There are various risk assessment systems for determining the risk of coronary artery disease, with various emphasis on 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.

A coronary angiography is performed only after a stress test or ECG shows a sign of coronary ischemia or CAD. This test is very important in finding where the blockages are in the arteries.

This test helps determine if an angioplasty or bypass surgery is needed.

During this test the doctor makes a small incision in the patient's groin (femoral) or wrist (radial) and inserts a catheter. The catheter has a very small video camera on the end of it so that the doctor can find the arteries.

Once he has found the arteries, he injects a dye in them so that he/she can detect any blockages in the arteries. The dye is able to be seen on a special x-ray machine.

The test takes one to two hours.

A stress test, is just that, a test to put stress on the heart through exercise. A doctor will put a patient through a series of exercises to measure the tolerance for stress on the heart. This test uses an ECG to detect the electrical impulses of the heart during physical exertion.

During this test a patient is put on a treadmill or a stationary bike. The incline or resistance of the bike are steadily increased until the patient reaches the target heart rate for the patient's age and weight.

An exercise stress test is not always accurate in determining if one has a blockage in the arteries. Women and those who are young may show abnormalities on their test even though no signs of coronary ischemia or CAD are present.

In "stable" angina, chest pain with typical features occurring at predictable levels of exertion, 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.

Stable coronary artery disease (SCAD) is also often called stable ischemic heart disease (SIHD). A 2015 monograph explains that "Regardless of the nomenclature, stable angina is the chief manifestation of SIHD or SCAD." There are U.S. and European clinical practice guidelines for SIHD/SCAD.

Although Prinzmetal's angina has been documented in between 2% to 10% of angina patients, it can be overlooked by cardiologists who stop testing protocol after ruling out typical angina. Rarely, an ECG can capture diffuse ST elevations.

Patients who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome", and are generally tested for cardiac enzymes such as creatine kinase isoenzymes or troponin I or T. These may or may not show a degree of positivity, as coronary spasm too can cause myocardial damage or may leave the arteries undamaged. Echocardiography or thallium scintigraphy is often performed.

The gold standard is coronary angiography with injection of provocative agents into the coronary artery. Rarely, an active spasm can be documented angiographically (e.g. if the patient receives an angiogram with intent of performing a primary coronary intervention with angioplasty). Depending on the local protocol, provocation testing may involve substances such as ergonovine, methylergonovine or acetylcholine and hyperventilation. Exaggerated spasm is diagnostic of Prinzmetal angina.

One of the most important features differentiating ischemic cardiomyopathy from the other forms of cardiomyopathy is the shortened, or worsened all-cause mortality in patients with ischemic cardiomyopathy. According to several studies, coronary artery bypass graft surgery has a survival advantage over medical therapy (for ischemic cardiomyopathy) across varied follow-ups.

To discover the extent and severity of coronary artery ectasia there are a variety of diagnostic tools used. The most common method for discovering the disease is through angiography. Angiography is the procedure where a contrast dye is entered into the vessels and an x-ray is taken, which will allow the vessels to be seen on the x-ray. Using angiography clinicians are able to display the size, location and number of vessels affected by the disease. Is can also be analyzed through other methods such as intravascular ultrasound, and magnetic resonance imaging. Using these diagnostic methods, it has been discovered that the disease normally occurs most often in the right coronary artery, followed by the left anterior descending artery, and finally the left anterior circumflex artery. Using these methods Coronary artery ectasia can be divided into four different types: Type 1¬→diffuse ectasia in 2-3 different vessels, Type 2¬→ diffuse disease in 1 vessel and local disease in another, Type 3¬→ diffuse disease in one vessel and Type 4¬→ localized or segmental ectasia.

Ischemic cardiomyopathy can be diagnosed via magnetic resonance imaging (MRI) protocol, imaging both global and regional function. Also the Look-Locker technique is used to identify diffuse fibrosis; it is therefore important to be able to determine the extent of the ischemic scar. Some argue that only left main- or proximal-left anterior descending artery disease is relevant to the diagnostic criteria for ischemic cardiomyopathy. Myocardial imaging usually demonstrates left ventricular dilation, severe ventricular dysfunction, and multiple infarctions. Signs include congestive heart failure, angina edema, weight gain and fainting, among others.

Areas of severe narrowing, stenosis, detectable by angiography, and to a lesser extent "stress testing" have long been the focus of human diagnostic techniques for cardiovascular disease, in general. However, these methods focus on detecting only severe narrowing, not the underlying atherosclerosis disease. As demonstrated by human clinical studies, most severe events occur in locations with heavy plaque, yet little or no lumen narrowing present before debilitating events suddenly occur. Plaque rupture can lead to artery lumen occlusion within seconds to minutes, and potential permanent debility and sometimes sudden death.

Plaques that have ruptured are called complicated plaques. The extracellular matrix of the lesion breaks, usually at the shoulder of the fibrous cap that separates the lesion from the arterial lumen, where the exposed thrombogenic components of the plaque, mainly collagen will trigger thrombus formation. The thrombus then travels downstream to other blood vessels, where the blood clot may partially or completely block blood flow. If the blood flow is completely blocked, cell deaths occur due to the lack of oxygen supply to nearby cells, resulting in necrosis. The narrowing or obstruction of blood flow can occur in any artery within the body. Obstruction of arteries supplying the heart muscle results in a heart attack, while the obstruction of arteries supplying the brain results in a stroke.

Lumen stenosis that is greater than 75% was considered the hallmark of clinically significant disease in the past because recurring episodes of angina and abnormalities in stress tests are only detectable at that particular severity of stenosis.

However, clinical trials have shown that only about 14% of clinically debilitating events occur at sites with more than 75% stenosis. The majority of cardiovascular events that involve sudden rupture of the atheroma plaque do not display any evident narrowing of the lumen.

Thus, greater attention has been focused on "vulnerable plaque" from the late 1990s onwards.

Besides the traditional diagnostic methods such as angiography and stress-testing, other detection techniques have been developed in the past decades for earlier detection of atherosclerotic disease. Some of the detection approaches include anatomical detection and physiologic measurement.

Examples of anatomical detection methods include coronary calcium scoring by CT, carotid IMT (intimal media thickness) measurement by ultrasound, and intravascular ultrasound (IVUS). Examples of physiologic measurement methods include lipoprotein subclass analysis, HbA1c, hs-CRP, and homocysteine.

Both anatomic and physiologic methods allow early detection before symptoms show up, disease staging and tracking of disease progression. Anatomic methods are more expensive and some of them are invasive in nature, such as IVUS. On the other hand, physiologic methods are often less expensive and safer. But they do not quantify the current state of the disease or directly track progression. In recent years, developments in nuclear imaging techniques such as PET and SPECT have provided ways of estimating the severity of atherosclerotic plaques.

Diabetics, despite not having clinically detectable atherosclerotic disease, have more severe debility from atherosclerotic events over time than non-diabetics who have already had atherosclerotic events. Thus diabetes has been upgraded to be viewed as an advanced atherosclerotic disease equivalent.

The treatment of coronary artery ectasia is normally done in conjunction with therapies of other heart disorders such as atherosclerosis and hypertension. To prevent the formation of blood clots and the blockage of the vessels, patients are commonly placed on anticoagulant therapy (e.g. warfarin, and aspirin), as well as anti-spasm therapy of calcium channel blockers. Coronary artery ectasia also responds to statins and ACE inhibitors.

Prinzmetal's angina typically responds to nitrates and calcium channel blockers.

Use of a beta blocker such as propranolol is contraindicated in Prinzmetal's angina. Prazosin has also been found to be of value in some patients. Coronary revascularization is only useful when the patient shows concomitant coronary atherosclerosis on coronary angiogram.

Hospital admission for people with the following symptoms is recommended, as they may have unstable angina: pain at rest (which may occur at night), pain on minimal exertion, angina that seems to progress rapidly despite increasing medical treatment. All people with suspected angina should be urgently referred to a chest pain evaluation service, for confirmation of the diagnosis and assessment of the severity of coronary heart disease.

Angina should be suspected in people presenting tight, dull, or heavy chest discomfort that is:

1. Retrosternal or left-sided, radiating to the left arm, neck, jaw, or back.

2. Associated with exertion or emotional stress and relieved within several minutes by rest.

3. Precipitated by cold weather or a meal.

Some people present with atypical symptoms, including breathlessness, nausea, or epigastric discomfort or burning. These atypical symptoms are particularly likely in older people, women, and those with diabetes.

Anginal pain is not usually sharp or stabbing or influenced by respiration. Antacids and simple analgesics do not usually relieve the pain. If chest discomfort (of whatever site) is precipitated by exertion, relieved by rest, and relieved by glyceryl trinitrate, the likelihood of angina is increased.

In angina patients momentarily not feeling any chest pain, an electrocardiogram (ECG) is typically normal unless there have been other cardiac problems in the past. During periods of pain, depression, or elevation of the ST segment may be observed. To elicit these changes, an exercise ECG test ("treadmill test") may be performed, during which the patient exercises to his/her maximum ability before fatigue, breathlessness, or pain intervenes; if characteristic ECG changes are documented (typically more than 1 mm of flat or downsloping ST depression), the test is considered diagnostic for angina. Even constant monitoring of the blood pressure and the pulse rate can lead to some conclusion regarding angina. The exercise test is also useful in looking for other markers of myocardial ischemia: blood pressure response (or lack thereof, in particular, a drop in systolic blood pressure), dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram or sestamibi scintigram (in patients unable to exercise enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis or in whom the ECG is too abnormal at rest) or Stress Echocardiography.

In patients in whom such noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft (CABG), treatment only with medication, or other treatments. In hospitalized patients with unstable angina (or the newer term of "high-risk acute coronary syndromes"), those with resting ischaemic ECG changes or those with raised cardiac enzymes such as troponin may undergo coronary angiography directly.

The gold standard for measuring endothelial function is angiography with acetylcholine injection. Previously, this was not done outside of research because of the invasive and complex nature of the procedure. As mentioned above, the use of acetylcholine injections to test vasodilation is now safely used for procedures where arterial catheterization is employed (this method is less frequently used though, so overall acetylcholine is not used very often in this way).

A noninvasive method to measure endothelial dysfunction is % Flow Mediated Dilation (FMD) as measured by Brachial Artery Ultrasound Imaging (BAUI). Current measurements of endothelial function via FMD vary due to technical and physiological factors. For example, FMD is largely affected by hormones, especially for women. FMD values can differ for the same woman if she is in different phases of her menstrual cycle during the time of measurement. When using this technique on people who suffer from things like heart failure, renal failure, or hypertension, their increased sympathetic tone can often falsify the results. Furthermore, a negative correlation between percent flow mediated dilation and baseline artery size is recognised as a fundamental scaling problem, leading to biased estimates of endothelial function. For research on FMD an ANCOVA approach to adjusting FMD for variation in baseline diameter is more appropriate. Another challenge of FMD is variability across centers and the requirement of highly qualified technicians to perform the procedure.

A non-invasive, FDA-approved device for measuring endothelial function that works by measuring Reactive Hyperemia Index (RHI) is Itamar Medical's EndoPAT™. It has shown an 80% sensitivity and 86% specificity to diagnose coronary artery disease when compared against the gold standard, acetylcholine angiogram. This results suggests that this peripheral test reflects the physiology of the coronary endothelium. Endopat has been tested in several clinical trials at multiple centers (including major cohort studies such as the Framingham Heart Study, the Heart SCORE study, and the Gutenberg Health Study). The results from clinical trials have shown that EndoPAT™ is useful for risk evaluation, stratification and prognosis of getting major cardiovascular events (MACE).

Since NO maintains low tone and high compliance of the small arteries at rest a reduction of age-dependent small artery compliance is a marker for endothelial dysfunction that is associated with both functional and structural changes in the microcirculation that are predictive of subsequent morbid events Small artery compliance or stiffness can be assessed simply and at rest and can be distinguished from large artery stiffness by use of pulsewave analysis with the CV Profilor.

Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk. This includes those who are young without risk factors. In those at higher risk the evidence for screening with ECGs is inconclusive.

Additionally echocardiography, myocardial perfusion imaging, and cardiac stress testing is not recommended in those at low risk who do not have symptoms.

Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the clinical value of some biomarkers is questionable.

The NIH recommends lipid testing in children beginning at the age of 2 if there is a family history of heart disease or lipid problems. It is hoped that early testing will improve lifestyle factors in those at risk such as diet and exercise.

Screening and selection for primary prevention interventions has traditionally been done through absolute risk using a variety of scores (ex. Framingham or Reynolds risk scores). This stratification has separated people who receive the lifestyle interventions (generally lower and intermediate risk) from the medication (higher risk). The number and variety of risk scores available for use has multiplied, but their efficacy according to a 2016 review was unclear due to lack of external validation or impact analysis. Risk stratification models often lack sensitivity for population groups and do not account for the large number of negative events among the intermediate and low risk groups. As a result, future preventative screening appears to shift toward applying prevention according to randomized trial results of each intervention rather than large-scale risk assessment.

In order to treat acute limb ischaemia there are a series of things that can be done to determine where the occlusion is located, the severity, and what the cause was. To find out where the occlusion is located one of the things that can be done is simply a pulse examination to see where the heart rate can be detected and where it stops being sensed. Also there is a lower body temperature below the occlusion as well as paleness. A Doppler evaluation is used to show the extent and severity of the ischaemia by showing flow in smaller arteries. Other diagnostical tools are duplex ultrasonography, computed tomography angiography (CTA), and magnetic resonance angiography (MRA). The CTA and MRA are used most often because the duplex ultrasonography although non-invasive is not precise in planning revascularization. CTA uses radiation and may not pick up on vessels for revascularization that are distal to the occlusion, but it is much quicker than MRA. In treating acute limb ischaemia time is everything.

In the worst cases acute limb ischaemia progresses to critical limb ischaemia, and results in death or limb loss. Early detection and steps towards fixing the problem with limb-sparing techniques can salvage the limb. Compartment syndrome can occur because of acute limb ischaemia because of the biotoxins that accumulate distal to the occlusion resulting in edema.

A selective coronary angiogram is the most common method to diagnose the condition, although it is sometimes not recognised until after death. Intravascular ultrasound (IVUS) is also used as it is able to more easily differentiate the condition from atherosclerotic disease.

A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body.

While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.

Treatment is varied depending upon the nature of the case. In severe cases, coronary artery bypass surgery is performed to redirect blood flow around the affected area. Drug-eluting stents and thrombolytic drug therapy are less invasive options for less severe cases.

The use of heparin following surgery is common if there are no issues with bleeding. Generally, a risk-benefit analysis is required, as all anticoagulants lead to an increased risk of bleeding. In people admitted to hospital, thrombosis is a major cause for complications and occasionally death. In the UK, for instance, the Parliamentary Health Select Committee heard in 2005 that the annual rate of death due to thrombosis was 25,000, with at least 50% of these being hospital-acquired. Hence "thromboprophylaxis" (prevention of thrombosis) is increasingly emphasized. In patients admitted for surgery, graded compression stockings are widely used, and in severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend low molecular weight heparin (LMWH) administration, mechanical calf compression or (if all else is contraindicated and the patient has recently suffered deep vein thrombosis) the insertion of a vena cava filter. In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis, and in the United Kingdom the Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines.

Surgery for symptomatic myocardial bridge of the LAD may include myotomy, coronary artery bypass surgery, or both.

Procedure selection is based on the size of the underlying artery during diastole, the presence of concomitant proximal coronary artery disease, and the presence of anatomic factors that would increase the risk of myotomy. Surgical strategy for the management should be customized, and the treatment

of choice is myotomy but bypass surgery can be added

when there is proximal coronary obstruction or anatomic

anomalies that increase the risk of recurrence of the

obstruction.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

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

The major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.