Objective Patients with cancer may display elevated levels of B-type natriuretic peptide (BNP) and high-sensitive troponin T (hsTnT) without clinical manifestation of cardiac disease. This study aimed to evaluate circulating cardiovascular hormones and hsTnT and their association with mortality in cancer. Methods We prospectively enrolled 555 consecutive patients with a primary diagnosis of cancer and without prior cardiotoxic anticancer therapy. N-terminal pro BNP (NT-proBNP), mid-regional pro-atrial natriuretic peptide (MR-proANP), mid-regional pro-adrenomedullin (MR-proADM), C-terminal pro-endothelin-1 (CT-proET-1), copeptin, hsTnT, proinflammatory markers interleukin 6 (IL-6) and C reactive protein (CRP), and cytokines serum amyloid A (SAA), haptoglobin and fibronectin were measured. All-cause mortality was defined as primary endpoint. Results During a median follow-up of 25 (IQR 16–31) months, 186 (34%) patients died. All cardiovascular hormones and hsTnT levels rose with tumour stage progression. All markers were significant predictors of mortality with HRs per IQR of 1.54 (95% CI 1.24 to 1.90, p Conclusions Circulating levels of cardiovascular peptides like NT-proBNP, MR-proANP, MR-proADM, CT-pro-ET-1 and hsTnT were elevated in an unselected population of patients with cancer prior to induction of any cardiotoxic anticancer therapy. The aforementioned markers and copeptin were strongly related to all-cause mortality, suggesting the presence of subclinical functional and morphological myocardial damage directly linked to disease progression.

/pdf/cardiovascular-biomarkers-in-patients-with-cancer-and-their-1ri5fozlm5.pdf

Cardiovascular biomarkers in patients with cancer and their association with all-cause mortality

Aspirin, heparin, or both to treat acute unstable angina

Mineralocorticoid receptor antagonists (MRAs) improve survival and reduce morbidity in patients with heart failure, reduced ejection fraction (HF–REF), and mild-to-severe symptoms, and in patients with left ventricular systolic dysfunction and heart failure after acute myocardial infarction. These clinical benefits are observed in addition to those of angiotensin converting enzyme inhibitors or angiotensin receptor blockers and beta-blockers. The morbidity and mortality benefits of MRAs may be mediated by several proposed actions, including antifibrotic mechanisms that slow heart failure progression, prevent or reverse cardiac remodelling, or reduce arrhythmogenesis. Both eplerenone and spironolactone have demonstrated survival benefits in individual clinical trials. Pharmacologic differences exist between the drugs, which may be relevant for therapeutic decision making in individual patients. Although serious hyperkalaemia events were reported in the major MRA clinical trials, these risks can be mitigated through appropriate patient selection, dose selection, patient education, monitoring, and follow-up. When used appropriately, MRAs significantly improve outcomes across the spectrum of patients with HF–REF.

Mineralocorticoid receptor antagonists for heart failure with reduced ejection fraction: integrating evidence into clinical practice

Objectives This study aimed to evaluate the specific role of the 2 available mineralocorticoid receptor antagonists (MRAs), eplerenone and spironolactone, on the modulation of galectin-3 (Gal-3) and interleukin (IL)-33/ST2 signaling in an experimental model of left ventricular systolic dysfunction after acute myocardial infarction (MI). Background The molecular mechanisms of benefits of MRAs in patients with left ventricular systolic dysfunction after MI not well understood. Methods MI and left ventricular systolic dysfunction were induced by permanent ligation of the anterior coronary artery in 45 male Wistar rats, randomly assigned to no therapy (MI group, n = 15) or to receive MRAs (100 mg/kg/day) for 4 weeks; either eplerenone (n = 15) or spironolactone (n = 15) was used. A sham group was used as a control (n = 8). Elements of the pathway for Gal-3 including transforming growth factor (TGF)-β and SMAD3, as well as that for IL-33/ST2 (including IL-33 and soluble ST2 [sST2]) were analyzed in the infarcted and noninfarcted myocardium by quantitative real-time reverse transcription polymerase chain reaction. Expression of markers of fibrosis (collagen types I and III, tissue inhibitor of metalloproteinase-1) and inflammation (IL-6, tumor necrosis factor-α, monocyte chemotactic protein-1) was also examined. Results In the infarcted myocardium, compared with sham animals, the MI group had higher concentrations of Gal-3, TGF-β, SMAD3, IL-33, and sST2, as well as higher concentrations of markers of fibrosis and inflammation. Treatment with MRAs down-regulated Gal-3, TGF-β, and SMAD3 and enhanced IL-33/ST2 signaling with lower expression of sST2; protective IL-33 up-regulation was unaffected by MRAs. Modulation of Gal-3 and IL-33/ST2 signaling induced by MRAs correlated with lower expression levels of fibrosis and inflammatory markers. No differences were found between eplerenone and spironolactone. In the noninfarcted myocardium, compared with sham animals, the MI group exhibited a higher expression of Gal-3 and IL-33, but no signs of inflammation or fibrosis were observed; in the presence of MRAs, IL-33 expression was significantly up-regulated, but Gal-3 was unaffected. Conclusions MRAs play a pivotal role in the Gal-3 and IL-33/ST2 modulation in post-MI cardiac remodeling.

Mineralocorticoid receptor antagonists modulate galectin-3 and interleukin-33/ST2 signaling in left ventricular systolic dysfunction after acute myocardial infarction.

Mechanistic Biomarkers Informative of Both Cancer and Cardiovascular Disease: JACC State-of-the-Art Review

Aldosterone antagonists represented by nonselective spironolactone and mineralocorticoid-selective eplerenone are approved for treatment of symptomatic heart failure with reduced systolic function. Their cardioprotective, antifibrotic, and antiarrhythmic effects have been proven in animal experiments, and their effects on morbidity and mortality have been demonstrated in randomized clinical trials. Yet, they remain the most underutilized of all classes of medications for heart failure, primarily because of fear of hyperkalemia. Thorough patient screening and selection is the key for minimizing risks and optimizing benefits from these drugs. Ongoing trials will demonstrate whether the indication for aldosterone antagonists can be expanded to less severe heart failure or patients with preserved systolic function.

Aldosterone Antagonists in Heart Failure

The acute coronary syndrome is most often caused by plaque rupture and can result in a variety of clinical conditions. There are two general strategies (early invasive versus conservative) currently employed in the treatment of unstable angina or non-ST elevation myocardial infarction. Pooled data from recent clinical trials have demonstrated that high-risk patients benefit from a routine or early invasive approach while certain low-risk subgroups have similar outcomes with a conservative approach. Most patients in the USA are treated aggressively given advances in technology and the relative ease of interventional therapy. The routine invasive approach, however, remains controversial and has important limitations that are not well identified in trials. Furthermore, data from trials are difficult to interpret given their relevance to contemporary practice in today's cost conscious, health care environment. The decision to pursue an invasive or conservative approach should be based upon an individual patient's risk profile, and the level of medical therapy should be based on the underlying pathophysiology. The best strategy incorporates aggressive anti-atherosclerotic therapy with early risk stratification and invasive therapy when appropriate-the so-called hybrid approach. Identifying plaque rupture helps identify patients that would benefit from potent antiplatelet, antithrombotic, and anti-inflammatory therapies, and further insight into the natural history of coronary artery disease coupled with continued advances in diagnostic and interventional approaches will hopefully help guide long-term primary and secondary management.

/pdf/routine-invasive-versus-conservative-management-strategies-4vq0b6d2qs.pdf

Routine Invasive Versus Conservative Management Strategies in Acute Coronary Syndrome: Time for a “Hybrid” Approach

High levels of B-type natriuretic peptide in cancer patients are poorly studied. Previously published data suggest that they are not related to fluid overload and are encountered mostly in solid cancers. The authors investigated the distribution of amino terminal pro-brain natriuretic peptide (NT-proBNP) between hematologic and solid organ malignancies and the relationship of NT-proBNP with volume status in oncologic patients. A total of 145 consecutive patients with at least one occurrence of NT-proBNP exceeding the upper normal range 10-fold were identified. The authors retrospectively reviewed their records including clinical, laboratory, and radiological data and echocardiograms. More than 70% of patients had hematologic malignancies. Patients with NT-proBNP >50,000 pg/mL had only hematologic malignancies, primarily multiple myeloma. There was no association between M-spike proteins and NT-proBNP. About 80% of patients had signs of fluid overload. The magnitude of NT-proBNP elevation was similar between those with and without heart failure or volume overload, as well as with solid cancers vs hematologic malignancies. Contrary to prior reports, it was found that very high NT-proBNP in cancer patients is usually encountered in the context of fluid overload and most often in hematologic malignancies.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/chf.12018

What Is Causing Extremely Elevated Amino Terminal Brain Natriuretic Peptide in Cancer Patients

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Aldosterone Antagonists in Heart Failure

Routine Invasive Versus Conservative Management Strategies in Acute Coronary Syndrome: Time for a “Hybrid” Approach

What Is Causing Extremely Elevated Amino Terminal Brain Natriuretic Peptide in Cancer Patients