Why the study?
Male sex in takotsubo syndrome has a low incidence and remains not well characterized, prompting this study to describe sex differences.
Does male sex worsen clinical outcomes and mortality in patients with Takotsubo syndrome?
Cohort (n=2,531)
No
Does male sex worsen clinical outcomes and mortality in patients with Takotsubo syndrome?
Male patients with Takotsubo syndrome represent a high-risk phenotype with significantly higher in-hospital and long-term mortality compared to female patients.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Male patients can have Takotsubo, and if they have it, they have a very high risk of long-term MACE. These patients should have aggressive follow-up in the first few months following the event and then every 6 months thereafter.”
“The study's observations may seem paradoxical at first, but they may actually provide important clues about the pathophysiologic mechanisms of this disorder. There is increasing evidence that the transient myocardial dysfunction observed in Takotsubo syndrome is the result of sympathetically mediated microvascular ischemia.”
“There's something about the autonomic nervous system control mechanism that's different between the two sexes. The whole gender thing is fascinating to me just as to why it would be that way. Why would a woman's heart be much more susceptible to this than a man's heart? Why is it that men can still get it, obviously, but it takes a much greater stress to provoke it?”
Supports male sex as mortality predictor in Takotsubo syndrome; hypothesis-generating for sex-specific risk models.
BACKGROUND: Male sex in takotsubo syndrome (TTS) has a low incidence and it is still not well characterized. OBJECTIVES: The aim of the present study is to describe TTS sex differences. METHODS: TTS patients enrolled in the international multicenter GEIST (GErman Italian Spanish Takotsubo) registry were analyzed. Comparisons between sexes were performed within the overall cohort and using an adjusted analysis with 1:1 propensity score matching for age, comorbidities, and kind of trigger. RESULTS: In total, 286 (11%) of 2,492 TTS patients were men. Male patients were younger (age 69 ± 13 years vs 71 ± 11 years; P = 0.005), with higher prevalence of comorbid conditions (diabetes mellitus 25% vs 19%; P = 0.01; pulmonary diseases 21% vs 15%; P = 0.006; malignancies 25% vs 13%; P < 0.001) and physical trigger (55 vs 32% P < 0.01). Propensity-score matching yielded 207 patients from each group. After 1:1 propensity matching, male patients had higher rates of cardiogenic shock and in-hospital mortality (16% vs 6% and 8% vs 3%, respectively; both P < 0.05). Long-term mortality rate was 4.3% per patient-year (men 10%, women 3.8%). Survival analysis showed higher mortality rate in men during the acute phase in both cohorts (overall: P < 0.001; matched: P = 0.001); mortality rate after 60 days was higher in men in the overall (P = 0.002) but not in the matched cohort (P = 0.541). Within the overall population, male sex remained independently associated with both in-hospital (OR: 2.26; 95% CI: 1.16-4.40) and long-term mortality (HR: 1.83; 95% CI: 1.32-2.52). CONCLUSIONS: Male TTS is featured by a distinct high-risk phenotype requiring close in-hospital monitoring and long-term follow-up.
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Arcari et al. (2022) conducted a cohort in COVID-19 (n=2,531). Elevated cardiac troponin-T (> 0.014 ng/ml) vs. Normal cardiac troponin-T was evaluated on All-cause mortality (p=<0.001).
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