Acute heart failure and/or cardiogenic shock are frequently triggered by ischemic coronary events. Yet, there is a paucity of randomized data on the management of patients with heart failure complicating acute coronary syndrome, as acute coronary syndrome and cardiogenic shock have frequently been defined as exclusion criteria in trials and registries. As a consequence, guideline recommendations are mostly driven by observational studies, even though these patients have a particularly poor prognosis compared to heart failure patients without signs of coronary artery disease. In acute heart failure, and especially in cardiogenic shock related to ischemic conditions, vasopressors and inotropes are used. However, both pathophysiological considerations and available clinical data suggest that these treatments may have disadvantageous effects. The inodilator levosimendan offers potential benefits due to a range of distinct effects including positive inotropy, restoration of ventriculo-arterial coupling, increases in tissue perfusion, and anti-stunning and anti-inflammatory effects. In clinical trials levosimendan improves symptoms, cardiac function, hemodynamics, and end-organ function. Adverse effects are generally less common than with other inotropic and vasoactive therapies, with the notable exception of hypotension. The decision to use levosimendan, in terms of timing and dosing, is influenced by the presence of pulmonary congestion, and blood pressure measurements. Levosimendan should be preferred over adrenergic inotropes as a first line therapy for all ACS-AHF patients who are under beta-blockade and/or when urinary output is insufficient after diuretics. Levosimendan can be used alone or in combination with other inotropic or vasopressor agents, but requires monitoring due to the risk of hypotension.

Introduction: Serum levels of CA125 are often high in advanced heart failure (AHF) patients. Aim: To determine the predictive value of CA125 in forecasting the occurrence of death or cardiac transplantation in an AHF population. Methods: 88 AHF patients referred for heart transplantation were divided into 2 groups based on CA125 levels: normal (CA125 b 38 U/mL) and elevated (≥ 38 U/mL). Events (death or heart transplant) were monitored over a period of 13 ± 7 months after CA125 determination. Results: Patients with elevated CA125 (n = 65) had significantly lower blood pressure, body mass index, serum sodium and peak exercise oxygen consumption, while B-type natriuretic peptide levels were significantly higher. The combined primary endpoint (death or heart transplant) rate was 39.4% and 62.3% in normal and elevated CA125 groups, respectively (p = 0.029). Multivariate regression analysis showed that CA125 and sodium levels were the only independent predictors of the combined endpoint. Conclusion: In AHF patients, plasma CA125 was an effective prognostic marker. Its determination may contribute to better risk stratification in this population.

No abstract

Introduction Acute appendicitis is a major cause of acute abdomen. Although its diagnosis is clinical, it is often supported by complementary diagnostic tests. Sometimes, delay in diagnosis can lead to worsening of the clinical picture, resulting in a complicated acute appendicitis. Some series have studied some clinical and analytical parameters as possible predictors of complicated acute appendicitis. Study design A retrospective analysis of patients admitted for acute appendicitis and undergoing appendectomy between January 2014 and December 2017 was performed in order to assess the possible existence of preoperative analytical predictive factors for complicated acute appendicitis (such as leukocytosis, C-reactive protein and ratio between neutrophils and lymphocytes). Results 841 patients underwent emergency appendectomy during the analysed period. This initial sample was divided into two groups: Group 1 with patients with uncomplicated acute appendicitis and Group 2 with patients with complicated acute appendicitis. Group 2's presentation age, duration of symptoms and hospital stay was significantly higher than Group 1. Regarding analytical parameters, the measurement of leukocytes, C-reactive protein and ratio between neutrophils and lymphocytes was significantly higher in patients with complicated acute appendicitis. After a multivariate analysis, it was found that only C-reactive protein was a good predictor of complicated acute appendicitis. Conclusion Several publications have studied and demonstrated the possible use of certain analytical parameters as predictors of complicated acute appendicitis. In our study, C-reactive protein proved to be a good independent predictor of complicated acute appendicitis and, therefore, when an assay of this protein exceeds 63.3 mg/L, faster surgical approach should be considered due to the high probability of the presence of a complicated picture of this clinical entity.

Venlafaxine is a serotonin-norepinephrine reuptake inhibitor used as an antidepressant. Interindividual variability and herb-drug interactions can lead to drug-induced toxicity. We report the case of a 35-year-old female patient diagnosed with synchronous pneumonitis and acute cardiomyopathy attributed to venlafaxine. The patient sought medical attention due to dyspnea and dry cough that started three months after initiating treatment with venlafaxine for depression. The patient was concomitantly taking Centella asiatica and Fucus vesiculosus as phytotherapeutic agents. Chest CT angiography and chest X-ray revealed parenchymal lung disease (diffuse micronodules and focal ground-glass opacities) and simultaneous dilated cardiomyopathy. Ecocardiography revealed a left ventricular ejection fraction (LVEF) of 21%. A thorough investigation was carried out, including BAL, imaging studies, autoimmune testing, right heart catheterization, and myocardial biopsy. After excluding other etiologies and applying the Naranjo Adverse Drug Reaction Probability Scale, a diagnosis of synchronous pneumonitis/cardiomyopathy associated with venlafaxine was assumed. The herbal supplements taken by the patient have a known potential to inhibit cytochrome P450 enzyme complex, which is responsible for the metabolization of venlafaxine. After venlafaxine discontinuation, there was rapid improvement, with regression of the radiological abnormalities and normalization of the LVEF. This was an important case of drug-induced cardiopulmonary toxicity. The circumstantial intake of inhibitors of the CYP2D6 isoenzyme and the presence of a CYP2D6 slow metabolism phenotype might have resulted in the toxic accumulation of venlafaxine and the subsequent clinical manifestations. Here, we also discuss why macrophage-dominant phospholipidosis was the most likely mechanism of toxicity in this case.