Stress Cardiomyopathy: A Syndrome of Catecholamine-Mediated Myocardial Stunning?

Wittstein, Ilan S.

doi:10.1007/s10571-012-9804-8

Cited by 155 publications

(114 citation statements)

References 69 publications

(90 reference statements)

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“…LV myocardial dysfunction of TTC characterized by symmetric WMAs including the mid-ventricular segments of the anterior, inferior, and lateral walls (segment 7-12 based on the ASE guideline) over the apical segment (segment 13-17 based on the ASE guideline) should be considered peculiar to TTC and included in the differential diagnosis of TTC and acute coronary syndromes (31). These findings support the hypothesis of diffuse ventricular dysfunction secondary to myocardial stunning underlying the pathogenesis of TTC (32). Some earlier studies reported that advanced echocardiographic techniques, such as tissue Doppler imaging and speckle tracking imaging, could provide new insights into LV wall motion and systolic function assessment (33)(34)(35)(36).…”

Section: Wall Motion and Systolic Functionmentioning

confidence: 55%

Role of echocardiography for takotsubo cardiomyopathy: clinical and prognostic implications

Izumo¹,

Akashi²

2018

Cardiovasc. Diagn. Ther.

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Takotsubo cardiomyopathy (TTC) is newly-described secondary cardiomyopathy characterized by transient left ventricular (LV) dysfunction, which is increasingly recognized in the field of cardiology.TTC occurs in approximately 2% of the patients with acute coronary syndrome. Its onset is rare; however, its specific features play a crucial role in diagnosing the chest pain in clinical practice. TTC has generally favorable outcome with rapid recovery of LV function; however, an increasing evidence suggests that it should be regarded as a more serious acute cardiac disorder with a variety of complications. Owing to its widespread availability, even in emergency settings, transthoracic echocardiography plays a key role in the diagnostic assessment of TTC and contributes to an increased number of disease detection and incidence reports in contemporary clinical practice. This review focuses on the role of echocardiography in understanding the clinical prognostic implications in patients with TTC.

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Section: Wall Motion and Systolic Functionmentioning

confidence: 55%

Role of echocardiography for takotsubo cardiomyopathy: clinical and prognostic implications

Izumo¹,

Akashi²

2018

Cardiovasc. Diagn. Ther.

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“…Serum catecholamine concentration may be up to two to three times higher in patients with takotsubo cardiomyopathy compared to patients with myocardial infarction [17,20]. We postulate that as our patient was withdrawing from clonidine, he most likely had high serum catecholamine concentrations which precipitated the takotsubo cardiomyopathy variant.…”

Section: Reports Of Clonidine Withdrawalmentioning

confidence: 78%

Intrathecal Clonidine Pump Failure Causing Acute Withdrawal Syndrome With ‘Stress-Induced’ Cardiomyopathy

2015

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Clonidine is a central alpha(2)-agonist antihypertensive used widely for opioid/alcohol withdrawal, attention deficit hyperactivity disorder and chronic pain management. We describe a case of clonidine withdrawal causing lifethreatening hypertensive crisis and stress-induced cardiomyopathy. A 47-year-old man with chronic back pain, treated with clonidine for many years via intrathecal pump (550 mcg/24 h), presented following a collapse and complaining of sudden worsening of back pain, severe headache, diaphoresis, nausea and vomiting. A few hours prior to presentation, his subcutaneous pump malfunctioned. On presentation, vital signs included pulse 100 bpm, BP 176/103 mmHg, temperature 37.8°C and O 2 saturation 100 % (room air). Acute clonidine withdrawal with hypertensive crisis was suspected. Intravenous clonidine loading dose and a 50 mcg/h infusion were commenced. Five hours later, severe chest pain, dyspnoea, tachycardia, hypoxia, with BP 180/120 mmHg and pulmonary edema ensued. ECG showed sinus tachycardia with no ST elevation. Repeated intravenous clonidine doses were given (25 mcg every 5-10 min), with ongoing clonidine infusion to control blood pressure. Glyceryl trinitrate infusion, positive pressure ventilation and intravenous benzodiazepines were added. Bedside echocardiogram showed stress-induced cardiomyopathy pattern. Serum troponin-I was markedly elevated. His coronary angiography showed minor irregularities in the major vessels. Over the next 3 days in the ICU, drug infusions were weaned. Discharge was 12 days later on oral clonidine, metoprolol, perindopril, aspirin and oxycodone-SR. Two months later, his echocardiogram was normal. The intrathecal pump was removed. We report a case of stressinduced cardiomyopathy resulting from the sudden cessation of long-term intrathecal clonidine. This was managed by reinstitution of clonidine and targeted organ-specific therapies.

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“…The time that myocardium is at risk of being stunned is when it has a low reserve flow [4]. Acute emotional or physical stress can trigger a catecholamine-mediated myocardial stunning [5]. Extremely high plasma catecholamine levels and their metabolites elevation can cause stress cardiomyopathy resulting in stunned myocardium with transient ischemic change [6].…”

Section: Discussionmentioning

confidence: 99%

Stunned Myocardium due to Decompensation from Hypovolemic Shock in a Pregnant Woman with Uterine Atony Following Cesarean Section

Hs¹,

Hans²

2016

J Clin Exp Cardiolog

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Transient post ischemic left ventricular dysfunction has been called stunned myocardium. The stunned myocardium can lead cardiac problems such as arrhythmias, left ventricular dysfunction, and a myocardial infarction. Stunned myocardium is a reversible condition. In this case, a 25 year old female patient with a history of mild intermittent asthma became hypovolemic and got into shock after developing uterine atony following a cesarean section. The patient did not respond to rapid volume replacement therapy. Subsequently, the patient had acute pulmonary edema, hypotension, and tachycardia developed. Echocardiogram was done showing severe left ventricular dysfunction (ejection fraction (EF), 25-35%) with left inferobasal wall hypokinesis and no right ventricular dysfunction or severe tricuspid regurgitation or right ventricular hypertrophy. Chest x-ray showed newly diagnosed cardiomegaly and bilateral pulmonary congestion. Initial troponin I was elevated, however, the level of troponin I remained stable with the same baseline value. Patient was at high risk for pulmonary embolism (PE) based on risk assessment, therefore, anticoagulation was started. Chest CT for pulmonary embolism was performed, and the result was negative. Two days after, repeated echocardiogram showed improved EF was 35%. Patient was discharged with beta -blocker to reduce oxygen demand of myocardium. This case supports hypovolemic shock not responding to volume replacement therapy can cause myocardium damage which is able to be diagnosed with stunned myocardium. Keywords: Hypovolemic shock; Stunned myocardium; Pulmonary embolism Case ReportA 25 year old Hispanic female with history mild intermittent asthma was admitted for normal vaginal delivery. Obstetrician converted it to cesarean section due to severe bleeding secondary to uterine atony and inversion. Patient was already intubated for the cesarean section. Heart rate were 150/ min , O 2 saturation was 81% on FIO 2 100% , and systolic blood pressure was checked at 84 mmHg and diastolic was 40 mmHg, therefore, 2 units of packed red blood cell and 4 liters of Ringer lactate were given for hypovolemic shock secondary to bleeding. Blood pressure was not returned to normal range even if transfusion and intravenous fluid were given. Endotracheal tube position was checked by laryngoscopy, glydescope and fiber optic bronchoscopy. After completion of cesarean section in the operation room, patient was transferred to surgical intensive care unit (SICU) for post-surgical care. Patient was still tachycardic and hypotensive, therefore, patient was transferred to medical intensive care unit (MICU) for acute respiratory distress syndrome (ARDS) and presumed diagnosis of PE, which might be developed during cesarean section. Chest x-ray at that time showed bilateral pulmonary edema with cardiomegaly. Electrocardiogram (EKG) showed sinus tachycardia without specific ischemic changes (Figure 2). Initial troponin I was elevated up to 0.21, however, it was post-operative, moreover, the peak of troponin...

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Stress Cardiomyopathy: A Syndrome of Catecholamine-Mediated Myocardial Stunning?

Cited by 155 publications

References 69 publications

Role of echocardiography for takotsubo cardiomyopathy: clinical and prognostic implications

Role of echocardiography for takotsubo cardiomyopathy: clinical and prognostic implications

Intrathecal Clonidine Pump Failure Causing Acute Withdrawal Syndrome With ‘Stress-Induced’ Cardiomyopathy

Stunned Myocardium due to Decompensation from Hypovolemic Shock in a Pregnant Woman with Uterine Atony Following Cesarean Section

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