS - PART
III
COMMONLY ASKED QUESTIONS
WHAT IS THE RECUPERATION PERIOD AFTER AN ANGIOPLASTY?
USUALLY THE RECUPERATION PERIOD WILL BE A FEW DAYS WITH GRADUAL INCREASE
IN ACTIVITY. YOU ARE USUALLY DISCHARGED THE NEXT DAY AS LONG AS THERE
WERE NO COMPLICATIONS. THE TIME TO RETURN TO WORK OR STRENUOUS ACTIVITY
MAY BE LONGER DEPENDING ON WHETHER YOU HAD A RECENT HEART ATTACK OR
NOT PRIOR TO THE ANGIOPLASTY.
HOW MANY TIMES CAN YOU HAVE AN ANGIOPLASTY DONE IF THE BLOCKAGE
COMES BACK?
THERE IS NO LIMIT. EACH CASE IS DIFFERENT. SOME VESSELS CAN BE DONE
MULTIPLE TIMES IF NEEDED AND SOME MAY BE BEST TREATED WITH BYPASS
IF THEY RENARROW.
HOW WILL I KNOW IF THE BLOCKAGE IS COMING BACK OR NOT?
YOU MAY START TO DEVELOP SYMPTOMS SIMILAR TO THOSE YOU HAD PRIOR TO
THE ANGIOPLASTY. YOU MAY HAVE NO SYMPTOMS AND EARLY DETECTION MAY
BE ON THE SURVEILLANCE STRESS TEST YOU USUALLY WILL HAVE A FEW WEEKS
AFTER THE ANGIOPLASTY. YOU WILL NOT NECESSARILY HAVE A HEART ATTACK
IF RENARROWING OCCURS, (EVEN IF YOUR FIRST PRESENTATION PRIOR TO YOUR
PROCEDURE WAS A HEART ATTACK) .
IF I HAVE A STENT, WILL IT MOVE?
NO. ONCE IT IS EXPANDED AND EMBEDDED IN THE ARTERY WALL IT SHOULDN'T
MOVE. TISSUE WILL GROW AROUND IT WITHIN THE FIRST WEEK OR TWO TO FURTHER
ANCHOR IT. THE HIGHEST RISK OF THE STENT MOVING OR SLIPPING IS DURING
IMPLANTATION. STENTS ARE PERMANENT. THEY WILL NOT COLLAPSE, BUT TISSUE
CAN POTENTIALLY GROW ACROSS THEM TO RENARROW THE VESSEL.
CAN I HAVE AN MRI OR GO THROUGH A METAL DETECTOR AT THE AIRPORT
WITH A STENT?
YES AND YES. WE USUALLY ADVISE TO WAIT A FEW WEEKS BEFORE AN MRI SO
THE STENT IS WELL ANCHORED BY TISSUE OVERGROWTH. AIRPORT METAL DETECTORS
ARE NOT A PROBLEM.
At no time should any individual use this information to diagnose
or treat themselves. Any questions or concerns which may arise from
any of this material should be discussed with your family physician.
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