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Mitral regurgitation (MR) is a common valvular disorder that can arise from abnormalities of any part of the mitral valve apparatus.

These include the valve leaflets, annulus, chordae tendineae, and papillary muscles. The ventricular myocardium adjacent to the papillary muscles are also integrally involved with mitral valve function.


The prevalence of MR varies inversely with severity. A trivial amount of MR is detectable with sensitive Doppler techniques in up to 70 percent of healthy adults; this is often termed "physiologic" MR.

The etiology of mitral regurgitation (MR) may be due to a primary abnormality of the valve apparatus or may be secondary to another cardiac disease.

The major etiologies of MR are rheumatic heart disease, mitral valve prolapse and coronary heart disease.

Chronic mitral regurgitation (MR) is a relatively common valvular disorder that can progress to ventricular decompensation and the need for mitral valve surgery.


Mitral stenosis (MS), resulting from thickening and immobility of the mitral valve leaflets causes an obstruction in blood flow from the left atrium to left ventricle. As a result, there is an increase in pressure within the left atrium, pulmonary vasculature, and right side of the heart, while the left ventricle is unaffected in isolated MS. Mitral stenosis, however, often coexists with mitral regurgitation and occasionally with aortic valve dysfunction, which may cause left ventricular dysfunction.

In the great majority of cases, mitral stenosis is caused by rheumatic involvement of the mitral valve followed by degenerative mitral calcification.

Management options for moderate-to severe stenosis include transcathether balloon valvotomy and mitral valve surgery.


Aortic valve stenosis (AS, aortic stenosis) is the most common cause of left ventricular outflow obstruction in children and adults. Aortic valve sclerosis is defined as aortic valve thickening and calcification without a significant obstruction. Aortic stenosis (AS) is present when the velocity across an abnormal valve increases as obstruction increases. The progression of AS are defined by symptoms, valve anatomy and hemodynamics, and left ventricular function.

Worldwide, rheumatic valve disease is most common and mitral valve involvement invariably accompanies rheumatic aortic valve disease. In North America and Europe, aortic valve disease is primarily due to calcific disease of a native valve or a congenitally bicuspid valve.

There are three primary causes of valvular aortic stenosis (AS):

1. A congenitally abnormal valve with superimposed calcification (unicuspid or bicuspid).

2. Degenerative calcific disease of a trileaflet valve

3. Rheumatic valve disease


Aortic regurgitation (AR, also called aortic insufficiency) is caused by inadequate closure of the aortic valve leaflets. It can be induced either by disease of the aortic valve leaflets or by distortion or dilation of the aortic root and ascending aorta.

All forms of aortic regurgitation (AR) produce a similar hemodynamic abnormality. The inability of the aortic valve leaflets to remain closed during diastole results in a portion of the left ventricular stroke volume leaking back from the aorta into the left ventricle.

Patients with aortic regurgitation (AR) may remain asymptomatic for decades, even if there is progressive ventricular dilation. Symptoms that develop in some patients with severe AR include exertional dyspnea, angina, and other symptoms of heart failure.

Exertional dyspnea develops in some patients with severe AR. More severe heart failure symptoms such as orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema may develop without appropriate treatment.


Ischemic heart disease, also referred to as coronary heart disease, is present when a patient has one or more symptoms or signs from an inadequate supply of blood to the heart muscle. This is most commonly due to obstruction of the coronary arteries due to atherosclerosis.

Angina pectoris, occurs when myocardial oxygen demand exceeds oxygen supply; the clinical manifestation is often chest discomfort. Stable angina pectoris, refers to chest discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerine. Most patients with ischemic heart disease will experience angina as part of the clinical manifestations of the disease.

The care of patients with ischemic heart disease includes ascertainment of the diagnosis and its severity, control of symptoms, and therapies to improve survival. These include medical management, percutaneous interventions and coronary artery surgery.

An aortic aneurysm is defined as a segmental, full thickness, dilation of a blood vessel having at least a 50 percent increase in diameter compared with the expected normal diameter. True aneurysms involve all three layers of the arterial wall (intima, media, adventitia). Norma thoracic aortic diameter varies according to the location within the aorta and also with body habitus, gender, and age.

Thoracic aortic aneurysm (TAA) represents about one-third of aortic aneurysm admissions with the remainder of cases related to abdominal aortic disease. Most patients with TAA have no symptoms and are silent until a complication occurs. Aneurysms that produce symptoms are typically very large and are at an increased risk for rupture, which is associated with high mortality rates. When symptoms do occur, patients can present with chest or upper back pain, or with symptoms related to compression of surrounding structures leading to nerve dysfunction, or arterial compression causing vascular compromise.

There is a strong familial component to acute thoracic aortic disease.



Aortic dissection is a relatively uncommon but catastrophic illness, often presenting with severe chest pain and sudden hemodynamic instability. Early and accurate diagnosis and treatment are fundamental for survival.

The initial event in aortic dissection is a tear in the aortic intima (innermost layer). Blood passes into the aortic media through the tear, separating the intima from the surrounding media and/or adventitia, and creating a false lumen. Propagation of the dissection can occur, involving branch vessels, the aortic valve and/ or entering the pericardial space. Such propagation is responsible for many of the associated clinical manifestations and cause of early mortality, including variable organ ischemia, aortic regurgitation, and cardiac tamponade.

The most important predisposing factor for acute aortic dissection is systemic hypertension.

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