What is coronary artery disease?
Coronary artery disease (CAD; sometimes called coronary heart disease, or CHD) is the most common kind of heart disease. It happens when the arteries that feed blood to the heart muscles harden and get clogged through atherosclerosis. This process starves the heart of the oxygen and nutrients it needs to function well. Worsening CAD can lead to permanent heart damage and ultimately death. [1]
What are the main signs and symptoms of coronary artery disease?
Damage to the coronary arteries begins early in life, and is usually without major symptoms until things get pretty bad. At that point, one of the main symptoms of CAD is chest pain (angina) that lasts on the order of minutes (as opposed to hours or seconds)[2]. However, the specifics of how this feels, when it occurs, and what’s associated with the pain depend on the specifics of the clinical disease; heart attacks (where a clot breaks off from a ruptured athrosclerotic plaque and blocks a narrower downstream artery) are different from, say, stable ischemic heart disease (where pain appears upon exertion and settles down afterwards).
How is coronary artery disease diagnosed?
The specifics of how chest pain feels, along with risk factors such as high cholesterol, high blood pressure, diabetes, lifestyle factors such as smoking, and a family history of cardiovascular diseases is often enough to raise a strong suspicion of CAD. Physical examination and additional testing by a medical professional such as imaging studies and blood work can provide further evidence.[3]
What are some of the main medical treatments for coronary artery disease?
The specifics of medical treatment ultimately depends on the specifics of the person and the clinical disease they have. The treatments tend to fall into a few categories:
- Medically treating underlying risk factors to slow CAD progression. For instance, statins can be used to lower cholesterol and prevent further heart damage
- Drugs for symptom relief. For example, nitroglycerin can be used in people with stable ischemic heart disease to reduce short-term chest pain. Drugs that work on the heart like beta-blockers and calcium-channel blockers are often used to control pain and discomfort in the longer term, and also may help improve other outcomes in people who have established clinical disease[3]
- In severe cases, invasive procedures like coronary artery catheterizations with stenting, or surgeries such as coronary artery bypass grafting (CABG) are sometimes used
Medical treatments are ideally added on top of lifestyle changes that can help slow CAD progression. Things like quitting smoking and exercise can help a lot.
Have any supplements been studied for coronary artery disease?
Yes, many supplements have been studied for both preventing clinical CAD as well as in people who already have CAD.[4] Given that high blood pressure and high cholesterol cause CAD, supplements that affect those outcomes may also affect the risk of CAD progression.
How could diet affect coronary artery disease?
There’s a big connection, although there’s still some controversy around the details, such as whether or not limiting saturated fat without considering what it’s being replaced with will do much.[5][6][7] Just like with atherosclerosis, guidelines suggest that a diet abundant in vegetables, fruits, legumes, nuts, whole grains, can help reduce the risk of CAD.[8] Weight loss for people with higher BMIs may also play a role in preventing CAD, although the current evidence suggests that modest weight loss (in the 5-10 kg range) may have limited benefits.[9]
Are there any other treatments for coronary artery disease?
Exercise can play a big role in preventing CAD[8] and also can help people who have CAD improve their health.[10] Guidelines suggest that the role of resistance training in preventing CAD is unclear, but resistance training is still encouraged.[8]
What causes coronary artery disease?
Examine Database: Coronary Artery Disease (CAD)
Research FeedRead all studies
Frequently asked questions
Coronary artery disease (CAD; sometimes called coronary heart disease, or CHD) is the most common kind of heart disease. It happens when the arteries that feed blood to the heart muscles harden and get clogged through atherosclerosis. This process starves the heart of the oxygen and nutrients it needs to function well. Worsening CAD can lead to permanent heart damage and ultimately death. [1]
Damage to the coronary arteries begins early in life, and is usually without major symptoms until things get pretty bad. At that point, one of the main symptoms of CAD is chest pain (angina) that lasts on the order of minutes (as opposed to hours or seconds)[2]. However, the specifics of how this feels, when it occurs, and what’s associated with the pain depend on the specifics of the clinical disease; heart attacks (where a clot breaks off from a ruptured athrosclerotic plaque and blocks a narrower downstream artery) are different from, say, stable ischemic heart disease (where pain appears upon exertion and settles down afterwards).
The specifics of how chest pain feels, along with risk factors such as high cholesterol, high blood pressure, diabetes, lifestyle factors such as smoking, and a family history of cardiovascular diseases is often enough to raise a strong suspicion of CAD. Physical examination and additional testing by a medical professional such as imaging studies and blood work can provide further evidence.[3]
The specifics of medical treatment ultimately depends on the specifics of the person and the clinical disease they have. The treatments tend to fall into a few categories:
- Medically treating underlying risk factors to slow CAD progression. For instance, statins can be used to lower cholesterol and prevent further heart damage
- Drugs for symptom relief. For example, nitroglycerin can be used in people with stable ischemic heart disease to reduce short-term chest pain. Drugs that work on the heart like beta-blockers and calcium-channel blockers are often used to control pain and discomfort in the longer term, and also may help improve other outcomes in people who have established clinical disease[3]
- In severe cases, invasive procedures like coronary artery catheterizations with stenting, or surgeries such as coronary artery bypass grafting (CABG) are sometimes used
Medical treatments are ideally added on top of lifestyle changes that can help slow CAD progression. Things like quitting smoking and exercise can help a lot.
Yes, many supplements have been studied for both preventing clinical CAD as well as in people who already have CAD.[4] Given that high blood pressure and high cholesterol cause CAD, supplements that affect those outcomes may also affect the risk of CAD progression.
There’s a big connection, although there’s still some controversy around the details, such as whether or not limiting saturated fat without considering what it’s being replaced with will do much.[5][6][7] Just like with atherosclerosis, guidelines suggest that a diet abundant in vegetables, fruits, legumes, nuts, whole grains, can help reduce the risk of CAD.[8] Weight loss for people with higher BMIs may also play a role in preventing CAD, although the current evidence suggests that modest weight loss (in the 5-10 kg range) may have limited benefits.[9]
Exercise can play a big role in preventing CAD[8] and also can help people who have CAD improve their health.[10] Guidelines suggest that the role of resistance training in preventing CAD is unclear, but resistance training is still encouraged.[8]
Atherosclerosis of the coronary arteries leads to CAD.
ApoB commonly refers to the liver-derived apolipoprotein B-100 protein which is embedded in every circulating fatty molecule aside from HDL-C, although it can also refer to the small intestine-derived apolipoprotein B-48 protein found in some chylomicrons, or both.[11] These non-HDL fat molecules — VLDL-C, LDL-C, IDL-C, remnant particles, LP(a), and chylomicrons — are contributors to atherosclerosis[12]. ApoB is the protein of lipoprotein cholesterol molecules, which binds to the LDL receptor and allows the fats in cholesterol particles to be taken up by tissues. Because the conventional risk marker for heart disease, LDL-C, is usually a calculated measure of blood concentration that cannot tell you the total number of particles nor the density of individual particles — key factors in cholesterol particle’s ability to do damage — and because there is exactly one ApoB per lipoprotein molecule, ApoB is emerging as a marker of cardiovascular disease risk that provides added detail when LDL-C is insufficient.[11][13]
Chronic stress is implicated in the development and progression of CAD over time, and acute bouts of stress can trigger rapid progression of CAD or the underlying atherosclerosis.[14] When your fight-or-flight response is dialed up constantly, it can increase white blood cells called leukocytes, which play a direct role in advancing atherosclerosis and increase inflammation throughout the body and the inflammation of the clogged arteries.[15] Acute and chronic stress raises blood pressure — which encourages atherosclerosis — and acute stress can precipitate a blockage of the heart (A.K.A. thrombosis) leading to decreased blood flow, reduced oxygenation, and damage to the heart itself. [16] Meditation and interventions to lower stress may reduce the risk of getting CAD in the first place, as well as reducing downstream effects of CAD like stroke and heart attacks.[17][18]
Genes account for roughly 40-60% of the risk for developing Coronary Artery Disease (CAD).[19] Genetic studies have helped clarify the causes of atherosclerotic heart disease like Coronary Artery Disease for decades. The way LDL particles are made and the role they play in causing atherosclerosis, for example, were uncovered from early studies on people with genetically raised cholesterol levels.[20]
Familial hypercholesterolemia (“FH”) is a condition in which a collection of different genetic variants cause elevated LDL cholesterol levels in the blood. [21] Having a non-functional gene that codes for either Apolipoprotein B (ApoB), PCSK9, or the LDL-receptor protein will raise blood LDL-C level and increases risk for atherosclerosis and Coronary Artery Disease. Having multiple variants in different genes, and especially having two of the same variant in the same gene, increases heart disease risk to an even greater extent.[21] Globally, about 1 in 300 people have familial hypercholesterolemia, although the prevalence can be higher or lower depending on the population (i.e., the prevalence of FH among French-Canadians is about 1 in 80; a similar estimate exists for South African Afrikaners). [22]
Another development in identifying genetic risk factors for atherosclerotic heart disease risk is recent research on the role of Lipoprotein a (LP(a), not to be confused with LPA, the gene encoding the LP(a) protein). LP(a) levels vary considerably between people, and the differences in levels of this lipoprotein have been reliably shown to determine atherosclerosis risk.[23] LP(a) levels are 80-90% determined by genetics, and elevated LP(a) levels are found in about 20% of the global population.[24]
Genetic variants in inflammation-regulation pathways (i.e., 5′-lipoxygenase) also appear to affect the risk for atherosclerosis and Coronary Artery Disease.[25]
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- ^Arne Astrup, Faidon Magkos, Dennis M Bier, J Thomas Brenna, Marcia C de Oliveira Otto, James O Hill, Janet C King, Andrew Mente, Jose M Ordovas, Jeff S Volek, Salim Yusuf, Ronald M KraussSaturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art ReviewJ Am Coll Cardiol.(2020 Aug 18)
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- ^Allan D Sniderman, George Thanassoulis, Tamara Glavinovic, Ann Marie Navar, Michael Pencina, Alberico Catapano, Brian A FerenceApolipoprotein B Particles and Cardiovascular Disease: A Narrative ReviewJAMA Cardiol.(2019 Dec 1)
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- ^Kivimäki M, Steptoe AEffects of stress on the development and progression of cardiovascular disease.Nat Rev Cardiol.(2018-04)
- ^Libby P, Nahrendorf M, Swirski FKLeukocytes Link Local and Systemic Inflammation in Ischemic Cardiovascular Disease: An Expanded "Cardiovascular Continuum".J Am Coll Cardiol.(2016-Mar-08)
- ^Vaccarino V, Almuwaqqat Z, Kim JH, Hammadah M, Shah AJ, Ko YA, Elon L, Sullivan S, Shah A, Alkhoder A, Lima BB, Pearce B, Ward L, Kutner M, Hu Y, Lewis TT, Garcia EV, Nye J, Sheps DS, Raggi P, Bremner JD, Quyyumi AAAssociation of Mental Stress-Induced Myocardial Ischemia With Cardiovascular Events in Patients With Coronary Heart Disease.JAMA.(2021-11-09)
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