• -Real time measurement of pressure & volume within left ventricle
  • -It gives information on stroke volume, cardiac output, ejection fraction, and myocardial contractility
  • -The LV pressure is plotted against the LV volume at multiple points during a single cardiac cycle

1 → 2 (isovolumetric contraction). The cycle begins at the end of diastole at point 1. Ventricular pressure is low because the ventricular muscle is relaxed. On excitation, the ventricle contracts and ventricular pressure increases. The mitral valve closes when left ventricular pressure is greater than left atrial pressure. Because all valves are closed, no blood can be ejected from the ventricle (isovolumetric).

2 → 3 (ventricular ejection). The aortic valve opens at point 2 when pressure in the left ventricle exceeds pressure in the aorta. Blood is ejected into the aorta, and ventricular volume decreases. The volume that is ejected in this phase is the stroke volume. Thus, stroke volume can be measured graphically by the width of the pressure–volume loop. The volume remaining in the left ventricle at point 3 is end-systolic volume.

3 → 4 (isovolumetric relaxation). At point 3, the ventricle relaxes. When ventricular pressure decreases to less than aortic pressure, the aortic valve closes. Because all of the valves are closed again, ventricular volume is constant (isovolumetric) during this phase.

4 → 1 (ventricular filling). Once left ventricular pressure decreases to less than left atrial pressure, the mitral valve opens and filling of the ventricle begins. During this phase, ventricular volume increases to about 140 mL (the end-diastolic volume).

Loops Based off Drugs

Increased Preload/ Intravenous Fluids

  • -Increases end diastolic volume and increases stroke volume
  • -Increases width of pressure-volume loop

Decreased Afterload – ACE-inhibitors, ARB’s

  • -Increased stroke volume because ventricle ejects blood against a lower pressure in the systemic vasculature
  • -Causes increased width of pressure-volume loop
  • -Decreases end systolic volume

Increased Contractility/Positive Inotropes – Dobutamine, Dopamine

  • -Ventricle develops more tension during systole, leads to an increase in stroke volume
  • -Decreases end systolic volume






















Deaths due to Alzheimer’s disease have sky-rocketed by 89% since the year 20001. Currently, 5 million Americans have Alzheimer’s disease with 16 million projected to have it by 20501. Alzheimer’s is an insidious, chronic disease that affects patients and their families for about a decade before killing them. It puts extreme emotional and financial stress, not only on the patient, but also on the family members and caregivers who look after patients during their illness.

Emerging research comparing plant based diets, like the vegan diet, to the average American diet show that a plant based diet has neuroprotective effects for the brain. For example, a recent study from California showed that vegan subjects were half as likely to become demented compared to those who ate meat, including poultry and fish. Cumulative data on vegetarians show a trend of delayed onset of dementia overall2. Harvard University researchers found that older women who eat foods containing monounsaturated fats, such as avocado, nuts, and seeds, are less likely to develop Alzheimer’s disease than those who eat foods high in saturated fats, like meat and butter.3

The typical Western diet consists of high carbohydrates, high saturated fats, and refined sugars, increases oxidative stress in the body, which significantly contributes to cardiac and cerebrovascular disease. Both of these disease states are caused by fat and cholesterol plaques building up along the sides of blood vessels walls throughout the body. Poor diet doesn’t just affect the vessels in your heart; it affects the vessels in your brain too! The small vessels of the brain can become clogged leading to small areas of brain death. Eventually these damaged areas can cause dementia and cognitive defects. Along these lines, a study from the Mayo Clinic discovered women with heart disease are three times more likely to develop cognitive problems associated with dementia.3

The evidence is clear: our typical Western Diet is linked with the development of dementia and Alzheimer’s disease. We need a diet shift that supports a plant based diet to prevent heart disease, diabetes mellitus, and dementia. Foods that decrease oxidative stress like fruits, vegetables, seeds, and nuts can protect our brain health in addition to helping us lose weight, reduce fatigue and medications. Your physical health and mental health will both be improved by the significant antioxidant properties of the plant based diet. So head to the produce isle today!


  1. Alzheimer’s Association.
  2. Giem, P., W.L. Beeson, and G.E. Fraser. “The incidence of dementia and intake of animal products: preliminary findings from the Adventist Health Study.” Neuroepidemiology. U.S. National Library of Medicine, 1993. Web. 08 Aug. 2017.
  3. “New Link Between Dementia and Diet.” PETA Prime. Mayo Clinic, 27 Feb. 2013. Web. 08 Aug. 2017.
  4. Solfrizzi, V., et. al. “Relationships of Dietary Patterns, Foods, and Micro- and Macronutrients with Alzheimer’s Disease and Late-Life Cognitive Disorders: A Systematic Review.” Journal of Alzheimer’s Disease, Volume 59 (2017), pp 815-849.
















Close your eyes for a moment. Imagine your wife or husband is told by your doctor that you had a significant heart attack. He explains that you may not survive the night and your wife or husband should bring your teenaged children to the hospital to say, “Good bye”. And if you do survive your family, the people you love the most in the world can be consoled by the fact that you will most likely be a vegetable and unable to take care of yourself. Now how do you feel? It could happen to you, G-d forbid. It happened to me. Please read my story below so you won’t have to live with the same guilt I now live with for the rest of my life.

My name is Leibel Winegard and I usually don’t like to write about myself nor do I typically engage in social media. However, I believe it is vital for me to spread my story because it may help someone out there. I have told my story several times and several cardiologists have suggested that I need to make sure that as many people as possible understand that what happened to me, can easily happen to you. I write this story with tears. This account originates from multiple sources because candidly, I lost six days of my life that I cannot account for today. I simply don’t have any recall of even leaving my home, much less all that happened to me and my family once my heart attack started. I’ve done the best to be as accurate and as detailed as possible.

Los Angeles Marathon- Sunday- 2017. In the morning, I attended the open house of a new building my client built where our firm was the Construction Manager. I remember the celebration and the joy as this was a relatively large building built just a few miles from my home. When I got home, I was hot and felt exhausted. Sitting on the couch in the living room, I didn’t even have the energy to change out of my suit and tie and I asked my son to go get me a change of clothes. My last memory for the next six days was sitting on the couch feeling hot and out of breath.

After I woke up in the hospital, I was told that my sons who are trained in first aid, CPR, and are almost Eagle Scouts knew I was in trouble and needed urgent medical assistance. They said I got sick to my stomach and I told them that I would not let them call 911. Instead, they told me that I thought I was having an asthma attack and I suggested that they get our neighbor, who is a trained first responder to drive me to Dr. Ben Zur because he was open on Sundays. I DON’T REMEMBER LEAVING MY HOME AND GETTING IN THE CAR. As we were driving and speaking with Ramiro navigating to Dr. Ben Zur’s office, I am told I developed severe chest pain and then slumped over. My son knew he needed to keep my airway open and grabbed my head from behind so I could breathe. My neighbor told Ramiro that I was nearby Sherman Oaks Hospital in Sherman Oaks, CA. and that he was taking me there because he didn’t think I would survive the drive through heavy traffic to Dr. Ben Zur’s office. By the time I was at the hospital parking lot I had gone into cardiac arrest, my heart stopped and I understand I took my last breath of oxygen for probably at least 5 minutes. Worse, I was told by an LA County Deputy Sherriff that it is very important if you have an emergency because it significantly delays the Emergency Room’s response to starting the necessary treatment.

Because my treatment was somewhat delayed, the ER (emergency room) staff had to perform CPR on me for between 30 and 40 minutes. Thank G-d, after the third and final electric shock, I was revived from death.

My wife immediately notified Dr. Ben Zur’s office which was about 6 miles away in Tarzana, CA. Because it was a Sunday and probably because it was the marathon day, all the streets and the freeways were virtual parking lots. Cars were standing still in all directions. This was especially the case for Ventura Boulevard and the Ventura Freeway which are the only ways to rapidly get from Tarzana to Sherman Oaks. Suddenly, Dr. Ben-Zur appeared in the Sherman Oaks emergency room and took control of the situation. My wife was astonished because she knew that they had just spoken with Dr. Ben-Zur by phone and he was in his Tarzana office. One of the nurses looked at Dr. Ben-Zur and said “you must have superpowers” I just spoke with you and you were in Tarzana. But, I know how he did it, his genuine care and love for his patients provides him with unique abilities. That is the secret superpower that God has bestowed upon Dr. Ben-Zur.

When Dr. Ben-Zur arrived I was in cardiac shock with a very poor blood pressure and I was on a respiratory machine. The staff of the hospital informed my family that my chances of survival were dismal. Apparently, Sherman Oaks Hospital does not have the ability to operate on my condition. Thank G-d, Dr. Ben-Zur ordered an ambulance to Sherman Oaks Hospital while he was driving. The ambulance immediately came to where I was located and transported me to Tarzana Hospital. Dr. Ben-Zur also asked the great one, Ramiro, (SM) to call ahead of time to Tarzana Hospital. The entire Tarzana Hospital ER and operating room staff were all there waiting for the ambulance to arrive. One of the ER doctors commented that for the past 20 years Dr. Ben-Zur has always arrived before the ambulances. “Every second counts,” said Dr. Ben-Zur, the difference between life and death may be a matter of only a few minutes. One of the ambulance crew members said to Dr. Ben-Zur “I know you left after us, I saw you! How is it possible that you got here before us?” Apparently, caring gives you higher powers than the wailing sirens of the Los Angeles Fire Department. Now every time I hear sirens I think of Dr. Ben-Zur and where he might be. Perhaps he’s flying overhead?

I subsequently made a full recovery and I am back with my family, my wife and three children. My daughter Shira does not allow people to refer to Dr. Ben-Zur as Dr. Ben-Zur. She insists that we all call him Abba’s Dr. Ben-Zur and all of us occasionally call him Rabbi Ben Zur as a measure of added respect. Whenever she sees Dr. Ben-Zur she runs over to give him a deep hug. She too has become a vegetarian (at 14 years old) and my 15 and 17-year-old sons now are more conscious of our family history and try to exercise more and more.

When I come to the office I’m greeted by an incredible staff. People who go above and beyond to love and respect each and every one of their patients. What an incredibly loving atmosphere. A team that saves lives for a living and cares and truly cares about each and every individual person. When I tell you that I love going to the office, I know you’ll think I’m crazy, but it’s the truth. My doctor and his staff are special. Please, If you see Dr. Ben-Zur or any of his staff members, please give them a big hug. Tell them Leibel sends his love and gratitude for keeping his family together.

The purpose of this letter is to help save lives. You need to understand how lucky I was that I was a patient of Dr. Ben Zurs and the Cardiac Institute. Once I woke up six days later, I had several doctors and nurses at the Tarzana Hospital coming in to see me and they called me a miracle. I thought they were being kind and encouraging me to help. The truth is that a very close friend of mine is a cardiac care specialist who has won fellowships and publishes and delivers papers at prestigious cardiac conferences. He explained to me three months after my heart attack just how lucky I was to have Dr. Ben Zur provide the care he did when I needed it. My friend explained that because I went so long without oxygen from not breathing and because it took precious moments to start CPR which lasted so long, the statistics of my survival, particularly that I, thank G-d, didn’t have any loss of mental capacity nor physical complications were probably 1 in 1 million. Yes – I am a miracle. What that means is that there are 999,999 others most-likely that given the same situation would be dead or a vegetable.

So what do you do? Please, I beg of you do the following:

1.Go to Dr. Ben Zur for a check-up.
2.Start a vegetarian diet. Get your family, including your children to start eating properly, especially if you have a family history of cardiac disease.
3.Exercise. It is the summer now and my wife and I walk laps at the mall. It is air conditioned with flat surfaces and there are bathrooms and chairs available to sit down if you need them.
4.Take your blood pressure and start a record of your daily BP, weight, medications, and exercise so you and Dr. Ben Zur can see how you are doing over time.
5.Realize that while your work is important, your family is more important. I wore my strong work ethic like a badge of honor. I used to be so proud that I was one of the first in the office in the morning and always the last to leave Working 60 or more hours on a salaried job where you are not paid a dollar more over 40 hours indicates you have your priorities wrong.
6.Take vacations. Give your family the memories they can share with their children and grandchildren.
7.Sleep. Again, I used to be so proud of myself that I was able to work an extremely long day on four hours of sleep. Lack of sleep plays a major role in weight gain, stress, and heart disease. To quote Forrest Gump, “Stupid is as stupid does.”
8.Love yourself. Dr. Ben Zur almost always greets you with a hug because he knows that in today’s high energy environment, we rarely take care of ourselves. When Dr. Ben Zur hugs me, it brings me back to a reality that I too have to hug myself. I have to love myself because I deserve to be loved.
9. Finally, if you ever find yourself in a situation where you MIGHT need emergency medical attention, call 9-1-1 immediately. I was the 1 in a million chance that survived cardiac arrest after waiting far too long to get treatment and you and your family will have a much higher rate of survival if you go into the emergency room from an ambulance than if you drive in yourself.
10.Have your family and friends learn CPR and the signs of cardiac arrest and stroke. Seconds mean lives.

Thank G-d I don’t have any recollection of the physical pain associated with my heart attack. Having said that, however, knowing that I cause my wife and children such pain hearing I may die and seeing me on life support is horrible. I live with this guilt every day. But I use this guilt as the motivation to exercise more, eat a vegetarian diet, and walk away from stress at work and home. I want to become their role model of healthy living. That is the only way I can bear the guilt of having given them such a scare.

Thank you very much for reading my letter. I would be glad to further discuss my near-death experience, as well as how I am making the necessary changes in my life to beat heart disease. I suggest you reach out to Dr. Ben Zur and Ramiro to get a hold of me.

Wishing you the good health.

Leibel Winegard.













This is our story about when my husband had his heart attack. My husband developed chest pain. We went to the local emergency room, where a doctor told me my husband was having a major heart attack. A cardiologist had been called. Fear and panic overwhelmed me. My husband was 47 years old at the time. We have three children. Thoughts began taking root in my head: What will happen to him, my life-long friend? What will be with our children? Amazingly within minutes, a tall gentleman arrived. He said, “Hi my name is Dr. Ben-Zur, and I’ll be taking care of your husband.” He was obviously hurried and intensely focused on the problem, but his gentle eyes were calming. Within seconds I felt at ease. It was if an older brother had come to save us while we were drowning.

Almost immediately Dr. Ben-Zur rushed my husband to the operating room. This was at about 1:30 AM. At about 4:30 AM Dr. Ben-Zur emerged and came out to the waiting area. He had a glowing look, a big smile, and two thumbs up. His clothing was wet from perspiration. It was obvious that he had worked very hard. My husband was fine and he Would be going home in a few days, he said. My husband was then seen in. Dr. Ben-Zur’s office over the next several months. Dr. Ben-Zur and his amazing staff completely changed our lifestyle. My husband is now eating healthy food and is in the best shape he has been in a very long time.

After meeting with many of Dr. Ben-Zur’s patients, I realized that our story was not unique. Hundreds of them have similar stories. Dr. Ben-Zur has been a tremendous addition to our lives. My youngest son said it best: “Our doctor is special.” Even though I’m busy with my husband and raising three children, I take two cups of green juice to Dr. Ben-Zur every morning. (I worry that he does not always eat on time.)

My name is Azita and I look forward to meeting you at Dr. Ben-Zur’s office some day.

















My sister is a physician who worked with Dr. Ben-Zur, back when she was a medical student. Our family is well acquainted with Dr. Ben-Zur and his office staff. We have the highest regard for everyone there. I always thought that I was taking care of my health; being that I have been eating properly and exercising daily. On June 26th, 2017 I had a stress test at Dr. Ben-Zur’s office. This was the first stress test I’d ever undergone. I questioned whether I really needed it, but for the two weeks prior I was having chest pain. A lot of the features of the chest pain I was having were not typical for heart disease. During the stress test, however, I developed severe problems – my artery closed off. Within seconds, Dr. Ben-Zur and the entire team at the Cardiovascular Institute were activated. Within minutes I was at the hospital and less than 20 minutes later my arteries were open. It turned out that two of my main arteries were severely diseased. I truly believe that Dr. Ben-Zur and his staff saved my life that day. They not only saved my life, but they did so in the most rapid fashion. I was top priority and they stopped everything and focused only on helping me. It seemed like everybody knew who to call and how to get things done. It was as if a tornado was set off, but one which was carefully orchestrated and precisely choreographed. The doctors and nurses at the hospital were already waiting for me upon my arrival. How Dr. Ben-Zur arrived at the hospital before the ambulance is still beyond me. The Cardiovascular Institute is a great place for medical care. Many years ago I lost my father to heart disease. He was approximately the same age I am today. I will, hopefully, get to see my children grow and develop – something my father was not as fortunate to have.

Andre Shamalian










































The year was 1942. My father’s father, Meir Nuri, the man who I am named after, underwent a “minor procedure” in Iraq. Complications ensued immediately after the procedure and, as a result, my grandfather lost his life the very next day. My father was now in charge of raising his ten young siblings. His mother was very loving but her husband had been the one in charge of the finances. My father wept without end. At age 16 his best friend, the center of his universe, was gone. He walked out of the hospital and knelt on the sand. Drawing a puzzle made up of 12 pieces, similar to the 12 tribes of Israel, he then removed the center piece of the puzzle. The piece that represented his father. Sitting up all night, terrified and sobbing, he tried to figure out how to rebuild that puzzle on his own. In the morning he got up and decided to change his life. He left school and started to work, at times, 20 hours per day, to support his brothers, sisters, and mother. He promised himself that he would make sure that each of his siblings would receive an education and get married before he would consider his job complete.

Twenty years ago today, the doors to the Cardiovascular Institute opened. As my father stood proudly on that day, in that first small office, he recounted the events of the night after his father had passed. Our mission, like his, would be to keep all of the families of our patients together. To keep the puzzle of each family that puts its trust in us together. That is our mission.

As I stand here today, I cannot be more proud of what we have accomplished. After years of work from morning to night, and on occasion 24 hours a day, we have assembled a team of people of whom I am extremely proud. “The best people in the world,” my father always says.  From my father, who built and currently manages the office, to my colleague, Ramiro, to Bhagat, Martha, Tatyana, Vladimir, Leslie, Mariana, Marissa, Sylvia, Aida, Liora, Elizabeth, Lana, Ofir, Jessie, and all of our wonderful students.

In those twenty years, we have often received many thoughtful and heartwarming gifts from our patients. All of them carry great meaning. But, every morning I arrive 30 minutes before everyone else to look at one particular gift. Another puzzle.

Several years ago a beautiful family came to us. The family consisted of a loving mother, who relied on her husband, a father, and a severely autistic young woman. The father had been having a very difficult time with his health and they had driven a great distance to see us. He was the sole provider for his family and had been sick for several months. After repeatedly passing out, he had been seen by multiple doctors and hospitalized on multiple occasions without any formal diagnosis. After careful evaluation, we discovered the problem and were able to correct it with a surgical procedure. His daughter, the autistic child, understood exactly what had happened, and its significance to her and to her family.

As her mother later recounted to me, as soon as her dad came home she grabbed her mother’s hand and dragged her to a store. Once inside she stopped in front of a particularly complex puzzle. Pointing to it, she said with enthusiasm, “Dr. Ben-Zur!”  They returned home with the puzzle and she immediately put it together with incredible speed. The same puzzle would’ve taken me many months to assemble. When she brought it to the office she gave me a big hug. The normally very shy girl, who her parents said, rarely demonstrated any affection, showed me the meaning of warmth. Her mother explained that her daughter meant for the puzzle to represent all the pieces of her family, with the face being her father. Now, my puzzle is back in one piece. Tears of joy filled my eyes and my throat constricted.  It took me immediately back to the night my dad was putting his pieces together.

And so, for all those who ask me, “Why do you get up so early?” and “Why do you put so much effort into what you do?” and “Why don’t you ever go on vacation?” I stand back, and point to that puzzle, and say, “Today I’m assembling a puzzle!”

Sincerely yours,

Uri Meir Nuriel Ben-Zur, M.D., F.A.C.C.

And the loving members of the Cardiovascular InstituteFullSizeRender (2)












With All of My Love, Pauline Bustamante


From the Bustamante Family:

I have never met a doctor so dedicated to helping, caring, saving, guiding, and supporting his patients the way Dr. Uri Ben-Zur does.

I had a condition no other doctor knew how to treat. The doctors (cardiologists, neurologists, etc.) told me my heart was fine and that they couldn’t find anything abnormal.

My daughter, Annie, received a referral for Dr. Ben-Zur. She called his office and immediately made an appointment.

When I arrived at his office, I waited no more than 2 minutes before the doctor greeted me and my family. He took me into a room where his friendly staff ran tests and asked me questions.

Going to an appointment with Dr. Ben-Zur is completely different than going to any other doctor appointment. The tranquil atmosphere and harmony that one feels is incredibly relaxing. I sometimes spend hours at his office (with all the testing that needs to be done) but time passes quickly and it’s always a pleasure since it’s such a calm environment.

For me, it was a blessing from G-d to have found Dr. Uri Ben-Zur. Not only did he save my life, but I had the opportunity to meet such an extraordinary and charitable man. My family and I are profoundly grateful for all of his help and for the compassion he shows for my special needs daughter, Pauline.

From the bottom of my heart, thank you doctor.
May G-d bless you.

Eternally Grateful,

Jose Bustamante & Family



















Thank you for saving our Papi, The Bustamante Family



Save A Life, Share This Story!


Acute Coronary Syndrome

            ASC is the classification used to describe a range of conditions associated with suddenly reduced blood flow to the heart such as a myocardial infarction and/or unstable angina. This is when blood that is supposed to be supplied to the heart is suddenly blocked. Atherosclerosis is the primary cause of acute coronary syndrome. It is known as the buildup of fats, cholesterol, and other foreign particles that are clogged in the artery walls. ASC symptoms include chest pain, nausea, excessive sweating, dizziness, jaw/neck pain with radiation in the arm, and dyspnea. Acute Coronary Syndrome mainly affects those of older age.

Acute coronary syndrome can be diagnosed by a blood test, it can display evidence that heart cells are dying by looking at the blood count. An ECC can diagnose ACS by measuring the heart’s electrical activity of the AV and SV nodes and how the atria and ventricles contract. An echo as well can diagnose ACS because it uses sound waves to produce live images of the heart and can determine if it is pumping properly. Other diagnostic tests that could help diagnose ASC include coronary angiograms, myocardial perfusion imaging, and a stress test.

The cause of acute coronary syndrome is when a blood clot forms after a plaque deposit ruptures, the clot then obstructs the flow of blood to heart muscles. The low supply of oxygen to cells is too low, then causing cells of the heart muscles to die thus causing a myocardial infarction. Treatment of acute coronary syndrome includes an angioplasty, medications, or stent. Medications include statins, nitrates, beta blockers, clopidogrel, etc. High-risk factors of acute coronary syndrome include high blood pressure, obesity, unhealthy dieting, diabetes, high blood sugar levels, lack of physical activity, and smoking.

According to the 2013 AHA/ACC Lifestyle Management Guidelines, adults (>21 years of age) are recommended to use a high dose statin (daily dose lowers LDL0C by approximately >50%) if any of the following criteria are met:

  1. Clinical ASCVD*
  2. LDL-C ≥190 mg/dL**
  3. Diabetic, age 40-75 years old, with an LDL-C of 70-189 mg/dL, and an estimated ASCVD risk of ≥7.5%
  4. Non-diabetic, age 40-75 years old, with and LDL-C of 70-189, with an estimated ASCVD risk of ≥7.5%

*Clinical ASCVD includes acute coronary syndrome, or a history of myocardial infarction, stable or unstable angina, coronary or other arterial revascularization, stroke, transient ischemic attack, or peripheral arterial disease presumed to be of atherosclerotic origin.

** Consider LDL-C-lowering non-statin therapy to further reduce LDL-C

According to the 2013 AHA/ACC Lifestyle Management Guidelines, adults (>21 years of age) are recommended to use a moderate dose statin (daily dose lowers LDL0C by approximately 30% to <50%) if any of the following criteria are met:

  1. Age >75 OR if not candidate for high-intensity statin
  2. Diabetic, age 40-75 years old, with an LDL-C of 70-189 mg/dL, and an estimated ASCVD risk of <7.5%
  3. Non-diabetic, age 40-75 years old with and LDL-C of 70-189 mg/dL and an estimated ASCVD risk of 5% to <7.5%

Myocardial infarction:


According to the third universal definition (released in 2012 by theESC/ACCF/AHA/WHF), any one of the following criteria meets the diagnosis of MI:

  •         Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin)

AND at least one of the following:

  1.   Symptoms of ischemia
  2.   Development of pathologic Q waves on EKG
  3.   New or presumed new significant ST changes or new LBBB
  4.   Identification of an intracoronary thrombus by angiography or autopsy
  5.   Imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality
  6. STEMI:
  7.  Definition:  ST-segment elevation of at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads is present.
  8. Profound ST elevation or depression in multiple leads usually indicates very severe ischemia.
  9.                                    From a clinical viewpoint, the division of acute myocardial infarction into ST-segment elevation and non-ST elevation types is useful since the efficacy of acute reperfusion therapy is limited to the former group.
  10.  Etiology: STEMI usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis. Slowly developing, high-grade coronary artery stenoses do not typically precipitate STEMI because of the development of a rich collateral network over time. Instead, STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury. This injury is produced or facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation. In most cases, STEMI occurs when the surface of an atherosclerotic plaque becomes disrupted (exposing its contents to the blood) and conditions (local or systemic) favor thrombogenesis. The amount of myocardial damage caused by coronary occlusion depends on
  11.                                the territory supplied by the affected vessel
  12.                                whether or not the vessel becomes totally occluded

iii.      the duration of coronary occlusion

  1.                                the quantity of blood supplied by collateral vessels to the affected tissue
  2.                                the demand for oxygen of the myocardium whose blood supply has been suddenly limited

Vi.      endogenous factors that can produce early spontaneous lysis of the occlusive thrombus

vii.      the adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery.

  1.        Signs and sxs:
  2.                           Pain is the most common presenting complaint in patients with STEMI. The pain is deep and visceral; adjectives commonly used to describe it are heavy, squeezing, and crushing. Typically, the pain involves the central portion of the chest and/or the epigastrium, and, on occasion, it radiates to the arms. Less common sites of radiation include the abdomen, back, lower jaw, and neck. It is often accompanied by weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom. The pain may commence when the patient is at rest, but when it begins during a period of exertion, it does not usually subside with cessation of activity, in contrast to angina pectoris.
  3.       Diagnostics:
  4.                              EKG:   Severe, acute ischemia lowers the resting membrane potential and shortens the duration of the action potential. Such changes cause a voltage gradient between normal and ischemic zones. As a consequence, current flows between those regions. These currents of injury are represented on the surface ECG by deviation of the ST segment. When the acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves over the ischemic zone.
  5.                                    Serum Biomarkers:  Certain proteins, called serum cardiac biomarkers, are released from necrotic heart muscle after STEMI. The rate of liberation of specific proteins differs depending on their intracellular location, their molecular weight, and the local blood and lymphatic flow. Cardiac biomarkers become detectable in the peripheral blood once the capacity of the cardiac lymphatics to clear the interstitium of the infarct zone is exceeded and spillover into the venous circulation occurs. The temporal pattern of protein release is of diagnostic importance. The criteria for AMI require a rise and/or fall in cardiac biomarker values with at least one value above the 99th percentile of the upper reference limit for normal individuals.
  6.   Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) have amino-acid sequences different from those of the skeletal muscle forms of these proteins.  These differences permitted the development of quantitative assays for cTnT and cTnI with highly specific monoclonal antibodies. Since cTnT and cTnI are not normally detectable in the blood of healthy individuals but may increase after STEMI to levels many times higher than the upper reference limit  the measurement of cTnT or cTnI is of considerable diagnostic usefulness, and they are now the preferred biochemical markers for MI.
  7.  CK rises within 4–8 h and generally returns to normal by 48–72 h. An important drawback of total CK measurement is its lack of specificity for STEMI, as CK may be elevated with skeletal muscle disease or trauma, including intramuscular injection. The MB isoenzyme of CK has the advantage over total CK that it is not present in significant concentrations in extracardiac tissue and, therefore, is considerably more specific. However, cardiac surgery, myocarditis, and electrical cardioversion often result in elevated serum levels of the MB isoenzyme.


iii.    Imaging:  Abnormalities of wall motion on two-dimensional echocardiography are almost universally present. Although acute STEMI cannot be distinguished from an old myocardial scar or from acute severe ischemia by echocardiography, the ease and safety of the procedure make its use appealing as a screening tool in the Emergency Department setting. When the ECG is not diagnostic of STEMI, early detection of the presence or absence of wall motion abnormalities by echocardiography can aid in management decisions, such as whether the patient should receive reperfusion therapy

  1.  Treatment:

INITIAL THERAPY — The patient with acute ST elevation myocardial infarction (STEMI) should have continuous cardiac monitoring, oxygen, and intravenous access. Therapy should be started to relieve ischemic pain, stabilize hemodynamic status, and reduce ischemia while the patient is being assessed as a candidate for fibrinolysis or primary percutaneous coronary intervention (PCI), with a goal of initiating PCI within 120 min of first medical contact.. Other routine hospital measures include anxiolytics, serial electrocardiograms, and blood pressure monitoring.


  1.   M:  Morphine may be given for the relief of chest pain in the setting of acute myocardial infarction. We generally reserve its use for patients with an unacceptable level of pain, due to evidence of worse outcomes in patients receiving the drug. We give intravenous morphine sulfate at an initial dose of 2 to 4 mg, with increments of 2 to 8 mg repeated at 5- to 15-minute intervals.
  2.   O:   Oxygen, when hypoxemia is present, O2 should be administered by nasal prongs or face mask (2–4 L/min) for the first 6–12 h after infarction.
  3.   N:  Nitrates, intravenous nitroglycerin is useful in patients with persistent chest pain after three sublingual nitroglycerin tablets, as well as in patients with hypertension or heart failure. Nitrates must be used with caution or avoided in settings in which hypotension is likely or could result in serious hemodynamic decompensation, such as right ventricular infarction or severe aortic stenosis. In addition, nitrates are contraindicated in patients who have taken a phosphodiesterase inhibitor for erectile dysfunction (or pulmonary hypertension) within the previous 24 hours.
  4.   A:  Aspirin, There is strong evidence to support the early initiation of dual antiplatelet therapy with aspirin and a platelet P2Y12 receptor blocker, irrespective of treatment strategy (fibrinolysis, PCI, or medical therapy), in patients with acute-STEMI.

STEMI EKG Changes:

The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease. The findings depend on several key factors: the nature of the process (reversible [i.e., ischemia] versus irreversible [i.e., infarction]), the duration (acute versus chronic), the extent (transmural versus subendocardial), and localization (anterior versus inferoposterior), as well as the presence of other underlying abnormalities (ventricular hypertrophy, conduction defects).

Acute ischemia causes a current of injury. With predominant subendocardial ischemia (A), the resultant ST vector will be directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore will record ST depression. With ischemia involving the outer ventricular layer (B) (transmural or epicardial injury), the ST vector will be directed outward. Overlying leads will record ST elevation.

ST-elevation MI evolution — The classic (but not invariable) sequence of ECG changes in patients with STEMI is as follows:

  1.  The first change may be a hyperacute T wave. It is tall, peaked, and symmetric (the normal T wave is asymmetric with an upstroke that is slower than the downstroke) in at least two contiguous leads.
  2.  Initially, there is elevation of the J point and the ST segment retains its concave configuration but may become convex or rounded upward.
  3.   Over time, the ST-segment elevation becomes more pronounced and the ST segment changes its morphology, becoming more convex or rounded upward.
  4.   The ST segment eventually merges with the T wave and the ST-segment and T wave become indistinguishable. The QRS-T complex can actually resemble a monophasic action potential. This is a “current of injury” or so-called “tombstone” pattern. Reciprocal ST-segment depressions are usually observed in other leads.
  5.   The ST-segment returns to baseline, an initial Q wave develops, and there is a loss of R wave amplitude. When the ST segment elevation persists for greater than three weeks after the event, a ventricular aneurysm in the area may be suspected.
  6.   The T wave becomes inverted and it may remain inverted or return to upright
  7.   Over time, there is continued evolution of ECG changes. The R wave amplitude becomes markedly reduced, the Q wave deepens, and the T wave remains inverted or becomes positive. These changes generally occur within the first two weeks after the event; however, in some patients, they occur within a few hours of presentation.

ST-segment elevation, associated with epicardial coronary vasospasm or actual occlusion, is a relatively specific sign of acute transmural ischemia. ST-T wave abnormalities that are suggestive of acute myocardial ischemia in the earliest phase of ST elevation MI are usually localized to those leads that reflect the involved regions of the myocardium:

  1.        V1-V2 – Anteroseptal
  2.       V3-V4 – Anteroapical
  3.        V5-V6 – Anterolateral
  4.       I, aVL – Lateral
  5.       II, III, aVF – Inferior
  6.       Acute Anterior Wall MI:  An acute anterior wall MI presents with the changes in some or all of the precordial chest leads V1 to V6. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting most often as depressions of the ST segments in the inferior leads (II, III, and aVF). Reciprocal changes are actually the same ST segment shifts as seen from a different angle or direction.
  7.   Anteroseptal MI:  An acute anteroseptal MI presents with the changes in leads V1 to V2. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segments in the inferior (II, II, aVF) or lateral leads (I, aVL, V5, and V6).
  8.   Anterioapical wall MI:  An acute anteroapical MI presents with the changes in leads V3 and V4. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segment in the inferior leads (II, III, aVF).
  9.  Anterolateral wall MI :   An acute anterolateral MI presents with the changes in leads V5 and V6, often in association with changes in leads I and aVL (waveform 6). Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segment in the inferior leads (II, III, aVF), and in some cases in leads V1 and V2.
  10.  Lateral wall MI:   An acute lateral MI presents with the changes confined to leads I and aVL (waveform 7). Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as ST segment depressions in the inferior leads (II, III, and aVF) or leads V1 and V2.
  11.  Inferior wall MI – An acute inferior wall MI presents with the changes in leads II, III, and aVF. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting with ST segment depressions in leads I and aVL. The ST segment depression in the precordial leads V1 to V2 may be reciprocal, but more likely represents true posterior wall involvement (which may be diagnosed by ST elevation in leads V7 to V9) [4]. In addition, there may be the presence of ST elevation in the precordial chest leads V1 to V2. Involvement of the right ventricle may occur with an inferior wall MI and is confirmed by the presence of ST segment elevation in V3R and V4R. The duration of ST elevation in the right precordial leads may be shorter compared to the inferior leads, and, therefore, a right-sided ECG should be obtained as soon as possible after inferior wall ST elevation is noted.
  12.  Posterior wall MI — An acute posterior wall transmural MI reflecting left circumflex coronary artery involvement may be missed on a typical ECG. Posterior lead ECG (leads V7 to V9) should be completed if there is a high degree of suspicion or if ST depression is present in V1 to V3. The criteria for ST elevation in leads V7 to V9 are ≥0.05 mV in men over 40 years and women and ST elevation of ≥0.1 mV for men <40 years.
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