Systemic inflammatory response syndrome is a major determinant of late cardiovascular outcome in Takotsubo syndrome

Abstract

Recent advances regarding the pathophysiology of Takotsubo Syndrome (TTS) have underlined a key role for inflammation. To assess the impact of Systemic Inflammatory Response Syndrome (SIRS) on in-hospital, mid and long-term outcomes after TTS, and to determine its predictors. A total of 215 patients with TTS were included between September 2008 and January 2018. SIRS was defined by the presence of at least two of the three following criteria: (1) white blood cells count < 4 or > 12.10 9 /L, (2) heart rate > 90 bpm, (3) temperature < 36 or > 38 °C. A total of 96 out of 215 patients (44.7%) developed SIRS within the first 48 h after TTS diagnosis. Follow-up was obtained in 178 patients (82.8%) after a median of 518 days (128–1004). SIRS patients were more likely to be male, with a history of cancer or chronic obstructive pulmonary disease and presenting a physical trigger. They showed lower Left Ventricular Ejection Fraction (LVEF) on admission (34.5% ± 11.8 vs. 41.9% ± 10.6; P < 0.001) and higher Brain Natriuretic Peptide (BNP) and troponin peak values. In-hospital death (14.6% vs. 5.0%; P = 0.019), cardiogenic shock (26.0% vs. 5.0%; P < 0.001) and supraventricular arrythmia (33.3% vs. 16.0%; P = 0.003) occurred more frequently in patients with SIRS. SIRS was associated with increased 30-days (12.6% vs. 3.4%; P = 0.017) and 1-year mortality (29.4% vs. 10.8%; P = 0.002). History of cancer and LVEF < 40% at admission were evidenced as independent predictors of SIRS. SIRS (HR 12.844; 95% CI (1.583–104.177); P = 0.017) was evidenced as an independent predictor of cardiac death. SIRS was found in a large proportion of TTS patients and was associated with enhanced myocardial damage and adverse outcome at the acute phase. At long-term follow-up, SIRS was still evidenced as an independent factor of cardiac death. All together these findings underline SIRS patients as a high-risk subgroup, to target in future clinical trials with specific therapies to attenuate SIRS.