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We thank Dr. Sun and colleagues for their interest in our publication (1) and for their questions that highlight important pathophysiological phenomena that appear unique to Tako-tsubo cardiomyopathy (TTC).
It is true that for the same extent of left ventricular (LV) systolic impairment and indeed for the same degree of elevation of LV end-diastolic pressure (2), patients appear to have lesser degrees of pulmonary edema in acute TTC compared with those experiencing a large acute myocardial infarction (AMI). However, this does not mean that the clinical course in the early stages of acute TTC is “benign.” Conversely, there are significant hemodynamic, arrhythmic, and embolic complications, all of which are life threatening and place the early in-hospital mortality of acute TTC on par with that of AMI.
We entirely agree with the patterns of myocardial contraction described by Sun et al. in the apical variant of TTC. Their proposed concept of a “hyperkinetic basal myocardial conduit” that helps maintain cardiac output is an appealing one. However, the determinants of hemodynamic compromise in TTC are likely to be multifactorial. Differences in myocardial functional reserve will rely at least in part on different pathophysiologies: in AMI, the microcirculation/myocytes carry an atherosclerotic burden that attenuates the myocardial contractile reserve; in hemodynamically significant pulmonary embolism, there is a sudden/significant pressure overload in the right heart and a degree of hypoxia that also has the potential to adversely impact myocardial contractility. Despite initial reports of high levels of catecholamines in patients with TTC compared with those with AMI and the overwhelming evidence from basic science reports of a dose-dependent biased agonism of epinephrine for beta2-adrenergic receptors, in our experience, patients with TTC do not appear to have either tachycardia or hypertension in the acute stage. This may represent yet unrecognized pathophysiological responses of the peripheral nervous system, leading to a deficient chronotropic reserve in those developing cardiogenic shock. In addition, there is some evidence that patients with TTC have impaired vascular reactivity.
Finally, cardiac energetic impairment has been previously observed in hyperkinetic myocardium, and the classical example of this is hypertrophic cardiomyopathy. The concept of a hyperkinetic basal myocardial conduit in apical variant TTC is therefore compatible with energetic impairment because the latter refers to a deficiency in trafficking high-energy phosphates in the myocyte with residual ability to generate ATP to various extents. Whether there is a base-apex or left-right gradient of this energetic machinery in the myocardium remains to be established in future work, and such investigations will require significant refinement of current magnetic resonance spectroscopy methods.
