Coronary artery disease

Short description: Reduction of blood flow to the heart

Coronary artery disease

Other names| Arteriosclerotic heart disease, atherosclerotic heart disease,[1] atherosclerotic vascular disease,[2] coronary heart disease.[3]
Illustration depicting two arteries: the one on the left is a normal artery and the one on the right is an atherosclerotic coronary artery disease
Specialty| Cardiology, cardiothoracic surgery
Symptoms| Chest pain, shortness of breath[4]
Complications| Heart failure, abnormal heart rhythms, heart attack, cardiogenic shock, cardiac arrest[5]
Causes| Atherosclerosis of the arteries of the heart[6]
Risk factors| High blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol[6][7]
Diagnostic method| Electrocardiogram, cardiac stress test, coronary computed tomographic angiography, coronary angiogram[8]
Prevention| Healthy diet, regular exercise, maintaining a healthy weight, not smoking[9]
Treatment| Percutaneous coronary intervention (PCI), coronary artery bypass surgery (CABG)[10]
Medication| Aspirin, beta blockers, nitroglycerin, statins[10]
Frequency| 110 million (2015)[11]
Deaths| 8.9 million (2015)[12]

Coronary artery disease (CAD), also called coronary heart disease (CHD), or ischemic heart disease (IHD),[13] is a type of heart disease involving the reduction of blood flow to the cardiac muscle due to a build-up of atheromatous plaque in the arteries of the heart.[5][6][14] It is the most common of the cardiovascular diseases.[15] CAD can cause stable angina, unstable angina, myocardial ischemia,[16] and myocardial infarction.[17]

A common symptom is angina, which is chest pain or discomfort that may travel into the shoulder, arm, back, neck, or jaw.[4] Occasionally it may feel like heartburn. In stable angina, symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest.[4] Shortness of breath may also occur and sometimes no symptoms are present.[4] In many cases, the first sign is a heart attack.[5] Other complications include heart failure or an abnormal heartbeat.[5]

Risk factors include high blood pressure, smoking, diabetes mellitus, lack of exercise, obesity, high blood cholesterol, poor diet, depression, and excessive alcohol consumption.[6][7][18] A number of tests may help with diagnosis including electrocardiogram, cardiac stress testing, coronary computed tomographic angiography, biomarkers (high-sensitivity cardiac troponins) and coronary angiogram, among others.[8][19] Ways to reduce CAD risk include eating a healthy diet, regularly exercising, maintaining a healthy weight, and not smoking.[20][9] Medications for diabetes, high cholesterol, or high blood pressure are sometimes used.[9] There is limited evidence for screening people who are at low risk and do not have symptoms.[21] Treatment involves the same measures as prevention.[10][22] Additional medications such as antiplatelets (including aspirin), beta blockers, or nitroglycerin may be recommended.[10] Procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG) may be used in severe disease.[10][23] In those with stable CAD it is unclear if PCI or CABG in addition to the other treatments improves life expectancy or decreases heart attack risk.[24]

In 2015, CAD affected 110 million people and resulted in 8.9 million deaths.[11][12] It makes up 15.6% of all deaths, making it the most common cause of death globally.[12] The risk of death from CAD for a given age decreased between 1980 and 2010, especially in developed countries.[25] The number of cases of CAD for a given age also decreased between 1990 and 2010.[26] In the United States in 2010, about 20% of those over 65 had CAD, while it was present in 7% of those 45 to 64, and 1.3% of those 18 to 45;[27] rates were higher among males than females of a given age.[27]

## Contents

* 1 Signs and symptoms
* 1.1 Symptoms in females
* 2 Risk factors
* 2.1 Air pollution
* 2.2 Blood fats
* 2.3 Genetics
* 2.4 Transcriptome
* 2.5 Other
* 3 Pathophysiology
* 4 Diagnosis
* 4.1 Stable angina
* 4.2 Acute coronary syndrome
* 4.3 Risk assessment
* 5 Prevention
* 5.1 Diet
* 5.2 Secondary prevention
* 5.3 Neuropsychological assessment
* 6 Treatment
* 6.1 Medications
* 6.1.1 Aspirin
* 6.1.2 Anti-platelet therapy
* 6.2 Surgery
* 7 Epidemiology
* 8 Society and culture
* 8.1 Names
* 8.2 Support groups
* 8.3 Industry influence on research
* 9 Research
* 10 See also
* 11 References
* 12 External links

## Signs and symptoms

Illustration of someone suffering coronary artery disease

The most common symptom is chest pain or discomfort that occurs regularly with activity, after eating, or at other predictable times; this phenomenon is termed stable angina and is associated with narrowing of the arteries of the heart. Angina also includes chest tightness, heaviness, pressure, numbness, fullness, or squeezing.[28] Angina that changes in intensity, character, or frequency is termed unstable. Unstable angina may precede myocardial infarction. In adults who go to the emergency department with an unclear cause of pain, about 30% have pain due to coronary artery disease.[29] Angina, shortness of breath, sweating, nausea or vomiting, and lightheadedness are signs of a heart attack or myocardial infarction, and immediate emergency medical services are crucial.[28]

With advanced disease, the narrowing of coronary arteries reduces the supply of oxygen-rich blood flowing to the heart, which becomes more pronounced during strenuous activities, during which the heart beats faster and has an increased oxygen demand.[30] For some, this causes severe symptoms, while others experience no symptoms at all.[4]

### Symptoms in females

Symptoms in females can differ from those in males, and the most common symptom reported by females of all races is shortness of breath.[31] Other symptoms more commonly reported by females than males are extreme fatigue, sleep disturbances, indigestion, and anxiety.[32] However, some females experience irregular heartbeat, dizziness, sweating, and nausea.[28] Burning, pain, or pressure in the chest or upper abdomen that can travel to the arm or jaw can also be experienced in females, but females less commonly report it than males.[32] Generally, females experience symptoms 10 years later than males.[33] Females are less likely to recognize symptoms and seek treatment.[28]

## Risk factors

Illustration depicting atherosclerosis in a coronary artery

Coronary artery disease is characterized by heart problems that result from atherosclerosis.[34] Atherosclerosis is a type of arteriosclerosis which is the "chronic inflammation of the arteries which causes them to harden and accumulate cholesterol plaques (atheromatous plaques) on the artery walls".[35] CAD has several well-determined risk factors contributing to atherosclerosis. These risk factors for CAD include "smoking, diabetes, high blood pressure (hypertension), abnormal (high) amounts of cholesterol and other fat in the blood (dyslipidemia), type 2 diabetes and being overweight or obese (having excess body fat)" due to lack of exercise and a poor diet.[36] Some other risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, family history, psychological stress and excessive alcohol.[6][7][18] About half of cases are linked to genetics.[37] Apart from these classical risk factors, several unconventional risk factors have also been studied including high serum fibrinogen, high c-reactive protein (CRP), chronic inflammatory conditions, hypovitaminosis D, high lipoprotein A levels, serum homocysteine etc.[38][39] Smoking and obesity are associated with about 36% and 20% of cases, respectively.[40] Smoking just one cigarette per day about doubles the risk of CAD.[41] Lack of exercise has been linked to 7–12% of cases.[40][42] Exposure to the herbicide Agent Orange may increase risk.[43] Rheumatologic diseases such as rheumatoid arthritis, systemic lupus erythematosus, psoriasis, and psoriatic arthritis are independent risk factors as well.[44][45][46][47][excessive citations]

Job stress appears to play a minor role, accounting for about 3% of cases.[40] In one study, females who were free of stress from work life saw an increase in the diameter of their blood vessels, leading to decreased progression of atherosclerosis.[48] In contrast, females who had high levels of work-related stress experienced a decrease in the diameter of their blood vessels and significantly increased disease progression.[48]

### Air pollution

Air pollution, both indoor and outdoor, is responsible for roughly 28% of deaths from CAD. This varies by region: In highly developed areas, this is approximately 10%, whereas in Southern, East and West Africa, and South Asia, approximately 40% of deaths from CAD can be attributed to unhealthy air.[49] In particular, fine particle pollution (PM2.5), which comes mostly from the burning of fossil fuels, is a key risk factor for CAD.[50]

### Blood fats

The consumption of different types of fats including trans fat (trans unsaturated), and saturated fat, in a diet "influences the level of cholesterol that is present in the bloodstream".[51] Unsaturated fats originate from plant sources (such as oils). There are two types of unsaturated fats, cis and trans isomers. Cis unsaturated fats are bent in molecular structure and trans are linear. Saturated fats originate from animal sources (such as animal fats) and are also molecularly linear in structure.[52] The linear configurations of unsaturated trans and saturated fats allow them to easily accumulate and stack at the arterial walls when consumed in high amounts (and other positive measures towards physical health are not met).

* Fats and cholesterol are insoluble in blood and thus are amalgamated with proteins to form lipoproteins for transport. Low-density lipoproteins (LDL) transport cholesterol from the liver to the rest of the body and raise blood cholesterol levels. The consumption of "saturated fats increases LDL levels within the body, thus raising blood cholesterol levels".[51]
* High-density lipoproteins (HDL) are considered 'good' lipoproteins as they search for excess cholesterol in the body and transport it back to the liver for disposal. Trans fats also "increase LDL levels whilst decreasing HDL levels within the body, significantly raising blood cholesterol levels".[51]

High levels of cholesterol in the bloodstream lead to atherosclerosis. With increased levels of LDL in the bloodstream, "LDL particles will form deposits and accumulate within the arterial walls, which will lead to the development of plaques, restricting blood flow".[51] The resultant reduction in the heart's blood supply due to atherosclerosis in coronary arteries "causes shortness of breath, angina pectoris (chest pains that are usually relieved by rest), and potentially fatal heart attacks (myocardial infarctions)".[36]

### Genetics

The heritability of coronary artery disease has been estimated between 40% and 60%.[53] Genome-wide association studies have identified over 160 genetic susceptibility loci for coronary artery disease.[54]

### Transcriptome

Several RNA Transcripts associated with CAD - FoxP1, ICOSLG, IKZF4/Eos, SMYD3, TRIM28, and TCF3/E2A are likely markers of regulatory T cells (Tregs), consistent with known reductions in Tregs in CAD.[55]

Transcripts associated with CAD identified by RNA-seq. The differentially expressed genes identified by RNAseq were curated by automated and manual analysis to identify the molecular pathways involved. The resulting pattern points to changes in the 'immune synapse', which involves both endocytic pathways of T cell receptor-containing vesicles, as well as ciliary protrusions that couple to intracellular signaling pathways.

The RNA changes are mostly related to ciliary and endocytic transcripts, which in the circulating immune system would be related to the immune synapse.[56] One of the most differentially expressed genes, fibromodulin (FMOD), which is increased 2.8-fold in CAD, is found mainly in connective tissue[57] and is a modulator of the TGF-beta signaling pathway. However, not all RNA changes may be related to the immune synapse. For example, Nebulette, the most down-regulated transcript (2.4-fold), is found in cardiac muscle; it is a 'cytolinker' that connects actin and desmin to facilitate cytoskeletal function and vesicular movement. The endocytic pathway is further modulated by changes in tubulin, a key microtubule protein, and fidgetin, a tubulin-severing enzyme that is a marker for cardiovascular risk identified by genome-wide association study. Protein recycling would be modulated by changes in the proteasomal regulator SIAH3 and the ubiquitin ligase MARCHF10. On the ciliary aspect of the immune synapse, several of the modulated transcripts are related to ciliary length and function. Stereocilin is a partner to mesothelin, a related super-helical protein, whose transcript is also modulated in CAD. DCDC2, a double-cortin protein, modulates ciliary length. In the signaling pathways of the immune synapse, numerous transcripts are directly related to T-cell function and the control of differentiation. Butyrophilin is a co-regulator for T cell activation. Fibromodulin modulates the TGF-beta signaling pathway, a primary determinant of Tre differentiation. Further impact on the TGF-beta pathway is reflected in concurrent changes in the BMP receptor 1B RNA (BMPR1B), because the bone morphogenic proteins are members of the TGF-beta superfamily, and likewise impact Treg differentiation. Several of the transcripts (TMEM98, NRCAM, SFRP5, SHISA2) are elements of the Wnt signaling pathway, which is a major determinant of Treg differentiation.

### Other

* Endometriosis in females under the age of 40.[58]
* Depression and hostility appear to be risks.[59]
* The number of categories of adverse childhood experiences (psychological, physical, or sexual abuse; violence against mother; or living with household members who used substances, mentally ill, suicidal, or incarcerated) showed a graded correlation with the presence of adult diseases including coronary artery (ischemic heart) disease.[60]
* Hemostatic factors: High levels of fibrinogen and coagulation factor VII are associated with an increased risk of CAD.[61]
* Low hemoglobin.[62]
* In the Asian population, the b fibrinogen gene G-455A polymorphism was associated with the risk of CAD.[63]
* Patient-specific vessel ageing or remodelling determines endothelial cell behaviour and thus disease growth and progression. Such 'hemodynamic markers' are patient-specific risk surrogates.[64]
* HIV is a known risk factor for developing atherosclerosis and coronary artery disease.[65]

## Pathophysiology

Micrograph of a coronary artery with the most common form of coronary artery disease (atherosclerosis) and marked luminal narrowing. Masson's trichrome.

Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the heart's muscle cells. The heart's muscle cells may die from lack of oxygen and this is called a myocardial infarction (commonly referred to as a heart attack). It leads to damage, death, and eventual scarring of the heart muscle without regrowth of heart muscle cells. Chronic high-grade narrowing of the coronary arteries can induce transient ischemia, which leads to the induction of a ventricular arrhythmia, which may terminate in a dangerous heart rhythm known as ventricular fibrillation, which often leads to death.[66]

Typically, coronary artery disease occurs when part of the smooth, elastic lining inside a coronary artery (the arteries that supply blood to the heart muscle) develops atherosclerosis. With atherosclerosis, the artery's lining becomes hardened, stiffened, and accumulates deposits of calcium, fatty lipids, and abnormal inflammatory cells – to form a plaque. Calcium phosphate (hydroxyapatite) deposits in the muscular layer of the blood vessels appear to play a significant role in stiffening the arteries and inducing the early phase of coronary arteriosclerosis. This can be seen in a so-called metastatic mechanism of calciphylaxis as it occurs in chronic kidney disease and hemodialysis. Although these people have kidney dysfunction, almost fifty percent of them die due to coronary artery disease. Plaques can be thought of as large "pimples" that protrude into the channel of an artery, causing partial obstruction to blood flow. People with coronary artery disease might have just one or two plaques or might have dozens distributed throughout their coronary arteries. A more severe form is chronic total occlusion (CTO) when a coronary artery is completely obstructed for more than 3 months.[67]

Microvascular angina is a type of angina pectoris in which chest pain and chest discomfort occur without signs of blockages in the larger coronary arteries of their hearts when an angiogram (coronary angiogram) is being performed.[68][69] The exact cause of microvascular angina is unknown. Explanations include microvascular dysfunction or epicardial atherosclerosis.[70][71] For reasons that are not well understood, females are more likely than males to have it; however, hormones and other risk factors unique to females may play a role.[72]

## Diagnosis

Coronary angiogram of a male Coronary angiogram of a female

The diagnosis of CAD depends largely on the nature of the symptoms and imaging. The first investigation when CAD is suspected is an electrocardiogram (ECG/EKG), both for stable angina and acute coronary syndrome. An X-ray of the chest, blood tests, and resting echocardiography may be performed.[73][74]

For stable symptomatic patients, several non-invasive tests can diagnose CAD depending on pre-assessment of the risk profile. Noninvasive imaging options include; Computed tomography angiography (CTA) (anatomical imaging, best test in patients with low-risk profile to "rule out" the disease), positron emission tomography (PET), single-photon emission computed tomography (SPECT)/nuclear stress test/myocardial scintigraphy and stress echocardiography (the three latter can be summarized as functional noninvasive methods and are typically better to "rule in"). Exercise ECG or stress test is inferior to non-invasive imaging methods due to the risk of false-negative and false-positive test results. The use of non-invasive imaging is not recommended on individuals who are exhibiting no symptoms and are otherwise at low risk for developing coronary disease.[75][76] Invasive testing with coronary angiography (ICA) can be used when non-invasive testing is inconclusive or show a high event risk.[74]

The diagnosis of microvascular angina (previously known as cardiac syndrome X – the rare coronary artery disease that is more common in females, as mentioned, is a diagnosis of exclusion. Therefore, usually, the same tests are used as in any person suspected of having coronary artery disease:[77]

* Intravascular ultrasound
* Magnetic resonance imaging (MRI)

### Stable angina

Stable angina is the most common manifestation of ischemic heart disease, and is associated with reduced quality of life and increased mortality. It is caused by epicardial coronary stenosis, which results in reduced blood flow and oxygen supply to the myocardium.[78] Stable angina is short-term chest pain during physical exertion caused by an imbalance between myocardial oxygen supply and metabolic oxygen demand. Various forms of cardiac stress tests may be used to induce both symptoms and detect changes by way of electrocardiography (using an ECG), echocardiography (using ultrasound of the heart) or scintigraphy (using uptake of radionuclide by the heart muscle). If part of the heart seems to receive an insufficient blood supply, coronary angiography may be used to identify stenosis of the coronary arteries and suitability for angioplasty or bypass surgery.[79]

In minor to moderate cases, nitroglycerine may be used to alleviate acute symptoms of stable angina or may be used immediately before exertion to prevent the onset of angina. Sublingual nitroglycerine is most commonly used to provide rapid relief for acute angina attacks and as a complement to anti-anginal treatments in patients with refractory and recurrent angina.[80] When nitroglycerine enters the bloodstream, it forms free radical nitric oxide, or NO, which activates guanylate cyclase and in turn stimulates the release of cyclic GMP. This molecular signaling stimulates smooth muscle relaxation, resulting in vasodilation and consequently improved blood flow to heart regions affected by atherosclerotic plaque.[81]

Stable coronary artery disease (SCAD) is also often called stable ischemic heart disease (SIHD).[82] A 2015 monograph explains that "Regardless of the nomenclature, stable angina is the chief manifestation of SIHD or SCAD."[82] There are U.S. and European clinical practice guidelines for SIHD/SCAD.[83][84][74] In patients with non-severe asymptomatic aortic valve stenosis and no overt coronary artery disease, the increased troponin T (above 14 pg/mL) was found associated with an increased 5-year event rate of ischemic cardiac events (myocardial infarction, percutaneous coronary intervention, or coronary artery bypass surgery).[85]

### Acute coronary syndrome

Main article: Medicine:Acute coronary syndrome

### Risk assessment

There are various risk assessment systems for determining the risk of coronary artery disease, with various emphases on the different variables above. A notable example is Framingham Score, used in the Framingham Heart Study. It is mainly based on age, gender, diabetes, total cholesterol, HDL cholesterol, tobacco smoking, and systolic blood pressure. When predicting risk in younger adults (18–39 years old), the Framingham Risk Score remains below 10–12% for all deciles of baseline-predicted risk.[86]

Polygenic score is another way of risk assessment. In one study, the relative risk of incident coronary events was 91% higher among participants at high genetic risk than among those at low genetic risk.[87]

## Prevention

Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided.[88][89] Prevention involves adequate physical exercise, decreasing obesity, treating high blood pressure, eating a healthy diet, decreasing cholesterol levels, and stopping smoking. Medications and exercise are roughly equally effective.[90] High levels of physical activity reduce the risk of coronary artery disease by about 25%.[91] Life's Essential 8 are the key measures for improving and maintaining cardiovascular health, as defined by the American Heart Association. AHA added sleep as a factor influencing heart health in 2022.[92]

Most guidelines recommend combining these preventive strategies. A 2015 Cochrane Review found some evidence that counseling and education to bring about behavioral change might help in high-risk groups. However, there was insufficient evidence to show an effect on mortality or actual cardiovascular events.[93]

In diabetes mellitus, there is little evidence that very tight blood sugar control improves cardiac risk, although improved sugar control appears to decrease other problems such as kidney failure and blindness.[94]

A 2024 study published in The Lancet Diabetes & Endocrinology found that the oral glucose tolerance test (OGTT) is more effective than hemoglobin A1c (HbA1c) for detecting dysglycemia in patients with coronary artery disease.[95] The study highlighted that 2-hour post-load glucose levels of at least 9 mmol/L were strong predictors of cardiovascular outcomes, while HbA1c levels of at least 5.9% were also significant but not independently associated when combined with OGTT results.[96]

### Diet

A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death.[97] Vegetarians have a lower risk of heart disease,[98][99] possibly due to their greater consumption of fruits and vegetables.[100] Evidence also suggests that the Mediterranean diet[101] and a high fiber diet lower the risk.[102][103]

The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause a precursor to atherosclerosis[104] and increase the risk of coronary artery disease.[105]

Evidence does not support a beneficial role for omega-3 fatty acid supplementation in preventing cardiovascular disease (including myocardial infarction and sudden cardiac death).[106][107]

### Secondary prevention

Secondary prevention is preventing further sequelae of already established disease. Effective lifestyle changes include:

* Weight control
* Smoking cessation
* Avoiding the consumption of trans fats (in partially hydrogenated oils)
* Decreasing psychosocial stress[108][109]
* Exercise

Aerobic exercise, like walking, jogging, or swimming, can reduce the risk of mortality from coronary artery disease.[110] Aerobic exercise can help decrease blood pressure and the amount of blood cholesterol (LDL) over time. It also increases HDL cholesterol.[111]

Although exercise is beneficial, it is unclear whether doctors should spend time counseling patients to exercise. The U.S. Preventive Services Task Force found "insufficient evidence" to recommend that doctors counsel patients on exercise, but "it did not review the evidence for the effectiveness of physical activity to reduce chronic disease, morbidity, and mortality", only the effectiveness of counseling itself.[112] The American Heart Association, based on a non-systematic review, recommends that doctors counsel patients on exercise.[113]

Psychological symptoms are common in people with CHD. Many psychological treatments may be offered following cardiac events. There is no evidence that they change mortality, the risk of revascularization procedures, or the rate of non-fatal myocardial infarction.[109]

Antibiotics for secondary prevention of coronary heart disease

Early studies suggested that antibiotics might help patients with coronary disease reduce the risk of heart attacks and strokes.[114] However, a 2021 Cochrane meta-analysis found that antibiotics given for secondary prevention of coronary heart disease are harmful to people with increased mortality and occurrence of stroke.[114] So, antibiotic use is not currently supported for preventing secondary coronary heart disease.

### Neuropsychological assessment

A thorough systematic review found that indeed there is a link between a CHD condition and brain dysfunction in females.[115] Consequently, since research is showing that cardiovascular diseases, like CHD, can play a role as a precursor for dementia, like Alzheimer's disease, individuals with CHD should have a neuropsychological assessment.[116]

## Treatment

There are a number of treatment options for coronary artery disease:[117]

* Lifestyle changes
* Medical treatment – commonly prescribed drugs (e.g., cholesterol lowering medications, beta-blockers, nitroglycerin, calcium channel blockers, etc.);
* Coronary interventions as angioplasty and coronary stent;
* Coronary artery bypass grafting (CABG)

### Medications

* Statins, which reduce cholesterol, reduce the risk of coronary artery disease[118]
* Nitroglycerin[119]
* Calcium channel blockers and/or beta-blockers[120]
* Antiplatelet drugs such as aspirin[120][121]

It is recommended that blood pressure typically be reduced to less than 140/90 mmHg.[122] The diastolic blood pressure should not be below 60 mmHg. Beta-blockers are recommended first line for this use.[122]

#### Aspirin

In those with no previous history of heart disease, aspirin decreases the risk of a myocardial infarction but does not change the overall risk of death.[123] Aspirin therapy to prevent heart disease is thus recommended only in adults who are at increased risk for cardiovascular events, which may include postmenopausal females, males above 40, and younger people with risk factors for coronary heart disease, including high blood pressure, a family history of heart disease, or diabetes. The benefits outweigh the harms most favorably in people at high risk for a cardiovascular event, where high risk is defined as at least a 3% chance over five years, but others with lower risk may still find the potential benefits worth the associated risks.[124]

#### Anti-platelet therapy

Clopidogrel plus aspirin (dual anti-platelet therapy) reduces cardiovascular events more than aspirin alone in those with a STEMI. In others at high risk but not having an acute event, the evidence is weak.[125] Specifically, its use does not change the risk of death in this group.[126] In those who have had a stent, more than 12 months of clopidogrel plus aspirin does not affect the risk of death.[127]

### Surgery

Revascularization for acute coronary syndrome has a mortality benefit.[128] Percutaneous revascularization for stable ischaemic heart disease does not appear to have benefits over medical therapy alone.[129] In those with disease in more than one artery, coronary artery bypass grafts appear better than percutaneous coronary interventions.[130] Newer "anaortic" or no-touch off-pump coronary artery revascularization techniques have shown reduced postoperative stroke rates comparable to percutaneous coronary intervention.[131] Hybrid coronary revascularization has also been shown to be a safe and feasible procedure that may offer some advantages over conventional CABG though it is more expensive.[132]

## Epidemiology

Deaths due to ischaemic heart disease per million persons in 2012

160–288

289–379

380–460

461–576

577–691

692–894

895–1,068

1,069–1,443

1,444–2,368

2,369–7,233

Disability-adjusted life year for ischaemic heart disease per 100,000 inhabitants in 2004.[133]

no data

<350

350–700

700–1,050

1,050–1,400

1,400–1,750

1,750–2,100

2,100–2,450

2,450–2,800

2,800–3,150

3,150–3,500

3,500–4,000

>4,000

As of 2010, CAD was the leading cause of death globally resulting in over 7 million deaths.[134] This increased from 5.2 million deaths from CAD worldwide in 1990.[134] It may affect individuals at any age but becomes dramatically more common at progressively older ages, with approximately a tripling with each decade of life.[135] Males are affected more often than females.[135]

The World Health Organization reported that: "The world's biggest killer is ischemic heart disease, responsible for 13% of the world's total deaths. Since 2000, the largest increase in deaths has been for this disease, rising by 2.7 million to 9.1 million deaths in 2021."[136]

It is estimated that 60% of the world's cardiovascular disease burden will occur in the South Asian subcontinent despite only accounting for 20% of the world's population. This may be secondary to a combination of genetic predisposition and environmental factors. Organizations such as the Indian Heart Association are working with the World Heart Federation to raise awareness about this issue.[137]

Coronary artery disease is the leading cause of death for both males and females and accounts for approximately 600,000 deaths in the United States every year.[138] According to present trends in the United States, half of healthy 40-year-old males will develop CAD in the future, and one in three healthy 40-year-old females.[139] It is the most common reason for death of males and females over 20 years of age in the United States.[140]

After analysing data from 2 111 882 patients, the recent meta-analysis revealed that the incidence of coronary artery diseases in breast cancer survivors was 4.29 (95% CI 3.09–5.94) per 1000 person-years.[141]

## Society and culture

### Names

Other terms sometimes used for this condition are "hardening of the arteries" and "narrowing of the arteries".[142] In Latin it is known as morbus ischaemicus cordis (MIC).

### Support groups

The Infarct Combat Project (ICP) is an international nonprofit organization founded in 1998 which tries to decrease ischemic heart diseases through education and research.[143]

### Industry influence on research

In 2016 research into the internal documents of the Sugar Research Foundation, the trade association for the sugar industry in the US, had sponsored an influential literature review published in 1965 in the New England Journal of Medicine that downplayed early findings about the role of a diet heavy in sugar in the development of CAD and emphasized the role of fat; that review influenced decades of research funding and guidance on healthy eating.[144][145][146][147]

## Research

Research efforts are focused on new angiogenic treatment modalities and various (adult) stem-cell therapies. A region on chromosome 17 was confined to families with multiple cases of myocardial infarction.[148] Other genome-wide studies have identified a firm risk variant on chromosome 9 (9p21.3).[149] However, these and other loci are found in intergenic segments and need further research in understanding how the phenotype is affected.[150]

A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[151] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive regarding whether it can be considered a causative factor.[152] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[153]

Myeloperoxidase has been proposed as a biomarker.[154]

Plant-based nutrition has been suggested as a way to reverse coronary artery disease,[155] but strong evidence is still lacking for claims of potential benefits.[156]

Several immunosuppressive drugs targeting the chronic inflammation in coronary artery disease have been tested.[157]

## See also

* Mental stress-induced myocardial ischemia

## References

1. ↑ "Coronary heart disease – causes, symptoms, prevention". https://www.southerncross.co.nz/AboutTheGroup/HealthResources/MedicalLibrary/tabid/178/vw/1/ItemID/191.
2. ↑ "Atherosclerotic Vascular Disease Conference: Executive summary: Atherosclerotic Vascular Disease Conference proceeding for healthcare professionals from a special writing group of the American Heart Association". Circulation 109 (21): 2595–604. June 2004. doi:10.1161/01.CIR.0000128517.52533.DB. PMID 15173041.
3. ↑ MedlinePlus Encyclopedia Coronary heart disease
4. ↑ 4.0 4.1 4.2 4.3 4.4 "What Are the Signs and Symptoms of Coronary Heart Disease?". 29 September 2014. http://www.nhlbi.nih.gov/health/health-topics/topics/cad/signs.
5. ↑ 5.0 5.1 5.2 5.3 "Coronary Artery Disease (CAD)". 12 March 2013. https://www.cdc.gov/heartdisease/coronary_ad.htm.
6. ↑ 6.0 6.1 6.2 6.3 6.4 Global atlas on cardiovascular disease prevention and control. World Health Organization. 2011. pp. 3–18. ISBN 978-92-4-156437-3.
7. ↑ 7.0 7.1 7.2 "Ischemic heart disease in women: a focus on risk factors". Trends in Cardiovascular Medicine 25 (2): 140–51. February 2015. doi:10.1016/j.tcm.2014.10.005. PMID 25453985.
8. ↑ 8.0 8.1 "How Is Coronary Heart Disease Diagnosed?". 29 September 2014. http://www.nhlbi.nih.gov/health/health-topics/topics/cad/diagnosis.
9. ↑ 9.0 9.1 9.2 "How Can Coronary Heart Disease Be Prevented or Delayed?". http://www.nhlbi.nih.gov/health/health-topics/topics/cad/prevention.
10. ↑ 10.0 10.1 10.2 10.3 10.4 "How Is Coronary Heart Disease Treated?". 29 September 2014. http://www.nhlbi.nih.gov/health/health-topics/topics/cad/treatment.
11. ↑ 11.0 11.1 "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet 388 (10053): 1545–1602. October 2016. doi:10.1016/S0140-6736(16)31678-6. PMID 27733282.
12. ↑ 12.0 12.1 12.2 "Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet 388 (10053): 1459–1544. October 2016. doi:10.1016/S0140-6736(16)31012-1. PMID 27733281.
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15. ↑ Murray, Christopher J. L. (January 2015). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet 385 (9963): 117–71. doi:10.1016/S0140-6736(14)61682-2. PMID 25530442.
16. ↑ "Myocardial ischemia – Symptoms and causes" (in en). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/myocardial-ischemia/symptoms-causes/syc-20375417.
17. ↑ "Epidemiological studies of CHD and the evolution of preventive cardiology". Nature Reviews. Cardiology 11 (5): 276–89. May 2014. doi:10.1038/nrcardio.2014.26. PMID 24663092.
18. ↑ 18.0 18.1 "The contribution of major depression to the global burden of ischemic heart disease: a comparative risk assessment". BMC Medicine 11. November 2013. doi:10.1186/1741-7015-11-250. PMID 24274053.
19. ↑ "2023 ESC Guidelines for the management of acute coronary syndromes". Eur Heart J 44 (38): 3720–3826. October 2023. doi:10.1093/eurheartj/ehad191. PMID 37622654.
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22. ↑ "Exercise as a therapeutic intervention in patients with stable ischemic heart disease: an underfilled prescription". The American Journal of Medicine 127 (10): 905–11. October 2014. doi:10.1016/j.amjmed.2014.05.007. PMID 24844736.
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29. ↑ "Emergency department and office-based evaluation of patients with chest pain". Mayo Clinic Proceedings 85 (3): 284–99. March 2010. doi:10.4065/mcp.2009.0560. PMID 20194155.
30. ↑ "Coronary artery disease – Symptoms and causes" (in en). https://www.mayoclinic.org/diseases-conditions/coronary-artery-disease/symptoms-causes/syc-20350613.
31. ↑ "Racial differences in women's prodromal and acute symptoms of myocardial infarction". American Journal of Critical Care 19 (1): 63–73. January 2010. doi:10.4037/ajcc2010372. PMID 20045850.
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33. ↑ "Women & Cardiovascular Disease". https://my.clevelandclinic.org/health/diseases/17645-women--cardiovascular-disease.
34. ↑ Institute of Medicine (US) Committee on Social Security Cardiovascular Disability Criteria. (2010). Cardiovascular Disability: Updating the Social Security Listings. "Ischemic Heart Disease". NCBI, National Academies Press (US).
35. ↑ Tenas, M. S. & Torres, M. F. (2018) "What is Ischaemic Heart Disease?" Clinic Barcelona.
36. ↑ 36.0 36.1 Nordestgaard, B. G. & Palmer, T. M. & Benn, M. & Zacho, J & Tybjærg-Hansen, A. & Smith, G. D. & Timpson, N. J. (2012). "The Effect of Elevated Body Mass Index on Ischemic Heart Disease Risk: Causal Estimates from a Mendelian Randomisation Approach". PLoS Medicine vol. 9,5 e1001212. doi:10.1371/journal.pmed.1001212.
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38. ↑ Ullah, Himayat (2022-04-29). "High Sensitivity C-Reactive Protein Level and Ischemic Heart Disease" (in en). Pakistan Journal of Medical & Health Sciences 16 (4): 34–35. doi:10.53350/pjmhs2216434. ISSN 2957-899X. https://pjmhsonline.com/index.php/pjmhs/article/view/648.
39. ↑ Yuan, Deshan; Jiang, Ping; Zhu, Pei; Jia, Sida; Zhang, Ce; Liu, Yue; Liu, Ru; Xu, Jingjing et al. (2021-07-16). "Prognostic value of fibrinogen in patients with coronary artery disease and prediabetes or diabetes following percutaneous coronary intervention: 5-year findings from a large cohort study". Cardiovascular Diabetology 20 (1): 143. doi:10.1186/s12933-021-01335-1. ISSN 1475-2840. PMID 34271936.
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42. ↑ "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". Lancet 380 (9838): 219–29. July 2012. doi:10.1016/S0140-6736(12)61031-9. PMID 22818936.
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44. ↑ "Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus". Arthritis and Rheumatism 44 (10): 2331–37. October 2001. doi:10.1002/1529-0131(200110)44:10<2331::aid-art395>3.0.co;2-i. PMID 11665973.
45. ↑ "How early in the course of rheumatoid arthritis does the excess cardiovascular risk appear?". Annals of the Rheumatic Diseases 71 (10): 1606–15. October 2012. doi:10.1136/annrheumdis-2012-201334. PMID 22736093.
46. ↑ "The effects of tumour necrosis factor inhibitors, methotrexate, non-steroidal anti-inflammatory drugs and corticosteroids on cardiovascular events in rheumatoid arthritis, psoriasis and psoriatic arthritis: a systematic review and meta-analysis". Annals of the Rheumatic Diseases 74 (3): 480–89. March 2015. doi:10.1136/annrheumdis-2014-206624. PMID 25561362.
47. ↑ "The Use of Primary Prevention Statin Therapy in Those Predisposed to Atherosclerosis". Current Atherosclerosis Reports 19 (12). October 2017. doi:10.1007/s11883-017-0685-7. PMID 29038899.
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50. ↑ Montone, Rocco A.; Rinaldi, Riccardo; Bonanni, Alice; Severino, Anna; Pedicino, Daniela; Crea, Filippo; Liuzzo, Giovanna (2023-02-01). "Impact of air pollution on ischemic heart disease: Evidence, mechanisms, clinical perspectives" (in English). Atherosclerosis 366: 22–31. doi:10.1016/j.atherosclerosis.2023.01.013. ISSN 0021-9150. PMID 36696748.
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52. ↑ "Types of Fatty Acids | BioNinja". https://ib.bioninja.com.au/standard-level/topic-2-molecular-biology/23-carbohydrates-and-lipids/types-of-fatty-acids.html.
53. ↑ "Genetics of Coronary Artery Disease". Circulation Research 118 (4): 564–78. February 2016. doi:10.1161/circresaha.115.306566. PMID 26892958.
54. ↑ "Identification of 64 Novel Genetic Loci Provides an Expanded View on the Genetic Architecture of Coronary Artery Disease". Circulation Research (Ovid Technologies (Wolters Kluwer Health)) 122 (3): 433–43. February 2018. doi:10.1161/circresaha.117.312086. PMID 29212778.
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56. ↑ "RNAseq profiling of blood from patients with coronary artery disease: Signature of a T cell imbalance". Journal of Molecular and Cellular Cardiology Plus 4. June 2023. doi:10.1016/j.jmccpl.2023.100033. PMID 37303712.
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79. ↑ "Coronary Angiography". https://www.nhlbi.nih.gov/health/health-topics/topics/ca.
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119. ↑ MedlinePlus Encyclopedia Nitroglycerin Sublingual
120. ↑ 120.0 120.1 "Clinical Practice: Chronic Stable Angina". The New England Journal of Medicine 374 (12): 1167–76. March 2016. doi:10.1056/NEJMcp1502240. PMID 27007960.
121. ↑ "Antiplatelet therapy in acute coronary syndromes". Expert Opinion on Pharmacotherapy 16 (14): 2133–47. 2015. doi:10.1517/14656566.2015.1079619. PMID 26293612.
122. ↑ 122.0 122.1 "Treatment of hypertension in patients with coronary artery disease: a scientific statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension". Circulation 131 (19): e435–70. May 2015. doi:10.1161/cir.0000000000000207. PMID 25829340.
123. ↑ "Aspirin for the Primary Prevention of Cardiovascular Events: A Systematic Evidence Review for the U.S. Preventive Services Task Force". Annals of Internal Medicine 164 (12): 804–13. June 2016. doi:10.7326/M15-2113. PMID 27064410.
124. ↑ U.S. Preventive Services Task Force (January 2002). "Aspirin for the primary prevention of cardiovascular events: recommendation and rationale". Annals of Internal Medicine 136 (2): 157–60. doi:10.7326/0003-4819-136-2-200201150-00015. PMID 11790071.
125. ↑ "Clopidogrel plus aspirin versus aspirin alone for preventing cardiovascular events". The Cochrane Database of Systematic Reviews 2017 (12). December 2017. doi:10.1002/14651858.CD005158.pub4. PMID 29240976.
126. ↑ "FDA Drug Safety Communication: FDA review finds long-term treatment with blood-thinning medicine Plavix (clopidogrel) does not change risk of death". 6 November 2015. https://www.fda.gov/Drugs/DrugSafety/ucm471286.htm.
127. ↑ "Extended duration dual antiplatelet therapy and mortality: a systematic review and meta-analysis". Lancet 385 (9970): 792–98. February 2015. doi:10.1016/S0140-6736(14)62052-3. PMID 25467565.
128. ↑ "ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—2002: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina)". Circulation 106 (14): 1893–900. October 2002. doi:10.1161/01.CIR.0000037106.76139.53. PMID 12356647.
129. ↑ "Percutaneous coronary intervention outcomes in patients with stable obstructive coronary artery disease and myocardial ischemia: a collaborative meta-analysis of contemporary randomized clinical trials". JAMA Internal Medicine 174 (2): 232–40. February 2014. doi:10.1001/jamainternmed.2013.12855. PMID 24296791.
130. ↑ "Coronary artery bypass grafting vs percutaneous coronary intervention and long-term mortality and morbidity in multivessel disease: meta-analysis of randomized clinical trials of the arterial grafting and stenting era". JAMA Internal Medicine 174 (2): 223–30. February 2014. doi:10.1001/jamainternmed.2013.12844. PMID 24296767.
131. ↑ "Coronary Artery Bypass Grafting With and Without Manipulation of the Ascending Aorta: A Network Meta-Analysis". Journal of the American College of Cardiology 69 (8): 924–36. February 2017. doi:10.1016/j.jacc.2016.11.071. PMID 28231944.
132. ↑ "Hybrid coronary revascularization versus conventional coronary artery bypass grafting: Systematic review and meta-analysis". Medicine 97 (33). August 2018. doi:10.1097/MD.0000000000011941. PMID 30113498.
133. ↑ "WHO Disease and injury country estimates". 2009. https://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html.
134. ↑ 134.0 134.1 "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet 380 (9859): 2095–128. December 2012. doi:10.1016/S0140-6736(12)61728-0. PMID 23245604. PMC 10790329. https://repozitorij.upr.si/Dokument.php?id=7123&dn=.
135. ↑ 135.0 135.1 "Mortality from ischaemic heart disease by country, region, and age: statistics from World Health Organisation and United Nations". International Journal of Cardiology 168 (2): 934–45. September 2013. doi:10.1016/j.ijcard.2012.10.046. PMID 23218570.
136. ↑ "The top 10 causes of death" (in en). https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death.
137. ↑ Indian Heart Association Why South Asians Facts , 29 April 2015; accessed 26 October 2015.
138. ↑ "Deaths: final data for 2009". National Vital Statistics Reports 60 (3): 1–116. December 2011. PMID 24974587. https://www.cdc.gov/nchs/https://www.cdc.gov/nchs/data/nvsr/nvsr60/nvsr60_03.pdf.
139. ↑ "Heart disease and stroke statistics—2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee". Circulation 115 (5): e69–171. February 2007. doi:10.1161/CIRCULATIONAHA.106.179918. PMID 17194875.
140. ↑ "Heart Disease and Stroke Statistics | American Heart Association (AHA)". 2007. http://www.americanheart.org/presenter.jhtml?identifier=3000090.
141. ↑ Galimzhanov, Akhmetzhan; Istanbuly, Sedralmontaha; Tun, Han Naung; Ozbay, Benay; Alasnag, Mirvat; Ky, Bonnie; Lyon, Alexander R; Kayikcioglu, Meral et al. (2023-07-27). "Cardiovascular outcomes in breast cancer survivors: a systematic review and meta-analysis" (in en). European Journal of Preventive Cardiology 30 (18): 2018–31. doi:10.1093/eurjpc/zwad243. ISSN 2047-4873. PMID 37499186. https://academic.oup.com/eurjpc/advance-article/doi/10.1093/eurjpc/zwad243/7232455.
142. ↑ "Other Names for Coronary Heart Disease". 29 September 2014. http://www.nhlbi.nih.gov/health/health-topics/topics/cad/names.
143. ↑ "Our Mission". http://www.infarctcombat.org/OurMission.html.
144. ↑ O'Connor, Anahad, "How the Sugar Industry Shifted Blame to Fat" , The New York Times, 12 September 2016. Retrieved 12 September 2016.
145. ↑ "Food Industry Funding of Nutrition Research: The Relevance of History for Current Debates". JAMA Internal Medicine 176 (11): 1685–86. November 2016. doi:10.1001/jamainternmed.2016.5400. PMID 27618496.
146. ↑ "Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents". JAMA Internal Medicine 176 (11): 1680–85. November 2016. doi:10.1001/jamainternmed.2016.5394. PMID 27617709.
147. ↑ "How the sugar industry paid experts to downplay health risks". PBS NewsHour. 13 September 2016. https://www.pbs.org/newshour/show/sugar-industry-paid-experts-downplay-health-risks.
148. ↑ "Genome-wide mapping of susceptibility to coronary artery disease identifies a novel replicated locus on chromosome 17". PLOS Genetics 2 (5). May 2006. doi:10.1371/journal.pgen.0020072. PMID 16710446.
149. ↑ "9p21 and the genetic revolution for coronary artery disease". Clinical Chemistry 58 (1): 104–12. January 2012. doi:10.1373/clinchem.2011.172759. PMID 22015375.
150. ↑ "Genomics in coronary artery disease: past, present and future". The Canadian Journal of Cardiology 26 (Suppl A): 56A–59A. March 2010. doi:10.1016/s0828-282x(10)71064-3. PMID 20386763.
151. ↑ "Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study". Annals of Internal Medicine 116 (4): 273–78. February 1992. doi:10.7326/0003-4819-116-4-273. PMID 1733381.
152. ↑ "Infection with Chlamydia pneumoniae as a cause of coronary heart disease: the hypothesis is still untested". Pathogens and Disease 73 (1): 1–9. February 2015. doi:10.1093/femspd/ftu015. PMID 25854002.
153. ↑ "Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials". JAMA 293 (21): 2641–47. June 2005. doi:10.1001/jama.293.21.2641. PMID 15928286.
154. ↑ "Myeloperoxidase: a new biomarker of inflammation in ischemic heart disease and acute coronary syndromes". Mediators of Inflammation 2008. 2008. doi:10.1155/2008/135625. PMID 18382609.
155. ↑ "A way to reverse CAD?". The Journal of Family Practice 63 (7): 356–64b. July 2014. PMID 25198208. https://cdn.mdedge.com/files/s3fs-public/Document/September-2017/JFP_06307_Article1.pdf.
156. ↑ "Trending Cardiovascular Nutrition Controversies". Journal of the American College of Cardiology 69 (9): 1172–87. March 2017. doi:10.1016/j.jacc.2016.10.086. PMID 28254181.
157. ↑ "Immunomodulatory and immunosuppressive therapies in cardiovascular disease and type 2 diabetes mellitus: A bedside-to-bench approach". Eur J Pharmacol 925. 2022. doi:10.1016/j.ejphar.2022.174998. PMID 35533739.

## External links

* Risk Assessment of having a heart attack or dying of coronary artery disease, from the American Heart Association.
* "Coronary Artery Disease". MedlinePlus. U.S. National Library of Medicine. https://medlineplus.gov/coronaryarterydisease.html.
* Norman, James (2019-10-07). "Managing Diabetes with Blood Glucose Control". https://www.endocrineweb.com/conditions/diabetes/assessing-how-well-diabetes-controlled.

Classification|

* ICD-11: BA40–BA60, BA81–BA86, BE1A
* ICD-10: I20-I25
* ICD-9-CM: 410-414, 429.2
* MeSH: D003324

|

External resources|

* MedlinePlus: 007115
* eMedicine: radio/192

* v
* t
* e

Cardiovascular disease (heart) (I00–I52, 390–429)

Ischaemic|

| Coronary disease|

* Coronary artery disease (CAD)
* Coronary artery aneurysm
* Spontaneous coronary artery dissection (SCAD)
* Coronary thrombosis
* Coronary vasospasm
* Myocardial bridge

|

Active ischemia|

* Angina pectoris
* Prinzmetal's angina
* Stable angina
* Acute coronary syndrome
* Myocardial infarction
* Unstable angina

Sequelae|

* hours
* Hibernating myocardium
* Myocardial stunning
* days
* Myocardial rupture
* weeks
* Aneurysm of heart / Ventricular aneurysm
* Dressler syndrome

Layers|

| Pericardium|

* Pericarditis
* Acute
* Chronic / Constrictive
* Pericardial effusion
* Cardiac tamponade
* Hemopericardium

|

Myocardium|

* Myocarditis
* Chagas disease
* Cardiomyopathy
* Dilated
* Alcoholic
* Hypertrophic
* Tachycardia-induced
* Restrictive
* Loeffler endocarditis
* Cardiac amyloidosis
* Endocardial fibroelastosis
* Arrhythmogenic right ventricular dysplasia

Endocardium /
valves|

| Endocarditis|

* infective endocarditis
* Subacute bacterial endocarditis
* non-infective endocarditis
* Libman–Sacks endocarditis
* Nonbacterial thrombotic endocarditis

|

Valves|

* mitral
* regurgitation
* prolapse
* stenosis
* aortic
* stenosis
* insufficiency
* tricuspid
* stenosis
* insufficiency
* pulmonary
* stenosis
* insufficiency

Conduction /
arrhythmia|

| Bradycardia|

* Sinus bradycardia
* Sick sinus syndrome
* Heart block: Sinoatrial
* AV
* 1°
* 2°
* 3°
* Intraventricular
* Bundle branch block
* Right
* Left
* Left anterior fascicle
* Left posterior fascicle
* Bifascicular
* Trifascicular
* Adams–Stokes syndrome

|

Tachycardia
(paroxysmal and sinus)|

| Supraventricular|

* Atrial
* Multifocal
* Junctional
* AV nodal reentrant
* Junctional ectopic

|

Ventricular|

* Accelerated idioventricular rhythm
* Catecholaminergic polymorphic
* Torsades de pointes

Premature contraction|

* Atrial
* Junctional
* Ventricular

Pre-excitation syndrome|

* Lown–Ganong–Levine
* Wolff–Parkinson–White

Flutter / fibrillation|

* Atrial flutter
* Ventricular flutter
* Atrial fibrillation
* Familial
* Ventricular fibrillation

Pacemaker|

* Ectopic pacemaker / Ectopic beat
* Multifocal atrial tachycardia
* Pacemaker syndrome
* Parasystole
* Wandering atrial pacemaker

Long QT syndrome|

* Andersen–Tawil
* Jervell and Lange-Nielsen
* Romano–Ward

Cardiac arrest|

* Sudden cardiac death
* Asystole
* Pulseless electrical activity
* Sinoatrial arrest

Other / ungrouped|

* hexaxial reference system
* Right axis deviation
* Left axis deviation
* QT
* Short QT syndrome
* T
* T wave alternans
* ST
* Osborn wave
* ST elevation
* ST depression
* Strain pattern

Cardiomegaly|

* Ventricular hypertrophy
* Left
* Right / Cor pulmonale
* Atrial enlargement
* Left
* Right
* Athletic heart syndrome

Other|

* Cardiac fibrosis
* Heart failure
* Diastolic heart failure
* Cardiac asthma
* Rheumatic fever

* v
* t
* e

Cardiovascular disease (vessels) (I70–I99, 440–456)

Arteries, arterioles
and capillaries|

| Inflammation|

* Arteritis
* Aortitis
* Buerger's disease

|

Peripheral artery disease|

| Arteriosclerosis|

* Atherosclerosis
* Foam cell
* Fatty streak
* Atheroma
* Intermittent claudication
* Critical limb ischemia

* Monckeberg's arteriosclerosis
* Arteriolosclerosis
* Hyaline
* Hyperplastic
* Cholesterol
* LDL
* Oxycholesterol
* Trans fat

|

Stenosis|

* Carotid artery stenosis
* Renal artery stenosis

Other|

* Aortoiliac occlusive disease
* Degos disease
* Erythromelalgia
* Fibromuscular dysplasia
* Raynaud's phenomenon

Aneurysm / dissection /
pseudoaneurysm|

* torso: Aortic aneurysm
* Abdominal aortic aneurysm
* Thoracic aortic aneurysm
* Aneurysm of sinus of Valsalva
* Aortic dissection
* Aortic rupture
* Coronary artery aneurysm
* head / neck
* Intracranial aneurysm
* Intracranial berry aneurysm
* Carotid artery dissection
* Vertebral artery dissection
* Familial aortic dissection

Vascular malformation|

* Arteriovenous fistula
* Arteriovenous malformation
* Telangiectasia
* Hereditary hemorrhagic telangiectasia

Vascular nevus|

* Cherry hemangioma
* Halo nevus
* Spider angioma

Veins|

| Inflammation|

* Phlebitis

|

Venous thrombosis /
Thrombophlebitis|

* primarily lower limb
* Deep vein thrombosis
* abdomen
* Hepatic veno-occlusive disease
* Budd–Chiari syndrome
* May–Thurner syndrome
* Portal vein thrombosis
* Renal vein thrombosis
* upper limb / torso
* Mondor's disease
* Paget–Schroetter disease
* head
* Cerebral venous sinus thrombosis
* Post-thrombotic syndrome

Varicose veins|

* Gastric varices
* Portacaval anastomosis
* Caput medusae
* Esophageal varices
* Hemorrhoid
* Varicocele

Other|

* Chronic venous insufficiency
* Chronic cerebrospinal venous insufficiency
* Superior vena cava syndrome
* Inferior vena cava syndrome
* Venous ulcer

Arteries or veins|

* Angiopathy
* Macroangiopathy
* Microangiopathy
* Embolism
* Pulmonary embolism
* Cholesterol embolism
* Paradoxical embolism
* Thrombosis
* Vasculitis

Blood pressure|

| Hypertension|

* Hypertensive heart disease
* Hypertensive emergency
* Hypertensive nephropathy
* Essential hypertension
* Secondary hypertension
* Renovascular hypertension
* Benign hypertension
* Pulmonary hypertension
* Systolic hypertension
* White coat hypertension

|

Hypotension|

* Orthostatic hypotension

* v
* t
* e

Cigarettes

Types|

* Fashion
* Fire safe
* Kretek
* Lights
* Menthol
* Beedi

Components|

* Tobacco
* Rolling paper
* Filter
* Additives

Peripherals|

* Ashtray
* Case
* Holder
* Lighter
* Pack
* Receptacles
* Vending machine

Culture|

* Cigarette card
* Cigarette smoking among college students
* Loosie
* Smoking fetishism
* Tobacco smoking

Health issues|

* Chain smoking
* Cigarette smoking for weight loss
* Nicotine poisoning
* Passive smoking
* Third-hand smoke
* Schizophrenia and smoking
* Sidestream smoke
* Smoking cessation
* Tobacco harm reduction

Related products|

* Electronic cigarette
* E-liquid
* Candy cigarette
* Herbal cigarette
* Heat-not-burn product
* Nicotine patch
* Nicotine gum
* Nicotine inhaler
* Nicotine lozenge
* Nicotine pouch

Tobacco industry|

* Cultivation of tobacco
* Egyptian cigarette industry
* History of commercial tobacco in the United States
* Tobacco advertising

Government
and the law|

* Cigarette smuggling
* Plain cigarette packaging
* Smoking age
* Smoking bans in private vehicles
* Tobacco control movement
* Tobacco Master Settlement Agreement
* Tobacco packaging warning messages
* Tobacco politics
* WHO Framework Convention on Tobacco Control
* Protocol to Eliminate Illicit Trade in Tobacco Products

Lists|

* Cigarette brands
* Cigarette smoke carcinogens
* Countries by cigarette consumption per capita
* Rolling papers
* Smoking bans

* v
* t
* e

Electronic cigarettes

General topics|

* Construction
* Usage
* Marketing
* Regulation
* Safety
* Cloud-chasing
* Composition of electronic cigarette aerosol
* Composition of heat-not-burn product emissions
* Flavored tobacco
* Heat-not-burn product
* Pod mod
* Vape shop

Brands and companies|

* Blu eCigs
* Dragonite International
* Juul
* LOGIC
* NJOY
* Openvape
* Pax Labs
* R. J. Reynolds Vapor Company
* Ten Motives
* Vuse

Controversy|

* Adverse effects of electronic cigarettes
* Vaping-associated pulmonary injury
* Effects of electronic cigarettes on human brain development
* Positions of medical organizations on electronic cigarettes
* List of vaping bans in the United States
* 2019–20 vaping lung illness outbreak
* Hospitalized cases in the vaping lung illness outbreak
* Nicotine poisoning
* Nicotine salt

Lists|

* List of electronic cigarette and e-cigarette liquid brands
* List of heat-not-burn products

* Category

* Category
* Commons

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