3. INTRODUCTION
Broken heart syndrome is a group of symptoms similar to those of a heart attack,
occurring in response to a physical or emotional stress.
Most people affected by broken heart syndrome think they are having a heart
attack because symptoms, such as shortness of breath and chest pain, are similar
in both conditions. However, those with broken heart syndrome do not have
blocked coronary arteries, and usually make a fast and full recovery.
Broken heart syndrome is also called Takotusubo cardiomyopathy and stress-
induced cardiomyopathy, meaning that stress has caused dysfunction or failure of
the heart muscle.
4. How common is broken heart syndrome?
According to the National Heart, Lung and Blood
Institute an estimated 1.2 million people in the
United States in 2007 would have a myocardial
infarction (an interruption of blood supply to the
heart).
About 1 percent of this estimate, or 12,000 people
would have experienced broken heart syndrome.
5. What causes broken heart syndrome?
The cause of broken heart syndrome is not fully understood. In most cases,
symptoms are brought on by emotional or physical stress such as the death
of a loved one, a divorce, the breakup of a romantic relationship, an asthma
attack, an exhausting physical event, or even happy occurrences such as a
surprise, a reunion, or being a big lottery winner.
A person’s reaction to such events causes a release of stress hormones
(catechol amines) that temporarily reduce the effectiveness of the heart’s
pumping action, or cause it to contract too forcefully or wildly instead of in
a steady pattern.
6. In rare cases, certain drugs may trigger broken heart syndrome, because
they may cause hormones to surge in your body. Such drugs include:
Epinephrine, which treats severe allergic reactions
Duloxetine (Cymbalta), which can treat nerve problems among people
with diabetes and is also an antidepressant
Venlafaxine (Effexor XR), an antidepressant
Levothyroxine (Synthroid, Levoxyl), which can treat thyroid problems
Methamphetamine
Cocaine
7.
8. Diagnostics
Diagnostic tests include:
Physical exam and a review of the patient’s medical history.
An EKG (electrocardiogram) to measure the heart’s electrical activity.
Coronary angiography (uses dye and a type of X-ray to get a picture inside
the heart’s arteries).
Echocardiography (uses sound waves to create moving images of the
heart’s pumping action).
9. Chest X-ray (analyzes the structure of the heart, lungs and
blood vessels).
Cardiac MRI (magnetic resonance imaging) (produces both still
and moving pictures of the heart).
Ventriculogram (uses a dye injected into the heart’s left
ventricle to take X-rays that will show the size and pumping
efficiency of this chamber in the heart).
10. Based on test results, a number of clues help differentiate broken
heart syndrome from a heart attack:
Symptoms of broken heart syndrome appear suddenly, following a
stressful event.
An EKG will show the heart’s electrical activity is not normal but is
not the same as the changes seen during a heart attack.
Blood tests show no damage to the heart.
The arteries of the heart are not blocked.
11. The left ventricle (lower left chamber of the heart) shows
enlargement and unusual contractions that are not present in a
heart attack.
Cardiac biomarkers (substances released into the blood when
the heart is damaged or stressed) are higher than normal, but
are not as high as when having a heart attack.
12. The most common acute ECG findings of Takotusubo
cardiomyopathy are ST segment elevation in the precordial leads
and T-wave inversion in most leads.
Unlike in acute myocardial infarction, ECG changes in Takotusubo
cardiomyopathy are not limited to one coronary vascular
territory.
16. VENTRICULOGRAM OF CONTRACTILE PHASE OF NORMAL LEFT VENTRICLE
(LEFT) CONTRASTED AGAINST A TAKOTSUBO CARDIOMYOPATHY
VENTRICULOGRAM SHOWING APICAL BALLOONING OF THE LEFT
VENTRICLE (RIGHT)
17. Complications of Takotusubo
cardiomyopathy include:
left heart failure with and without pulmonary oedema
cardiogenic shock
dynamic intraventricular obstruction with left ventricular intracavitary pressure gradient
generation
mitral regurgitation resulting from chordal tethering and systolic anterior motion of the mitral
valve apparatus
ventricular arrhythmias
left ventricular mural thrombus formation
left ventricular free-wall rupture
death.
18. TREATment
Broken heart syndrome is mostly treatable.
The doctor will prescribe medicines used to treat things like heart failure. For
example:
ACE inhibitors: benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec),
fosinopril (Monopril)
Angiotensin II receptor blockers (ARBs): Azilsartan (Edarbi) Candesartan
(Atacand) Eprosartan. Irbesartan (Avapro)
Beta-blockers:Acebutolol (Sectral), Atenolol (Tenormin), Bisoprolol (Zebeta),
Metoprolol (Lopressor, Toprol XL)
19. Diuretics: Chlorthalidone (Hygroton), Chlorothiazide (Diuril)
Anti-anxiety medications: benzodiazepines; among them are
alprazolam (Xanax), clonazepam (Klonopin), chlordiazepoxide
(Librium), diazepam (Valium), and lorazepam (Ativan).
Treatments such as angioplasty, stent placement, and surgery are
used to treat a heart attack but are NOT used in cases of broken heart
syndrome because they address the problem of blocked arteries,
which is not found in broken heart syndrome.
20. Key points
Takotusubo cardiomyopathy should be suspected in any postmenopausal
woman presenting with chest pain and dyspnea following intense
emotional or physical stress.
ECG changes are often dramatic and not in proportion with the rise in
troponin levels.
Acute coronary syndrome is an important differential diagnosis and
suspected cases should be referred to hospital.
Diagnosis can be confirmed by findings of normal coronary arteries and
apical ballooning of the left ventricle on coronary angiography.
21. Heart failure with or without pulmonary edema is the most
common clinical complication of takotsubo cardiomyopathy.
The prognosis of takotsubo cardiomyopathy is usually good,
with a mortality rate of 0–8%. Most patients that survive the
initial episode will regain normal ventricular function with 1–4
weeks and have a good long term prognosis.
22. Without the use of coronary angiography it can be difficult to objectively
distinguish takotsubo cardiomyopathy from acute coronary syndrome.
When the diagnosis is in doubt, takotsubo cardiomyopathy should be
treated as acute coronary syndrome until proven otherwise. Most patients
should be hospitalized for confirmation of the diagnosis and subsequent
management.
Treatment of takotsubo cardiomyopathy is usually supportive. Despite the
fact that a ß-blockade is widely considered to have an important role in
treatment, there is a lack of large randomized controlled trials to support
its routine use.
23. In haemodynamically stable patients, a ß-blocker should be considered and
diuretics given as necessary for volume overload. ß-blockers may block the effects
of the catecholamine excess, which is a potential mechanism of takotsubo
cardiomyopathy. Moreover, ß-blockers have an essential role in reducing left
ventricular outflow tract obstruction by decreasing basal segment hyper
contractility.
Patients without a left ventricular outflow tract gradient should be prescribed an
angiotensin converting enzyme inhibitor (ACEI) or an angiotensin receptor
antagonist to prevent cardiac remodeling. In a rodent model, takotsubo
cardiomyopathy could be prevented with an α-blockade or ß-blockade.
24. The prognosis of takotsubo cardiomyopathy is generally good. Patients
that survive the acute episode typically recover normal ventricular function
within 1–4 weeks. Reported inpatient mortality rates for takotsubo
cardiomyopathy range from 0–8%. In a study with a mean follow up of 4.4–
4.6 years, there was no difference in survival for patients with an acute
episode of takotsubo cardiomyopathy compared to an age and gender
matched population.9
Heart failure with or without pulmonary edema is the most common clinical
complication and was reported in 38 of 215 patients (17.7%).
