Acute myocardial infarction (MI), including ST-segment elevation MI, non-ST-segment elevation MI, and unstable angina are part of a group of diseases called acute coronary syndrome (ACS). Patients with ACS have some degree of coronary artery occlusion. Development begins with a rupture or erosion of plaque. The rupture results in platelet adhesions, fibrin clot formation, and activation of thrombin.

A thrombus progresses and occludes blood flow, although an early thrombus doesn’t necessarily block blood flow. The effect is an imbalance in myocardial oxygen supply and demand. Depending on the degree of occlusion, ACS is defined as three types.

If the patient has unstable angina, a thrombus partially occludes a coronary vessel. This thrombus is full of platelets. The partially occluded vessel may have distal microthrombi that cause necrosis in some myocytes.

If smaller vessels infarct, the patient is at higher risk for MI, which may progress to a non-Q-wave MI. Usually, only the innermost layer of the heart is damaged.

A Q-wave MI results when reduced blood flow through one of the coronary arteries causes myocardial ischemia, injury, and necrosis. The damage extends through all myocardial layers. The destruction of healthy cardiac tissue from myocardial ischemia varies with the severity of the ACS involved and the promptness of effective diagnosis and treatment.

An aneurysm is a localized outpouching or abnormal dilation of a weakened arterial wall of the aorta. When developing, lateral pressure increases, causing the vessel lumen to widen and blood flow to slow. An aortic aneurysm may result in hemodynamic forces that can create pulsatile stresses on the weakened wall and press on the small vessels that supply nutrients to the arterial wall, causing the aorta to become bowed and torturous.

An aortic aneurysm may rupture or tear suddenly, possibly causing death. Rupture of an aortic aneurysm is a medical emergency requiring prompt treatment.

Aortic aneurysms are classified according to their anatomical location along the aorta, their shape, and how they are formed. Abdominal aneurysms are located along the portion of the aorta that passes through the abdomen. Ascending aneurysms are located in the ascending aorta and descending in the descending aorta.

Cardiac tamponade is a rapid, unchecked increase in pressure in the pericardial sac. It usually results from blood or fluid that accumulates in the sac and compresses the heart. This compression obstructs blood flow to the ventricles and reduces the amount of blood pumped out of the heart with each contraction. Possible causes include malignant disease, dissecting aorta, heart surgery, trauma or radiation to the chest, heart tumor, placement of a central line, myocardial infarction, pericarditis, or a reaction to certain drugs, such as procainamide or hydralazine.

Cardiomyopathy is a disease of the heart where the heart muscle tissue can’t work properly or as efficiently as it should. Cardiomyopathy can be classified as primary or secondary.

Primary cardiomyopathy refers to changes in the heart muscle without a specific cause. Secondary cardiomyopathy results from disorders that involve other organs as well as the heart.

There are four types of cardiomyopathy—dilated, restrictive, hypertrophic, and arrhythmogenic right ventricular dysplasia. Dilated or congestive cardiomyopathy (most common) and restrictive cardiomyopathy are discussed here.

Restrictive cardiomyopathy is characterized by restricted ventricular filling (the result of left ventricular hypertrophy) and endocardial fibrosis and thickening. It’s severe and irreversible, and the average survival after diagnosis is 9 years.

Coronary artery disease (CAD) occurs when the arteries that supply blood to the heart muscle harden and narrow. The result is the loss of oxygen and nutrients to myocardial tissue because of diminished coronary blood flow. This reduction in blood flow can lead to coronary syndrome (angina or myocardial infarction).

Endocarditis (also known as infective or bacterial endocarditis) is an infection of the endocardium, heart valves, or cardiac prosthesis resulting from bacterial or fungal invasion. Even transient bacteremia after dental or urogenital procedures can introduce the pathogen into the bloodstream. This infection causes fibrin and platelets to aggregate on the valve tissue and engulf circulating bacteria or fungi that flourish and form friable, wartlike vegetative growths on the heart valves, the endocardial lining of a heart chamber, or the epithelium of a blood vessel. Such growths may cover the valve surfaces, causing ulceration and necrosis; they may also extend to the chordae tendineae, leading to rupture and subsequent valvular insufficiency. Ultimately, they may embolize to the spleen, kidneys, central nervous system, and lungs.

Untreated, endocarditis is usually fatal, but with proper treatment, 70% of patients recover. The prognosis is worst when endocarditis causes severe valvular damage, leading to insufficiency and heart failure, or when it involves a prosthetic valve.

Heart failure is a syndrome characterized by myocardial dysfunction that leads to impaired pump performance (diminished cardiac output) or to frank heart failure and abnormal circulatory congestion. Heart failure can be classified according to its pathophysiology. It may be right-sided or left-sided, systolic or diastolic, and acute or chronic.

Congestion of systemic or venous circulation may result in peripheral edema or hepatomegaly; congestion of pulmonary circulation may cause pulmonary edema, an acute life-threatening emergency. Pump failure usually occurs in a damaged left ventricle (left-sided heart failure) but may occur in the right ventricle (right-sided heart failure) either as a primary disorder or secondary to left-sided heart failure. Sometimes, left- and right-sided heart failure develop simultaneously.

Hypertension is an intermittent or sustained elevation in diastolic or systolic blood pressure. It may occur as essential (primary, idiopathic) where there is no identifiable cause, or secondary, resulting from an identifiable cause. Primary hypertension occurs in 90% to 95% of cases and tends to develop gradually over many years. Risk factors include obesity, stress, sedentary lifestyle, and smoking. Secondary hypertension tends to appear suddenly and causes higher blood pressure than does primary. Various conditions can lead to secondary hypertension, including renal disease, adrenal gland tumors, congenital coarctation, and obstructive sleep apnea. Medications that can cause secondary hypertension include hormonal contraceptives, cold remedies, certain pain relievers, and illegal drugs, such as cocaine and amphetamines. Malignant hypertension is a severe, fulminant form of hypertension common to both types. Hypertension is a major cause of stroke, cardiac disease, and renal failure. The prognosis is good if this disorder is detected early and treatment begins before complications develop. Severely elevated blood pressure (hypertensive crisis) may be fatal.