Sunday, August 24, 2014

Cardiac Enzymes

Enzymes are found throughout the body and are released to enable chemical reactions and responses to take place.Cardiac enzymes are chemical substances made up of proteins that are essential to enable function of the heart muscle.
These enzymes are always present in the blood, even in those with good health, but they are released to higher concentrations when the heart tissues become damaged or have to work harder.

What Are The Main Cardiac Enzymes In The Body?

The main cardiac enzymes found in the heart tissues are troponin T, troponin I, creatine kinase (CK), aspartate aminotranferase (AST) and lactate dehydrogenase (LDH).These enzymes all rise and peak at differing times after heart muscle injury and the elevations can remain peaked for several days, though these times are also variable with the different enzymes.

Are Cardiac Enzymes Important?

These enzymes are extremely important and testing for them can tell doctors whether or not the cardiac muscle has been damaged in some way, for example when a heart attack has taken place.
When the cells of the heart become damaged, the membranes within the cell become weakened causing the enzymes contained in the cell to seep out into the blood stream.The more damaged sustained by the heart, the greater the concentrations of the enzymes in most cases.

Cardiac Enzyme Tests.

Testing for cardiac enzymes is a routine part of diagnosing damage to the heart, particularly when a heart attack is suspected. The test is not carried out alone and a full examination of the patient will be needed along with other tests such as an electrocardiogram (ECG). This is because raised levels of cardiac enzymes does not automatically mean that a person had suffered a heart attack as raised levels are also present in many other conditions of the heart also.
The testing is performed by obtaining a blood sample and finding out if there are high concentration levels of the enzymes in the blood. As these concentration levels can rise slowly as more leak into the blood stream. It is often common practice to repeat the test after some time has lapsed and levels reassessed.
The results from the tests are usually available quite quickly (often within an hour or two) due to their use in emergency patients and the need for physicians to make a fast and accurate diagnosis.
Separate tests are usually carried out also to test for levels of the different types of cardiac enzymes and some are more reliable than others.Testing for troponin T and I are becoming the most popular testing techniques as the results are more accurate and specific to heart injury and the levels remain raised for longer periods of time, though most doctors will also routinely test for the other enzymes as well.
Cardiac enzymes are chemicals that are found naturally in the blood. Their levels become raised as a result of injury to the heart muscle and a simple blood test can be performed to help make a diagnosis. The test is commonly performed if a heart attack is suspected and has become a routine part of making such a diagnosis.
Unfortunately some heart attacks can be immediately fatal, and those that aren't need immediate medical attention, but the chances of survival of these people can be greatly increased by ensuring that some basic life support techniques are carried out whilst waiting for medical assistance.Every second is vital in ensuring good recovery rates with a lower chance of long term problems.Heart attacks do not have to be sudden and intense, they can in fact develop slowly, worsening gradually.

Is it a Heart Attack?

The most obvious signs that someone is having an intense sudden heart attack include:
  • Clutching of the chest; this pain can be centralised in the chest cavity or radiate to the left shoulder and down the left arm.
  • Painful expressions; many people will show an immediate sign of intense pain and facial expressions will easily convey this.
  • Shortness of breath; this can include gasping or short sharp intake of breath.Collapse; the person falls to the ground.
Signs of a heart attack that worsens over time include:
  • Complaining of persistent heart burn or indigestion.
  • Sweating but shivering at the same time.
  • Looking pale.
  • Feeling nauseous.
  • Chest pain develops slowly.

Immediate First Aid

These guidelines are in no way to act as an alternative to professional medical help and should be used whilst waiting for help to arrive. They apply to adult life support only as paediatric guidelines vary.
First of all, it is essential to determine whether the area around the person is safe for you to enter. Electric shocks can cause a cardiac arrest so ensure there are no live electrics around. Make sure there is no broken glass or other obstacles in the way.
Initially, discover if the person is responsive. Gently shake them and ask if they can hear you. Do not do this too violently in case of injury or if the person has fallen hard and fractured their skull. Find out if the person is breathing or not. Watch for signs of the chest cavity rising and falling and feel for exhaled air from the nose or mouth.
Check for a pulse using either the pulse point on the wrist or on the side of the neck. Do this using two fingers placed directly but not too hard onto the area and leave in place for at least 30 seconds. A pulse can be weak, intermittent or very slow in these cases.If a pulse is present try and determine why the person is not breathing. Is their airway obstructed by something? Is there a tightly fitting tie around their neck? Tilting the head back and gently opening the mouth using two fingers observe for anything that may have become lodged in the throat.
If the airway is clear, run and call for help. Assess regularly.
Find out if anyone around is familiar with CPR techniques.Whilst the casualty is laid on their back, tilt the head and chin upwards and slightly back to open the airway.Placing the hands, one on top of the other, to the centre of the chest give 30 compressions to 2 breaths. Try and find someone to help do this as it can be exhausting for one person.
To give a breath, tilt the head back and block the nose by pinching with finger and thumb, give one deep breath into the persons mouth. Whilst doing this look for the chest rising informing you that the air has gone into the lungs.Repeat the pattern of 30 compressions to 2 breaths until help arrives.
The methods given are to be used in an emergency only. Always try and find a medically trained person as this will increase the chances of the person surviving.The methods detailed were as per government guidelines at the time of publication, but are subject to frequent change as research provides more information on which to base the guidelines on.
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Cardiomyopathy

Cardiomyopathy (literally "heart muscle disease") is the measurable deterioration of the function of the myocardium (the heart muscle) for any reason, usually leading to heart failure; common symptoms are dyspnea (breathlessness) and peripheral edema(swelling of the legs). People with cardiomyopathy are often at risk of dangerous forms of irregular heart beat and sudden cardiac death.[1] The most common form of cardiomyopathy is dilated cardiomyopathy.[2][3]

Classification[edit]

Although in theory the term "cardiomyopathy" could apply to almost any disease affecting the heart, in practice it is usually reserved for "severe myocardial disease leading to heart failure".[4]
  • An extrinsic cardiomyopathy is a cardiomyopathy where the primary pathology is outside the myocardium itself. Most cardiomyopathies are extrinsic, by far the most common cause of an extrinsic cardiomyopathy is ischemia. Ischemia can be understood as poor oxygen supply of the heart muscle (the demand for oxygen is higher than the current supply). The World Health Organization calls these specific cardiomyopathies:[5]
  • An intrinsic cardiomyopathy is defined as weakness in the muscle of the heart not due to an identifiable external cause. This definition was used to categorize previously idiopathic cardiomyopathies although specific external causes have since been identified for many. For example, alcoholism has been identified as a cause for some forms of dilated cardiomyopathy. To make a diagnosis of an intrinsic cardiomyopathy, significant coronary artery disease should be ruled out first (amongst other causes). The term intrinsic cardiomyopathy does not describe the specific etiology of weakened heart muscle. The intrinsic cardiomyopathies consist of a variety of disease states, each with their own causes. Many intrinsic cardiomyopathies now have identifiable external causes including drug and alcohol toxicity, certain infections (including Hepatitis C), and variousgenetic and idiopathic (i.e., unknown) causes. For example mutations in the cardiac desmosomal genes as well as in the DES gene might cause arrhythmogenic right ventricular cardiomyopathy (ARVC).[6][7]
It is also possible to classify cardiomyopathies functionally, as involving dilation, hypertrophy, or restriction.[8]

Types[edit]

Signs and symptoms[edit]

Symptoms and signs may mimic those of almost any form of heart disease. Chest pain is common. Mild myocarditis or cardiomyopathy is frequently asymptomatic; severe cases are associated with heart failure, arrhythmias, and systemic embolization. Manifestations of the underlying disease (e.g., Chagas' disease) may be prominent. Most patients with biopsy-proven myocarditis report a recent viral prodrome preceding cardiovascular symptoms.
ECG abnormalities are often present, although the changes are frequently nonspecific. A pattern characteristic of left ventricular hypertrophy may be present. Flat or inverted T waves are most common, often with low-voltage QRS complexes. Intraventricular conduction defects and bundle branch block, especially left bundle branch block, are also common. An echocardiogram is useful to detect wall motion abnormalities or a pericardial effusion. Chest radiographs can be normal or can show evidence of congestive heart failure with pulmonary edema or cardiomegaly.

Images[edit]

  • (HE stain).

Treatment[edit]

Treatment depends on the type of cardiomyopathy and condition of disease, but may include medication (conservative treatment) or iatrogenic/implanted pacemakers for slow heart rates, defibrillators for those prone to fatal heart rhythms, ventricular assist devices (LVADs) for severe heart failure, or ablation for recurring dysrhythmias that cannot be eliminated by medication or cardioversion. The goal of treatment is often symptom relief, and some patients may eventually require a heart transplant. Treatment of cardiomyopathy (and other heart diseases) using alternative methods such as stem cell therapy is commercially available but is not supported by convincing evidence.

References[edit]

  1. Jump up^ Kasper, Denis Lh. et al. (2005). Harrison's Principles of Internal Medicine, 16th edn. McGraw-Hill. ISBN 0-07-139140-1.
  2. Jump up^ Cardiopulmonary Pharmacology for Respiratory Care, Jahangir Moini, Ch.2; page 24
  3. Jump up^ http://www.nhlbi.nih.gov/health/health-topics/topics/cm/types.html
  4. Jump up^ Gabriel A. Adelmann; McKenna, W; Bristow, M; Maisch, B; Mautner, B; O'Connell, J; Olsen, E; Thiene, G et al. (1996). "Cardiology Essentials in Clinical Practice".Circulation 93 (5). pp. 841–2. doi:10.1161/01.CIR.93.5.841. ISBN 9781849963053.PMID 8598070. Retrieved 11he 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies. (Full text)
  5. Jump up^ Richardson, P. et al.; McKenna, W; Bristow, M; Maisch, B; Mautner, B; O'Connell, J; Olsen, E; Thiene, G et al. (1996). "Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies". Circulation 93 (5): 841–2.doi:10.1161/01.CIR.93.5.841. PMID 8598070. (Full text)
  6. Jump up^ Klauke B, Kossmann S, Gaertner A, Brand K, Stork I, Brodehl A, Dieding M, Walhorn V, Anselmetti D, Gerdes D, Bohms B, Schulz U, Zu Knyphausen E, Vorgerd M, Gummert J, Milting H (2010). "De novo desmin-mutation N116S is associated with arrhythmogenic right ventricular cardiomyopathy". Hum. Mol. Genet. 19 (23): 4595–607.doi:10.1093/hmg/ddq387. PMID 20829228.
  7. Jump up^ Brodehl A, Hedde PN, Dieding M, Fatima A, Walhorn V, Gayda S, Å arić T, Klauke B, Gummert J, Anselmetti D, Heilemann M, Nienhaus GU, Milting H (2012). "Dual color photoactivation localization microscopy of cardiomyopathy-associated desmin mutants". J. Biol. Chem. 287 (19): 16047–57. doi:10.1074/jbc.M111.313841
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Myocardial Ischemia

Myocardial ischemia occurs when blood flow to your heart muscle is decreased by a partial or complete blockage of your heart's arteries (coronary arteries). The decrease in blood flow reduces your heart's oxygen supply.
Myocardial ischemia, also called cardiac ischemia, can damage your heart muscle, reducing its ability to pump efficiently. A sudden, severe blockage of a coronary artery may lead to a heart attack. Myocardial ischemia may also cause serious abnormal heart rhythms.
Treatment for myocardial ischemia is directed at improving blood flow to the heart muscle and may include medications, a procedure to open blocked arteries or coronary artery bypass surgery. Making heart-healthy lifestyle choices is important in treating and preventing myocardial ischemia.
    Symptoms
    Some people who have myocardial ischemia don't experience any signs or symptoms (silent ischemia). When myocardial ischemia does cause signs and symptoms, they may include:
  • Chest pressure or pain, typically on the left side of the body (angina pectoris)
  • Neck or jaw pain
  • Shoulder or arm pain
  • A fast heartbeat
  • Shortness of breath
  • Nausea and vomiting

When to see a doctor

If you have chest discomfort, especially if it's accompanied by one or more of the other signs and symptoms listed above, seek medical care immediately. Call 911 or your local emergency number. If you don't have access to emergency medical services, have someone drive you to the nearest hospital. Drive yourself only as a last resort, if there are absolutely no other options. Driving yourself puts you and others at risk if your condition suddenly worsens.
CMyocardial ischemia occurs when the blood flow through one or more of the blood vessels that lead to your heart (coronary arteries) is decreased. This decrease in blood flow leads to a decrease in the amount of oxygen your heart muscle (myocardium) receives. Myocardial ischemia may occur slowly as arteries become blocked over time, or it may occur quickly when an artery becomes blocked suddenly.
Conditions that may cause myocardial ischemia include:
  • Coronary artery disease (atherosclerosis). Atherosclerosis occurs when plaques made of cholesterol and waste products build up on your artery walls and restrict blood flow. Atherosclerosis of the heart arteries is called coronary artery disease and is the most common cause of myocardial ischemia.
  • Blood clot. The plaques that develop in atherosclerosis can rupture, causing a blood clot, which may lead to sudden, severe myocardial ischemia, resulting in a heart attack.
  • Coronary artery spasm. A coronary artery spasm is a brief, temporary tightening (contraction) of the muscles in the artery wall. This can narrow and briefly decrease or even prevent blood flow to part of the heart muscle.
Things that may trigger chest pain associated with myocardial ischemia include:
  • Physical exertion
  • Emotional stress
  • Cold temperatures
  • Lying down
  • Cocaine use
ausesFactors that may increase your risk of developing myocardial ischemia include:
  • Tobacco. Both smoking and long-term exposure to secondhand smoke can damage the interior walls of arteries — including arteries in your heart — allowing deposits of cholesterol and other substances to collect and slow blood flow. Smoking also increases the risk of blood clots forming in the arteries that can cause myocardial ischemia.
  • Diabetes. Diabetes is the inability of your body to adequately produce or respond to insulin properly. Insulin, a hormone secreted by your pancreas, allows your body to use glucose, which is a form of sugar from foods. Both type 1 and type 2 diabetes are linked to an increased risk of myocardial ischemia, heart attack and other heart problems.
  • High blood pressure. Over time, high blood pressure can damage arteries that feed your heart by accelerating atherosclerosis. High blood pressure is more common in those who are obese. Eating a diet high in salt also may increase your risk of high blood pressure.
  • High blood cholesterol or triglyceride levels. Cholesterol is a major part of the deposits that can narrow arteries throughout your body, including those that supply your heart. A high level of "bad" (low-density lipoprotein, or LDL) cholesterol in your blood is linked to an increased risk of atherosclerosis and myocardial ischemia. A high LDL level may be due to an inherited condition or a diet high in saturated fats and cholesterol. A high level of triglycerides, another type of blood fat, may also contribute to atherosclerosis. However, a high level of high-density lipoprotein (HDL) cholesterol (the "good" cholesterol), which helps the body clean up excess cholesterol, is desirable and lowers your risk of heart attack.
  • Lack of physical activity. An inactive lifestyle contributes to obesity and is associated with higher cholesterol and triglycerides and an increased risk of atherosclerosis. People who get regular aerobic exercise have better cardiovascular fitness, which is associated with a decreased risk of myocardial ischemia and heart attack. Exercise also lowers high blood pressure.
  • Obesity. Obese people have a high proportion of body fat, often with a body mass index of 30 or higher. Obesity raises the risk of myocardial ischemia because it's associated with high blood cholesterol levels, high blood pressure and diabetes.
  • Waist circumference. A waist circumference of more than 35 inches (88 centimeters) for women and 40 inches (102 cm) or more in men increases the risk of heart disease.
  • Family history. If you have a family history of heart attack or coronary artery disease, you may be at increased risk of myocardial ischemia.

  • Complications

    Myocardial ischemia can lead to a number of serious complications, including:
    • Heart attack (myocardial infarction). If a coronary artery becomes completely blocked, the lack of blood and oxygen can lead to a heart attack that destroys part of the heart muscle, causing serious and in some cases fatal heart damage.
    • Irregular heart rhythm (arrhythmia). Your heart muscle needs sufficient oxygen to beat properly. When your heart doesn't receive enough oxygen, the electrical impulses in your heart that coordinate your heartbeats may malfunction, causing your heart to beat too fast, too slow or irregularly. In some cases, arrhythmias can be life-threatening.
    • Heart failure. Myocardial ischemia can damage the heart muscle itself, leading to a reduction in its ability to effectively pump blood to the rest of your body. Over time, this damage may lead to heart failure

    • Tests and diagnosis

      Appointments & care

      At Mayo Clinic, we take the time to listen, to find answers and to provide you the best care.
      Learn more. Request an appointment.
      Along with a review of your medical history and a thorough physical exam, the tests and procedures used to diagnose myocardial ischemia include:
      • Electrocardiogram (ECG).This test records the electrical activity of your heart via electrodes attached to your skin. Certain abnormalities in your heart's electrical activity may indicate myocardial ischemia.
      • Echocardiogram. This test uses sound waves to produce an image of your heart. During an echocardiogram, sound waves are directed at your heart from a wand-like device (transducer) held on your chest. The sound waves bounce off your heart and are reflected back through your chest wall and processed electronically to provide video images of your heart. An echocardiogram can help identify whether an area of your heart has been damaged and isn't pumping normally.
      • Nuclear scan. This test helps identify blood flow problems to your heart. Small amounts of radioactive material are injected into your bloodstream. Special cameras can detect the radioactive material as it flows through your heart and lungs. Areas of reduced blood flow to the heart muscle — through which less of the radioactive material flows — appear as dark spots on the scan.
      • Coronary angiography. Coronary angiography uses X-ray imaging to examine the inside of your heart's blood vessels. During coronary angiography, a type of dye that's visible by X-ray machine is injected into the blood vessels of your heart. The X-ray machine rapidly takes a series of images (angiograms), offering a detailed look at the inside of your blood vessels.
      • Cardiac CT scan. CT scans can determine if you have coronary artery calcification — a sign of coronary atherosclerosis. The heart arteries also can be seen using CT scanning (coronary CT angiogram).
      • Stress test. A stress test usually involves walking on a treadmill or riding a stationary bike while your heart rhythm, blood pressure and breathing are monitored. Because exercise makes your heart pump harder and faster than it does during most daily activities, a stress test can reveal problems within your heart that might not be noticeable otherwise. It can be particularly useful if your doctor suspects you may have myocardial ischemia but you don't have any signs or symptoms.
      • Holter monitoring. A Holter monitor is a small, wearable device that records your heart rhythm. You usually wear a Holter monitor for one to two days. During that time, the device will record all of your heartbeats. A Holter monitor test is usually performed if an electrocardiogram isn't able to give your doctor enough information about your heart's condition or if your doctor suspects silent myocardial ischemia

Treatments and drugs

Appointments & care

At Mayo Clinic, we take the time to listen, to find answers and to provide you the best care.
Learn more. Request an appointment.
Treatment of myocardial ischemia is directed at improving blood flow to the heart muscle. Depending on the severity of your condition, you may be treated with medications, undergo a surgical procedure or both.

Medications

Medications that can be used to treat myocardial ischemia include:
  • Aspirin. Your doctor may recommend taking a daily aspirin or other blood thinner. This can reduce the tendency of your blood to clot, which may help prevent obstruction of your coronary arteries. There are some cases where aspirin isn't appropriate, such as if you have a bleeding disorder or if you're already taking another blood thinner, so ask your doctor before starting to take aspirin.
  • Nitroglycerin. This medication temporarily opens arterial blood vessels, improving blood flow to and from your heart.
  • Beta blockers. These medications help relax your heart muscle, slow your heartbeat and decrease blood pressure so blood can flow to your heart more easily.
  • Cholesterol-lowering medications. By decreasing the amount of cholesterol in your blood, especially low-density lipoprotein (LDL), or "bad," cholesterol, these drugs decrease the primary material that deposits on the coronary arteries.
  • Calcium channel blockers. Calcium channel blockers, also called calcium antagonists, relax and widen blood vessels by affecting the muscle cells in the arterial walls. This increases blood flow in your heart. Calcium channel blockers also slow your pulse and reduce the workload on your heart.
  • Angiotensin-converting enzyme (ACE) inhibitors. These drugs help relax blood vessels and lower blood pressure. ACE inhibitors prevent an enzyme in your body from producing angiotensin II, a substance in your body that affects your cardiovascular system in numerous ways, including constricting your blood vessels.
  • Ranolazine (Ranexa). This medication helps relax your heart arteries. Ranolazine is an anti-angina medication that may be prescribed with other angina medications, such as calcium channel blockers, beta blockers or nitroglycerin.

Procedures to improve blood flow

Sometimes more aggressive treatment is needed to improve blood flow. Surgical procedures that may help include:
  • Angioplasty and stenting. During angioplasty — also called a percutaneous coronary intervention (PCI) — your doctor inserts a long, thin tube (catheter) into the narrowed part of your artery. A wire with a tiny, deflated balloon is passed through the catheter to the narrowed area. The balloon is inflated to widen the artery, and then a small wire mesh coil (stent) is usually inserted to keep the artery open. Some stents slowly release medication to help keep the artery open. This procedure improves blood flow in your heart, reducing or eliminating myocardial ischemia.
  • Coronary artery bypass surgery. During this procedure, a surgeon creates a graft to bypass blocked coronary arteries using a vessel from another part of your body. This allows blood to flow around the blocked or narrowed coronary artery. Because this requires open-heart surgery, it's typically reserved for cases of multiple narrowed coronary arteries.


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Takotsubo Cardiomyopathy

Takotsubo Cardiomyopathy: A Unique Cardiomyopathy With Variable Ventricular Morphology 

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J Am Coll Cardiol Img. 2010;3(6):641-649. doi:10.1016/j.jcmg.2010.01.009
Article
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  Takotsubo cardiomyopathy is an important differential diagnosis of acute coronary syndrome. It is characterized by normal (or near-normal) coronary arteries, regional wall motion abnormalities that extend beyond a single coronary vascular bed, and often, a precipitating stressor. Variants of the classical left ventricular apical ballooning, including mid- or basal left ventricular wall motion abnormalities, are increasingly recognized. Takotsubo cardiomyopathy is not rare, and heightened awareness of this unique cardiomyopathy likely will lead to a higher reported incidence. Diagnosis of takotsubo cardiomyopathy has important implications for clinical management at presentation and afterward. The long-term prognosis is generally favorable; however, a small subset has potentially life-threatening complications during the initial presentation. The pathophysiologic mechanism is unknown, but catecholamine excess likely has a central role.
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Figures in this Article
Takotsubo cardiomyopathy is a novel cardiomyopathy that has been recently recognized as an important consideration in the differential diagnosis of acute coronary syndrome. The presenting features of takotsubo cardiomyopathy are similar to those of myocardial ischemia after acute plaque rupture, but the characteristic distinctions are regional wall motion abnormalities that extend beyond a single coronary vascular bed and the absence of epicardial coronary occlusion. A preceding emotional or physical stressor is common. Although the acute presentation can include life-threatening symptoms and hemodynamic compromise, the long-term prognosis is more benign than that of traditional acute coronary syndrome (1-6). Although this cardiomyopathy classically is described as “apical ballooning syndrome,” emerging data show variant forms that include isolated basal, mid-ventricular, or apical segment involvement. The pathophysiology underlying takotsubo cardiomyopathy is not known, but the most compelling evidence suggests a catecholamine excess.
Takotsubo cardiomyopathy first was described in a case series of 5 Japanese patients in 1991 (7). The name of the syndrome was coined (8) on the basis of similarities between the appearance of the left ventricle in systole (narrow neck and wide base; Figure 1A and Figure 1B) and the shape of a Japanese octopus trap. Other suggested names are “transient ventricular ballooning syndrome,” “left ventricular apical ballooning syndrome,” “stress-induced cardiomyopathy,” “ampulla cardiomyopathy,” and “broken heart syndrome.”
Figure 1
Radiograph of the Left Ventricle
(A) Left ventriculogram in diastole. (B) Left ventriculogram in systole shows preserved contraction of the base of the ventricle and apical ballooning. (C) Right anterior oblique view in diastole. (D) Right anterior oblique view in systole. Note the hypercontractility of the basal and apical segments and ballooning of the mid-ventricular segments. (E) After methamphetamine use in end-diastole. (F) After methamphetamine use in end-systole. Basal segments are akinetic, the papillary level shows normal contractility, and the apex is hypercontractile. (G) Cardiac magnetic resonance image. Hypotension may be due to dynamic outflow tract obstruction caused by hyperkinesis of the basal left ventricle segments and systolic anterior motion of the mitral valve. Four-chamber, steady-state, free-precession image: end-diastole (left) and end-systole (center) show left and right ventricular apical akinesis.(Right) Three-chamber image in systole shows systolic anterior motion of the mitral leaflets (*) with dynamic left ventricular outflow tract obstruction; left ventricular apical mass consistent with thrombus(**). Panels C and D are adapted, with permission from Hurst et al. (31). Panels E and F are adapted, with permission from Reuss et al. (34). Panel G is adapted, with permission from Syed IS, et al. (38). Apical ballooning syndrome or aborted myocardial infarction? Insights from cardiovascular magnetic resonance imaging. Int J Cardiovasc Imaging 2008;24:875–82. Ao = aorta; LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.
Image not available.
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Patient characteristics
Takotsubo cardiomyopathy represents an estimated 1% to 2% of patients who present with an acute coronary syndrome (1), although this estimate may be low because of under-recognition. The age range of patients with takotsubo cardiomyopathy extends from the first to the ninth decade (4), and patients are usually female and most commonly post-menopausal, whereas men account for less than 10% of cases. In the first large Japanese series describing takotsubo cardiomyopathy, 76 patients were women, 12 were men, and the median age was 67 ± 13 years (4). Forty-three percent had a preceding acute medical condition (surgical procedure, cerebrovascular accident, asthma exacerbation), and 27% had a severe emotional or physical stressor. The in-hospital course was complicated by pulmonary edema (22%), cardiogenic shock (15%), ventricular tachycardia or fibrillation (9%), or death (1%). However, 85 of 88 patients were New York Heart Association functional class I at discharge, with a mean left ventricular ejection fraction that improved from 41% ± 11% at admission to 64% ± 10% at discharge. During a mean follow-up of 13 ± 14 months, 2 patients had recurrence and 1 had sudden death. Similar findings have been reported in subsequent case series from around the world, including Europe (9) and the U.S. (1,6).
Presentation
The most common presenting symptom is chest pain (70% to 90%). Less common symptoms such as dyspnea (approximately 20%) and pulmonary edema may occur, but cardiac arrest, cardiogenic shock, and serious ventricular arrhythmias are rare (4,6,10-11). Nonspecific symptoms such as syncope, weakness, cough, and fever also have been reported (12). An emotional, psychological, or physical stressor (or a combination) is typical, although not always present (1). Commonly reported precipitating stressors include being informed of the death of a loved one, social events such as public speaking or a surprise birthday party, and anxiety or pain related to a medical procedure (1-6,9). Other situations that are less common, but still considered possible triggers of takotsubo cardiomyopathy, include cocaine use (13), opiate withdrawal (14), stress testing (15) (with dobutamine [16]), lightning strike (17), ergonovine injection (18), and thyrotoxicosis (19). A chronobiological pattern has also been reported by a multicenter Italian study, with increased frequency of presentation in the summer months and in the morning hours (20). As our experience and knowledge of takotsubo cardiomyopathy has increased, the proposed Mayo diagnostic criteria for the syndrome have evolved. Table 1 shows updated criteria (21).
Table 1Proposed Mayo Clinic Criteria for Diagnosis of Takotsubo Cardiomyopathy
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Takotsubo cardiomyopathy should be considered in the differential diagnosis of acute myocardial infarction for a post-menopausal woman who presents with symptoms of myocardial ischemia after acute emotional or physical stress. For such patients, emergent transfer to a center with primary angioplasty capabilities may lead to the diagnosis of takotsubo cardiomyopathy, thereby avoiding the administration of fibrinolytic therapy and the potential, subsequent complications. However, such transfers should only be considered when transfer and angiography can be performed within recommended door-to-balloon guidelines (22). Furthermore, such a strategy must not be implemented at the expense of withholding life-saving reperfusion therapy from patients with ST-segment elevation myocardial infarction.
Electrocardiography, coronary angiography, and left ventriculography
Electrocardiogram findings in patients with takotsubo cardiomyopathy vary at presentation. ST-segment elevation is present in approximately one-third of patients, with the anterior leads most commonly involved (Figure 2) (23-24). However, deep T-wave inversion and nonspecific ST-T wave changes may also be seen on the electrocardiogram at presentation. Common changes observed with serial electrocardiograms include prolongation of the QT interval and deep, symmetric T-wave inversion (1,3) that may take several weeks or months to resolve (Figure 2) (12,25). Despite the long QT interval, torsades de pointes rarely is reported (26-27). Individuals who present with ST-segment elevation have a higher likelihood of undergoing coronary angiography, which is required for the diagnosis of takotsubo cardiomyopathy. Thus, the high percentage of patients with takotsubo cardiomyopathy and ST-segment elevation in some series may be due to selection bias.
Figure 2
Longitudinal Left Ventricular Strain in Stress Cardiomyopathy
A 73-year-old woman presented with chest pain and normal coronary arteries (as determined by coronary angiography). End-systolic (A) and end-diastolic (B) frames are diagnostic of apical ballooning syndrome. Bull's-eye view of left ventricle shows longitudinal strain on day 1 (C) and day 2 (D). Contracting segments are in red, akinetic and dyskinetic segments are in blue. Note the early appearance of red in basal and mid-ventricular segments of the inferior wall and septum, indicating recovery of myocardial shortening strain on day 2. ANT = anterior; ANT_SEPT = anterior septal; INF = inferior; LAT = lateral; POST = posterior; SEPT = septal.
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The absence of obstructive coronary artery disease or evidence of acute plaque rupture has been proposed as a diagnostic criterion (23). However, there is no reason that an individual with established, stable coronary artery disease would not also be at risk of having takotsubo cardiomyopathy. A recent case series of 97 Japanese patients with takotsubo cardiomyopathy noted a 10% incidence of incidental coronary artery disease (>75% stenosis of a major epicardial coronary artery) (28). Another case series described 7 patients with presentations consistent with takotsubo cardiomyopathy, and at least 1 epicardial coronary artery with 50% or greater stenosis (29). In our experience, severe coronary stenosis is uncommon, and when identified in patients with takotsubo cardiomyopathy, it is rarely in a multivessel distribution (30).
Classically, the apical or mid-ventricular segments (or both) of the left ventricle are akinetic (Figure 3). However, other patterns of left ventricular wall motion abnormality have been reported. Takotsubo cardiomyopathy with mid-ventricular akinesis and apical sparing has been described (Figure 1C and Figure1D) (31-32) and may not be uncommon. A recent report suggested that as many as 40% of patients with takotsubo cardiomyopathy have a mid-ventricular variant (33). Basal akinesis with mid-ventricular and apical sparing (Figure 1E and Figure 1F) also has been reported (34). We have occasionally noted a changing pattern of wall motion abnormality (i.e., from mid-ventricular to apical variant) in the same patient, as have other investigators (35).
Figure 3
Short-Axis Images From a Patient With Takotsubo Cardiomyopathy at 2 Days and 6 Weeks After Presentation With Stress-Induced Cardiomyopathy
(A) Myocardial blood flow (13N-ammonia). (B)11C hydroxyephedrine positron emission tomography shows preserved perfusion but transiently abnormal sympathetic activity. Adapted with permission from Prasad et al. (54).
Image not available.
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Cardiac biomarkers
Biomarkers of cardiac myonecrosis generally are elevated at presentation (1-6). This is almost always the case for cardiac troponin. Usually, the biomarker levels peak within 24 h after presentation, but the levels are markedly lower than would be anticipated on the basis of the extent of wall motion abnormalities and electrocardiogram findings. The absence of clinically significant myocardial necrosis has been confirmed in several case series in which cardiac magnetic resonance examination has shown the absence of gadolinium hyperenhancement (3).
Acute care
Initial clinical management of patients with takotsubo cardiomyopathy is similar to that of patients with acute coronary syndrome. The diagnosis must be confirmed with coronary artery and left ventricular imaging. A high index of suspicion is required because early recognition can affect management; this is particularly true when fibrinolytic therapy is being considered for patients presenting with ST-segment elevation.
Hypotension occurs frequently, and it is important to identify the cause of hypotension to determine appropriate management. Acute pump failure may require intravenous pressor support, but given the evidence of catecholamine excess in the origin of this syndrome, mechanical support with an intra-aortic balloon pump may be preferred. In addition, hypotension may be due to dynamic outflow tract obstruction caused by hyperkinesis of the basal left ventricular segments and systolic anterior motion of the mitral valve (Figure 1G) (1,36-38). In this situation, intravenous inotropic agents would be contraindicated; to reduce outflow obstruction, short-acting β-blockers (39) and intravenous fluids could be used cautiously to decrease contractility and increase cavity size, respectively. Peripheral vasoconstrictors such as phenylephrine may be considered if β-blockers and fluid administration are contraindicated or ineffective.
Arrhythmias such as atrial fibrillation, ventricular tachycardia, and ventricular fibrillation are not rare in takotsubo cardiomyopathy and are likely attributable to high levels of circulating catecholamines. Mechanical complications such as left ventricular rupture are rare (40-42).
Right ventricular involvement in takotsubo cardiomyopathy has been reported (10,43-45), and right ventricle involvement at presentation may be an important predictor of adverse outcome. In a study of 30 patients with takotsubo cardiomyopathy (10), right ventricular dysfunction (involving apical or mid-ventricular segments [or both], similar to the left ventricle) was highly associated with longer hospitalization, severe congestive heart failure, the use of intra-aortic balloon pumps, or performance of cardiopulmonary resuscitation.
Subacute and long-term care
In-hospital death is rare (4,10); if it occurs, it may be attributable to the underlying stressor rather than to the cardiomyopathy itself (6,46). Only a relatively small number of cases of takotsubo cardiomyopathy–related death have been reported in the literature to date. The incidence of sudden death caused by takotsubo cardiomyopathy before evaluation in a hospital or emergency department is unknown, of course, but it has been described (47).
Complete recovery of left ventricular systolic function is necessary to confirm the diagnosis of takotsubo cardiomyopathy. The recovery time varies and can be as short as several days or as long as several weeks (6). Our practice uses an empirical approach, treating individuals with takotsubo cardiomyopathy as those with other causes of cardiomyopathy (with angiotensin-converting enzyme inhibitors and β-blockers), at least until left ventricular systolic function recovers. Left ventricular thrombus (6,48) and systemic thromboembolism have been reported. Anticoagulation therapy, at least until recovery of the wall motion abnormality, should be considered for those with clinically significant apical hypokinesis or akinesis that persists 2 to 3 days after presentation. Systemic thromboembolism has been reported in takotsubo cardiomyopathy (49).
Recurrence occurs in approximately 10% of patients (1,6). Comprehensive follow-up of 100 patients for a mean of 4.4 ± 4.6 years at the Mayo Clinic showed a recurrence rate of 11.4% (5). In that study, the mortality rate was 16%, which was similar to an age- and sex-matched local population.
Long-term β-blockade and combined α- and β-blockade are attractive therapies given the putative association between takotsubo cardiomyopathy and a catecholamine surge. Such strategies have been advocated if patients have no contraindications, but few trial data show efficacy of these strategies (32,50).
The pathophysiology of takotsubo cardiomyopathy is not established but is likely multifactorial, involving the vascular, endocrine, and central nervous systems (51). The instigating factor for most patients is an emotional or physical stressor that commonly is associated with a “fight or flight” hypersympathetic response. Most evidence suggests a major contribution from catecholamine excess and exaggerated stimulation of the sympathetic nervous system. Abraham et al. (52) described 9 cases of takotsubo cardiomyopathy precipitated by epinephrine or dobutamine infusion. All morphologic variants of takotsubo cardiomyopathy (apical, mid-, and basal) were observed, suggesting a common causality of excessive sympathetic stimulation. Wittstein et al. (3) determined that norepinephrine, epinephrine, and dopamine levels were approximately 2 to 3 times higher in patients with takotsubo cardiomyopathy than in patients with clinically significant left ventricular dysfunction due to acute myocardial infarction. Biopsy findings from the same study showed mononuclear cell infiltrate and contraction band necrosis, which are consistent with catecholamine-induced myocardial injury. In a study of 8 patients with takotsubo cardiomyopathy (53), myocardial scintigraphy with 123I-meta-iodobenzylguanidine showed evidence of cardiac sympathetic hyperactivity, which improved after 3 months. Transient abnormal cardiac sympathetic activity was also shown by 11C-hydroxyephedrine imaging with positron emission tomography (Figure 3) (54). An animal model of takotsubo cardiomyopathy with immobilized rats showed that the abnormal findings typically observed in electrocardiograms and left ventriculograms were mitigated by α- and β-blockade and partially attenuated by estrogen (55-56). More recently, increased local release of catecholamines from the hearts of patients with takotsubo cardiomyopathy has been documented (57).
It is difficult to ignore the similar cardiac manifestations of takotsubo cardiomyopathy and other disease entities with heightened catecholamine and sympathetic discharge such as subarachnoid hemorrhage (58-59) and pheochromocytoma (60-61). Animal models of subarachnoid hemorrhage have shown a correlation between catecholamine levels and the extent of myocardial damage (62). Lyon et al. (63) recently proposed that a switch in intracellular signal trafficking protects cells against proapoptotic effects of catecholamines but is negatively inotropic when the β1-adrenoceptor is intensely activated, thereby causing myocardial stunning when high levels of epinephrine are circulating. A catecholamine-induced disorder in glucose metabolism has been suggested on the basis of decreased left ventricular apical 18F-fluorodeoxyglucose uptake on positron emission tomography of 15 patients with the apical variant of takotsubo cardiomyopathy (64).
Some investigators have reported coronary microvascular dysfunction in patients with takotsubo cardiomyopathy (1,65-69), which may either cause or be caused by the sympathetic response. Mayo Clinic investigators evaluated coronary angiograms of 42 consecutive patients with takotsubo cardiomyopathy and found abnormal myocardial perfusion in 69%, as determined by Thrombolysis In Myocardial Infarction myocardial perfusion grade (70).
Myocarditis as a cause of takotsubo cardiomyopathy is not well supported by the data. Viral titers do not rise after the initial event (71), and biopsy findings are not suggestive of myocarditis (71-72). Cardiac magnetic resonance imaging of a limited number of patients has shown no evidence of myocarditis or infarction (3,6).
Multivessel epicardial coronary artery spasm as a cause of takotsubo cardiomyopathy is not strongly supported in the literature, despite isolated reports (72-73). ST segments commonly remain elevated in patients with takotsubo cardiomyopathy, even when coronary angiography shows no spasm. Spontaneous or invoked coronary artery spasm is an infrequent observation (12).
The reason why the cardiomyopathy predominately occurs in post-menopausal women is also unexplained. A unifying mechanism of disease will need to explain why women, most commonly post-menopausal women, are predisposed to takotsubo cardiomyopathy development after heightened sympathetic discharge. A deficiency in estrogen activity may have a role, as suggested by the higher incidence in post-menopausal women and the evidence of estrogen supplementation attenuating takotsubo cardiomyopathy in an animal model (56). Endothelial dysfunction may be a mechanism, given the influence of sex hormones on endothelial function (74). Interestingly, a study of 72 individuals (47% women) with subarachnoid hemorrhage reported that left ventricular wall motion abnormality occurred only in women (59). Cardiac syndrome X also is most common in post-menopausal women, and endothelial dysfunction is thought to affect the underlying pathophysiology (75-76). A genetic component is suggested by the observation of takotsubo cardiomyopathy occurrence in 2 sisters and in a mother–daughter pair (77-78).
There is no evidence documenting different pathophysiologic mechanisms in the various morphologic variants of takotsubo cardiomyopathy. A common mechanism is suggested by the finding of 2 morphologic variants in the same individual (35) and the finding of multiple morphologic variants with epinephrine or dobutamine infusion (52).
Takotsubo cardiomyopathy is important in the differential diagnosis of acute coronary syndrome. It is characterized by normal (or near-normal) coronary arteries, regional wall motion abnormalities that extend beyond a single coronary vascular bed, and often, a precipitating stressor. Variants of the classical left ventricular apical ballooning, including mid- or basal left ventricular wall motion abnormalities, are increasingly recognized. Takotsubo cardiomyopathy is not rare, and heightened awareness of this unique cardiomyopathy likely will lead to a higher reported incidence. Diagnosis of takotsubo cardiomyopathy has important implications for clinical management at presentation and afterward. The long-term prognosis is generally favorable; however, a small subset has potentially life-threatening complications during the initial presentation. The pathophysiologic mechanism is unknown, but catecholamine excess likely has a central role.
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