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Purpose Acute heart failure (AHF) causes high burden of mortality, morbidity, and repeated hospitalizations worldwide. This guidance paper describes the tailored treatment approaches of different clinical scenarios of AHF and CS, focusing on the needs of professionals working in intensive care settings. Results Tissue congestion and hypoperfusion are the two leading mechanisms of end-organ injury and dysfunction, which are associated with worse outcome in AHF. Diagnosis of AHF is based on clinical assessment, measurement of natriuretic peptides, and imaging modalities. Simultaneously, emphasis should be given in rapidly identifying the underlying trigger of AHF and assessing severity of AHF, as well as in recognizing end-organ injuries. Early initiation of effective treatment is associated with superior outcomes. Oxygen, diuretics, and vasodilators are the key therapies for the initial treatment of AHF. In case of respiratory distress, non-invasive ventilation with pressure support should be promptly started. In patients with severe forms of AHF with cardiogenic shock (CS), inotropes are recommended to achieve hemodynamic stability and restore tissue perfusion. In refractory CS, when hemodynamic stabilization is not achieved, the use of mechanical support with assist devices should be considered early, before the development of irreversible end-organ injuries. Conclusion A multidisciplinary approach along the entire patient journey from pre-hospital care to hospital discharge is needed to ensure early recognition, risk stratification, and the benefit of available therapies. Medical management should be planned according to the underlying mechanisms of various clinical scenarios of AHF., Author(s): A. Mebazaa [sup.1] [sup.2] [sup.3], H. Tolppanen [sup.1] [sup.4], C. Mueller [sup.5], J. Lassus [sup.4], S. DiSomma [sup.6], G. Baksyte [sup.7], M. Cecconi [sup.8], D. J. Choi [sup.9], A. [...]

Byline: Afzal. Azim, Sunil. Jena The 108-amino acid prohormone, B-type natriuretic peptide (BNP), is released during hemodynamic stress and, once in the circulation, it gets cleaved by endopeptidase, corin, into [...]

Childhood cancer survivors can develop significant cardiac dysfunction in adulthood as a consequence of their cancer treatment. Studies have linked heart failure during pregnancy to childhood doxorubicin (DOX) exposure. We hypothesized that DOX injection would reduce cardiac function peripartum and that DOX-treated dams would show greater cardiac remodeling postweaning. Weanling female Sprague-Dawley rats were injected with phospate-buffered saline, DOX (3 mg/kg), or DOX plus the cardioprotectant dexrazoxane (DEX; 60 mg/kg) and followed for 2 pregnancies. DOX and DOX:DEX dams were fertile, but had fewer pups and more pup losses. Echocardiography, 1-day postpartum after each pregnancy, revealed greater increases in cardiac mass and eccentric hypertrophy in DOX-treated dams and early dilation in DOX:DEX dams. The expression of calcium homeostasis proteins can change after DOX treatment and cardiac remodeling. SERCA2a expression did not change. Reductions in phospholamban and phospho-serine 16-specific phospholamban expression in DOX dams were not relieved by DEX coinjection. DOX binds and inactivates calsequestrin 2 expression so increased calsequestrin 2 expression in DOX:DEX-treated dams suggests some DEX compensation. The eccentric hypertrophy and dilation development, despite compensatory changes in proteins controlling calcium cycling, suggest DOX damage with repeat pregnancy that was not alleviated fully by DEX. Key words: Sprague-Dawley rat, pregnancy, echocardiography, SERCA2a, phospholamban, calsequestrin 2. Les survivants d'un cancer pediatrique peuvent developper une dysfonction cardiaque importante en consequence a leur traitement contre le cancer. Des etudes ont relie l'insuffisance cardiaque lors de la grossesse a une exposition a la doxorubicine (DOX) durant l'enfance. Nous avons emis l'hypothese que l'injection de DOX reduirait la fonction cardiaque peri-partum et que les meres traitees a la DOX montreraient un accroissement du remodelage cardiaque apres le sevrage. Des rats femelles Sprague Dawley sevrees ont recu une injection de PBS, de DOX seule (3 mg/kg) ou de DOX et du cardioprotecteur dexrazoxane (DEX, 60 mg/kg), traitements suivis de deux gestations. Les meres des groupes DOX et DOX :DEX etaient fertiles mais leurs portees etaient plus petites et la mortalite a la naissance plus elevee. L'echocardiographie effectuee un jour post-partum apres chaque gestation, revelait des augmentations plus elevees de la masse cardiaque et une hypertrophie excentrique chez les meres traitees a la DOX et une dilatation precoce chez les meres traitees au DOX : DEX. L'expression de proteines de l'homeostasie du calcium peut changer a la suite du traitement a la DOX et du remodelage cardiaque. L'expression de SERCA2a ne changeait pas. Des reductions de l'expression de phospholamban (PLB) et de [pS.sup.16]-PLB chez les meres du groupe DOX n'etaient pas affectees par la co-injection de DEX. La DOX lie et inactive la calsequestrine 2 (CSQ2) faisant en sorte que l'augmentation de l'expression de CSQ2 chez les meres traitees au DOX :DEX suggere une certaine compensation par le DEX. L'hypertrophie excentrique et le developpement de la dilatation, malgre les changements compensateurs dans les proteines controlant le cycle du calcium suggerent que la DOX induit un dommage lors de gestations repetees qui n'etait pas attenue completement par le DEX. Mots-cles : rat Sprague-Dawley, gestation, echocardiographie, SERCA2a, phospholamban, calsequestrine 2. [Traduit par la Redaction], Introduction Many childhood cancer survivors have at least one chronic illness (Oeffinger et al. 2006; Diller 2011; Trachtenberg et al. 2011). Reductions in cardiac function may be due to anthracycline-induced [...]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2010.07.033 Byline: Kirkwood F. Adams, Mandeep R. Mehra, Ron M. Oren, Christopher M. O'Connor, Jun R. Chiong, Jalal K. Ghali, Daniel J. Lenihan, Stephanie H. Dunlap, J. Herbert Patterson, Todd A. Schwartz, G. Michael Felker Abstract: Elevated cardiac troponin T is a well-documented marker of cardiomyocyte damage and poor prognosis in patients with heart failure. We prospectively evaluated the relationship between this marker and hematopoietic disturbances in heart failure. Article History: Received 25 November 2009; Accepted 30 July 2010

A literature review on dental care for patients with heart failure research between 2000 and 2009 brings up over 23,000 articles. Since it is more probable that dentists will encounter patients with this condition, it is important for dentists to be know how to treat and diagnose this disease.

Chronic heart failure (CHF) remains the only cardiovascular disease with an increasing hospitalization burden and an ongoing drain on health care expenditures. The prevalence of CHF increases with advancing life [...]

The case of a 74-year-old man with a history of hypertension and myocardial infarction discussed to better understand the causes, diagnosis, treatment and management methodologies for systolic heart failure. The need for participation in a disease-management program for the patient and family is encouraged to provide them with adequate knowledge about self-care interventions.

Am J Physiol Heart Circ Physiol 298: H158-H162, 2010. First published October 23, 2009; doi: 10.1152/ajpheart.00654.2009.--In the failing myocardium a subendocardial plexus can develop. Detection of the presence or function, however, of such a plexus does not form part of the present diagnostic spectrum for heart failure. This may now change as new methods for high-resolution imaging of myocardial perfusion distribution are being developed. A severely hypertrophic heart was harvested during transplantation and analyzed for morphology of the intramural coronary arterial vasculature. The heart only had one coronary ostium, and the main branches of the coronary artery were cannulated. A fluorescent casting material was infused that was allowed to harden under physiological pressure. The entire heart was frozen and placed in a novel imaging cryomicrotome and sequentially cut in 25-[micro]m slices. High-resolution images of each cutting plane were acquired, allowing a detailed three-dimensional reconstruction of the arterial vasculature. The epicardial layer of the free wall demonstrated a normal vasculature with penetrating branching arteries. The endocardial layer and the septum revealed a highly interconnected vascular plexus with large vessels oriented parallel to the apicobasal axis. An extensive endocardial network with collaterals was detected, forming connections between the main epicardial branches. We conclude that an outward remodeling of transmural vessels did not prevent the generation and growth of subendocardial conduit arteries. The orientation and vascular volume in the plexus provides an opportunity for detection by novel techniques of MRI contrast imaging currently developed. Knowledge of the effect on perfusion studies is required to prevent a misinterpretation of subendocardial perfusion images in heart failure. imaging cryomicrotome; collateral; vascular plexus; hypertrophy

From bone marrow transplants 5 decades ago to the most recent stem cell-derived organ transplants, regenerative medicine is increasingly recognized as an emerging core component of modern practice. In cardiovascular [...]