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Slow continuous ultrafiltration (SCUF) is an extracorporeal therapy able to reduce fluid overload in chronic or acute heart failure resistant to diuretics. An in-vitro study demonstrated the SCUF feasibility using a standard fluid infusion central venous catheter (CVC). We describe the clinical application of this SCUF in regional citrate anticoagulation (SCUF-RCA) in a patient admitted to the Intensive Care Unit for acute decompensate heart failure with severe systemic fluid overload resistant to diuretics. To avoid risks deriving from a new catheterization, we used a pre-existing multi-lumen CVC for drug administration to provide 10 h of SCUF-RCA with a blood flow of 35 mL/min and 100 mL/h of ultrafiltration with a final weight loss of 1 Kilogram without technical and clinical complications. The patient had a hemodynamics improvement with the diuresis recovery from the previous oliguria after the SCUF-RCA. This clinical case can open the use of the SCUF-RCA in the clinical practice to treat the fluid overload unresponsive to maximal diuretic therapy not exposing the patient to the risks and complications related to the use of SCUF with CVC for dialysis and systemic anticoagulation with heparin. Accordingly, this technique may be useful in the treatment of fluid overload in outpatients.

Background The spectrum of Coronavirus Disease 2019 (COVID-19) is broad and thus early appropriate risk stratification can be helpful. Our objectives were to define the frequency of myocardial injury using high-sensitivity cardiac troponin I (hs-cTnI) and to understand how to use its prognostic abilities. Methods Retrospective study of patients with COVID-19 presenting to an Emergency Department (ED) in Italy in 2020. Hs-cTnI was sampled based on clinical judgment. Myocardial injury was defined as values above the sex-specific 99th percentile upper reference limits (URLs). Most data is from the initial hospital value. Results 426 unique patients were included. Hs-cTnI was measured in 313 (73.5%) patients; 85 (27.2%) had myocardial injury at baseline. Patients with myocardial injury had higher mortality during hospitalization (hazard ratio = 9 [95% confidence interval (CI) 4.55–17.79], p 13 [OR (95% CI): 0.48 (0.08, 2.65), p = 0.40]. Initial hs-cTnI

High-sensitivity cardiac troponin (hs-cTnT) is often increased in patients with atrial fibrillation/flutter, portending a poor prognosis. The etiologies for these increases have not been systematically investigated. Our aim was to define prevalence/significance of structural cardiac abnormalities in patients with atrial fibrillation/flutter and high-sensitivity cardiac troponin T (hs-cTnT) increases.This is a retrospective observational cohort study of patients with atrial fibrillation/flutter diagnosis with hs-cTnT measurements, echocardiograms, and coronary angiograms. Myocardial injury was defined as hs-cTnT10 ng/L for women and15 ng/L for men. Cases with myocardial injury were adjudicated according to the Fourth Universal Definition of Myocardial Infarction.Patients with definite causes for increased hs-cTnT (n = 875) were tabulated but not evaluated further; common diagnoses were type 1 myocardial infarction, critical illness, and known heart failure. Of the remaining 401, increased hs-cTnT was present in 336 (84%) patients. Of those, 78% had nonischemic myocardial injury, the remaining (n = 75, 22%) had type 2 myocardial infarction. Patients with elevated hs-cTnT had greater left ventricular mass index, left ventricular filling pressures, and right ventricular systolic pressure. They more frequently had significant coronary artery disease (47% vs 31%, P = .016), especially in type 2 myocardial infarction. With logistic regression, age, sex (F), diabetes, left ventricular mass index, e' medial velocity, and right ventricular systolic pressure were independent determinants of myocardial injury. One-year mortality was higher in patients with myocardial injury.Structural heart abnormalities are common in patients with atrial fibrillation/flutter and increased hs-cTnT. Causes of myocardial injury should be elucidated in each patient to craft appropriate therapies.

Background Although oral P2Y12 inhibitors are key in the management of patients with non-ST elevation acute coronary syndrome (NSTE-ACS), the optimal timing of their administration is not well defined. Objective to compare downstream and upstream oral P2Y12 inhibitors administration strategies in NSTE-ACS patients undergoing invasive management. Methods We performed a randomized, adaptive, open-label, multi-center, clinical trial. Patients were randomly assigned to receive pre-treatment with ticagrelor before angiography (upstream group) or no pre-treatment (downstream group). Patients in the downstream group undergoing percutaneous coronary intervention (PCI) were further randomized to receive ticagrelor or prasugrel. The primary hypothesis was superiority of the downstream over the upstream strategy on the combination of efficacy and safety events (net clinical benefit). Results We randomized 1449 patients to downstream or upstream oral P2Y12 inhibitor administration. A prespecified stopping rule for futility at interim analysis led the trial to be stopped. The rate of the primary endpoint, a composite of death due to vascular causes, non-fatal myocardial infarction or non-fatal stroke, and Bleeding Academic Research Consortium (BARC) type 3, 4 and 5 bleedings through day 30, did not differ significantly between the downstream and upstream groups (Absolute Risk Reduction (ARR%) -0.46 [-2.90; 1.90]).These results were confirmed among patients undergoing PCI (72% of population) and regardless of the timing of coronary angiography (within or after 24 hours from enrolment). Conclusions Downstream and upstream oral P2Y12 inhibitors administration strategies were associated with low incidence of ischemic and bleeding events and minimal numerical difference of event rates between treatment groups. These findings led to premature interruption of the trial and suggest the unlikelihood of enhanced efficacy of one strategy over the other. [Funded by the Italian Society of Interventional Cardiology (SICI-GISE)]

A 61-year-old man suffering from myasthenia gravis with predominant bulbar involvement since 10 months before admission, was diagnosed with thymoma in April 2021. He had no relevant comorbidities except for history of polymorphic ventricular ectopic beats. In this regard, in 2019 he had undergone transthoracic echocardiogram and coronary computed tomography angiography, which resulted both normal. After 1 month, due to poor response to standard medical therapy with prednisone and pyridostigmine and in preparation for thymectomy, an intravenous immunoglobulins (IVIG) treatment was prescribed leading to mild clinical improvement (Myasthenia Gravis Foundation of America Clinical Classification IIIA—MGFA). Two weeks later, the patient underwent robotic-assisted thoracoscopic thymectomy without complications. Pathological findings were consistent with type B1 Thymoma classified as Masaoka Stage IIB (TNM Stage pT1a). After discharge the patient complained a rapid worsening of neurological symptoms (MGFA IIIB) leading to an urgent hospitalization for Myasthenia Gravis exacerbation in the middle of June. On admission Intravenous Immunoglobulins (IVIG) treatment was immediately started. After administration of the second IVIG dose, he had a myasthenic crisis complicated by refractory heart failure with significant increase of cardiac troponin up to 5.768 ng/L, requiring invasive ventilation, inotropic support and urgent transfer to the Cardiac Intensive Care Unit (CICU). The 2D echo showed severe left ventricular systolic dysfunction (LVEF 20%) with diffuse hypokinesis. The patient underwent cardiac catheterization and coronary angiography that confirmed severe reduction of the LVEF (LVEF 23%) with embolic occlusion of the distal posterior descending coronary artery (PDA) without other significant coronary artery stenosis. An endomyocardial biopsy was performed, which revealed cardiomyocytes of normal dimensions with sporadic cytoplasmic vacuolization and excluded signs of inflammation, fibrosis, necrosis and viral myocarditis. The day after the patient completed IVIG treatment. During the following days, despite persistence of severe left ventricular systolic dysfunction, he was successfully weaned form inotropic and ventilatory support. At neurological evaluation he reported persistence of severe bulbar involvement with upper and lower limbs weakness. Five days later, the patient had a sudden cardiac arrest for pulseless electrical activity. Advanced cardiac life support requiring inotropes and invasive ventilation was performed for 28 min before returning to spontaneous circulation. The echocardiogram excluded pulmonary embolism and mechanical complications but showed severe left ventricular systolic dysfunction. A new coronary angiography showed clear coronary arteries including PDA. Because of severe haemodynamic compromise, an Impella CP device was implanted and set at maximum support level (P8 flow, >3 L/min). A neurological exam revealed no severe neurological sequelae. As a result of the long CPR the patient had a massive left haemothorax, initially treated with multiple blood transfusions and pleural drainage. Two days later, due to persistence of haemodynamic instability and active pleural bleeding with incessant severe anaemia the case underwent a Heart Team discussion where it was decided to escalate Impella CP device to Veno-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO) and then perform a video-assisted thoracoscopic evacuation of the haemothorax. Both procedures were carried out without complications. The patient had an immediate haemodynamic improvement which led to rapid weaning from inotropic support. Haemoglobin was stable. The 2D echo showed significant improvement of the LVEF (40%). After 3 days, given the persistence of haemodynamic stability, ECMO device was removed and invasive ventilation stopped shortly afterwards. Eleven days later, another 2D echo demonstrated complete recovery of left ventricular systolic function (LVEF 59%). Notwithstanding, the patient reported a progressive worsening of neurological symptoms with generalized myasthenia and severe bulbar involvement (MGFA IVB) along with episodes of respiratory muscle fatigue requiring non-invasive ventilation. For this reason, the patient was transferred to Subintensive Respiratory Unit and the case underwent a new multidisciplinary discussion involving neurologists, cardiologists and haematologists. Specialists agreed upon potential causal role of IVIG treatment in transient left ventricular dysfunction and considered re-administration absolutely contraindicated. Thus, they prescribed five plasmapheresis treatments and up-titration of corticosteroid therapy (methylprednisolone up to 60 mg od). An immediate and outstanding improvement of neurological symptoms was obtained (MGFA IIIA) and the patient was discharged from hospital 1 week later.

Aims Out-of-hospital cardiac arrest (OHCA) affects around 1/1000 person-years. Following return of spontaneous circulation (ROSC), the patient can manifest neurological impairment. A targeted temperature management (TTM) protocol is recommended to prevent hypoxic–ischaemic brain damage in patients with coma after cardiac arrest. Neuro-prognostication remains substantial for the prediction of clinical outcomes. To study clinical characteristics, overall survival, and neurological outcome of patients with Glasgow Coma Scale (GCS) Methods Observational retrospective study evaluating all patients with OHCA of presumed cardiac cause and with GCS Results One-hundred and five patients out of 107 patients initially selected were included in the study (77% male, mean age 67 years). At 30 days, mortality was 41% and 53% of patients had a poor neurological outcome (Cerebral Performance Category, CPC, 3–5). Sixty-nine patients (66%) underwent TTM. In regard of the circumstances of OHCA, index event in a private place [OR = 3.12 (1.43–7.11), P = 0.005], ineffective rhythm changes during resuscitation manoeuvres [OR = 2.40 (1.05–5.47), P = 0.037] and a greater amount of adrenaline administered during resuscitation [OR = 1.62 (1.27–2.06), P Conclusions In our population, at 30 days after cardiac arrest, survival rate and the rate of good neurological outcome were comparable to those of the major international registries and studies. Even though patients treated with TTM did not demonstrate significant differences in terms of neurological outcome, this might be related to study-sample size and patient selection. Results in the literature are still controversial on this topic. The MIRACLE score showed a good performance, making it suitable for clinical use in our population. Similarly, the proposed multivariate models are potentially useful for the elaboration of simple and effective prognostic scores in neurological risk stratification.

Patients admitted with acute medical conditions are at prolonged risk for venous thrombosis. The efficacy and safety, and the appropriate duration of thromboprophylaxis have not been clearly determined. In recent years, direct coagulation factor inhibitors have been successfully tested for the prevention and treatment of arterial and venous thromboembolism. Betrixaban is a novel direct inhibitor of factor Xa with a noteworthy pharmacological feature: limited renal clearance. Areas covered: This review focuses on the pharmacological profile of Betrixaban, including its clinical efficacy and safety. It also covers the results of the pivotal APEX trial assessing the safety and efficacy of betrixaban for extended thromboprophylaxis in patients with acute medical conditions. Expert opinion: The role of extended thromboprophylaxis in acutely ill medical patients is subject to debate. The beneficial results in terms of VTE prevention were offset by the relevant increase in major bleeding. Betrixaban is the only direct oral anticoagulant to have shown a favorable risk-benefit profile in this setting especially in patients at higher risk for thrombosis.

We present the case of a 18-year-old female with fulminant lymphocytic myocarditis caused by Parvovirus B19 (PVB19), successfully treated using temporary LVAD. In the literature there is no consensus on the surgical strategy. While some surgeons prefer to use a single device supporting only the LV, others prefer to start immediately with a biventricular supporting. At pre-procedural ultrasound evaluation, her anatomical features were not suitable for a percutaneous device such as the Impella. Thus, a temporary paracorporeal continuous flow LVAD was inserted. The heart recovery allowed LVAD removal 9 days after the implant. Supplementary Information The online version contains supplementary material available at 10.1007/s10047-021-01247-7.

Highlights • Several papers have reported increased concentrations of cardiac biomarkers in patients with COVID-19 disease, being elevated cardiac troponin values associated with disease severity and a poor prognosis, as in many other non-ACS pathologies. • Our study aimed to evaluate if the kinetic release of the troponin I concentrations in SARS-CoV-2 patients, evaluated with an high-sensitivity method (hs-TnI) might provide additional, clinically useful information in identifying the underlying mechanisms of troponins release. • The obtained results shows different patterns in troponin I kinetics, suggesting different types of myocardial injury of varying severity associated to COVID 19, providing clinical data for stratifying risk, establishing the prognosis and gaining relevant epidemiological insight., Background Major cardiac complications have been described in SARS-CoV-2 patients. The study of cardiac troponin’ kinetic release is the recommended approach to differentiate acute from chronic injury, in order to clinically manage different cardiac diseases. Aim To investigate whether serial measurements of high sensitivity troponin I (hs-cTnI) might provide additional information in SARS-CoV-2 patients’s clinical management. Methods 113 consecutive patients suffering from microbiology proven SARS-CoV2-infection have been studied. Hs-cTnI has been measured in lithium-heparin plasma samples using STAT High Sensitive Troponin I (Architect i2000, Abbott Diagnostics), being 99th percentiles 16 and 34 ng/L for females and males respectively. Results In 69 out of 113 patients hs-cTnI has been measured, showing in 31 (45%) values higher than 99th percentiles in at least one occasion. In 50 patients (72%) a kinetic evaluation (at least 2 measurements during 24 h) has been carried out. Patients were subdivided into five groups: 1 (n=44) and 2 (n=19) no measurement of hs-cTnI or no monitoring respectively; 3 (n=15) no significant variations during monitoring; 4 (n=8) and 5 (n=27) significant variations with values persistently below or sometimes higher than 99th percentiles, respectively. Group 5 patients had a longer hospital stay (median 37 days, p=0.0001), a more aggressive disease (6 out of 27, 22%, died), more often need admission to ICU (n=25, 92.6%, p

Although oral P2YThe purpose of this study was to compare downstream and upstream oral P2YWe performed a randomized, adaptive, open-label, multicenter clinical trial. Patients were randomly assigned to receive pre-treatment with ticagrelor before angiography (upstream group) or no pre-treatment (downstream group). Patients in the downstream group undergoing percutaneous coronary intervention were further randomized to receive ticagrelor or prasugrel. The primary hypothesis was the superiority of the downstream versus the upstream strategy on the combination of efficacy and safety events (net clinical benefit).We randomized 1,449 patients to downstream or upstream oral P2YDownstream and upstream oral P2Y

Reduction of kidney function and heart disease frequently coexisted in the seam patient. The relation between renal and heart function is quite complex and bring out some unresolved questions about diagnosis (mostly related to the biomarkers levels interpretation), pharmacological therapy (mostly related to drugs kinetics and efficacy), and non-pharmacological therapy. Patients with kidney dysfunction (KD) are frequently excluded and underrepresented in the large trials. It is well-known that coronary revascularization reduces mortality also in KD patients presenting with acute coronary syndrome. However, acute kidney injury (AKI), primarily related at contrast medium administration, is worse prognosis. For this reason, prevention, early diagnosis, and effective therapy of ACK are key elements in assistance of these patients. In this context, recently, some new biomarkers of renal function have been proposed. Frequently, patients with acute coronary syndromes and kidney disease are undertreated, worsening their prognosis. Undertreatment and comorbidities associated with renal dysfunction explain the higher mortality of these patients.

Poor exercise capacity, abnormal heart rate responses, and electrocardiographic abnormalities during treadmill exercise testing independently predict mortality. The combined relationship of these 3 variables to determine the incremental increase in mortality was compared in groups with and without known cardiovascular disease (CVD).Patients referred for treadmill exercise testing during 1986 to 1991 were included. Exercise capacity74% (of age- and gender-predicted value), heart rate reserve of68 beat/min, and horizontal or down-sloping ST depression ofor =1 mm were considered abnormal. Cox proportional hazards regression was used to determine all-cause mortality (average follow-up of 16 years) based on the number of exercise test abnormalities (0, 1, 2, or all 3).Among 10,897 patients, 20.9% (n = 2,277) had CVD. Poor exercise capacity and limited heart rate reserve were associated with increased risk of mortality (P.0001) in both groups; however, abnormal exercise electrocardiogram was associated with an increased risk of mortality in the no-CVD group only (P.0001). A graded increase in mortality was observed with increase in number of abnormal exercise test results in both groups. Patients without CVD having 2 or 3 abnormal exercise test results had a similar age-adjusted risk of long-term mortality as those with CVD but normal exercise test results, with a hazard ratio comparing these groups = 1.01 (95% CI 0.79-1.28).The combinatorial approach validates the prognostic significance of multiple exercise test variables. The presence ofor =2 exercise test abnormalities may constitute a "CVD risk equivalent" in patients without CVD.

It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease. Troponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated.

To the Editor: Constrictive pericarditis (CP) often is a challenging diagnosis despite sophisticated modalities ([1–4][1]). If a simple test could alert physicians to the possibility of CP in patients with evidence of heart failure, it would be valuable. Recent data ([5][2]) suggest that brain

Refractory cardiogenic shock is characterized by severe hemodynamic instability with high mortality rate. In most critical patients extracorporeal membrane oxygenation (ECMO) is the only therapy available nowadays that gives a possibility to survive. It guarantees continuous organs perfusion with

Elevations in troponin level have prognostic importance in critically ill patients, including those with gastrointestinal (GI) bleeding. However, there are no data addressing the independent association of troponin levels and mortality, adjusted for the severity of the underlying disease, in patients with GI bleeding.This study was designed to determine whether troponin T elevations are independently associated with in-hospital, short-term (30 days), and long-term mortality in medical intensive care unit patients with GI bleeding after adjusting for the severity of disease measured by the Acute Physiology, Age, and Chronic Health Evaluation score prognostic system.Retrospective study.We examined the Acute Physiology, Age, and Chronic Health Evaluation III database and cardiac troponin T levels from patients consecutively admitted to the medical intensive care unit at Mayo Clinic, Rochester, MN, with acute GI bleeding.Between August 2000 and July 2005, 1076 patients with acute GI bleeding consecutively admitted to the medical intensive care units.In-hospital, short-term (30 days), and long-term all-cause mortality.During hospitalization, 8.0% of deaths occurred in patients with troponin T0.01% and 11.9% with troponin Tor = 0.01 (p = 0.083). At 30 days, mortality was 10.1% and 18.8% in patients without and with elevations of troponins, respectively (p0.001). The Kaplan-Meier expected probability of survival at 1-, 2-, and 3-yr follow-up was 54.2%, 40.8%, and 30.4% with troponin Tor = 0.01 microg/L and 78.3%, 69.3%, and 61.5% with troponin T0.01 microg/L (p0.001). After adjustment for severity of disease and baseline characteristics, cardiac troponin levels were associated only with long-term mortality (p0.001).This is a retrospective, single-center study which included only patients in whom troponin level was determined upon admission.In patients with GI bleeding severe enough to require admission to the medical intensive care unit, admission troponin T elevations are associated with long-term but not short-term mortality.

Background Cardiac troponins are the markers of choice for the diagnosis of acute myocardial infarction. The objective of this study was to compare the frequency of “aborted myocardial infarction” (no detectable myocardial injury) determined by measurement of troponin versus that determined by creatine kinase (CK) and creatine kinase–muscle brain (CK-MB) measurement criteria among patients with ST-elevation myocardial infarction (STEMI) who received reperfusion therapy. Methods Since 2004, the Mayo Clinic (Rochester, MN) has had a standard reperfusion protocol for the treatment of patients with STEMI. During the study period, 767 patients presented with new or presumed new ST elevation or left bundle block. Results The diagnosis of STEMI was confirmed in 765 (99.7%) patients. Using the 99th percentile cutoff value, troponin T elevations occurred in 765 (100%) of 765 patients when serial samples were available. Creatine kinase–MB levels of twice or more the upper limit of normal occurred in 681 (90.1%) of 749 patients with serial samples for CK-MB, and CK equal or greater than twice the gender-specific upper limits of normal occurred in 521 (78.8%) of 661 patients with serial samples for CK available. Conclusion The frequency of aborted myocardial infarction is 0% when using troponin at the 99th percentile cutoff as recommended by contemporary guidelines from the European Society of Cardiology (Nice, France) and American College of Cardiology (Washington, DC).

Troponin elevations are common in critically ill patients. Whether they are predictors of mortality independent of the severity of the underlying disease is unclear.To determine whether troponin elevations predict in-hospital, short-term, and long-term mortality in medical intensive care unit patients independent of the severity of the underlying disease as measured by Acute Physiology and Chronic Health Evaluation III prognostic system.Retrospective study.We examined the Acute Physiology and Chronic Health Evaluation III database and cardiac troponin T levels of medical intensive care unit patients at Mayo Clinic, Rochester, MN.In all, 1,657 patients consecutively admitted to medical intensive care units between August 2000 and December 2001.In-hospital, short-term (30-day), and long-term all-cause mortality.During hospitalization, 12.5% of patients with a cardiac troponin T0.01 microg/L suffered deaths compared with 29.5% among those with cardiac troponin Tor = 0.01 microg/L (p.001). At 30 days, mortality was 13.7% without and 34.6% with elevations (p.001). The expected probability of survival at 1-, 2-, and 3-yr follow-up was 43.7%, 33.8%, and 25.7% among patients with cardiac troponin Tor = 0.01 microg/L and 75.3%, 67.6%, and 62.9% in those with cardiac troponin T0.01 microg/L, respectively (p.001). After adjustment for the severity of disease and baseline characteristics, cardiac troponin levels were still associated with in-hospital, short-term, and long-term mortality (p = .006, p = .007, and p = .001, respectively).This is a single-site retrospective study that included only patients in whom a troponin level was obtained on admission.In medical intensive care unit patients, admission troponin levels are independently associated with short- and long-term mortality, even after adjustment for severity of disease.

We recently cared for several patients with chest discomfort characteristic of coronary disease, electrocardiogram (ECG) changes, and increasing troponin concentrations. Coronary angiography revealed mild or no coronary artery disease (CAD), so we evaluated these patients with contrast-enhanced cardiac MRI. Our data suggest that these patients had myocardial infarction (MI). With Institutional Review Board permission, we reviewed our angiography database for patients with normal coronary arteries or mild coronary artery disease during the period from January 2005 to November 1, 2006, to augment those cases we found clinically. Inclusion criteria included presentation with acute coronary syndrome, increased serum troponin T concentration (>0.01 μg/L), or mild or absent CAD by angiography and a contrast-enhanced cardiac MRI (CE-CMR) considered diagnostic for infarction. Patients with prior infarction, known CAD, heart failure, pulmonary embolism, or suspected pericarditis/myocarditis were excluded. Eight patients met these criteria. All angiogram results were reviewed by one of the investigators (V.M.). CE-CMR studies performed on a GE Signa CVi system …

We evaluated relationships among two circulating molecular forms of brain natriuretic peptide (BNP32 and NT-proBNP), severity of hypertension (HTN), and cardiac hypertrophy in subjects with mild, moderate, and severe HTN. We prospectively studied 78 patients (43 males; mean age 51.4 ± 11 yr) with essential HTN and 28 age- and sex-matched controls. BNP32 and NT-proBNP were measured by radioimmunoassay. In grade 1 HTN, BNP32 was not elevated and NT-proBNP was reduced ( P = 0.030) compared with controls. However, log-transformed values of BNP32 and NT-proBNP were both increased with severity of HTN from grade 1 to 3 ( P

The diagnosis of acute myocardial infarction (AMI) as defined by the World Health Organization (WHO) was based for many years on the presence of two of three possible criteria: clinical symptoms compatible with AMI, typical electrocardiogram changes, and increases in markers of cardiac injury. However, because of the very good sensitivity and specificity of creatine kinase-MB (CK-MB), it eventually became rare to diagnose AMI in the absence of elevations of this biomarker. Thus, although never formally embraced by WHO, the clinical diagnosis of AMI became dependent on elevation of a biomarker of myocardial injury in the appropriate clinical setting. This approach evolved further with the development of cardiac troponin and its integration into the definition of MI by the European Society of Cardiology and the American College of Cardiology. The present diagnostic standard for MI is thus based on the following biomarker criteria: Maximal concentration of troponin T or I exceeding the decision limit (99th percentile of the values for a reference control group) manifesting a dynamic pattern on at least one occasion during the first 24 h after the index clinical event; if the value is between the 99th percentile and the 10% coefficient of variation level, caution is warranted because analytic false-positive results can occur. In the unusual situation in which troponin assays are not available, the value of CK-MB (preferably CK-MB mass) exceeding the 99th percentile of the value for a reference control group and manifesting a dynamic pattern can be used for diagnosis.

Aims The objectives of this study are to evaluate the prognostic role of pre-operative stratification in patients undergoing elective major vascular surgery, the timing of adverse outcomes, and the predictive role of troponin (cTn). Methods and results Consecutive vascular surgery candidates (n ¼ 391) were prospectively stratified and treated according to the ACC/AHA guidelines. The patients were categorized into three groups: (1) with coronary revascularization in the past 5 years, (2) with intermediate clinical risk predictors, and (3) with minor or no clinical risk predictors. cTnI was measured post-operatively. By 18 months, 18.7% of subjects had experienced death or acute myocardial infarction (MI) (by the ACC/ESC criteria). The hazard ratio (HR) was 5.21 (95% CI ¼ 2.60–10.43; P , 0.0001) in group 1 and 2.58 (95% CI ¼ 1.27–4.38; P ¼ 0.004) in group 2 when compared with group 3. Most events occurred within 30 days. Elevations of cTnI were associated with adverse outcomes even after multivariable adjustment at long-term (adjusted overall HR ¼ 4.73, 95% CI ¼ 2.92–7.65; P , 0.0001) and at 30 days (adjusted HR ¼ 5.52, 95%CI ¼ 3.23–9.42; P , 0.0001). Conclusion After pre-operative stratification, patients undergoing elective major vascular surgery remain at high risk of MI and death. Events occur mainly early after surgery. cTnI elevations are frequent and independently associated with increased risk. These findings suggest the need for a major re-evaluation of our approach to these patients.