Multivessel coronary artery disease (MVCAD) is found in approximately 50% of patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). Although we have data showing the benefits of revascularization of significant non-culprit coronary lesions in patients with AMI, the optimal timing of angioplasty remains unclear. The most common reason for postponing subsequent percutaneous treatment is the fear of contrast-induced acute kidney injury (CI-AKI). Acute kidney injury (AKI) is common in patients with AMI undergoing PCI, and its etiology appears to be complex and incompletely understood. In this review, we discuss the definition, pathophysiology and risk factors of AKI in patients with AMI undergoing PCI. We present the impact of AKI on the course of hospitalization and distant prognosis of patients with AMI. Special attention was paid to the phenomenon of AKI in patients undergoing multivessel revascularization. We analyze the correlation between increased exposure to contrast medium (CM) and the risk of AKI in patients with AMI to provide information useful in the decision-making process about the optimal timing of revascularization of non-culprit lesions. In addition, we present diagnostic tools in the form of new biomarkers of AKI and discuss ways to prevent and mitigate the course of AKI.

Background: Proper prognostication is critical in clinical decision-making following out-of-hospital cardiac arrest (OHCA). However, only a few prognostic tools with reliable accuracy are available within the first 24 h after admission. Aim: To test the value of neuron-specific enolase (NSE) and S100B protein measurements at admission as early biomarkers of poor prognosis after OHCA. Methods: We enrolled 82 consecutive patients with OHCA who were unconscious when admitted. NSE and S100B levels were measured at admission, and routine blood tests were performed. Death and poor neurological status at discharge were considered as poor clinical outcomes. We evaluated the optimal cut-off levels for NSE and S100B using logistic regression and receiver operating characteristic (ROC) analyses. Results: High concentrations of both biomarkers at admission were significantly associated with an increased risk of poor clinical outcome (NSE: odds ratio [OR] 1.042 per 1 ng/dL, [1.007–1.079; p = 0.004]; S100B: OR 1.046 per 50 pg/mL [1.004–1.090; p < 0.001]). The dual-marker approach with cut-off values of ≥27.6 ng/mL and ≥696 ng/mL for NSE and S100B, respectively, identified patients with poor clinical outcomes with 100% specificity. Conclusions: The NSE and S100B-based dual-marker approach allowed for early discrimination of patients with poor clinical outcomes with 100% specificity. The proposed algorithm may shorten the time required to establish a poor prognosis and limit the volume of futile procedures performed.

The use of impedance cardiography (ICG) revealed to provide beneficial blood pressure (BP) lowering effect. However, the follow-up in previous trials was short and brachial BP was the only evaluated hemodynamic variable. Thus, we aimed to estimate the influence of ICG-guided therapy on brachial and central BP, impedance-derived hemodynamic profile and echocardiographic features after 12 months in a randomized, prospective and controlled trial (NCT01996085). One hundred and forty-four hypertensives were randomly assigned to groups of empiric (GE) and ICG-guided therapy (HD). Office BP, ambulatory BP monitoring, central BP and echocardiography (left ventricular hypertrophy and diastolic function assessment) were performed before and after 12 months of treatment. Blood pressure reduction was higher in HD (office BP: 21.8/14.1 vs. 19.9/11.8 mm Hg; mean 24-h BP: 19.0/10.9 vs. 14.4/9.2 mm Hg). However, the only statistically significant differences were: percentage of patients achieving BP reduction of minimum 20 mm Hg for of-fice diastolic BP (27.3% vs. 12.1%; p = 0.034) and mean 24-h systolic BP (49.1% vs. 27.3%; p = 0.013). More pronounced improvement in the left ventricular diastolic dysfunction (delta E/A 0.34 vs. 0.12, p = 0.017) was the only other beneficial hemodynamic effect. Beneficial BP lowering effect of hemodynamically-guided pharmacotherapy, observed previously in short-term observation, persists over time. Hemodynamic effects of such a treatment approach, especially those of prognostic value (central BP, myocardial hypertrophy), should be evaluated in further studies including patients with resistant hypertension, heart failure, diabetes mellitus and chronic kidney disease.

Background: Heart failure (HF) is associated with high mortality, morbidity, and frequent hospitalizations due to acute HF (AHF) and requires immediate diagnosis and individualized therapy. Some differences between acutely decompensated chronic heart failure (ADCHF) and de novo HF (dnHF) patients in terms of clinical profile, comorbidities, and outcomes have been previously identified, but the hemodynamics related to both of these clinical states are still not well recognized. Purpose: To compare patients hospitalized with ADCHF to those with dnHF, with a special emphasis on hemodynamic profiles at admission and changes due to hospital treatment. Methods: This study enrolled patients who were at least 18 years old, hospitalized due to AHF (both ADCHF and dnHF), and who underwent detailed assessments at admission and at discharge. The patients’ hemodynamic profiles were assessed by impedance cardiography (ICG) and characterized in terms of heart rate (HR), blood pressure (BP), systemic vascular resistance index (SVRI), cardiac index (CI), stroke index (SI), and thoracic fluid content (TFC). Results: The study population consisted of 102 patients, most of whom were men (76.5%), with a mean left ventricle ejection fraction (LVEF) of 37.3 ± 14.1%. The dnHF patients were younger than the ADCHF group and more frequently presented with palpitations (p = 0.041) and peripheral hypoperfusion (p = 0.011). In terms of hemodynamics, dnHF was distinguished by higher HR (p = 0.029), diastolic BP (p = 0.029), SVRI (p = 0.013), and TFC (only numeric, p = 0.194) but lower SI (p = 0.043). The effect of hospital treatment on TFC was more pronounced in dnHF than in ADCHF, and this was also true of N-terminal pro-brain natriuretic peptide (NT-proBNP) and body mass. Some intergroup differences in the hemodynamic profile observed at admission persisted until discharge: higher HR (p = 0.002) and SVRI (trend, p = 0.087) but lower SI (p < 0.001) and CI (p = 0.023) in the dnHF group. Conclusions: In comparison to ADCHF, dnHF is associated with greater tachycardia, vasoconstriction, depressed cardiac performance, and congestion. Despite more effective diuretic therapy, other unfavorable hemodynamic features may still be present in dnHF patients at discharge.