The role of antimicrobial resistance on long-term mortality and quality of life in critically ill patients: a prospective longitudinal 2-year study.

BACKGROUND: In the recent era, antimicrobial resistance has been identified as one of the most important threats to human health worldwide. The rapid emergence of antibiotic-resistant pathogens (ABRP) in the modern intensive care unit (ICU) also represents a "nightmare scenario" with unknown clinical consequences. In the Greek ICU, in particular, gram negative ABRPs are now considered endemic. However, the possible longitudinal impact of ABRPs on long-term outcomes of ICU patients has not yet been determined. METHODS: In this two-year (January 2014-December 2015) single-centre observational longitudinal study, 351 non-neurocritical ICU patients ≥ 18 year-old were enrolled. Patients' demographic, clinical and outcome data were prospectively collected. Quality-adjusted life years (QALY) were calculated at 6, 12, 18 and 24 months after ICU admission. RESULTS: Fifty-eight patients developed infections due to ABRP (ABRP group), 57 due to non-ABRP (non-ABRP group), and 236 demonstrated no infection (no-infection group) while in ICU. Multiple regression analysis revealed that multiple organ dysfunction syndrome score (OR: 0.676, 95%CI 0.584-0.782; P < 0.001) and continuous renal replacement therapy (OR: 4.453, 95%CI 1.805-10.982; P = 0.001) were the only independent determinants for ABRP infections in ICU. Intra-ICU, 90-day and 2-year mortality was 27.9%, 52.4% and 61.5%, respectively. Compared to the non-ABRP and no-infection group, the ABRP group demonstrated increased intra-ICU, 90-day and 2-year mortality (P ≤ 0.022), worse 2-year survival rates in ICU patients overall and ICU survivor subset (Log-rank test, P ≤ 0.046), and poorer progress over time in 2-year QALY kinetics in ICU population overall, ICU survivor and 2-year survivor subgroups (P ≤ 0.013). ABRP group was further divided into multi-drug and extensively-drug resistant subgroups [MDR (n = 34) / XDR (n = 24), respectively]. Compared to MDR subgroup, the XDR subgroup demonstrated increased ICU, 90-day and 2-year mortality (P ≤ 0.031), but similar 90-day and 2-year QALYs (P ≥ 0.549). ABRP infections overall (HR = 1.778, 95% CI 1.166-2.711; P = 0.008), as well as XDR [HR = 1.889, 95% CI 1.075-3.320; P = 0.027) but not MDR pathogens, were independently associated with 2-year mortality, after adjusting for several covariates of critical illness. CONCLUSIONS: The present study may suggest a significant association between ABRP (especially XDR) infections in ICU and increased mortality and inability rates for a prolonged period post-discharge that requires further attention in larger-scale studies.

Thrombolysis in severe COVID-19 pneumonia with massive pulmonary embolism.

OBJECTIVE: No guidelines exist for the management of massive pulmonary embolism (PE) in COVID-19. We present a COVID-19 patient with refractory acute respiratory syndrome (ARDS), and life-threatening PE who underwent successful thrombolysis. CASE PRESENTATION: A previously healthy 47 year old male was admitted to our hospital due to severe COVID-19 pneumonia [confirmed by Real-Time-Polymerase-Chain-Reaction (RT-PCR)]. He had rapidly evolving ARDS [partial arterial pressure of oxygen to fractional inspired concentration of oxygen ratio: 175], and sepsis. Laboratory results showed lymphocytopenia, and increased D-dimer levels (7.7 µg/ml; normal: 0-0.5 µg/ml). The patient was treated in the intensive care unit. On day-1, ARDS-net/prone positioning ventilation, and empiric anti-COVID treatment integrating prophylactic anticoagulation was administered. On hospital day-2, the patient developed shock with worsening oxygenation. Point-of-care-ultrasound depicted a large thrombus migrating from the right atrium to the pulmonary circulation. Intravenous alteplase (100 mg over 2 h) was administered as rescue therapy. The patient made an uneventful recovery, and was discharged to home isolation (day-20) on oral rivaroxaban. CONCLUSION: Thrombolysis may have a critical therapeutic role for massive PE in COVID-19; however the risk of potential bleeding should not be underestimated. Point-of-care ultrasound has a pivotal role in the management of refractory ARDS in COVID-19.

Reverse takotsubo cardiomyopathy in fulminant COVID-19 associated with cytokine release syndrome and resolution following therapeutic plasma exchange: a case-report.

BACKGROUND: Fulminant (life-threatening) COVID-19 can be associated with acute respiratory failure (ARF), multi-system organ failure and cytokine release syndrome (CRS). We present a rare case of fulminant COVID-19 associated with reverse-takotsubo-cardiomyopathy (RTCC) that improved with therapeutic plasma exchange (TPE). CASE PRESENTATION: A 40 year old previous healthy male presented in the emergency room with 4 days of dry cough, chest pain, myalgias and fatigue. He progressed to ARF requiring high-flow-nasal-cannula (flow: 60 L/minute, fraction of inspired oxygen: 40%). Real-Time-Polymerase-Chain-Reaction (RT-PCR) assay confirmed COVID-19 and chest X-ray showed interstitial infiltrates. Biochemistry suggested CRS: increased C-reactive protein, lactate dehydrogenase, ferritin and interleukin-6. Renal function was normal but lactate levels were elevated. Electrocardiogram demonstrated non-specific changes and troponin-I levels were slightly elevated. Echocardiography revealed left ventricular (LV) basal and midventricular akinesia with apex sparing (LV ejection fraction: 30%) and depressed cardiac output (2.8 L/min) consistent with a rare variant of stress-related cardiomyopathy: RTCC. His ratio of partial arterial pressure of oxygen to fractional inspired concentration of oxygen was < 120. He was admitted to the intensive care unit (ICU) for mechanical ventilation and vasopressors, plus antivirals (lopinavir/ritonavir), and prophylactic anticoagulation. Infusion of milrinone failed to improve his cardiogenic shock (day-1). Thus, rescue TPE was performed using the Spectra Optia™ Apheresis System equipped with the Depuro D2000 Adsorption Cartridge (Terumo BCT Inc., USA) without protective antibodies. Over 5 days he received daily TPE (each lasting 4 hours). His lactate levels, oxygenation, and LV function normalized and he was weaned off vasopressors. His inflammation markers improved, and he was extubated on day-7. RT-PCR was negative on day-17. He was discharged to home isolation in good condition. CONCLUSION: Stress-cardiomyopathy may complicate the course of fulminant COVID-19 with associated CRS. If inotropic therapy fails, TPE without protective antibodies may help rescue the critically ill patient.

Malignant mesothelioma cells secrete natriuretic peptides: Data and diagnostic clinical implications.

BACKGROUND AND OBJECTIVE: Mesothelial cells and cardiomyocytes have shared embryonic mesodermal origin. Cardiomyocytes release BNP under stretch. We searched whether malignant mesothelioma cells also secrete BNP and if so, this has a meaningful impact. METHODS: Part I: Prospectively, patients with pleural lesions on CT having malignant mesothelioma effusions (MME, n = 13) were compared to patients with malignant effusions with pleural lesions (MEa, n = 14). Age-matched patients with ME without pleural lesions (MEb, n = 16) and non-malignant effusions (NME, n = 25) were analysed. Part II: Retrospectively, samples from patients with mesothelioma (n = 14), lung cancer (n = 8) or heart failure (n = 9) were used. BNP was measured in pleural fluid and blood/plasma. Part III: BNP was assessed in the culture supernatants of benign (MeT-5A) and malignant mesothelioma cell lines (M14K-epithelioid, MSTO-biphasic and ZL34-sarcomatoid) (n = 10 per cell line in three different biological replicates). RESULTS: In vitro, BNP concentration was significantly higher in the supernatant of all malignant cell lines than benign ones (P < 0.01), denoting BNP's production from the former. The pleural fluid to blood BNP ratio in MME was extremely high in Part I and Part II subjects (28.3 ± 12.1 and 25.9 ± 8.6, respectively) versus 1.1 ± 0.3 and 0.4 ± 0.1 in Part I ME and NME, respectively (P < 0.0001), and 0.8 ± 0.1 and 0.4 ± 0.1 in Part II ME and NME, respectively (P < 0.0001). BNP ratio ≥2.11 in Part I had 92% sensitivity and 94.5% specificity for MME (P < 0.0001). CONCLUSION: BNP is secreted from malignant mesothelial cells. In clinical practice, the pleural fluid to blood BNP ratio can help in the diagnosis of malignant mesothelioma.

The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study.

BACKGROUND: The aim was to investigate whether the use of N-acetylcysteine and ascorbic acid reduce contrast-induced nephropathy incidence in critical care patients. METHODS: This was a one-center, two-arm, prospective, randomized, open-label, controlled trial in the Intensive Care Unit of the University Hospital of Larissa, Greece. Patients with stable renal function, who underwent non urgent contrast-enhanced computed tomography for diagnostic purposes, were included in the study. Patients in the treatment group (NacA, n = 60) received intravenously N-acetylcysteine (1200 mg) and ascorbic acid (2 g) dissolved separately in 100 ml of normal saline 2 hours before, and at 10 hours and 18 hours following the infusion of contrast agent, while control group patients (CG, n = 64) received only normal saline. All patients received additional hydration. Contrast-induced nephropathy was defined as relative increase by 25% of the baseline values of serum creatinine. RESULTS: Contrast-induced nephropathy in NacA and CG were 18.33% and 15.6%, respectively (p = 0.81). The percentage change median (interquartile range (IR)) of serum cystatin-C (mg/L) from baseline in patients who underwent contrast-induced tomography, were 37.23% (28.53) and 93.20% (46.90) in NacA and in CG, respectively (p = 0.03). The 8-isoprostane serum levels in NacA were significantly lower compared to CG at 2 hours (p = 0.012) and 24 hours (p = 0.006) following radiocontrast infusion. Multivariate analysis revealed that contrast-induced nephropathy was independently associated with a higher baseline ratio of serum urea/creatinine (odds ratio, 1.02; 95 CI%, 1.00-1.05) and with the use of nephrotoxic medications (odds ratio, 0.24; 95 CI%, 0.06-0.94). CONCLUSION: Intravenous administration of N-acetylcysteine and ascorbic acid failed to reduce contrast-induced nephropathy in critically ill patients who underwent contrast-enhanced computed tomography, despite a significant reduction of 8-isoprostane levels in treated patients. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01017796 . Registered on 20 November 2009.

Post-partum hemorrhage complicated by reverse-Takotsubo cardiogenic shock; a novel therapeutic approach.

Takotsubo Cardiomyopathy (TTC) is a type of transient, yet severe left ventricular systolic dysfunction, rarely complicating extreme emotional stress ("primary" TTC) or critical medical/surgical illness ("secondary" TTC forms). Although usually reversible, TTC may result in cardiogenic shock with dismal prognosis. "Secondary" TTC forms are particularly in danger for this complication, bearing significantly worse short and long-term prognosis. Herein, we report a rare case of a life-threatening "secondary" TTC in a patient with post-cesarean section severe hemorrhage, and we point out that early co-administration of esmolol and levosimendan might be an effective and safe therapeutic approach in "reversing" TTC-induced cardiogenic shock, especially when invasive therapeutic strategies are practically unfeasible.

The role of nuclear cardiac imaging in redefining neurogenic stunned myocardium in subarachnoid hemorrhage: a deeper look into the heart.

Subarachnoid hemorrhage may be complicated by neurogenic stunned myocardium, a catecholamine-induced transient cardiomyopathy that displays a wide clinical spectrum of cardiac abnormalities, including electrocardiographic changes, arrhythmias, myocardial necrosis, and left ventricular systolic and diastolic dysfunction. However, less is known about the cardiac metabolic consequences of acute subarachnoid hemorrhage. Prunet and coworkers' recent study provides scintigraphic evidence suggesting that glucose metabolism and sympathetic cardiac innervation are severely and globally depressed during the acute phase of the disease. Metabolic and innervation abnormalities are largely overlapped and are probably not causally related to myocardial ischemia, suggesting that impaired glucose metabolism is probably neurogenic in nature. The scintigraphic defects seem to reverse slowly, within months of the onset of cerebral bleeding. Interestingly, scintigraphic evidence of metabolic myocardial alterations may exist even in the absence of clinical features of cardiac disease, possibly representing a subclinical type of neurogenic stunned myocardium.

New insights into the mechanisms involved in B-type natriuretic peptide elevation and its prognostic value in septic patients.

INTRODUCTION: Elevated plasma B-type natriuretic peptide (BNP) levels in patients with critical sepsis (severe sepsis and septic shock) may indicate septic cardiomyopathy. However, multiple heterogeneous conditions may also be involved in increased BNP level. In addition, the prognostic value of BNP in sepsis remains debatable. In this study, we sought to discover potential independent determinants of BNP elevation in critical sepsis. The prognostic value of BNP was also evaluated. METHODS: In this observational study, we enrolled mechanically ventilated, critically septic patients requiring hemodynamic monitoring through a pulmonary artery catheter. All clinical, laboratory and survival data were prospectively collected. Plasma BNP concentrations were measured daily for five consecutive days. Septic cardiomyopathy was assessed on day 1 on the basis of left and right ventricular ejection fractions (EF) derived from echocardiography and thermodilution, respectively. Mortality was recorded at day 28. RESULTS: A total of 42 patients with severe sepsis (N = 12) and septic shock (N = 30) were ultimately enrolled. Daily BNP levels were significantly elevated in septic shock patients compared with those with severe sepsis (P ≤0.002). Critical illness severity (assessed by Acute Physiology and Chronic Health Evaluation II and maximum Sequential Organ Failure Assessment scores), and peak noradrenaline dose on day 1 were independent determinants of BNP elevation (P <0.05). Biventricular EFs were inversely correlated with longitudinal BNP measurements (P <0.05), but not independently. Pulmonary capillary wedge pressures (PCWP) and volume expansion showed no correlation with BNP. In septic shock, increased central venous pressure (CVP) and CVP/PCWP ratio were independently associated with early BNP values (P <0.05). CONCLUSIONS: The severity of critical illness, rather than septic cardiomyopathy, is probably the major determinant of BNP elevation in patients with critical sepsis. Daily BNP values are of limited prognostic value in predicting 28-day mortality; however, fast BNP decline over time and a decrease in BNP <500 pg/ml may imply a favorable outcome.

Aspiring use of a thrombectomy catheter for coronary air embolism aspiration.

A 52-year-old man with a history of percutaneous coronary intervention (PCI) in the left anterior descending (LAD) coronary artery was admitted for a facilitated PCI following an anterior ST-elevation myocardial infarction treated with thrombolysis at a nearby clinic.

Comprehensive temporal analysis of right ventricular function and pulmonary haemodynamics in mechanically ventilated COVID-19 ARDS patients.

BACKGROUND: Cardiac injury is frequently reported in COVID-19 patients, the right ventricle (RV) is mostly affected. We systematically evaluated the cardiac function and longitudinal changes in severe COVID-19 acute respiratory distress syndrome (ARDS) admitted to the intensive care unit (ICU) and assessed the impact on survival. METHODS: We prospectively performed comprehensive echocardiographic analysis on mechanically ventilated COVID-19 ARDS patients, using 2D/3D echocardiography. We defined left ventricular (LV) systolic dysfunction as ejection fraction (EF) < 40%, or longitudinal strain (LS) > - 18% and right ventricular (RV) dysfunction if two indices among fractional area change (FAC) < 35%, tricuspid annulus systolic plane excursion (TAPSE) < 1.6 cm, RV EF < 44%, RV-LS > - 20% were present. RV afterload was assessed from pulmonary artery systolic pressure (PASP), PASP/Velocity Time Integral in the right ventricular outflow tract (VTIRVOT) and pulmonary acceleration time (PAcT). TAPSE/PASP assessed the right ventriculoarterial coupling (VACR). RESULTS: Among 176 patients included, RV dysfunction was common (69%) (RV-EF 41.1 ± 1.3%; RV-FAC 36.6 ± 0.9%, TAPSE 20.4 ± 0.4mm, RV-LS:- 14.4 ± 0.4%), usually accompanied by RV dilatation (RVEDA/LVEDA 0.82 ± 0.02). RV afterload was increased in most of the patients (PASP 33 ± 1.1 mmHg, PAcT 65.3 ± 1.5 ms, PASP/VTIRVOT, 2.29 ± 0.1 mmHg/cm). VACR was 0.8 ± 0.06 mm/mmHg. LV-EF < 40% was present in 21/176 (11.9%); mean LV-EF 57.8 ± 1.1%. LV-LS (- 13.3 ± 0.3%) revealed a silent LV impairment in 87.5%. A mild pericardial effusion was present in 70(38%) patients, more frequently in non-survivors (p < 0.05). Survivors presented significant improvements in respiratory physiology during the 10th ICU-day (PaO2/FiO2, 231.2 ± 11.9 vs 120.2 ± 6.7 mmHg; PaCO2, 43.1 ± 1.2 vs 53.9 ± 1.5 mmHg; respiratory system compliance-CRS, 42.6 ± 2.2 vs 27.8 ± 0.9 ml/cmH2O, all p < 0.0001). Moreover, survivors presented significant decreases in RV afterload (PASP: 36.1 ± 2.4 to 20.1 ± 3 mmHg, p < 0.0001, PASP/VTIRVOT: 2.5 ± 1.4 to 1.1 ± 0.7, p < 0.0001 PAcT: 61 ± 2.5 to 84.7 ± 2.4 ms, p < 0.0001), associated with RV systolic function improvement (RVEF: 36.5 ± 2.9% to 46.6 ± 2.1%, p = 0.001 and RV-LS: - 13.6 ± 0.7% to - 16.7 ± 0.8%, p = 0.001). In addition, RV dilation subsided in survivors (RVEDA/LVEDA: 0.8 ± 0.05 to 0.6 ± 0.03, p = 0.001). Day-10 CRS correlated with RV afterload (PASP/VTIRVOT, r: 0.535, p < 0.0001) and systolic function (RV-LS, 0.345, p = 0.001). LV-LS during the 10th ICU-day, while ΔRV-LS and ΔPASP/RVOTVTI were associated with survival. CONCLUSIONS: COVID-19 improvements in RV function, RV afterload and RV-PA coupling at day 10 were associated with respiratory function and survival.

Cath lab activation with smartwatch's electrocardiogram tracings.

A 67-year-old man with a history of smoking, hyperlipidemia, and hypertension complained of central chest pain radiating to his left arm for 2 hours and contacted the attending cardiologist. Based on medical history and symptom description, the physician urged him to undergo a complete cardiac evaluation to rule in or out an acute coronary syndrome. Interestingly, the patient insisted on sending digitally for tele-consultation a lead-I tracing recorded by his Samsung Galaxy Watch 4 (Samsung Electronics) worn on his left wrist.

MACULAR HOLE HYDRODISSECTION TECHNIQUE WITH HUMAN AMNIOTIC MEMBRANE FOR REPAIR OF LARGE MACULAR HOLES.

PURPOSE: To describe a combined surgical technique using the macular hole hydrodissection (MHH) with human amniotic membrane for repair of large macular holes. METHODS: A step-by-step procedure and a surgical video using the combined MHH and human amniotic membrane technique are presented. DESCRIPTION AND TECHNIQUE: As the first step, the MHH separates the adhesions of the macular hole to the underlying retinal pigment epithelium with a soft-tipped cannula through proportional reflux followed by gentle passive aspiration. The human amniotic membrane graft is marked to identify the nonsticky epithelial side and ensure that the stromal layer (sticky and nonshinny) is facing downward toward the retinal pigment epithelium. The graft is then tucked into the space created with MHH between the macular hole edges and the retinal pigment epithelium with closed forceps to decrease the likelihood of the graft from dislocating postoperatively. CONCLUSION: The MHH in combination with the human amniotic membrane is a practical and effective technique for addressing challenging large macular holes.

Radial Artery Spasm, Excision of Avulsed Fragment and Uncompromised Flow: An Oxymoron in Invasive Cardiology.

Transradial access may lead to anatomical and functional changes on the vessel wall due to puncture or material-associated trauma, inflammation and loss of endothelium's nitric oxide vasodilatory response. Despite the superficial and palpable radial artery course, caution and dexterity are important assets when puncturing, wiring, inserting the sheath, or maneuvering the catheters. Radial artery anatomic variations, tortuosity, and radial artery spasm are related with femoral access switch. The outer diameter of sheaths and catheters needs to match radial artery internal diameter; otherwise, friction or vascular stretch will occur, activating the surface endothelium and the coagulation cascade. Friction between the arterial wall and the equipment worsens endothelial function and precipitates patient discomfort, radial artery spasm, and ultimately, radial artery occlusion.

Levosimendan in the Treatment of Patients with Severe Septic Cardiomyopathy.

(1) Background: The optimal treatment of septic cardiomyopathy (SCM) remains questionable. The aim of the study was to compare the treatment of SCM based on levosimendan versus the best available therapy. (2) Methods: We conducted an observational study including patients with severe septic cardiomyopathy and circulatory failure. (3) Results: Fourteen patients (61%) received levosimendan, and nine received other treatments. The patients in the levosimendan group were more severely ill [APACHE II: 23.5 (14, 37) vs. 14 (13, 28), respectively, p = 0.012], and there was a trend for more decompensated LV function depicted by the LVEF [15% (10, 20) vs. 25% (5, 30), respectively, p = 0.061]. However, they presented a significantly higher increase in LVEF after seven days [15% (10, 20) to 50% (30, 68) (p < 0.0001) vs. 25% (5, 30) to 25% (15, 50) (p = 0.309), and a significantly higher decrease in lactate levels during the first 24 h [4.5 (2.5, 14.4) to 2.85 (1.2, 15), p = 0.036 vs. 2.9 (2, 18.9) to 2.8 (1, 15), p = 0.536]. Seven-day survival (64.3% vs. 33.3%, p = 0.424) and ICU survival (50% vs. 22.2%, p = 0.172) were higher in the first group, although differences did not reach statistical significance. The degree of left ventricular impairment and the magnitude of EF improvement by the seventh-day post-SCM onset were associated with mortality in regression analysis. (4) Conclusions: Our study presents main hemodynamic data supporting the possible efficacy of levosimendan treatment in patients with severe SCM.

Cardiac and central vascular functional alterations in the acute phase of aneurysmal subarachnoid hemorrhage.

OBJECTIVES: To investigate aortic functional alterations in the acute phase of aneurysmal subarachnoid hemorrhage and to evaluate the relationship between potential cardiovascular alterations and delayed cerebral infarctions or poor Glasgow Outcome Scale score at discharge from critical care unit. DESIGN: Prospective observational study. SETTING: Critical Care Departments of two tertiary centers. PATIENTS: Thirty-seven patients with aneurysmal subarachnoid hemorrhage. INTERVENTIONS: Patients were evaluated at two time points: on admission (acute aneurysmal subarachnoid hemorrhage phase) and at least 21 days later (stable aneurysmal subarachnoid hemorrhage state). At baseline, the severity of aneurysmal subarachnoid hemorrhage was assessed clinically (Hunt and Hess scale) and radiologically (brain computed tomography Fisher grading). Aortic elasticity was evaluated by Doppler-derived pulse-wave velocity and left ventricular function by echocardiography. Serum B-type natriuretic peptide and troponin I were also assessed at the same time points. MEASUREMENTS AND MAIN RESULTS: At the acute phase, 23 patients (62%) were found to present supranormal pulse-wave velocity and 14 patients (38%) presented left ventricular systolic dysfunction; there were significant associations between pulse-wave velocity values and left ventricular ejection fraction (p < .001). Left ventricular ejection fraction and pulse-wave velocity were both associated with Hunt and Hess (p ≤ .004) and Fisher grading (p ≤ .03). Left ventricular ejection fraction and pulse-wave velocity were improved between acute aneurysmal subarachnoid hemorrhage and stable state (p ≤ .005); changes (Δ%) were greater in patients who initially had regional wall motion abnormalities compared to patients who had not (28.7% ± 10.2% vs. 2.4% ± 1.8% [p = .002] and -17.9% ± 3.7% vs. -3.5% ± 4.7% [p = .045], respectively). Pulse-wave velocity/left ventricular ejection fraction ratio was the only independent predictor for delayed cerebral infarctions. Left ventricular ejection fraction, B-type natriuretic peptide, pulse-wave velocity, and pulse-wave velocity/left ventricular ejection fraction showed significant diagnostic performance for predicting delayed cerebral infarctions or poor Glasgow Outcome Scale score (1-3). CONCLUSIONS: Our findings suggest that significant cardiovascular alterations in left ventricular function and in aortic stiffness occur during the early phase of aneurysmal subarachnoid hemorrhage. These phenomena were associated with adverse outcomes in this study and their role in the pathogenesis of delayed neurologic complications warrants further investigation.

Sepsis-associated takotsubo cardiomyopathy can be reversed with levosimendan.

Sepsis is a stressful physical condition, and at the acute phase, overstimulation of the sympathetic nervous system may occur; these events have the potential to induce cardiomyopathy. Takotsubo cardiomyopathy (TTC) is a form of catecholamine-induced cardiomyopathy, which occurs very rarely in sepsis. However, TTC management in critically ill patients with sepsis may be challenging because the use of exogenous catecholamines for circulatory support might augment further TTC. Herein, we report a rare case of TTC after urosepsis; and we point out that cardiac function may improve after catecholamine withdrawal and the application of calcium channel sensitizer levosimendan.