Thursday, February 23, 2017

Point of care chest ultrasound

Here is a review of its usefulness as a clinical tool, excluding cardiac applications.

Wednesday, February 22, 2017

Pnuemonia in comatose patients post cardiac arrest

75% of patients developed pneumonia!

Methods: We identified consecutive patients undergoing targeted temperature management following OHCA secondary to a shockable rhythm (ventricular tachycardia or fibrillation). To address survival bias we excluded patients who died within 48 hours of hospital admission. We then compared clinical outcomes between patients with and without pneumonia. The primary outcome was severe neurologic dysfunction as defined by a cerebral performance category (CPC) ≥3; secondary outcomes included duration of mechanical ventilation and length of stay in hospital and in the cardiac intensive care unit (CICU).

Results: Of 116 patients included (mean age 57 years, mean downtime 24 min, 22% female, 47% STEMI), 87 (75%) developed pneumonia. Patients who developed pneumonia were older; baseline patient and index event characteristics were otherwise comparable between the two cohorts. The most common pathogens isolated included Staphylococcus aureus, Haemophilus influenza, Streptococcal species and Klebsiella species. Piperacillin/tazobactam and cephalosporins were used to treat the majority of patients. The incidence of the primary outcome (28%) was comparable in patients with versus without pneumonia. However, compared to patients without pneumonia, OHCA patients with pneumonia required longer periods of mechanical ventilation and longer lengths of stay in hospital and in the CICU.

Tuesday, February 21, 2017

Your GI bleeding patient is on antiplatelet therapy. Should you transfuse platelets?

From a recent retrospective cohort study:

Background & Aims

Antiplatelet agents decrease cardiovascular events but increase gastrointestinal bleeding (GIB). Guidelines propose platelet transfusion for patients who take antiplatelet agents and have serious GIB. We investigated whether such patients are at decreased risk for rebleeding or increased risk for cardiovascular events after platelet transfusion.


We performed a retrospective cohort study of patients with GIB admitted to Yale-New Haven Hospital from 2008 to 2013 who were taking antiplatelet agents and had platelet counts higher than 100 × 109/L. Cases (patients who received platelet transfusion, n = 204) were matched with controls (no platelet transfusions, n = 204) for sex, age, and GIB location. The primary outcome was recurrent GIB. Multivariable regression analyses were performed to adjust for differences in baseline characteristics.


Cases and controls had similar proportions of GIB due to non-variceal upper GIB (117 of 204, 57% vs 115 of 204, 56%) and colonic GIB (80 of 204, 39% vs 81 of 204, 40%). Cases had more severe GIB than controls, which was based on lower blood pressure and hemoglobin levels and higher heart rates and the proportion admitted to intensive care. Univariate analyses showed that higher proportions of cases had major cardiovascular events (23% vs 13% for controls), died (7% vs 1% for controls), or had hospital stay longer than 4 days (47% vs 33% for controls). However, multivariable analyses showed a significant difference between cases and controls in only risk of death (odds ratio, 5.57; 95% confidence interval, 1.52–27.1). The adjusted odds ratio for recurrent bleeding was 1.47 (95% confidence interval, 0.73–3.05) for cases vs controls.


The use of platelet transfusions in patients with GIB who are taking antiplatelet agents without thrombocytopenia did not reduce rebleeding but was associated with higher mortality. At least some of the increase in mortality could be due to the residual bias of an observational study, but because of the lack of benefit, we do not support the use of platelet transfusions in patients with GIB who are taking antiplatelet agents.

Sunday, February 19, 2017

Genetic variants and the efficacy of clopidogrel in stroke and TIA

Background: The association of genetic polymorphisms and clopidogrel efficacy in patients with ischemic stroke or transient ischemic attack (TIA) remains controversial. We performed a systematic review and meta-analysis to assess the association between genetic polymorphisms, especially CYP2C19 genotype, and clopidogrel efficacy for ischemic stroke or TIA.

Methods: We conducted a comprehensive search of PubMed and EMBASE from their inceptions to June 24, 2016. Studies that reported clopidogrel-treated patients with stroke or TIA and with information on genetic polymorphisms were included. The end points were stroke, composite vascular events, and any bleeding.

Results: Among 15 studies of 4762 patients with stroke or TIA treated with clopidogrel, carriers of CYP2C19 loss-of-function alleles (*2, *3, and *8) were at increased risk of stroke in comparison with noncarriers (12.0% versus 5.8%; risk ratio, 1.92, 95% confidence interval, 1.57–2.35; P less than 0.001). Composite vascular events were also more frequent in carriers of CYP2C19 loss-of-function alleles than in noncarriers (13.7% versus 9.4%; risk ratio, 1.51, 95% confidence interval, 1.10–2.06; P=0.01), whereas bleeding rates were similar (2.4% versus 3.1%; risk ratio, 0.89, 95% confidence interval, 0.58–1.35; P=0.59). There was no evidence of statistical heterogeneity among the included studies for stroke, but there was for composite vascular events. Genetic variants other than CYP2C19 were not associated with clinical outcomes, with the exception that significant associations of PON1, P2Y12, and COX-1 with outcomes were observed in 1 study.

Conclusions: Carriers of CYP2C19 loss-of-function alleles are at greater risk of stroke and composite vascular events than noncarriers among patients with ischemic stroke or TIA treated with clopidogrel.

Saturday, February 18, 2017

More evidence for obesity as a risk factor for atrial fibrillation

From a recently published study:


We analyzed data from 2,717 participants of the Health, Aging, and Body Composition Study. Adiposity measures were BMI, abdominal circumference, subcutaneous and visceral fat area, and total and percent fat mass. We determined the associations between the adiposity measures and 10-year incidence of AF using Cox proportional hazards models and assessed for their racial differences in these estimates.


In multivariable-adjusted models, 1-SD increases in BMI, abdominal circumference, and total fat mass were associated with a 13% to 16% increased AF risk (hazard ratio [HR] 1.14, 95% CI 1.02-1.28; HR 1.16, 95% CI 1.04-1.28; and HR 1.13, 95% CI 1.002-1.27). Subcutaneous and visceral fat areas were not significantly associated with incident AF. We did not identify racial differences in the associations between the adiposity measures and AF.


Body mass index, abdominal circumference, and total fat mass are associated with risk of AF for 10 years among white and black older adults. Obesity is one of a limited number of modifiable risk factors for AF; future studies are essential to evaluate how obesity reduction can modify the incidence of AF.

The evidence is mounting that obesity is a risk factor for atrial fibrillation. The extent to which weight loss intervention will impact atrial fibrillation is less clear.

Friday, February 17, 2017

Performance linked to MI survival???

The title to a recent NEJM paper, Life Expectancy after Myocardial Infarction, According to Hospital Performance, (and there was a positive correlation) is deceptive. From the paper:


We analyzed data from the Cooperative Cardiovascular Project, a study of Medicare beneficiaries who were hospitalized for acute myocardial infarction between 1994 and 1996 and who had 17 years of follow-up. We grouped hospitals into five strata that were based on case-mix severity. Within each case-mix stratum, we compared life expectancy among patients admitted to high-performing hospitals with life expectancy among patients admitted to low-performing hospitals. Hospital performance was defined by quintiles of 30-day risk-standardized mortality rates. Cox proportional-hazards models were used to calculate life expectancy.


The study sample included 119,735 patients with acute myocardial infarction who were admitted to 1824 hospitals. Within each case-mix stratum, survival curves of the patients admitted to hospitals in each risk-standardized mortality rate quintile separated within the first 30 days and then remained parallel over 17 years of follow-up. Estimated life expectancy declined as hospital risk-standardized mortality rate quintile increased. On average, patients treated at high-performing hospitals lived between 0.74 and 1.14 years longer, depending on hospital case mix, than patients treated at low-performing hospitals. When 30-day survivors were examined separately, there was no significant difference in unadjusted or adjusted life expectancy across hospital risk-standardized mortality rate quintiles.


In this study, patients admitted to high-performing hospitals after acute myocardial infarction had longer life expectancies than patients treated in low-performing hospitals. This survival benefit occurred in the first 30 days and persisted over the long term.

The time in question for this study, 1994-1996, was quite a bit before what we know today as the performance movement, in the forms of public reporting and pay incentives, was underway. So what is termed performance in this paper has little to do with performance as the phony surrogate for quality as we know it today. What this study really shows is that hospitals with good overall outcomes also have better outcomes in the more narrowly focused category of myocardial infarction.