3 research outputs found
Inotropes in cardiac patients: update 2011
Purpose of review
ICU patients frequently develop low output syndromes due to cardiac
dysfunction, myocardial injury, and inflammatory activation.
Conventional inotropic agents seem to be useful in restoring hemodynamic
parameters and improving peripheral organ perfusion, but can increase
short-term and long-term mortality in these patients. Novel inotropes
may be promising in the management of ICU patients, having no serious
adverse effects. This review summarizes all the current knowledge about
the use of conventional and new inotropic agents in various clinical
entities of critically ill patients.
Recent findings
In recent European Society of Cardiology guidelines, inotropic agents
are administered in patients with low output syndrome due to impaired
cardiac contractility, and signs and symptoms of congestion. The most
recommended inotropes in this condition are levosimendan and dobutamine
(both class of recommendation: IIa, level of evidence: B). Recent data
indicate that levosimendan may be useful in postmyocardial infarction
cardiac dysfunction and septic shock through increasing coronary flow
and attenuating inflammatory activation, respectively. Furthermore,
calcium sensitizing by levosimendan can be effectively used for weaning
of mechanical ventilation in postcardiac surgery patients and has also
cardioprotective effect as expressed by the absence of troponin release
in this patient population. Finally, new agents, such as istaroxime and
cardiac myosin activators may be safe and improve central hemodynamics
in experimental models of heart failure and heart failure patients in
phase II clinical trials; however, large-scale randomized clinical
trials are required.
Summary
In an acute cardiac care setting, short-term use of inotropic agents is
crucial for the restoration of arterial blood pressure and peripheral
tissue perfusion, as well as weaning of cardiosurgery. New promising
agents should be tested in randomized clinical trials
Serum levels of retinol-binding protein-4 are associated with the presence and severity of coronary artery disease
Background: The interplay between the novel adipokine retinol-binding
protein-4 (RBP4) and coronary artery disease (CAD) is still obscure. We
investigated the relationship between RBP4 levels and the presence and
severity of angiographically proven CAD and determined its possible role
in acute myocardial infarction (AMI).
Methods: 305 individuals with angiographically proven CAD
(CAD-patients), were classified into 2 subgroups: 1) acute myocardial
infarction (AMI, n = 141), and 2) stable angina (SA, n = 164).
Ninety-one age-and sex-matched individuals without CAD, but with at
least 2 classical cardiovascular risk factors, served as controls
(non-CAD group). RBP4 serum levels were measured at hospital admission
and were analyzed in relation to the coronary severity stenosis,
assessed by the Gensini-score and the number of coronary narrowed
vessels. Other clinical parameters, including insulin levels, HOMA-IR,
hsCRP, glycaemic and lipid profile, and left-ventricular ejection
fraction were also assessed.
Results: Serum RBP4 levels were significantly elevated in patients with
CAD compared to non-CAD patients (39.29 +/- 11.72 mg/L vs. 24.83 +/-
11.27 mg/L, p < 0.001). We did not observe a significant difference in
RBP4 levels between AMI and SA subgroups (p = 0.734). Logistic
regression analysis revealed an independent association of CAD presence
with serum RBP4 (beta = 0.163, p = 0.006), and hsCRP (beta = 0.122, p =
0.022) levels, in the whole study group. Among variables, hsCRP (beta =
0.220), HDL (beta = -0.150), and RBP4 (beta = 0.297), correlated in both
univariate and multivariate analysis with CAD severity (R-2 = 0.422, p <
0.001). Similarly, RBP4 concentrations increased with the number of
coronary narrowed vessels (p < 0.05).
Conclusion: Patients with CAD, both SA and AMI, showed elevated RBP4
serum levels. Notably, increased RBP4 concentration seemed to
independently correlate with CAD severity, but no with AMI