Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Unlike other causes of acute coronary syndromes, such as unstable angina, a myocardial infarction occurs when there is cell death, as measured by a blood test for biomarkers (the cardiac protein troponin or the cardiac enzyme CK-MB). When there is evidence of an MI, it may be classified as an ST elevation myocardial infarction (STEMI) or Non-ST elevation myocardial infarction (NSTEMI) based on the results of an ECG.

The phrase "heart attack" is often used non-specifically to refer to a myocardial infarction and to sudden cardiac death. An MI is different from—but can cause—cardiac arrest, where the heart is not contracting at all or so poorly that all vital organs cease to function, thus causing death. It is also distinct from heart failure, in which the pumping action of the heart is impaired. However, an MI may lead to heart failure.

Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen. The pain most suggestive of an acute MI, with the highest likelihood ratio, is pain radiating to the right arm and shoulder. Similarly, chest pain similar to a previous heart attack is also suggestive. The pain associated with MI is usually diffuse, does not change with position, and lasts for more than 20 minutes. Levine's sign, in which a person localizes the chest pain by clenching one or both fists over their sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a poor positive predictive value. Pain that responds to nitroglycerin does not indicate the presence or absence of a myocardial infarction.

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.

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.

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.

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 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.

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.

The risk of PVF during acute myocardial infarction is related to the amount of ST elevation, the presence of hypokalemia, the absence of pre-infarction angina, the size of the infarction, and the presence of a blocked left coronary artery. Other risk factors could include younger age, male gender, and history of sudden cardiac death in first degree relatives.

A myocardial infarction may compromise the function of the heart as a pump for the circulation, a state called heart failure. There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided coronary occlusion that disrupts the blood supply of the papillary muscles. The incidence of heart failure is particularly high in patients with diabetes and requires special management strategies.

Approximately 10% of all myocardial infarctions lead to PVF. The incidence peaks between 20 and 50 minutes after the start of the MI. 2/3 of events occur before medical attendance, and of these medically unattended events, 2/3 occur after more than 30 minutes of warning symptoms.

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.

Loss of consciousness, headache, and vomiting usually occur more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

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 symptoms and signs of hypertensive heart disease will depend on whether or not it is accompanied by heart failure. In the absence of heart failure, hypertension, with or without enlargement of the heart (left ventricular hypertrophy) is usually symptomless.

Symptoms, signs and consequences of Congestive heart failure can include:

- Fatigue

- Irregular pulse or palpitations

- Swelling of feet and ankles

- Weight gain

- Nausea

- Shortness of breath

- Difficulty sleeping flat in bed (orthopnea)

- Bloating and abdominal pain

- Greater need to urinate at night

- An enlarged heart (cardiomegaly)

- Left ventricular hypertrophy and left ventricular remodeling

- Diminished coronary flow reserve and silent myocardial ischemia

- Coronary heart disease and accelerated atherosclerosis

- Heart Failure With Normal Left Ventricular Ejection Fraction (HFNEF), often termed diastolic heart failure

- Atrial fibrillation, other cardiac arrhythmias, or sudden cardiac death

Heart failure can develop insidiously over time or patients can present acutely with acute heart failure or acute decompensated heart failure and pulmonary edema due to sudden failure of pump function of the heart. Sudden failure can be precipitated by a variety of causes, including myocardial ischemia, marked increases in blood pressure, or cardiac arrhythmias.

Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and the posterior column–medial lemniscus pathway, symptoms may include:

- hemiplegia and muscle weakness of the face

- numbness

- reduction in sensory or vibratory sensation

- initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies.

In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is "usually" on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.In addition to the above CNS pathways, the "brainstem" gives rise to most of the twelve cranial nerves. A brainstem stroke affecting the brainstem and brain, therefore, can produce symptoms relating to deficits in these cranial nerves:

- altered smell, taste, hearing, or vision (total or partial)

- drooping of eyelid (ptosis) and weakness of ocular muscles

- decreased reflexes: gag, swallow, pupil reactivity to light

- decreased sensation and muscle weakness of the face

- balance problems and nystagmus

- altered breathing and heart rate

- weakness in sternocleidomastoid muscle with inability to turn head to one side

- weakness in tongue (inability to stick out the tongue or move it from side to side)

If the "cerebral cortex" is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

- aphasia (difficulty with verbal expression, auditory comprehension, reading and writing; Broca's or Wernicke's area typically involved)

- dysarthria (motor speech disorder resulting from neurological injury)

- apraxia (altered voluntary movements)

- visual field defect

- memory deficits (involvement of temporal lobe)

- hemineglect (involvement of parietal lobe)

- disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)

- lack of insight of his or her, usually stroke-related, disability

If the "cerebellum" is involved, ataxia might be present and this includes:

- altered walking gait

- altered movement coordination

- vertigo and or disequilibrium

Symptoms of TIAs can last on the order of minutes to 1-2 hours, but occasionally may last for a longer period of time. TIAs used to be defined as ischemic events in the brain that last less than 24 hours, but given the variation in duration of symptoms, this definition holds less significance. A pooled study of 808 patients with TIAs from 10 hospitals showed that 60% lasted less than 1 hour, 71% lasted less than 2 hours, and 14% lasted greater than 6 hours . Importantly, patients with symptoms that last more than one hour are more likely to have permanent neurologic damage, making prompt diagnosis and treatment important to maximize recovery.

Hypertensive heart disease includes a number of complications of high blood pressure that affect the heart. While there are several definitions of hypertensive heart disease in the medical literature, the term is most widely used in the context of the International Classification of Diseases (ICD) coding categories. The definition includes heart failure and other cardiac complications of hypertension when a causal relationship between the heart disease and hypertension is stated or implied on the death certificate. In 2013 hypertensive heart disease resulted in 1.07 million deaths as compared with 630,000 deaths in 1990.

According to ICD-10, hypertensive heart disease (I11), and its subcategories: hypertensive heart disease with heart failure (I11.0) and hypertensive heart disease without heart failure (I11.9) are distinguished from chronic rheumatic heart diseases (I05-I09), other forms of heart disease (I30-I52) and ischemic heart diseases (I20-I25). However, since high blood pressure is a risk factor for atherosclerosis and ischemic heart disease, death rates from hypertensive heart disease provide an incomplete measure of the burden of disease due to high blood pressure.

Signs and symptoms of TIA are widely variable and can mimic other neurologic conditions, making the clinical context and physical exam crucial in ruling in or out the diagnosis. The most common presenting symptoms of TIA are focal neurologic deficits, which can include, but are not limited to :

- Amaurosis fugax (painless, temporary loss of vision)

- One-sided facial droop

- One-sided motor weakness

- Diplopia (double vision)

- Problems with balance and spatial orientation

A detailed neurologic exam, including a thorough cranial nerve exam, is important to identify these findings and to differentiate them from mimickers of TIA. Symptoms such as unilateral weakness, amaurosis fugax, and double vision have higher odds of representing TIA compared to memory loss, headache, and blurred vision. Below is a table of symptoms at presentation, and what percentage of the time they are seen in TIAs versus conditions that mimic TIA. In general, focal deficits make TIA more likely, but the absence of focal findings do not exclude the diagnosis and further evaluation may be warranted if clinical suspicion for TIA is high (see “Diagnosis” section below).

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

Symptoms may begin quickly or slowly depending on the size of the embolus and how much it blocks the blood flow. Symptoms of embolisation in an organ vary with the organ involved but commonly include:

- Pain in the involved body part

- Temporarily decreased organ function

Later symptoms are closely related to infarction of the affected tissue. This may cause permanently decreased organ function.

For example, symptoms of myocardial infarction mainly include chest pain, dyspnea, diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations.

Symptoms of limb infarction include coldness, decreased or no pulse beyond the site of blockage, pain, muscle spasm, numbness and tingling, pallor and muscle weakness, possibly to the grade of paralysis in the affected limb.

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