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PERM STATE MEDICAL

UNIVERSITY
BROKEN HEART
SYNDROME:
DIAGNOSTICS
JOISY ALOOR
5TH YEAR
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.
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.
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.
 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
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).
 Chest X-ray (analyzes the structure of the heart, lungs and blood
vessels).
 CardiacMRI (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).
 Basedon 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.
 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.
 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.
ECG CHANGES IN
TAKOTUSUBO
CARDIOMYOPATHY (TTC)
ECG SHOWING DEEP T-WAVE INVERSION IN ALL LEADS
ANGIOGRAM SHOWING NORMAL CORONARY ARTERIES
VENTRICULOGRAM OF CONTRACTILE PHASE OF NORMAL LEFT
VENTRICLE (LEFT) CONTRASTED AGAINST A TAKOTSUBO
CARDIOMYOPATHY VENTRICULOGRAM SHOWING APICAL
BALLOONING OF THE LEFT VENTRICLE (RIGHT)
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.
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)
 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.
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.
 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.
 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.
 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.
 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%).
DIFFERNTIAL DIAGNOSIS

 Acute Coronary Syndrome


 Angina Pectoris
 Aortic Dissection
 Boerhaave Syndrome
 Cardiac Tamponade
 Cardiogenic Shock
 Cocaine-Related Cardiomyopathy
 Coronary Artery Vasospasm
 Dilated Cardiomyopathy
 Hypertrophic Cardiomyopathy

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