Outcomes of extracorporeal membrane oxygenation support in the cardiac catheterization laboratory.

OBJECTIVES: The aims of this single-center retrospective study were to characterize and determine predictors of 30-day survival in a cohort of patients requiring venoarterial extracorporeal membrane oxygenation (VA-ECMO) supported cardiopulmonary resuscitation (E-CPR) in the cardiac catheterization laboratory (CCL) for cardiac arrest (CA) or refractory cardiogenic shock (CS). BACKGROUND: While safety in the CCL has improved, periprocedural mortality from CA remains high. The application of VA-ECMO is an emerging form of resuscitation with a paucity of data evaluating its use in the CCL for CA or CS. METHODS: All consecutive patients aged 18 years or older presenting to a single CCL from October 2010 to May 2018 who required E-CPR for CA or refractory CS were included. The primary outcome of our study was overall survival 30 days from VA-ECMO initiation. Secondary outcomes included 1-year survival, hospital length of stay, and ECMO related complications. RESULTS: Sixty-two patients with a mean age of 60 ± 9 years, 63% male, were included. VA-ECMO was initiated for CA in 39 patients (63%) and for CS in 23 patients (37%). The median ECMO duration was 48 hr. Overall 30-day survival was 47% (CA group 44% vs. CS group 52%; p = .414). One-year survival was 44%. Initial serum creatinine (OR 1.18 per 10 µmol/L increase; p = .016; AUC = 0.65) was the only multivariate predictor of 30-day mortality. CONCLUSIONS: The use of VA-ECMO in the CCL is feasible, demonstrating 47% 30-day survival, largely persistent to 1 year, in a cohort that otherwise has extremely high mortality.

The biofilm-specific antibiotic resistance gene ndvB is important for expression of ethanol oxidation genes in Pseudomonas aeruginosa biofilms.

Bacteria growing in biofilms are responsible for a large number of persistent infections and are often more resistant to antibiotics than are free-floating bacteria. In a previous study, we identified a Pseudomonas aeruginosa gene, ndvB, which is important for the formation of periplasmic glucans. We established that these glucans function in biofilm-specific antibiotic resistance by sequestering antibiotic molecules away from their cellular targets. In this study, we investigate another function of ndvB in biofilm-specific antibiotic resistance. DNA microarray analysis identified 24 genes that were responsive to the presence of ndvB. A subset of 20 genes, including 8 ethanol oxidation genes (ercS', erbR, exaA, exaB, eraR, pqqB, pqqC, and pqqE), was highly expressed in wild-type biofilm cells but not in ΔndvB biofilms, while 4 genes displayed the reciprocal expression pattern. Using quantitative real-time PCR, we confirmed the ndvB-dependent expression of the ethanol oxidation genes and additionally demonstrated that these genes were more highly expressed in biofilms than in planktonic cultures. Expression of erbR in ΔndvB biofilms was restored after the treatment of the biofilm with periplasmic extracts derived from wild-type biofilm cells. Inactivation of ethanol oxidation genes increased the sensitivity of biofilms to tobramycin. Together, these results reveal that ndvB affects the expression of multiple genes in biofilms and that ethanol oxidation genes are linked to biofilm-specific antibiotic resistance.

Using the Zwolle Risk Score at Time of Coronary Angiography to Triage Patients With ST-Elevation Myocardial Infarction Following Primary Percutaneous Coronary Intervention or Thrombolysis.

Background The Zwolle Risk Score was designed to identify the risk of complications in patients with ST-segment‒elevation myocardial infarction (STEMI) following percutaneous coronary intervention (PCI). Its utility following PCI in STEMI treated with thrombolysis is unknown. The objective was to evaluate the safety of using the Zwolle Risk Score to triage patients with STEMI following PCI, including patients receiving thrombolysis. Methods and Results Patients aged ≥18 years with STEMI and primary PCI or PCI after thrombolysis were included. A triage protocol was developed, with high-risk patients those with Zwolle Risk Score ≥4 triaged to the cardiac intensive care unit. A prospective evaluation of the triaging protocol was performed on 452 patients, mean age 65±12 years, 73% men. Median Zwolle Risk Score was 3 (interquartile range, 2‒5), with 257 low-risk (57%), and 195 high-risk (43%) patients. Adherence to the protocol was 91%. In-hospital mortality was 0.4% in low-risk and 13% in high-risk patients (P<0.001). Seventy-two patients (16%) received thrombolysis. Median time post-thrombolysis to PCI was 281 minutes (interquartile range, 219‒376). In-hospital mortality was 0% versus 9% (P=0.083) for low- and high-risk patients, respectively. High-risk patients had higher rates of cardiogenic shock (34% versus 1%, P<0.001), pulmonary edema (60% versus 9%, P<0.001), arrhythmia (25% versus 2%, P<0.001), blood transfusion (10% versus 2%, P<0.001), and stroke (4% versus 0.4%, P=0.011). Median hospital costs decreased by $1419 per low-risk patient after protocol implementation. Conclusions For patients with STEMI following primary PCI or PCI following thrombolysis, a Zwolle-based triaging system is safe and may decrease cardiac intensive care unit usage costs.

Spinal Epidural Hematoma Secondary to Tenecteplase for ST-Elevation Myocardial Infarction in the Setting of Trauma and Cervical Endplate Fracture.

A 78-year-old woman presented with an inferior ST-segment elevation myocardial infarction in the setting of a fall resulting in facial trauma causing an unrecognized C6 cervical endplate fracture. After administration of tenecteplase, she developed a spinal epidural hematoma requiring intubation for airway protection and cessation of antiplatelet therapies. The need to delay coronary intervention in this setting led to a recurrent inferolateral ST-segment elevation myocardial infarction that eventually required coronary bypass grafting. In the first report of a spinal epidural hematoma after tenecteplase for ST-segment elevation myocardial infarction, we emphasize the need for imaging after significant trauma before initiating thrombolysis.

Une femme de 78 ans a été vue en consultation pour un infarctus du myocarde inférieur avec élévation du segment ST, dans un contexte de trauma facial entraîné par une chute, causant une fracture du plateau vertébral de C6 non diagnostiquée. Après avoir reçu du ténectéplase, la patiente a présenté un hématome épidural rachidien ayant nécessité l'intubation pour protéger les voies respiratoires et l'arrêt des traitements antiplaquettaires. La nécessité de retarder l'intervention coronarienne dans ce contexte a entraîné un nouvel infarctus du myocarde inférolatéral avec élévation du segment ST, ayant par la suite nécessité un pontage aortocoronarien. Relativement au premier rapport d'hématome épidural rachidien survenu après l'administration de ténectéplase pour le traitement de l'infarctus du myocarde avec élévation du segment ST, nous insistons sur l'importance de procéder, avant d'instaurer la thrombolyse, à des examens d'imagerie chez les patients ayant subi un trauma important.

Apical hypertrophic cardiomyopathy treated as ST-elevation myocardial infarction.

Electrocardiographic changes resulting from apical hypertrophic cardiomyopathy may mimic an acute coronary syndrome. A 67-year-old Sudanese male without cardiac risk factors presented to hospital with chest pain and electrocardiographic findings of septal ST-segment elevation, ST-segment depression in V4-V6, and diffuse T-wave inversion. He was treated as an acute ST-elevation myocardial infarction with thrombolytics. There was no cardiac biomarker rise and coronary angiography did not reveal evidence of significant coronary arterial disease. Ventriculography, transthoracic echocardiography, and cardiac magnetic resonance imaging were consistent with apical hypertrophic cardiomyopathy. The patient was discharged three days later with outpatient cardiology follow-up. We highlight the clinical and electrocardiographic findings of apical hypertrophic cardiomyopathy, with an emphasis on distinguishing this from acute myocardial infarction.