Stress CardiomyopathyStress Cardiomyopathy

Presented by Brittney Howard, PA-S

Advised by Bill Grimes, Dmin, PA-C

Presented by Brittney Howard, PA-S

Advised by Bill Grimes, Dmin, PA-C

Me and Granny

What is Stress Cardiomyopathy?What is Stress Cardiomyopathy?

• Cardiac syndrome

• Reversible

• Left ventricular apical ballooning

• Mimics myocardial infarction

• Cardiac syndrome

• Reversible

• Left ventricular apical ballooning

• Mimics myocardial infarction

• Signs & Symptoms

Onset following extreme stress

Chest pain Dyspnea ST-segment elevation

T wave changes Elevated cardiac biomarkers

• Signs & Symptoms

Onset following extreme stress

Chest pain Dyspnea ST-segment elevation

T wave changes Elevated cardiac biomarkers

BackgroundBackground

• First recognized in Japan during 1990s

• Originally known as takotsubo-like left ventricular dysfunction due to apical response during syndrome

• Colloquially known as Broken Heart Syndrome

• First recognized in Japan during 1990s

• Originally known as takotsubo-like left ventricular dysfunction due to apical response during syndrome

• Colloquially known as Broken Heart Syndrome

Takotsubo-LikeLeft Ventricular

Dysfunction

Takotsubo-LikeLeft Ventricular

Dysfunction

www.grangeblanche.hautetfort.com

takotsubo fishing pot

left ventricular apical ballooning

Why is Stress Cardiomyopathy Important?

Why is Stress Cardiomyopathy Important?

• Mimics myocardial infarction

• Differentiate from grief response

• Educate patients on favorable prognosis

• Protect patients from exposure to unnecessary treatments

• Mimics myocardial infarction

• Differentiate from grief response

• Educate patients on favorable prognosis

• Protect patients from exposure to unnecessary treatments

Stress Cardiomyopathy vs. Myocardial Infarction

Stress Cardiomyopathy vs. Myocardial Infarction

Stress Cardiomyopathy

Normal coronary arteries, no blockage

Results in stunning of cardiac muscle

Reversible condition

Stress Cardiomyopathy

Normal coronary arteries, no blockage

Results in stunning of cardiac muscle

Reversible condition

Myocardial Infarction

Caused by blockages in coronary arteries

Results in death of cardiac muscle

Permanent, irreversible damage

Myocardial Infarction

Caused by blockages in coronary arteries

Results in death of cardiac muscle

Permanent, irreversible damage

Possible Causes of Stress Cardiomyopathy?

Possible Causes of Stress Cardiomyopathy?

• Catecholamine excess?

• Lack of estrogen?

• Or both?

• Catecholamine excess?

• Lack of estrogen?

• Or both?

Diagnostic Criteria Proposed by

The Mayo Clinic

Diagnostic Criteria Proposed by

The Mayo Clinic1. Transient loss or decreased movement of

the left ventricular apical and mid-ventricular segments with regional wall-motion abnormalities extending beyond a single region supplied by a coronary vessel

2. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture

3. New EKG abnormalities - either ST-segment elevation or T-wave inversion

4. Absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, and hypertrophic cardiomyopathy

1. Transient loss or decreased movement of the left ventricular apical and mid-ventricular segments with regional wall-motion abnormalities extending beyond a single region supplied by a coronary vessel

2. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture

3. New EKG abnormalities - either ST-segment elevation or T-wave inversion

4. Absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, and hypertrophic cardiomyopathy

Decreased Left Ventricular Function

Decreased Left Ventricular Function

• Ejection fraction in healthy individual• >0.55

• Average ejection fraction at presentation• 0.39 - 0.49

• Average ejection fraction at follow-up• 0.60-0.79

• Ejection fraction in healthy individual• >0.55

• Average ejection fraction at presentation• 0.39 - 0.49

• Average ejection fraction at follow-up• 0.60-0.79

Treatment ModalitiesTreatment Modalities• Alpha Blockers

• Help small blood vessels remain open

• Beta Blockers• Reduce catecholamine effects

• Short-term Anticoagulants• Prevent thrombus formation until function improves

• Supportive Treatment• ACE inhibitor, aspirin, IV diuretics

• Contraindications• Synthetic catecholamines• Thrombolysis in ST-segment elevation• ACE inhibitors in increased pressure gradients

• Alpha Blockers• Help small blood vessels remain open

• Beta Blockers• Reduce catecholamine effects

• Short-term Anticoagulants• Prevent thrombus formation until function improves

• Supportive Treatment• ACE inhibitor, aspirin, IV diuretics

• Contraindications• Synthetic catecholamines• Thrombolysis in ST-segment elevation• ACE inhibitors in increased pressure gradients

The Future of Stress Cardiomyopathy

The Future of Stress Cardiomyopathy

» Importance of ESTROGEN in stress response

» Identifiable DIAGNOSTIC measures

» RECOGNITION in medical community

» More EDUCATION about differences of cardiac symptoms in women vs. men

» Importance of ESTROGEN in stress response

» Identifiable DIAGNOSTIC measures

» RECOGNITION in medical community

» More EDUCATION about differences of cardiac symptoms in women vs. men

The Take Home MessageThe Take Home Message

•Primarily affects postmenopausal females

•Often precipitated by severe stress

•Severe reversible left ventricular dysfunction

•Mimics myocardial infarction• Increased catecholamines and lack of estrogen thought to play a role

• Alpha and beta blockers the best treatment

•Primarily affects postmenopausal females

•Often precipitated by severe stress

•Severe reversible left ventricular dysfunction

•Mimics myocardial infarction• Increased catecholamines and lack of estrogen thought to play a role

• Alpha and beta blockers the best treatment

REFERENCESREFERENCESBybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004; 141(11):858-65.

Grawe H, Katoh M, Kuhl HP. Stress cardiomyopathy mimicking acute coronary syndrome: case presentation and review of the literature. Clinical Research in Cardiology. 2006; 95(3):179-185.

John Hopkins Medicine. Frequently asked questions about broken heart syndrome. Available at: http://www.hopkinsmedicine.org/asc/faqs.html. Accessed February 10, 2007. Korlakunta HL, Thambidorai SK, Denney SD, Khan IA. Transient left ventricular apical ballooning: a novel heart syndrome. Int J Cardiol. 2005; 102(2):351-3.

Matsuoka K, Okubo S, Fujii E, Uchida F, Kasai A, Aoki T, et al. Evaluation of the arrhythmogenecity of stress-induced “Takotsubo cardiomyopathy” from the time course of the 12-lead surface electrocardiogram. Am J Cardiol. 2003; 92(2):230-3. Reichman, Judith. Estrogen and your heart: Does it help or hurt? November 2005. Available at: http://www.msnbc.msn.com/id/10034785/. Accessed February 12, 2007.

Soni A, LeLorier P. Sudden death in nondilated cardiomyopathies: pathophysiology and prevention. Curr Heart Fail Rep. 2005; 2(3):118-23.

Ueyama T1. Emotional stress-induced Takotsubo cardiomyopathy: animal model and molecular mechanism. Ann N Y Acad Sci. 2004; 1018:437-44.

Ueyama T2, Senba E, Kasamatsu K, Hano T, Yamamoto K, Nishio I, et al. Molecular mechanism of emotional stress-induced and catecholamine-induced heart attack. J Cardiovasc Pharmacol. 2003; 41:S115-8.

Questions?Questions?