There is varying evidence about the importance of saturated fat in the development of myocardial infarctions. Eating polyunsaturated fat instead of saturated fats has been shown in studies to be associated with a decreased risk of myocardial infarction, while other studies find little evidence that reducing dietary saturated fat or increasing polyunsaturated fat intake affects heart attack risk. Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed. Trans fats do appear to increase risk. Acute and prolonged intake of high quantities of alcoholic drinks (3–4 or more) increases the risk of a heart attack.

The most prominent risk factors for myocardial infarction are older age, actively smoking, high blood pressure, diabetes mellitus, and total cholesterol and high-density lipoprotein levels. Many risk factors of myocardial infarction are shared with coronary artery disease, the primary cause of myocardial infarction, with other risk factors including male sex, low levels of physical activity, a past family history, obesity, and alcohol use. Risk factors for myocardial disease are often included in risk factor stratification scores, such as the Framingham risk score. At any given age, men are more at risk than women for the development of cardiovascular disease. High levels of blood cholesterol is a known risk factor, particularly high low-density lipoprotein, low high-density lipoprotein, and high triglycerides.

Many risk factors for myocardial infarction are potentially modifiable, with the most important being tobacco smoking (including secondhand smoke). Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease. Lack of physical activity has been linked to 7–12% of cases. Less common causes include stress-related causes such as job stress, which accounts for about 3% of cases, and chronic high stress levels.

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.

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.

After return of heart function, there has been a moderately higher risk of death in the hospital when compared to MI patients without PVF. Whether this still holds true with the recent changes in treatment strategies of earlier hospital admission and immediate angioplasty with thrombus removal is unknown. PVF does not affect the long-term prognosis.

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.

The survival of PVF largely depends on the promptness of defibrillation. The success rate of prompt defibrillation during monitoring is currently higher than 95%. It is estimated that the success rate decreases by 10% for each additional minute of delay.

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.

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.

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.

Ischemic cardiomyopathy is the cause of more than 60% of all cases of systolic congestive heart failure in most countries of the world. A chest radiography that demonstrates coronary artery calcification is a probable indication of ischemic cardiomyopathy.

The following are causes of ischemic cardiomyopathy:

- Diabetes

- Atherosclerosis

- Vasospasm

- Inflammation of arteries

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.

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.

Myocardial rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later. In the modern era of early revascularization and intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture is about 1% of all MIs. This may occur in the free walls of the ventricles, the septum between them, the papillary muscles, or less commonly the atria. Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm, a localized dilation or ballooning of the heart chamber.

Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction. In addition, the risk of rupture is higher in individuals who are revascularized with a thrombolytic agent than with PCI. The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.

Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac tamponade, in which blood accumulates within the pericardium or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a ventricular septal defect with shunting of blood through the defect from the left side of the heart to the right side of the heart, which can lead to right ventricular failure as well as pulmonary overcirculation. Rupture of the papillary muscle may also lead to acute mitral regurgitation and subsequent pulmonary edema and possibly even cardiogenic shock.

Risk factors for thromboembolism, the major cause of arterial embolism, include disturbed blood flow (such as in atrial fibrillation and mitral stenosis), injury or damage to an artery wall, and hypercoagulability (such as increased platelet count). Mitral stenosis poses a high risk of forming emboli which may travel to the brain and cause stroke. Endocarditis increases the risk for thromboembolism, by a mixture of the factors above.

Atherosclerosis in the aorta and other large blood vessels is a common risk factor, both for thromboembolism and cholesterol embolism. The legs and feet are major impact sites for these types. Thus, risk factors for atherosclerosis are risk factors for arterial embolisation as well:

- advanced age

- cigarette smoking

- hypertension (high blood pressure)

- obesity

- hyperlipidemia, e.g. hypercholesterolemia, hypertriglyceridemia, elevated lipoprotein (a) or apolipoprotein B, or decreased levels of HDL cholesterol)

- diabetes mellitus

- Sedentary lifestyle

- stress

Other important risk factors for arterial embolism include:

- recent surgery (both for thromboembolism and air embolism)

- previous stroke or cardiovascular disease

- a history of long-term intravenous therapy (for air embolism)

- Bone fracture (for fat embolism)

A septal defect of the heart makes it possible for paradoxical embolization, which happens when a clot in a vein enters the right side of the heart and passes through a hole into the left side. The clot can then move to an artery and cause arterial embolisation.

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.

Angina results when there is an imbalance between the heart's oxygen demand and supply. This imbalance can result from an increase in demand (e.g., during exercise) without a proportional increase in supply (e.g., due to obstruction or atherosclerosis of the coronary arteries).

However, the pathophysiology of angina in females varies significantly as compared to males. Non-obstructive coronary disease is more common in females.

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

HIV is a major cause of cardiomyopathy – in particular dilated cardiomyopathy. Dilated cardiomyopathy can be due to pericardial effusion or infective endocarditis, especially in intravenous drug users which are common in the HIV population. However, the most researched causes of cardiomyopathy are myocardial inflammation and infection caused by HIV-1. Toxoplasma gondii is the most common opportunistic infectious agent associated with myocarditis in AIDS. Coinfection with viruses (usually, coxsackievirus B3 and cytomegalovirus) seems to have an important affect in myocarditis. HIV-1 infection produces additional virus and cytokines such as TNF-α. This induces cardiomyocyte apoptosis. TNF-α causes a negative inotropic effect by interfering with the intracellular calcium ion concentrations. The intensity of the stains for TNF-α and iNOS of the myocardium was greater in patients with HIV associated cardiomyopathy, myocardial viral infection and was inversely correlated with CD4 count with antiretroviral therapy having no effect. Cardiac autoimmunity affects the pathogenesis of HIV-related heart disease as HIV-infected patients with dilated cardiomyopathy are more likely to have cardiac-specific autoantibodies than HIV-infected patients with healthy hearts and HIV-negative controls. Many patients with HIV have nutritional deficiencies which have been linked to left ventricular dysfunction. HIV-infected patients with encephalopathy are more likely to die of congestive heart failure than are those without encephalopathy. HAART has reduced the incidence of myocarditis thus reducing the prevalence of HIV-associated cardiomyopathy. Intravenous immunoglobulins (IVIGs) can also help patients with HIV-associated myocarditis.

Cardiogenic shock is caused by the failure of the heart to pump effectively. It can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes include abnormal heart rhythms, cardiomyopathy, heart valve problems, ventricular outflow obstruction (i.e. aortic valve stenosis, aortic dissection, cardiac tamponade, constrictive pericarditis, systolic anterior motion (SAM) in hypertrophic cardiomyopathy), or ventriculoseptal defects.

It can also be caused by a sudden decompressurization (e.g. in an aircraft), where air bubbles are released into the bloodstream (Henry's Law), causing heart failure.

The prevalence of LVT with AMI is 5-15%. The rates of AMI associated with LVT is declining due to the use of better therapies and percutaneous coronary intervention used to treat myocardial infarction. LVT formation has been found to be higher in anterior wall AMI than other types of AMI.

The cause of takotsubo cardiomyopathy is not fully understood, but several mechanisms have been proposed.

1. Transient vasospasm: Some of the original researchers of takotsubo suggested that multiple simultaneous spasms of coronary arteries could cause enough loss of blood flow to cause transient stunning of the myocardium. Other researchers have shown that vasospasm is much less common than initially thought. It has been noted that when there are vasospasms, even in multiple arteries, that they do not correlate with the areas of myocardium that are not contracting.

2. Microvascular dysfunction: The theory gaining the most traction is that there is dysfunction of the coronary arteries at the level where they are no longer visible by coronary angiography. This could include microvascular vasospasm, however, it may well have some similarities to diseases such as diabetes mellitus. In such disease conditions the microvascular arteries fail to provide adequate oxygen to the myocardium.

3. Mid-ventricular obstruction, apical stunning: It has been suggested that a mid-ventricular wall thickening with outflow obstruction is important in the pathophysiology.

4. Catecholamine-induced myocyte injury: It has been suggested that the response to catecholamines (such as epinephrine and norepinephrine, released in response to stress) leads to heart muscle dysfunction that contributes to takotsubo cardiomyopathy.

It is likely that there are multiple factors at play that could including some amount of vasospasm and a failure of the microvasculature

Case series looking at large groups of patients report that some patients develop takotsubo cardiomyopathy after an emotional stress, while others have a preceding clinical stressor (such as an asthma attack or sudden illness). Roughly one-third of patients have no preceding stressful event. A 2009 large case series from Europe found that takotsubo cardiomyopathy was slightly more frequent during the winter season. This may be related to two possible/suspected pathophysiological causes: coronary spasms of microvessels, which are more prevalent in cold weather, and viral infections – such as Parvovirus B19 – which occur more frequently during the winter.

Takotsubo cardiomyopathy is rare, affecting between 1.2% and 2.2% of people in Japan and 2% to 3% in western countries who suffer a myocardial infarction. It also affects far more women than men with 90% of cases being women, most postmenopausal. Scientists believe one reason is that estrogen causes the release of catecholamine and glucocorticoid in response to mental stress. It is not likely for the same recovered patient to experience the syndrome twice, although it has happened in rare cases. The average ages at onset are between 58 and 75 years. Less than 3% of cases occurred in patients under age 50.

The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial infarction. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction. On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered. The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.

The most common cause of myocardial rupture is a recent myocardial infarction, with the rupture typically occurring three to five days after infarction. Other causes of rupture include cardiac trauma, endocarditis (infection of the heart), cardiac tumors, infiltrative diseases of the heart, and aortic dissection.

Risk factors for rupture after an acute myocardial infarction include female gender, advanced age of the individual, first ischemic event, and a low body mass index. Other presenting signs associated with myocardial rupture include a pericardial friction rub, sluggish flow in the coronary artery after it is opened i.e. revascularized with an angioplasty, the left anterior descending artery being often the cause of the acute MI, and delay of revascularization greater than 2 hours.