Risk factors contributing to PAD are the same as those for atherosclerosis:

- Smoking – tobacco use in any form is the single most important modifiable cause of PAD internationally. Smokers have up to a tenfold increase in relative risk for PAD in a dose-response relationship. Exposure to second-hand smoke from environmental exposure has also been shown to promote changes in blood vessel lining (endothelium) which is a precursor to atherosclerosis. Smokers are 2 to 3 times more likely to have lower extremity peripheral arterial disease than coronary artery disease. More than 80%-90% of patients with lower extremity peripheral arterial disease are current or former smokers. The risk of PAD increases with the number of cigarettes smoked per day and the number of years smoked.

- Diabetes mellitus – causes between two and four times increased risk of PAD by causing endothelial and smooth muscle cell dysfunction in peripheral arteries. The risk of developing lower extremity peripheral arterial disease is proportional to the severity and duration of diabetes.

- Dyslipidemia – a high level of low-density lipoprotein (LDL cholesterol) and a low level of high-density lipoprotein (HDL cholesterol) in the blood) - elevation of total cholesterol, LDL cholesterol, and triglyceride levels each have been correlated with accelerated PAD. Correction of dyslipidemia by diet and/or medication is associated with a major improvement in rates of heart attack and stroke.

- Hypertension – elevated blood pressure is correlated with an increase in the risk of developing PAD, as well as in associated coronary and cerebrovascular events (heart attack and stroke). Hypertension increased the risk of intermittent claudication 2.5- to 4-fold in men and women, respectively.

- Risk of PAD also increases in individuals who are over the age of 50, male, obese, heart attack, or stroke or with a family history of vascular disease.

- Other risk factors which are being studied include levels of various inflammatory mediators such as C-reactive protein, fibrinogen, hyperviscosity, hypercoagulable state.

Peripheral arterial disease is more common in the following populations of people:

- All people who have leg symptoms with exertion (suggestive of claudication) or ischemic rest pain.

- All people aged 65 years and over regardless of risk factor status.

- All people between the age of 50 to 69 and who have a cardiovascular risk factor (particularly diabetes or smoking).

- Age less than 50 years, with diabetes and one other atherosclerosis risk factor (smoking, dyslipidemia, hypertension, or hyperhomocysteinemia).

- Individuals with an abnormal lower extremity pulse examination.

- Those with known atherosclerotic coronary, carotid, or renal artery disease.

- All people with a Framingham risk score 10%-20%

- All people who have previously experienced chest pain

A study showed that those who quit smoking reduced their risk of being hospitalized over the next two years.

Smoking increases blood pressure, as well as increases the risk of high cholesterol. Quitting can lower blood pressure, and triglyceride levels.

Secondhand smoke is also bad for the heart health.

CTEPH is an orphan disease with an estimated incidence of 5 cases per million, but it is likely that CTEPH is under-diagnosed as symptoms are non-specific. Although a cumulative incidence of CTEPH between 0.1% and 9.1% within the first 2 years after a symptomatic PE has been reported, it is currently unclear whether acute symptomatic PE begets CTEPH. Routine screening for CTEPH after PE is not recommended because a significant number of CTEPH cases develops in the absence of previous acute symptomatic PE. In addition, approximately 25% of patients with CTEPH do not present with a clinical history of acute PE. The median age of patients at diagnosis is 63 years (there is a wide age range, but paediatric cases are rare), and both genders are equally affected.

Historically the prognosis for patients with untreated CTEPH was poor, with a 5-year survival of 40 mmHg at presentation. More contemporary data from the European CTEPH registry have demonstrated a 70% 3-year survival in patients with CTEPH who do not undergo the surgical procedure of pulmonary endarterectomy (PEA). Recent data from an international CTEPH registry demonstrate that mortality in CTEPH is associated with New York Heart Association (NYHA) functional class IV, increased right atrial pressure, and a history of cancer. Furthermore, comorbidities such as coronary disease, left heart failure, and chronic obstructive pulmonary disease (COPD) are risk factors for mortality.

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.

Coronary artery disease has a number of well determined risk factors. These include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, family history, and excessive alcohol. About half of cases are linked to genetics. Smoking and obesity are associated with about 36% and 20% of cases, respectively. Lack of exercise has been linked to 7–12% of cases. Exposure to the herbicide Agent orange may increase risk. Both rheumatoid arthritis and systemic lupus erythematosus are independent risk factors as well.

Job stress appears to play a minor role accounting for about 3% of cases.

In one study, women who were free of stress from work life saw an increase in the diameter of their blood vessels, leading to decreased progression of atherosclerosis. In contrast, women who had high levels of work-related stress experienced a decrease in the diameter of their blood vessels and significantly increased disease progression. Having a type A behavior pattern, a group of personality characteristics including time urgency, competitiveness, hostility, and impatience is linked to an increased risk of coronary disease.

Diet is a very important factor in getting coronary ischemia or coronary artery disease and preventing it.

A heart healthy diet is low in saturated fat and cholesterol and high in complex carbohydrates.

Complex carbohydrates include fruits, vegetables, and whole grains. These food choices can reduce the risk of a heart attack or any other congestive heart failure event.

A heart healthy diet also includes low sodium intake and a higher potassium intake. A low potassium intake raises blood pressure, as does a diet high in sodium.

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.

Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. Some of these risk factors are related to inflammation. "Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wall injury, and altered blood coagulation. Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis.

Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed. Saturated fat is still a concern.

Coronary thrombosis is the formation of a blood clot inside a blood vessel of the heart. This blood clot restricts blood flow within the heart. It is associated with narrowing of blood vessels subsequent to clotting. The condition is considered as a type of ischaemic heart disease, also known as a heart attack or myocardial infarction.

Thrombosis in the heart can lead to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes used as synonyms, although this is technically inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart contains many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms. Coronary thrombosis is caused by atherosclerosis.This is when there is build up of cholesterol and fats in the artery walls. So the blood will clot because there isn't enough room for it to flow. The main causes of coronary thrombosis are stress, smoking, high blood pressure, and lack of exercise. Symptoms are sharp pains around the chest area, breathing difficulties, dizziness, and fainting. This is treated by taking Aspirin, Nitrates, or Beta Blockers.

Coronary thrombosis can be a complication associated with drug-eluting stents.

The relation between dietary fat and atherosclerosis is controversial. Writing in "Science", Gary Taubes detailed that political considerations played into the recommendations of government bodies. The USDA, in its food pyramid, promotes a diet of about 64% carbohydrates from total calories. The American Heart Association, the American Diabetes Association and the National Cholesterol Education Program make similar recommendations. In contrast, Prof Walter Willett (Harvard School of Public Health, PI of the second Nurses' Health Study) recommends much higher levels of fat, especially of monounsaturated and polyunsaturated fat. These differing views reach a consensus, though, against consumption of trans fats.

The role of dietary oxidized fats/lipid peroxidation (rancid fats) in humans is not clear.

Laboratory animals fed rancid fats develop atherosclerosis. Rats fed DHA-containing oils experienced marked disruptions to their antioxidant systems, and accumulated significant amounts of phospholipid hydroperoxide in their blood, livers and kidneys.

Rabbits fed atherogenic diets containing various oils were found to undergo the greatest amount of oxidative susceptibility of LDL via polyunsaturated oils. In another study, rabbits fed heated soybean oil "grossly induced atherosclerosis and marked liver damage were histologically and clinically demonstrated." However, Fred Kummerow claims that it is not dietary cholesterol, but oxysterols, or oxidized cholesterols, from fried foods and smoking, that are the culprit.

Rancid fats and oils taste very bad even in small amounts, so people avoid eating them.

It is very difficult to measure or estimate the actual human consumption of these substances. Highly unsaturated omega-3 rich oils such as fish oil are being sold in pill form so that the taste of oxidized or rancid fat is not apparent. The health food industry's dietary supplements are self regulated and outside of FDA regulations. To properly protect unsaturated fats from oxidation, it is best to keep them cool and in oxygen free environments.

In 2011, coronary atherosclerosis was one of the top ten most expensive conditions seen during inpatient hospitalizations in the U.S., with aggregate inpatient hospital costs of $10.4 billion.

The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow.

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

Patients can lower their risk for vulnerable plaque rupture in the same ways that they can cut their heart attack risk: Optimize lipoprotein patterns, keep blood glucose levels low normal (see HbA1c), stay slender, eat a proper diet, quit smoking, and maintain a regular exercise program. Researchers also think that obesity and diabetes may be tied to high levels of C-reactive protein.

Trauma to the lung can also cause an air embolism. This may happen after a patient is placed on a ventilator and air is forced into an injured vein or artery, causing sudden death. Breath-holding while ascending from scuba diving may also force lung air into pulmonary arteries or veins in a similar manner, due to the pressure difference.

It is associated with dipyridamole. Hence, dipyridamole is a pharmacological success diagnostically, but a therapeutic failure because of the coronary steal phenomenon.

Coronary steal is also the mechanism in most drug-based cardiac stress tests; When a patient is incapable of doing physical activity they are given a vasodilator that produces a "cardiac steal syndrome" as a diagnostic procedure. The test result is positive if the patient's symptoms reappear or if ECG alterations are seen.

It is also associated with the administration of Isoflurane, which is an inhaled anesthetic. Hydralazine can potentially cause this condition as well, as it is a direct arteriolar vasodilator.

It has been associated with nitroprusside.

Air can be injected directly into a vein or artery accidentally during clinical procedures. Misuse of a syringe to meticulously remove air from the vascular tubing of a hemodialysis circuit can allow air into the vascular system. Venous air embolism is a rare complication of diagnostic and therapeutic procedures requiring catheterization of a vein or artery. If a significant embolism occurs, the cardiovascular, pulmonary, or central nervous system may be affected. Interventions to remove or mitigate the embolism may include procedures to reduce bubble size, or withdrawal of air from the right atrium.

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.

Newer clinical trial results (2007), e.g. the COURAGE trial, have demonstrated that aggressively treating some of the physiologic behavioral factors that promote atheromas with "optimal medical therapy" (not opening narrowing(s), a.k.a. stenoses, per se) produced the most effective results in terms of improving human survival and quality of life for those identified as having already developed advanced cardiovascular disease with many vulnerable plaques.

Routine counselling of adults to advise them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended.

- Conditions that exacerbate or provoke angina:

One study found that smokers with coronary artery disease had a significantly increased level of sympathetic nerve activity when compared to those without. This is in addition to increases in blood pressure, heart rate, and peripheral vascular resistance associated with nicotine, which may lead to recurrent angina attacks. In addition, the Centers for Disease Control and Prevention (CDC) reports that the risk of CHD (Coronary heart disease), stroke, and PVD (Peripheral vascular disease) is reduced within 1–2 years of smoking cessation. In another study, it was found that, after one year, the prevalence of angina in smoking men under 60 after an initial attack was 40% less in those having quit smoking compared to those that continued. Studies have found that there are short-term and long-term benefits to smoking cessation.

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.

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.