Cardiovascular effects of breath-hold diving at altitude.

Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e' ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema.

Can catheter-based renal denervation reduce frequency of hospitalization in patients who have resistant hypertension and heart failure with reduced ejection fraction?

Hypertension is one of the most powerful and modifiable risk factors for the development, progression and even decompensation of heart failure. Uncontrolled hypertension increases to frequency of heart failure hospitalizations by increase sympathetic tone. Catheter-based renal denervation has been shown to reduce blood pressure in the treatment of multidrug-resistant hypertension. We report the improvement in clinical status after renal denervation in a 47-year-old male patient with a history of hypertension, chronic ischemic heart failure, and recurrent hospitalizations for acute hypertensive pulmonary edema despite optimal medical therapy.

Safety of midodrine in patients with heart failure with reduced ejection fraction: a retrospective cohort study.

Background: Heart failure with reduced ejection fraction (HFrEF) poses significant health risks. Midodrine for maintaining blood pressure in HFrEF, requires further safety investigation. This study explores midodrine's safety in HFrEF through extensive matched analysis. Methods: Patients with HFrEF (LVEF <50%) without malignancy, non-dialysis dependence, or non-orthostatic hypotension, were enrolled between 28 August 2013, and 27 August 2023. Propensity score matching (PSM) created 1:1 matched groups. Outcomes included mortality, stage 4 and 5 chronic kidney disease (CKD), emergency room (ER) visits, intensive care unit (ICU) admissions, hospitalizations, and respiratory failure. Hazard ratios (HR) with 95% confidence intervals (95% CI) were calculated for each outcome, and Kaplan-Meier survival analysis was performed. Subgroup analyses were conducted based on gender, age (20-<65 vs. ≥65), medication refill frequency, and baseline LVEF. Results: After 1:1 PSM, 5813 cases were included in each group. The midodrine group had higher risks of respiratory failure (HR: 1.16, 95% CI: 1.08-1.25), ICU admissions (HR: 1.14, 95% CI: 1.06-1.23), hospitalizations (HR: 1.21, 95% CI: 1.12-1.31), and mortality (HR: 1.090, 95% CI: 1.01-1.17). Interestingly, midodrine use reduced ER visits (HR: 0.77, 95% CI: 0.71-0.83). Similar patterns of lower ER visit risk and higher risks for ICU admissions, respiratory failure, and overall hospitalizations were observed in most subgroups. Conclusion: In this large-scale study, midodrine use was associated with reduced ER visits but increased risks of respiratory failure, prolonged ICU stays, higher hospitalizations, and elevated mortality in HFrEF patients. Further research is needed to clarify midodrine's role in hemodynamic support and strengthen existing evidence.

Safety of prehospital intravenous bolus dose nitroglycerin in patients with acute pulmonary edema: A 4-year review.

Background: Intravenous nitrates are a primary therapy for hypertensive congestive heart failure (CHF) with acute pulmonary edema (APE) in the hospital setting. Historically, sublingual nitrates are the mainstay of emergency medical services (EMS) pharmacologic therapy for these patients. We aimed to evaluate the safety of prehospital bolus dose intravenous nitroglycerin in patients with APE. Methods: This is a retrospective evaluation of EMS data between March 15, 2018, and March 15, 2022, where CHF with APE was suspected and bolus-dose intravenous nitroglycerin was administered. Protocol inclusion criteria were hypertension (systolic blood pressure [SBP] >160 mmHg) and acute respiratory distress, with a presumption of decompensated CHF with APE. These patients received 1 mg intravenous nitroglycerin, with the option to repeat once for ongoing distress if the SBP remained >160 mmHg. The primary outcomes were adverse events, defined as hypotension (SBP <90 mmHg), syncope, vomiting, or dysrhythmia. Results: The final analysis included 235 patients. In patients receiving intravenous bolus nitroglycerin, the median (interquartile range [IQR]) initial and final EMS SBP values decreased from 198 mmHg (180-218) to 168 (148-187), respectively. The median (IQR) pulse decreased from 108 (92-125) to 103 (86-119), and the median oxygen saturation increased from 89% (82-95) to 98% (96-99). Three episodes (1.3%) of asymptomatic hypotension occurred, and none required intervention. Conclusion: This study supports a favorable safety profile for prehospital bolus-dose intravenous nitroglycerin for decompensated CHF with APE. Blood pressure, heart rate, and oxygen saturation improvements are also demonstrated. Further, prospective studies are needed to confirm these findings.

Atosiban-induced acute pulmonary edema: A rare but severe complication of tocolysis.

Background: Atosiban is commonly used to delay premature labor in pregnant women and is thought to have few side effects. Objectives: To report a case of acute pulmonary edema (APE) following administration of atosiban and conduct a systematic review to identify common characteristics and risk factors of atosiban-associated APE. Methods: Searches were performed in Pubmed, Embase, and Web of Science using the keyword "Atosiban" combined with the terms "Pulmonary edema" or "Dyspnea" or "Hypoxia" on 9th July 2022. Only case reports of atosiban-associated APE were included without language restrictions. Data were extracted from the reports, and median, range, and percentages were calculated as applicable. The risk of bias was assessed using the Joanna Briggs Institute critical appraisal checklist for case reports. Results: Seven cases of atosiban-associated APE were included in the systematic review, including our case. APE occurred at a median gestational age of 32 + 6 weeks. Most patients were nulliparous (6/7, 85.7%) and were in multiple pregnancies (5/7, 71.4%). All patients were prescribed antenatal corticosteroids and tocolytics, with three (42.9%) receiving only atosiban and four (57.1%) receiving atosiban and other tocolytics. The median interval from starting atosiban administration to APE onset was about 40 h, and three patients (42.9%) showed symptoms 2-10 h after the end of atosiban treatment. Radiographic examinations (chest X-ray and/or computer tomography scan) confirmed APE in all patients and pleural effusion in four patients (57.1%). Five patients (71.4%) underwent emergency cesarean section, one patient (14.3%) with twin pregnancy had vaginal delivery with the help of suction cup and forceps, and another patient (14.3%) continued the pregnancy. All patients recovered well after administration of oxygen, diuresis, and other supportive therapy. Conclusion: Atosiban may cause acute pulmonary edema in patients with underlying risk factors. This complication remains rare, but caution during tocolytic treatment using atosiban is recommended.

Acute Pulmonary Edema After Hyperbaric Oxygen Treatment: A Case Report Written With ChatGPT Assistance.

Acute pulmonary edema is a rare but severe complication of hyperbaric oxygen therapy. While patients with known cardiovascular problems may be able to withstand this therapy, rapid decompensation can still occur. Here, we present a case of a patient with known low ejection fraction and severe mitral regurgitation who developed acute pulmonary edema during the first hyperbaric treatment for a foot ulcer. This case highlights the importance of identifying patients that are high risk, such as those with moderate-to-severe cardiac disease, and pursuing other treatment options to avoid this complication.

Taming the Tiger: Ultra high dose nitroglycerin in managing sympathetic crashing acute pulmonary edema patient.

INTRODUCTION: Sympathetic Crashing Acute Pulmonary Edema (SCAPE) lies on the end of the acute heart failure syndrome spectrum with pulmonary edema in all lung zones. NTG at lower doses (10-20 µg/min) cause preload reduction, and at higher doses (> 100 µg/min) causes after-load reduction by arterial dilatation. The main aim is to decrease the afterload at the earliest to cut the vicious cycle caused by sudden sympathetic upsurge. To our knowledge, this is the highest nitroglycerin dose usage in the literature. CASE: A 60-year-old male with no known prior co-morbidities presented to our Emergency with complaints of acute onset severe shortness of breath, which was also associated with extreme diaphoresis, agitation, anxiety, and palpitations. On Examination, the patient was hypoxic and hypertensive with severe tachypnea and tachycardia. On Auscultation, diffuse bilateral crackles in all areas were heard. Point of care ultrasound showed bilateral B-profile in all lung zones, inferior vena cava was >50% collapsible. We managed the patient with non-invasive ventilation and ultrahigh dose nitroglycerin/ highest ever- 9 mg intravenous bolus with 76 mg infusion. The patient had improved within hours and did not require oxygen. The patient was discharged from the emergency after a few hours of observation. DISCUSSION: SCAPE occurs due to a vicious spiral involving increasing sympathetic outflow, excessive afterload, and worsening heart failure. The central, defining pathophysiological feature of SCAPE is pathologically elevated afterload due to systemic vasoconstriction and hypertension. SCAPE patients may be euvolemic, hypovolemic or hypervolemic. The problem is shift of fluid into the lungs rather than hypervolemia. The emphasis on treating pulmonary edema has shifted from diuretics to vasodilators, especially high-dose nitrates, combined with non-invasive positive pressure ventilation. CONCLUSION: This is the first report describing the safe and effective administration of ultra-high dose bolus/ highest dose ever and prolonged high-dose infusion for SCAPE, along with Non-invasive ventilation, which has prevented mechanical ventilation and mortality. High doses of intravenous NTG are extremely effective and safe for SCAPE patients.

Acute Pulmonary Edema as a Cardiovascular Manifestation of Pheochromocytoma.

Pheochromocytoma most commonly presents with the triad of paroxysms of headache, palpitations, and diaphoresis. Pheochromocytoma crisis, caused by a supra-physiological surge of catecholamine release, is an endocrine emergency that can present with various clinical manifestations. Acute pulmonary edema is one of the manifestations of pheochromocytoma crisis and can be either cardiogenic or non-cardiogenic. Here, we report cases of acute pulmonary edema of each type, related to pheochromocytoma crisis, which were presented to our district general hospital in 2020.

Effects of midazolam vs morphine in patients with acute pulmonary edema with left ventricular systolic dysfunction: a secondary analysis of data from the MIMO trial. / Efectos del midazolam frente a la morfina en pacientes con edema agudo de pulmón con disfunción sistólica ventricular izquierda: un análisis secundario del ensayo MIMO.

OBJECTIVES: The midazolam vs morphine (MIMO) trial showed that patients treated with midazolam had fewer serious adverse events than those treated with morphine. In many patients with acute pulmonary edema, the left ventricular ejection fraction (LVEF) is preserved, at 50% or higher. We aimed to determine whether left ventricular (LV) systolic dysfunction (D), defined by an LVEF of less than 50%, modifies the protective effect of midazolam vs morphine. MATERIAL AND METHODS: The MIMO trial randomized 111 patients with acute pulmonary edema to receive intravenous midazolam in 1-mg doses to a maximum of 3 mg (n = 55) or morphine in 2- to 4-mg doses to a maximum of 8 mg (n= 56). We calculated the relative risk (RR) for a serious adverse event in patients with and without systolic LVD. RESULTS: LVEF was preserved in 84 (75.7%) of the patients with acute pulmonary edema. In patients with systolic LVD, 4 patients (26.9%) in the midazolam arm vs 6 (50%) in the morphine arm developed serious adverse events (RR, 0.53; 95% CI, 0.2-1.4). In patients without systolic LVD, 6 patients (15%) in the midazolam arm vs 18 (40.9%) in the morphine arm experienced such events (RR, 0.37; 95% CI, 0.16-0.83). The presence of systolic LVD did not modify the protective effect of midazolam on serious adverse effects (P=.57). CONCLUSION: The effect of midazolam vs morphine in protecting against the development of serious adverse events or death is similar in patients with and without systolic LVD.

OBJETIVO: El ensayo clínico MIMO demostró que los pacientes con edema agudo de pulmón (EAP) tratados con midazolam tenían menos eventos adversos graves (EAG) que los tratados con morfina. Muchos pacientes con EAP tienen fracción de eyección del ventrículo izquierdo (FEVI) preservada ($ 50%). El objetivo fue conocer si la disfunción sistólica ventricular izquierda (DSVI) (fracción eyección ventrículo izquierdo 50%) modifica el efecto protector del midazolam frente a la morfina. METODO: El estudio MIMO asignó al azar 111 pacientes con EAP a tratamiento con midazolam (dosis de 1 mg intravenosa, hasta una dosis máxima de 3 mg, n = 55) o morfina (dosis de 2-4 mg, hasta una dosis máxima de 8 mg, n = 56). Se calculó el riesgo relativo (RR) de padecer un EAG en pacientes con y sin DSVI. RESULTADOS: La FEVI preservada estuvo presente en 84 (75,7%) pacientes con EAP. En el grupo con DSVI, 4 pacientes (26,9%) en el brazo midazolam frente a 6 (50%) en el brazo morfina presentaron EAG (RR = 0,53; IC 95: 0,2-1,4). En el grupo sin DSVI 6 pacientes (15%) del brazo midazolam frente a 18 (40,9%) del brazo morfina presentaron EAG (RR = 0,37; IC 95: 0,16-0,83). La DSVI no modificó el efecto protector del midazolam en la aparición de EAG con respecto a la morfina (p = 0,57). CONCLUSIONES: En pacientes con EAP el efecto protector del midazolam sobre la morfina en la aparición de EAG y EAG o muerte fue similar en pacientes con y sin DSVI.

Efectos del midazolam frente a la morfina en pacientes con edema agudo de pulmón con disfunción sistólica ventricular izquierda: un análisis secundario del ensayo MIMO / Effects of midazolam vs morphine in patients with acute pulmonary edema with left ventricular systolic dysfunction: a secondary analysis of data from the MIMO trial

Objetivo. El ensayo clínico MIMO demostró que los pacientes con edema agudo de pulmón (EAP) tratados con midazolam tenían menos eventos adversos graves (EAG) que los tratados con morfina. Muchos pacientes con EAP tienen fracción de eyección del ventrículo izquierdo (FEVI) preservada ($ 50%). El objetivo fue conocer si la disfunción sistólica ventricular izquierda (DSVI) (fracción eyección ventrículo izquierdo < 50%) modifica el efecto protector del midazolam frente a la morfina.Método. El estudio MIMO asignó al azar 111 pacientes con EAP a tratamiento con midazolam (dosis de 1 mg intravenosa, hasta una dosis máxima de 3 mg, n = 55) o morfina (dosis de 2-4 mg, hasta una dosis máxima de 8 mg, n = 56). Se calculó el riesgo relativo (RR) de padecer un EAG en pacientes con y sin DSVI.Resultado. La FEVI preservada estuvo presente en 84 (75,7%) pacientes con EAP. En el grupo con DSVI, 4 pacientes (26,9%) en el brazo midazolam frente a 6 (50%) en el brazo morfina presentaron EAG (RR = 0,53; IC 95: 0,2-1,4). En el grupo sin DSVI 6 pacientes (15%) del brazo midazolam frente a 18 (40,9%) del brazo morfina presentaron EAG (RR = 0,37; IC 95: 0,16-0,83). La DSVI no modificó el efecto protector del midazolam en la aparición de EAG con respecto a la morfina (p = 0,57)Conclusiones. En pacientes con EAP el efecto protector del midazolam sobre la morfina en la aparición de EAG y EAG o muerte fue similar en pacientes con y sin DSVI. (AU)

Background and objective. The midazolam vs morphine (MIMO) trial showed that patients treated with midazolam had fewer serious adverse events than those treated with morphine. In many patients with acute pulmonary edema, the left ventricular ejection fraction (LVEF) is preserved, at 50% or higher. We aimed to determine whether left ventricular (LV) systolic dysfunction (D), defined by an LVEF of less than 50%, modifies the protective effect of midazolam vs morphine. Methods. The MIMO trial randomized 111 patients with acute pulmonary edema to receive intravenous midazolam in 1-mg doses to a maximum of 3 mg (n = 55) or morphine in 2- to 4-mg doses to a maximum of 8 mg (n= 56). We calculated the relative risk (RR) for a serious adverse event in patients with and without systolic LVD. Results. LVEF was preserved in 84 (75.7%) of the patients with acute pulmonary edema. In patients with systolic LVD, 4 patients (26.9%) in the midazolam arm vs 6 (50%) in the morphine arm developed serious adverse events (RR, 0.53; 95% CI, 0.2-1.4). In patients without systolic LVD, 6 patients (15%) in the midazolam arm vs 18 (40.9%) in the morphine arm experienced such events (RR, 0.37; 95% CI, 0.16-0.83). The presence of systolic LVD did not modify the protective effect of midazolam on serious adverse effects (P=.57). Conclusions. The effect of midazolam vs morphine in protecting against the development of serious adverse eventsor death is similar in patients with and without systolic LVD. (AU)

Temporary balloon occlusion test can overestimate the risk of acute pulmonary edema after transcatheter atrial septal defect closure.

BACKGROUND: Atrial septal defect (ASD) closure can cause acute pulmonary edema. Before transcatheter closure is performed, temporary balloon occlusion test (BOT) is recommended in patients with left ventricular dysfunction to predict the risk of pulmonary edema. However, the accuracy of BOT has not been verified. This study aimed to compare hemodynamic differences between BOT and transcatheter closure. METHODS: A total of 42 patients with a single ASD over age 18 years who underwent BOT before transcatheter ASD closure between October 2010 and May 2020 were analyzed. Pulmonary capillary wedge pressure (PCWP) was measured using a Swan-Ganz catheter placed in the pulmonary artery at baseline, after 10 min of BOT, and after transcatheter closure. Amplatzer septal occluder was used for all transcatheter closures. RESULTS: Mean patient age was 64 ± 18 years (range, 18-78). Mean ASD diameter and pulmonary to systemic flow ratio were 18 ± 5 and 2.8 ± 1.0 mm, respectively. Mean PCWP at baseline, during BOT, and after transcatheter closure was 8.9 ± 2.9, 13.5 ± 4.2, and 9.5 ± 2.6 mmHg, respectively. The difference between BOT and after transcatheter closure values was significant (p < 0.001). During BOT, PCWP increased ≥18 mmHg in 7 patients, whereas after ASD closure, PCWP was <18 mmHg in all 7 and none developed acute pulmonary edema. CONCLUSION: Temporary balloon occlusion of an ASD and transcatheter ASD closure result in different hemodynamic change. BOT overestimates increase of PCWP after transcatheter ASD closure and requires careful interpretation. Well-designed, larger studies in higher-risk patients are warranted to verify the clinical implications of BOT in more detail.

The Development of Pulmonary Edema after Recombinant Tissue Plasminogen Activator in Acute Ischemic Stroke Patient; Neurogenic or Non-Neurogenic?

Recombinant tissue plasminogen activator (r-tPA) is the first-line drug for the treatment of acute ischemic stroke, despite it may lead to a variety of complications in some cases. In patients with extensive stroke, infarction of the brain can cause suppression of the respiratory center in the brain leading to neurogenic pulmonary edema that potentially causes respiratory failure. Its etiology is either due to a neurogenic or non-neurogenic process. Nevertheless, the definite pathophysiology of these circumstances remains unclear. In this study, we reported four cases of post-thrombolytic ischemic stroke patients who suffer from pulmonary edema with different symptoms and onset times as well as we discuss the possible explanation behind these different outcomes.

Just an Acute Pulmonary Edema? Paraneoplastic Thyroid Storm Due to Invasive Mole.

Hydatidiform mole is a malignant entity included in the gestational trophoblastic diseases. It usually produces pregnancy hormones such as beta-human chorionic gonadotropin (ß-hCG), which in turn stimulates endogenous thyroid hormone production. We report the case of a high-risk complete invasive hydatidiform mole with pulmonary metastasis and associated paraneoplastic syndrome. The patient is a 30-year-old woman who presented symptoms of pregnancy and metrorrhagia. A uterine mass was detected. Urine ß-hCG was found negative. In serum, 2,662,000 mIU/mL (normal range: <5) was found, together with parameters of severe hyperthyroidism. The patient underwent uterine curettage with diagnostic and therapeutic means. At that precise moment, her pregnancy-like symptoms worsened and she developed restlessness, tachycardia, diaphoresis, dyspnea at rest, and peripheral edema. A scan showed bilateral pulmonary nodules suggestive of metastasis, acute pulmonary edema, and bilateral pleural effusion without signs of pulmonary thromboembolism. At that time, she presented a free T4 of 2.34 ng/dL (normal range: 0.8-1.8 ng/dL), causing a thyroid storm with secondary cardiac dysfunction. The patient was treated with corticosteroid therapy to decrease peripheral conversion of thyroid hormone T4 to active T3. Her symptoms remitted within 8 h. After 48 h, T4 level was 1.2 ng/dL while serum ß-hCG was 80,000 mIU/mL, with a positive urine result. The change in the urine analysis is due to the "hook effect" of the reactive test. An effective chemotherapy treatment was started according to the EMA-CO scheme, remaining free of disease at present. Knowing paraneoplastic syndromes is necessary to achieve the best clinical management and to start treatment early.

Safety of a Cardiac Resynchronization Therapy Device Implantation in a Patient with Unstable Heart Failure Who Require Impella-Device Assistance.

Implantation of a cardiac resynchronization therapy (CRT) device is usually scheduled in the compensated phase of heart failure; however, procedural safety may be sometimes disturbed in the decompensated phase. We report a case of a successful semi-urgent implantation of a CRT device temporary assisted with Impella in a patient with the decompensated phase of severe heart failure dependent on inotropic agents and who cannot maintain the supine position. Impella assistance with left ventricular (LV) unloading and maintenance of end-organ perfusion contributed to early recovery from acute heart failure. Furthermore, an acute effect of mechanical resynchronization by biventricular pacing plays an important role in weaning from the mechanical support or inotropic dependence. These mutual effects of mechanical support and CRT might contribute to a decrease in LV end-diastolic pressure and to a remarkable early recovery from a severely decompensated condition.

Fatal noncardiogenic pulmonary edema related to nonionic, iso-osmolar iodine contrast medium: one case report.

BACKGROUND: Noncardiogenic pulmonary edema (NCPE) is a rare and life-threatening allergy-like reaction to the intravascular injection of a nonionic radiographic agent. We first describe a very rare case of fatal NCPE after the intravenous injection of nonionic, iso-osmolar iodine contrast media. Case presentation A 55-year-old male patient was admitted to the hospital with esophageal cancer. After the intravenous administration of 100 mL iodixanol, the patient first exhibited digestive tract symptoms, including abdominal pain, diarrhea, and vomiting, with no dyspnea, rash, itching, or throat edema. He received anti-allergy treatment, but his symptoms did not improve; instead, he further developed pulmonary edema. Arterial blood gas analysis results were as follows: pH, 7.08; PO2, 70 mm Hg; PCO2, 40 mm Hg; and SaO2, 52%. Then, the patient received emergent tracheal intubation and ventilation to assist breathing, and he was transferred to the intensive care unit (ICU) for further treatment. In the ICU, the patient developed shock and respiratory and circulatory failure; therefore, he received shock resuscitation, acidosis correction, muscle relaxants to lower the work of breathing, and cardiotonic therapy. The patient eventually died. During the ICU period, emergency bedside color ultrasound showed a diffuse B line in both lungs, and the size of the cardiac cavity was normal, but the ventricular rate was extremely fast. Chest radiography showed pulmonary edema with a normal cardiac silhouette, and the brain natriuretic peptide (BNP) level was in the normal range. CONCLUSIONS: NCPE is a rare and critical allergy-like reaction to the use of a nonionic iso-osmolar radiocontrast contrast medium. Clinicians should pay very close attention to digestive tract manifestations during the medical observation of patients, as gastrointestinal manifestations may be the prodromal symptoms of NCPE caused by iso-osmolar contrast medium injection.

Uric acid associated with acute heart failure presentation in Acute Coronary Syndrome patients.

We focused on the role of Uric Acid (UA) as a possible determinant of Heart Failure (HF) related issues in Acute Coronary Syndromes (ACS) patients. Main outcomes were acute HF and cardiogenic shock at admission, secondary outcomes were the use of Non Invasive Ventilation (NIV) and the admission Left Ventricular Ejection Fraction (LVEF). We consecutively enrolled 1269 ACS patients admitted to the cardiological Intensive Care Unit of the Niguarda and San Paolo hospitals (Milan, Italy) from June 2016 to June 2019. Median age was 68 (first-third quartile 59-77) years and males were 970 (76%). All the evaluated outcomes occurred more frequently in the hyperuricemic subjects (UA higher than 6 mg/dL for females and 7 mg/dL for males, n = 292): acute HF 35.8 vs 11.1% (p < 0.0001), cardiogenic shock 10 vs 3.1% (p < 0.0001), NIV 24.1 vs 5.1% (p < 0.0001) and lower admission LVEF (42.9±12.8 vs 49.6±9.9, p < 0.0001). By multivariable analyses, UA was confirmed to be significantly associated with all the outcomes with the following Odds Ratio (OR): acute HF OR = 1.119; 95% CI 1.019;1.229; cardiogenic shock OR = 1.157; 95% CI 1.001;1.337; NIV use OR = 1.208; 95% CI 1.078;1.354; LVEF ß = -0.999; 95% CI -1.413;-0.586. We found a significant association between UA and acute HF, cardiogenic shock, NIV use and LVEF. Due to the cross-sectional nature of our study no definite answer on the direction of these relationship can be drawn and further longitudinal study on UA changes over time during an ACS hospitalization are needed.

Elevated admission C-reactive protein to albumin ratios are associated with disease severity and respiratory complications in adults with imported falciparum malaria.

BACKGROUND: In imported falciparum malaria, systemic inflammation with increased capillary permeability can cause life-threatening complications, such as acute pulmonary edema (APO) or adult respiratory distress syndrome (ARDS). This observational study assessed the association of the admission serum albumin level (ALB) and C-reactive protein to albumin ratio (CRP/ALB) with disease severity and these respiratory complications. METHODS: All adult cases hospitalized during 2001-2015 in the Charité University Hospital, Berlin, with ALB and CRP values measured upon admission, were retrospectively analysed. RESULTS: Seventy-six patients were enrolled (26 female, median age: 37 y), 60 with uncomplicated malaria and 16 with severe malaria (SM). SM was associated with lower ALB (p<0.0001) and higher CRP/ALB (p<0.0001) values; the areas under the receiver operator curves (AUROCs) were 0.85 (95% CI 0.74 to 0.96) for ALB and 0.88 (95% CI 0.80 to 0.97) for CRP/ALB. Radiologic changes consistent with APO/ARDS were detectable in 5 of 45 admission chest X-rays performed (11.1%); the AUROCs were 0.86 (95% CI 0.74 to 0.99) for ALB and 0.91 (95% CI 0.82 to 0.99) for CRP/ALB. CONCLUSIONS: Diminished admission ALB levels and elevated CRP/ALB ratios are associated with disease severity and respiratory complications in imported falciparum malaria. These readily and ubiquitously available markers may facilitate early identification of at-risk patients.