On the first day of basketball practice, Elizabeth Pearlman passed out with a heart condition, but an AED saved her life. “What if it happened somewhere where an AED wasn’t available?” she asked.

Chicago native Elizabeth Pearlman was taking part in a conditioning drill with her college basketball team last October when she collapsed.

If an automated external defibrillator -- an AED is a portable device that can detect cardiac arrhythmias and shock the heart back into rhythm -- hadn't been available, she likely would have died. Pearlman hopes that by sharing her story she might raise awareness -- and ultimately help save others.

"It was the first day of practice," the Aurora University senior said. "At the end of practice, we were doing sprints. On the last sprint, I suddenly felt like I had to stop running. Did I feel faint? No. I just knew that I didn't feel right. The next thing I saw was the floor coming to my face."

Fortunately, Aurora head athletic trainer Terry Smith was at the practice. He saw Pearlman go down. Was she just tired? He doubted that. He sensed something was wrong, and went directly over to her. He saw that she was having a hard time breathing and was hyperventilating. Then he saw her eyes roll back in her head.

"It went downhill real quick," Smith said.

He told one coach to call 911, and told another to get an AED. He immediately began performing CPR. But Pearlman didn't respond to the CPR. Smith had to use the AED to restore her heart rhythm. He had to shock her twice.

"I don't know how much time passed," Smith said. "But time flew. Then the ambulance came."

Pearlman, 21, remembers being in a state of euphoria before regaining full consciousness in the ambulance.

"I was in a great place -- it was deep and solid," she said. "Then I started feeling pricks and pokes, and I woke up to [the paramedics] putting needles in my veins."

Pearlman would spend the next week in the intensive care unit. She would learn that she suffers from a previously undiagnosed genetic heart disease called arrhythmogenic right ventricular dysplasia. She also had suffered a pulmonary embolism. In the months that followed she would undergo several medical procedures, including having an implantable cardioverter defibrillator, or ICD, put in her chest. She has become an expert on her heart condition. She knows she had a close call. Make that a very close call.

"If not for the AED, you're dead," she said. "Growing up, I played basketball in some pretty tough city neighborhoods. I played pick-up games with guys, and we were always running. What if it had happened then? What if it had happened somewhere where an AED wasn't available?"

If it were up to organizations such as the American Red Cross, you would find an AED on every playground and in every home. Because CPR alone isn't always enough. AEDs are not useful for every arrhythmia, but they can detect two that are frequently implicated in sudden cardiac arrest, ventricular fibrillation and ventricular tachycardia.

"If you have an AED, it can increase your chance [of survival]," said Theresa Rees, manager of instruction and development for the Red Cross of Greater Chicago.

Fortunately, you can find AEDs in more places than ever before. They're small, light and easy to use.

"They are in all sporting facilities, government buildings, airports, schools, police cars, ambulances [and other places, as well]," Rees said.

Even those without training should not hesitate to use one in a crisis. But ideally everyone would learn from a professional.

Paramedic Lisa Krch, the CPR training coordinator for Advocate Christ Medical Center's Center for Prehospital Care in southwest suburban Oak Lawn, has taught thousands of people how to use an AED.

"You can teach anyone to use them," Krch said. "I've taught Boy Scouts -- 8-year-old kids. You just follow the prompts. Turn the machine on, then one prompt at a time. It won't go to the next step until you've completed the step you're on."

Advocate Christ has for the past two years gone into high schools to teach CPR, AED and basic first aid.

"Last year alone we taught 1,000 people," Krch said. "I wish they would make it a requirement of high school graduation that you need to know CPR and AED. It's less than eight hours, and it could save a life."

Twelve months ago, Pearlman's life changed drastically. She can no longer play basketball -- her heart condition won't allow it. But she's on target to graduate with her class, and she hopes to attend veterinary school. She's not only alive, she is full of life. Spread the word.

"AEDs are very, very important," she said.

suntimes.com

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For the past 30 years, Peter Gorevic, now director of rheumatology at Mount Sinai, has been treating patients with immune and arthritis-related disorders. One of his main research interests is looking at what causes the group of disorders known as amyloid diseases, and what doctors can do to treat them.

Who's at risk

Amyloid disease is hardly a household word, despite the fact that one of the 26 types is Alzheimer’s disease — which affects about 4 million Americans. "Amyloid diseases, or amyloidosis, are conditions in which the abnormal amyloid proteins build up in organs and tissues," says Gorevic. "During a biopsy, the pathologist sees a pinkish amorphous material that is the sign of an unhealthy mutation," he says.

These amyloid deposits can occur anywhere in the body and cause different symptoms, depending on which organ is primarily affected. Doctors divide amyloid disease into systemic and localized disease, with localized disease often related to Alzheimer’s.

"Systemic amyloid falls into three groups: primary, secondary and familial amyloid," says Gorevic, "While these diseases are relatively uncommon, they do occur in certain settings more often than others."

For instance, one type of amyloid is a frequent complication resulting from long-term dialysis.

"Some researchers think that 60%-80% of patients who are on dialysis for more than 10 years may have amyloid," says Gorevic. "We estimate that about 250,000 Americans fall into this high-risk category."

Another common disease linked to amyloid is chronic inflammatory arthritis, which can cause secondary amyloid disease. "As many as 5%-10% of those people might develop amyloid if their arthritis isn’t kept under control," says Gorevic.

Familial amyloid is the rarest disorder, with only 10,000 to 15,000 people affected worldwide.

"The genetic mutation that causes it is widely represented in Western Africa, and as a result more prevalent in African-Americans," says Gorevic. "Some researchers think 1 million people carry the mutation that can lead to familial amyloid."

Signs and symptoms

Amyloid diseases present themselves differently, depending on the system that is primarily affected.

"Often patients end up with symptoms related to the kidney, heart, nervous system or GI tract," says Gorevic. "The symptoms may not be specific to amyloid, but they would lead the patient to come to the doctor, who runs a biopsy that catches the amyloid," he says.

For instance, amyloid patients commonly see a nephrologist if they are retaining fluid, losing protein in their urine or experiencing shortness of breath. Cardiologists more often find amyloid in patients who have swollen legs, chest palpitations and shorter and shorter breath. "Sometimes they can’t lie flat because fluid accumulates in their lungs," says Gorevic.

Neurological symptoms can include neuropathy (which cause numbness and tingling in the legs), carpal-tunnel syndrome or weakness in the legs and arms. In the GI system, red flags can come from the sense that the stomach fills up too quickly, trouble swallowing, dry mouth, diarrhea or constipation.

Traditional treatment

A thorough diagnosis is the key first step to treating amyloid disease.

"Traditionally, treatment is, first of all, figuring out what organ is involved and how it should be handled," says Gorevic. "For instance, if heart failure, what could you do? If the kidneys, how do we conserve function?" In this approach, cardiac patients might be helped by certain drugs and the need to avoid others.

Kidney patients would take "standard meds" like ACE inhibitors or ARBs (angiotensin receptor blockers). In both cases, organ transplant can be an option down the line. One of the primary objectives is that the treatment has to be tailored to the particular type of amyloid.

"For primary amyloid, we must first evaluate the patient for the bone marrow cancer multiple myeloma, which occurs in 10% of these patients," says Gorevic. "The treatment is chemotherapy."

In secondary amyloid, the amyloid results from another health problem, such as chronic inflammatory arthritis. Treating the underlying disease aggressively has great results in managing the amyloid." Familial amyloid is the most frustrating," says Gorevic. "It affects the nervous system or heart, and until recently we had no therapeutics."

New drugs are rapidly changing the landscape of treatments available for all three types of amyloid, with more rapid chemo and an improved understanding of bone marrow transplantation changing the prognosis for patients with primary amyloid.

New therapeutics can prevent secondary amyloid from forming, or prevent the need for kidney transplant.

Research breakthroughs

Doctors expect that two new drugs approved for rheumatoid arthritis will dramatically cut down on the resulting amyloid. In the past year, doctors have discovered a new therapeutic, diflunisal.

"It seems to inhibit this form of amyloid from occurring," says Gorevic. "It’s going through testing now, and we're very optimistic."

Questions for your doctor

If you’re diagnosed with amyloid disease, start out by asking "How much of my body is affected?" Be sure to consider the range of treatments by asking "What are my options?"

If your doctor recommends a medical treatment, ask, "What side effects can I expect from these drugs?" Many of the drugs that doctors prescribe to patients can be part of a study or involve an off-label use, "so it’s important for the patients to understand the risks and benefits," says Gorevic.


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It’s the latest wrinkle in acne treatments -- an at-home kit that uses LED light therapy by exposing the skin to various wavelengths of colored light in an attempt to clear up blemishes.

LED treatments aren’t just favored by dermatologists and facialists, but by high-profile celebs like Carla Bruni, Sienna Miller and Natalie Imbruglia, reports The Daily Mail. In salons, a light treatment could cost well over $100 and take more than six sessions.

But a hand-held device for home use actually mimics the treatments that the pros pay top dollar for, at a much smaller price.

The Tanda Light Therapy Skincare System, created in Canada, is a minimachine for home use that has two separate devices. One, the Tanda Clear, employs blue LED light to zap bacteria that cause acne. Red LED light is used in the Tanda Regenerate, said to enliven collagen-producing cells, with the goal of fewer wrinkles and firmer skin. Studies found that users experienced a "significant" reduction in pimples, reports The Daily Mail.

So is a device like this safe for those who like the idea of a do-it-yourself acne treatment?

"It appears to be safe, but I would be skeptical of the findings of any of these studies," says Dr. David Avram, a dermatologist at Long Island College Hospital. "They are not doubleblinded studies that meet the criteria for good scientific studies."

Those who use the at-home LED system may discover that it "will probably help on inflamed lesions," Avram says. "It will wipe away acne on the surface of the skin. It works very superficially on very mild cases, but in significant acne, it really does not have much of a role."

Adds Dr. Maria Tsoukas, a dermatologist at the University of Chicago, "The LED lights have been shown to be effective in acne therapy, but you have to be careful. Anytime someone uses something like this they should carefully follow the instructions."

Dr. Doris Day, dermatologist and an attending physician at Lenox Hill Hospital, predicts that more products like the Tanda will make their way onto the market. But, she says, people should think of at-home acne treatments as an adjunct to the treatment they receive from a physician.

There is no true "cure" for acne, she explains, and it can be scarring. "The earlier and more appropriately you treat it, the greater chance that you will be able to clear the acne without leaving marks behind," Day explains. "Systems like these are okay as part of a treatment, because very often a combination of treatments is needed for acne. In any case, they should be used under the guidance of your dermatologist."

Avram says of the at-home treatments, "They are not dangerous, but people who use them should be realistic. People probably will just see a limited improvement. For those with more significant acne, it may just be a waste of their time."


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Definition

Acne is a skin condition that causes whiteheads, blackheads, and inflamed red lesions (papules, pustules, and cysts) to form. These growths are commonly called pimples or "zits."
Alternative Names

Acne vulgaris; Cystic acne; Pimples; Zits
Causes, incidence, and risk factors

Acne occurs when tiny holes on the surface of the skin, called pores, become clogged. Each pore is an opening to a canal called a follicle, which contains a hair and an oil gland. Normally, the oil glands help keep the skin lubricated and help remove old skin cells. When glands produce too much oil, the pores can become blocked, accumulating dirt, debris, and bacteria. The blockage is called a plug or comedone.

The top of the plug may be white (whitehead) or dark (blackhead). If it ruptures, the material inside, including oil and bacteria, can spread to the surrounding area and cause an inflammatory reaction. If the inflammation is deep in your skin, the pimples may enlarge to form firm, painful cysts.

Acne commonly appears on the face and shoulders, but may also occur on the trunk, arms, legs, and buttocks.

Acne is most common in teenagers, but it can happen at any age, even as an infant. Three out of four teenagers have acne to some extent, probably caused by hormonal changes that stimulate oil production. However, people in their 30s and 40s may also have acne.

Acne tends to run in families and can be triggered by:

* Hormonal changes related to menstrual periods, pregnancy, birth control pills, or stress
* Greasy or oily cosmetic and hair products
* Certain drugs (such as steroids, testosterone, estrogen, and phenytoin)
* High levels of humidity and sweating

Despite the popular belief that chocolate, nuts, and other foods cause acne, research does not confirm this idea.
Symptoms

* Blackheads
* Crusting of skin eruptions
* Cysts
* Pustules
* Redness around the skin eruptions
* Scarring of the skin
* Whiteheads

Signs and tests

Your doctor can diagnose acne based on the appearance of the skin. Testing is usually not required.
Treatment

Take the following self-care steps to lessen the effects of acne:

* Clean your skin gently with a mild, non-drying soap (such as Dove, Neutrogena, or Basics). Remove all dirt or make-up. Wash once or twice a day, including after exercising. However, avoid excessive or repeated skin washing.
* Shampoo your hair daily, especially if it's oily. Comb or pull your hair back to keep the hair out of your face. Avoid tight headbands.
* Try not to squeeze, scratch, pick, or rub the pimples. Although it might be tempting to do this, it can lead to skin infections and scarring.
* Avoid touching your face with your hands or fingers.
* Avoid greasy cosmetics or creams. Look for water-based or "non-comedogenic" formulas. Take make-up off at night. Non-comedogenic products have been tested and proven not to clog pores and cause acne.

If these steps do not clear up the blemishes to an acceptable level, try over-the-counter acne medications. These products are applied directly to the skin. They may contain benzoyl peroxide, sulfur, resorcinol, or salicylic acid. They work by killing bacteria, drying up the oil, and causing the top layer of your skin to peel. They may cause redness or peeling of the skin.

If pimples are still a problem, a dermatologist can prescribe stronger medications and discuss other options with you.

Prescription medicines include:

* Oral antibiotics (taken by mouth) such as minocycline, doxycycline, tetracycline, erythromycin, and amoxicillin
* Topical antibiotics (applied to the skin) such as clindamycin, erythromycinm or dapsone
* Retinoic acid cream or gel (Retin-A) and isotretinoin pills (Accutane) -- pregnant women and sexually active adolescent females should NOT take Accutane, as it causes severe birth defects. Women taking Accutane must use two forms of birth control before starting the drug and enroll in the iPledge program.
* Prescription formulas of benzoyl peroxide, sulfur, resorcinol, salicylic acid
* A pill called spironolactone may help women with hormonally controlled acne.
* A laser procedure called photodynamic therapy may also be helpful.

Birth control pills can sometimes help clear up acne. (In some cases, though, they may make it worse.)

Your doctor may also suggest chemical skin peeling, removal of scars by dermabrasion, or removal, drainage, or injection of cysts.

A small amount of sun exposure may improve acne. However, excessive exposure to sunlight or ultraviolet rays is not recommended because it increases the risk of skin cancer.
Expectations (prognosis)

Acne usually subsides after adolescence, but may last into middle age. The condition generally responds well to treatment after 6 - 8 weeks, but may flare up from time to time. Scarring may occur if severe acne is not treated. Some people, especially teenagers, can become significantly depressed if acne is not treated.
Complications

Possible complications include:

* Changes in skin color
* Cysts
* Damage to self-esteem, confidence, personality, and social life
* Permanent facial scars
* Side effects of Accutane (including very dry skin and mucus membranes, high triglyceride levels, liver damage, and birth defects in an unborn baby; call your doctor right away if you become pregnant while taking this drug)
* Side effects of other medications

Calling your health care provider
Call your doctor or a dermatologist if:

* Self-care measures and over-the-counter medicine have not helped after several months
* Your acne is severe (for example, you have lots of redness around the pimples or you have cysts) or getting worse
* You develop scars as your acne clears up

Call your pediatrician if your baby has acne that does not clear up on its own within 3 months.
References

Acne, rosacea, and related disorders. In: Habif TP, ed. Clinical Dermatology. 5th ed. Philadelphia, Pa: Saunders Elsevier; 2009:chap 7.

Adam.

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The initial diagnosis of acute coronary syndrome (ACS) is based on history, risk factors, and, to a lesser extent, ECG findings. The symptoms are due to myocardial ischemia, the underlying cause of which is an imbalance between supply and demand of myocardial oxygen.

Patients with ACS include those whose clinical presentations cover the following range of diagnoses: unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). This ACS spectrum concept is a useful framework for developing therapeutic strategies.

A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and ECG changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta-blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.

[ CLOSE WINDOW ]

A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and ECG changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta-blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.

A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure 140/90 mm Hg and heart rate is 98. Her ECG is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.

[ CLOSE WINDOW ]

A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure 140/90 mm Hg and heart rate is 98. Her ECG is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.

Pathophysiology

Myocardial ischemia is most often due to atherosclerotic plaques, which reduce the blood supply to a portion of myocardium. Initially, the plaques allow sufficient blood flow to match myocardial demand. When myocardial demand increases, the areas of narrowing may become clinically significant and precipitate angina. Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest, and without recent change in frequency or severity of activity that produce symptoms, is called chronic stable angina. Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombus forms. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina.

Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery. Angiographic evidence of coronary thrombus formation may be seen in more than 90% of patients with STEMI but in only 1% of patients with stable angina and about 35-75% of patients with unstable angina or NSTEMI. However, not every STEMI evolves into a Q-wave MI; likewise, a patient with NSTEMI may develop Q waves.

The excessive mortality rate of coronary heart disease is primarily due to rupture and thrombosis of the atherosclerotic plaque. Inflammation plays a critical role in plaque destabilization and is widespread in the coronary and remote vascular beds. Systemic inflammatory, thrombotic, and hemodynamic factors are relevant to the outcome. Evidence indicates that platelets contribute to promoting plaque inflammation as well as thrombosis. A new theory of unbalanced cytokine-mediated inflammation is emerging, providing an opportunity for intervention.

A less common cause of angina is dynamic obstruction, which may be caused by intense focal spasm of a segment of an epicardial artery (Prinzmetal angina). Coronary vasospasm is a frequent complication in patients with connective tissue disease. Other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, such as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina as a baseline medical condition.

Spontaneous and cocaine-related coronary artery dissection remains an unusual cause of ACS and should be included in the differential diagnosis, especially when a younger female or cocaine user is being evaluated. An early clinical suspicion of this disease is necessary for a good outcome. Cardiology consultation should be obtained for consideration for urgent percutaneous coronary intervention.

Although rare, pediatric and adult ACS may result from the following (see Myocardial Infarction in Childhood):

• ACS may occur with Marfan syndrome; Kawasaki disease; Takayasu arteritis; or cystic medial necrosis with aortic root dilatation, aneurysm formation, and dissection into the coronary artery.
• Anomalous origin of the left coronary artery from the pulmonary artery may occur as unexplained sudden death in a neonate.
• Coronary artery ostial stenosis may occur after repair of a transposition of the great arteries in the neonatal period.
• An aberrant left main coronary artery with its origin at the right sinus of Valsalva may cause ACS, especially with exertion.
• Traumatic myocardial infarction can occur in patients at any age.
• Accelerated atherosclerosis is known to occur in cardiac transplant recipients on immunosuppressive therapy.
• ACS may occur with progeria.

Irrespective of the cause of unstable angina, the result of persistent ischemia is myocardial infarction (MI).

Frequency

United States

Although the exact incidence of ACS is difficult to ascertain, hospital discharge data indicate that 1,680,000 unique discharges for ACS occurred in 2001.

International

In Britain, annual incidence rate of angina is estimated at 1.1 cases per 1000 males and 0.5 cases per 1000 females aged 31-70 years. In Sweden, chest pain of ischemic origin is thought to affect 5% of all males aged 50-57 years. In industrialized countries, annual incidence rate of unstable angina is approximately 6 cases per 10,000 people.

Mortality/Morbidity

When the only therapy for angina was nitroglycerin and limitation of activity, patients with newly diagnosed angina had a 40% incidence of MI and a 17% mortality rate within 3 months. A recent study shows that the 30-day mortality rate from ACS has decreased as treatment has improved, a statistically significant 47% relative decrease in 30-day mortality rate among newly diagnosed ACS from 1987-2000. This decrease in mortality rate is attributed to aspirin, glycoprotein (GP) IIb/IIIa blockers, and coronary revascularization via medical intervention or procedures.

Clinical characteristics associated with a poor prognosis include advanced age, male sex, prior MI, diabetes, hypertension, and multiple-vessel or left-mainstem disease.

Sex

Incidence is higher in males among all patients younger than 70 years. This is due to the cardioprotective effect of estrogen in females. At 15 years postmenopause, the incidence of angina occurs with equal frequency in both sexes. Evidence exists that women more often have coronary events without typical symptoms, which might explain the frequent failure to initially diagnose ACS in women.

Age

ACS becomes progressively more common with increasing age. In persons aged 40-70 years, ACS is diagnosed more often in men than in women. In persons older than 70 years, men and women are affected about equally.

Clinical

History

• Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It is usually described as a sensation of chest pressure or heaviness, which is reproduced by activities or conditions that increase myocardial oxygen demand.
• Not all patients experience chest pain. Some present with only neck, jaw, ear, arm, or epigastric discomfort.
• Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalents.
• A patient may present to the ED because of a change in pattern or severity of symptoms. A new case of angina is more difficult to diagnose because symptoms are often vague and similar to those caused by other conditions (eg, indigestion, anxiety).
• Patients may have no pain and may only complain of episodic shortness of breath, weakness, lightheadedness, diaphoresis, or nausea and vomiting.
• Patients may complain of the following:
  • Palpitations
  • Pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm
  • Exertional dyspnea that resolves with pain or rest
  • Diaphoresis from sympathetic discharge
  • Nausea from vagal stimulation
  • Decreased exercise tolerance
  • Patients with diabetes and elderly patients are more likely to have atypical presentations and offer only vague complaints, such as weakness, dyspnea, lightheadedness, and nausea.
• Stable angina
  • Involves episodic pain lasting 5-15 minutes
  • Provoked by exertion
  • Relieved by rest or nitroglycerin
• Unstable angina: Patients have increased risk for adverse cardiac events, such as MI or death. Three clinically distinct forms exist, as follows:
  • New-onset exertional angina
  • Angina of increasing frequency or duration or refractory to nitroglycerin
  • Angina at rest
• Variant angina (Prinzmetal angina)
  • Occurs primarily at rest
  • Triggered by smoking
  • Thought to be due to coronary vasospasm
• Elderly persons and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. Elderly persons may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.
• As many as half of cases of ACS are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. Maintain a high index of suspicion for ACS especially when evaluating women, patients with diabetes, older patients, patients with dementia, and those with a history of heart failure.

Physical

• Physical examination results are frequently normal. If chest pain is ongoing, the patient will usually lie quietly in bed and may appear anxious, diaphoretic, and pale.
• Hypertension may precipitate angina or reflect elevated catecholamine levels due to either anxiety or exogenous sympathomimetic stimulation.
• Hypotension indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvular dysfunction.
• Jugular venous distention
• Third heart sound (S₃) may be present.
• A new murmur may reflect papillary muscle dysfunction.
• Rales on pulmonary examination may suggest left ventricular (LV) dysfunction or mitral regurgitation.
• Presence of a fourth heart sound (S₄) is a common finding in patients with poor ventricular compliance due to preexisting ischemic heart disease or hypertension.

Causes

• Atherosclerotic plaque is the predominant cause. Coronary artery vasospasm is less common.
• Alternative causes of angina include the following:
  • Ventricular hypertrophy due to hypertension, valvular disease, or cardiomyopathy
  • Embolic occlusion of the coronary arteries
  • Hypoxia, as in carbon monoxide poisoning or acute pulmonary disorders
  • Cocaine and amphetamines, which increase myocardial oxygen demand and may cause coronary vasospasm
  • Underlying coronary artery disease, which may be unmasked by severe anemia
  • Inflammation of epicardial arteries
  • Coronary artery dissection
• Risk factors for ACS should be documented and include the following:
  • Male gender
  • Diabetes mellitus (DM)
  • Smoking history
  • Hypertension
  • Increased age
  • Hypercholesterolemia
  • Hyperlipidemia
  • Prior cerebrovascular accident (CVA) - These patients constitute 7.5% of patients with ACS and have high-risk features.
  • Inherited metabolic disorders
  • Methamphetamine use
  • Occupational stress
  • Connective tissue disease

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