Right Ventricular Enlargement within Months of Arteriovenous Fistula

Creation in 2 Hemodialysis Patients

Summary:

In this topic they are using mixed effects models, they observed

adverse changes in rMSSD , SDNN, TpTe, heart rate turbulence, systolic and
diastolic blood pressures, C-reactive protein, and fibrinogen associated with
interquartile range increases in UFP, AMP, and PM2.5 at 1 or more lag times
within the previous 5 days. Acute increases in blood pressure increase myocardial
work and oxy gen consumption, and together with increased coagulation and
inflammation, may worsen cardiac ischemia in post infarction patients. The
magnitudes of estimated effects for individual outcomes were small, but in
combination may increase the risk of myocardial ischemia, contribute to parasym
pathetic withdrawal, and increase myocardial vulnerability to arrhythmias and
post infarction adverse remodeling that increase the risk of CV events in this
susceptible population.
Reaction:

In ARSHF its been observed that there is acute increases in blood

pressure and increases in blood pressure and increase myocardial work and may
lead to poor oxygenation. While in consumed the heart to pump more it is also
increases its coagulation at may cause to inflammation and this will leads to be
worsen cardiac ischemia in post myocardial infarction in patients with RSHF. It is

concluded that increase myocardial ischemia will manifest parasympathetic

withdrawal of blood at it will increase myocardial infarction to arrhythmias.

The effects of iodixanol and iopamidol on adhesion molecule serum levels in

patients with angina pectoris undergoing coronary angiography: a
randomized study

SUMMARY: For these reasons in their study, peripheral venous blood samples
to measure the CAM serum levels were taken just before and 12 hours after CAG.
In a previous different study, inflammatory markers increased following exposure
to both ionic and non-ionic RCM during CAG. The level of increase was lower
with non-ionic RCM. In current study's subgroup analyses; in patients who
received non-ionic RCM, LO iopamidol during CAG, levels of both ICAM-1 and
VCAM-1 increased significantly in patients with USAP and increased with a
borderline significance in patients with SAP. These findings suggest that LO
iopamidol may induce release of both AMs in patients with unstable and stable
atherosclerotic plaque. Although associations between increments in soluble
ICAM-1 or VCAM-1 levels following percutaneous coronary intervention and
restenosis have been detected, there have been studies about the relationship
between AM levels and stent thrombosis; clinical significance of proinflammatory or AM inducing effects of CAG and its long-term consequences
have not been studied. This is the first study which indicates, ICAM-1 and
VCAM-1 inducing effect of diagnostic CAG in patients with SAP or USAP and

differential effects of iodixanol and iopamidol on ICAM-1 and VCAM-1 serum

levels.
REACTION: This article is good because they aimed to compare the baseline
ICAM-1 and VCAM-1 serum levels between patients with SAP and USAP
undergoing diagnostic CAG, to investigate effects of CAG on basal ICAM-1
and/or VCAM-1 levels in patients with SAP and USAP; probable different effects
of non-ionic RCM, IO iodixanol and LO iopamidol, on these sCAMs. If a lower
impact on the CAMs can be detected for one of these RCM, it may be reasonable
to prefer that agent for coronary procedures. This study is more useful parameter
for detecting increased inflammation, plaque destabilization and culprit lesion.