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Biomedical subjects

Marco Maggiorini

Publications and source records attributed to Marco Maggiorini.

At least 19 recordsLinked to original sources
PubMed2006

Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema: a randomized trial.

BACKGROUND: High-altitude pulmonary edema (HAPE) is caused by exaggerated hypoxic pulmonary vasoconstriction associated with decreased bioavailability of nitric oxide in the lungs and by impaired reabsorption of alveolar fluid. OBJECTIVE: To investigate whether dexamethasone or tadalafil reduces the incidence of HAPE and acute mountain sickness (AMS) in adults with a history of HAPE. DESIGN: Randomized, double-blind, placebo-controlled study performed in summer 2003. SETTING: Ascent from 490 m within 24 hours and stay for 2 nights at 4559 m. PATIENTS: 29 adults with previous HAPE. INTERVENTION: Prophylactic tadalafil (10 mg), dexamethasone (8 mg), or placebo twice daily during ascent and stay at 4559 m. MEASUREMENTS: Chest radiography was used to diagnose HAPE. A Lake Louise score greater than 4 defined AMS. Systolic pulmonary artery pressure was measured by using Doppler echocardiography, and nasal potentials were measured as a surrogate marker of alveolar sodium transport. RESULTS: Two participants who received tadalafil developed severe AMS on arrival at 4559 m and withdrew from the study; they did not have HAPE at that time. High-altitude pulmonary edema developed in 7 of 9 participants receiving placebo and 1 of the remaining 8 participants receiving tadalafil but in none of the 10 participants receiving dexamethasone (P = 0.007 for tadalafil vs. placebo; P < 0.001 for dexamethasone vs. placebo). Eight of 9 participants receiving placebo, 7 of 10 receiving tadalafil, and 3 of 10 receiving dexamethasone had AMS (P = 1.0 for tadalafil vs. placebo; P = 0.020 for dexamethasone vs. placebo). At high altitude, systolic pulmonary artery pressure increased less in participants receiving dexamethasone (16 mm Hg [95% CI, 9 to 23 mm Hg]) and tadalafil (13 mm Hg [CI, 6 to 20 mm Hg]) than in those receiving placebo (28 mm Hg [CI, 20 to 36 mm Hg]) (P = 0.005 for tadalafil vs. placebo; P = 0.012 for dexamethasone vs. placebo). No statistically significant difference between groups was found in change in nasal potentials and expression of leukocyte sodium transport protein messenger RNA. LIMITATIONS: The study involved a small sample of adults with a history of HAPE. CONCLUSIONS: Both dexamethasone and tadalafil decrease systolic pulmonary artery pressure and may reduce the incidence of HAPE in adults with a history of HAPE. Dexamethasone prophylaxis may also reduce the incidence of AMS in these adults. ClinicalTrials.gov identifier: NCT00274430.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2006

High altitude-induced pulmonary oedema.

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.

Acclimatization↗
PubMed2006

Long-term experience with oral or inhaled vasodilator combination therapy in patients with pulmonary hypertension.

BACKGROUND: Disease progression in pulmonary hypertension (PH) is common despite standard vasodilator monotherapy with iloprost, bosentan or sildenafil. OBJECTIVE: To investigate if the combination of these non-invasively applicable treatments is an effective option to address the multiple pathophysiological mechanisms present in PH. METHODS: We analysed the clinical course of 23 patients with PH, diagnosed as idiopathic (n = 15), chronic thromboembolic (n = 4), and associated with collagen vascular disease (n = 4), receiving combination vasodilator therapy at our institution. RESULTS: Vasodilator therapy before combination therapy consisted of inhaled iloprost (I; n = 12), or oral bosentan (B; n = 6) at a mean duration of 19 +/- 3 months. The combination therapy added was B (n = 8), sildenafil (S; n = 6) or I (n = 4) and in five patients, combination therapy was given from the beginning (3x BS, 1x IS, 1x IBS). Under combination therapy, the 6-minute walk distance (6MWD) increased significantly by 46.7 +/- 24.8 m (p = 0.02) after three months, and after six months it was still 38.3 +/- 28.3 m (p = 0.17) longer than before combination therapy. Respective changes in the Borg Scale and the NYHA functional class were -1.05 +/- 0.49 (p = 0.014) and -0.42 +/- 0.19 (p = 0.02) after three months and -0.21 +/- 0.65 (p = 0.61) and -0.38 +/- 0.29 (p = 0.26) after six months. Only minor side effects were reported. CONCLUSION: Combination vasodilator therapy in severe PH is safe and well tolerated. It significantly improves exercise capacity and stabilises the functional class in patients with severe PH deteriorating under single-agent therapy.

Administration, Inhalation↗
PubMed2006

Changes in cerebral glucose metabolism after an expedition to high altitudes.

The possibility of persistent cerebral impairment due to exposure to extreme altitude and resulting hypoxic conditions is of great concern to both high altitude mountaineers and researchers. The aim of the present study was to investigate the effect of prolonged exposure to hypoxia on cerebral glucose metabolism, which probably precedes structural and functional impairment. Positron emission tomography (PET) employing [18F]-2-deoxy-2-fluoro-D-glucose (FDG) was performed, and the normobaric hypoxic ventilatory response (HVR) was assessed in 11 mountaineers before (pre) and after (post) climbing Mount Shisha Pangma (8048 m). During the climb, acute mountain sickness (AMS) symptoms were recorded and heart rate and oxygen saturation (SaO2) were measured daily. Neuropsychological evaluations were conducted at different heights. The difference FDGpost- FDGpre was analyzed voxel by voxel using statistical parametric mapping (SPM) and volumes of interest (VOI). SPM revealed two areas of increased cerebral FDG uptake after the expedition, one localized in the left cerebellum (+9.4%) and one in the white matter lateral of the left thalamus (+8.3%). The VOI analysis revealed increased postexpeditional metabolism in an area of the right cerebellum (+11%) and of the thalamus bilaterally (+3.7% on the left, +4.6% on the right). FDG-PET alterations did not correlate with changes in SaO2, HVR, or AMS scores. All neuropsychological test results during the climb were unremarkable. We conclude that a prolonged stay at an extreme altitude leads to regional specific changes in the cerebral glucose metabolism without any signs of neuropsychological impairment during the climb.

Acute Disease↗
PubMed2006

Comparable increase of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide levels in patients with severe sepsis, septic shock, and acute heart failure.

OBJECTIVE: B-type natriuretic peptide (BNP) and N-terminal pro-BNP measurements are used for the diagnosis of congestive heart failure (HF). However, the diagnostic value of these tests is unknown under septic conditions. We compared patients with severe sepsis or septic shock and patients with acute HF to unravel the influence of the underlying diagnosis on BNP and N-terminal pro-BNP levels. DESIGN: Prospective, clinical study. SETTING: Academic medical intensive care unit (ICU). PATIENTS: A total of 249 consecutive patients were screened for the diagnosis of sepsis or HF. Sepsis was defined according to published guidelines. HF was diagnosed in the presence of an underlying heart disease and congestive HF, pulmonary edema, or cardiogenic shock. INTERVENTIONS: BNP and N-terminal pro-BNP were measured from blood samples that were drawn daily for routine analysis. MEASUREMENTS AND MAIN RESULTS: We identified 24 patients with severe sepsis or septic shock and 51 patients with acute HF. At admission, the median (range) BNP and N-terminal pro-BNP levels were 572 (13-1,300) and 6,526 (198-70,000) ng/L in patients with sepsis and 581 (6-1,300) and 4,300 (126-70,000) ng/L in patients with HF. The natriuretic peptide levels increased during the ICU stay, but the differences between the groups were not significant. Nine patients with sepsis and eight patients with HF were monitored with a pulmonary artery catheter. Mean (sd) pulmonary artery occlusion pressure were 16 (4.2) and 22 (5.3) mm Hg (p = .02), and cardiac indexes were 4.6 (2.8) and 2.2 (0.6) L/min/m (p = .03) in patients with sepsis and HF, respectively. Despite these clear hemodynamic differences BNP and N-terminal pro-BNP levels were not statistically different between the two groups. CONCLUSION: In patients with severe sepsis or septic shock, BNP and N-terminal pro-BNP values are highly elevated and, despite significant hemodynamic differences, comparable with those found in acute HF patients. It remains to be determined how elevations of natriuretic peptide levels are linked to inflammation and sepsis-associated myocardial dysfunction.

Acute Disease↗
PubMed2006

Do changes in lung function predict high-altitude pulmonary edema at an early stage?

PURPOSE: Ascent to high altitude is associated with alterations in lung function. The mechanisms of these changes and whether they reflect early stages of high-altitude pulmonary edema (HAPE) has been debated. Therefore, we investigated the time course of pulmonary function in relation to hemodynamics and clinical symptoms in mountaineers ascending rapidly to high altitude. METHODS: In 26 unacclimatized subjects we assessed spirometry, single-breath nitrogen washout, diffusing capacity (DLCO), and Doppler echocardiography in Zurich, 490 m, after climbing within 24 h to Monte Rosa, 4559 m, and after one night at 4559 m. RESULTS: Mean (+/- SD) FVC fell from 103 +/- 9% predicted in Zurich to 96 +/- 10% predicted at 4559 m, FEV1/FVC increased from 0.82 +/- 0.06 to 0.84 +/- 0.08, and closing volume increased from 0.35 +/- 0.14 to 0.44 +/- 0.11 L above residual volume (P < 0.05, all changes). On the following day at 4559 m, closing volume remained elevated in 9 of 21 subjects who had a lower DLCO but similar pulmonary artery systolic pressures compared with the remaining 12 subjects (40 +/- 8 vs 43 +/- 7 mm Hg, P = NS). None of the subjects had overt HAPE. CONCLUSION: We conclude that changes in pulmonary function after rapid ascent to high altitude were consistent with interstitial fluid accumulation, but they were not related to changes in pulmonary artery pressure. Individual lung function responses to high-altitude exposure varied largely and did not predict subsequent HAPE.

Adolescent↗
PubMed2006

Chronic thromboembolic and pulmonary arterial hypertension share acute vasoreactivity properties.

BACKGROUND: Pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) are the major classes of pulmonary hypertensive disorders according to the World Health Organization; both lead to right heart failure and death. A better understanding of disease mechanisms has led to the suggestion that the thromboembolic and nonthromboembolic types of pulmonary hypertension may share pathophysiologic features. We therefore compared acute vasoreactivity and proximal pulmonary artery compliance in patients with PAH and CTEPH during the initial diagnostic heart catheterization. METHODS: Right heart catheterization using a flow-directed Swan-Ganz catheter was performed in patients with CTEPH (n = 22) and PAH (n = 35). Pulmonary hemodynamics were assessed at baseline, during the inhalation of 40 ppm of nitric oxide, and 30 min after the inhalation of 10 mug of iloprost. To assess the proximal pulmonary artery compliance, the pulse pressure (PP) [systolic-diastolic pressure] and the fractional PP (PPf) [divided by the mean pressure] were calculated. RESULTS: Both vasodilators produced similar hemodynamic improvement, and the difference between CTEPH and PAH was not significant. The baseline PP and PPf did not vary between the two groups. CONCLUSION: Patients with PAH and CTEPH show similar acute vasoreactivity to inhaled nitric oxide and iloprost, and have similar pulmonary artery compliance. These findings support the presence of some shared pathophysiologic pathways in both disorders and may lead to therapeutic implications in patients with inoperable CTEPH.

Adult↗
PubMed2005

Inhaled nitric oxide therapy in adults: European expert recommendations.

BACKGROUND: Inhaled nitric oxide (iNO) has been used for treatment of acute respiratory failure and pulmonary hypertension since 1991 in adult patients in the perioperative setting and in critical care. METHODS: This contribution assesses evidence for the use of iNO in this population as presented to a expert group jointly organised by the European Society of Intensive Care Medicine and the European Association of Cardiothoracic Anaesthesiologists. CONCLUSIONS: Expert recommendations on the use of iNO in adults were agreed on following presentation of the evidence at the expert meeting held in June 2004.

Administration, Inhalation↗
PubMed2005

Effects of high altitude exposure on cerebral hemodynamics in normal subjects.

BACKGROUND AND PURPOSE: Acute mountain sickness (AMS) may be an early stage of high altitude cerebral edema. If so, AMS could result from an alteration of dynamic autoregulation of cerebral blood flow resulting in overperfusion of capillaries and vasogenic cerebral edema. METHODS: We measured middle cerebral artery blood flow velocity (Vmca) by transcranial Doppler and arterial blood pressure by finger plethysmography at 490 m and 20 hours after arrival at 4559 m in 35 volunteers who had been randomized to tadalafil, dexamethasone, or placebo in a study on the pharmacological prevention of high altitude pulmonary edema. A dynamic cerebral autoregulation index (ARI) was calculated from continuous recordings of Vmca and blood pressure during transiently induced hypotension. RESULTS: Altitude was associated with an increase in a cerebral-sensible AMS (AMS-C) score (P<0.001) and with a decrease in arterial oxygen saturation (Sao2), whereas average Vmca or ARI did not change. However, at altitude, the subjects with the lowest ARI combined with the lowest Sao2 presented with the highest AMS-C score (P<0.03). In addition, a stepwise multiple linear regression analysis on arterial Pco2, Sao2, and baseline or altitude ARI identified altitude ARI as the only significant predictor of the AMS-C score (P=0.01). The AMS-C score was lower in dexamethasone-treated subjects compared with high altitude pulmonary edema-susceptible untreated subjects. Neither tadalafil nor dexamethasone had any significant effect on Vmca or ARI. CONCLUSIONS: High altitude hypoxia is associated with impairment in the regulation of the cerebral circulation that might play a role in AMS pathogenesis.

Adult↗
PubMed2005

Consensus statement on chronic and subacute high altitude diseases.

This is an international consensus statement of an ad hoc committee formed by the International Society for Mountain Medicine (ISMM) at the VI World Congress on Mountain Medicine and High Altitude Physiology (Xining, China; 2004) and represents the committee's interpretation of the current knowledge with regard to the most common chronic and subacute high altitude diseases. It has been developed by medical and scientific authorities from the committee experienced in the recognition and prevention of high altitude diseases and is based mainly on published, peer-reviewed articles. It is intended to include all legitimate criteria for choosing to use a specific method or procedure to diagnose or manage high altitude diseases. However, the ISMM recognizes that specific patient care decisions depend on the different geographic circumstances involved in the development of each chronic high altitude disease. These guidelines are established to inform the medical services on site who are directed to solve high altitude health problems about the definition, diagnosis, treatment, and prevention of the most common chronic high altitude diseases. The health problems associated with life at high altitude are well documented, but health policies and procedures often do not reflect current state-of-the-art knowledge. Most of the cases of high altitude diseases are preventable if on-site personnel identify the condition and implement appropriate care.

Acclimatization↗
PubMed2005

Determinants of acute mountain sickness and success on Mount Aconcagua (6962 m).

To investigate the determinants of acute mountain sickness (AMS) and of summiting in expedition-style mountaineering, 919 mountaineers (15.4% female) leaving Aconcagua Provincial Park at the end of an expedition to Mt. Aconcagua (6962 m) via the normal route were retrospectively evaluated by questionnaires. Symptoms of AMS were reported from the day when mountaineers felt worst. The prevalence of AMS, defined as a Lake Louise Score (self-assessment) > 4, was 39%. Low AMS scores were associated with faster ascent rates. The following parameters were independent predictors for AMS: no susceptibility for AMS (odds ratio, OR, 0.24; 95% confidence interval 0.17 to 0.35) more than 10 exposures per year above 3000 m (OR 0.60; 0.41 to 0.86), and previous exposures above 6000 m (OR, 0.48; 0.33 to 0.68). This last variable increased the OR for summiting 3.7-fold while female gender reduced this OR to 0.41 (0.25 to 0.67). Susceptibility and few exposures to high altitude are major predictors for AMS on Aconcagua, but AMS does not substantially reduce the chances for summiting. Those who are often in the mountains and who have already climbed to altitudes above 6000 m and are not susceptible for AMS have the best options for summiting Aconcagua.

Acclimatization↗
PubMed2005

Physiological aspects of high-altitude pulmonary edema.

High-altitude pulmonary edema (HAPE) develops in rapidly ascending nonacclimatized healthy individuals at altitudes above 3,000 m. An excessive rise in pulmonary artery pressure (PAP) preceding edema formation is the crucial pathophysiological factor because drugs that lower PAP prevent HAPE. Measurements of nitric oxide (NO) in exhaled air, of nitrites and nitrates in bronchoalveolar lavage (BAL) fluid, and forearm NO-dependent endothelial function all point to a reduced NO availability in hypoxia as a major cause of the excessive hypoxic PAP rise in HAPE-susceptible individuals. Studies using right heart catheterization or BAL in incipient HAPE have demonstrated that edema is caused by an increased microvascular hydrostatic pressure in the presence of normal left atrial pressure, resulting in leakage of large-molecular-weight proteins and erythrocytes across the alveolarcapillary barrier in the absence of any evidence of inflammation. These studies confirm in humans that high capillary pressure induces a high-permeability-type lung edema in the absence of inflammation, a concept first introduced under the term "stress failure." Recent studies using microspheres in swine and magnetic resonance imaging in humans strongly support the concept and primacy of nonuniform hypoxic arteriolar vasoconstriction to explain how hypoxic pulmonary vasoconstriction occurring predominantly at the arteriolar level can cause leakage. This compelling but as yet unproven mechanism predicts that edema occurs in areas of high blood flow due to lesser vasoconstriction. The combination of high flow at higher pressure results in pressures, which exceed the structural and dynamic capacity of the alveolar capillary barrier to maintain normal alveolar fluid balance.

Altitude↗
PubMed2005

Monitoring carbon dioxide tension and arterial oxygen saturation by a single earlobe sensor in patients with critical illness or sleep apnea.

OBJECTIVES: The purpose of the study was to evaluate a novel, combined sensor for transcutaneous monitoring of arterial oxygen saturation and carbon dioxide tension. DESIGN: The new monitoring technique was compared to established reference methods. SETTING: ICU and sleep laboratory of a university hospital. PATIENTS: Eighteen critically ill adult patients with acute respiratory failure or heart failure, and 12 patients with sleep apnea (mean [+/- SD] apnea/hypopnea index, 43 +/- 24 events per hour). MEASUREMENTS: Continuous measurements were performed over several hours by the novel heated (temperature, 42 degrees C) earlobe sensor (TOSCA; Linde Medical Sensors; Basel, Switzerland), incorporating electrochemical and optical elements for carbon dioxide measurement (PtcCO2) and pulse oximetry (SpO2), respectively. The data were compared to the results of repeated arterial blood gas analyses in critically ill patients and to simultaneous nocturnal pulse oximetry performed with different devices with earlobe or finger sensors in sleep apnea patients. RESULTS: In critically ill patients, the mean difference and limits of agreement (bias +/- 2 SDs) of transcutaneous PtcCO2 vs arterial PaCO2 were 3 +/- 7 mm Hg; the corresponding values for changes in PtcCO2 vs PaCO2 were 1 +/- 6 mm Hg. The bias +/- 2 SDs for pulse oximetric SpO2 vs arterial oxygen saturation (SaO2) were 1 +/- 4%. In sleep apnea patients, the combined earlobe sensor identified more transient oxygen desaturations, and the rate of change in oxygen saturation during events was greater compared to those with other tested pulse oximeters, indicating a faster response. CONCLUSIONS: Due to its ability to accurately assess both ventilation and oxygenation by a single transcutaneous sensor, the described noninvasive monitoring technique is a valuable tool for respiratory monitoring with potential applications in critical care and sleep medicine.

Acute Disease↗
PubMed2004

Identification and quantitation of novel metabolites of amiodarone in plasma of treated patients.

In mammals, mono-N-desethylamiodarone (MDEA) is the only known metabolite of amiodarone. Our previous experiments demonstrated that in vitro MDEA may be hydroxylated, N-dealkylated, and deaminated. In this report, we investigated the concentration of these microsomal metabolites in the plasma of patients receiving amiodarone. The presence of the hydroxy-amiodarone and deiodinated amiodarone was also additionally investigated. A high-performance liquid chromatography-atmospheric pressure chemical ionization tandem mass spectrometry (HPLC-APCI-MS/MS) quantitative assay using morpholine-amiodarone as internal standard was developed for measuring these metabolites in the range of 3-250 ng ml(-1). In the concentration ranges 5-50 and 50-250 ng ml(-1), the coefficients of variation of the measurements were less than 14 and 7%, respectively. The concentrations of investigated compounds in plasma of patients (n=14) receiving amiodarone (0.2 g day(-1), orally for >2 months) varied inter-individually and were 140.0+/-85.2, 39.1+/-20.8, and 26.2+/-15.2 ng ml(-1) for 3'OH-mono-N-desethylamiodarone, di-N-desethylamiodarone, and deaminated amiodarone, respectively. The concentrations of MDEA and amiodarone in these samples were 970+/-347 and 11163+/-435 ng ml(-1), respectively. In contrast, the studied compounds were not detectable in plasma samples from eight patients receiving amiodarone intravenously. Qualitatively, in the plasma of patients receiving amiodarone orally, hydroxylated amiodarone was also positively detected by assaying the [M+H](+) ions at m/z 662, but the deiodo-metabolites of amiodarone were not detected using mass spectrometry. Thus, in humans, amiodarone and MDEA were biotransformed by dealkylation, hydroxylation, and deamination.

Aged↗
PubMed2003

High altitude pulmonary oedema.

Altitude, speed and mode of ascent and, above all, individual susceptibility are the most important determinants for the occurrence of high altitude pulmonary oedema (HAPE). This illness usually develops only within the first 2-5 days after acute exposure to altitudes above 2500-3000 m. An excessive rise in pulmonary artery pressure preceding oedema formation is the crucial pathophysiological factor. Recent investigations using right heart catheterisation and bronchoalveolar lavage (BAL) in incipient pulmonary oedema have shown that HAPE is a hydrostatic oedema in the presence of normal left atrial pressure with non-inflammatory high permeability leakage of the alveolocapillary barrier and mild alveolar haemorrhage. An inflammatory response may develop later in more advanced cases, as has been documented by BAL. Furthermore, decreased fluid clearance from the alveoli may contribute to such non-cardiogenic pulmonary oedema. Supplemental oxygen is the primary treatment in areas with medical facilities, while the treatment of choice in remote mountain areas is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible. Even susceptible individuals can avoid HAPE if they ascend slowly with an average gain of altitude not exceeding 300-350 m/day above an altitude of 2500 m.

Altitude Sickness↗
PubMed2003

Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes.

OBJECTIVES: We sought to assess the mechanism and prognostic value of elevated troponins in patients without acute coronary syndromes (ACS). BACKGROUND: Cardiac troponins are used as specific markers for the diagnosis of ACS. Recent studies reported a considerable number of critically ill patients without ACS as being troponin-positive, especially patients with sepsis, pulmonary embolism, renal failure, and stroke. METHODS: We analyzed 58 consecutive, critically ill patients admitted for reasons other than ACS, according to their troponin status. Thirty-day mortality, left ventricular ejection fraction (LVEF), and a panel of inflammatory cytokines were compared between troponin-positive and troponin-negative patients. Relevant coronary artery disease was excluded either by stress echocardiography or autopsy. RESULTS: Of the 58 critically ill patients, 32 (55%) without evidence of ACS were troponin-positive. Positive troponin levels were associated with higher mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006). Troponin-positive patients had significantly higher median levels of tumor necrosis factor (TNF)-alpha, its soluble receptor, and interleukin (IL)-6. A subgroup of 10 aplastic patients was troponin-negative at study entry. Three became troponin-positive during leukocyte recovery and subsequently died, whereas all the others stayed troponin-negative and survived. Flow-limiting coronary artery disease was not demonstrable at autopsy or stress echocardiography in 72% of troponin-positive patients. CONCLUSIONS: Elevated troponin is a mortality risk factor for medical intensive care patients admitted for reasons other than ACS. It is associated with decreased left ventricular function and higher levels of TNF-alpha and IL-6.

Acute Disease↗