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Stress (Takotsubo) Cardiomyopathy -- A Novel Pathophysiological Hypothesis to Explain Catecholamine-induced Acute Myocardial Stunning : The Triggering Event


The Triggering Event

The common etiologic feature of stress cardiomyopathy is sudden physical or emotional stress as the precipitant. Two reports demonstrated an increased incidence of the syndrome after earthquakes in Japan.[7,8] The condition has also been reported in patients undergoing noncardiac surgery[9,10] and in patients with noncardiac medical emergencies.[11–15] If measured early after the triggering event, a substantial increase in plasma catecholamine levels is reported in many patients following stress cardiomyopathy. Serum catecholamine levels are not usually measured in routine clinical practice, but, when measured, the catecholamine levels seen in this syndrome are significantly higher than those found in conditions such as acute myocardial infarction or cardiac failure and up to 34 times higher than normal resting values.[16,17] This issue is still a subject of debate, however, because the plasma half-life of epinephrine is approximately 3 min,[18] and most patients present to emergency departments at least 30 min (>10 half-lives), and in some cases several hours, after symptom onset. The peak epinephrine level to which the myocardium is exposed at the point of stress will, therefore, be several logfold higher than any measurement of serum epinephrine level taken on admission to an emergency department, which could have returned to basal levels after the delay in presentation.

The surge in catecholamine levels results in cardiac dysfunction similar to that often classified as 'stunning with normal coronary blood flow'. This phenomenon is a relatively common finding in patients with acute intracranial injury, particularly acute subarachnoid hemorrhage, who also have surges in sympathetic activity in response to acute hemorrhage.[19] Approximately 10% of patients with acute intracranial injury have acute ischemic electrocardiographic changes, raised levels of cardiac enzymes, and acute, but reversible, left ventricular impairment, all in the presence of normal coronary arteries.[20–22] The pathology of the myocardium in such patients is similar to that sometimes seen in individuals with stress cardiomyopathy, with leukocyte infiltration and contraction-band necrosis.[23] The acute clinical instability during the early phase of a major neurological event means that optimum myocardial assessment (e.g. angiography, cardiac MRI) is rarely performed until after recovery. The same clinical picture is seen in patients with surges in catecholamine levels secondary to pheochromocytomas.[24,25]

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