INTRO

Hehehehehehehe ……………..The one thing which has made a substitute for INSULIN…………….the only drug of choice for a early diagnosed and well diet controlled patient with Non insulin diabetes mellitus  ……….

Oral hypoglycemic agents commonly are referred to as sulfonylureas, a class of compounds. Sulfonylurea compounds are among the most widely prescribed medications in the world. The drugs are frequently used to treat patients with type II diabetes. Wide availability of these medications increases potential for either intentional or unintentional overdose in pediatric and adult populations.

First-generation sulfonylurea compounds became widely available in 1955. They are acetohexamide, chlorpropamide, tolazamide, and tolbutamide. First-generation agents have longer half-lives (eg, 49 hours for chlorpropamide). Second-generation sulfonylureas were introduced in 1984. Known as glipizide, glyburide, and glimepiride, second-generation sulfonylureas are more potent and have shorter half-lives than the first-generation sulfonylureas.

Other agents besides sulfonylureas are used to treat type II diabetes, including biguanides, alpha-glucosidase inhibitors, and troglitazone. Metformin (Glucophage in the United States) is one such agent. Even in excessive dosage, these agents do not decrease serum glucose below euglycemia; consequently, they are referred to appropriately as antihyperglycemic agents rather than hypoglycemic agents.

The Joslin Diabetes Center released a clinical guideline for the pharmacological management of type II diabetes in 2007.

CLASSIFICATION OF DRUGS

1. SULFONYL UREA’S
2. BIGUANIDES
3. ALPHA GLUCOSIDASE INHIBHITORS
4. MEGLITINIDES
5. THIAZOLINEDIONES

SULFONYLUREA’S

Sulfonylureas work primarily by stimulating pancreatic insulin secretion, which in turn reduces hepatic glucose output and increases peripheral glucose disposal.

preparation of sulfonylurea

The sulfonylureas are often classified as belonging to the first or second generation.

The First generation sulfonylureas:

• Acetohexamide
• Chlorpropamide
• Tolazamide
• Tolbutamide.

The Second generation sulfonylureas :

• Glibenclamide
• Glyburide
• Glipizide
• Glicazide
• Glimepiride

The first generation sulfonylureas are rarely used now.

NEWER DRUGS ARE Glimipiride (Amaryl) and Glicazide MR and XR ………Nowadays new medicine is used vastly in the practice of longterm NIDDM cases (Non insulin dependant Diabetes Mellitus)……..

Also available in 60 mg and even in XR(xtended release)

The SU class of oral hypoglycemic agents (insulin secretagogues) has been in existence since tolbutamide was introduced in 1956.

The sulfonylurea drugs have effects which are still not completely understood. Initially, they work primarily by stimulating pancreatic insulin secretion, which in turn reduces hepatic glucose output and increases peripheral glucose disposal. They are potassium channel blockers whose effect on the pancreatic beta-islet cells is to allow an influx of calcium into the cell, which causes an increase in the release of insulin.

depletion of Beta cells

However, after several months, blood levels of insulin return to pre-medication levels, yet blood glucose levels remain reduced. Clearly, the sulfonylurea drugs must have other effects. Several have been identified, among them: sulfonylurea medications slow the rate at which the liver releases glucose into the bloodstream, and they increase the number of insulin receptors on cell membranes, thus increasing insulin efficiency.

The efficacy of the first- and second-generation sulfonylureas is similar, although second-generation agents are better formulated and, although costlier than the older sulfonylureas, have some advantages. Second-generation sulfonylureas:

Are more potent on a per milligram basis
Tend to produce fewer side effects
In addition, the pharmacokinetics of these second-generation agents allows for more effective once-a-day dosing, which enhances compliance.

Although some consider SUs to be dated compared with the newer oral hypoglycemic drugs, there remains a large number of patients that will continue to benefit from them.

BIGUANIDES

Two drugs in this category are phenformin and metformin.

Metformin_500mg_Tablets

Biguanides work mainly by

• Suppressing excessive hepatic glucose production
• Increasing glucose utilization in peripheral tissues to a lesser degree.
• Possibly reduce food intake and thus reduce intestinal glucose absorption

Metformin structure

As the biguanides do not stimulate endogenous insulin secretion, hypoglycemia does not occur when they are used alone and therefore they are sometimes called anti-hyperglycemic agents rather hypoglycemic agents.

The use of phenformin has decreased considerably and it is usually metformin that is now used when a biguanide is prescribed.

The biguanides were introduced in 1957. Both phenformin and metformin have been widely used here, although in recent times, the use of phenformin has decreased significantly and most people now use metformin when a biguanide is to be used.

Metformin works mainly by suppressing excessive hepatic glucose production, although it may increase glucose utilization in peripheral tissues to a lesser degree, by decreasing insulin resistance in muscle cells. Metformin may also improve glucose levels by reducing intestinal glucose absorption.

Metformin is not metabolized and is excreted unchanged by the kidneys.

Metformin effects

Metformin has many characteristics that are ideal for treating type 2 diabetes, including weight loss, insulin sensitization, positive lipid effect, mild hypotensive effect, and low or no incidence of hypoglycemia.

Because metformin does not stimulate endogenous insulin secretion, hypoglycemia does not occur when this dose is used alone, although hypoglycemia may occur if metformin is taken with insulin, a sulfonylurea, or an excessive amount of alcohol.

Treatment with metformin has beneficial effects on plasma lipids (it lowers triglyceride and low-density lipoprotein [LDL] cholesterol levels while increasing high-density lipoprotein [HDL] cholesterol) that are greater than expected from improved glucose control alone.

In addition, metformin therapy has been associated with weight loss or no weight gain. This may be particularly helpful in obese patients with type II diabetes.

Metformin is effective as monotherapy or in combination with sulfonylureas, alpha-glucosidase inhibitors, and insulin. The combination of metformin and troglitazone has also been shown to be safe and effective, although this combination is not an USA FDA- approved indication and extensive published data on this combination is lacking.

ALFA GLUCOSIDASE INHIBHITORS

miglitol structure

There are Acarbose and Miglitol. Acarbose (Precose) is an alpha-glucosidase inhibitor that slows down the breakdown of disaccharides and polysaccharides and other complex carbohydrates into monosaccharides. The enzymatic generation and subsequent absorption of glucose is delayed and the postprandial blood glucose values, which are characteristically high in patients with type II diabetes, are reduced with acarbose. AGIs do not prevent the absorption of carbohydrates and complex sugars, but they do delay their absorption.

Acarbose structure

Delaying the absorption of carbohydrates is a unique mechanism among oral diabetic medications for lowering HgbA1c levels. The effectiveness of this mechanism is one of the physiologic characteristics of type 2 diabetes. Patients with type 2 diabetes demonstrate a delayed or sluggish insulin response from the pancreas to a glucose (a meal) load. By delaying the absorption of glucose, the insulin response is more matched to the serum glucose, resulting in less postprandial hyperglycemia and a lowering of the HbA1c. The AGIs also demonstrate a lowering of total insulin output of the pancreas, increased insulin sensitivity, a variable but mild decrease in triglycerides, with no effect on patient weight.

One disadvantage with the use of acarbose is that it is to be taken along with the first bite of a meal. Moreover, it has to be taken three times daily with meals. These factors often lead to non compliance and a decrease in the efficacy of the drug.

MEGLITINIDES +AMINOACID DERIVATIVES

A very recent addition to the OHA group. It is a ultra short acting drug which acts directly on the the beta cells of the pancreas and increases the secretion of insulin. It also corrects the problems with the pulsatile release of insulin which is seen in Type II diabetes.

Repaglinide from the meglitinide drug class, acts like an extremely short-acting SU (an insulin secretagogue) and is potentially useful as a SU replacement. The effect of repaglinide on the pancreas is very similar to that of the SUs. Repaglinide, like the SUs, blocks the potassium channels on the pancreatic islet beta-cells, which causes an influx of calcium into the cell and increasing the secretion of insulin. There appears to be 2 similar potassium channels on islet beta-cells, one of which is predominantly affected by repaglinide and the other is predominantly affected by SUs.

Repaglinide structure

The repaglinide-affected potassium channel appears to be glucose dependent, which may partially explain why repaglinide is associated with a much lower incidence of hypoglycemia.

novonorm- repaglinide

What makes repaglinide clinically different from the SUs is its ultra-short half-life (1 hour). Repaglinide is taken just before or with meals, and the stimulation of the pancreas is limited only to a brief time around meals. Because of the short duration, the patient does not have continuous high levels of insulin and the resulting adverse effects.

Its biggest advantage over the other oral hypoglycemic medications is that it allows for flexible timing and missed meals.

Repaglinide has been approved for use with metformin, and the combination appears to be a very effective. There are no clinical trials of repaglinide with the alpha-glucosidase inhibitors, and of the TZD class, only 1 clinical trial with troglitazone has been reported. There are theoretical interactions between repaglinide and the TZDs through their common metabolism in the P450 pathway, so more clinical trials are clearly needed.

THIAZOLIDINEDIONES

Rosiglitazone structure

Thiazolidinediones are a new class of oral antidiabetic agents (commercially known as glitazones) that enhance insulin sensitivity in peripheral tissues. Troglitazone was the first glitazone introduced to the market, and though widely used, it has now been withdrawn from the market as its use has been linked with hepatocellular injury and death secondary to liver failure.

Rosiglitazone and Pioglitazone are now available for clinical use and are extremely potent in reducing peripheral insulin resistance.

The thiazolidinedione (TZD) class of oral hypoglycemics ( popularly known as glitazones) was developed in 1997 and offers a new mechanism for treatment of type 2 diabetes. The first, troglitazone was taken off the market in 1999 because of its association with hepatic toxicity. Rosiglitazone and pioglitazone have been available since 1999, and have recently been introduced in the Indian market.

The primary effect of TZDs is peripheral, with increasing insulin sensitivity and increased glucose uptake. The TZDs have some effect on hepatic glucose uptake and sensitivity to a lesser degree. They do not stimulate the pancreas to produce more insulin.

TZDs are hepatically metabolized and thus can be used safely in patients with renal dysfunction. They can be dosed once daily, although rosiglitazone works better with twice-daily dosing. Reports have suggested that rosiglitazone works better in women, but the reason for this is not known.

Both pioglitazone and rosiglitazone are approved for monotherapy and in combination with metformin, SUs, and insulin.

Besides their effect in lowering the blood glucose levels, both drugs also have notable effects on lipids. The current data show that pioglitazone has a minimal effect on low-density lipoprotein (LDL) cholesterol levels and a favorable effect on high-density lipoprotein (HDL) cholesterol and triglyceride levels. Rosiglitazone has a favorable effect on HDL cholesterol levels but a negative effect on LDL cholesterol levels.

With use of glitazones, patience is required. Blood sugar levels may show a significant reduction statistically in as little as two to four weeks, but the maximum effects are not seen until two or three months have passed.

CONCLUSION

So i dont have a conclusin yet……………………Postin it soon !!!!!!!!!!!!!!!!!!!!!!!!

Y suffer when u know the Better

What is gonorrhea ?????

A sexually transmitted Disease (STD) caused by the bacterium Neisseria gonorrhoea. Although gonorrhea is known primarily as a sexually transmitted Disease (STD), it is not exclusively so, but can also be transmitted to the newborn during the birthing process.

What was it called Before ????

Gonorrhea is sometimes also known as “the clap”. This moniker may seem a bit strange but is has actually been around since 1587. It comes from the French word “clapoir” which was commonly used to describe gonorrhea in the late sixteenth century.

How is it spread????

Contrary to popular belief, gonorrhea cannot be transmitted from toilet seats or door handles. The bacterium Neisseria gonorrhea requires very specific conditions to grow and to reproduce. It cannot live outside the body for more than a few minutes at most, nor can it live on the skin of the hands, arms, or legs. It survives only on moist surfaces within the body and is found most commonly in the vagina and, especially the cervix. The bacterium can also live in the urethra. Gonorrhea can even exist in the back of the throat (from oral-genital contact) and in the rectum.

Gonorrhea is not a small problem ????

Left untreated, gonorrhea can lead to a severe painful pelvic infection with inflammation of the fallopian tubes and ovaries, a form of pelvic inflammatory disease, or PID. Symptoms of PID include fever, pelvic cramping, abdominal pain, and pain with intercourse. PID can lead to difficulty in becoming pregnant or even sterility.

Can Gonorrhea Complicate ????

The complications of gonorrhea can include inflammation of the heart valves, arthritis, and eye infections. If the infection is severe enough, a localized area of infection and pus (an abscess) forms, and major surgery may be necessary and even life-saving. Gonorrheal infection in people with diminished immune function, such as from chemotherapy or AIDS, can also be extremely serious.

Gonorrhea can also cause eye Infections !!!!!

Gonorrhea can cause eye infections in babies born to infected mothers, even if the mother has no symptoms at the time of delivery. Chlamydia can also be passed from mother to child during birth. Infected newborn infants develop drainage from the eyes within 2 weeks of birth and the eyelids become puffy, red, and tender. Gonorrhea may cause perforation of the cornea and very significant destruction of the deeper eye structures while chlamydia is somewhat less destructive. Hospitals require silver nitrate or, more often today, antibiotic drops in a newborn’s eyes to prevent these diseases.

Symptoms of Gonorrhea ???

The early symptoms of gonorrhea often are mild, and some people who are infected have no symptoms of the disease; this is one reason why it is so readily transmitted. If symptoms of gonorrhea develop, they usually appear within 2 to 10 days of sexual contact with an infected partner, although a small percentage of patients may be infected for several months without showing symptoms.

The initial symptoms in women include a painful or burning sensation when urinating or a yellowish vaginal discharge. More advanced symptoms include abdominal pain, bleeding between menstrual periods, vomiting, or fever.

Men usually have a whitish-yellowish discharge from the penis and a burning sensation during urination that may be severe. Symptoms of rectal infection include anal itching, and sometimes painful bowel movements.

Diagnosis of gonorrhea ???

Testing for gonorrhea is done by swabbing the infected site and culturing the bacteria on the swab in the laboratory. The culture is positive when the gonorrhea bacteria are found to be growing on a culture plate. A newer test can detect both gonorrhea and chlamydia in a urine sample. Up to 40% of women with gonorrhea are also infected with chlamydia.

How silent is it ???

Gonorrhea is often silent in women. Over half of infected women have no symptoms in the early stages of gonorrheal infection. If symptoms do occur, there may be burning on urination, frequent urination, yellowish vaginal discharge, redness of the genitals, swelling of the genitals, and a burning or itching of the vaginal area.

Treatment ?????

Because a high proportion of men and women who have gonorrhea also have chlamydia, the goal of treatment is to cure both infections. Your partner(s) should be treated at the same time you are.

Treatment for uncomplicated gonorrhea consists of antibiotics, including ceftriaxone, cefixime, ciprofloxacin, or ofloxacin for gonorrhea along with azithromycin, doxycycline, or erythromycin for chlamydia.

Prevention Of Gonorrhea ???

All sexually active persons should consider using latex condoms to prevent STDs and HIV infection, even if they are using another form of contraception. Latex condoms used consistently and correctly are an effective means for preventing disease (and pregnancy). Talk openly with your partner about STDs, HIV, and hepatitis B infection, and the use of contraception.

Can i treat a Pregnant woman with Gonorrhea ????

If you become infected with gonorrhea while you are pregnant, it is important that you seek treatment quickly. Not only is it possible to transmit the infection to your child during childbirth, but this common sexually transmitted disease can also cause complications in your pregnancy.

Questions U can ask ur Family Doctor!!!

1. Should the sexual partner be alerted so that they can be tested?
2. Has the gonorrhea progressed into Pelvic Inflammatory Disease (PID)?
3. Can the gonorrhea come back without additional exposure?
4. Do any of the internal contraceptive gels, ointments, devices, etc. help prevent gonorrhea?
5. What type of medication will you be prescribing?
6. Are there any side effects?
7. Can I tell if a sexual partner has gonorrhea before having sexual intercourse?

WAT IS IT????

Stroke is a disease that affects the arteries leading to and within the brain. It is the No. 3 cause of death in the United States, behind diseases of the heart and cancer. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts. When that happens, part of the brain cannot get the blood (and oxygen) it needs, so it starts to die.

Is it similar to brain hemorrhage ???

Brain Hemorrhage is a condition caused due to a sudden stroke to a person after blood leaks out from the blood vessels in the brain. This situation occurs due to the break in the wall of blood vessel, the blood spills out of the blood vessel and enters the area where vital tissues and cells of brain reside, killing those tissues and cells; this causes the patient to become seriously ill and needs immediate medication/treatment.

Symptoms ???

Symptoms

If you have symptoms of a stroke, seek emergency medical care. General symptoms of a stroke include:

• Sudden numbness, paralysis, or weakness in your face, arm, or leg, especially on only one side of your body.
• New problems with walking or balance.
• Sudden vision changes.
• Drooling or slurred speech.
• New problems speaking or understanding simple statements, or feeling confused.
• A sudden, severe headache that is different from past headaches.

Symptoms vary depending on whether the stroke is caused by a clot or bleeding. The location of the blood clot or bleeding and the extent of brain damage can also affect symptoms.

1)Symptoms of an ischemic stroke (caused by a clot blocking a blood vessel) usually occur in the side of the body opposite from the side of the brain where the clot occurred. For example, a stroke in the right side of the brain affects the left side of the body.

2)Symptoms of a hemorrhagic stroke (caused by bleeding in the brain) can be similar to those of an ischemic stroke but may be distinguished by symptoms relating to higher pressure in the brain, including severe headache, nausea and vomiting, neck stiffness, dizziness, seizures, irritability, confusion, and possibly unconsciousness.

Symptoms of a stroke may progress over minutes, hours, or days, often in a stepwise fashion. For example, mild weakness may progress to an inability to move the arm and leg on one side of the body.

• If a stroke is caused by a large blood clot (ischemic stroke) or bleeding (hemorrhagic stroke), symptoms occur suddenly, within seconds.
• When an artery that is narrowed by atherosclerosis becomes blocked, stroke symptoms usually develop gradually over minutes to hours, or (in rare cases) days.
• If several smaller strokes occur over time, the person may have a more gradual change in walking, balance, thinking, or behavior (multi-infarct dementia).

It is not always easy for people to recognize symptoms of a small stroke. They may mistakenly think the symptoms can be attributed to aging, or the symptoms may be confused with those of other conditions that cause similar symptoms.

Risk Factors??

1)Controllable

• Hypertension
• Atrial Fibrillation
• High Cholesterol
• Diabetes Mellitus
• Smoking and Tobacco chewing
• Alcohol Use
• Obesity or Overweight

2)Non- controllable

• Age >55
• Gender – Males most common , but more women die of stroke
• Race – African American>Hispanic>Asians>caucasions
• Family History
• Previous Stroke or Transient Ischemic attacks or Thrombosis or Embolism

What Are the Types of Stroke?

Stroke can be caused either by a clot obstructing the flow of blood to the brain (called an ischemic stroke) or by a blood vessel rupturing and preventing blood flow to the brain (called a hemorrhagic stroke).

Diagnosis of Stroke??

When someone has shown symptoms of a stroke or a TIA (transient ischemic attack or mini stroke), a doctor will gather information and make a diagnosis. A doctor may use many different tests. The ones listed here are just some of the more common options.

Treatment !!!!

Ischemic Stroke

Acute Treatment

• Clot busters, e.g., tPA
  The most promising treatment for ischemic stroke is the FDA-approved clot-busting drug tPA (tissue plasminogen activator), which must be administered within a three-hour window from the onset of symptoms to work best. Administering tPA or other clot-dissolving agents is complex and is done through an intravenous (IV) line in the arm by hospital personnel. If given promptly, tPA can significantly reduce the effects of stroke and reduce permanent disability. Generally, only 3 to 5 percent of those who suffer a stroke reach the hospital in time to be considered for this treatment.

Preventive Treatment

• 	Click to enlarge

  Anticoagulants/Antiplatelets
  Antiplatelet agents such as aspirin and anticoagulants such as warfarin interfere with the blood’s ability to clot and can play an important role in preventing stroke. click here for  anticoagulants.

• Carotid Endarterectomy
  Carotid endarterectomy is a procedure in which blood vessel blockage is surgically removed from the carotid artery. View a detailed illustration of carotid endarterectomy.

• Angioplasty/Stents
  Doctors sometimes use balloon angioplasty and implantable steel screens called stents to treat cardiovascular disease and reduce fatty buildup clogging a vessel. View a detailed illustration of carotid stent.

Hemorrhagic Stroke (Subarachnoid hemorrhage or AVM)

• Surgical Intervention
  For hemorrhagic stroke (specifically for a subarachnoid hemorrhage), surgical treatment is often recommended to either place a metal clip at the base, called the neck, of the aneurysm or to remove the abnormal vessels comprising an arteriovenous malformation (AVM). Learn more about AVM.

• Endovascular Procedures, e.g., “coils”
  Endovascular procedures are less invasive and involve the use of a catheter introduced through a major artery in the leg or arm, guided to the aneurysm or AVM where it deposits a mechanical agent, such as a coil, to prevent rupture. (wat is  aneurysms).

What is Heart Attack

INTRODUCTION

A heart attack (also called “myocardial infarction”) occurs when a blood vessel supplying blood to a part of the heart becomes blocked, resulting in permanent damage to the heart muscle due to the lack of blood flow. The blood vessel can become blocked from advancing atherosclerotic plaque lesions, a sudden formation of a blood clot, or from the spasming of a coronary artery – an artery that supplies blood to the heart.

Most people believe that a heart attack is caused by a slow, progressive build-up of plaque, comforting themselves that it takes a lifetime to become completely clogged – but this just isn’t true for a majority of heart attacks. Heart specialists now believe that most heart attacks occur when an unstable, atherosclerotic plaque lesion, filled with cholesterol and fat, suddenly breaks apart, thus forming an open wound within the artery wall. Blood platelets and clotting proteins rush to the wound and form a clot — called a thrombus. The clot can enlarge in a matter of moments, causing obstruction of blood flow to the heart with resultant angina (chest pain). If the blood flow becomes completely obstructed, a heart attack ensues.

Surprisingly, it is the small plaques that can be the most lethal. A person with a 50% blockage who suddenly becomes obstructed is at much greater risk of having a large amount of heart damage than a person with a slowly progressive blockage. A person with a 90% blockage that was slow to progress has probably had a chance to develop “collaterals”–– smaller blood vessels that grow to take over the job of the big vessel that has been gradually closing down.

Is it an Emergency ?????

Every Second Counts
A heart attack is a life–threatening event. With immediate medical intervention — preferably within the first hour of onset of symptoms – heart damage may be averted or reduced. A new blood test measuring “troponin” – a chemical released into the blood during a heart attack – allows doctors to diagnose a heart attack more quickly and accurately than ever before. Time equals muscle is the theme that resounds in emergency rooms and treatment is aimed at quickly restoring blood flow to the heart muscle to prevent permanent damage.

Risk Factors ????

1) Increased LDL/HDL ratios (i.e.,, elevated LDL and low HDL levels)Cholesterol

2) Smoking

3) Diabetes

4) Hypertension

5) Obesity

6)  Stress (i.e., stress or depression)

7) Failure to eat fruits and vegetables daily

Failure to Exercise

9) Failure to drink Moderate Alcohol (complex relationship between alcohol and the heart.)

10) Metabolic syndrome.

11) Increased CRP ( C reactive Protein)

12) Taking Birth Control Pills

13) Complicated Pregnancy

Non modifiable Risk factors?????????

• A family history of premature CAD (generally, CAD that has occurred in male relatives before the age of 50, or in female relatives before the age of 60.)
• Age 55 or older (men), or 65 or older (women)
• For women, being post-menopausal, or having your ovaries removed.
• Chronic kidney disease.

Is there a recent rise Of Heart Attack patients in INDIA???

Yes Bcoz of the Follwing Reasons :

1. Economic Progress

2. Better standard living

3. Westernisation

4. Change of food habits

5. More prone genetics

6. Small vessel Coronary Artery Disease

7. High incidence of Diabetes

8. More Smokers

Symptoms ?????

A unique fact about heart disease is that, in general, the more serious the condition the more remote from the heart are the symptoms.   Amongst danger signals that may, but not necessarily do, betoken heart disease and invite prompt medical attention are:

1 Shortness of breath after slight exertion.

2  Pain or tightness in the chest, often running down the left arm.

3  Swelling in the ankles and abdomen.

4  Dizziness, light-headedness, or vertigo.

5  Seeing double (a particularly dangerous sign).

6  Indigestion that is vague and hangs on.

7  Persistent head-ache.

8  Fatigue without otherwise explained origin.

SIGNS?????

• Bradycardia to Tachycardia
• Angina
• Arrythmia
• Low cardiac Output
• Rales in case of Pulmonary edema
• Cyanosis
• Cold extremities

DIAGNOSIS ???

Essentials of Diagnosis

• Sudden but not instantaneous development of prolonged (> 30 minutes) anterior chest discomfort (sometimes felt as “gas” or pressure) that may produce arrhythmias, hypotension, shock, or cardiac failure.
• Sometimes painless, masquerading as acute CHF, syncope, stroke, or shock.
• ECG: ST-segment elevation or depression, evolving Q waves, symmetric inversion of T waves.
• Elevation of cardiac markers (CK-MB, troponin T, or troponin I).
• Appearance of segmental wall motion abnormality by imaging techniques.

Treatment ????

1)Aspirin and Clopidogrel All patients with definite or suspected myocardial infarction should receive aspirin at a dose of 162 mg or 325 mg at once regardless of whether thrombolytic therapy is being considered or the patient has been taking aspirin. Chewable aspirin provides more rapid blood levels. Patients with a definite aspirin allergy should be treated with clopidogrel; a 300 mg (or 600 mg) loading dose will result in faster onset of action than the standard 75 mg dose.

2) Thrombolytic Therapy: Streptokinase is not commonly used for treatment of acute myocardial infarction since it is less effective at opening occluded arteries and less effective at reducing mortality. It is non-fibrin-specific, causes depletion of circulating fibrinogen, and has a tendency to induce hypotension, particularly if infused rapidly. This can be managed by slowing or interrupting the infusion and administering fluids. There is controversy as to whether adjunctive heparin is beneficial in patients given streptokinase, unlike its administration with the more clot-specific agents. Allergic reactions, including anaphylaxis, occur in 1–2% of patients, and this agent should generally not be administered to patients with prior exposure.

3) Nitrates: Nitroglycerin is the agent of choice for continued or recurrent ischemic pain and is useful in lowering BP or relieving pulmonary congestion. However, routine nitrate administration is not recommended, since no improvement in outcome has been observed in the ISIS-4 or GISSI-3 trials, in which a total of over 70,000 patients were randomized to nitrate treatment or placebo. Nitrates should be avoided in patients who received phosphodiesterase inhibitors (sildenafil, vardenafil, and tadalafil) in the prior 24 hours.

4) Beta Blockers  : Although trials have shown modest short-term benefit from intravenous -blockers given immediately after acute myocardial infarction, it has not been clear that this provides a major advantage over simply beginning an oral -blocker. The Chinese COMMIT/CCS-2 trial involving 45,000 patients found no overall benefit to intravenous followed by oral metoprolol; the aggressive dosing (three 5 mg intravenous boluses followed by 200 mg/d orally) appeared to prevent reinfarction at the cost of increasing shock in patients presenting with heart failure. Thus, -blockade should be avoided in patients with decompensated heart failure, decompensated asthma, or high degrees of AV block. The CAPRICORN trial showed the benefits of carvedilol following the acute phase of large myocardial infarction with contemporary care.

5)ACE Inhibitors: A series of trials (SAVE, AIRE, SMILE, TRACE, GISSI-III, and ISIS-4) have shown both short- and long-term improvement in survival with ACE inhibitor therapy. The benefits are greatest in patients with low EFs, large infarctions, or clinical evidence of heart failure. Because substantial amounts of the survival benefit occur on the first day, ACE inhibitor treatment should be commenced early in patients without hypotension, especially patients with large or anterior myocardial infarction.

6) Calcium Channel Blockers : There are no studies to support the use of calcium channel blockers in most acute myocardial infarction patients—and indeed, they have the potential to exacerbate ischemia and cause death from reflex tachycardia or myocardial depression. One exception is that diltiazem and verapamil appear to prevent reinfarction and ischemia in the subset of patients with non-Q wave infarction. Diltiazem is preferable because it causes less myocardial depression. The dosage is 240–360 mg daily. Otherwise, long-acting calcium channel blockers should be reserved for management of hypertension or ischemia as second- or third-line drugs after -blockers and nitrates

7) Surgery:

Prevention>>>

How Can a Heart Attack Be Prevented?

Lowering your risk factors for coronary artery disease (CAD) can help you prevent a heart attack. (See “Who Is At Risk for a Heart Attack?“) Even if you already have CAD, you can still take steps to lower your risk of heart attack.

Reducing the risk of heart attack usually means making healthy lifestyle choices. You also may need treatment for medical conditions that raise your risk.

Healthy Lifestyle Choices

Healthy lifestyle choices to help prevent heart attack include:

• Following a low-fat diet rich in fruits and vegetables. Pay careful attention to the amounts and types of fat in your diet. Lower your salt intake. These changes can help lower high blood pressure and high blood cholesterol.
• Losing weight if you’re overweight or obese.
• Quitting smoking.
• Doing physical activity to improve heart fitness. Ask your doctor how much and what kinds of physical activity are safe for you.

Treat Related Conditions

In addition to making lifestyle changes, you can help prevent heart attacks by treating conditions you have that make a heart attack more likely:

• High blood cholesterol. You may need medicine to lower your cholesterol if diet and exercise aren’t enough.
• High blood pressure. You may need medicine to keep your blood pressure under control.
• Diabetes (high blood sugar). If you have diabetes, control your blood sugar levels through diet and physical activity (as your doctor recommends). If needed, take medicine as prescribed.

Have an Emergency Action Plan

Make sure that you have an emergency action plan in case you or someone else in your family has a heart attack. This is especially important if you’re at high risk or have already had a heart attack.

Talk with your doctor about the signs and symptoms of heart attack, when you should call 9–1–1, and steps you can take while waiting for medical help to arrive.