No abstract

Objective We aimed to determine if the severity of inhalation injury evokes an immune response measurable at the systemic level and to further characterize the balance of systemic pro- and anti-inflammation early after burn and inhalation injury. Summary Background Data Previously we reported that the pulmonary inflammatory response is enhanced with worse grades of inhalation injury, and that those who die from their injuries have a blunted pulmonary immune profile compared to survivors. Methods From August 2007 to June 2011, bronchoscopy was performed on 80 patients admitted to the burn intensive care unit when smoke inhalation was suspected. Of these, inhalation injury was graded into one of five categories (0, 1, 2, 3, and 4), with Grade 0 being the absence of visible injury and Grade 4 corresponding to massive injury. Plasma was collected at the time of bronchoscopy and analyzed for 28 immunomodulating proteins via multiplex bead array or ELISA. Results The concentrations of several plasma immune mediators were increased with worse inhalation injury severity, even after adjusting for age and % TBSA. These included interleukin (IL)-1RA (p=0.002), IL-6 (p=0.002), IL-8 (p=0.026), granulocyte colony stimulating factor (p=0.002), and monocyte chemotactic protein (MCP)-1 (p=0.007). Differences in plasma immune mediator concentrations in surviving and deceased patients were also identified. Briefly, plasma concentrations of IL-1RA, IL-6, IL-8, IL-15, Eotaxin, and MCP-1 were higher in deceased patients compared to survivors (p<0.05 for all), while IL-4 and IL-7 were lower (p<0.05). After adjusting for the effects of age, % TBSA, and inhalation injury grade, plasma IL-1RA remained significantly associated with mortality (OR 3.12, 95% CI 1.03–9.44). Plasma IL-1RA also correlated with % TBSA, inhalation injury grade, fluid resuscitation, Baux score, revised Baux score, Denver score, and the Sequential Organ Failure Assessment score. Conclusion The severity of smoke inhalation injury has systemically reaching effects, which argues in favor of treating inhalation injury in a graded manner. Additionally, several plasma immune mediators measured early after injury were associated with mortality. Of these, IL-1RA appeared to have the strongest correlation with injury severity and outcomes measures, which may explain the blunted pulmonary immune response we previously found in non-survivors.

; societ a Italiana di cardiologia and the CCU academy investigators group. Reduction of hospitalizations for myocardial infarction in Italy in the COVID-19 era.

No abstract

Patients with chronic kidney disease (CKD) are at increased risk for stroke. High-sensitivity troponin (hsTP), a marker of myocardial injury, has been associated with stroke risk in patients without CKD, but whether this applies to patients with CKD is not known. We assessed whether hsTP levels is associated with incident stroke in patients with mild-to-moderate CKD without a history of stroke enrolled in the Chronic Renal Insufficiency Cohort. Patients were followed for incident stroke, and the association with hsTP was assessed. A total of 3477 patients without prior stroke were included in this investigation. Over a median follow-up of 7.3 years, 101 (2.8%) patients had an incident stroke. Baseline hsTP was associated with a 9-year risk of stroke (quartile 1: 1.8%, quartile 2: 3.8%, quartile 3: 4.9%, quartile 4: 7.3%; P < .001). After adjusting for traditional stroke risk factors, patients in the fourth quartile (hazard ratio: 2.52, 95% CI: 1.10-5.76, P = .021) had higher risk of stroke when compared with the lowest quartile of hsTP. In conclusion, hsTP levels are associated with increased risk of incident stroke in patients with mild to moderate CKD, and this association remains significant despite the adjustment for traditional risk factors and CKD.

Background The global pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused significant morbidity and mortality, not only through devastating lung injury, but also due to multiple malfunctions in the cardiovascular system. The primary aetiology is believed to be mediated through lung alveolar injury; however, a few published reports have linked SARS-CoV-2 to significant organ dysfunction, venous thrombo-embolism, and coagulopathy. In view of the fact that the utility of tissue plasminogen activator in this population is not well studied, we present this case of rapid improvement in oxygenation after successful lytic therapy for thrombus in transit in this patient with SARS-CoV-2. Case summary We discuss a patient admitted with SARS-CoV-2 pneumonia. Due to the development of dramatic hypoxia, he underwent echocardiography which demonstrated extensive thrombus in transit. He received successful thrombolytic therapy with tissue plasminogen activator, with subsequent improvement in oxygenation. The patient was successfully discharged home on 2 L of oxygen via nasal cannula, and continues to improve at follow-up with his cardiologist and primary care physician. Conclusion This case not only highlights embolic causes of hypoxia in SARS-CoV-2, but demonstrates the important utility of an echocardiogram and tissue plasminogen activator in this population.

Heart failure (HF) is one of the leading causes of cardiovascular morbidity and mortality in the ever-growing population of patients with chronic kidney disease (CKD). There is a need to enhance early prediction to initiate treatment in CKD. We sought to study the feasibility of a multi-variable biomarker approach to predict incident HF risk in CKD.

No abstract