Takotsubo Cardiomyopathy: What Is Behind the Octopus Trap?

摘要: During the 15 years that have passed since introduction of term “takotsubo” transient apical cardiomyopathy (TAC), rich literature on this confusing syndrome has contained little definitively clarifies any fundamental aspect except for meaning Japanese word tako-tsubo (“octopus trap”). The accompanying article by Lee and colleagues1 regarding 2 cases “inverted TAC” proposes more questions than answers, but are also part learning process, so they welcome. Like better-known frequent “midventricular variety” TAC, inverted TAC is an important alternative manifestation what frequently claimed to be a continuous spectrum which includes typical variety. Phenotypically, defined following features: a) event; b) sudden onset severe segmental left ventricular (LV) dysfunction, may affect different areas LV commonly independent territory single coronary branch; c) evolution ST-segment changes (elevation, depression, or both); d) mild elevation cardiac enzyme levels with respect dysfunctional area; e) absence obstructive lesions capable explaining patterns early angiography. The only mechanism known cardiologists cause similar dysfunction clearly myocardial stunning,2 usually related occlusion. One suggested explanation direct, simple catecholamine overload, as “catecholamine heart” “broken in English-language medical literature. Actually, infusion endogenous hyperactivity does not either ST hypotension (mild) hypertension, tachycardia. Some patients increased load vasospasm (although never been well demonstrated), great majority spontaneous pharmacologic overload do present TAC.3 The most credible (and spontaneously resolving) stunning spasm, hemodynamic metabolic stress. In thousands case reports short series current literature, authors quickly dismissed—on basis few retrospective studies had inadequate descriptions testing protocols—the hypothesis spasm pathophysiologic TAC.4 In contrast, our group5–7 recently resurrected reporting pilot who were prospectively subjected acetylcholine (ACh) during recovery period after presented TAC. series, such endothelial function8,9 consistently resulted substantially abnormal response characterized (subtotal) spastic narrowing extensive territories, accompanied echocardiographic documentation observed original, presentation TAC.4–6 Our experience admittedly preliminary (we currently pursuing goal performing larger, controlled study), it strongly suggests typical, form, midventricular variety, disappears days clinical presentation. Also, intracoronary administration nitroglycerin results safe, dependable, total resolution both dysfunction.4,5 On ACh testing, we proposed seems result from combination precipitating factors (mental physical stress, pain, some other crisis), mediated excessive production. Those rare, well-described, (approximately 10% those TAC) recurrent presentations seem ones predominantly pattern (as reflected persistently positive test over months). behavior condition Prinzmetal angina, well-known involves can reproduced testing. substantial difference between conditions segment (typically proximal anterior descending artery) shows enhanced spasticity, likely secondary specific its neural control. A probably exists angina.4 In addition, tests, documented TAC,5 varying involvement branches arteries. Whereas involve critical, diffuse all mid- distal artery, relative sparing territory, leading contractile preservation5 monitoring (Fig. 1). We yet observe TAC,” would interesting know how respond challenge. remaining question concerns whether possible patient “global” (generalized dysfunction). Most probably, occur; but, if sustained, lead death. Not even necropsy able reveal death (the arteries intact, myocardium “normal” routine examination). Additional fascinating are, “Why rarely recurrent?” “What leads cancellation recovery?” Surely, (pain, dyspnea, anxiety, stressors) improve rather, tend persist. For example, reported here, indicate sepsis presence metastatic cancer first unclear second case; patients, remained active TAC. Fig. 1 Schematic representation responses evaluated angiography. Drawing baseline, lumen. P1 followed ... In conclusion, essential better qualify mechanisms individual TAC,7 especially order document common baseline characteristics, effect treatment, prognosis (tendency recur). Moreover, at experienced centers, need emergency catheterization evolving toward elective (pre-discharge) catheterization, including test. phenotypic diagnosis can, fact, established simply echocardiography presentation; doubtful cases, computed axial tomographic angiography used rule out significant occlusive disease. Because mechanistic prognostic information provide, endothelial-function appears worth limited discomfort, risk, cost entails.