Chest pain is a major indication of coronary ischemia. If chest pain occurs while exercising, or during sex, but it doesn't persist after rest, it may be coronary ischemia, or what is called, "angina". Some people characterize the pain they feel as though an elephant is sitting on their chest.

Other typical symptoms include diaphoresis which is sweaty palms, and clammy skin, nausea or vomiting, or shortness of breath. Chest pain radiating down the left arm is also a symptom of coronary ischemia and the pain can also be radiating directly to the back in some instances.

The symptoms of coronary ischemia can last for a short period of time. The other symptoms that last for a longer period of time may suggest a myocardial infarction.

Symptoms of coronary ischemia can be classified as typical or atypical.

Signs and symptoms of ischemic cardiomyopathy include sudden fatigue, shortness of breath, dizziness and palpitations.

Prinzmetal's or Prinzmetal angina (, sounds like "prints metal") (also known as variant angina, vasospastic angina (VSA), angina inversa, or coronary vessel spasm) is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in cycles. It is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than directly by atherosclerosis (buildup of fatty plaque and hardening of the arteries).

For a portion of patients Prinzmetal's angina may be a manifestation of vasospastic disorder and is associated with migraine, Raynaud's phenomenon or aspirin-induced asthma.

In contrast to patient with unstable angina secondary to coronary atherosclerosis, patients with variant angina are generally younger and have fewer coronary risk factors (except smoking). Episode of chest pain usually does not progress from a period of chronic stable angina. Cardiac examination is usually normal in the absence of ischemia.

Symptoms typically occur at rest, rather than on exertion (thus attacks usually occur in early morning hours). Two-thirds of patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of symptoms.

Prinzmetal's should be suspected by a cardiologist when the pain occurs at rest and/or in clusters, and in the absence of a positive treadmill stress test, as Prinzmetal's is exercise tolerant and can generally only be diagnosed after other forms of cardiac disease have been ruled out.

It is associated with specific ECG changes (elevation rather than depression of the ST segment) together with small elevation of cardiac enzymes (especially with long attacks). However, in order to be diagnosed, these ECG changes can only be tracked when the electrocardiogram occurs while the patient is experiencing an attack. Therefore, many experts recommend provocative testing during electrocardiogram testing to attempt to induce an attack when Prinzmetal's is suspected.

Coronary steal (with its symptoms termed coronary steal syndrome or cardiac steal syndrome) is a phenomenon where an alteration of circulation patterns leads to a reduction in the blood directed to the coronary circulation. It is caused when there is narrowing of the coronary arteries and a coronary vasodilator is used – "stealing" blood away from those parts of the heart. This happens as a result of the narrowed coronary arteries being always maximally dilated to compensate for the decreased upstream blood supply. Thus, dilating the resistance vessels in the coronary circulation causes blood to be shunted away from the coronary vessels supplying the ischemic zones, creating more ischemia.

The pathophysiology of unstable angina is controversial. Until recently, unstable angina was assumed to be angina pectoris caused by disruption of an atherosclerotic plaque with partial thrombosis and possibly embolization or vasospasm leading to myocardial ischemia. However, sensitive troponin assays reveal rise of cardiac troponin in the bloodstream with episodes of even mild myocardial ischemia. Since unstable angina is assumed to occur in the setting of acute myocardial ischemia without troponin release, the concept of unstable angina is being questioned with some calling for retiring the term altogether.

Unstable angina (UA) is a type of angina pectoris that is irregular. It is also classified as a type of acute coronary syndrome (ACS).

It can be difficult to distinguish unstable angina from non-ST elevation (non-Q wave) myocardial infarction (NSTEMI). They differ primarily in whether the ischemia is severe enough to cause sufficient damage to the heart's muscular cells to release detectable quantities of a marker of injury (typically troponin T or troponin I). Unstable angina is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponin, with or without ECG changes indicative of ischemia (e.g., ST segment depression or transient elevation or new T wave inversion). Since an elevation in troponin may not be detectable for up to 12 hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation.

The symptoms are often very similar to those of myocardial infarction (heart attack), with the most common being persistent chest pain.

Also known as 'effort angina', this refers to the classic type of angina related to myocardial ischemia. A typical presentation of stable angina is that of chest discomfort and associated symptoms precipitated by some activity (running, walking, etc.) with minimal or non-existent symptoms at rest or after administration of sublingual nitroglycerin. Symptoms typically abate several minutes after activity and recur when activity resumes. In this way, stable angina may be thought of as being similar to intermittent claudication symptoms. Other recognized precipitants of stable angina include cold weather, heavy meals, and emotional stress.

Ischemic cardiomyopathy is a type of cardiomyopathy caused by a narrowing of the coronary arteries which supply blood to the heart. Typically, patients with ischemic cardiomyopathy have a history of acute myocardial infarction, however, it may occur in patients with coronary artery disease, but without a past history of acute myocardial infarction. This cardiomyopathy is one of the leading causes of sudden cardiac death.

Up to 50% of people with PAD may have no symptoms. Symptoms of PAD in the legs and feet are generally divided into 2 categories:

1. Intermittent claudication—pain in muscles when walking or using the affected muscles that is relieved by resting those muscles. This is due to the unmet oxygen demand in muscles with use in the setting of inadequate blood flow.

2. Critical limb ischemia, consisting of:

Medical signs of PAD in the legs, due to inadequate perfusion, include:

- Noticeable change in color – blueness, or in temperature (coolness) when compared to the other limb.

- Buerger's test can check for pallor on elevation of limb and redness (rubor) on a change to a sitting position, in an assessment of arterial sufficiency.

- Diminished hair and nail growth on affected limb and digits

PAD in other parts of the body depends on the organ affected. Renal artery stenosis can cause renovascular hypertension.

Carotid artery disease can cause strokes and transient ischemic attacks.

Unstable angina (UA) (also ""crescendo angina""; this is a form of acute coronary syndrome) is defined as angina pectoris that changes or worsens.

It has at least one of these three features:

1. it occurs at rest (or with minimal exertion), usually lasting more than 10 minutes

2. it is severe and of new onset (i.e., within the prior 4–6 weeks)

3. it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than before).

UA may occur unpredictably at rest, which may be a serious indicator of an impending heart attack. What differentiates stable angina from unstable angina (other than symptoms) is the pathophysiology of the atherosclerosis. The pathophysiology of unstable angina is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms, or coronary thrombosis. The process starts with atherosclerosis, progresses through inflammation to yield an active unstable plaque, which undergoes thrombosis and results in acute myocardial ischemia, which, if not reversed, results in cell necrosis (infarction). Studies show that 64% of all unstable anginas occur between 22:00 and 08:00 when patients are at rest.

In stable angina, the developing atheroma is protected with a fibrous cap. This cap may rupture in unstable angina, allowing blood clots to precipitate and further decrease the area of the coronary vessel's lumen. This explains why, in many cases, unstable angina develops independently of activity.

Chest pain that occurs regularly with activity, after eating, or at other predictable times is termed stable angina and is associated with narrowings of the arteries of the heart.

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.

Coronary arteriovenous fistula between coronary artery and another cardiac chamber, like, the coronary sinus, right atrium, or right ventricle may cause steal syndrome under conditions like myocardial infarction and possible angina or ventricular arrhythmias, if the shunt is large in magnitude.

It can also be associated with new patterns of blood vessel growth.

Acquired causes include atherosclerosis, Kawasaki disease and coronary catheterization.

It can also be congenital.

For most people, the first symptoms result from atheroma progression within the heart arteries, most commonly resulting in a heart attack and ensuing debility. However, the heart arteries, because (a) they are small (from about 5 mm down to microscopic), (b) they are hidden deep within the chest and (c) they never stop moving, have been a difficult target organ to track, especially clinically in individuals who are still asymptomatic. Additionally, all mass-applied clinical strategies focus on both (a) minimal cost and (b) the overall safety of the procedure. Therefore, existing diagnostic strategies for detecting atheroma and tracking response to treatment have been extremely limited. The methods most commonly relied upon, patient symptoms and cardiac stress testing, do not detect any symptoms of the problem until atheromatous disease is very advanced because arteries enlarge, not constrict in response to increasing atheroma. It is plaque ruptures, producing debris and clots which obstruct blood flow downstream, sometimes also locally (as seen on angiograms), which reduce/stop blood flow. Yet these events occur suddenly and are not revealed in advance by either stress testing, stress tests or angiograms.

Subclavian steal syndrome (SSS), also called subclavian steal phenomenon or subclavian steal steno-occlusive disease, is a constellation of signs and symptoms that arise from retrograde (reversed) blood flow in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. The arm may be supplied by blood flowing in a retrograde direction down the vertebral artery at the expense of the vertebrobasilar circulation. This is called the "subclavian steal". It is more severe than typical vertebrobasilar insufficiency.

Coronary artery ectasia is a rare disease that occurs in only 0.3-4.9% of people in North America. Coronary artery ectasia is characterized by the enlargement of a coronary artery to 1.5 times or more than its normal diameter. The disease is commonly asymptomatic and is normally discovered when performing tests for other conditions such as coronary artery disease, stable angina and other acute coronary syndromes. Coronary artery ectasia occurs 4 times more frequently in males than in females and in people who have risk factors for heart disease such as smokers. While the disease is commonly found in patients with atherosclerosis and coronary artery disease, it can occur by itself and in both cases it can cause health problems. The disease can cause the heart tissue to be deprived of blood and die due to decreased blood flow, and blockages due to blood clots or spasms of the blood vessel. This blood flow disruption can cause permanent damage to the muscle if the deprivation is prolonged. Coronary artery ectasia also increases the chance of developing large weak spots in the affected coronary arteries, or aneurysms that can rupture and result in death. The damage can result in angina which is pain in the chest and is a common complaint in these patients.

Generally, it has a good prognosis. In Kawasaki's disease, untreated, there is a 1–2% death rate, from cardiac causes.

Coronary artery disease (CAD), also known as ischemic heart disease (IHD), refers to a group of diseases which includes stable angina, unstable angina, myocardial infarction, and sudden cardiac death. It is within the group of cardiovascular diseases of which it is the most common type. A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. Occasionally it may feel like heartburn. Usually symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest. Shortness of breath may also occur and sometimes no symptoms are present. Occasionally, the first sign is a heart attack. Other complications include heart failure or an abnormal heartbeat.

Risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, and excessive alcohol. The underlying mechanism involves reduction of blood flow and oxygen to the heart muscle due to atherosclerosis of the arteries of the heart. A number of tests may help with diagnoses including: electrocardiogram, cardiac stress testing, coronary computed tomographic angiography, and coronary angiogram, among others.

Ways to reduce CAD risk include eating a healthy diet, regularly exercising, maintaining a healthy weight, and not smoking. Medications for diabetes, high cholesterol, or high blood pressure are sometimes used. There is limited evidence for screening people who are at low risk and do not have symptoms. Treatment involves the same measures as prevention. Additional medications such as antiplatelets (including aspirin), beta blockers, or nitroglycerin may be recommended. Procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG) may be used in severe disease. 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.

In 2015 CAD affected 110 million people and resulted in 8.9 million deaths. It makes up 15.9% of all deaths making it the most common cause of death globally. The risk of death from CAD for a given age has decreased between 1980 and 2010, especially in developed countries. The number of cases of CAD for a given age has also decreased between 1990 and 2010. 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. Rates are higher among men than women of a given age.

The healthy epicardial coronary artery consists of three layers, the intima, media, and adventitia. Atheroma and changes in the artery wall usually result in small aneurysms (enlargements) just large enough to compensate for the extra wall thickness with no change in the lumen diameter. However, eventually, typically as a result of rupture of vulnerable plaques and clots within the lumen over the plaque, stenosis (narrowing) of the vessel develops in some areas. Less frequently, the artery enlarges so much that a gross aneurysmal enlargement of the artery results. All three results are often observed, at different locations, within the same individual.

This condition can cause complications such as vasospasm, angina pectoris, arrhythmia, ventricular tachycardia. Additionally many patients express discomfort in specific positions, (i.e. lying on the left side for a prolonged period of time).

A spontaneous coronary artery dissection (SCAD) (occasionally coronary artery dissection) is a rare, sometimes fatal traumatic condition, with eighty percent of cases affecting women. One of the coronary arteries develops a tear, causing blood to flow between the layers which forces them apart. Studies of the disease place the mortality rate at around 70%.

SCAD is a primary cause of myocardial infarction (MI) in young, fit, healthy women (and some men) with no obvious risk factors. These can often occur during late pregnancy, postpartum and peri-menopausal periods.

In cardiology, stunned myocardium is a state when some section of the myocardium (corresponding to area of a major coronary occlusion) shows a form of contractile abnormality. This is a segmental dysfunction which persists for a variable period of time, about two weeks, even after ischemia has been relieved (by for instance angioplasty or coronary artery bypass surgery). In this situation, while myocardial blood flow (MBF) returns to normal, function is still depressed for a variable period of time.

Myocardial stunning is the reversible reduction of function of heart contraction after reperfusion not accounted for by tissue damage or reduced blood flow.

After total ischemia occurs, the myocardium switches immediately from aerobic glycolysis to anaerobic glycolysis resulting in the reduced ability to produce high energy phosphates such as ATP and Creatinine Phosphate. At this point, the lack of the energy and lactate accumulation results in cessation of contraction within 60 seconds of ischemia (i.e. Vessel Occlusion). Subsequent to this is a period of "myocardial stunning," in which reversible ischemic damage is taking place. At approximately 30 minutes after the onset of total ischemia the damage becomes irreversible, thereby ending the phase of myocardial stunning.

Clinical situations of stunned myocardium are:

- acute myocardial infarction (AMI)

- after percutaneous transluminal coronary angioplasty (PTCA)

- after cardiac surgery

- 'neurogenic' stunned myocardium following an acute cerebrovascular event such as a subarachnoid hemorrhage