Controlling axillary intra‐aortic balloon pump inflation is a viable option for turning an acute heart failure patient into a chronic one

Intra‐aortic balloon pump (IABP) is often used to support patients in decompensated heart failure. Placement of the IABP via the axillary artery facilitates long‐term support with the device and may allow for the conversion of an acute heart failure (HF) patient into a chronic HF patient using a modified weaning protocol; allowing for medical symptom management and removal of mechanical support. We will discuss strategies for supporting these complicated patients.     

Drugs acting on the heart: heart failure and coronary insufficiency

Heart failure (HF) and coronary insufficiency are common among intensive care patients or those undergoing surgery. Both conditions can present as an acute decompensated state with high mortality or with a more stable, chronic course. Although similar drugs can be used to treat both conditions, an understanding of the respective pathological processes enables better targeting of treatment. Several drugs have been recently developed for HF and coronary insufficiency. It is increasingly appreciated that HF is not a single entity: the pathophysiology, treatment and prognosis depend on whether systolic or diastolic dysfunction predominates, and whether the condition is stable and compensated or acute and decompensated. Acute decompensated heart failure (ADHF) is treated with diuretics, vasodilators and positive inotropes in some cases. It is better to treat decompensated systolic HF with reduced left ventricular ejection fraction (LVEF; < 40%) with arterial dilators, whereas diastolic HF with intact LVEF responds better to venodilators. After an episode of ADHF, treatment for chronic HF (diuretics, angiotensin-converting enzyme inhibitors (ACEIs) and β-blockers unless contraindicated) should be initiated before hospital discharge and continued. ACEIs and β-blockers slow the progression of chronic HF and reduce mortality. Ischaemic heart disease is managed with nitrates, β-blockers, ACEIs, statins and anti-platelet drugs. In the acute coronary syndrome, thrombolytic agents are still used.     

Drugs acting on the heart: heart failure and coronary insufficiency

Heart failure (HF) and coronary insufficiency are common amongst surgical and critical care patients. Both are chronic conditions interrupted by acute episodes. HF activates neurohormonal mechanisms that worsen renal and cardiac function. Acute heart failure (AHF) commonly presents with dyspnoea as a consequence of systolic and/or diastolic dysfunction. Goals of treatment are symptom relief, to maintain tissue perfusion and optimize cardiac function. Diuretics and vasodilators are used early; positive inotropic drugs are reserved for when other treatment has failed. Chronic heart failure (CHF) is treated using changes in lifestyle and drugs to manage symptoms. ACE inhibitors and beta-blockers are effective in systolic heart failure and are associated with improved mortality. HF with preserved ejection fraction (HFPEF) is less responsive to drug therapy, though outcomes are better than for systolic HF. Coronary insufficiency occurs because of an imbalance of myocardial oxygen balance, leading to symptoms of ischaemic heart disease (IHD). Treatment goals are maintaining coronary blood flow and reducing myocardial oxygen demand. Beta-blockers and anti-platelet drugs improve outcomes; modern anti-platelets are more effective but are associated with risks of haemorrhage. Statins are effective for primary and secondary prevention of myocardial infarction; they have additional anti-inflammatory properties.     

Drugs acting on the heart: heart failure and coronary insufficiency

Heart failure (HF) and coronary insufficiency are common amongst surgical and critical care patients. Both are chronic conditions interrupted by acute episodes. HF activates neurohormonal mechanisms that worsen renal and cardiac function. Acute heart failure (AHF) commonly presents with dyspnoea as a consequence of systolic and/or diastolic dysfunction. Goals of treatment are symptom relief to maintain tissue perfusion and optimize cardiac function. Diuretics and vasodilators are used early; positive inotropic drugs are reserved for when other treatment has failed. Chronic heart failure (CHF) is treated using changes in lifestyle and drugs to manage symptoms. ACE inhibitors and beta-blockers are effective in systolic heart failure and are associated with improved mortality. HF with preserved ejection fraction (HFPEF) is less responsive to drug therapy, though outcomes are better than for systolic HF. Coronary insufficiency occurs because of an imbalance of myocardial oxygen balance, leading to symptoms of ischaemic heart disease (IHD). Treatment goals are maintaining coronary blood flow and reducing myocardial oxygen demand. Beta-blockers and anti-platelet drugs improve outcomes; modern anti-platelets are more effective but are associated with risks of haemorrhage. Statins are effective for primary and secondary prevention of myocardial infarction; they have additional anti-inflammatory properties.     

Role of bioimpedance vectorial analysis in cardio-renal syndromes

The cardio-renal syndromes (CRS) are the result of complex bidirectional organ cross-talk between the heart and kidney, with tremendous overlap of diseases such as coronary heart disease, heart failure (HF), and renal dysfunction in the same patient. Volume overload plays an important role in the pathophysiology of CRS. The appropriate treatment of overhydration, particularly in HF and in chronic kidney disease, has been associated with improved outcomes and blood pressure control. Clinical examination alone is often insufficient for accurate assessment of volume status because significant volume overload can exist even in the absence of peripheral or pulmonary edema on physical examination or radiography. Bioelectrical impedance techniques increasingly are being used in the management of patients with HF and those on chronic dialysis. These methods provide more objective estimates of volume status in such patients. Used in conjunction with standard clinical assessment and biomarkers such as the natriuretic peptides, bioimpedance analysis may be useful in guiding pharmacologic and ultrafiltration therapies and subsequently restoring such patients to a euvolemic or optivolemic state. In this article, we review the use of these techniques in CRS.     

New directions in the medical management of heart failure

Like the introduction of digitalis more than 200 years ago, novel medical therapies today have the potential to significantly alter the course of heart failure (HF) and save thousands of lives. This review outlines new directions in HF medical management beyond the foundation of neurohormonal blockade. Furthermore, the role of novel risk factors in HF such as chronic renal insufficiency, anemia, and sleep apnea present tantalizing therapeutic targets to extend the morbidity and mortality benefits of current therapies. The course of time will tell which of these risk factors and therapies can hold promise, given the recent litany of negative trials in the HF arena. Advancements in molecular and genetic techniques have allowed us to begin to consider patient specific therapies and lay the groundwork for even further improvements in treatment of symptomatic HF. Finally, advances in telemedicine and device technology will allow the clinician to remotely monitor useful clinical parameters such as heart rate variability and pulmonary filling pressures to make more informed clinical decision-making and improve outcomes.     

Neurohumoral activation in heart failure: the role of adrenergic receptors

Heart failure (HF) is a common endpoint for many forms of cardiovascular disease and a significant cause of morbidity and mortality. The development of end-stage HF often involves an initial insult to the myocardium that reduces cardiac output and leads to a compensatory increase in sympathetic nervous system activity. Acutely, the sympathetic hyperactivity through the activation of beta-adrenergic receptors increases heart rate and cardiac contractility, which compensate for decreased cardiac output. However, chronic exposure of the heart to elevated levels of catecholamines released from sympathetic nerve terminals and the adrenal gland may lead to further pathologic changes in the heart, resulting in continued elevation of sympathetic tone and a progressive deterioration in cardiac function. On a molecular level, altered beta-adrenergic receptor signaling plays a pivotal role in the genesis and progression of HF. beta-adrenergic receptor number and function are decreased, and downstream mechanisms are altered. In this review we will present an overview of the normal beta-adrenergic receptor pathway in the heart and the consequences of sustained adrenergic activation in HF. The myopathic potential of individual components of the adrenergic signaling will be discussed through the results of research performed in genetic modified animals. Finally, we will discuss the potential clinical impact of beta-adrenergic receptor gene polymorphisms for better understanding the progression of HF.     

Cardorenal syndrome: an emerging problem in pediatric critical care

The cardiorenal syndrome (CRS) refers to a complex pathophysiologic state in which heart and kidney dysfunction coexist. Although a robust amount of adult literature exists, limited reports have been made regarding CRS in pediatric patients. However, CRS is increasingly being recognized as an impactful clinical problem that can have important implications regarding the need for treatment and prognosis. Although wide acceptance of a unified definition of CRS is lacking, a general consensus exists that CRS can be either primarily caused by cardiac disease with secondary effects on the kidney, or vice versa, as well as systemic conditions in which cardiac and renal disease are both considered to be secondary. Convincing data in the pediatric perioperative population have been reported, but there is a paucity of information in acute and chronic heart failure (HF), as well as acute kidney injury (AKI) and chronic kidney disease (CKD). Herein, we briefly report on the adult literature and summarize the current pediatric experience.     

The natriuretic peptide system: kidney and cardiovascular effects

PURPOSE OF REVIEW: The natriuretic peptide (NP) system is primarily an endocrine system that maintains fluid and pressure homeostasis by modulating cardiac and renal function. The physiologic functions of the NP system in healthy humans and in patients with cardiovascular disease are not fully understood. NP levels are elevated in patients with heart failure (HF) and other cardiac diseases; measurement of NPs may be used in the clinical setting to aid diagnosis and prognosis. In addition, synthetic NPs such as nesiritide are available for use in management of patients with acutely decompensated congestive HF. RECENT FINDINGS: Not only do NPs modulate volume and pressure homeostasis, but they also exert important anti-proliferative, anti-fibrotic effects in the heart. Thus, NPs may prove useful for prevention of remodeling after myocardial infarction and in advanced HF. BNP is emerging as an important biomarker in patients with HF and other cardiovascular diseases, such as pulmonary hypertension and atherosclerotic vascular disease. Elevated NP levels may serve as an early warning system to help to identify patients at high risk for cardiac events. Recombinant human ANP (carperitide) and BNP (nesiritide) are useful for management of acutely decompensated HF; these drugs are also being investigated for myocardial and renal protection in the setting of cardiac surgery and for prevention of cardiac remodeling. SUMMARY: The clinical application of NPs is expanding rapidly. Recent basic science and clinical research findings continue to improve our understanding of the NP system and guide use of ANP and BNP as biomarkers and as therapeutic agents.     

Anti-HLA antibody analysis and crossmatching in heart and lung transplantation

Although the clinical significance of anti-HLA antibodies in heart and lung transplantation is less well studied than in renal transplantation, several studies have shown that heart and lung recipients transplanted in the presence of donor-specific antibodies are at increased risk for early acute rejection and have a lower graft survival. In an effort to avoid any increase in organ ischemia time, heart and lung candidates with anti-HLA antibodies have to be identified prior to transplantation and crossmatches performed with donor materials obtained prior to organ recovery. Both class I and II antibodies have been found to be associated with chronic rejection, defined in heart transplantation as transplant-related coronary artery disease (TRCAV) and in lung transplantation as obliterative bronchiolitis (OB) or bronchiolitis obliterative syndrome (BOS). Post-transplant de novo development of donor antigen-specific class II antibodies has been found to be especially deleterious, significantly increasing the risk of chronic rejection and poor graft outcome. Based on the review of studies regarding the development of anti-HLA antibodies and thoracic organ allograft rejection several conclusions can be drawn. The presence of class I and II-directed anti-HLA antibodies, detected by any method, are associated with acute and chronic rejection in heart and lung transplantation. Different therapeutic strategies have been used pre-transplantation to decrease the level of anti-HLA antibodies and post-transplantation to maintain low antibody levels or treat rejection, thereby improving graft outcome. Thus, monitoring the presence and the level of anti-HLA antibodies is prognostic of graft outcome and allows for measurement of therapeutic efficacy.     

C34T AMP deaminase 1 gene mutation protects cardiac function in donors

Dysfunction of the donor heart is an important clinical problem that could be affected by genetic factors. We tested the hypothesis that possession of the C34T nonsense mutation in AMPD1 gene, which is known to improve survival in chronic heart failure, protects against cardiac dysfunction in donors. Genetic analysis for C34T mutation was performed by single-stranded conformational polymorphism (SSCP) in 22 donor hearts used for transplantation, 10 unused donor hearts with acute heart failure (HF), 37 patients with chronic HF, and 207 healthy controls. We found a significantly higher frequency of the mutation among donors with healthy hearts used for transplantation (31.8%) as compared to control population (13.5%, P < 0.001) and a lower frequency in dysfunctional donor hearts (5.0% P = 0.025); the frequency of the C34T mutation in patients with chronic heart failure (14.8%) was not different from that of a control population. The presence of the C34T mutation in AMPD1 gene appears to be protective against acute heart failure in cardiac donors.     

Liver disease related to the heart

In this article, we review both acute and chronic liver diseases that occur as a result of heart or circulatory system failure. Ischemic hepatitis, congestive hepatopathy, cardiac cirrhosis, and Fontan liver disease are reviewed. We review clinical presentation, diagnostic data, prognosis, and available therapeutic strategies for these entities. We aim to increase awareness about cardio-hepatic disease as the prevalence of this disorder in adults is increasing. Due to advances in medical and surgical care, patients with heart disease are living longer and thus exposing long-term effects on the liver that are clinically relevant. There may be a role for dual organ transplantation in some cases, but this is a very challenging endeavor, and newer ideas about treatment or prevention are needed.     

Induction of chronic cardiac insufficiency by arteriovenous fistula and doxorubicin administration

OBJECTIVES: Large animal experimental models of chronic heart failure (HF) permit repeated invasive assessment of cardiovascular function, and evaluation of new medical or surgical therapies. The existing models however fail to achieve stable and long-term HF. The aim of this study was to create a simple and stable chronic model of HF in goat, using both arteriovenous fistula and weekly intravenous doxorubicin injections. METHODS: After a preliminary experiment on four goats receiving weekly 1 to 2 mg/kg of doxorubicin, six adult female goats, having had an arteriovenous fistula without signs or symptoms of heart failure, received weekly two different dosages of doxorubicin for 13 weeks: group A (n = 3) received 0.5 mg/kg and group B (n = 3) received 1 mg/kg. After a three-month period without medication, both groups received again 1 mg/kg for four weeks. Cardiac function was assessed by repeated electrocardiographic and echocardiographic examinations. RESULTS: Four goats died during the medication period (one in group A, three in group B). During the period without medication a stable ventricular hypocontractility with left ventricular dilation was observed. Left ventricular dysfunction was more pronounced in group B, and was associated with clinical symptoms of HF. CONCLUSIONS: Arteriovenous fistula alone did not produce HF. Its association with doxorubicin injections provides a simple and stable chronic model of HF. This association allows reduction of the required doxorubicin dose and toxicity in animals and in the environment. Depending of the dose of doxorubicin, it is possible to obtain a model of heart dilatation and ventricular hypokinesia with or without clinical symptoms of HF, with a different mortality.     

Drugs acting on the heart: heart failure and coronary insufficiency

Heart failure (HF) and coronary insufficiency are common amongst surgical and critical care patients. Both are chronic conditions interrupted by acute episodes. HF activates neurohormonal mechanisms that worsen renal and cardiac function. Acute heart failure (AHF) commonly presents with dyspnoea as a consequence of systolic and/or diastolic dysfunction. Goals of treatment are symptom relief, maintenance of tissue perfusion, and optimizing cardiac function. Diuretics and vasodilators are used early; inotropes are reserved for when other treatment has failed.Chronic heart failure (CHF) is treated by changes in lifestyle and drugs to manage symptoms. ACE inhibitors and β-blockers are effective in systolic heart failure and are associated with improved mortality. HF with preserved ejection fraction (HFPEF) is less responsive to drug therapy, though outcomes are better than for systolic HF.Coronary insufficiency occurs when myocardial oxygen delivery is inadequate, leading to symptoms of ischaemic heart disease (IHD). Treatment goals are maintaining coronary blood flow and reducing myocardial oxygen demand. β-blockers and anti-platelet drugs improve outcomes; modern anti-platelets are more effective but associated with risks of haemorrhage. Statins are effective for primary and secondary prevention of myocardial infarction; they have additional anti-inflammatory properties.     

Perinatal cocaine exposure impairs myocardial beta-adrenoceptor signaling in the neonatal rat

Cardiac dysfunction occurs in infants with prenatal cocaine exposure, and gestational cocaine exposure induces presynaptic and postsynaptic changes in the central monoaminergic receptor pathways. The hypothesis of this study is that prenatal cocaine exposure adversely affects the peripheral adrenergic receptor (betaAR) signaling pathway in the neonatal rat heart. Timed pregnant rats received daily intragastric treatment with saline or cocaine 20 mg/kg or 60 mg/kg from Gestational Day 2 until parturition. After birth, nursing mothers either continued to receive the same treatment or received no treatment. Adenylyl cyclase activity, betaAR density, and the amount of immunoreactive G proteins were measured in myocardial membranes obtained from the offspring on Postnatal Day 1 or 7. On Postnatal Day 1, prenatal cocaine exposure increased the betaAR number but did not affect isoproterenol-stimulated adenylyl cyclase activity. On Postnatal Day 7, perinatal cocaine exposure significantly attenuated isoproterenol-stimulated adenylyl cyclase activity in the absence of betaAR up-regulation. Prenatal cocaine exposure also significantly increased Gi protein and reduced GTP-stimulated adenylyl cyclase activity in Postnatal Day 1 cocaine (20 mg/kg) pups compared with saline (P < 0.05). Therefore, perinatal cocaine exposure impaired the myocardial betaAR-cAMP signaling pathway during the first week of postnatal life in the rat. IMPLICATIONS: This study shows that maternal cocaine use during pregnancy impairs the beta-adrenoceptor signaling pathway in the rat during the first week of life. Abnormal cardiac function in the cocaine-exposed neonate may be related to a defect in beta-adrenoceptors, because they regulate cardiac function.     

Bacteriophage therapy in infection after fracture fixation (IAFF) in orthopaedic surgery

Infection after fracture fixation (IAFF) in orthopaedic surgery is a significant complication that can lead to disability due to chronic infection and/or relapsing disease, non-union necessitating revision surgery. Management of IAFF is a major challenge facing orthopaedic surgeons across the world due to two key pathogenic mechanisms of Biofilm formation and antimicrobial resistance (AMR) against traditional antibiotics. Advanced prophylactic and treatment strategies to help eradicate established infections and prevent the development of such infections are necessary. Bacteriophage therapy represents an innovative modality to treat IAFF due to multi-drug resistant organisms. We assess the current role and potential therapeutic applications of the novel bacteriophage therapy in the management of these recalcitrant infections to achieve a successful outcome.     

Predictors of haemodynamic instability and heart rate variability during haemodialysis.

BACKGROUND: The pathogenesis of haemodialysis-induced hypotension is multifactorial and may include autonomic nervous system dysfunction. The present study was undertaken to (i) determine heart rate variability (HRV) in chronic haemodialysis patients without and with haemodynamic instability (hypotension-prone) during ultrafiltration and (ii) identify patients at risk and the predictors of dialysis-related hypotension. METHODS: HRV was evaluated in 56 chronic haemodialysis patients without (stable; n = 27) and with symptomatic hypotension episodes (unstable; n = 29) during daytime, haemodialysis and night-time periods. Logistic regression analysis was performed in a model that included clinical and biochemical data and HRV measurements. RESULTS: HRV was significantly reduced in haemodynamically unstable as compared with the stable patients. LF/HF ratio, an index representative of sympathovagal balance, was significantly lower in unstable patients, especially in those with ischaemic heart disease and diabetes mellitus. In a logistic regression model including clinical data and HRV measurements, ischaemic heart disease and left ventricular systolic dysfunction were found to be the main predictors of haemodynamic instability. CONCLUSIONS: These data suggest that haemodynamic instability is strongly associated with a decreased HRV and an impaired sympathovagal balance, suggesting disturbed autonomic control in uraemic patients with cardiac damage. Patients with ischaemic heart disease, reduced left ventricular systolic function and decreased HRV may be at the highest risk to be haemodynamically unstable during haemodialysis. The role of early detection and treatment of ischaemic heart disease in preventing symptomatic hypotensive episodes in these patients remains to be determined.     

Atrial fibrillation in intensive care units

Atrial fibrillation (AF) is an abnormal irregular heart rhythm whereby electrical signals are generated apparently randomly throughout the atria. It is the most common of all cardiac arrhythmias. The occurrence of AF has been poorly studied in general intensive care units (ICUs), but extensively studied in the postoperative period, when it is a cause of admission to surgical ICUs (S-ICUs) or can delay patient transfer from S-ICUs. The most frequently identified risk factors are increased age, valvular heart disease, atrial enlargement, preoperative atrial arrhythmias, and chronic lung diseases. Ischaemic heart disease is probably the most common cause of AF, followed by hypertension, rheumatic heart disease, thyrotoxicosis, cardiomyopathy, mitral valve disease, haemochromatosis and infection (e.g. pneumonia or systemic sepsis). The onset of AF or faster rates of chronic AF may be precipitated by acid–base disturbances, electrolyte abnormalities (in particular, hypokalaemia or hypomagnesaemia), hypovolaemia, myocardial ischaemia, and surgical manipulation in the thorax. Postoperative AF resolves spontaneously in most patients, but can recur. Two main therapeutic strategies can be adopted in perioperative AF: rhythm control and rate control. The former is based on electrical or pharmacological treatment, while the latter is only pharmacological. No clear superiority has been pointed out by comparative studies, but the choice is influenced by clinical conditions. Rhythm control strategy should be chosen in the presence of contraindications to anticoagulation, which is indicated if spontaneous conversion to sinus rhythm does not occur within 48 h.     

Cardiac failure in the newborn. Diagnostic pitfalls

Echocardiography commonly represents the diagnostic clue in neonatal heart failure (HF). Congenital heart diseases are the most frequent causes of HF in this age group. Arterio-venous malformations are the most common noncardiac causes of HF. Normal cardiac structural findings on echocardiography require further investigations in order to exclude other causes of HF. We present three male patients admitted in the interval 2003-2007 with neonatal HF, systolic murmur, cardiomegaly, normal cardiac structure on echocardiography and intracranial bruit. All three cases were diagnosed with vein of Galen aneurysmal malformation (VGAM) by head ultrasound. According to age and malformation type, different presentation patterns were noticed: early neonatal intractable HF mimicking aortic coarctation, postnatal HF stabilized by drug treatment, and chronic HF in a VGAM with tendency to spontaneous regression. Both head ultrasound and cranial auscultation are mandatory in newborns or infants with no cardiac primary cause of HF.