Unfaithfulness in men may be associated with higher risk of cardiovascular events

How common is unfaithfulness in men?

As expected the results were variable. Some surveys reported that 1.5–4% of married men had extramarital coitus in any given year, others that 23.2% of men have cheated during their current relationship.

Lifetime prevalence of unfaithfulness was between 15% and 50%.

What are the factors related to unfaithfulness?

Men with extramarital affairs more frequently have a dysfunctional primary relationship.

Parenthood and conflicts within the family are associated with a higher risk of having an affair.

Unfaithful men display a higher androgenization, larger testis volume, higher sexual desire, and better sexual functioning.

What are the clinical implications of unfaithfulness in men?

Some studies have suggested that having an extramarital affair could have a negative impact on cardiac morbidity and mortality. Unfaithfulness in men seems to be associated with a higher risk of major cardiovascular events.

References

Fisher AD, Bandini E, Rastrelli G, Corona G, Monami M, Mannucci E, and Maggi M. Sexual and cardiovascular correlates of male unfaithfulness.

Ischemia

Ischemia symptoms can vary based on where in the body the condition occurs, and many times no
symptoms are present until a health complication arises. Chest pain, shortness of breath, and heaviness in the chest can be potential symptoms of ischemia occurring at the heart muscle. Bowel ischemia can cause digestive upset and discomfort, while dizziness, confusion, and dementia can occur in the brain. These symptoms can be severe or minor, although they generally worsen if not treated promptly.

Ischemia is a condition which is characterized by a lack of blood flow to a particular organ or system of the body, which often results in tissue damage. There are both reversible and irreversible varieties of this condition, and there are a number of potential causes and treatments. Sometimes tissue damage is so severe it cannot be fully corrected.

What is a Cardiopathy

Cardiopathy is a medical term that can refer to several different types of heart disease. The condition can involve the weakening of the heart muscle, a structural abnormality, or a blockage that affects the heart's ability to pump blood throughout the body. Cardiopathy can arise because of inherited and congenital disorders, unhealthy lifestyle choices, and acquired medical conditions like high blood pressure. Without an accurate diagnosis and treatment, heart disease is usually fatal. There are many different medical and treatment options, however, that can improve a person's chances of overcoming cardiopathy.

Heart disease may be caused by a number of different factors. Some defects are present at birth, while other conditions do not arise until later in life. Consuming excessive amounts of alcohol, smoking, and eating unhealthy foods greatly increases the risk of developing high blood pressure and atherosclerosis, a condition in which arteries become blocked with buildups of hardened cholesterol. Arterial blockages are a leading cause of heart problems because blood cannot be efficiently pumped through the heart. Cardiomyopathy is another common form of heart disease in which the heart muscle is weakened and thereby inhibited from functioning properly.

Too Little Salt Can Also Be A Problem

We've been bombarded for more than two decades with scientists and doctors telling us to eat less salt. Statistics show that those eating excessive salt in their diets are far more likely to suffer from cardiovascular problems, but as with any nutritional or diet information, moderation and balance is the key. Everyone is familiar with the active salt intake in hot countries like Mexico and Spain, where more salt is lost through perspiration, so it should come as no surprise that too little salt can also be a problem.

A study in the November 23 issue of JAMA shows that too high or too low sodium levels in urine carries a far higher risk for cardiovascular events (for higher levels), or cardiovascular death and hospitalization for congestive heart failure for lower levels.

Researchers also found higher estimated urinary potassium excretion was associated with a reduced risk of stroke.

The exact daily recommended salt intake is still not precisely clear, and would be an academic number, since it would be fairly difficult for the average person to accurately measure how much salt they eat on a day to day basis. A lot would also depend on the climate they live in and how active they are.

Researchers say that :

"Clarifying the optimal daily intake of sodium is particularly important in patients with established Cardiovascular (CV) disease, where it has been inadequately studied. Patients with CV disease may be especially vulnerable to the CV effects of high and low sodium intake and are most likely to receive recommendations on restricting sodium intake."


The authors also note that the optimal level of daily potassium intake, a proposed modifier of the association between sodium intake and CV disease, has not been established.

Martin J. O'Donnell, M.B., Ph.D., and Salim Yusuf, D.Phil., F.R.C.P.C., F.R.S.C., of McMaster University, Hamilton, Ontario, Canada, and colleagues examined the association between sodium and potassium excretion (markers of intake) and CV events and mortality.

The study consisted of an observational analyses of 2 cohorts (n = 28,880) included in the ONTARGET and TRANSCEND trials (November 2001-March 2008 from initial recruitment to final follow-up). The researchers estimated 24-hour urinary sodium and potassium excretion from a morning fasting urine sample. Multivariable models were used to determine the association of urinary sodium and potassium with CV events (myocardial infarction [MI; heart attack], stroke, and hospitalization for congestive heart failure (CHF) and mortality.

At study entry, the average estimated 24-hour excretion for sodium was 4.77 g and 2.19 g for potassium. After a median (midpoint) follow-up of 56 months, the composite outcome occurred in 4,729 (16.4 percent) participants. The researchers found that after multivariable analysis, compared with baseline sodium excretion of 4 to 5.99 g per day (n = 14,156 [15.2 percent with the composite outcome]), higher baseline sodium excretion (18.4 percent for 7-8 g/d and 24.1 percent for greater than 8 g/d) and lower sodium excretion (18.2 percent for 2-2.99 g/d and 20.2 percent for less than 2g/d) were associated with an increased risk of the composite of CV death, heart attack, stroke, and hospitalization for CHF.

Compared with the reference group, higher baseline sodium excretion was associated with an increased risk of CV death (9.7 percent for 7-8 g/day; and 11.2 percent for greater than 8 g/day), MI (6.8 percent for greater than 8 g/day), stroke (6.6 percent for greater than 8 g/day), and hospitalization for CHF (6.5 percent for greater than 8 g/day). Lower sodium excretion was associated with an increased risk of CV death (8.6 percent for 2-2.99 g/day; 10.6 percent for less than 2 g/day), and hospitalization for CHF (5.2 percent for 2-2.99 g/day) on multivariable analysis. Compared with an estimated potassium excretion of less than 1.5 g per day, higher potassium excretion was associated with a reduced risk of stroke on multivariable analysis.

The researchers conclude that :

"Discrepant findings of previous studies are likely due to differences in ranges of sodium intake, study populations, methods of measurement, and failure to explore a nonlinear association ... Compared with moderate sodium excretion, we found an association between high sodium excretion and CV events and low sodium excretion and CV death and hospitalization for CHF, which emphasizes the urgent need to establish a safe range for sodium intake in randomized controlled trials.

Higher urinary potassium excretion was associated with lower stroke risk and is a potential intervention that merits further evaluation for stroke prevention."


They also mention that previous individual prospective cohort studies have either reported a positive association, no association, or an inverse relationship between sodium intake and CV mortality, and that this area clearly needs further investigation.

What Is Heart Rate? What Is A Healthy Heart Rate?

A person's heart rate, also known as their pulse, refers to how many times their heart beats per minute. Our heart rates vary tremendously, depending on the demands we make on our bodies - a person who is sleeping will have a much lower heart rate compared to when he/she is doing exercise.

There is a technical difference between heart rate and pulse, although they both should come up with the same number:
Heart rate - how many times the heart beats in a unit of time, nearly always per minute. The number of contractions of the lower chambers of the heart (the ventricles).
Pulse (pulse rate) - as the blood gushes through the artery from a heart beat, it creates a bulge in the artery. The rate at which the artery bulges can be measured by touching it with your fingers, as on the wrist or neck.
According to Medilexicon's medical dictionary:

Heart beat is "A complete cardiac cycle, including spread of the electrical impulse and the consequent mechanical contraction."

Pulse is "Rhythmic dilation of an artery, produced by the increased volume of blood thrown into the vessel by the contraction of the heart. A pulse may also at times occur in a vein or a vascular organ, such as the liver."


Doctors and other healthcare professionals measure patients' heart rates when monitoring their health, gauging the effectiveness of certain treatments, or making a diagnosis.

Athletes and sports people usually measure their heart beats so that they can gain maximum efficiency from their training regimes.
What is a normal resting heart rate (pulse rate)?
For a human aged 18 or more years, a normal resting heart rate can be anything between 60 and 100 beats per minute. Usually the healthier or fitter you are, the lower your rate. A competitive athlete may have a resting heart rate as low as 40 beats per minute.

Champion cyclist, Lance Armstrong has had a resting heart rate of about 32 beats per minute (bpm). Fellow cyclist Miguel Indurain once had a resting heart rate of 29 bpm.

According to the National Health Service, UK, the following are ideal normal pulse rates at rest, in bpm (beats per minute):
Newborn baby - 120 to 160
Baby aged from 1 to 12 months - 80 to 140
Baby/toddler aged from 1 to 2 years - 80 to 130
Toddler/young child aged 2 to 6 years - 75 to 120
Child aged 7 to 12 years - 75 to 110
Adult aged 18+ years - 60 to 100
Adult athlete - 40 to 60
(There is a considerable amount of overlap from 14 to 17 years of age, with younger and older ages, depending on which health authorities you use for data)

Checking your own heart rate:
The wrist (the radial artery) - place the palm of your hand facing upward. Place two fingers on the thumb side of your wrist gently, you will sense your pulse beating there. Either count them for up to one minute, or thirty seconds and then multiply by two. Counting for 15 seconds and then multiplying by four is less accurate. It is also possible to test the pulse by touching the other side of the wrist, where the ulnar artery is.
The neck (the carotid artery) - place the index and third fingers on the neck, next to your windpipe. When you feel your pulse, either count for the whole sixty seconds, or do it in a 30 or 15 second spell and multiply by two or four.
The human heart rate may also be measured at the following points:

The brachial artery - under the biceps or inside the elbow
Abdominal aorta - over the abdomen
Apex of the heart - by placing your hand or fingers on the chest
Basilar artery - at the side of the head, close to the ear
Dorsalis pedis - the middle of dorsum of the foot
Superficial temporal artery - the temple
The facial artery - the lateral edge of the mandible
The femoral artery - in the groin
The posterior tibial artery - behind the medial malleoulus of the feet


Testing the pulse rate at the radial artery


An electrocardiograph, also known as an ECG or EKG is a more accurate way of checking a patient's heartbeat. ECGs are commonly used in critical care medicine, and many other fields of medicine.

Sports shops sell heart-rate watches that communicate with a device you strap around your chest. The readings on your watch tell you what your heart rate is - some can even work out heart-rate averages over set periods, such as the whole of an exercise session.

Bear in mind that your heart rate can be influenced by several factors, such as:
Your level of physical activity at the time
How fit you are
The ambient temperature
The position of your body - standing, sitting, lying down, etc.
Your mental and/or emotional state - excitement, anger, fear, anxiety, and other factors can raise your heart beat
The size of your body
Some medications
Bradycardia - a medical term that refers to a heart beat that is too slow, such as below 60 beats per minute (for a non-athlete)

Tachycardia - a medical term that refers to a resting heart beat of more than 100 beats per minute, an excessively fast heart beat for an adult

If you think you have bradycardia or tachycardia, see your doctor, especially if you are also short of breath, feel dizzy, and/or have fainting episodes.
What is your maximum heart rate?
This is the maximum number of times your heart can beat per minute. It is a useful measure for sports people, so they can gauge their training intensities.

There are two ways you can find out what your maximum heart rate is:
Have it clinically tested - usually by a cardiologist or an exercise physiologist. People over 35 years of age who are overweight or have not done exercise for a long time are advised to have their maximum heart rates clinically tested by a trained health care professional. The health care professional may use a treadmill and a electrocardiograph.
Predicted maximum heart rate - this involves using a mathematical formula, called the age-adjusted formula.

For adult males: 220 minus your age. For a 25 year-old man it would be 195 bpm (220 minus 25)

For adult females: 226 minus your age. For a 25 year-old woman it would be 201 bpm (226 minus 25)

It is important to remember that this formula gives a rough figure, a ballpark figure. Ideally, you should have your maximum heart beat measured clinically.

Atherosclerosis Pathology

Definition

The term atherosclerosis is derived from the Greek "athero," meaning gruel, or wax, corresponding to the necrotic core area at the base of the atherosclerotic plaque, and "sclerosis" for hardening, or induration, referring to the fibrous cap of the plaque's luminal edge.

The earliest pathologic descriptions of atherosclerotic lesions focused on morphologies of fatty streaks to fibroatheromas (FAs) and advanced plaques complicated by hemorrhage, calcification, ulceration, and thrombosis. In the mid 1990s the terminology used to define atheromatous plaques was refined by the American Heart Association (AHA) Consensus Group headed by Dr. Stary.{{Ref2}

The classification consists of 6 different numeric categories to include early lesions of initial type I, adaptive intimal thickening; type II, fatty streak; and type III, transitional or intermediate lesions; and advanced plaques characterized as type IV, atheroma; type V, fibroatheroma or atheroma with thick fibrous cap; and type VI, complicated plaques with surface defects, and/or hematoma-hemorrhage, and/or thrombosis.

A modified version of the AHA classification was developed by our laboratory to include important pathologic lesions responsible for luminal thrombosis other than plaque rupture, such as plaque erosion and calcified nodule.[1] In this modified classification, numeric AHA lesions types I to IV are replaced by descriptive terminology to include adaptive intimal thickening, intimal xanthoma, pathologic intimal thickening (PIT), and fibroatheroma, as shown in the table below.

Lesion reference to AHA types V and VI was discarded, because it failed to account for the 3 different morphologies (rupture, erosion, and calcified nodule) that give rise to acute coronary thrombosis.

Epidemiology

Coronary artery disease remains the leading cause of death in the Western world. A new or recurrent myocardial infarction afflicts approximately 1.1 million people in the USA per year, of which 40% are fatal. Sudden cardiac death as a first manifestation of the atherosclerotic process occurs in >450,000 individuals annually. The vast majority of acute myocardial infarctions (approximately 75%) occur from plaque rupture; other causes of coronary thrombosis include erosion and calcified nodules.[3]

Although lesions with rupture occur in men of all ages (this is consistent for all plaque morphologies with thrombi), the frequency of sudden coronary death decreases with advancing age. The incidence of rupture varies with each decade, and the highest incidence of plaque rupture is seen in the 40s in men, whereas in women the incidence increases beyond age 50 years. Approximately 80% of coronary thrombi in women older than 50 years occur from plaque rupture, and there is a strong association with circulating cholesterol. In acute myocardial infarction or sudden coronary death, plaque erosion occurs primarily in patients younger than 50 years and represents the majority of acute coronary thrombi in premenopausal women. Furthermore, 20-25% of acute myocardial infarcts occurring in hospitalized patients are due to plaque erosion.

The etiology of atherosclerosis is unknown, but there are multiple factors that contribute to atherosclerotic plaque progression. These include genetic and acquired factors. Processes involved in atherosclerosis include coagulation, inflammation, lipid metabolism, intimal injury, and smooth muscle cell proliferation (see the image below).

Factors that affect these processes may inhibit or accelerate atherosclerosis. The most common risk factors are family history, hyperlipidemia, diabetes mellitus, cigarette smoking, hypertension, and dietary deficiencies of antioxidants.[4] Early lesion development is marked by lipid retention with activation of endothelial adhesion molecules. Inflammatory macrophages play a significant role throughout all phases of atherosclerotic progression; hyperlipidemia-induced macrophage infiltration of the arterial intima is one of the earliest pathologic changes.

A major event in atherosclerotic plaque progression is thrombosis, which may occur in any arterial bed (coronary, aorta, carotid, etc.) Three different morphologies (rupture, erosion and calcified nodule) may give rise to acute coronary thrombosis. Plaque rupture is defined by fibrous cap disruption or fracture, whereby the overlying thrombus is in continuity with the underlying necrotic core. Plaque erosion is identified when serial sectioning through a thrombus fails to show communication with a necrotic core or deep intima; the endothelium is absent, and the thrombus is superimposed on a plaque substrate primarily composed of smooth muscle cells and proteoglycans. Calcified nodules are characterized by eruptive dense calcified bodies protruding into the luminal space and represent the least frequent morphology associated with luminal thrombosis. See the following diagram.
Atherosclerosis occurs in elastic and muscular arteries and may occur iatrogenically in vein grafts interposed in the arterial circulation. The aorta is affected earliest, followed by the carotid arteries, coronary arteries, and iliofemoral arteries. Initially, lesions are most common at branch points, at sites of low shear, where a predilection to plaque formation has been observed. Coronary lesions, including thrombi occuring at atherosclerotic sites, are most prevalent in the proximal coronary arteries: the proximal left anterior descending coronary artery, followed by the right and left circumflex coronary arteries.

Atherosclerosis causes symptoms by arterial obstruction, embolization of plaque material, and weakening with rupture of the arterial wall. Obstruction with or without embolization causes ischemia of the circulation supplied by the vessel. Ischemic strokes result from atherosclerosis of the carotid arteries and aortic arch, which embolize thrombi and atherosclerotic material, as well as local atherosclerosis of the cerebral vessels.

Obstruction of coronary arteries causes myocardial ischemia. Myocardial ischemia may present as acute coronary syndromes (acute ST elevation infarct, non-ST elevation infarct, and unstable angina), sudden death, or chronic congestive heart failure. Obstruction of iliac vessels results in ischemia of the lower extremities (claudication). Atherosclerotic aneurysms show a predilection for the aorta, especially the abdominal aorta. Aortic aneurysms may rupture and cause death by hemorrhage into the retroperitoneal space or pleural cavities, depending on the location.

The gold standard for imaging atherosclerotic lesions of the coronary circulation is angiography. Newer imaging modalities, such as cardiac magnetic resonance imaging (MRI), are being developed that may provide less invasive methods of determining sites of stenosis. Imaging of atherosclerotic lesions of the carotid circulation include carotid ultrasonography, a noninvasive technique.


Gross Findings

In the aorta, atherosclerotic lesions have been classified largely on gross findings. Fatty streaks are yellow, minimally raised lesions that demonstrate abundant lipid when stained with oil red O. Fibrous plaques are raised, white, firmer areas that are relatively well demarcated. Ulcerated plaques demonstrate surface thrombosis and represent ruptured fibroatheromas.

Coronary lesions, when cut on cross-section, show bright yellow cores when there is abundant extracellular lipid, as in fibroatheromas. Ruptured or eroded plaques demonstrate a luminal thrombus, which is pale red or tan in the unfixed state, depending on the proportion of fibrin, platelets, and entrapped red blood cells. Calcified plaques are hard and brittle, are difficult to cute with a scalpel blade, and must be decalcified during or after fixation so that sections for microscopy may be performed.

The gross findings of carotid plaques are similar to those of the coronary arteries. There is often calcification, which can be seen and felt as mineral deposits. Atheromas are bright yellow on cross-section, and atheromas with intraplaque hemorrhage show a more variegated yellow-red cut surface. Fibrous plaques are homogeneous, firm and white, and often show areas of calcification.

Atrial fibrillation

Introduction

Atrial fibrillation is a condition in which there is disorganized atrial activity resulting in loss of effective atrial contraction. The atria beat between 350 and 600 times per minute. These rapid, irregular impulses pass through the AV node of the heart to the ventricles and result in a rapid and "irregularly irregular" ventricular response. There are paroxysmal and persistent forms.

Epidemiology

Incidence and prevalence

AF is the most common sustained arrhythmia.
Approximately 2.2 million individuals in the United States and 4.5 million individuals in the European Union have atrial fibrillation.[1,2]

Gender

Men are more likely than women to develop AF, but women diagnosed with it carry a longer-term risk of premature death.

Age

The incidence of atrial fibrillation increases with age. The prevalence in individuals over the age of 80 is about 8%.[3] In developed countries, the number of patients with atrial fibrillation is likely to increase during the next 50 years, due to the growing proportion of elderly individuals.[4]

Race

Blacks have half the age adjusted incidence when compared to Caucasians.

Causes of AF

1. Coronary heart disease
2. Congestive heart failure
3. Pericarditis
4. Myocarditis
5. Rheumatic heart disease
6. Hypoxia
7. Hypertrophic cardiomyopathy
8. Hypertensive cardiomyopathy
9. Dilated cardiomyopathy
10. Pulmonary embolism
11. Alcohol
12. Lone atrial fibrillation
13. Thyrotoxicosis
14. Theophylline
15. Blunt trauma
16. Sick sinus syndrome
17. Sympathomimetic toxicity
18. Post-CABG surgery

Risk factors

Risk factors for development of AF include:

1. Those who have had coronary heart disease, heart attack or heart failure.
2. It's also found in people with heart valve disease, an inflamed heart muscle or lining (endocarditis) or
3. Recent heart surgery
4. People with atherosclerosis and angina
5. Congenital heart defects
6. People with chronic lung disease, emphysema and asthma
7. Thyroid disorders
8. Diabetes
9. High blood pressure
10. Excessive consumption of alcohol, cigarette or stimulant drugs, including caffeine.

Pathogenesis

Atrial fibrillation is caused by multiple re-entrant circuits or "wavelets" of activation sweeping around the atrial myocardium. These are often triggered by rapid firing foci. Conduction of atrial impulses to the ventricles is variable and unpredictable. Only a few of the impulses transmit through the atrioventricular node to produce an irregular ventricular response. Wavelength is critical in the pathogenesis of AF. Increased wavelength may prevent or end AF. This can be produced by antiarrhythmic drugs.

• Paroxysmal AF is characterized by brief episodes of the arrhythmia, which can resolve by themselves.
• In persistent AF, the episodes require some form of intervention to return the heart rhythm back to normal.
• For those with permanent AF, intervention (if successful at all) only restores normal heart rhythm for a brief time.

As the uncoordinated atrial depolarizations from various places within the atria in AF causes blood in the upper chambers of the heart not to be carried through in a regular manner, there is a tendency for blood clots to form in these chambers. These clots may then be swept into the ventricles and pumped into the lungs from the right side of the heart and into the general circulation from the left ventricle. Sometimes, clotted blood dislodges from the atria and results in a stroke.

Symptoms and signs

The symptoms of atrial fibrillation (AF) include palpitations, irregular heart beat, shortness of breath, chest discomfort, dizziness and syncopal attacks. Many patients experience feelings of weakness, exercise intolerance, caused by the heart�s diminished pumping ability. The awareness of a rapid and/or irregular heart beat also may lead to anxiety. Systemic embolization may result as well as precipitation or intensification of heart failure.
Patients who have otherwise healthy hearts may be better able to tolerate AF. People with underlying heart disease are generally less able to tolerate AF without complication. Once AF becomes symptomatic, it becomes more serious as it indicates that the heart is failing to pump adequate amounts of blood to the body.
The ventricular rate depends on the degree of atrioventricular block, but when 1:1 conduction occurs a rapid ventricular response may result. Increasing the degree of block with carotid sinus massage or adenosine may aid the diagnosis.

Complications

• Stroke: The relative risk for the development of stroke can be determined by assessing the patient's CHADS2 score.
• Heart failure: Heart failure and pulmonary edema can be precipitated or aggravated by AF.
• Cardiac ischemia: Tachy-arrhythmia can precipitate ischemic heart disease.

Diagnosis

Atrial fibrillation can be strongly suspected simply by feeling the pulse, but a complete diagnosis calls for full medical investigation.

EKG

One of the most important tests is the electrocardiograph (EKG), which can also give evidence of any previous heart disease that may have been the cause of the condition. If the AF is intermittent, it may be necessary for the patient to wear a Holter monitor for an extended period of time in order to catch one or more episodes of AF. Often the EKG and Holter are used in conjunction with a chest x-ray and echocardiogram, which shows the heart walls as they are beating. EKG features in AF include:

• P waves absent; oscillating baseline f (fibrillation) waves
• Atrial rate 350-600 beats/min
• Irregular ventricular rhythm
• Ventricular rate 100-180 beats/min

Fast atrial fibrillation may be difficult to distinguish from other tachycardias. The RR interval remains irregular, however, and the overall rate often fluctuates. Mapping R waves against a piece of paper or with calipers usually confirms the diagnosis.

Imaging

A chest X-ray in a young patient may suggest the presence of congenital heart disease. In an older patient it can give information on the size of the heart and whether heart failure is present. The echocardiogram is useful in ruling out thrombus formation as well as determining the diameter of the left atrium (> 4.5 cm).

Blood tests

Routine blood tests can also be useful in the diagnosis. They may show anemia, which may be complicating the situation, impaired kidney function, or thyroid gland overactivity (thyrotoxicosis).

Treatment

Left untreated, the overactive heart muscle can weaken and stretch out. This makes it harder for the atria to contract properly, so blood backs up even more. This problem not only increases the risk of stroke, but it can also lead to congestive heart failure. Treating AF correctly is the best way to reduce stroke risk. Therapy is indicated in patients with persistent, permanent or recurrent paroxysmal AF. The goals of treatment plans for AF are:

• Prevent blood clots from forming
• Heart rate control within a relatively normal range
• Restore a normal heart rhythm, if symptomatic

1. Medicine to prevent clots

To lower the risk of stroke either aspirin or Warfarin are generally prescribed. Aspirin has an antiplatelet effect and is less likely to cause abnormal bleeding, but Warfarin seems to be more effective at preventing clot-caused strokes. Regular INR tests are carried out to monitor the dose of Warfarin. INR should usually test between 2.0 and 3.0.
The choice of giving a patient Warfarin or aspirin depends on the patient's risk factors for development of thromboembolic disease. This can be determined by assessing a patient's CHADS2 score.[5]

• CHF (1 point)
• Hypertension (1 point)
• Age 75 (1 point)
• Diabetes (1 point)
• Second stroke (2 points)

A patient with a low score (0) can receive aspirin 325 mg daily for prophylaxis against coagulation. Those with an intermediate score (1-2) can receive either aspirin or Warfarin depending on the patient's preference. Those with a high CHADS2 score (3 or more) should receive Warfarin prophylaxis to maintain an INR of 2.0-3.0, unless contraindicated (e.g., history of falls, clinically significant GI bleeding, inability to obtain regular INR screening).

2. Rate control

• Beta-blockers (like metoprolol, carvedilol or propanolol) and calcium-channel blockers (like verapamil or diltiazem), which slow the heart rate;
• Digoxin, which slows the heart rate through the AV node, therefore decreasing the rate at which the electrical impulses conduct from the atria to the ventricles.
• In cases who are refractory to the above measures or in those with heart failure or pre-exitation syndrome, use amiodarone, consider cardiac consultation,

3. Rhythm control (cardioversion)

Cardioversion changes an abnormal heart rate back to a normal one. Cardioversion can be done through medication or through electricity.
Based on the AFFIRM, RACE and STAF trials rate control with anticoagulation is the preferred treatment. Rhythm control (cardioversion) in asymptomatic patients does not appear to affect survival. Electrical or chemical cardioversion may be required in symptomatic cases or in emergency situations such as those with cardiovascular instability and heart failure.

• Chemical cardioversion

Medicines include amiodarone, dofetilide, disopyramide, flecainide and procainamide.

• Electrical cardioversion

Electrical cardioversion is typically used to treat cases of persistent or permanent AF, and it is often used with medication.
There are two types of electrical cardioversion: external and internal. For external cardioversion, two external paddles are placed on the patient�s chest or on the chest and back. A high-energy electrical shock is sent through the patches, through the body to the heart. The energy shocks the heart out of AF and back into normal rhythm.
Internal cardioversion uses a similar approach, but instead of using paddles on the outside of the body, a catheter is inserted through a vein to the heart. The electrical energy is delivered through the catheter to the inside of the heart to stop the AF. Internal cardioversion has met with high success and provides an alternative to external cardioversion.

4. Ablation

Cardiac ablation is a medical procedure performed to prevent abnormal electrical impulses from ever beginning in the first place. In an ablation procedure, the electrophysiologist first does mapping, which means the precise area in the heart at which the abnormal signals start are pin-pointed. The electrophysiologist then eliminates the small area of tissue that is causing the arrhythmia.
There is also a procedure called AV nodal ablation. This involves ablating the AV node, keeping the abnormal impulses from traveling to the heart�s lower chambers. A pacemaker is used to regulate the heartbeat after this therapy.

5. AF Suppression

AF Suppression is designed to suppress atrial fibrillation (AF). An implanted pacemaker stimulates the heart in a way that preempts any irregular rhythms.
A clinical study has found that a software-based AF Suppression algorithm can suppress symptomatic paroxysmal and persistent AF better than standard pacing. The AF Suppression algorithm is available in certain ICDs and pacemakers manufactured by St. Jude Medical.

Prognosis and survival

Prognosis is related to the underlying cause; it is excellent when due to idiopathic atrial fibrillation and relatively poor when due to ischemic cardiomyopathy. Healthy life style, regular checks on blood pressure and treatment for raised blood pressure can reduce the chances of developing the heart problems that cause atrial fibrillation.

Some study results

Among people with atrial fibrillation who not are taking the anticoagulant drug Warfarin, women are more likely to form dangerous blood clots than men, according to a study.
Men who explode with anger or expect the worst from people are more likely to develop an irregular heart rhythm called atrial fibrillation, according to another study report.

Aortic valve stenosis

Introduction

The aortic valve is a flap-like opening located between the left side of the heart and the aorta. The aorta is the main artery carrying blood from the heart. Blood is pumped by the left ventricle across the aortic valve into the aorta and the arteries of the body. Aortic stenosis causes restricted systolic opening of the valve leaflets, with a mean transvalvular pressure gradient of at least 5-10 mmHg. When the degree of narrowing becomes significant enough to impede the flow of blood from the left ventricle to the arteries, heart problems develop.
In the Euro Heart Survey on Valvular Heart Disease, aortic valve stenosis was the most common valve abnormality. Aortic valve sclerosis is commonly defined as a focal or diffuse thickening of the aortic cusps with calcific nodules generally at the base of leaflets and transvalvular velocity at Doppler still in the normal range (Vmax <2 m/s).

Epidemiology

Prevalence

Rheumatic valve disease has declined dramatically in the United States during the past 50 years, and isolated rheumatic aortic valve is unusual in any event. With our aging population, calcific aortic stenosis accounts for the vast majority of aortic valve disease. In the elderly, mild thickening and/or calcification of a trileaflet aortic valve without restricted leaflet motion (ie, aortic sclerosis) affects about 25% of the population > 65 years of age. Calcific aortic stenosis, however, affects approximately 2% to 3% of those > 75 years. Thus not all patients with aortic sclerosis will go on to develop obstructive aortic valve disease.

Incidence

The approximate overall incidence of an anatomic bicuspid aortic valve is 1% to 2% of the population. Of these individuals, most will go on to present with aortic stenosis, while a minority will develop a regurgitant lesion. Particularly, the aortic valve sclerosis (aortic valve thickening and calcification without pressure gradient) seem to affect about one fourth of adults over 65 years of age, while the aortic valve stenosis is present in 2�9% of general population over 65 years of age; an increased prevalence of both sclerosis and stenosis with aging (48% and 4% in those over 85 years) is observed.
The relative frequency of the postinflammatory disease (i.e. post-rheumatic) decreased from 30% to 18% and the relative frequency of the bicuspid aortic valve changed from 37% to 33%; in contrast, the relative frequency of degenerative-calcific aortic stenosis (an "atherosclerotic" form of disease, see below) increased from 30% to 46%. These differences were striking in subjects older than 70 years.

Gender

Aortic stenosis due to bicuspid valves affects males three times more often than females, but late-life calcific disease of a trileaflet valve involves both sexes equally.

Age

Aortic stenosis can occur at any age (because the causes are different) but is usually asymptomatic until middle or old age. Until few years ago, aortic stenosis was considered a physiologic process related to aging without clinical relevance. However, aortic valve sclerosis is not observed in about 50% of people over 80 years old.

Causes and risk factors

A number of conditions contribute towards aortic stenosis. Three conditions that are known to cause aortic stenosis are:

Valvular causes

1. Calcification of a bicuspid valve

Bicuspid aortic valve is the most common cause of aortic stenosis in patients under age 65. Normal aortic valves have 3 thin leaflets called cusps. About 2% of people are born with aortic valves that have only 2 cusps (bicuspid valves). Although bicuspid valves usually do not impede blood flow when the patients are young, they do not open as widely as normal valves with 3 cusps. The turbulent blood flow causes excessive wear and tear leading to calcification, scarring, and reduced mobility of the valve leaflets over time. About 10% of bicuspid valves become significantly narrowed, resulting in the symptoms and heart problems of aortic stenosis.

2. Senile calcific aortic stenosis

The most common cause of aortic stenosis in patients 65 years and over is called "senile calcific aortic stenosis." With aging, protein collagen of the valve leaflets is destroyed, and calcium is deposited on the leaflets. Once valve leaflet mobility is reduced by calcification, turbulence across the valve increases, causing scarring, thickening, and stenosis of the valve. Why this aging process progresses to cause significant aortic stenosis in some patients but not in others is not known.

3. Rheumatic fever

Rheumatic fever rarely causes isolated aortic stenosis. Rheumatic fever is a condition resulting from untreated infection by group A streptococcal bacteria. Damage to valve leaflets from rheumatic fever causes increased turbulence across the valve and more damage. The narrowing from rheumatic fever occurs from the fusion of the commissures of the valve leaflets. Rheumatic aortic stenosis usually occurs with some degree of aortic regurgitation. Under normal circumstances, the aortic valve closes to prevent blood in the aorta from flowing back into the left ventricle. In aortic regurgitation, the diseased valve allows leakage of blood back into the left ventricle as the ventricular muscles relax after pumping. These patients also have some degree of rheumatic damage to the mitral valve.

Subvalvular causes

• Subvalvular aortic stenosis
• Hypertrophic obstructive cardiomyopathy

Pathogenesis

Valvular aortic stenosis results in chronic left ventricular pressure overloading. At any stage of life, however, the natural history of aortic stenosis largely reflects the functional integrity of the mitral valve. As long as adequate mitral valve function is maintained, the pulmonary bed is protected from the systolic pressure overloading imposed by aortic stenosis. In contrast to mitral valve disease where the pulmonary circuit is directly involved, compensatory concentric left ventricular hypertrophy allows the pressure overloaded ventricle to maintain stroke volume with modest increases in diastolic pressure, and patients can remain asymptomatic for many years.Eventually, left ventricular hypertrophy results in either diastolic dysfunction with the onset of congestive symptoms or myocardial oxygen needs in excess of supply with the onset of angina.

Symptoms

Most patients with calcific aortic stenosis report knowing of a cardiac murmur for many years. Common symptoms of aortic stenosis include: coughing at night; fainting, especially with physical activity; fatigue; shortness of breath that worsens at night or with exertion; angina; and, visual impairments. Some patients may also experience exertional syncope, probably reflecting the inability to increase cardiac output and maintain blood pressure in response to vasodilation. Vasodepressor syncope, however, may be an operative mechanism in a portion of these syncopal episodes.

Signs

On physical examination, the harsh systolic diamond shaped (crescendo-decrescendo) murmur of aortic stenosis, loudest at the base of the heart and radiating to the carotids, is often, but not always, prominent. Low output states, obesity, or chronic lung disease may mask the findings. The murmur may radiate toward the cardiac apex, in which case the harsh component is lost; this finding may be mistaken for a second murmur. Other hallmarks of significant aortic valve stenosis include a single (pulmonic) component of the second heart sound and a sustained left ventricular apical impulse with a fourth heart sound. The slowly rising, low volume carotid arterial pulses of severe aortic stenosis may be noted in younger patients, but changes in arterial compliance often mask these findings in the elderly.

Assessment

Patients with typical findings of aortic stenosis should have a detailed history-taking session with inquiry into habitual activity levels and any changes in exercise tolerance. The onset of any of the classic symptoms of left ventricular outflow obstruction, namely angina, syncope, or heart failure, in a patient with valvular aortic stenosis indicates advanced valve disease and should be carefully and promptly evaluated. The severity of symptoms is not always related to the severity of the disease. In fact, people sometimes die suddenly from aortic stenosis without having had symptoms. Symptoms usually occur when the aortic valve area narrows to less than 1 square centimeter. Critical aortic stenosis is present when the valve area is less than 0.7 square centimeters.

Diagnosis

The electrocardiogram often shows changes of left ventricular hypertrophy. In rare instances, electrical conduction abnormality can also been seen.
The chest X-ray is seldom helpful, although occasionally heavy calcification of the valve or post-stenotic ascending aortic dilation may be seen.
With its widespread availability, two-dimensional and Doppler echocardiography has become the study of choice in the evaluation of patients with suspected valvular disease. Echocardiography allows assessment of the anatomy of the valve as well as chamber size and ventricular function. Doppler studies permit estimation of pressure gradients, as well as aortic valve area by employing the continuity equation.
With good quality echocardiography, cardiac catheterization is usually not required for diagnosis of patients with aortic stenosis. However, a cardiac catheterization is the gold standard in evaluating aortic stenosis. A pre-operative coronary angiography is generally performed in men over 40 years old and women over 50.

Treatment

Patients with (predominant) aortic stenosis fall into one of four categories of severity:

1. valve area > 1.2 cm2����������.mild
2. valve area 1.0 to 1.2 cm2��������.moderate
3. valve area 0.7 to 1.0 cm2��������.severe
4. valve area < 0.7 cm2����������.critical

1. Observation

Asymptomatic patients with mild to moderate aortic stenosis should have medical follow-up with regular inquiry as to changes in exercise tolerance or other symptoms. Serial echocardiographic examination should be based on an understanding of the natural history of the lesion, as outlined below. Patients should avoid strenuous activity, and particularly avoid post-prandial exertion. Infective endocarditis precautions following American Heart Association guidelines must be emphasized at each visit.

2. Antihypertensives

Hypertension occurs in about 20% to 30% of patients with mild to moderate aortic stenosis and should be managed with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers titrated slowly. Selected patients may be given modest doses of concomitant beta-blockers.
A supervised exercise tolerance test may provide helpful objective assessment in patients with echocardiographic evidence of moderate aortic stenosis who report atypical symptoms, who minimize complaints, or who are sedentary and therefore might not experience exercise intolerance. Functional limitation with inability to exercise to levels greater than 6 metabolic equivalents (METs) may, in some cases, be viewed as a "symptom." Stress testing is not advocated for patients with very severe left ventricular outflow obstruction.

2. Valve replacement

Symptomatic patients, ie, those with angina, syncope, dyspnea, with moderate, severe, or critical aortic stenosis should undergo valve replacement. Indications for aortic valve surgery include moderate aortic stenosis in patients requiring coronary bypass grafting and/or any other cardiac surgery, exercise-induced hypotension, and asymptomatic severe aortic stenosis with evidence of left ventricular dysfunction. Smoking cessation and diabetic control are mandatory after the replacement. Dental care should be completed with antibiotic prophylaxis before surgery.
The advantages and drawbacks of mechanical versus bioprosthetic valves should be discussed with the patient and his or her family. Often the choice of prosthesis is straightforward, but younger patients in particular may have special needs, which should be addressed Bioprosthetic valves offer the advantage of not requiring long-term oral anticoagulation, but have the drawback of relatively limited durability. In contrast, mechanical valves offer long-term durability, but require lifelong warfarin therapy. The generally accepted risk of serious bleeding with warfarin is on the order of 3% per year. Childbearing in women and vigorous sports activities in men are contra-indications to chronic oral anticoagulation with warfarin, and may figure importantly in the choice of valves. In general, bioprosthetic valves are preferred in patients over the age of 60 years and mechanical valves under the age of 50. Homograft aortic valve replacement with a cryopreserved cadaveric valve may offer specific advantages in patients with infective endocarditis or with disease of the aortic root. If significant narrowing of the coronary arteries is found, coronary artery bypass graft surgery (CABG) can be performed during aortic valve replacement surgery.

3. Balloon valvuloplasty

Balloon valvuloplasty is a technique that lowers the pressure across the valve by slightly enlarging the opening. This is usually done when someone is not stable enough for corrective surgery.
Current evidence indicates that calcific aortic stenosis progresses, on the average, at a rate of about 0.1 cm2 per year decline in valve area. To date, no medical therapy exists for the treatment of degenerative aortic stenosis. The possible impact of 'secondary prevention' measures, particularly lipid lowering with HMG-CoA reductase inhibitors (statins), on the progression of aortic stenosis is under investigation.

Follow up

Successful replacement of the valve restores normal blood flow. The long-term outcome is usually very good. Artificial valves wear out over a period of years. Their function is monitored, and the valves are replaced as necessary. A prosthetic heart valve commits a patient to continued infective endocarditis prophylaxis, regular cardiac follow-up, and often to continued medical therapy, including anticoagulation with warfarin for those with mechanical prostheses. Re-operation may be required for malfunction of the prosthetic valve. In addition, a small but not insignificant subset of patients may require implantation of a permanent pacemaker after valve surgery.

Prognosis and survival

Serious long-term effects of aortic stenosis without timely treatment include:

• congestive heart failure
• coronary heart disease
• enlargement of the left ventricle
• pulmonary edema
• sudden death (occurs in less than 1%)

With surgery, the patient can expect to live a normal life with necessary precautions as explained above.

Aortic aneurysm

 

 

Introduction

An aortic aneurysm is an abnormal bulge in the wall of the aorta. Enlargement of the aorta may be only mild in degree and termed "ectasia." In general, if the diameter of the aneurysm is more than 1.5 times the size of the normal aorta, it is called an aneurysm.
Although an aneurysm can develop anywhere along the aorta, abdominal aneurysms are more common than thoracic ones. An aortic aneurysm is serious because - depending on its size - it may rupture, causing life-threatening internal bleeding. The risk of an aneurysm rupturing increases as the aneurysm gets larger. The risk of rupture also depends on the location of the aneurysm. When detected in time, an aortic aneurysm can usually be repaired with surgery.

Epidemiology

Incidence

• Ruptured aortic aneurysm is the 13th leading cause of death in the US.
• More than 15,000 Americans die each year due to ruptured aneurysms, many of them needlessly.
• The number of aneurysms in the United States is increasing as the population increases.
• Many people don't even make it to the hospital, and those who do often die of complications.

Gender

Aneurysm is 5 times more common in men than in women.

Age

Clinically important aneurysms over 4 cm in diameter are present in about 1 percent of men between the ages of 55 and 64; the prevalence increases by 2 to 4 percent per decade thereafter.

Race and ethnicity

The disease is predominant in men of the white race. In black men, black and white women the incidence of aortic artery aneurysm (AAA) is identical.

Morbidity

38 to 50 percent of the AAA patients suffer from hypertension, 33 to 60% from coronary artery disease, 28% from cerebrovascular diseases and 25% from peripheral occlusive disease.

Causes and risk factors

• Age over 55 years (Risk increases with age)
• A family history of AAA is particularly concerning
• Smoking
• High blood pressure

Pathogenesis

Most aneurysms are caused by a breakdown in the proteins that provide the structural strength to the wall of the aorta. These proteins, called collagen and elastin can gradually deteriorate with age, but inflammation that is associated with atherosclerosis can accelerate this process even in younger people. There are also naturally occurring enzymes that cause the breakdown of collagen and elastin. An excess of these enzymes or other conditions that activate these enzymes may also contribute to the formation of an aneurysm, or its sudden growth. In rare cases an aneurysm may be caused by infection (mycotic aneurysms). There is still much to be learned about the cause of aneurysms and their growth, but fortunately we have successful, permanent treatments for AAA when they occur. Vascular surgeons have performed much of the basic research on aneurysm formation.

Types of Aortic Aneurysms

Aortic aneurysms are classified by shape, location along the aorta, and how they are formed.

True aneurysms and pseudoaneurysms

The wall of the aorta is made up of three layers: a thin inner layer of smooth cells called the endothelium, a muscular middle layer which has elastic fibers in it called the media, and a tough outer layer called the adventitia. When the walls of the aneurysm have all three layers, they are called true aneurysms. If the wall of the aneurysm has only the outer layer remaining, it is called a pseudoaneurysm. Pseudoaneurysms may occur as a result of trauma when the inner layers are torn apart.

Shape

• Fusiform aneurysms

Most fusiform aneurysms are true aneurysms. The weakness is often along an extended section of the aorta and involves the entire circumference of the aorta. The weakened portion appears as a generally symmetrical bulge.

• Saccular aneurysms

Occasionally an aneurysm may occur because of a localized weakness of the artery wall (saccular). Saccular aneurysms appear like a small blister or bleb on the side of the aorta and are asymmetrical. Typically they are pseudoaneurysms caused either by trauma (such as a car accident) or as the result of a penetrating aortic ulcer.

Location

• Thoracic aortic aneurysm (TAA)

A TAA is a diseased, weakened, and bulging section of the aorta in the chest. This condition, if not treated, could result in a rupture of the aorta, leading to life-threatening internal bleeding. The aneurysm may be caused by vascular disease, injury, or a genetic defect of the tissue. TAA is sometimes found in people with Marfan�s syndrome, which is characterized by many anomalies including elongated bones. It is also associated with Turner syndrome, which results from a missing X chromosome and is associated with dwarfism and arrested sexual development in addition to aortic aneurysm. TAA also can run in families independent of those two syndromes. Because it is difficult to diagnose victims often die young. People with TAA remain unaware of the risk they face because the slowly enlarging aorta does not cause any symptoms until it has reached a critical diameter. At that point, the aorta dissects or ruptures, both of which are life-threatening. Typically, the patient develops chest pain and usually goes to an emergency department to seek treatment.

• Abdominal aortic aneurysm (AAA)

More than 90% of abdominal aortic aneurysms originate below the renal arteries. The diameter is the most important predictor of aneurysm rupture with up to a 40% risk of rupture over 5 years for aneurysm > 5 cm. When they do rupture they tend to rupture leftward and posteriorly.

Symptoms and signs

Most aortic aneurysms have no symptoms. In fact, most are diagnosed on a chest X-ray or computerized tomography (CT) scan performed for evaluation of another condition, such as lung disease, or during routine exams. Symptoms may occur, however, due to the aneurysm pressing on nearby organs or tissue, or if the aneurysm leads to dissection. Symptoms of dissection include severe tearing pain in the chest or back, stroke, cold or numb extremities, or abdominal pain.

Screening

When aortic aneurysms are diagnosed early, treatment is safe and effective and the aneurysm is cured. AAA can be diagnosed by a simple ultrasound scan that can be performed in a few minutes without risk or discomfort.
Men between the ages of 65 and 75 who are or have been smokers should have a one-time ultrasound to screen for abdominal aortic aneurysm, according to a new recommendation from the U.S. Preventive Services Task Force. Nearly 70 percent of men in this age group have smoked and would benefit from routine screening to check for aneurysms.

Diagnosis

Most patients have no symptoms at the time an AAA is discovered. Aneurysms are often detected on tests that were performed for entirely different reasons. Abdominal aortic aneurysms may be diagnosed by a doctor during a physical exam, or sometimes patients notice a pulsating mass in their abdomen. The first hint of an aortic aneurysm may be an abnormal chest X-ray. Although AAA can be detected by physical examination, most are diagnosed today using an ultrasound scan or CAT scan, simple exams that are non-invasive and can be done as an outpatient. Magnetic resonance imaging (MRI) can also help. These exams also tell us about the size of the aneurysms � the key element to determine the need for treatment. Since major surgery was required in the past to repair an aortic aneurysm, that decision depended upon a comparison of the risk of rupture with risk of the surgery itself. Most doctors agree that for someone in good health, an AAA larger than 5 centimeters in diameter (about the size of a lemon) needs treatment. Smaller aneurysms may also need treatment if they cause symptoms (like back pain or abdominal pain), or tests show that the aneurysm has rapidly grown larger.

Treatment

1. Watch and wait

When detected in time, most ruptures can be prevented by repairing the aneurysms with an operation. Treatment for an aneurysm depends on its size and location and the general health of the person. If the aneurysm is small and without symptoms, a "watch-and-wait" approach may be suggested with regularly scheduled images of the aneurysm to check the size. However, if the aneurysm is large enough, or if the aneurysm is growing more than 1 centimeter per year, surgery may be the best option.
Women are more likely than men to die from aortic dissection according to one of the first studies of its kind reported. Aortic dissections may involve the ascending aorta alone, the descending thoracic and abdominal aorta alone, or the entire aorta. The risk of death depends on the extent of the dissection. It is highest for those aneurysms involving the ascending aorta. For that reason, most of these aneurysms are treated surgically as an emergency.

2. Medical treatment

Dissections of the descending thoracic aorta can often be treated with blood pressure control. The medical treatment of aortic dissection includes aggressive control of blood pressure and heart rate while the aorta heals. The risk of death with medical treatment of descending thoracic aortic dissection is about 10 percent. If surgery is required, however, the risk is higher at about 30 percent. Every effort is therefore made to treat these patients with medication.

3. Endovascular repair of AAA

Recent advances in catheter-based technologies have led to exciting new treatments for aortic aneurysms. Now, endovascular grafting technology allows surgeons to repair the AAA by delivering a graft through a small incision in the groin, rather than the traditional major open surgery. The endovascular method, approved by the FDA in 1999, allows the graft to be delivered via a catheter (tube) inserted in a groin artery. In the operating room, x-ray guidance is used for proper positioning of the graft. The graft is then expanded inside the aorta and held in place with metallic hooks rather than sutures. The hospital stay is usually only one or two days, and most patients can return to work or normal daily activities in about a week. Even patients with serious medical problems, once thought to be too sick, or too frail to have surgery for AAA, may have their aneurysm repaired using an endovascular graft. This can avoid the need for major open surgery and also eliminate the risk of fatal rupture if the AAA was not treated at all. It�s very important for patients to know that endovascular grafting may not be possible in every case. Endovascular grafts are specially manufactured and don�t �fit� for every case. Also, in many cases, standard surgery is still the best since we don�t have 50 years of experience with these newer procedures like we do with surgery. There may still be serious problems we haven�t anticipated.

4. Surgical resection

Surgery is usually required to repair an AAA, but modern, catheter-based technologies using endovascular grafts have made treatment less invasive in many cases. The combination of early diagnosis and modern treatment of aortic aneurysms can save countless lives lost due to aneurysm rupture each year.
Surgical treatment of AAA has been performed for almost 50 years and is a successful and durable procedure. In surgery the diseased part of the aorta is replaced with a Dacron or Teflon graft that is carefully matched to the normal aorta and is sewn in place by the surgeon. While ultimately curative, this operation requires a major abdominal incision and general anaesthesia, and the hospital stay averages 7-10 days for most patients. Even after uncomplicated surgery, it is often a month or two before patients can return to a full and normal life. Nevertheless, more than 90% of patients make a full recovery from surgery. After more than half a century of experience with these procedures we know that once patients have recovered, their aneurysms are permanently cured.

Follow up

Once the acute dissection has healed, adequate control of blood pressure may eliminate the need for surgery. Lifelong monitoring of diameter of the aorta is required because a previously dissected descending thoracic aorta may enlarge and rupture.

Prognosis and survival

Because the abdominal aorta is such a large blood vessel, a ruptured abdominal aneurysm is a life-threatening event. Fortunately, not all aneurysms rupture. Many grow very slowly and cause no symptoms or problems for many years. However, all have the potential to rupture and thus must be identified and treated or watched very carefully. The combination of earlier diagnosis with safer, simpler, and ever more successful treatments can prevent needless deaths due to ruptured abdominal aortic aneurysms. Timely suspicion and consultation with the family doctor and a simple ultrasound test can tell whether a person has aneurysm.
The length of the operation and the risks involved depends on the extent of the repair required, and on the patient's general health. Recovery time varies. Most people need at least a month or six weeks to recover from aneurysm surgery. The length of the hospital stay depends on the patient's condition and the operation performed, but it is typically a week.
Although endovascular surgery reduces recovery time to a few days, it still carries risk. And because the procedure is fairly new, long-term results are unknown. Complications can occur with this procedure, namely blood leaking from the graft, known as endoleak. For this reason, patients who have repair of their aortic aneurysms with stent-grafts are initially required to return for monitoring every six months.

Recent news and research

Cocaine users in their mid-40s are found to have more than four times the risk of coronary artery aneurysms as non-users as per the Journal of the American Heart Association. It is believed that cocaine predisposes to coronary artery aneurysms, and then the aneurysms themselves may predispose to heart attacks.
The Food and Drug Administration has approved a new device called GORE TAG Endoprosthesis System that is intended to prevent ruptures of descending thoracic aneurysms by making a new path for blood flow. It is the first endovascular grafting system approved to treat aneurysms of the thoracic aorta.