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Occasionally, a heart attack happens without causing any pain. This is usually diagnosed when you have a heart tracing (electrocardiogram, or ECG) at a later stage.

Some people collapse and die suddenly if they have a large portion of heart muscle damaged. This is not very common.

Dial 999/112/911 for an ambulance immediately .

Dial 999/112/911 for an ambulance immediately

Then, if you have some, take one aspirin tablet (see below for the reason for this). You will normally be admitted straight to hospital.

If you think someone is having a heart attack, look for the four Ps:

Many people develop chest pains that are not due to a heart attack. For example, you can have quite bad chest pains with heartburn, and with gallbladder problems or with pains from conditions of the muscles in the chest wall. Therefore, tests are usually done to confirm a heart attack. These are:

A rough idea as to the severity of the heart attack (the amount of heart muscle that is damaged) can be gauged by:

Another chemical that may be measured in a blood test is called creatine kinase. This too is released from heart muscle cells during a heart attack.

Your ECG will be monitored for a few days to check on the heart rhythm. Various blood tests will be done to check on your general well-being.

Other tests may be done in some cases. This may be to clarify the diagnosis (if the diagnosis is not certain) or to diagnose complications such as heart failure if this is suspected. For example, an ultrasound scan of the heart (echocardiogram, or 'echo') or a test called a myocardial perfusion scan may be done.

Also, before discharge from hospital, you may be advised to have tests to assess the severity of the fatty patches or plaques (atheroma) in the coronary arteries - for example:

The following is a typical situation and mentions the common treatments that are usually offered. However, each case is different and treatments may vary depending on your situation.

As soon as possible after a heart attack is suspected you will be given a dose of aspirin. Aspirin reduces the stickiness of platelets. Platelets are tiny particles in the blood that trigger the blood to clot. It is the platelets that become stuck on to a patch of atheroma inside an artery that go on to form the clot.

Other antiplatelet medicines called latest for sale for sale Skechers equalizer 20 True Balance Mens Sneakers Black/Charcoal outlet store online CdptLoguQ
or ticagrelor may be given. They work in a different way to aspirin and help reduce platelet stickiness.

See separate leaflet calledAspirin and other Antiplatelet Medicines .

These are usually given for a few days to help prevent further blood clots from forming.

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Two UCLA economists say they have figured out why the Great Depression dragged on for almost 15 years, and they blame a suspect previously thought to be beyond reproach: President Franklin D. Roosevelt.
After scrutinizing Roosevelt's record for four years, Harold L. Cole and Lee E. Ohanian conclude in a new study that New Deal policies signed into law 71 years ago thwarted economic recovery for seven long years.
"Why the Great Depression lasted so long has always been a great mystery, and because we never really knew the reason, we have always worried whether we would have another 10- to 15-year economic slump," said Ohanian, vice chair of UCLA's Department of Economics. "We found that a relapse isn't likely unless lawmakers gum up a recovery with ill-conceived stimulus policies."
In an article in the August issue of the Journal of Political Economy, Ohanian and Cole blame specific anti-competition and pro-labor measures that Roosevelt promoted and signed into law June 16, 1933.
"President Roosevelt believed that excessive competition was responsible for the Depression by reducing prices and wages, and by extension reducing employment and demand for goods and services," said Cole, also a UCLA professor of economics. "So he came up with a recovery package that would be unimaginable today, allowing businesses in every industry to collude without the threat of antitrust prosecution and workers to demand salaries about 25 percent above where they ought to have been, given market forces. The economy was poised for a beautiful recovery, but that recovery was stalled by these misguided policies."
Using data collected in 1929 by the Conference Board and the Bureau of Labor Statistics, Cole and Ohanian were able to establish average wages and prices across a range of industries just prior to the Depression. By adjusting for annual increases in productivity, they were able to use the 1929 benchmark to figure out what prices and wages would have been during every year of the Depression had Roosevelt's policies not gone into effect. They then compared those figures with actual prices and wages as reflected in the Conference Board data.
In the three years following the implementation of Roosevelt's policies, wages in 11 key industries averaged 25 percent higher than they otherwise would have done, the economists calculate. But unemployment was also 25 percent higher than it should have been, given gains in productivity.
Meanwhile, prices across 19 industries averaged 23 percent above where they should have been, given the state of the economy. With goods and services that much harder for consumers to afford, demand stalled and the gross national product floundered at 27 percent below where it otherwise might have been.
"High wages and high prices in an economic slump run contrary to everything we know about market forces in economic downturns," Ohanian said. "As we've seen in the past several years, salaries and prices fall when unemployment is high. By artificially inflating both, the New Deal policies short-circuited the market's self-correcting forces."
The policies were contained in the National Industrial Recovery Act (NIRA), which exempted industries from antitrust prosecution if they agreed to enter into collective bargaining agreements that significantly raised wages. Because protection from antitrust prosecution all but ensured higher prices for goods and services, a wide range of industries took the bait, Cole and Ohanian found. By 1934 more than 500 industries, which accounted for nearly 80 percent of private, non-agricultural employment, had entered into the collective bargaining agreements called for under NIRA.
Cole and Ohanian calculate that NIRA and its aftermath account for 60 percent of the weak recovery. Without the policies, they contend that the Depression would have ended in 1936 instead of the year when they believe the slump actually ended: 1943.
Roosevelt's role in lifting the nation out of the Great Depression has been so revered that Time magazine readers cited it in 1999 when naming him the 20th century's second-most influential figure.
"This is exciting and valuable research," said Robert E. Lucas Jr., the 1995 Nobel Laureate in economics, and the John Dewey Distinguished Service Professor of Economics at the University of Chicago. "The prevention and cure of depressions is a central mission of macroeconomics, and if we can't understand what happened in the 1930s, how can we be sure it won't happen again?"
NIRA's role in prolonging the Depression has not been more closely scrutinized because the Supreme Court declared the act unconstitutional within two years of its passage.
"Historians have assumed that the policies didn't have an impact because they were too short-lived, but the proof is in the pudding," Ohanian said. "We show that they really did artificially inflate wages and prices."
Even after being deemed unconstitutional, Roosevelt's anti-competition policies persisted — albeit under a different guise, the scholars found. Ohanian and Cole painstakingly documented the extent to which the Roosevelt administration looked the other way as industries once protected by NIRA continued to engage in price-fixing practices for four more years.
The number of antitrust cases brought by the Department of Justice fell from an average of 12.5 cases per year during the 1920s to an average of 6.5 cases per year from 1935 to 1938, the scholars found. Collusion had become so widespread that one Department of Interior official complained of receiving identical bids from a protected industry (steel) on 257 different occasions between mid-1935 and mid-1936. The bids were not only identical but also 50 percent higher than foreign steel prices. Without competition, wholesale prices remained inflated, averaging 14 percent higher than they would have been without the troublesome practices, the UCLA economists calculate.
NIRA's labor provisions, meanwhile, were strengthened in the National Relations Act, signed into law in 1935. As union membership doubled, so did labor's bargaining power, rising from 14 million strike days in 1936 to about 28 million in 1937. By 1939 wages in protected industries remained 24 percent to 33 percent above where they should have been, based on 1929 figures, Cole and Ohanian calculate. Unemployment persisted. By 1939 the U.S. unemployment rate was 17.2 percent, down somewhat from its 1933 peak of 24.9 percent but still remarkably high. By comparison, in May 2003, the unemployment rate of 6.1 percent was the highest in nine years.
Recovery came only after the Department of Justice dramatically stepped up enforcement of antitrust cases nearly four-fold and organized labor suffered a string of setbacks, the economists found.
"The fact that the Depression dragged on for years convinced generations of economists and policy-makers that capitalism could not be trusted to recover from depressions and that significant government intervention was required to achieve good outcomes," Cole said. "Ironically, our work shows that the recovery would have been very rapid had the government not intervened."
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Figure 2. DVA causing mechanical compression. The patient had severe trigeminal pain in the distribution of left V2 and V3. A (contrast-enhanced T1-weighted axial section), the enlarged venous collector of a transpontine DVA encroaches on the trigeminal nerve at its exiting zone from the brain stem (arrow). B–C, Vertebral artery angiograms in anteroposterior and lateral views in the venous phase demonstrate a classical umbrella-shaped pattern of the DVA with the medullary vein draining into an enlarged collector that further drained into the superior petrosal vein. D–E, Surgical view with compression of the left trigeminal nerve (arrow in E). A Teflon patch to separate the nerve from the vein was placed with excellent results and complete recovery from the trigeminal pain immediately after surgery.

Flow-related complications were characterized as a misbalance of the in- and outflow of blood in the DVA system raising the pressure in the DVA either due to an increased inflow or a restricted outflow and were present in 49 patients.

Increase of Developmental Venous Anomalies’ Inflow

An augmentation of inflow into the DVA was either due to microshunts into the DVA or AVMs that used the DVA as the drainage route. We found 4 cases in our databank and 15 cases in the literature with a mean age of 28.5 years ranging from 1 to 62 years and a discrete male predominance (male:female=12:7; Womens Relaxed Fit Upgrades Be Jeweled sale purchase clearance ebay fRP2z3
). The initial clinical presentations included headaches (n=11 [61%]), neurological deficits (n=7 [38%]), seizures (n=4 [22.2%]), and coma (n=4 [22.2%]). The morphological presentation was mainly hemorrhages in 12 cases (66.6%), including intraparenchymal (n=8 [66%]), intraventricular (n=2 [17%]), and both (n=2 [17%]). The remaining 6 cases (33.3%) had venous infarction in the drainage territory of the DVA, presumably due to venous congestion after arterialization. Thirteen lesions (72%) were located supratentorially and 6 lesions (28%) infratentorially. The angioarchitectural aspects were microshunts into capillary veins at the medullary zone of the DVA (n=11 [55%]; Figures 3 and 4 ) and typical nidal-type AVMs draining through the venous collector (n=8 [45%]). Among them, only 3 cases were larger than 5 cm and had complex venous drainage with no relationship with the clinical manifestation. Asymmetrical dilatation of the capillary veins in the medullary zone of the DVA of the patients with microshunts was observed in 76% (8 of 11). This finding helped to support the diagnosis in some cases, which was subsequently confirmed by superselective injections.

View this table:

Table 3. Findings in All Patients Reported in the Literature With Increased Inflow Into the DVA

Figure 3. Flow-related complication of a DVA due to a microshunt into the DVA. This 25-year-old man experienced a sudden onset of left hemiparesis associated with severe headaches. A (axial nonenhanced coronal CT), a right frontoparietal atypical hemorrhage. B (contrast-enhanced T1-weighted MRI), the venous collector of a DVA lateral to the hematoma. Within the hematoma, medullary vessels are demonstrated as small enhancing areas. C–D (3-dimensional reconstruction of a right internal carotid artery angiography, including blowup in D), the communication of a branch of the pericallosal artery with the DVA (arrow). In the lateral view of the late arterial phase (E and blowup in G), the microshunt can be demonstrated at the level of the dorsal medullary zone (arrow). Transarterial embolization with glue was carried out (F) that resulted in complete obliteration of the microshunt and preservation of the DVA (H).

Figure 4. Flow-related complication of a DVA due to a microshunt into the DVA. This 9-year-old boy presented with his first-ever seizure that was preceded by severe headaches. A (axial T2*-weighted MRI), a hematoma in the right forceps major. B–C, left internal carotid artery angiography in lateral view in the arterial (B) and venous phase (C) demonstrate a large temporooccipital DVA draining superficially into the vein of Labbé. There is contrast stagnation in the medullary zone of the DVA. D–E, after injection into the left vertebral artery (anteroposterior view, in arterial phase, D; capillary phase, E) demonstrate a false aneurysm (arrow) as the point of rupture of a microshunt into the DVA. The gluecast (F) penetrates through the lateral posterior choroidal branch into the pseudoaneurysm and the early part of the venous drainage of the microshunt.

Treatment strategies were extremely variable according to architecture, morphological presentation, and the treating center. Radiosurgery was the most frequent option (n=7 [38.8%]), even for hemorrhagic or ischemic presentations, and was focused on the AVM and DVA (70%) or on the AVM alone (30%). Five patients (including all 4 cases from our series) were treated with endovascular embolization of the lesion (microshunt or AVM) with careful preservation of the patency of the DVA using transarterial glue (n-butyl cyanoacrylate, Histoacryl; B. Brain, Melsungen, Germany) injections. All patients recovered from their bleeding without new neurological deficits.

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What is diabetic retinopathy?

Diabetic retinopathy (DR) is the most common type of diabetic eye disease and the leading cause of blindness in American adults. Diabetes causes damage to the blood vessels of the retina, a thin and delicate tissue that is responsible for vision. In some people suffering from DR, blood vessels swell and leak fluid. In others, abnormal new blood vessels grow on the surface of the retina that can lead to bleeding and retinal detachment. A healthy retina is necessary for good vision.

If you have diabetic retinopathy, at first you may not notice changes to your vision. Yet over time, the condition can worsen and cause vision loss. Diabetic retinopathy usually affects both eyes, but early detection and prompt treatment can minimize vision loss.

Here's what a person with normal vision sees
This is what that same image looks like to a person with diabetic retinopathy

The features of mild nonproliferative retinopathy are some of the earlier stages of diabetic retinopathy. At this point, small areas of balloon-like dilation of blood vessels, called microaneurysms, start to appear along with other findings such as small spot hemorrhages and cotton wool spots. It's important to note that not all patients with mild nonproliferative retinopathy will notice a change in their vision.

Moderate nonproliferative retinopathy is essentially a progression from the mild stage. Many more microaneurysms, hemorrhages and cotton wool spots emerge and there is further damage to the retinal blood vessels. The danger is that such damage can result in reduced blood flow to the surrounding retinal tissue leading to vision loss.

Proliferative diabetic retinopathy

At this advanced stage, the signals sent by the retina for nourishment trigger the growth of new blood vessels that grow along the retina and into other parts of the eye. These blood vessels are abnormal and fragile, often leading to the development of new or worsening existing symptoms and frequent vision loss. Left untreated, severe vision loss and even permanent blindness can result.

Damaged blood vessels from diabetic retinopathy can cause vision loss in several ways:

Diabetic macular edema

All diabetics—both Types 1 2—are at risk, which is why everyone with diabetes should get a comprehensive dilated eye exam at least once a year. The longer someone has diabetes, the more likely he or she will develop diabetic retinopathy. It's fortunate that in most cases diabetic retinopathy is a treatable condition. Your doctor can recommend treatment to help prevent its progression.

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