Broken Heart Syndrome, Neurogenic Stunned Myocardium and Stroke

Abstract

The diagnosis of stress cardiomyopathy is often made during coronary angiography. At this point hemodynamic parameters should be assessed; a right heart catheterization with measurement of cardiac output by Fick and thermodilution methods is helpful. Patients with acute neurologic pathology who develop left ventricular dysfunction (neurogenic stunned myocardium) may not be candidates for coronary angiography and in such cases real-time myocardial contrast echocardiography or nuclear perfusion scan can be used to exclude obstructive coronary disease. Hypotension and shock can be due to low output state or left ventricular outflow tract obstruction. Low output state can be managed with diuretics and vasopressor support. Refractory shock and/or severe mitral regurgitation may require an intra-aortic balloon pump for temporary support. In patients with intraventricular gradient intravenous beta-blockers have been used safely. Hemodynamically unstable patients should be managed in a critical care unit and stable patients should be monitored on a telemetry unit as arrhythmias may occur. An echocardiogram should be performed to look for intraventricular gradient, mitral regurgitation, or left ventricular thrombus. If left ventricular thrombus is seen or suspected anticoagulation with warfarin or low molecular weight heparin is generally advised until recovery of myocardial function and resolution of thrombus occurs. In patients with subarachnoid hemorrhage the use of vasopressors to reduce cerebral vasospasm may worsen left ventricular outflow tract gradient. In hemodynamically stable patients, a beta-blocker or combined alpha/beta blocker should be initiated. Myocardial function generally recovers within days to weeks with supportive treatment in most patients. The use of a standard heart failure regimen including an angiotensin-converting enzyme inhibitor or aldosterone receptor antagonist, beta-blocker titrated to maximal dose, diuretics, and aspirin is common until complete recovery of myocardial function occurs. Chronic therapy with a beta-blocker may be advisable. The underlying diagnosis that precipitated stress cardiomyopathy such as critical illness, neurologic injury, or medication exposure should be identified and treated.

The pathogenesis of reversible T-wave inversions or large upright peaked T-waves: Sympathetic T-waves

“…TS, also described as broken heart syndrome, or acute cardiac sympathetic disruption syndrome is an acute cardiac disease entity, which presents with a clinical picture resembling that of acute coronary syndrome (ACS) [22][23][24]. The disease is characterized by a unique pattern of reversible usually regional circumferential (bi-) LVWMA resulting in a conspicuous left ventricular ballooning.…”

Case report: Naturally occurring neurogenic stunned myocardium in a dog secondary to status epilepticus

“…Neurogenic stunned myocardium (NSM) is defined as cardiovascular dysfunction after a neurologic event causing autonomic dysregulation (1). A variety of neurological insults, such as seizures or subarachnoid hemorrhage, have the potential to lead to significant catecholamine surges (1,2). At high concentrations, catecholamines exhibit cardiotoxic effects and may cause infarction-like changes such as arrhythmias and ventricular wall motion abnormalities (1,2).…”

“…A variety of neurological insults, such as seizures or subarachnoid hemorrhage, have the potential to lead to significant catecholamine surges (1,2). At high concentrations, catecholamines exhibit cardiotoxic effects and may cause infarction-like changes such as arrhythmias and ventricular wall motion abnormalities (1,2). These changes can be life-threatening if not promptly identified and managed (2).…”

Tit for Tat Brain versus Heart: A Case of Status Epilepticus, Cardiomyopathy, and Stroke

“…In some institutions, the practice is to treat with anticoagulation once an LV thrombus or a low ejection fraction has been identified. 7 There is little evidence base to support this, likely because of the rare occurrence of neurogenic cardiomyopathy. In this case, it is unlikely that anticoagulation would have prevented the stroke, because the ventricular dysfunction was not identified until after the stroke had occurred.…”

“…In some institutions, the practice is to treat with anticoagulation once an LV thrombus or a low ejection fraction has been identified 7 . There is little evidence base to support this, likely because of the rare occurrence of neurogenic cardiomyopathy.…”