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The relation of high-sensitivity cardiac troponin I (hs-cTnI) concentration and presence of obstructive coronary artery disease (CAD) in patients without myocardial infarction (MI) is unclear. Study participants selected from patients free of MI who underwent coronary angiography with or without intervention were enrolled, and hs-cTnI measured. A gradient boosting model was implemented to build a model for detection of CAD. Cox proportional hazard regression was used to assess the association of hs-cTnI and adverse cardiovascular (CV) outcome. Among 978 study participants, 607 patients (62%) had CAD. Higher concentrations of hs-cTnI were associated with chronic kidney disease, heart failure, CAD, male gender, current tobacco use, anemia, age, and low-density lipoprotein cholesterol. History of CAD, male gender, type 2 diabetes mellitus, hs-cTnI, anemia, age, and high-density lipoprotein cholesterol were the most influential factors for detection of CAD. The gradient boosting model had an area under the curve of 0.82, accuracy of 75%, sensitivity of 88%, specificity of 52%, positive predictive value of 76%, and negative predictive value of 72% for detection of CAD. Increase in 1 log unit of hs-cTnI was significantly associated with increased risk of incident MI (hazard ratio [HR] 1.34, 95% confidence interval [CI] 1.22 to 1.47, p0.001), CV mortality (HR 1. 24, 95% CI 1.11 to 1.39, p0.001), and composite of incident MI or CV mortality (HR 1.29, 95% CI 1.20 to 1.40, p0.001). In conclusion, among patients without acute MI and CAD, higher concentrations of hs-cTnI were associated with the presence of CAD and linked to increased risk of future CV events. ClinicalTrials.gov Identifier: NCT00842868.

BACKGROUND: Immune checkpoint inhibitors (ICI) are widely used cancer treatments. There are limited data the risk for developing venous thromboembolism (VTE) among patients on an ICI. METHODS: This was a retrospective study of 2854 patients who received ICIs at a single academic center. VTE events, defined as a composite of deep vein thrombosis (DVT) or pulmonary embolism (PE), were identified by individual chart review and were blindly adjudicated using standard imaging criteria. A self-controlled risk-interval design was applied with an “at-risk period” defined as the two-year period after, and the “control period”, defined as the two-year prior to treatment. The hazard ratio (HR) was calculated using a fixed-effect proportional hazards model. RESULTS: Of the 2854 patients, 1640 (57.5%) were men; mean age was 64±13 years. The risk for VTE was 7.4% at 6 months and 13.8% at 1 year after starting an ICI. The rate of VTE was >4-fold higher after starting an ICI (HR 4.98, 95% CI 3.65 – 8.59, p

Background Coronary vasospasm is a recognized side effect of 5-fluorouracil (5-FU). There are limited and conflicting data on the incidence, risk factors, and prognostic effect of 5-FU–associated vasospasm. Objectives This study sought to assess the incidence, risk factors, and prognostic implications of 5-FU coronary vasospasm among patients receiving 5-FU regimens at a single tertiary care center. Methods The study conducted a retrospective analysis of all patients who received 5-FU at a single academic center from January 2009 to July 2019. Vasospasm was defined as the occurrence of a typical chest pain syndrome in the presence of 5-FU. The presence of associated electrocardiogram changes or elevated biomarkers was used to further confirm the diagnosis. Patients with vasospasm were compared with patients treated with 5-FU without vasospasm in a 1:2 ratio. Data regarding demographics, medical history, and follow-up were collected by manual chart review. Results From approximately 4,019 individual patients who received 5-FU from 2009 to 2019 at a single center, 87 (2.16%) developed vasospasm. Patients who developed vasospasm were younger (age 58 ± 13 years vs. 64 ± 13 years; p = 0.001) and were less likely to have any cardiovascular risk factors (70.1% vs. 84.5%; p = 0.007). Patients with vasospasm and patients without vasospasm were otherwise similar in terms of types of cancer, stage of cancer, sex, and race. There was no significant difference in progression-free survival, overall mortality or cancer specific mortality between patients who developed vasospasm versus those who did not. Conclusions In a large, single-center report of 5-FU–associated vasospasm, patients who developed vasospasm were younger, had lower rates of traditional cardiovascular risk factors, and had no significant difference in progression-free or overall survival compared with those who did not develop vasospasm.

This study sought to assess associations between longitudinal change in atrial natriuretic peptide (ANP) and reverse cardiac remodeling following initiation of sacubitril/valsartan in patients with heart failure with reduced ejection fraction (HFrEF).Neprilysin inhibition results in an increase of several vasoactive peptides that may mediate the beneficial effects of sacubitril/valsartan, including ANP.In a prospective study of initiation and titration of sacubitril/valsartan in patients with HFrEF, blood was collected at scheduled time points into tubes containing protease inhibitors. This pre-specified exploratory analysis included patients in whom ANP was measured at baseline and serially through 12 months of treatment.Among 144 participants (mean age: 64.5 years; left ventricular ejection fraction: 30.8%), following initiation of sacubitril/valsartan, there was an early and significant increase in ANP, with the majority of rise from 99 pg/ml at baseline to 156 pg/ml at day 14 (p 0.001). There was a further trend toward a second increase from day 30 to day 45 (p = 0.07). At maximal rise, ANP had doubled. In longitudinal analyses, early rise in ANP was followed by a subsequent increase in urinary cycle guanosine monophosphate. Larger early increase in ANP was associated with larger later improvements in left ventricular ejection fraction and left atrial volume index (p 0.001 for both).Concentrations of ANP doubled after initiation of sacubitril/valsartan in patients with HFrEF. Larger early increases in ANP were associated with a greater magnitude of subsequent reverse cardiac remodeling. (Effects of Sacubitril/Valsartan Therapy on Biomarkers, Myocardial Remodeling and Outcomes [PROVE-HF]; NCT02887183).

It has long been observed that heart failure (HF) is associated with measures of systemic inflammation. In recent years, there have been significant advancements in our understanding of how inflammation contributes to the pathogenesis and progression of HF. However, although numerous studies have validated the association between measures of inflammation and HF severity and prognosis, clinical trials of anti-inflammatory therapies have proven mostly unsuccessful. On this backdrop emerges the yet unmet goal of targeting precise phenotypes within the syndrome of HF; if such precise definitions can be realized, and with better understanding of the roles played by specific inflammatory mediators, the expectation is that targeted anti-inflammatory therapies may improve prognosis in patients whose HF is driven by inflammatory pathobiology. Here, the authors describe mechanistic links between inflammation and HF, discuss traditional and novel inflammatory biomarkers, and summarize the latest evidence from clinical trials of anti-inflammatory therapies.

Left ventricular (LV) thrombus is a feared complication of LV dysfunction associated with high rates of systemic embolism, morbidity, and mortality. Traditionally, LV thrombus has been associated with acute myocardial infarction (MI). However, with improvements in percutaneous coronary intervention

Although the concept of myocardial infarction (MI) occurring in the absence of coronary thrombus was first identified in 1939, it was 2007 before the term type 2 MI , referring to infarctions related to supply–demand imbalance, was first introduced into clinical practice [(1)][1]. Since then, our

Background: Sacubitril/valsartan (S/V) treatment is associated with reverse cardiac remodeling and reductions in biomarkers reflecting ventricular wall stress and myocardial injury, such as NT-proB...

Introduction Sacubitril/valsartan (S/V) promotes reverse cardiac remodeling in patients with HFrEF. Neprilysin inhibition results in increase of several vasoactive peptides that may mediate effects of S/V, however its effects on atrial natriuretic peptide (ANP) are largely unknown. Effects of ANP are mediated by cyclic guanosine monophosphate (cGMP). Hypothesis Longitudinal change in ANP concentration following initiation of S/V is associated with reverse cardiac remodeling. Methods Within a prospective open-label study of initiation and titration of S/V in patients with HFrEF, this pre-specified sub-study included patients in whom ANP was measured from samples collected in protease inhibitors to minimize its degradation. Concentrations of ANP and cGMP were measured at baseline and serially through 12 months of treatment. Echocardiographic assessment of LVEF and left atrial volume index (LAVi) was performed at baseline, 6 and 12 months. Results Among 144 participants (mean age 64.5 years; LVEF 30.8%), median ANP concentration at baseline was 102 pg/mL. Following initiation of S/V, ANP increased steeply and consistently during the first 2 months, with a significant increase in log-transformed ANP concentration at Day 14 (from 4.60 pg/mL to 5.05 pg/mL; Δ = 0.453; P Conclusions Concentrations of ANP increase substantially after initiation of S/V in patients with HFrEF. Larger early increases in ANP after S/V initiation were associated with greater magnitude of reverse cardiac remodeling (PROVE-HF; NCT02887183).

Patients with type 2 myocardial infarction (MI) related to supply-demand inequity are frequently encountered in clinical practice but, in the absence of evidence-based therapies, their prognosis remains poor; 5-year survival is less than 40%. Cardiac rehabilitation is associated with reduced all

Summary This outline suggests that the principal political parties in Quebec are committed to the position thatthe state and its functionaries are the primary authorities in education, including the moral, ethicaland religious education of children. They appear to relegate parents and subsidiary institutions -especially religious authorities - to what is, at best, a secondary role: one, moreover, that can beunilaterally defined and limited - perhaps even abolished - by state power.There is no reason to believe that health care workers and their associations will be treateddifferently. It is very doubtful that the government would afford state functionaries a deference thatit denies to parents in the education of their own children.Return to the question: will the government of Quebec - sooner or later - use its Charter of Values tosuppress freedom of conscience and religion among health care workers?The Quebec government's assumption of sovereignty over education and the religious and ethical

When the National Association for the Repeal of Abortion Laws opened its doors in the United States in 1969, the claim that abortion was a “right” was directed only at the repeal of laws against the procedure, so that women would be free to seek abortions and, as the Globe and Mail put it, so that physicians would be able “to perform their duties according to their conscience and their calling.” At that time, Canadians were repeatedly assured that “nobody would be forcing abortion procedures on anyone else.”Current rights claims must be distinguished from this early period. Contrary to early activist promises, current rights claims are meant to force health care workers and institutions to provide or at least facilitate abortion, contraception, and artificial reproduction, all of which remain morally controversial. A major “mover and shaker” in this project is the Center for Reproductive Rights (CRR), The ultimate goal of the CRR is to establish what it calls “hard norms” - treaty-based international laws - that recognize access to abortion as a fundamental human right. It plans to develop a “culture of enforcement” that will compel governments to respect this right and enforce it against physicians and other health care workers. Even as it works toward this end, it is cultivating “soft norms” in the form of statements by international, regional, and intergovernmental bodies.Canadian Professor Bernard M. Dickens appears to follow this strategy in a standard text, Canadian Health Law and Policy, in his chapter on Informed Consent, addressing the topic of conscientious objection and disclosure of relevant information to a patient. He very selectively borrows terms from the Treaty of Rome and arranges his material to make it appear that conscientious objection that delays access to the morning after pill or abortion is actually or very nearly a crime against humanity analogous to torture, or, at least, an egregious violation of human rights. He also leaves out everything necessary for a proper understanding of the Treaty of Rome, which, incidentally, includes everything that might cause a reader to question his claims. Professor Dickens’ polemic seamlessly weaves the agenda of the Center for Reproductive Rights into a standard Canadian reference work. There is no doubt that this is advantageous to the Center and its allies, but it brings into question the reliability of Canadian Health Law and Policy. Perhaps it is time for a third and more carefully revised edition of the book.