Heart–brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential


carotid stenosis :: Article Creator

Carotid Stenosis

Content

The goal of treatment for carotid artery disease is to reduce the possibility of TIA or stroke, or to prevent the recurrence of a stroke.

Medical Therapy - Medications such as aspirin, other antiplatelets agents (like Plavix), diabetic medications, and medications that lower cholesterol and blood pressure are commonly prescribed when the degree of narrowing is less than 60 percent. Smoking cessation, exercise, and a healthy diet is also important for managing carotid artery disease and preventing further narrowing.

Carotid Endarterectomy - For patients with significant carotid artery narrowing with or without stroke-like symptoms, surgery may be recommended. Carotid Endarterectomy surgery involves exposing the carotid artery in the neck, clamping the artery above and below the plaque buildup, opening up the artery with a knife while it is clamped and directly removing the plaque (Figure 2).

Carotid Stenting - Alternatively, for select patients, carotid angioplasty and stenting, may be recommended. This procedure involves placing a self-expanding stent in the artery at the site of the narrowing and the stent expands holding the artery open (Figure 3), thereby, reducing the risk of future strokes.


Carotid Artery Disease

Content

Carotid artery disease may be asymptomatic (without symptoms) or symptomatic (with symptoms). Asymptomatic carotid disease is the presence of a significant amount of atherosclerotic build-up without obstructing enough blood flow to cause symptoms. However, a sufficiently tight stenosis will not always cause symptoms. Symptomatic carotid artery disease may result in either a transient ischemic attack (TIA) and/or a stroke (brain attack).

A transient ischemic attack (TIA) is a sudden or a temporary loss of blood flow to an area of the brain, usually lasting a few minutes to one hour. Symptoms usually go away entirely within 24 hours, with complete recovery. Symptoms of a TIA may include, but are not limited to, the following:

  • Sudden weakness or clumsiness of an arm and/or leg on one side of the body
  • Sudden paralysis (inability to move) of an arm and/or leg on one side of the body
  • Loss of coordination or movement
  • Confusion, dizziness, fainting, and/or headache
  • Numbness or loss of sensation (feeling) in the face
  • Numbness or loss of sensation in an arm and/or leg
  • Temporary loss of vision or blurred vision
  • Inability to speak clearly or slurred speech
  • TIA may be related to severe narrowing or blockage or from small pieces of an atherosclerotic plaque breaking off, traveling through the bloodstream, and lodging in small blood vessels in the brain. With TIA, there is rarely permanent brain damage.

    Call for medical help immediately if you suspect a person is having a TIA, as it may be a warning sign that a stroke is about to occur. Not all strokes, however, are preceded by TIAs.

    Stroke is another indicator of carotid artery disease. The symptoms of a stroke are the same as for a TIA. A stroke is loss of blood flow (ischemia) to the brain that continues long enough to cause permanent brain damage. Brain cells begin to die after just a few minutes without oxygen. The area of dead cells in tissues is called an infarct.

    The area of the brain that suffered the loss of blood flow will determine what the physical or mental disability may be. This may include impaired ability with movement, speech, thinking and memory, bowel and bladder function, eating, emotional control, and other vital body functions. Recovery from the specific ability affected depends on the size and location of the stroke. A stroke may result in problems such as weakness in an arm or leg or may cause paralysis, loss of speech, or even death.

    The symptoms of carotid artery disease may resemble other medical conditions or problems. Always consult your physician for a diagnosis.


    Aortic Stenosis - Physical Exam

    Auscultation of the heart in patients with aortic stenosis can be very helpful in both the diagnosis and determining the severity of disease.

    The typical murmur of aortic stenosis is a high-pitched, "diamond shaped" crescendo-decrescendo, midsystolic ejection murmur heard best at the right upper sternal border radiating to the neck and carotid arteries (see figure below). In mild aortic stenosis, the murmur peaks in early systole. However, as the disease progresses the peak moves to later in systole since longer time is required to complete LV systole and aortic valve closure is delayed. The intensity of the murmur typically increases as disease progresses; however, when heart failure develops and cardiac output declines, the murmur becomes softer. Thus, the intensity of the murmur is not a good indicator of disease severity.

    Auscultation at the cardiac apex may reveal a murmur that may sound midsystolic or holosystolic and may mimic the murmur of mitral regurgitation. However, this is commonly the result of radiation of the murmur of aortic stenosis to the apex rather than coexistent mitral regurgitation. This finding is referred to as "Gallavardin dissociation." To determine if the apical murmur is indeed due to mitral regurgitation or radiation of the murmur of aortic stenosis, dynamic auscultation can be undertaken (see section on dynamic auscultation). At times, the murmur of hypertrophic cardiomyopathy can also mimic the murmur of aortic stenosis. The Valsalva maneuver decreases the murmur of aortic stenosis while it increases the murmur of hypertrophic cardiomyopathy.

    The S2 heart sound is often paradoxically split in patients with aortic stenosis due to the significantly delayed closure of the aortic valve, a result of the increased time needed to complete LV systole.

    As disease progresses and the aortic valve leaflets lose their mobility, the intensity of S2 decreases. When the S2 sound is no longer audible, it can be concluded that the aortic stenosis is relatively severe. An S4 heart sound is also often present due to the severe concentric left ventricular hypertrophy that develops in aortic stenosis. If an S3 heart sound is present, then significant systolic dysfunction has developed, which is common in end-stage aortic stenosis.

    Perhaps the best bedside method to estimate the severity of aortic stenosis is derived from evaluation of the carotid arteries. The phenomenon known as "pulsus parvus et tardus" refers to a weak (parvus) and delayed (tardus) carotid upstroke. To asses for "parvus," it is often helpful to palpate one's own carotid artery while concurrently palpating the patient's carotid artery. It is important to note that in some elderly individuals the carotids may be stiff due to calcification, which may falsely normalize the carotid upstroke. To assess for "tardus," auscultate the patient's S2 heart sound while palpating their carotid upstroke. The S2 and carotid upstroke should occur almost simultaneously. If the carotid upstroke comes significantly after the S2 heart sound, "tardus" is present indicating severe aortic stenosis. Other physical exam findings in patients with aortic stenosis include those of both right and left heart failure.






    Comments

    Popular Posts

    Diabetic vascular diseases: molecular mechanisms and therapeutic strategies

    Effects of hot weather, humidity on blood pressure, heart