Inflammation and heart disease -
Or what about the guy who ran a marathon on Saturday, never having any chest pain during the race, finished with a good time, and then three days later climbed a flight of stairs, felt a squeezing sensation in the middle of his chest, and suddenly dropped dead?
On Saturday, his coronary arteries had been wide open — open enough to push his heart to its max for 26 miles over 3. But just three days later, at least one artery became completely blocked: climbing one flight of stairs killed him. We now understand why. As cholesterol invades the wall of the artery, the immune system treats it like it treats other invaders.
Immune system cells infiltrate the wall of the artery. They release inflammation-producing chemicals and send signals calling for other cells to come remove the cholesterol from the artery wall. Then a fibrous cap forms over the plaque.
Inflammation inside the plaque can eventually eat away at that fibrous cap. If the cap ruptures, the cholesterol and the inflammatory cells and chemicals in the plaque suddenly spill into the artery, causing a blood clot to form and block blood flow.
If even a little plaque — one not large enough to block blood flow by itself — suddenly ruptures, it can stop blood flow completely. The test for inflammation your doctor probably used called hsCRP was first studied here at Harvard Medical School.
And it was researchers here who showed that statin drugs work by reducing inflammation as well as by lowering cholesterol; and that drugs that reduce inflammation only, and don't lower cholesterol, still reduce heart attack risk. In August , another drug that works only on inflammation called colchicine Colcrys, Gloperba also was shown to prevent heart disease.
So your doctor is right: inflammation is an important contributor to heart attacks. As a service to our readers, Harvard Health Publishing provides access to our library of archived content.
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Icy fingers and toes: Poor circulation or Raynaud's phenomenon? Inflammation grabbed the attention of researchers a couple of decades ago as a primary culprit in the progression of cardiovascular disease.
However, identifying a drug therapy that leverages this link has been more elusive. With the results of the recent Canakinumab Anti-inflammatory Thrombosis Outcomes Study CANTOS , published in the Sept. Peter Libby, a cardiologist at Harvard-affiliated Brigham and Women's Hospital.
Paul Ridker. Inflammation is part of the body's natural response to protect itself against harm. There are two types: acute and chronic. The acute type occurs when you have an injury or infection. This short-lived reaction rids the body of harmful intruders and repairs damaged cells.
Chronic inflammation, on the other hand, can develop as a response to long-term exposure to unwanted substances in the body, such as toxins from cigarette smoke or an excess of fat tissue, especially around the midriff. Chronic inflammation is important to heart health because it plays a pivotal role in the development of atherosclerosis — the buildup of fatty, cholesterol-rich plaque inside the arteries.
Your body perceives this plaque as foreign, so it initiates an inflammatory response to contain the damage. Chemical messengers called cytokines draw white blood cells to the area to consume the cholesterol particles and to wall off the plaque from the flowing blood.
But if that wall breaks down, the plaque may rupture. The contents then mingle with blood, forming a clot that could block blood flow. These clots are responsible for most heart attacks and strokes. The more than 10, patients enrolled in the CANTOS trial had already suffered a heart attack.
They also had high levels of C-reactive protein, a biomarker signaling bodywide inflammation see "What your CRP test results mean". All were taking standard heart drugs, but some also took varying doses of the drug canakinumab Ilaris.
Canakinumab was not originally developed as a heart medicine; it's a specialized monoclonal antibody used to treat a rare autoimmune disorder in children. It disrupts the inflammatory process by neutralizing a specific cytokine that is instrumental in the progression of atherosclerosis.
This held true even though the canakinumab did not lower lipid levels or affect any other traditional heart risk factor, says Dr. Your liver makes C-reactive protein CRP in response to inflammation.
Low levels of this protein indicate the subtle, chronic inflammation that reflects unhealthy changes in artery walls.
Doctors check for CRP levels using a high-sensitivity C-reactive protein hsCRP test, which requires only a small amount of blood. Nature Communications. Healthy habits to help prevent flu. Centers for Disease Control and Prevention. Cooper LT, et al. The role of endomyocardial biopsy in the management of cardiovascular disease: A scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology.
Braswell-Pickering EA. Allscripts EPSi. Mayo Clinic. Mankad R expert opinion. April 13, Cheng CY, et al. Myocarditis in systemic immune-mediated diseases: Prevalence, characteristics and prognosis.
A systematic review. Autoimmunity Reviews. Lopez-Jimenez F expert opinion. Myocarditis and pericarditis after mRNA COVID vaccination. Accessed April 13, Hause AM, et al.
Safety monitoring of COVID vaccine booster doses among persons aged 12—17 years — United States, December 9, February 20, MMWR Morbidity and Mortality Weekly Report.
Mouch SA, et al. Myocarditis following COVID mRNA vaccination. Mevorach D, et al. Myocarditis after BNTb2 mRNA vaccine against Covid in Israel. The New England Journal of Medicine. Lee ASY, et al. Myocarditis following COVID vaccination: A systematic review October October Heart, Lung and Circulation.
COVID Get the facts. Accessed April 14, Related Myocarditis. Associated Procedures Cardiac catheterization Chest X-rays Echocardiogram Electrocardiogram ECG or EKG Extracorporeal membrane oxygenation ECMO Heart transplant Holter monitor MRI Ventricular assist device Show more associated procedures.
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