Heart Failure Reviews

Heart rhythm problems are common among patients who are hospitalized with acute heart failure (HF). Although it is often difficult to determine whether a tachyarrhythmia is the major contributor to an acute HF decompensation or merely a consequence of the decompensation, both issues usually need to be addressed. There is also a subset of patients with HF who have a tachycardia-induced cardiomyopathy (TIC), where the sole cause of the ventricular dysfunction is the heart rhythm problem. In most cases, the management of a tachyarrhythmia in a patient with acute HF is not significantly different than the management of a heart rhythm problem in any patient, but there are several special clinical scenarios and important considerations. These considerations include the time urgency for an intervention, the usual need to be more aggressive and definitive, the need to stabilize a patient to allow for a heart rhythm intervention, such as catheter ablation to be performed safely, and the limitations of antiarrhythmic drugs in patients with ventricular dysfunction. Catheter ablation is a highly effective treatment option for many patients with supraventricular or ventricular tachycardias who are hospitalized with HF. This review will discuss the different types of tachyarrhythmias that can be associated with acute HF and are amenable to catheter ablation, and the assessment that needs to take place in potentially eligible patients to determine when catheter ablation is appropriate.

N-terminal fragment of pro B-type natriuretic peptide (NT-proBNP) has emerged as an important adjunct in the management of heart failure (HF) and other cardiovascular diseases. NT-proBNP is a 76-amino acid peptide created during cleavage of the precursor molecule, Pro B-type natriuretic peptide (ProBNP). NT-proBNP is of significant diagnostic value in patients presenting with possible HF and is an important prognostic factor in this condition and other cardiovascular diseases. Ongoing research supports the potential value of this biomarker in non-cardiovascular disease. This review will describe clinical applications of NT-proBNP in HF and a broad range of other conditions.

Despite significant advances in the prevention and treatment of heart failure (HF), the prognosis in patients who have been hospitalised on at least one occasion due to exacerbation of HF is still poor. Therefore, a better understanding of the underlying pathophysiological mechanisms of HF is crucial in order to achieve better results in the treatment of this clinical syndrome. One of the areas that, for years, has aroused the interest of researchers is the activation of the immune system and the elevated levels of biomarkers of inflammation in patients with both ischaemic and non-ischaemic HF. Additionally, it is intriguing that the level of circulating pro-inflammatory biomarkers correlates with the severity of the disease and prognosis in this group of patients. Unfortunately, clinical trials aimed at assessing interventions to modulate the inflammatory response in HF have been disappointing, and the modulation of the inflammatory response has had either no effect or even a negative effect on the HF prognosis. The article presents a summary of current knowledge on the role of immune system activation and inflammation in the pathogenesis of HF. Understanding the immunological mechanisms pathogenetically associated with left ventricular remodelling and progression of HF may open up new therapeutic possibilities for HF.

Cardiac resynchronization therapy (CRT) has been demonstrated to improve mortality and morbidity in patients with chronic, stable heart failure who have reduced left ventricular ejection fraction and prolonged QRS duration. Patients with acute heart failure syndromes (AHFS) have been excluded from major CRT trials. The potential benefits and risks of implementation of these devices in the AHFS setting are largely unknown. In this review, we discuss the role that early implementation of CRT may have in improving postdischarge outcomes. In addition, we also discuss the potential adverse consequences of inserting these devices in patients who are in the tenuous clinical state of AHFS.

An explanation of the molecular mechanisms that trigger the development of pathological cardiac fibrosis, myocyte hypertrophy, and heart failure associated with common ailments such as chronic postinfarction has been sought at the bench top and clinic for the past 40years, and is a current topic of intensive investigative activity. During the past several years, awareness of the important role of molecular alterations in the cardiac myocyte and interstitium in cardiac physiology has burgeoned among investigators, and this has led to a focus on the role of cardiac fibrosis and myocyte hypertrophy in the development of heart failure. Among the information garnered from these studies is that growth factors including angiotensin II (AII) and transforming growth factorβ1 (TGF-β1 ), in particular, are believed to be involved in modulation of gene products specifically expressed by cardiac fibroblasts and cardiac myocytes in vitro, and their enhanced presence has been associated with myocardial stress and inappropriate cardiac growth and fibrosis in vivo. Although these growth factors certainly may act on the myocardium alone via specific signaling pathways, we will review evidence that the signals modulated by AII and TGF-β may be coordinated among cardiac fibroblasts and myocytes. In this context, cardiac myocyte hypertrophy and alteration of the cardiac interstitium, i.e., cardiac fibrosis, are examined.

Many of the disorders and lesions leading to acute heart failure can be treated surgically. Modern surgical techniques like the off pump coronary surgery, newer techniques for the surgical treatment of the mechanical complications of acute MI and valvular reparative techniques have been added to the surgical armamentarium in recent years. Modern ventricular assist devices have started their career in the clinical arena promising to be less invasive. At the same time the spectrum of indications for mechanical circulatory support continues to witness a rapid expansion. Technical advances have led to an evolution of surgical strategies. Heart failure surgery is now in a position to offer improved outcomes, avoidance of recurrence of acute heart failure or the development of advanced chronic heart failure.

Chagas’ disease, caused by Trypanosoma cruzi infection, is ranked as the most serious parasitic disease in Latin America. Nearly 30% of infected patients develop life-threatening complications, and with a latency of 10–30 years, mostly Chagas’ heart disease which is currently the major cause of morbidity and mortality in Latin America, enormously burdening economic resources and dramatically affecting patients’ social and labor situations. Because of increasing migration, international tourism and parasite transfer by blood contact, intrauterine transfer and organ transplantation, Chagas’ heart disease could potentially become a worldwide problem. To raise awareness of this problem, we reflect on the epidemiology and etiopathology of Chagas’ disease, particularly Chagas’ heart disease. To counteract Chagas’ heart disease, in addition to the general interruption of the infection cycle and chemotherapeutic elimination of the infection agent, early and effective causal or symptomatic therapies would be indispensable. Prerequisites for this are improved knowledge of the pathogenesis and optimized patient management. From economic and logistics viewpoints, this last prerequisite should be performed using laboratory medicine tools. Consequently, we first summarize the mechanisms that have been suggested as driving Chagas’ heart disease, mainly those associated with the presence of autoantibodies against G-protein-coupled receptors; secondly, we indicate new treatment strategies involving autoantibody apheresis and in vivo autoantibody neutralization; thirdly, we present laboratory medicine tools such as autoantibody estimation and heart marker measurement, proposed for diagnosis, risk assessment and patient guidance and lastly, we critically reflect upon the increase in inflammation and oxidative stress markers in Chagas’ heart disease.