Pathophysiology
The cause of takotsubo cardiomyopathy is not fully understood, but several mechanisms have been proposed. It is well documented that elevated catecholamine levels have been implicated in the vast majority of TTS cases. Theories suggest a link between brain activation of stress-related biochemicals and the effects these chemicals have on areas of the heart. More specifically, adrenal stimulation by the sympathetic nervous system has been noted in cases ranging from physical events such as ischemic stroke, to emotional events such as depression or loss of a loved-one. How these increased levels of catecholamines act in the body to produce the changes seen with TTS is not clearly understood. Research supports the widely-held understanding that microvascular dysfunction and coronary vasospasm caused by a rapid influx of catecholamines to cardiac myocytes results in apical stunning and transient cardiomyopathy. Microvascular dysfunction/Transient vasospasm: Some of the original researchers of takotsubo suggested that multiple simultaneous spasms of coronary arteries could cause enough loss of blood flow to cause transient stunning of the myocardium. Other researchers have shown that vasospasm is much less common than initially thought. It has been noted that when there are vasospasms, even in multiple arteries, that they do not correlate with the areas of myocardium that are not contracting. However, the idea of coronary artery vasospasm is still believed to contribute to the TTS disease process. The theory of vasospasm is not easily separated from that of microvascular dysfunction and in fact, microvascular dysfunction could explain vasospasticity.
In anagen effluvium, histopathologic evaluation of a punch biopsy of the scalp will exhibit a normal anagen-to-telogen ratio, which is less than 15% telogen hair follicles. If greater than 15% of the hair follicles are in the telogen phase, this more supports a diagnosis of telogen effluvium. Treatment
The management of anagen effluvium should be aimed at limiting the amount of time the patient has alopecia. To date, several agents have been studied; unfortunately, no treatment appears to be effective in preventing or stopping the hair loss. Although the results have not been impressive in stopping or preventing hair loss, it has been postulated that topical minoxidil is effective in reducing the period of baldness by an average of fifty days. Several studies have described limiting drug delivery to the scalp by using a scalp tourniquet during chemotherapy. If scalp or brain metastases are a possibility, this method should not be used to allow penetration of the chemotherapeutic agent. Another method that has shown success is inducing scalp hypothermia (by keeping ice over the scalp) to a scalp temperature of fewer than 24° Celsius during chemotherapy with daunorubicin, doxorubicin, paclitaxel, vincristine, vinblastine, mechlorethamine, actinomycin D, and epirubicin.As pharmacologic agents successful in treating and preventing anagen effluvium have not been found, patient education and aesthetic advice on managing hair loss are fundamental to managing androgen effluvium.