A syndrome of transient left ventricular apical wall motion abnormality in the absence of coronary disease: a perspective from the United States.
BACKGROUND
The syndrome of chest pain associated with characteristic anterior electrocardiographic changes, moderate increases in cardiac enzymes, and a reversible apical wall motion abnormality in the absence of coronary artery disease has been documented in Japan, but has received relatively little attention in other countries.


METHODS
The clinical and echocardiographic data of 12 patients (11 women, mean age 64 +/-14 years) who presented with chest symptoms, electrocardiographic (ECG) changes indicative of an acute anteroapical myocardial infarction, abnormal cardiac enzyme levels and echocardiography showing an apical wall motion abnormality were collected. Coronary angiography was performed in 10 patients. A follow-up echocardiogram was obtained within 2 weeks of the initial diagnosis in most cases.


RESULTS
An identifiable, precipitating ("trigger") event could be identified in all 12 individuals. Respiratory distress was present in 7, the death of a relative in 3, in 4 a surgical or medical procedure had been performed, and in 1 a panic disorder was diagnosed. The echocardiograms showed a characteristic wall motion pattern of significant apical dysfunction. All of the patients who underwent coronary arteriography had noncritical coronary artery disease. Follow-up echocardiography showed normalization of the LV dysfunction in all instances.


CONCLUSIONS
We identified a syndrome of chest pain, dyspnea, ECG and enzyme changes mimicking acute myocardial infarction, similar to the "Takotsubo" syndrome described in Japan. It is likely that the widespread use of echocardiography, coupled with increased recognition of this syndrome, will result in this diagnosis being made more commonly.
Seth
Paula S
PS
Division of Cardiology, Department of Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.
Aurigemma
Gerard P
GP
Krasnow
Joshua M
JM
Tighe
Dennis A
DA
Untereker
William J
WJ
Meyer
Theo E
TE
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D003327:Coronary Disease / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D003402:Creatine Kinase / Q000097:blood / Q000378:metabolism; D052279:Creatine Kinase, MB Form; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D012206:Rhabdomyolysis / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology; D013577:Syndrome; D019210:Troponin I / Q000097:blood; D014481:United States / Q000453:epidemiology; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D007527:Isoenzymes; D019210:Troponin I; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form