Early left ventricular ejection fraction as a predictor of survival after cardiac arrest.

BACKGROUND: Cardiopulmonary resuscitation and early defibrillation have been shown to improve outcomes of cardiac arrest. The significance of the post-arrest echocardiogram, specifically the left ventricular ejection fraction (LVEF) is unknown. METHODS: We performed a retrospective cohort study of patients who suffered from cardiac arrest between 1 January 2009 and 31 December 2013. We included all patients who achieved return of spontaneous circulation (ROSC), and were admitted to the intensive care unit (ICU) or coronary care unit (CCU) of a tertiary care academic center. Patients who underwent echocardiography within 24 h of cardiac arrest were included for analysis. The primary outcome was survival. RESULTS: We identified 151 patients who achieved ROSC of which 97 underwent post-arrest echocardiogram within 24 h. 70.8% were males and the mean age was 67.8 years (SD: 15.9). The mean LVEF at 24 h was 35.7 (SD: 17.8). LVEF > 40% was not a predictor of survival at 30 days or hospital discharge. The only significant predictors on multivariate analyses were age, presence of shockable rhythm and time to ROSC. CONCLUSION: Although echocardiograms are frequently ordered, LVEF greater than 40% in patients who are resuscitated after a cardiac arrest is not a predictor of survival.

Mechanical ventilation with high tidal volume and associated mortality in the cardiac intensive care unit.

BACKGROUND AND OBJECTIVES: Use of protective ventilation has been shown to decrease mortality in medical-surgical ICUs. There is limited data on tidal volume use in ventilated patients in the cardiac intensive care unit (CICU). We hypothesized that large tidal volumes are used in the CICU and that they could contribute to an increase in morbidity and mortality. METHODS: We conducted a retrospective chart review of all mechanically ventilated patients with congestive heart failure or cardiac arrest in a single tertiary care CICU between April 2010 and February 2012. Ventilator settings were analyzed and tidal volume for predicted body weight (VT/PBW) was calculated for 51 patients. RESULTS: The median initial tidal volume was 525 ml (IQR: 500-600) and median VT/PBW was 9.3 ml/kg (IQR: 8.3-10.1). Overall mortality was 29.4%. On univariate analysis, patients that received a VT/PBW below the median, mortality was 23.1% (95% CI: 7.9-39.3) compared to 36.0% (95% CI: 17.2-55.0) in patients that received a VT/PBW above themedian (P = 0.31). On multivariate analysis, the OR for death was 9.0 (95% CI: 1.3-62.0, P = 0.03) with VT/PBW above the median. CONCLUSION: Mechanical ventilation with high tidal volumes was associated with increased mortality in patients with congestive heart failure and post cardiac arrest in our CICU.

APOE p.Leu167del mutation in familial hypercholesterolemia.

BACKGROUND: Autosomal dominant hypercholesterolemia (ADH) is caused by mutations in the low density lipoprotein receptor (LDLR), its ligand apoB (APOB) or proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. Yet DNA sequencing does not identify mutations in these genes in a significant number of cases, suggesting that ADH has multiple genetic etiologies. METHODS: Through a combination of clinical examination, biochemical analysis, candidate gene approach and next-generation exome sequencing we investigated the genetic basis of an ADH phenotype in a proband of an Italian origin. RESULTS: The proband presented with an acute myocardial infarction at age 43. He had tendinous xanthomas, xanthelasmas and elevated levels of total and LDL cholesterol, at 11.2 and 9.69 mmol/L, respectively, with normal levels of HDL cholesterol and triglycerides at 1.62 and 1.13 mmol/L, respectively. HPLC lipoprotein profile showed selective increase in LDL-C. DNA sequencing did not identify any mutation in the LDLR, PCSK9, LDLRAP1 and APOB gene. We then performed exome sequencing on three individuals from the family. The strongest evidence of association was found for the previously identified apolipoprotein E mutation (APOE, chromosome 19:45412053-55) known as APOE Leu167del, an in-frame three base-pair deletion. Computational biology confirmed the deleterious nature of this mutation. The Leu167del mutation is predicted to alter the protein structure of apoE near the α-helix within the receptor binding domain. CONCLUSIONS: This report confirms a previous report that ADH can be caused by mutations within the APOE gene and represents the 4th loci causing ADH. Standard screening for ADH should include APOE gene.