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Hemodynamic Assessment in Takotsubo Syndrome
Quick Takes
- Using invasive pressure-volume loops, takotsubo syndrome (TTS) is associated with impaired cardiac contractility and a shortened systolic interval (with increased LV diastolic volume compensating for increased systolic volume thereby preserving stroke volume), and diastolic function characterized by prolonged active relaxation but unaltered passive elastic properties.
- Myocardial energetics in TTS reveal an inefficient system with increased potential energy and decreased kinetic energy (stroke work).
- Additional studies could help define whether therapies targeted at lengthening the systolic interval could result in improved myofilament protein phosphorylation and improved clinical outcomes.
Study Questions:
What cardiac hemodynamic abnormalities occur during the acute phase of takotsubo syndrome (TTS)?
Methods:
OCTOPUS (Optimized Characterization of Takotsubo Syndrome by Obtaining Pressure Volume Loops) was a single-center trial. Left ventricular (LV) invasive pressure-volume loops were recorded and analyzed in 24 patients with confirmed TTS and in a control population of 20 participants without cardiovascular disease (CVD) in this trial.
Results:
TTS was associated with impaired LV contractility (end-systolic elastance [Ees] 1.74 vs. 2.35 mm Hg/mL, p = 0.02; maximal rate of change in systolic pressure over time [dP/dtmax] 1533 vs. 1763 mm Hg/s, p = 0.03; end-systolic volume at a pressure of 150 mm Hg [ESV150] 77.3 vs. 46.4 mL, p = 0.002) and a shortened systolic period (286 vs. 343 ms, p < 0.001). The pressure-volume diagram was shifted rightward with significantly increased LV end-diastolic (125 [104, 171] vs. 108 [89, 129] mL, p = 0.03) and end-systolic volumes (72 [52, 93] vs. 44 [39, 46] mL, p < 0.001), and preserved stroke volume (62 [49, 79] vs. 65 [54, 87] mL, p = 0.37) despite a lower ejection fraction (48 ± 10 vs. 62 ± 7%, p < 0.001). Diastolic function was characterized by prolonged active relaxation (relaxation constant [tau] 69.5 vs. 45.9 ms, p < 0.001; and minimal rate of change in diastolic pressure [-dP/dtmin] –1457 vs. –2192 mm Hg/s, p < 0.001), while diastolic stiffness (1/compliance) was not affected in TTS (end-diastolic volume at a pressure of 15 mm Hg [EDV15] 96.7 vs. 109.0 mL, p = 0.94). Mechanical efficiency was significantly reduced in TTS (p < 0.001) with reduced stroke work (p = 0.001), increased potential energy (p = 0.036), and a similar total pressure-volume area compared to controls (p = 0.36).
Conclusions:
TTS is characterized by reduced cardiac contractility, a shortened systolic period, inefficient energetics, and prolonged active relaxation but unaltered diastolic passive stiffness. The authors conclude that these findings may suggest decreased phosphorylation of myofilament proteins, which represents a potential therapeutic target in TTS.
Perspective:
The underlying pathophysiology of TTS is unclear, with potential interplay between changes in the central nervous system (with sympathetic overdrive and excessive release of catecholamines) and their downstream effects on the cardiovascular system. Invasive pressure-volume loops among 24 patients with TSS and a control population of 20 participants without CVD revealed that TTS was associated with severely impaired cardiac contractility and a shortened systolic interval, and prolonged diastolic relaxation but unaltered passive elastic properties; and an inefficient system with increased potential energy and decreased kinetic energy (stroke work). The results suggest that the impaired contractility and altered elastance-time curve could be due to decreased phosphorylation of myofilament proteins (e.g., cardiac myosin-binding protein-C). Cardiac metabolic dysregulation also could play a role in impaired mechanical efficiency in TTS, which could also help explain persistent symptoms in some patients with TTS despite recovery of LV systolic function. Additional studies could help define whether therapies targeted at lengthening the systolic interval could result in improved clinical outcomes potentially mediated by improved myofilament protein phosphorylation.
Clinical Topics: Heart Failure and Cardiomyopathies, Acute Heart Failure
Keywords: Catecholamines, Diastole, Heart Failure, Hemodynamics, Myocardial Contraction, Myofibrils, Myosins, Phosphorylation, Stroke Volume, Systole, Takotsubo Cardiomyopathy
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