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Right heart function is the main determinant of prognosis in pulmonary arterial hypertension (PAH). At present, no treatments are currently available that directly target the right ventricle, as we will demonstrate in this article. Meta-analysis of clinical trials in PAH revealed that current PAH medication seems to have limited cardiac-specific effects when analysed by the pump-function graph. Driven by the hypothesis that ''left'' and right heart failure might share important underlying pathophysiological mechanisms, we evaluated the clinical potential of left heart failure (LHF) therapies for PAH, based on currently available literature. As in LHF, the sympathetic nervous system and the renin-angiotension-aldosterone system are highly activated in PAH. From LHF we know that intervening in this process, e.g. by angiotensin- converting enzyme inhibition or b-blockade, is beneficial in the long run. Therefore, these medications could be also beneficial in PAH. Furthermore, the incidence of sudden cardiac death in PAH could be reduced by implantable cardioverter-defibrillators. Finally, pilot studies have demonstrated that interventricular dyssynchrony, present at end-stage PAH, responded favourably to cardiac resynchronisation therapy as well. In conclusion, therapies for LHF might be relevant for PAH. However, before they can be implemented in PAH management, safety and efficacy should be evaluated first in well-designed clinical trials.

Mock circulation loops are used to evaluate the performance of cardiac assist devices prior to animal and clinical testing. A compressible, translucent silicone ventricle chamber that mimics the exact size, shape and motion of a failing heart is desired to assist in flow visualization studies around inflow cannulae during VAD support. The aim of this study was therefore to design and construct a naturally shaped flexible left ventricle and evaluate its performance in a mock circulation loop. The ventricle shape was constructed by the use of CT images taken from a patient experiencing cardiomyopathic heart failure and used to create a 3D image and subsequent mould to produce a silicone ventricle. Different cardiac conditions were successfully simulated to validate the ventricle performance, including rest, left heart failure and VAD support.

Background: Low bone mineral density (BMD) is common in chronic lung diseases and associated with re- duced quality of life. Little is known about BMD in pulmonary hypertension (PH). Methods: Steroid-naive patients with PH (n=34; 19 idiopathic, 15 chronic thromboembolic) had BMD measured by DXA at the time of diagnostic right heart catheterization. Exercise capacity, quality of life and various parameters related to PH severity and bone metabolism were also assessed. 24 patients with left heart failure (LHF) were similarly assessed as con- trols. Results: The prevalence of osteopenia was high both in PH (80%) and in controls with LHF (75%). Low BMD was asso- ciated with lean body mass, age, lower BMI, impaired exercise capacity and in PH with higher pulmonary vascular resis- tance. Serum parathyroid hormone (PTH) was elevated and considerably higher in PH than in LHF (above normal, in 55 vs 29%). Secondary hyperparathyroidism was not related to impaired renal function but possibly to low vitamin D status. Conclusions: Osteopenia is common in PH and in chronically ill patients with LHF. Osteopenia is associated with known risk factors but in PH also with disease severity. Preventive measures in an increasingly chronic ill PH population should be considered. Secondary hyperparathyroidism is highly prevalent in PH and might contribute to bone and possibly pul- monary vascular disease. Whether adequate vitamin D substitution could prevent low BMD in PH remains to be deter- mined.

Summary Chronic pulmonary hypertension Pulmonary hypertension comprises a group of diseases in which various pathophysiological mechanisms trigger a rise in the pressure of the pulmonary arteries and secondarily an overload in the right heart. Echocardiography is the screening method of choice to evaluate right ventricular morphology and function and measure systolic pulmonary artery pressure. In practice the commonest causes of pulmonary hypertension are left heart failure and chronic obstructive lung diseases. Therapy is primarily targeted at these underlying disorders. To treat the rare pulmonary artery hypertension (PAH) very costly but effective drugs have become available in the last few years. Before initiating such treatments for PAH, careful diagnosis by way of right heart catheterisation and a search for causative factors is essential in order to differentiate between pre- and post-capillary pulmonary hypertension. Chronic thromboembolic pulmonary hypertension is secondary to recurrent, often unrecognised pulmonary emboli and is probably under-diagnosed. Here the therapeutic arsenal consists not only of thromboendarterectomy but also of newly available specific drugs. Investigations and treatment for patients with pulmonary hypertension should be in the hands of multidisciplinary PH centres in close cooperation with the patients’ physicians.

The acute respiratory distress syndrome (ARDS)/acute lung injury is a major cause of morbidity and mortality throughout the world. ARDS is an acute syndrome of lung inflammation and increased permeability associated with severe hypoxia and bilateral infiltrates on chest radiographs with no evidence of left heart failure. This chapter reviews the evidence for genetic determinants in acute lung injury and ARDS with a focus on potential candidate gene polymorphism that may be important in the development and outcome of ARDS.

Background Pulmonary Hypertension has a poor prognosis and therapy is limited to symptomatic relief. Apelin, a new therapy, has the potential to address the underlying pathology whilst also providing relief of symptoms. NT-proBNP a marker of disease severity is commonly used to assess treatment effect. Aims and objectives This study aimed to investigate, for the first time, the effects of apelin on serum NT-proBNP concentration in groups of pulmonary hypertension patients and controls. The hypothesis of the study was that apelin would cause a change in NT-proBNP. Methods Serum samples from patients recruited for a haemodynamic investigation of apelin were used. The groups studied were controls, pulmonary arterial hypertension and pulmonary hypertension due to left heart failure. In the haemodynamic study each patient was given an apelin and placebo infusion separately over a period of several minutes. Serum samples were taken pre and post infusion. NT-proBNP concentration in the samples was determined using the ABNOVA ELISA kit. Results There was no significant change in NT-proBNP levels due to apelin infusion across all groups (P = 0.830). On sub group analysis there was no significant change detected in any group as shown in Figure 1. Conclusion NT-proBNP levels do not immediately change in response to several minutes of apelin infusion. This is consistent amongst control and pulmonary hypertension patients. Despite the lack of change in NT-proBNP levels seen in this study, the haemodynamic response pattern reported for apelin1 has been associated with NT-proBNP changes in other drug studies. The main difference between these studies and this study was investigation of therapy effect over a longer time period. From our results we cannot conclude that apelin has no effect on NT-proBNP levels. Investigation of therapy over a longer time period is required. Reference 1 Brash L, Church C, Gibbs JS, Howard LSGE, Johnson MK, Welsh DJ, Wilkins MR, Newby DE, Peacock AJ. Apelin improves cardiac output in patients with pulmonary arterial hypertension. Submitted to ERS 2015 Conference

A 59-year-old woman with intractable left heart failure caused by severe aortic regurgitation underwent emergency aortic valve replacement. She had originally presented four months earlier with dyspnoea, pyrexia (38.8°C) and signs of pneumonia. Blood cultures were not taken and she was treated with intravenous antibiotics. After four weeks her dyspnoea improved but …

Pulmonary arterial hypertension complicated by decompensated cor pulmonale is a challenging clinical problem with few effective therapeutic options. B-type natriuretic peptide is a pluripotent hormone that promotes diuresis and natriuresis, vasodilates systemic and pulmonary vessels, and reduces circulating levels of endothelin and aldosterone. It may represent a possible therapeutic strategy for decompensated cor pulmonale in the same manner that it is used to treat decompensated left heart failure. The authors report their experience with B-type natriuretic peptide as adjunctive therapy for pulmonary arterial hypertension complicated by decompensated cor pulmonale. A detailed case report is presented followed by the evaluation of a series of 11 cases occurring in eight patients from December 2002 through April 2004.

The authors present a case of an 85-year-old woman known to suffer from severe congestive heart failure who presented with dyspnea and a unilateral infiltrate in the right lung on chest x-ray. Following clinical judgment, she was diagnosed with unilateral pulmonary edema and was treated accordingly, with rapid improvement of symptoms and disappearance of the infiltrate within 12 hours. The patient had been hospitalized many times during the previous years with pulmonary edema affecting both lung fields. Unilateral pulmonary edema is an unusual clinical condition that has been reported as a manifestation of left heart failure, mostly affecting the right lung. The authors emphasize the possible presentation of unilateral pulmonary edema in a patient with heart failure and recurrent bilateral pulmonary edema.

Patients undergoing bilateral lung transplantation for end-stage pulmonary hypertension may experience various complications. We describe a patient who underwent transplantation for chronic pigeon breeder's disease, who had secondary pulmonary hypertension and deteriorated right heart function, and who developed severe left heart failure during the weaning phase after successful double lung transplantation. The patient was stabilized with catecholamines and an intra-aortic balloon pump. Left heart function increased within 7 days and normalized at Day 18. Otherwise, the post-operative course was uneventful.

Spontaneous coronary artery dissection (SCAD) is a very rare cause of peripheral artery thromboembolism. It is especially rare to show symptoms of acute limb ischemia without chest symptoms during a hospital visit. In this case, a rare case of SCAD led to left heart failure and caused left ventricle thrombi, which in turn caused peripheral thromboembolism.

Secondary tricuspid regurgitation (TR) primarily develops due to left heart failure or primary pulmonary diseases. Tricuspid annular dilation, which is commonly caused by right ventricular volume and pressure overload followed by right ventricle dilation, is believed to be the main mechanism underlying secondary TR. It is reported that once the tricuspid annulus is dilated, its size cannot spontaneously return to normal, and it may continue to dilate. These reports also suggest the use of an aggressive surgical approach for secondary TR. In the present report, we describe a case of tachycardia-induced severe TR that was completely resolved without the need for surgery.

The authors have developed Doppler mitral flow velocity (mfv) indices to estimate peak atrio-ventricular pressure gradient (pg), its mean and peak rate of change with time (pag and mag) to assess left atrial contractility. The authors' indices were measured from the digitised mfv signals which were fitted to splines of polynomials in time to represent mitral inflow during atrial systole in 4 normals (GpA) and 10 patients with stable NYHA grade 3 heart failure (GpB). The means (standard deviations) for pg, pag and mag for GpA versus GpB were 4.04 (1.04) mm Hg, 417 [154] and 211.5 (79.7) mm Hg s/sup -1/ respectively versus 2.39 (1.06) mm Hg, 117 [111] and 43.5 (34) mm Hg s/sup -1/ respectively. Mean indices pg, pag and mag were significantly greater for GpA, t values at the 95% confidence interval=2.65, 3.91 and 5.73 respectively and p values=0.021, 0.003 and 0.0001 respectively.

Clinical experience is accumulating that coronary artery bypass grafting is of great benefit in patients with advanced ischemic cardiomyopathy. At Yale University, we have analyzed short- and long-term results in 188 consecutive patients with an ejection fraction (EF) of 30% or less undergoing coronary artery bypass grafting by a single surgeon. This experience permits the following conclusions: (1) Surgery can be performed safely (mortality 2.8% in elective patients); (2) Major improvement in left ventricular (LV) function is objectively demonstrable (EF change from 23.3% to 33.2%); (3) Symptomatic improvement is noted by patients (NYHA class change from 3.1 to 1.4); and (4) Good long-term survival is realized, relative to expectations with medical management alone (88%, 77%, and 60% at 1, 3, and 5 years). If coronary artery disease is severe and proximally situated and there are adequate target arteries, we do not deny patients surgery based on EF or LV size criteria, nor do we require objective demonstration of reversible ischemia. In fact, hearts in the largest size range (left ventricular end-systolic volume index > 100 mL) actually showed beneficial reverse remodeling subsequent to coronary artery bypass grafting. Surgical revascularization is recommended strongly for patients with advanced ischemic cardiomyopathy. Results rival those of transplantation. Copyright 2002, Elsevier Science (USA). All rights reserved.

Galectin-3 (Gal 3) is a novel marker of left heart failure and cardiovascular mortality. We tested the hypothesis that Gal-3 predicts pulmonary artery pressure and right ventricular (RV) function in pulmonary arterial hypertension (PAH). Using a prospective study, 15 subjects with right heart

IntroductionThe optimal timing of coronary intervention in patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACSs) is a matter of debate.PurposeWe proposed through this work to study the optimal time to coronary angiography in patients admitted for acute coronary syndrome without ST-segment elevation in the Tunisian context and its prognostic impact on inhospital mortality.Materials and methodsIt is about an observational study from MIRACOS registry that included 407 patients admitted for NSTE-ACS. We were interested to find general characteristics, the time to coronary angiography, mortality and in-hospital complications.ResultsA total of 407 patients were included in our study. Nearly half of our patients (49.5%) were considered at high cardiovascular risk. The average to coronary angiography was 5.09 days. Patients who underwent early coronary angiography were significantly younger (p=0.01), had a lower incidence of diabetes (p=0.01), left heart failure (p=0.0001) and electrical changes suggestive of ischemia (p=0.009). Patients who have undergone an invasive strategy had significantly lower levels of creatinine (p

Background . The bridge to transplantation with pulsatile mechanical assist devices became a standard procedure for patients deteriorating on the waiting list. Recently, continuous flow axial impeller pumps were introduced to clinical application offering new advantages. Methods . From November 1998 till September 2000, 6 male patients (mean age 53 plus or minus 11 years) with end-stage left heart failure were implanted with a DeBakey ventricular assist device (VAD) axial-flow pump for bridge to transplantation. Results . Three patients were successfully transplanted after 74, 115, and 117 days, respectively. Two other patients died after 25 and 133 days. One patient is still on the device after 108 days. Because of modification of the implantation technique after the first 2 patients, mean pump-flow within the first 3 weeks was increased from 4.3 ± 0.6 L/min to 6.7 ± 0.3 L/min. Patients were put on regular bicycle-ergometer training and improved their exercise capacities up to a mean maximum oxygen consumption of 20.2 mL/kg/min. Conclusions . Initial implants of the DeBakey VAD demonstrated support properties comparable to pulsatile pumps but without significant restrictions for extended use.

Patients admitted to the coronary care unit following either myocardial infarction, severe left heart failure or rhythm disturbances frequently have difficulty conceptualizing a ‘broken heart’. The aim of this paper is to provide a greater understanding of the term ‘trust’ in relation to patient care, utilizing the concept analysis framework of Walker & Avant. Trust has been identified as an essential element in the nurse—patient relationship; due to its abstract nature it would appear that we as critical care nurses have been naive and have over-simplified the concept. Indeed, it is suggested that we could learn from our patients, in order to contribute to an effective nurse—patient relationship.

A 25-year-old woman was admitted to our center for left heart failure. The clinical, electrocardiographic and bioptic findings suggested an acute lymphocytic myocarditis. One month later, paroxysmal hypertension and high urinary excretion of noradrenaline revealed the presence of a pheochromocytoma.

Hypertensive crisis is thought to be initiated by an abrupt increase in systemic vascular resistance, likely related to humoral vasoconstrictors. Left ventricular dilatation and failure may develop as a result of increased afterload due to hypertension. Left heart failure may result in secondary pulmonary hypertension by increasing pulmonary venous pressure. Here, we report the effects of sodium nitroprusside for treatment of hypertensive crisis complicated with acute left ventricular dilatation, heart failure, and pulmonary hypertension secondary to vesicoureteral reflux in a 10-year-old female patient. This article presents a complex clinical case treated by simple medication. Key Words: Hypertensive crisis, dilated cardiomyopathy, pulmonary hypertension, sodium nitroprusside, heart failure, vesicoureteral reflux

Purpose The influence of speed optimization on long term outcome among Continuous Flow (CF) Left Ventricular Assist Device (LVAD) pts is still unknown. Current guidelines recommend setting device speed that will ensure intermittent Aortic Valve (AV) opening during support. This study sought to determine the feasibility of achieving this parameter prior to discharge using a ramp test and its potential role in preventing long-term device complications. Methods and Materials A prospective study on pre-discharge speed optimization via Ramp Protocol was conducted post-device implantation. Right and left Heart Failure (HF), Gastrointestinal (GI) bleeding, arrhythmia, device thrombosis, and ECHO parameters of aortic insufficiency (AI) were collected. Results 37 pts had speed optimization Ramp tests before discharge with a mean follow-up time of 9.6±6.7 months. Mean age was 59±12 years old and 84% were male. 49% (n=18) were discharged with a speed that allowed for intermittent AV opening while 32% (n=12) were discharged with a closed AV. 19% (n=7) had AV surgery (Park stitch) at the time of implant. The frequency of right and left HF, ventricular arrhythmia and GI bleeding were similar among all 3 groups. 28% (n=5) of the AV opening group had device exchange due to obstruction to pump flow, whereas none of the 19 pts in the AV closed and AV surgery groups experienced device thrombosis (OR = 6.92, p=0.094). None of the pts in the AV opening group developed significant AI as compared to 1 pt who developed AI from the AV-closed group. Conclusions Intermittent opening of the AV via speed optimization was achieved in only 49% of the pts. Pts with AV opening may be at higher risk for developing obstructions to flow. Pts with intermittent AV opening may be better protected from developing significant AI. This study implies a differential speed setting for Bridge-To-Transplant pts since long-term consequences of AI is of less concern than protecting them from experiencing obstruction to pump flow events. Larger cohorts with longer follow up times are warranted.

The clinical syndrome of left heart failure (HF) is often simplistically characterized as dyspnea related to elevation of pulmonary venous pressure. In fact, left HF may manifest as one or a combination of several syndromes, including acute dyspnea, chronic fatigue, functional incapacity, and

Approximately two-thirds of the volume taken up by a normal lung is air, about one-sixth is blood and about one-sixth is extravascular water and tissue solids. The physical density of the normal lung is thus approximately 0.3 g/ml. An increase in intrapulmonary blood volume or accumulation of water in the interstitial or alveolar space causes an increase in lung density, and measurements of lung density may thus provide an index of the abnormalities in pulmonary oedema. Qualitative information about lung density is obtained in the standard chest radiograph. Quantitative measurements of lung density can be obtained with X-ray computed tomography, Compton-scatter techniques or transthoracic gamma-ray attenuation. These techniques provide information of overall lung density. It is clear, however, that any changes in overall lung density are the result of individual variations in the density of the vascular and extravascular compartments, and that a modest increase in the density of one could be masked by a corresponding decrease in the density of the other. Evaluation of water accumulation and changes in pulmonary blood volume should therefore ideally be made with a technique able to differentiate between the vascular and extravascular compartments. The paper looks briefly at one such method-positron emission tomography. >

“Heart failure may be defined as the pathophysiologic state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues. Heart failure occurs as the consequence of many forms of heart disease afflicting at least 4 million Americans of all ages.”1 Heart failure also occurs with the failure of compensatory mechanisms such as myocardial hypertrophy, which may accompany dilatation of the ventricular chambers. Heart failure can be divided into left and right heart failure, although if the heart failure becomes chronic then left heart failure can result in right heart failure, so that both can occur concomitantly. Heart failure may be due to failure of myocardial contraction or it may be due to an excessive hemodynamic burden. The heart will compensate for this physiologically, but also pathologically with myocyte hypertrophy with or without ventricular dilatation. The rate of onset of heart failure also will in fluence the clinical and pathological manifestations.

Objective To assess the exercise capacity of chronic left heart failure using cardiopulmonary exercise testing (CPET). Methods 20 patients with chronic left heart failure (CHF) from August 2010 to December 2010 in our department were enrolled in the current study. 27 matched subjects with normal cardiopulmonary function were enrolled as control group. CPET was performed to all patients, and clinical characteristics and routine tests results were collected. Results Compared with the control group, anaerobic threshold, peak VO 2 , peak VO 2 /HR, peak VO 2 /pred. and peak heart rate significantly increased (p 2 slope significantly decreased. In Pearson and partial correlation, NT-proBNP, LVEF, peak HR and peak SBP were all significantly correlated with AT, peak VO 2 , peak VO 2 /HR, peak VO 2 /pred and VE/VCO 2 slope. Conclusions The exercise capacity of patients with CHF is much poorer than control subjects. CPET variables are significantly correlated with the variables of regular clinical measurements and can objectively evaluate exercise capacity and cardiopulmonary function of CHF patients.

Although vasomotor activity in small pulmonary vessels has been studied extensively in the past, using the concept of resistance to flow, information on the distensibility of these vessels is very sparse. In an attempt to reduce this deficit, we adapted a theoretical method developed for small systemic vessels, to estimate distensibility of pulmonary resistance vessels in experimental animals and man. Pressure-flow data from 11 dogs and 10 human subjects (5 control subjects and 5 patients with long-standing left heart failure) were used to calculate distensibility of small pulmonary vessels. The conductance, G, was calculated from these data as the ratio of blood flow to driving pressure. The slope of the relationship between the logarithm of G1/4 and the average distending pressure (ADP) provides a graphic picture of circumferential extensibility, E, defined as percent change in radius for an infinitesimal change in ADP. Results indicate that: (1) the value of E in dogs was 1.85 ± .40 mmHg−1 for the control state, which decreased to 1.45 ± .43 mmHg−1 during norepinephrine administration; however, the decrease in the value was not statistically significant (p = 0.53); (2) the value of E in control human subjects was 3.38 ± .47 mmHg−1 and the value of E in patients with left heart failure was −0.64 ± 0.39 mmHg−1; the difference was significant (P = .0001). Moreover, at a given ADP in the range of overlapping pressures, the “average” radius of small pulmonary vessels in patients with left heart failure was smaller than that in the control subjects; and (3) small pulmonary vessels were more distensible than both the small systemic vessels and the large pulmonary arteries.

Introduction Although studies have shown that right ventricular ejection fraction (RVEF) is an independent predictor of survival in patients with myocardial infarction and moderate left heart failure, there is scant data available on the prognostic significance of RVEF in patients with preserved left ventricular ejection fraction (LVEF), partly due to challenges in imaging the right ventricle (RV) due to its amorphous geometry. Recent technological advances in cardiac magnetic resonance (CMR) have allowed the RVEF to be assessed with greater accuracy.

To detect congestive left heart failure radiologists must evaluate the diameter of blood vessels on chest radiographs. An automatic digital method to detect the vessels and to measure their diameter is presented in this paper. The vessels are detected by searching the areas which are conform to an ideal vessel model. Then the false vessels detected are eliminated.

The hemodynamic effects of nitrates in patients with left ventricular dysfunction and both acute and chronic heart failure are well documented [1,12]. However, the development of hemodynamic tolerance during long-term treatment with oral nitrates remains a subject of debate [6,7]. This has two clinically important implications [2–4]: 1. Cardiac unloading by long-acting nitrates would increase exercise tolerance. 2. The progression of the degree of heart failure would be prevented or delayed.

Summary Chronic use of digitalis is common amongst the institutionalized elderly. Associated with digitalis use is the potential for toxicity and/or adverse reactions. In this study maintenance digoxin was withdrawn from 14 elderly nursing home residents in sinus rhythm. Subjects were followed over 18 months for evidence of dysrhythmia or heart failure. One resident had an episode of supraventricular tachycardia which required digoxin to be restarted. One resident developed left heart failure, treated with oral diuretic. For 12 of the 14 residents, withdrawal of maintenance digoxin was achieved without deleterious effect. This study suggests that maintenance digoxin may be withdrawn safely in elderly nursing home residents in sinus rhythm and without history of atrial dysrhythmia.

A 48-year-old woman with congenital heart disease was referred to our centre for refractory right and left heart failure. She was born with a pulmonary stenosis associated with an atrial and ventricular septal defect and underwent a surgical repair at the age of 16. From the age of 44, she gave a history of decline …

Low cardiac output states, such as left heart failure, are characterized by a preserved oxygen extraction ratio compared with severe sepsis. Near-infrared spectroscopy (NIRS) allows noninvasive estimation of skeletal muscle tissue oxygenation (StO2). The aim of study was to determine relationship between StO2 and mixed venous oxygen saturation (SvO2) in patients with severe left heart failure with or without additional severe sepsis or septic shock.

Right-sided heart failure is a major problem among patients with congenital heart diseases, due to the prevalence of congenital heart defects and the association of pulmonary hypertension. More attention is focused on the structure of the right heart particularly in association with congenital heart defects and chronic lung disease. The right ventricle (RV) may support the pulmonary circulation, and sometimes the systemic circulation (systemic RV) in congenital heart defects. Despite major progress being made, assessing the RV remains challenging, often requiring a multi-imaging approach and expertise (echocardiography, magnetic resonance imaging, nuclear and cineangiography). Evidence is accumulating that RV dysfunction develops in many of these patients and leads to considerable morbidity and mortality. While there is extensive literature on the pathophysiology and treatment of left heart failure, the data for right-sided heart failure is scarce. Therefore RV function in certain groups of congenital heart disease patients needs close surveillance and timely and appropriate intervention to optimise outcomes. An understanding of RV physiology and hemodynamics will lead to a better understanding of current and future treatment strategies for right heart failure. This will review right-sided heart failure with the implications of volume and pressure loading of the RV in congenital heart diseases.

Background : The serum B-type natriuretic peptide (BNP) is released from the ventricles as a response to volume or pressure overload of the ventricles. A few studies have reported that the BNP measurements are useful in differentiating between heart failure and pulmonary causes in patients who visited the emergency department with dyspnea as the chief complaint. It is difficult to differentiate a right heart failure from a left heart failure in the emergency room. However, there is no report on the application of a BNP assay to differentiate in right heart failure from left heart failure. In this study, the BNP levels were measured from dyspneic patients in the emergency department to determine whether or not the BNP level would be useful in differentiating the cause of the dyspnea from right ventricular failure and left ventricular failure. Method : 89 patients who visited emergency department of the Bundang Cha Hospital with dyspnea from June 2002 to March 2003 were selected. The 29 patients from the outpatient clinics and inpatients

Against my better judgment, I was persuaded by two of my wife's elderly spinster aunts to examine their sister, another spinster. “She's just not right,” I was told by telephone. She arrived the following morning after a car journey of some 150 miles, and they had been correct—she was not right, she was in left heart failure. Subsequent examination in hospital also revealed that she had advanced syringomyelia and cancer of the breast, with widespread deposits. She died peacefully six days later. After passing on the sad news to the aunts, I was somewhat tartly told that she had willed her body to medical science, and would I kindly deal with it. Ella, for that was her name, proved difficult to deal with. Getting the correct forms signed and witnessed by her …

A 70-year-old woman wth a long history of ischaemic heart disease was admitted to hospital after a sudden onset of crushing central chest pain. 3 years previously a permanent transvenous pacemaker had been inserted following a bradycardic episode. On examination there were signs of left heart failure. Peripheral pulses were normal and equal and she was normotensive. An electrocardiogram showed no features of acute myocardial infarction. A chest radiograph demonstrated cardiomegaly and widening of the superior mediastinum. The patient was referred for contrast computed tomography (CT) examination of the chest (Figures 1 and 2) to exclude dissection of the thoracic aorta.