The treatment of melanoma in situ (MIS) is controversial with current standard of care being surgical excision with clear margins. Alternative topical therapy with imiquimod has been proposed in recent studies as a possible treatment for MIS. This study aimed to evaluate the use of topical 5% imiquimod as an alternative approach for the treatment of residual melanoma in situ after surgical resection of the primary lesion. A retrospective chart review of all patients treated with topical 5% imiquimod for residual MIS following standard resection with 5–10 mm margins at Yale-New Haven Hospital from 2008 through 2013 was performed. The pre- and posttreatment results were confirmed by diagnostic tissue biopsy. Twenty-two patients were included in the study. One of these 22 patients was lost to follow up. Twenty patients (95%) had complete resolution of their residual MIS and 1 patient did not respond to imiquimod (5%). No reports of recurrences were noted at the treatment sites. For patients with residual melanoma in situ after the initial excision, topical 5% imiquimod appears to be a reasonable alternative treatment with good clinical and histopathologic success rates.

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.

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Takotsubo cardiomyopathy is a phenomenon of transient acute left ventricular dysfunction without obstructive coronary disease seen predominantly in postmenopausal women in the setting of acute emotional or physical stress. Neurocardiogenic injury from acute neurologic events such as intracranial bleeding can precipitate transient left ventricular dysfunction (termed ‘neurogenic stunned myocardium’) that may be indistinguishable from takotsubo cardiomyopathy. There is controversy about the diagnosis of takotsubo cardiomyopathy in the setting of acute neurologic disorders. We describe a case of a 67-year-old female who initially presented with takotsubo cardiomyopathy due to an acute gastrointestinal illness and 4 years later developed a recurrence in the setting of an ischemic cerebrovascular accident that was associated with more prominent EKG changes and much higher cardiac biomarker release but similar degree of left ventricular dysfunction. This case suggests that susceptibility to this disorder is likely due to patient-specific factors rather than etiology, and acute neurologic disorders should be included as precipitants of takotsubo cardiomyopathy. We also theorize that there may be patients with milder forms of stress-related cardiac injury who do not develop left ventricular dysfunction, being similar to the wide range of cardiac manifestations in patients with acute neurologic disorders. We review published literature on neurologic precipitants of takotsubo cardiomyopathy.