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170 Cardio Diabetes Medicine 2017

cases, mechanical circulatory support. ;some of these patients may also present low systolic
blood pressure.
- Hemodynamic deterioration due to acute mechan-
ical cause (eg, acute interventricular septal or mi- ‘‘Vascular’’ Profile: This profile is characterized as
tral valve papillary rupture in ACS, acute valvular rapid clinical deterioration (typically within hours),
incompetence due to endocarditis). with severe dyspnea, evidence of pulmonary conges-
tion (in the most severe cases in a form of pulmonary
- Acute coronary syndrome as an underlying cause edema), with no (or only minimal) weight gain, where
for decompensation with urgent transfer for expe- fluid redistribution to the lungs is essential for symp-
diting coronary reperfusion.
toms and vasoconstriction plays a major role; these
As the AHF pathophysiology is a consequence of patients often have preserved LVEF and present with
elevated ventricular filling pressure and reduced car- normal or elevated systolic blood pressure.
diac output, hemodynamic profiling of a patient is
often used in clinical practice.Typically, it is based This explains the background for different treatment
on bedside evaluation of congestion and perfusion, strategies often applied for these clinical profiles:
which allows differentiation of 4 different ‘‘hemody- diuretics for those with the ‘‘cardiac’’ profile and a
namic’’ profiles: combination of vasoactive agents with diuretics for
those with the ‘‘vascular’’ profile.
- ‘‘Wet and warm’’. Most commonly present with pa-
tients demonstrating congestion (wet profile) and In-hospital Heart Failure Worsening: A
still adequate peripheral perfusion (warm profile). Newly Recognized Clinical Profile

- ‘‘Wet and cold’’. With congestion and inadequate The natural course of AHF can comprise a clinical
peripheral perfusion (cold profile). scenario characterized by initial stabilization with
- ‘‘Dry and cold’’. With impaired perfusion and lack symptomatic improvement, followed by often sudden
of congestion. and unexpected deterioration, worsening of symp-
toms and signs of AHF, requiring re-intensification
- ‘‘Dry and warm’’. Often with symptoms of AHF, of therapy. This clinical profile has only recently been
but compromised hemodynamics. recognized as worsening heart failure (WHF), which

Hemodynamic profiles are associated with outcome is associated with adverse outcomes. Between 10%
(patients with ‘‘wet and cold’’ characteristic having and 30% of AHF patients may develop WHF during
the worst prognosis) but more importantly they may hospital stay. WHF represents a meaningful change
also have important therapeutic and prognostic im- in clinical status, with variable clinical manifestations
plications. (from only symptomatic deterioration to severe he-
modynamic collapse) and should always be consid-
Clinical signs in Acute Heart Failure Patient ered in patients with changing hemodynamics.In the
With Congestion: Fluid Accumulation or RELAX-AHF study, treatment with serelaxin was as-
sociated with a 30% reduction in WHF at day 1442
Redistribution? whereas rolophylline, which enhances diuresis, failed
Signs and symptoms of fluid overload are present to prevent WHF in the PROTECT study, thus high-
in most patients hospitalized due to HF decompen- lighting that the clinical profile of WHF needs to be
sation, whereas only a minority demonstrate signifi- recognized pertinently.
cantly impaired peripheral perfusion and hypoten-
sion. This explains why the ‘‘wet and warm’’ pro- Clinical Profile and Comorbidities
file (depicting congestion with adequate peripheral The clinical presentation of an individual patient ad-
perfusion) is most commonly seen in these clinical mitted with AHF is often influenced by cardiovascular
settings. However, the ‘‘warm and wet’’ profile may and non-cardiovascular comorbidities. Recent data
comprise 2 groups of patients with different clinical from the ESC HF Registry demonstrate that atrial
characteristics and pathophysiological profiles: fibrillation is present in 44% of AHF patients, diabetes
‘‘Cardiac’’ Profile: This profile typically occurs in pa- mellitus in 39%, chronic obstructive pulmonary dis-
tients with a history of chronic HF, impaired LVEF, ease in 20%, and renal dysfunction in 26%. One study
slow symptomatic deterioration, gradual (over sever- showed that only 25% admitted with AHF tended to
al days-weeks) fluid accumulation with concomitant have preserved iron status indicating surrogately
weight gain and dominating signs of peripheral ede- that iron deficiency (irrespectively of the presence of
ma, jugular venous distension, and hepatomegaly anaemia) often coincides with HF decompensation.

GCDC 2017