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Objectives of this study were (1) to evaluate preoperative predictors of systolic and diastolic heart failure in patients undergoing liver transplantation (LT) and (2) to describe the prognostic implications of systolic and diastolic heart failure in these patients. The onset of heart failure after orthotopic LT remains poorly understood. Data were obtained for all LT recipients between January 2000 and December 2010. The primary outcome was post-LT heart failure: systolic (ejection fraction 50%), diastolic, or mixed heart failure. Patients underwent echocardiographic evaluation before and after LT. Pretransplant variables were evaluated as predictors of heart failure with Cox proportional hazards model. 970 LT recipients were followed for 5.3 6 3.4 years. Ninety-eight patients (10.1%) developed heart failure in the posttransplant period. There were 67 systolic (6.9%), 24 diastolic (2.5%), and 7 mixed systolic/diastolic (0.7%) heart failures. Etiology was ischemic in 18 (18.4%), tachycardia-induced in 8 (8.2%), valvular in 7 (7.1%), alcohol-related in 4 (4.1%), hypertensive heart disease in 3 (3.1%), and nonischemic in majority of patients (59.2%). Pretransplant grade 3 diastolic dysfunction, diabetes, hypertension, mean arterial pressure 65 mm Hg, mean pulmonary artery pressure 30 mm Hg, mean pulmonary capillary wedge pressure 15 mm Hg, hemodialysis, brain natriuretic peptide level and QT interval > 450 ms were found to be predictive for the development of new-onset systolic heart failure. However beta-blocker use before LT and tacrolimus after LT were associated with reduced development of new-onset systolic heart failure. In conclusion, pretransplant risk factors, hemodynamic variables, and echocardiographic variables are important predictors of post-LT heart failure. In patients undergoing LT, postoperative onset of systolic or diastolic heart failure was found to be an independent predictor of mortality.

Although there is a substantial amount of research on the neurological consequences of traumatic brain injury (TBI), there is a knowledge gap regarding the relationship between TBI and the pathophysiology of organ system dysfunction and autonomic dysregulation. In particular, the mechanisms or incidences of renal or cardiac complications after TBI are mostly unknown. Autonomic dysfunction following TBI exacerbates secondary injury and may contribute to nonneurologial complications that prolong hospital length of stay. Gaining insights into the mechanisms of autonomic dysfunction can guide advancements in monitoring and treatment paradigms to improve acute survival and long-term prognosis of TBI patients. In this paper, the authors will review the literature on autonomic dysfunction after TBI and possible mechanisms of paroxysmal sympathetic hyperactivity. Specifically, they will discuss the link among the brain, heart, and kidneys and review data to direct future research on and interventions for TBI-induced autonomic dysfunction.

Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the new coronavirus responsible for the coronavirus disease (COVID-19), characterized by acute respiratory distress syndrome and atypical pneumonia. In non-pregnant women, studies have shown that SARS-CoV-2 causes cardiac injury, which can result in myocardial inflammation and damage. Despite many studies investigating the extent of cardiac compromise in severely ill COVID-19 patients, little is known regarding its impact on pregnant women. Objective To illustrate the clinical, laboratory, radiological findings, and outcomes of COVID-19 pregnant patients who developed myocardial injury with ventricular dysfunction. Study Design We retrospectively reviewed the paper records of fifteen pregnant women with COVID-19, who developed myocardial injury on a single tertiary care hospital in the Dominican Republic. Patient's baseline characteristics, clinical picture, laboratory, and radiological findings were presented, and maternal and fetal outcomes were analyzed. Results Of 154 pregnant patients diagnosed with COVID-19 at our hospital during the study period, 15 (9.7%), developed myocardial injury. These patients' mean age and gestational age were 29.87 ± 5.83 and 32.31 ± 3.68, respectively. 66.7% of patients presented with shortness of breath and 16.3% with palpitations. All patients were admitted to the intensive care unit, and 86.6% needed intubation. Patients developed myocardial injury confirmed with highly elevated troponin (34.6 [14.4-55.5 ng/ml]), and pro-BNP concentrations (209 [184-246 pg/ml]). Additionally, all patients developed left ventricular dysfunction demonstrated by an echocardiogram with a mean left ventricular ejection fraction (LVEF) of 37.67 ± 6.4 %. Two patients that presented with palpitations passed away a few days after admission. Conclusion Our study showed COVID-19 induced myocardial injury and left ventricular dysfunction in pregnant women with a 13.3% mortality rate which was attributed to malignant arrhythmias.