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.

By increasing physical activity, it is possible to manage body weight, reduce blood pressure, and relieve stress.

The Center for Disease Control recommends 30 minutes of physical activity a day.

Instead of 30 minutes a day at one time, short bursts of physical activity for 8–10 minutes three times a day are also suitable. Exercising this way can reduce the risk of getting heart disease or coronary ischemia, if it is performed at moderate intensity.

Secondary prevention is preventing further sequelae of already established disease. Lifestyle changes that have been shown to be effective to this goal include:

- Weight control

- Smoking cessation

- Avoiding the consumption of trans fats (in partially hydrogenated oils)

- Decrease psychosocial stress.

- Exercise. Aerobic exercise, like walking, jogging, or swimming, can reduce the risk of mortality from coronary artery disease. Aerobic exercise can help decrease blood pressure and the amount of blood cholesterol (LDL) over time. It also increases HDL cholesterol which is considered as "good cholesterol". Separate to the question of the benefits of exercise; 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", it only examined the effectiveness of the counseling itself. The American Heart Association, based on a non-systematic review, recommends that doctors counsel patients on exercise.

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

- Lifestyle changes

- Medical treatment – 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)

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.

Nitroglycerin can be used immediately to widen the coronary arteries and help increase blood flow to the heart. In addition, nitroglycerin causes peripheral venous and artery dilation reducing cardiac preload and afterload. These reductions allow for decreased stress on the heart and therefore lower the oxygen demand of the heart's muscle cells.

Antiplatelet drugs such as aspirin and clopidogrel can help reduce the progression of atherosclerotic plaque formation, as well as combining these with an anticoagulant such as a low molecular weight heparin.

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.

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.

Changes in diet may help prevent the development of atherosclerosis. Tentative evidence suggests that a diet containing dairy products has no effect on or decreases the risk of cardiovascular disease.

A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death. Evidence suggests that the Mediterranean diet may improve cardiovascular results. There is also evidence that a Mediterranean diet may be better than a low-fat diet in bringing about long-term changes to cardiovascular risk factors (e.g., lower cholesterol level and blood pressure).

Restoring adequate blood flow to the heart muscle in people with heart failure and significant coronary artery disease is strongly associated with improved survival, some research showing up to 75% survival rates over 5 years. A stem cell study indicated that using autologous cardiac stem cells as a regenerative approach for the human heart (after a heart attack) has great potential.

American Heart Association practice guidelines indicate (ICD) implantable cardioverter-defibrillator use in those with ischemic cardiomyopathy (40 days post-MI) that are (NYHA) New York Heart Association functional class I. LVEF of >30% is often used to differentiate primary from ischemic cardiomyopathy, and a prognostic indicator. At the same time, people who undergo ventricular restoration on top of coronary artery bypass show improved postoperative ejection fraction as compared to those treated with only coronary artery bypass surgery. Severe cases are treated with heart transplantation.

Many approaches have been promoted as methods to reduce or reverse atheroma progression:

- eating a diet of raw fruits, vegetables, nuts, beans, berries, and grains;

- consuming foods containing omega-3 fatty acids such as fish, fish-derived supplements, as well as flax seed oil, borage oil, and other non-animal-based oils;

- abdominal fat reduction;

- aerobic exercise;

- inhibitors of cholesterol synthesis (known as statins);

- low normal blood glucose levels (glycosylated hemoglobin, also called HbA1c);

- micronutrient (vitamins, potassium, and magnesium) consumption;

- maintaining normal, or healthy, blood pressure levels;

- aspirin supplement

- cyclodextrin can solubilize cholesterol, removing it from plaques

Put simply, take steps to live a healthy, sustainable lifestyle.

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.

Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided. Medical management of atherosclerosis first involves modification to risk factors–for example, via smoking cessation and diet restrictions. Additionally, a controlled exercise program combats atherosclerosis by improving circulation and functionality of the vessels. Exercise is also used to manage weight in patients who are obese, lower blood pressure, and decrease cholesterol. Often lifestyle modification is combined with medication therapy. For example, statins help to lower cholesterol, antiplatelet medications like aspirin help to prevent clots, and a variety of antihypertensive medications are routinely used to control blood pressure. If the combined efforts of risk factor modification and medication therapy are not sufficient to control symptoms, or fight imminent threats of ischemic events, a physician may resort to interventional or surgical procedures to correct the obstruction.

Combinations of statins, niacin and intestinal cholesterol absorption-inhibiting supplements (ezetimibe and others, and to a much lesser extent fibrates) have been the most successful in changing common but sub-optimal lipoprotein patterns and group outcomes. In the many secondary prevention and several primary prevention trials, several classes of lipoprotein-expression-altering (less correctly termed "cholesterol-lowering") agents have consistently reduced not only heart attack, stroke and hospitalization but also all-cause mortality rates. The first of the large secondary prevention comparative statin/placebo treatment trials was the Scandinavian Simvastatin Survival Study (4S) with over fifteen more studies extending through to the more recent ASTEROID trial published in 2006. The first primary prevention comparative treatment trial was AFCAPS/TexCAPS with multiple later comparative statin/placebo treatment trials including EXCEL, ASCOT and SPARCL. While the statin trials have all been clearly favorable for improved human outcomes, only ASTEROID and SATURN showed evidence of atherosclerotic regression (slight). Both human and animal trials that showed evidence of disease regression used more aggressive combination agent treatment strategies, which nearly always included niacin.

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.

Aggressive risk factor modification is required for effective treatment of microvascular angina where exercise plays a major role. Several other treatment strategies including b-blockers, angiotensin-converting enzyme inhibitors, ranolazine, l-arginine, statin drugs and potentially estrogen replacement therapy have been shown to relieve anginal symptoms as well as improve vascular function. Nitrates may be effective for symptom relief. Further studies are required to determine whether specific treatments are associated with improved survival as well as decreased symptoms.

The most specific medicine to treat angina is nitroglycerin. It is a potent vasodilator that decreases myocardial oxygen demand by decreasing the heart's workload. Beta blockers and calcium channel blockers act to decrease the heart's workload, and thus its requirement for oxygen. Nitroglycerin should not be given if certain inhibitors such as sildenafil, tadalafil, or vardenafil have been taken within the previous 12 hours as the combination of the two could cause a serious drop in blood pressure. Treatments for angina are balloon angioplasty, in which the balloon is inserted at the end of a catheter and inflated to widen the arterial lumen. Stents to maintain the arterial widening are often used at the same time. Coronary bypass surgery involves bypassing constricted arteries with venous grafts. This is much more invasive than angioplasty.

The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and death. Beta blockers (e.g., carvedilol, propranolol, atenolol) have a large body of evidence in morbidity and mortality benefits (fewer symptoms, less disability and longer life) and short-acting nitroglycerin medications have been used since 1879 for symptomatic relief of angina. Calcium channel blockers (such as nifedipine (Adalat) and amlodipine), isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina. A new therapeutic class, called If inhibitor, has recently been made available: Ivabradine provides pure heart rate reduction leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit. Statins are the most frequently used lipid/cholesterol modifiers, which probably also stabilize existing atheromatous plaque. Low-dose aspirin decreases the risk of heart attack in patients with chronic stable angina, and was part of standard treatment. However, in patients without established cardiovascular disease, the increase in hemorrhagic stroke and gastrointestinal bleeding offsets any benefits and it is no longer advised unless the risk of myocardial infarction is very high.

Exercise is also a very good long-term treatment for the angina (but only particular regimens - gentle and sustained exercise rather than intense short bursts), probably working by complex mechanisms such as improving blood pressure and promoting coronary artery collateralisation.

Though sometimes used by patients, evidence does not support the use of Traditional Chinese Herbal Products (THCP) for angina

Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol and other fats in the blood, diabetes and hypertension (high blood pressure), and encouraging smoking cessation and weight optimization.

The calcium channel blocker nifedipine prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. New overt heart failures were reduced by 29% compared to placebo; however, the mortality rate difference between the two groups was statistically insignificant.

Treatment is often in the form of preventative measures of prophylaxis. Drug therapy for underlying conditions, such as drugs for the treatment of high cholesterol, drugs to treat high blood pressure (ACE inhibitors), and anti-coagulant drugs, are often prescribed to help prevent arteriosclerosis. Lifestyle changes such as increasing exercise, stopping smoking, and moderating alcohol intake are also advised. Experimental treatments include senolytic drugs, or drugs that selectively eliminate senescent cells, which enhance vascular reactivity and reduce vascular calcification in a mouse model of atherosclerosis, as well as improving cardiovascular function in old mice.

There are a variety of types of surgery:

- Angioplasty and stent placement: A catheter is first inserted into the blocked/narrowed part of your artery, followed by a second one with a deflated balloon which is passed through the catheter into the narrowed area. The balloon is then inflated, pushing the deposits back against the arterial walls, and then a mesh tube is usually left behind to prevent the artery from retightening.

- Coronary artery bypass surgery: This surgery creates a new pathway for blood to flow to the heart. Taking a healthy piece of vein, the surgeon attaches it to the coronary artery, just above and below the blockage to allow bypass.

- Endarterectomy: This is the general procedure for the surgical removal of plaque from the artery that has become narrowed, or blocked.

- Thrombolytic therapy: is a treatment used to break up masses of plaque inside the arteries via intravenous clot-dissolving medicine.

Cilostazol or pentoxifylline can improve symptoms in some. Cilostazol may improve walking distance for people who experience claudication due to peripheral artery disease, but there is no strong evidence to suggest that it improves the quality of life, decreases mortality, or decreases the risk of cardiovascular events.

Treatment with other drugs or vitamins are unsupported by clinical evidence, "but trials evaluating the effect of folate and vitamin B-12 on hyperhomocysteinemia, a putative vascular risk factor, are near completion".

In those who have developed critically poor blood flow to the legs, it is unclear if autotransplantation of autologous mononuclear cells is useful or not.

Only one randomized controlled trial has been conducted comparing vascular bypass to angioplasty for the treatment of severe PAD. The trial found no difference in amputation-free survival between vascular bypass and angioplasty at the planned clinical endpoint, however the trial has been criticized as being underpowered, limiting endovascular options, and comparing inappropriate endpoints. As of 2017, two randomized clinical trials are being conducted to better understand the optimal revascularization technique for severe PAD and critical limb ischemia (CLI), the BEST-CLI (Best Endovascular Versus Best Surgical Therapy for Patients With Critical Limb Ischemia) Trial, and the BASIL-2 (Bypass Versus Angio plasty in Severe Ischaemia of the Leg – 2 )Trial.

In 2011, pCMV-vegf165 was registered in Russia as the first-in-class gene therapy drug for treatment of peripheral artery disease, including the advanced stage of critical limb 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.

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.

Coronary vasospasm is a sudden, intense vasoconstriction of an epicardial coronary artery that causes occlusion (stoppage) or near-occlusion of the vessel.

It can cause Prinzmetal's angina.

It can occur in multiple vessels.

Atropine has been used to treat the condition.

In developed countries, with improved public health, infection control and increasing life spans, atheroma processes have become an increasingly important problem and burden for society.

Atheromata continue to be the primary underlying basis for disability and death, despite a trend for gradual improvement since the early 1960s (adjusted for patient age). Thus, increasing efforts towards better understanding, treating and preventing the problem are continuing to evolve.

According to United States data, 2004, for about 65% of men and 47% of women, the first symptom of cardiovascular disease is myocardial infarction (heart attack) or sudden death (death within one hour of symptom onset).

A significant proportion of artery flow-disrupting events occur at locations with less than 50% lumenal narrowing. Cardiac stress testing, traditionally the most commonly performed noninvasive testing method for blood flow limitations, generally only detects lumen narrowing of ~75% or greater, although some physicians advocate nuclear stress methods that can sometimes detect as little as 50%.

The sudden nature of the complications of pre-existing atheroma, vulnerable plaque (non-occlusive or soft plaque), have led, since the 1950s, to the development of intensive care units and complex medical and surgical interventions. Angiography and later cardiac stress testing was begun to either visualize or indirectly detect stenosis. Next came bypass surgery, to plumb transplanted veins, sometimes arteries, around the stenoses and more recently angioplasty, now including stents, most recently drug coated stents, to stretch the stenoses more open.

Yet despite these medical advances, with success in reducing the symptoms of angina and reduced blood flow, atheroma rupture events remain the major problem and still sometimes result in sudden disability and death despite even the most rapid, massive and skilled medical and surgical intervention available anywhere today. According to some clinical trials, bypass surgery and angioplasty procedures have had at best a minimal effect, if any, on improving overall survival. Typically mortality of bypass operations is between 1 and 4%, of angioplasty between 1 and 1.5%.

Additionally, these vascular interventions are often done only after an individual is symptomatic, often already partially disabled, as a result of the disease. It is also clear that both angioplasty and bypass interventions do not prevent future heart attack.

The older methods for understanding atheroma, dating to before World War II, relied on autopsy data. Autopsy data has long shown initiation of fatty streaks in later childhood with slow asymptomatic progression over decades.

One way to see atheroma is the very invasive and costly IVUS ultrasound technology; it gives us the precise volume of the inside intima plus the central media layers of about of artery length. Unfortunately, it gives no information about the structural strength of the artery. Angiography does not visualize atheroma; it only makes the blood flow within blood vessels visible. Alternative methods that are non or less physically invasive and less expensive per individual test have been used and are continuing to be developed, such as those using computed tomography (CT; led by the electron beam tomography form, given its greater speed) and magnetic resonance imaging (MRI). The most promising since the early 1990s has been EBT, detecting calcification within the atheroma before most individuals start having clinically recognized symptoms and debility. Interestingly, statin therapy (to lower cholesterol) does not slow the speed of calcification as determined by CT scan. MRI coronary vessel wall imaging, although currently limited to research studies, has demonstrated the ability to detect vessel wall thickening in asymptomatic high risk individuals. As a non-invasive, ionising radiation free technique, MRI based techniques could have future uses in monitoring disease progression and regression. Most visualization techniques are used in research, they are not widely available to most patients, have significant technical limitations, have not been widely accepted and generally are not covered by medical insurance carriers.

From human clinical trials, it has become increasingly evident that a more effective focus of treatment is slowing, stopping and even partially reversing the atheroma growth process. There are several prospective epidemiologic studies including the Atherosclerosis Risk in Communities (ARIC) Study and the Cardiovascular Health Study (CHS), which have supported a direct correlation of Carotid Intima-media thickness (CIMT) with myocardial infarction and stroke risk in patients without cardiovascular disease history. The ARIC Study was conducted in 15,792 individuals between 5 and 65 years of age in four different regions of the US between 1987 and 1989. The baseline CIMT was measured and measurements were repeated at 4- to 7-year intervals by carotid B mode ultrasonography in this study. An increase in CIMT was correlated with an increased risk for CAD. The CHS was initiated in 1988, and the relationship of CIMT with risk of myocardial infarction and stroke was investigated in 4,476 subjects ≤65 years of age. At the end of approximately six years of follow-up, CIMT measurements were correlated with cardiovascular events.

Paroi artérielle et Risque Cardiovasculaire in Asia Africa/Middle East and Latin America (PARC-AALA) is another important large-scale study, in which 79 centers from countries in Asia, Africa, the Middle East, and Latin America participated, and the distribution of CIMT according to different ethnic groups and its association with the Framingham cardiovascular score was investigated. Multi-linear regression analysis revealed that an increased Framingham cardiovascular score was associated with CIMT, and carotid plaque independent of geographic differences.

Cahn et al. prospectively followed-up 152 patients with coronary artery disease for 6–11 months by carotid artery ultrasonography and noted 22 vascular events (myocardial infarction, transient ischemic attack, stroke, and coronary angioplasty) within this time period. They concluded that carotid atherosclerosis measured by this non-interventional method has prognostic significance in coronary artery patients.

In the Rotterdam Study, Bots et al. followed 7,983 patients >55 years of age for a mean period of 4.6 years, and reported 194 incident myocardial infarctions within this period. CIMT was significantly higher in the myocardial infarction group compared to the other group. Demircan et al. found that the CIMT of patients with acute coronary syndrome were significantly increased compared to patients with stable angina pectoris.

It has been reported in another study that a maximal CIMT value of 0.956 mm had 85.7% sensitivity and 85.1% specificity to predict angiographic CAD. The study group consisted of patients admitted to the cardiology outpatient clinic with symptoms of stable angina pectoris. The study showed CIMT was higher in patients with significant CAD than in patients with non-critical coronary lesions. Regression analysis revealed that thickening of the mean intima-media complex more than 1.0 was predictive of significant CAD our patients. There was incremental significant increase in CIMT with the number coronary vessel involved. In accordance with the literature, it was found that CIMT was significantly higher in the presence of CAD. Furthermore, CIMT was increased as the number of involved vessels increased and the highest CIMT values were noted in patients with left main coronary involvement. However, human clinical trials have been slow to provide clinical & medical evidence, partly because the asymptomatic nature of atheromata make them especially difficult to study. Promising results are found using carotid intima-media thickness scanning (CIMT can be measured by B-mode ultrasonography), B-vitamins that reduce a protein corrosive, homocysteine and that reduce neck carotid artery plaque volume and thickness, and stroke, even in late-stage disease.

Additionally, understanding what drives atheroma development is complex with multiple factors involved, only some of which, such as lipoproteins, more importantly lipoprotein subclass analysis, blood sugar levels and hypertension are best known and researched. More recently, some of the complex immune system patterns that promote, or inhibit, the inherent inflammatory macrophage triggering processes involved in atheroma progression are slowly being better elucidated in animal models of atherosclerosis.

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

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