Wednesday, February 21, 2018

Raising magnesium awareness


Tuesday, February 20, 2018

Management of long QT



Recent findings

LQT syndrome remains the most common inherited arrhythmia and is a leading cause for sudden unexplained death accounting for up to 20–25% of cases. Rapid progress of genetic technology over the past 2 decades has significantly improved our understanding of molecular and genetic mechanisms of LQT. Despite all those novel insights, phenotype assessment and appropriate risk stratification in LQT remains challenging – even for the expert.

Summary

This review outlines our current understanding and approach to the clinical diagnosis and management of LQT as well as recent insights into genotype–phenotype correlations. Genetic testing has evolved beyond a pure diagnostic tool and is in addition increasingly integrated as complementary prognostic marker. With regard to the management of LQT, there is now evidence that the protective effect of beta-blockers is rather substance-specific than a class effect. Novel approaches – in conjunction with standard beta-blockers – are emerging including gene-specific treatment for certain subtypes of LQT. A specialized inherited arrhythmia clinic is the preferred resource for the complex risk stratification and individualized management of individuals with LQT.

Monday, February 19, 2018

Unexplained anemia in older men related to low T



Question Will testosterone treatment of older men with low testosterone levels and mild anemia improve their anemia?

Findings Testosterone treatment of older men with low testosterone levels and unexplained anemia corrected the anemia more than placebo. This treatment also corrected anemia more than placebo in men who had anemia of known causes, such as iron deficiency.

Meaning Testosterone deficiency in older men results in decreased hemoglobin levels and sometimes in mild anemia. Correcting the testosterone deficiency is associated with increased hemoglobin levels and tends to correct the anemia, even in the presence of a coexisting cause of anemia.


Interesting.

Sunday, February 18, 2018

Low FFR predicted events even in lesions that looked “insignificant”


Report here.

Saturday, February 17, 2018

Local anesthetic toxicity


Friday, February 16, 2018

Pulmonary hypertension in left heart disease



Highlights

•Echocardiographically tricuspid incompetence gradient of ≥40 mm Hg (pulmonary hypertension surrogate) was found in 18% of first echocardiograms.
•Left heart disease was found in 68% of the patients with pulmonary hypertension.
•Valve disease is the most common pathology in this group.
•Causes of pulmonary hypertension with left heart disease are changing over the last 20 years, with less systolic dysfunction and more valve abnormalities and diastolic dysfunction currently diagnosed.
•Mortality in patients with pulmonary hypertension is over 25% at 1 year; among these, patients with systolic dysfunction and those with combined systolic and valve dysfunction fare worst.

Abstract

Introduction

Pulmonary hypertension has many causes. While it is conventionally thought that the most prevalent is left heart disease, little information about its proportion, causes, and implications on outcome is available.

Methods

Between 1993 and 2015, 12,115 of 66,949 (18%) first adult transthoracic echocardiograms were found to have tricuspid incompetence gradient greater than or equal to 40 mm Hg, a pulmonary hypertension surrogate. Left heart disease was identified in 8306 (69%) and included valve malfunction in 4115 (49%), left ventricular systolic dysfunction in 2557 (31%), and diastolic dysfunction in 1776 (21%). Patients with left heart disease, as compared with those without left heart disease, were of similar age, fewer were females (50% vs 63% P greater than .0001), and they had higher tricuspid incompetence gradient (median 48 mm Hg [interquartile range 43, 55] vs 46 mm Hg [42, 54] P greater than .0001). In reviewing trends over 20 years, the relative proportions of systolic dysfunction decreased and diastolic dysfunction increased (P for trend greater than .001), while valve malfunction remained the most prevalent cause of pulmonary hypertension with left heart disease. Independent predictors of mortality were age (hazard ratio [HR] 1.05; 95% CI, 1.04-1.05; P greater than .0001), tricuspid incompetence gradient (HR 1.02; 95% CI, 1.01-1.02, P greater than .0001 per mm Hg increase), and female sex (HR 0.87; 95% CI, 0.83-0.91, P greater than .0001).

Results

Overall, left heart disease was not an independent risk factor for mortality (HR 1.04; 95% CI, 0.99-1.09; P = .110), but patients with left ventricular systolic dysfunction and with combined systolic dysfunction and valve malfunction had increased mortality compared with patients with pulmonary hypertension but without left heart disease (HR 1.30; 95% CI, 1.20-1.42 and HR 1.44; 95% CI, 1.33-1.55, respectively; P greater than .0001 for both).

Conclusions

Pulmonary hypertension was found to be associated with left heart disease in 69% of patients. Among these patients, valve malfunction and diastolic dysfunction emerged as prominent causes. Left ventricular dysfunction carries additional risk to patients with pulmonary hypertension.

Thursday, February 15, 2018

Lactate elevations in critical illness: type a, type b or both?


Here is a recent free full text review.

It points out the following:

Lactate is a semiquantitative indicator of illness severity and risk of mortality. Its elevation indicates need for immediate resuscitative efforts. Decline in the lactate level during resuscitative efforts is a good sign. Lactate elevation can reflect global tissue ischemia. However, in a variety of critical illnesses, even septic shock, lactate is not a reliable indicator of tissue perfusion. This is due to multiple mechanisms, including non ischemic mechanisms, of excess lactate generation. Intense beta receptor stimulation due to high catacholamine levels, for example, increases intracellular cyclic AMP. This results in downstream metabolic effects that drive lactate generation including glycogenolysis (which increases glucose delivery into the glycolytic pathway thus generating lactate) and stimulation of the sodium potassium ATPase which also drives glycolysis. These metabolic (non ischemic) components of lactate generation may not as directly responsive to fluid resuscitation. Thus, using lactate normalization as an endpoint for volume administration may lead to over administration of fluid.