Cardiac Chamber Enlargement Research Articles

Cirrhotic cardiomyopathy: Implications for liver transplantation.

The majority of patients on a waiting list for liver transplantation have end-stage liver disease. Because of the marked peripheral vasodilatation of end-stage cirrhosis that masks a latent myocardial dysfunction, cardiac abnormalities in the resting state are usually subclinical and escape the attention of physicians. However, when challenged, the systolic and diastolic contractile responses are attenuated. In addition to these contractile abnormalities, morphological changes, such as enlargement or hypertrophy of cardiac chambers, and electrophysiological repolarization changes, including a prolonged QT interval, can be observed. The constellation of these cardiac abnormalities is termed cirrhotic cardiomyopathy. Liver transplantation induces significant cardiovascular stress. Clamping of the inferior vena cava and portal vein, hemorrhage and blood/volume infusion, and ischemia/reperfusion all cause hemodynamic fluctuation. The changing cardiac preload and afterload status increases the cardiac workload, and thus, the previously subclinical ventricular dysfunction may manifest as overt heart failure during the operative and perioperative periods. Cardiac dysfunction contributes to morbidity and mortality associated with liver transplantation. Cardiovascular events are the third leading cause of death in liver recipients. However, because liver transplantation is the only definitive treatment for end-stage liver failure and also appears to reverse cardiac abnormalities, it is important to understand the challenges of the heart in liver transplantation. This review focuses on cardiac status before, during, and after liver transplantation. Liver Transplantation 23 826-835 2017 AASLD.

Clinical benefits, echocardiographic and MRI assessment after pulmonary sequestration treatment

BackgroundThis study aimed to explore systematically procedural results, clinical benefits with echocardiographic and chest-MRI assessment of pulmonary sequestration percutaneous treatment. Methods13 consecutive infants and children with diagnosis of isolated pulmonary sequestration (PS) had percutaneous closure of the aberrant artery supplying pulmonary sequestration between 2010 and 2015. By protocol, echocardiographic and chest-MRI assessment was performed before and respectively at 6–12months and 1year with the aim to study the effects of embolization on heart volume overload and regression of pulmonary sequestration. ResultsMedian age at diagnosis was 1year (95%CI 0–2.6); median age at treatment was 1.3years (95%CI1.01–2.85). In all pts the PS was confirmed by chest-MRI. Procedural success was 100%. After treatment, pts experiencing previously respiratory symptoms/infections remained asymptomatic at 2.9year follow-up. In pts with significant shunt due to PS, treatment resulted in amelioration in left or right cardiac chamber enlargement at 6 and 12month follow-up. At distance from PS closure (median 14months), chest-MRI confirmed the closure of the aberrant artery and PS regression in 12 patients. In one case, despite the acute procedural success and the supplying artery remained closed, MRI detected residual PS revascularization. ConclusionsPercutaneous PS closure in infants and children is safe and provide regression in respiratory symptoms and heart chamber dilatation if significant shunt is present. MRI is able to define aberrant artery course and PS parenchima, and might represent a valid instrument to study residual PS parenchima during growth.

Early sensitization of myofilaments to Ca2+ prevents genetically linked dilated cardiomyopathy in mice.

Dilated cardiomoypathies (DCM) are a heterogeneous group of inherited and acquired diseases characterized by decreased contractility and enlargement of cardiac chambers and a major cause of morbidity and mortality. Mice with Glu54Lys mutation in α-tropomyosin (Tm54) demonstrate typical DCM phenotype with reduced myofilament Ca2+ sensitivity. We tested the hypothesis that early sensitization of the myofilaments to Ca2+ in DCM can prevent the DCM phenotype. To sensitize Tm54 myofilaments, we used a genetic approach and crossbred Tm54 mice with mice expressing slow skeletal troponin I (ssTnI) that sensitizes myofilaments to Ca2+. Four groups of mice were used: non-transgenic (NTG), Tm54, ssTnI and Tm54/ssTnI (DTG). Systolic function was significantly reduced in the Tm54 mice compared to NTG, but restored in DTG mice. Tm54 mice also showed increased diastolic LV dimensions and HW/BW ratios, when compared to NTG, which were improved in the DTG group. β-myosin heavy chain expression was increased in the Tm54 animals compared to NTG and was partially restored in DTG group. Analysis by 2D-DIGE indicated a significant decrease in two phosphorylated spots of cardiac troponin I (cTnI) in the DTG animals compared to NTG and Tm54. Analysis by 2D-DIGE also indicated no significant changes in troponin T, regulatory light chain, myosin binding protein C and tropomyosin phosphorylation. Our data indicate that decreased myofilament Ca2+ sensitivity is an essential element in the pathophysiology of thin filament linked DCM. Sensitization of myofilaments to Ca2+ in the early stage of DCM may be a useful therapeutic strategy in thin filament linked DCM.

Understanding the ECG. Part 10: Pacing, drugs and electrolytes

Over the past nine months, this series has examined the most important topics in ECG interpretation. These include cardiac anatomy and physiology, arrhythmias, heart blocks, preexcitation, the cardiac axis, chamber enlargement, and myocardial ischaemia (Garcia, 2015). We have also discussed many of the key principles of electrocardiography, and emphasised the need for a structured approach to ECG evaluation (Gregory, 2006). Inevitably in such a large subject, there are topics that we have not touched on. Some of these are less relevant to cardiac nurses, and some more so. In this last instalment of the series, we address three issues that have particular relevance to practitioners caring for cardiac patients. These are  The recognition of cardiac pacing and pacing problems  The ECG in the management of cardiovascular drugs  And the diagnosis of electrolyte disturbances. As with previous articles in the series, we will place the ECG in the context of clinical practice, and consider important aspects of patient management.

Assessment for Pulmonary Artery Hypertension Using Clinical and Echocardiographic Criteria in Patients With Systemic Sclerosis

BackgroundPrognosis of systemic sclerosis (SSc) is affected by pulmonary artery hypertension (PAH). MethodsAmong 202 patients (mean age: 46.1 ± 13.3 years; 177 women) with SSc, those with a tricuspid regurgitation (TR) jet maximal velocity at 2D-echocardiography (2DE) < 2.8m/second were not considered at high risk for PAH, whereas those with a TR velocity >3m/second or between 2.8 and 3m/second and associated with dyspnea were. ResultsAmong 22 patients at risk, 15 (mean age: 50.4 ± 14.3 years) had definite precapillary PAH on right heart catheterization (RHC). The delay period between recognitions of SSc and PAH was 12.9 ± 5.2 years. Dyspnea was present in all 15 patients, 11 (73.3%) being in the New York Heart Association class III or IV. The 2DE showed normal left ventricular geometrics and function (n = 15), enlargement of the right-sided cardiac chambers (n = 12), increased pulmonary arterial resistances with a TR velocity to pulmonary time-velocity integral ratio of > 0.2 (n = 15) and impaired right ventricle function (n = 15). RHC showed severe PAH in all 15 patients (mean pulmonary artery pressure: 48 ± 17mmHg and mean right atrial pressure: 11.8 ± 4.4mmHg) and a reduced cardiac index (2.2L/m²). There was no statistical difference between patients with and without PAH regarding age, sex ratio, duration from onset of disease, diffuse or cutaneous limited type of SSc, Rodnan severity score and presence of digital ulcerations or autoantibodies. Telangiectasia (P = 0.01) and New York Heart Association class III or IV heart failure (P = 0.001) were more frequent in patients with PAH. ConclusionA combined clinical and Doppler-coupled 2DE screening of PAH risk in patients with SSc is useful to select those who can undergo RHC.

Illustrated Imaging Essay on Congenital Heart Diseases: Multimodality Approach Part II: Acyanotic Congenital Heart Disease and Extracardiac Abnormalities

Acyanotic heart disease constitutes a significant majority of patient who may present with non-cardiac symptoms. Either they are detected incidentally or present with respiratory complaints. Equipped with knowledge of anatomy by echocardiography and radiographic methods described in previous part of this presentation, diagnosis may be confidently attempted. On plain radiography acyanotic congenital heart diseases have variable appearance depending upon severity of disease. Cardiac size, chamber enlargement and pulmonary vascular pattern are key elements. Typically left to right shunts with large volume flow are associated with pulmonary plethora. Plain radiography has an important role in detecting manifestation of pulmonary arterial hypertension. Severe stenosis of pulmonary valve is associated with pulmonary oligemia. Small intra-cardiac shunts and anomalies of coronary arteries generally present with normal cardiac size and pulmonary arterial pattern. Disease spectrum presented in this illustration demands thorough scrutiny of pulmonary, osseous and abdominal abnormalities. This section illustrates some commonly encountered spectrum of acyanotic cardiac disease.

Associations between 'valentine' heart shape, atrial enlargement and cardiomyopathy in cats.

'Valentine' heart shape is a common qualifier used in veterinary radiology to describe a cardiac silhouette with focal enlargement at the level of the base of the heart in feline patients. Anecdotally, this sign has been thought to be related to biatrial enlargement and also to hypertrophic cardiomyopathy (HCM). However, to our knowledge, there has been no study performed to assess the association between cardiac chamber enlargement and cardiac disease with the 'valentine'-shaped heart. The aim of this study was to verify the association between the 'valentine' heart shape observed in ventrodorsal thoracic radiographs and the presence of singular or combined cardiac chamber enlargement, and also the presence and type of cardiomyopathy (CM) in cats. A search of the database of the Small Animal Veterinary Hospital of the University of Florida for cats with a radiology report of thoracic radiographs that contained the words 'valentine' and 'biatrial', and echocardiography performed within 1 week, was undertaken; 41 cases met the inclusion criteria. Eighty-two percent of the cats of the study sample had some form of CM. The 'valentine' heart shape was associated with biatrial enlargement in 41% of the patients in our study sample that had some form of CM and just 8% of cases diagnosed with HCM, suggesting that the 'valentine' heart shape has a low association with HCM or biatrial enlargement; however, it should be considered a sign of feline CM.

Partial pericardial defect with left auricular herniation in a dog with syncope

Pericardial defects are rare in both people and dogs. They may be congenital or acquired in origin, and partial or total in extent. Commonly, pericardial defects are incidental findings at autopsy; however, diagnostic methods such as thoracic radiography and echocardiography can be useful in the ante mortem diagnosis of pericardial defects. This report describes the first case of a dog with syncope, supraventricular tachycardia, and a partial left pericardial defect with herniation of the left auricle for which extensive ante mortem diagnostic information was available. Partial absence of the pericardium should be considered in dogs with disproportionate enlargement of cardiac chambers for which other congenital and acquired heart diseases are ruled out.

Left Ventricular Restoration Devices

Left ventricular (LV) remodeling results in continuous cardiac chamber enlargement and contractile dysfunction, perpetuating the syndrome of heart failure. With current exhaustion of the neurohormonal medical paradigm, surgical and device-based therapies have been increasingly investigated as a way to restore LV chamber architecture and function. Left ventricular restoration has been attempted with surgical procedures, such as partial left ventriculectomy, surgical ventricular restoration with or without revascularization, and devices, such as the Acorn CorCap, the Paracor HeartNet, and the Myocor Myosplint. Whereas all these techniques require surgical access, with or without cardiopulmonary bypass, a newer ventricular partitioning device (VPD) called Parachute, can be delivered percutaneously through the aortic valve. Designed to achieve LV restoration from within the ventricle, this VPD partitions the LV by isolating aneurysmal from normal myocardium thereby diminishing the functioning cavity. This review aims to critically appraise the above methods, with particular attention to device-based therapies.

Cardiovascular manifestations of hepatitis C virus infection

Introduction: Hepatitis C virus infection is a major global health problem being the second most common chronic virus infection. It is associated with numerous extra hepatic manifestations of which cardiovascular diseases constitute an important but under diagnosed aspect of the infection. Aim: This study was carried out to evaluate the association between cardiovascular manifestation and HCV seropositivity patients attending Regional Institute of Medical Sciences (RIMS) in Imphal, Manipur. Materials and Methods: From august 2009 to july 2011, 50 HCV seropositive patients in the department of Medicine, Regional Institute of Medical Sciences, Imphal were evaluated. They were subjected to thorough physical examination and baseline laboratory investigations. Above that, echocardiogram was done for each patient. For statistical analysis of data, statistical package for the social sciences (SPSS16.0 version) and student's t-test was used. Results: In this study, the average age of patients was 44 years, ratio of males to females was 3.5: 1. HCV infection is more common in males who are in the sexually active and married age group 30 to 49 years. In the laboratory parameters high serum glutamic pyruvic transaminase (SGPT) and high erythrocyte sedimentation rate (ESR) were significant indicators of cardiac chamber (left atrial and left ventricular) enlargement and left ventricular diastolic dysfunction in HCV seropositive patients. Conclusion: The result corroborated favorably that the more progressed is the inflammation and liver dysfunction due to HCV infection, the more likely to have cardiovascular changes of cardiac chamber enlargement and left ventricular diastolic dysfunction.

The LMNA mutation p.Arg321Ter associated with dilated cardiomyopathy leads to reduced expression and a skewed ratio of lamin A and lamin C proteins

Dilated cardiomyopathy (DCM) is a disease of the heart muscle characterized by cardiac chamber enlargement and reduced systolic function of the left ventricle. Mutations in the LMNA gene represent the most frequent known genetic cause of DCM associated with disease of the conduction systems. The LMNA gene generates two major transcripts encoding the nuclear lamina major components lamin A and lamin C by alternative splicing. Both haploinsuffiency and dominant negative effects have been proposed as disease mechanism for premature termination codon (PTC) mutations in LMNA. These mechanisms however are still not clearly established. In this study, we used a representative LMNA nonsense mutation, p.Arg321Ter, to shed light on the molecular disease mechanisms. Cultured fibroblasts from three DCM patients carrying this mutation were analyzed. Quantitative reverse transcriptase PCR and sequencing of these PCR products indicated that transcripts from the mutant allele were degraded by the nonsense-mediated mRNA decay (NMD) mechanism. The fact that no truncated mutant protein was detectable in western blot (WB) analysis strengthens the notion that the mutant transcript is efficiently degraded. Furthermore, WB analysis showed that the expression of lamin C protein was reduced by the expected approximately 50%. Clearly decreased lamin A and lamin C levels were also observed by immunofluorescence microscopy analysis. However, results from both WB and nano-liquid chromatography/mass spectrometry demonstrated that the levels of lamin A protein were more reduced suggesting an effect on expression of lamin A from the wild type allele. PCR analysis of the ratio of lamin A to lamin C transcripts showed unchanged relative amounts of lamin A transcript suggesting that the effect on the wild type allele was operative at the protein level. Immunofluorescence microscopy analysis showed no abnormal nuclear morphology of patient fibroblast cells. Based on these data, we propose that heterozygosity for the nonsense mutation causes NMD degradation of the mutant transcripts blocking expression of the truncated mutant protein and an additional trans effect on lamin A protein levels expressed from the wild type allele. We discuss the possibility that skewing of the lamin A to lamin C ratio may contribute to ensuing processes that destabilize cardiomyocytes and trigger cardiomyopathy

Pertinent reportable incidental cardiac findings on chest CT without electrocardiography gating: review of 268 consecutive cases

Pertinent reportable cardiac findings on non-electrocardiography (ECG)-gated chest CT examinations have become easier to detect given recent advancements in multidetector CT technology. However, those findings are easily overlooked on routine chest CT without ECG gating given residual inherent cardiac motion artifact and non-cardiac indications. To describe and quantify the types of pertinent reportable cardiac findings that can be detected on chest CT examinations without ECG gating and evaluate how often they were reported. Two radiologists retrospectively reviewed (blinded to the original interpretation) 268 consecutive routine adult chest CT examinations without ECG gating for the presence of pertinent reportable cardiac findings. Retrospective interpretations were then compared with the original radiological reports. One hundred and sixty-three patients (61%) had pertinent reportable cardiac findings. The findings encountered included: coronary artery disease (n = 131; 80.0%), coronary artery bypass grafts (n = 10; 6.1%), left ventricular aneurysm (n = 1; 0.6%), valve calcification (n = 131; 80.0%), valve repair/replacement (n = 5; 3.1%), pericardial effusion (n = 33; 20.2%), left atrial appendage thrombus (n = 1; 0.6%), cardiac mass (n = 1; 0.6%), and cardiac chamber enlargement (n = 29; 17.8%). On the original radiological reports 22.3% of the pertinent reportable cardiac findings, detected by the two radiologists retrospectively, were not reported. Detection of pertinent reportable cardiac findings on routine chest CT examinations without ECG gating is possible. The high volume of chest CT examinations without ECG gating represents an opportunity for radiologists to comment on the presence or absence of cardiac disease which may influence future clinical decisions.

Accuracy of Non-ECG–gated Computed Tomography Angiography of the Chest in Assessment of Left-sided Cardiac Chamber Enlargement

To determine whether measurement of left ventricular (LV) and left atrial (LA) diameters on nongated computed tomography angiography (CTA) can detect left atrial and left ventricular enlargement (LAE and LVE) with high specificity. Ninety-nine patients who had undergone both nongated CTA of the chest and echocardiography within 1 week constituted the pilot group. On CTA, LA and LV diameters were measured in the axial plane and on a 3-chamber-view multiplanar reconstruction. These measurements were compared with echocardiography results. Receiver operating characteristic (ROC) curves were then generated to determine optimal cutoff values for diagnosis of LAE and LVE. These thresholds were applied to a validation group (n = 203), and sensitivities and specificities for cutoff values were determined. Simple κ-coefficients were calculated for interobserver agreement. In the pilot group, axial measurements of the LA and LV diameters were superior to multiplanar reconstruction measurements based on areas under the ROC (LV: 0.82 vs. 0.76, LA: 0.87 vs. 0.82). Using the ROC results, cutoff values of 5.5 and 4.5 cm were chosen for LVE and LAE, respectively. These thresholds were applied to the validation group, achieving an average sensitivity and specificity for LAE of 53% [confidence interval (CI): 37%-71% and 94% (89%-97%)], respectively. Average sensitivity and specificity for LVE were 41% (CI: 23%-59%) and 99% (CI: 96%-100%), respectively. Kappa coefficients for diagnosis of LAE and LVE were 0.70 and 0.81, respectively. Thresholds for LA and LV diameter on nongated CTA can be chosen to provide specific, but not sensitive, detection of LAE and LVE.

Cardiac Remodeling Induced by Smoking: Concepts, Relevance, and Potential Mechanisms

Cardiac or ventricular remodeling is characterized by molecular, cellular, and interstitial alterations that lead to changes in heart size, mass, geometry and function in response to a given insult. Currently, tobacco smoke exposure is recognized as one of these insults. Indeed, tobacco smoke exposure induces the enlargement of the left-sided cardiac chambers, myocardial hypertrophy, and ventricular dysfunction. Potential mechanisms for these alterations include hemodynamic and neurohormonal changes, oxidative stress, inflammation, nitric oxide bioavailability, matrix metalloproteinases and mitogen-activated protein kinase activation. This review will focus on the concepts, relevance, and potential mechanisms of cardiac remodeling induced by tobacco smoke.

Rescue of a Dilated Cardiomyopathy Mouse Model Caused by a Mutation in Tropomyosin (E54K) by Expression of Slow Skeletal Troponin I

Dilated cardiomoypathy (DCM) is a disease characterized by decreased contractility and enlargement of cardiac chambers. We have previously shown that E54K mutation in α-tropomyosin (TM54) reduces myofilament Ca+2 sensitivity and causes DCM. Thus, we hypothesized that sensitization of the myofilament to Ca+2 in early phase of DCM would rescue the phenotype of the disease. Four groups were generated: non-transgenic (NTG), TM54,slow skeletal troponin I (ssTnI) and TM54/ssTnI. To sensitize TM54 myofilament we crossbred TM54 mice with ssTnI expressing mice, which increased Ca+2 sensitivity based on force pCa measurements.

The role of obesity and sleep apnea in atrial fibrillation

To discuss the relationship between obesity and obstructive sleep apnea as they relate to the growing atrial fibrillation epidemic, and to discuss possible mechanistic links and implications for treatment of atrial fibrillation. Increasing BMI plays an important role in development of atrial fibrillation in both men and women. Sleep-disordered breathing contributes to cardiac chamber enlargement, which may be responsible for increasing atrial fibrillation in this population. Patients with obstructive sleep apnea and/or obesity have less freedom from atrial fibrillation recurrence after catheter ablation for atrial fibrillation. BMI is a strong predictor of future development of atrial fibrillation and should be considered as a risk factor for atrial fibrillation. Patients with obstructive sleep apnea and/or obesity have high atrial fibrillation recurrence rates following atrial fibrillation ablation.

Right Aortic Arch With Isolation of the Left Innominate Artery Arising From the Pulmonary Artery and Atrial Septal Defect

A 6-month-old child (weight, 6.250 kg) was referred for evaluation of a systolic murmur and congestive heart failure. Echocardiography revealed right-sided cardiac chamber enlargement and an atrial septal defect, with right aortic arch and no clear visualization of the left pulmonary artery take-off. Angiography confirmed the diagnosis of right aortic arch, with the right carotid artery being the first branch and perfusing through the vertebrobasilar circulation the left carotid and subclavian vessels in a retrograde fashion. The former emptied through a left innominate artery into the pulmonary vessels, displaying a left-to-right shunt. In addition, the left subclavian artery was fed from a plexus of collaterals coming from the upper intercostal branches (Fig 1; A = aorta; AA = ascending aorta; IA = innominate artery; LBP = left branch-pulmonary; LCC = left common carotid; LDA = left descending coronary aorta; LSC = left subclavian; P = pulmonary artery; RDA = right descending coronary aorta; RPB = right pulmonary branch; RSC = right subclavian). On cardiopulmonary bypass, the atrial septal defect was closed. Then the ductus was transected, the pulmonary stump was oversewn, and the free end was reimplanted end-to-side to the ascending aorta, thus creating a mirror-like arrangement of the branches (Fig 2; LCC = left common carotid; LPA = left pulmonary artery; LS = left subclavian; RCC = right common carotid; RS = right subclavian). Edwards proposed in 1948 that all abnormalities of the aortic arch could be explained by a model involving a double aortic arch with right and left ductus, followed by resorption and remodeling of particular segments. In the case of our patient, the regression of the portion proximal to the left common carotid (so-called D) and the segment distal to the left subclavian (so-called A), plus the patency of the left ductus, gave rise to the arrangement of an isolated left innominate artery in the setting of a right-sided aorta (Fig 1). Because our patient presented an atrial septal defect, surgery was scheduled through a mid-sternotomy and under extracorporeal circulation. On reimplanting the left innominate artery in the ascending aorta, a physiological setting was achieved (ie, a right aortic arch with mirror-image arrangement of the neck vessels, plus interruption of the left-to-right shunt).

A high-fat diet increases adiposity but maintains mitochondrial oxidative enzymes without affecting development of heart failure with pressure overload

A high-fat diet can increase adiposity, leptin secretion, and plasma fatty acid concentration. In hypertension, this scenario may accelerate cardiac hypertrophy and development of heart failure but could be protective by activating peroxisome proliferator-activated receptors and expression of mitochondrial oxidative enzymes. We assessed the effects of a high-fat diet on the development of left ventricular hypertrophy, remodeling, contractile dysfunction, and the activity of mitochondrial oxidative enzymes. Mice (n = 10-12/group) underwent transverse aortic constriction (TAC) or sham surgery and were fed either a low-fat diet (10% of energy intake as fat) or a high-fat diet (45% fat) for 6 wk. The high-fat diet increased adipose tissue mass and plasma leptin and insulin. Left ventricular mass and chamber size were unaffected by diet in sham animals. TAC increased left ventricular mass (approximately 70%) and end-systolic and end-diastolic areas (approximately 100% and approximately 45%, respectively) to the same extent in both dietary groups. The high-fat diet increased plasma free fatty acid concentration and prevented the decline in the activity of the mitochondrial enzymes medium chain acyl-coenzyme A dehydrogenase (MCAD) and citrate synthase that was observed with TAC animals on a low-fat diet. In conclusion, a high-fat diet did not worsen cardiac hypertrophy or left ventricular chamber enlargement despite increases in fat mass and insulin and leptin concentrations. Furthermore, a high-fat diet preserved MCAD and citrate synthase activities during pressure overload, suggesting that it may help maintain mitochondrial oxidative capacity in failing myocardium.

Electrocardiographic manifestation of digoxin toxicity in a Pomeranian dog

This case report describes several electrocardiographic findings in an 8-years old female Pomeranian dog that was referred with a history of digoxin overdose. Electrocardiographic abnormalities detected in this case could be classified as primary electrocardiographic disturbances, reflecting cardiac chamber enlargement and secondary ECG changes, attributed to digoxin toxicity. ECG manifestations of digoxin toxicity such as first and second degree AV blocks completely disappeared following digoxin withdrawal. Therefore, veterinarians should be aware of the possibility of digoxin toxicity due to its narrow therapeutic margins. The purpose of this report is to increase awareness of small animal practitioners about adverse cardiotoxic effects of cardiac glycosides. It also highlights the significance of electrocardiographic monitoring for diagnosis and management of digoxin induced cardiac arrhythmias and conduction disturbances in small animal patients

MR Angiography of Renal-Hepatic Arteriovenous Malformation

WEB This is a Web exclusive article. rteriovenous fistulas secondary to arteriovenous malformations, iatrogenic intervention, and blunt and penetrating trauma have been described as a cause of hyperkinetic heart failure [1]. Cardiac chamber enlargement, systolic–diastolic murmurs, and varicose veins may be the earliest findings. Late complications include thrombosis and pseudoaneurysm. We describe a rare and, to our knowledge, previously unreported arteriovenous malformation arising from the right renal artery, draining into the right hepatic vein, and causing right atrial enlargement.