How fatal are heart attacks?

Are Heart Attacks Always Fatal?

The thought of having a heart attack is scary. Each year, you hear stories about people suffering fatal heart attacks at an age that always seems too young. But are all heart attacks fatal? The short answer is no, but it’s more complicated than that.

Are heart attacks always fatal? | Zinkevych/iStock/Getty Images

Heart attack symptoms may start weeks before you notice them

In the movies, it looks like heart attacks come on suddenly, with no signs or symptoms beforehand. While this is possible, most heart attacks show themselves before they become severe — and their signs and symptoms can start weeks in advance. If you start to feel recurrent chest pain that comes and goes, it may be a sign that a heart attack is on its way. It’s called angina, and it is pressure in your chest due reduced blood flow to the heart. Angina may start a few days or weeks before a severe heart attack hits, but some people confuse angina for indigestion and don’t seek help. Indigestion is common, but if you start to experience what you think is indigestion more frequently than normal, call your doctor — it could be something much more serious.

Today, only about 10% of heart attacks are fatal

Despite the common understanding that heart attacks are extremely deadly, roughly 90% of people survive heart attacks today. That’s in part due to medical advances that help doctors act quickly to stabilize the heart. But it’s also due to people becoming more aware of concerning symptoms. According to Harvard Health, at least a 50% reduction in heart attack deaths can be attributed to the use of aspirin during symptoms and procedures that open the arteries in ways they couldn’t decades earlier.

However, there is still more to be done to continue to make heart attacks less deadly. People should be getting annual physicals to check things such as blood pressure and cholesterol levels. Plus, most physicals give an electrocardiogram, which will point out any major issues with the heart. Also, if you notice anything unusual about your heart’s behavior, don’t hesitate. It’s always better get things checked out than potentially react too late.

But heart attacks can lead to more deadly heart problems, such as sudden cardiac arrest

Heart attacks, medically known as myocardial infarction, are much more curable than they once were. However, major heart problems can still stem from having a heart attack. Sudden cardiac arrest (SCA) occurs when the heart suddenly stops beating. And in 95% of cases, SCA is fatal. It often is caused by underlying heart damage, such as a past heart attack that has put added strain on the heart.

Heart disease is still the No. 1 cause of death in the United States. In 2016, 635,000 people died from heart disease, according to the CDC. Despite heart attacks having a 90% survival rate, taking care of your heart to ensure you don’t have a heart attack is extremely important. Consuming a diet heavy in sodium and fats plus not getting enough exercise is a recipe for problems such as high blood pressure and high cholesterol, which can eventually lead to heart attack. Make sure to eat plenty of fruits and vegetables each day and get at least 150 minutes of exercise per week to keep your heart as healthy as possible.

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Surviving Sudden Cardiac Arrest After Heart Attack

It sounds like a cruel joke — surviving a heart attack only to be felled by a second heart event, sudden cardiac arrest. Heart attack and sudden cardiac arrest are not the same thing, but the first can put you at increased risk of the other. A heart attack, also called a myocardial infarction, happens because of decreased blood supply to your heart’s muscle. Sudden cardiac arrest (SCA) occurs when your heart goes into a dangerous heart rhythm and suddenly stops working.

Heart attack is rarely fatal, but SCA is fatal in 95 percent of cases. SCA can follow a heart attack, and the greatest risk is during the first 30 days after a heart attack. SCA kills about 1,000 people a day, one person every 90 seconds — more than lung cancer and breast cancer combined.

When Darren Califano, 47, was driving to work in his truck on December 22, 2011, he had no way of knowing that over the next two weeks he would survive both a heart attack and an SCA. “At about 7 a.m., I started noticing indigestion; by 10, it had become chest tightness; by 11, I had jaw pain and cold sweats. I knew something was really wrong,” said Califano.

Califano got himself to a fire station where he had an EKG and a blood pressure reading. “Within one hour, I was told that I had suffered a heart attack, and I was at the hospital having a stent put in my heart,” he recalled.

Risk of Sudden Cardiac Arrest After Heart Attack

While recovering at the Highline Medical Center in Seattle, Califano met cardiologist Arun Kalyanasundaram, MD. “Dr. Kalyanasundaram told me that I was at risk for sudden cardiac arrest because my heart was not pumping blood efficiently enough yet,” said Califano.

Cardiologists measure heart-pumping efficiency by measuring the heart’s ejection fraction, the amount of blood pumped by each heartbeat. A normal heart pumps out about 60 to 65 percent of the blood on the left side of the heart with each beat. Califano’s ejection fraction showed that his heart was pumping at only 20 percent efficiency.

A study published in the European Heart Journal followed over 11,000 patients after heart attack. They found that the risk of SCA after heart attack was 8.6 percent, with the highest risk during the first 30 days after the patient leaves the hospital. One of the predictors of SCA was an ejection fraction of less than 40 percent — just what Califano was facing.

Guarding Against SCA After a Heart Attack

“Darren was a young man recovering from a serious heart attack, somewhat overweight, and his ejection fraction was only about 20 percent. I felt he was at significant risk for sudden cardiac arrest,” said Dr. Kalyanasundaram. “An implantable cardioverter defibrillator, or ICD, can protect a patient from SCA by recognizing a dangerous heart rhythm and shocking the heart back into normal rhythm. But it is too invasive a procedure to do right away because sometimes heart pumping ability improves.”

“Dr. Kalyanasundaram did not want me going home unprotected, so he suggested something called a ‘life vest.’ It sounded kind of crazy,” said Califano. The Zoll LifeVest is a temporary, wearable defibrillator that will recognize an SCA and shock the heart back to life. The LifeVest monitors the heart around the clock and can be worn underneath clothing.

Less than 10 days after leaving the hospital, at 5 a.m., Califano’s LifeVest saved his life. “The LifeVest had an alarm that would go off if my heart started to go into cardiac arrest. My wife heard the alarm and heard the vest give me two shocks. I only remember sitting up in bed. I was gone, and then I was back,” Califano said.

“Once your heart goes into sudden cardiac arrest, you only have about five minutes to get it back. That’s why a sudden cardiac arrest outside of a hospital is only survived less than five percent of the time,” explained Kalyanasundaram.

Today, Califano is back in his truck, and about 70 pounds lighter. He works as a project manager for a construction company and lives with his wife and four children south of Seattle. He has been fitted with an ICD and has not had any more cardiac events. “I am now a vegetarian, in great shape, and I have never felt better. I will always be grateful for Dr. Kalyanasundaram and for that LifeVest,” said Califano.

Nov. 4, 2008 — Heart attack patients face the highest risk of dying from sudden cardiac death within the first month after heart attack.

That’s according to a new study by researchers from the Veterans Affairs Medical Center and Mayo Clinic in Minnesota. The study appears in the Nov. 5 issue of TheJournal of the American Medical Association.

Since 1997, the risk of sudden cardiac death has steeply declined. Even so, it still causes about 325,000 adult deaths each year in the U.S., all linked to complications from heart attacks.

Sudden cardiac death occurs when the heart’s electrical system fails. The heart begins beating extremely fast, preventing the ventricles from allowing enough blood to flow throughout the body. Without blood going to the brain and other vital organs, a person quickly loses consciousness and soon dies.

To better understand this problem, as well as the impact of recurrent ischemia (an inadequate flow of blood to a part of the heart) and heart failure on sudden cardiac death, the researchers studied 2,997 residents who survived a heart attack in Olmsted County, Minn., between 1979 and 2005. On average, the patients were 67 years old, and 59% of them were men.

The researchers monitored the patients through their medical records until the time of their death or through the final follow-up in February 2008.

During this time, 1,160 patients died, with 282 of these deaths caused by sudden cardiac death. The rate of sudden cardiac death for patients who had suffered a heart attack within 30 days was four times higher than that seen in the general population. For each following year, however, the rate of sudden cardiac death was lower than expected.

The researchers also found that recurrent ischemia was not associated with sudden cardiac death. However, patients who experienced heart failure during the follow-up period had more than a fourfold risk of experiencing sudden cardiac death than the general population. This translates into an absolute increase in sudden cardiac death risk of 2.5% within 30 days of a heart attack and in each year thereafter.


Almost 20 percent of patients who’ve experienced one heart attack will have a second heart attack within the year, but whether follow-up heart attacks merely reflect worsening atherosclerotic disease, in which the accumulation of fatty materials such as cholesterol thicken artery walls, or whether heart attacks themselves instigate further heart problems has been unclear. Now, research published today (June 27) in Nature suggests that stress during the initial heart attack stimulates production of inflammatory cells that destabilize atherosclerotic plaques, increasing chances that existing plaques will rupture and cause more heart attacks. Researchers say this post-heart attack inflammatory process could provide a new therapeutic target for preventing future heart attacks.

“The findings are important because they clarify a situation we know from the clinics very well,” said Göran Hansson, who investigates the links between cardiovascular disease and inflammation at the Karolinska Institute in Sweden. The results provide a mechanism to understand why one heart attack often leads to accelerated atherosclerosis and more heart attacks, explained Hansson, who did not participate in the study. Stress is also a well-known factor in heart attacks, and the data provide a mechanism explaining “the role of stress… which was not completely understood,” he added.

Atherosclerotic plaques form when lipids accumulate in arterial walls and stimulate an inflammatory response. Macrophages arrive to engulf the lipids, creating plaques that harden and thicken vessel walls, constricting blood flow. Inflammatory macrophages can promote plaque rupture by secreting enzymes that destabilize the plaques. If the ruptured plaque blocks a coronary artery, a heart attack can ensue.

Macrophages are also part of the wound-healing process following a heart attack, explained senior author Matthias Nahrendorf of the Center for Systems Biology at Massachusetts General Hospital in Boston, and are recruited to the myocardial wound site to help repair the damaged tissue. But increased levels of macrophages and other white blood cells after heart attack is connected to increased risk of later heart attack and death.

To understand how heart attacks initiate inflammation that increases risk of subsequent heart attacks, Nahrendorf and his colleagues used a mouse model of atherosclerotic disease, and mimicked heart attacks by suturing the left coronary artery in mice with advanced atherosclerosis. Within 3 weeks, plaques in these mice had more inflammatory cytokines, more proteolytic enzyme activity, and more macrophage precursors called monocytes. Nahrendorf’s team also found that for several months after their heart attacks, mice had increased numbers of monocytes in the spleen, suggesting that the organ was hosting developing monocytes that could go on to worsen atherosclerosis. Sure enough, by removing the mice’s spleens just before promoting heart attacks, the researchers prevented worsening atherosclerosis.

Monocytes usually develop in the bone marrow, suggesting that this switch to splenic development was key to understanding how heart attacks accelerate atherosclerosis. Indeed, said Nahrendorf, preliminary studies examining spleens of patients killed by heart attack show higher numbers of monocyte progenitors in the spleen than victims of car accidents. Digging further into the mechanism of this shift to the spleen, Nahrendorf and his collaborators found that signals from the mice’s sympathetic nervous systems during heart attack caused monocyte progenitor cells to leave the bone marrow and accumulate in the spleen. Treating mice with beta blockers, which disrupt signaling involved in the fight-or-flight response and are often prescribed to cardiac patients to correct heart rhythm, prevented the cells from exiting the bone marrow and halted increased inflammation in their plaques after heart attack.

“We already use beta blockers to treat because they’re thought to treat imbalances in contractile machinery,” Hansson explained, but preventing release of monocyte progenitors from bone marrow “may be part of their benefit.”

Other researchers are also aiming to tame inflammation after heart attacks, though like the current study, so far these techniques have only been tested in mice. Armand Keating, a transplantation researcher at the University of Toronto, and colleagues showed that infusions of mesenchymal stromal cells (MSC), which are involved in tissue repair and immune modulation, can help convert macrophages to an anti-inflammatory phenotype in mice, which could help prevent secondary heart attacks, he said. “It would be very exciting if MSCs could make this switch in humans, too,” Keating said.

For now, Nahrendorf hopes that the research prompts investigators to take a more global look at heart attack treatment and prevention. Instead of looking just at the plaque, he says, “I hope they zoom out a little bit.”

P. Dutta et al., “Myocardial infarction accelerates atherosclerosis,” Nature, doi: 10.1038/nature11260, 2012.

How heart attacks became less deadly

Decades ago, a heart attack was often deadly, killing up to half of its victims within a few days. With only a vague understanding of the physiological processes underlying heart attacks, doctors couldn’t do much but let nature take its course. Doctors were taught that what they should do for people having heart attacks was to keep them calm and quiet, ease their chest pain, do whatever was possible to prevent heart rhythm problems, and hope that another heart attack wasn’t on its way.

Today, more than 90% of people survive myocardial infarction. That’s the technical term for heart attack; it means an area of damaged and dying heart muscle caused by an interruption in the blood supply. Some of the decline in deaths is due to doctors’ ability to diagnose and treat smaller, less deadly heart attacks. Some is due to the institution of specialized coronary care units in the early 1960s.

What changed?

Much of the improvement in heart-attack survival can be chalked up to the gradual understanding in the 1970s and 1980s that the main culprit behind heart attacks is the sudden formation of artery-blocking blood clots, and the new treatments that emerged from this knowledge. Growing use of aspirin, clot-busting drugs, and artery-opening angioplasty in the early stages of a heart attack account for more than half of the reduction in heart attack deaths since 1985, according to an analysis by Stanford researchers.

The improvement in survival hasn’t come without a cost. More people surviving heart attacks means more people living with scarred and damaged hearts. This has contributed to the steady increase in heart failure, which now accounts for more than one million hospitalizations a year in the U.S. and costs nearly $40 billion annually.

Although we have come a long way, there is still much to be done:

  • Get more heart attack victims to the hospital — and to treatment — within an hour of the start of symptoms.
  • Develop faster and more accurate techniques for determining who is having a heart attack.
  • Find ways to protect and support the heart during a heart attack.
  • Devise treatments to rebuild and regenerate heart muscle after a heart attack.

More important, of course, is finding ways to prevent heart attacks and strokes from happening in the first place.

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

Editor’s note: Alan Thicke’s cause of was a ruptured aorta, not a heart attack. The below article was written when reporting suggested Thicke died of a heart attack, but before the official cause of death was determined.

Actor Alan Thicke died after a heart attack on Tuesday, TMZ reported. But why do some people survive heart attacks, while others don’t?

Heart attacks occur when blood flow to the heart muscle is blocked, starving the muscle tissue of oxygen, which causes damage. Thicke, who was 69, was playing ice hockey with his son when he suffered his heart attack on Dec. 13. The “Growing Pains” star was pronounced dead shortly afterward in the hospital.

For a heart attack to quickly lead to death, the damage to the heart needs to be great enough to cause the heart to beat irregularly and eventually stop entirely, said Dr. Suzanne Steinbaum, a preventive cardiologist at Lenox Hill Hospital in New York City. Steinbaum was not involved in Thicke’s case.

The irregular heartbeats that result from the lack of oxygen start from the bottom of the heart, and aren’t strong enough to generate blood flow, Steinbaum told Live Science. When this occurs, “the heart becomes very agitated,” she said.

The heartbeat becomes more of a quiver than a decisive pump, which is also called fibrillation, and blood stops flowing, Steinbaum said. This can quickly lead to the heart stopping, she said.

But heart attacks don’t always kill instantly.

It’s also possible that the damage to the heart muscle doesn’t lead to an irregular heartbeat until a little while after the heart attack occurred, Steinbaum said.

And a person can also die from a heart attack that causes no irregular heartbeat at all — the heart muscle can be so damaged from the lack of oxygen that the heart can no longer pump enough blood, which can lead to death, she said.

For death to occur immediately or shortly after a heart attack, there had to be a very large blockage that damaged a lot of the heart muscle, Steinbaum added.

Risk factors and symptoms

It’s unclear what symptoms and risk factors Thicke had, if any, before his heart attack.

But people can have a heart attack even if there were no symptoms leading up to it, Steinbaum said.

Often when this happens, the heart attack is the result of a ruptured plaque in a person’s artery, Steinbaum said. Plaques are buildups of cholesterol and inflammatory cells that form along the wall of a blood vessel, partially blocking it. If a plaque ruptures, the body sends platelets to fix the rupture, which leads to more blockage that eventually cuts off blood flow to the heart, she said.

It is possible that exercise, which causes a person’s heart rate and blood pressure to increase, can lead to a ruptured plaque, she said.

But this doesn’t mean that people shouldn’t exercise, Steinbaum said. Rather, this is why you always hear, “Consult with your doctor before starting an exercise program,” she said. When a person exercises, the body’s demand for oxygen goes up, and if a person has a blockage in their arteries, it’s hard to get enough oxygen. This can cause symptoms of a heart attack, she said.

Steinbaum said that heart disease is preventable 80 percent of the time. Heart attacks usually stem from a person’s risk factors, such as high blood pressure, high cholesterol and a sedentary lifestyle, she said. Age also plays a role: For men, risk of a heart attack goes up after age 55, she said.

Originally published on Live Science.

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