Heart Failure With Preserved Ejection Fraction In Perspective

https://doi.org/10.1161/CIRCRESAHA.119.313572 - 2019;124:1598–1617

Heart failure (HF) was undoubtedly a major contributor to the centuries old
edematous condition, dropsy. As HF was recognized as a leading cause of edema and
dyspnea, the pathophysiologic role of the heart also emerged as is evident from the 1933
Lewis textbook definition of HF “a condition in which the heart fails to discharge its
contents adequately.”1 With the advent of hemodynamic measurements, it became clear that
congestion, the core of the HF syndrome regardless of the cause, was because of elevated
cardiac filling pressures. The more current HF definition “an inability of the heart to pump
blood to the body at a rate commensurate with its needs, or to do so only at the cost of high
filling pressures,” prominently adds this crucial aspect.

While this definition provides a reference standard against which other definitions
can be compared, it is much less transferable to clinical bedside practice where left
ventricular (LV) end-diastolic pressure is not directly measured. Multiple approaches have
been used to clinically define the syndrome of HF based on an integration of the patient’s
history, presentation, physical examination, and laboratory supportive findings to assess
whether HF is present, each with its own advantages and disadvantages. As in many aspects
of medicine, there is a range of diagnostic certainty about the time-honored constellation of
signs and symptoms attributed to HF. Dyspnea, for example, a critical component of HF can
also be a central manifestation of pulmonary disease rather than an aspect of impaired
cardiac performance. The judgment and experience needed to integrate the information
incorporated in the term HF challenges its diagnostic precision.

Despite the ambiguities and overlaps with other chronic conditions, the
unquestionable multifold higher risk for cardiovascular death as well as subsequent repeat
exacerbations of symptoms requiring hospitalizations for HF management of those with this
clinically determined diagnosis offers firm validation that the term has important specificity
and meaning. Indeed, the linkage between this longstanding clinical usage and heightened
risks for HF-specific major adverse events underscores that despite the seemingly inexact
diagnosis, HF denotes a most grave and identifiable medical disorder.

The adverse prognostic impact of a diagnosis of HF on an individual level is greatly

amplified on a population basis because its associated risk is matched by the relatively high
prevalence of HF in older individuals. In the Medicare population, HF is among the most
frequent reason to prompt an urgent hospitalization. The mortality occurring during a
hospitalization for HF is ≈4%. Despite major advances in HF management and care,
mortality within 1 month after discharge is 10%. Because 1 in 5 men and women over 40
years of age will develop HF during their lifetime, the public health burden, and cost to
society are staggering. These sobering statistics use the bedrock clinical definition of the
treating physicians for these assessments of the morbidity-mortality and economic impact
of a diagnosis of HF. It is important to note that neither the cause nor any measure of the
extent of cardiac dysfunction is incorporated into the broad overall definition or adverse
impact of a diagnosis of HF.
 Acute calculous cholecystitis: Review of current best practices
World J Gastrointest Surg. 2017 May 27; 9 (5): 118-126

Acute calculous cholecystitis (ACC) represents the second source of complicated

intra-abdominal infection (18.5%), according to the World Society of Emergency
Surgery complicated intra-abdominal infections Score study. Biliary stones are the main
etiology and are present in 6.5% of men and 10.5% of women. The risk of complications,
like ACC, gallstone pancreatitis, and choledocholithiasis is 1% to 4% per year.
Furthermore, it is recognized that patients with symptomatic cholecystolithiasis will
develop ACC more frequently than their asymptomatic counterparts; thereby, effectively
raising the risk of complications to five times higher.

ACC is the most common complication of cholecystolithiasis accounting for 14%

to 30% of cholecystectomies performed in many countries. The disease can be
diagnosed at any grade of severity including wall inflammation, local complication and
systemic organ dysfunction. Moreover, complicated grades of the disease increase with
age, with a peak between 70 and 75 years.The aim is of this manuscript is to provide a
practical and comprehensive review of the most important aspects of ACC and its
complications. In parallel, to highlight the current evidence that helps the surgeons
bedside decision making, on how best to manage the disease, to improve outcomes.

ACC is caused by an inflammatory/infectious process involving the gallbladder

wall, in many cases due to an impacted gallstone in the infundibulum or in the cystic
duct. The continued mucin production from epithelium and the gallbladder distention,
results in micro and macro circulatory perfusion deficits. The subsequent events are
serosa edema, mucosal sloughing, venous and lymphatic congestion, ischemia and
necrosis with regional or diffuse peritonitis. Acute inflammation may be complicated by
secondary bacterial infection, from the bile duct, via the portal lymphatic or vascular
system. The microorganisms present in the gastrointestinal tract are the most common
pathogens