Stress-induced cardiomyopathy, so-called Takotsubo cardiomyopathy, has recently been reported in Japan. Stress-induced cardiomyopathy is characterized by transient left ventricular apical dysfunction and ballooning, with normal coronary angiographic findings. We describe a rare case of stress-induced cardiomyopathy associated with lung adenocarcinoma presenting as hyponatremia.
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It is known that the morphologic expression or progression of hypertrophy in hyertrophic cardiomyopathy(HCMP) occurs mostly during childhood, when the body growth is considerable, but nearly not occurs in adult life. Apical hypertrophic cardiomyopathy is an uncommon variant of HCMP which is characteristic apical hypertrophy of the left ventricle showing characteristic ace of spade diastolic configuratioin of the left ventriculogram. It has not yet been clarified when the progression or development of hypertrophy occurs in apical HCMP. The possibliity of the morphologic changes in apical HCMP has been poposed in previous study, but not proved yet.
We experienced a case of apical HCMP in 62-year-old female, which evolved during 6 years from mild, diffuse left ventricular hypertrophy to more progressed diffuse hypertrophy associated with marked hypertrophy of the apex of left ventricle showing ventriculopraphic picture of apical HCMP. The present case shows the morphologic change in HCMP with progression of hypertrophy during adult life.
A 56-year-old man presented with sudden onset of congestive heart failure (New York Heart Association class III to IV) after mild stress and developed various cardiovascular manifestations. At first visit, cardiac enzyme elevation, regional left ventricular (LV) wall motion abnormality and pulmonary edema were evident. However, coronary angiography was normal. LV function was totally recovered at discharge, suspicious of fulminant myocarditis. During the hospital stay, acute non-obstructive stroke without neurologic sequelae occurred. After 3 years, he re-admitted because ventricular tachycardia and severe LV systolic dysfunction (ejection fraction, 15%) were developed. After 3 days of applying percutaneous cardiopulmonary bypass system, the patient was completely recovered. Suspicious of pheochromocytoma, we checked 24-hour urine catecholamines and metanephrines and abdomen computed tomography, which revealed pheochromocytoma. The patient underwent laparoscopic adrenalectomy.
Heat stoke is a life-threatening syndrome of multi-organ dysfunction caused by elevated body temperature. Reported mortality rate range from 17-70 percent. The heat stoke victim's circulatory pattern id defined low peripheral vascular resistance and high circulatory demand of other conditions involving tissue injury such as trauma or sepsis. Owing to either to direct thermal injury of the myocardium or to increased pulmonary vascular resistance, the heart may not meet the elevated circulatory demand. Heat stoke induced cardiomyopathy is diagnosed by pathlogy, EKG abnormality, LDH isoenzyme, echocardiography. Therapy was two purpose : rapid reduction of body temporature and support of the cardiovascular system. We experienced a case of heat stoke induced cardiomyopathy in a 21 year-old male who had been observed for 1 years. The Left Ventricular End-Diastolic Diameter(LVEDD) was 65mm, Ejection fraction(EF) was 35% initially and LVEDD was decreased 58mm, EF was 60% after 9 months. We report a case of heat stoke induced cardiomyopathy with brief review of literature.