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Aims Patients on chronic haemodialysis have a wide range of changes in cardiac function and structure, including left ventricular hypertrophy, dilation and diastolic dysfunction or pulmonary hypertension. All these changes were linked to increased mortality in previous studies. High-flow arteriovenous fistulas (AVF) are supposed to be a factor contributing to their development. This study investigated the early effect of surgical AVF blood flow (Qa) reduction on these changes in patients with or without heart failure changes. Methods and results Forty-two patients in chronic haemodialysis programme with high-flow AVF (Qa over 1500 mL/min), indicated for surgery for ≥1 of the following indications: 1.manifest heart failure; 2.hand ischemia; 3.advanced structural heart changes detected by echocardiography. The patients underwent echocardiography on selection visit, before blood flow reducing surgery and six weeks thereafter. The Qa reduction led to decrease of left ventricular mass (p = 0.02), end-diastolic volume (p = 0.008), end-diastolic diameter (p = 0.003) and left atrial volume (p = 0.0006). Diastolic function improved. Similarly, right ventricular diameter and right atrial volume decreased (p = 0.000001 and 0.00009, respectively) together with the decrease of estimated pulmonary artery systolic pressure. 81% of patients suffered from pulmonary hypertension prior to surgery, only 36% thereafter. Conclusion The surgical restriction of the hyperkinetic circulation leads to several improvements of heart structure and function, which was linked to higher mortality in other studies. The beneficial effect of Qa reduction is present even in patients without symptoms of heart failure. The contribution of AVF must be considered with structural or functional heart changes.

Iatrogenic complications may manifest in a variety of ways. We present the case of an 86-year-old woman who underwent a percutaneous coronary intervention with a drug-eluting stent for non–ST-segment elevation myocardial infarction followed by leadless pacemaker placement through a femoral approach. Her post-procedure course was complicated by new onset high-output heart failure secondary to iatrogenic arteriovenous fistula formation, requiring covered stent placement. (Level of Difficulty: Advanced.), Graphical abstract

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder characterized by the development of arteriovenous malformations. The arteriovenous shunts may result in high output heart failure, which predisposes to atrial dilatation and atrial fibrillation. Due to recurrent bleeding from epistaxis or the gastrointestinal tract, patients with HHT and atrial fibrillation are at high risk of bleeding if anticoagulated for stroke prevention. In this report, we present a case of a 74-year-old woman with a history of HHT and atrial fibrillation who developed a large left atrial thrombus that initially was thought to represent an atrial myxoma. The diagnosis was confirmed with cardiac magnetic resonance imaging, and the patient underwent surgical resection of the thrombus. This case demonstrates the role of different imaging modalities in the assessment of left atrial masses and presents an opportunity to review the data on safety of anticoagulation in patients with HHT.

Arteriovenous fistula is a rare complication of lumbar surgery that may cause high-output cardiac failure. We describe the case of a patient with treated lymphoma and recent spinal surgery who presented with heart failure. Logical deduction from clinical and imaging findings helped us arrive at this unusual diagnosis. (Level of Difficulty: Intermediate.), Central Illustration

Congenital renal arteriovenous fistula (rAVF) is a rare and often underdiagnosed clinical condition. Here, we present a case of a large congenital rAVF in an 81-year-old woman with a right flank bruit and high-output heart failure. The rAVF was successfully treated with percutaneous endovascular coil embolization. Complications included a small right renal hematoma, mild contrast-induced nephropathy, and small right renal infarct in the lower pole. Postoperatively, the patient had complete resolution of symptoms with salvage of the kidney. She has been observed annually for 5 years with computed tomography scan and ultrasound examination. Keywords: Congenital renal arteriovenous fistula, Coil embolization, High-output heart failure, Renal hematoma

Intra-cardiac shunt diseases may cause chronic ventricular volume overload, but extra-cardiac fistula could also cause high-output heart failure (HF). A patient presented with high-output HF and significant extra-cardiac shunt flow. Although the size and shape of the patient’s left ventricle suggested dilated cardiomyopathy, considerable origins were not identified except for a high-flow fistula between the right subclavian artery and right internal jugular vein. Right heart catheter examination revealed inappropriately high cardiac output. Left-to-right shunt ratio was calculated at 40.3% from an oximetry run, under the assumption that the left anonymous vein which was not contaminated with any shunt flow could be substituted for venous return from the upper body. We could determine the indication of fistula closure according to the estimated high left-to-right shunt ratio, reducing cardiac output by 42.7% which was similar to the pre-estimated left-to-right shunt ratio. Two months later, the patient’s serum B-type natriuretic peptide level and left ventricular end-diastolic and end-systolic diameters were decreased. The proposed method to estimate the left-to-right shunt ratio was useful in determining the indication for fistula closure in a patient with HF and a significant shunt fistula. Learning objective: A significant extracardiac left-to-right shunt more than 30–35% could cause heart failure with left ventricular dilatation similar to dilated cardiomyopathy. One can decide fistula closure with the finding of left-to-right shunt ratio calculated using a transcatheter oximetry run. It is mandatory that the venous oxygen saturation at the upper stream of fistula is determined precisely without the contamination of arterial blood. In this case, the oxygen saturation at the left anonymous vein substituted for it.>

Background Sudden Infant Death Syndrome (SIDS) mechanisms of death remains obscured. SIDS' Triple Risk Model assumed coexistence of individual subtle vulnerability, critical developmental period and stressors. Prone sleeping is a major risk factor but provide no clues regarding the mechanism of death. The leading assumed mechanisms of death are either an acute respiratory crisis or arrhythmias but neither one is supported with evidence, hence both are eventually speculations. Postmortem findings do exist but are inconclusive to identify the mechanism of death. What does the proposed hypothesis based on? 1. The stressors (suggested by the triple risk model) share a unified compensatory physiological response of decrease in systemic vascular resistant (SVR) to facilitate a compensatory increase in cardiac output (CO). 2. The cardiovascular/cardiorespiratory control of the vulnerable infant during a critical developmental period may be impaired. 3. A severe decrease in SVR is associated with hyper-dynamic state, high output failure and distributive shock. The hypothesis Infant who is exposed to one or more stressors responds normally by decrease in SVR which increases CO. In normal circumstances once the needs are met both SVR and CO are stabilized on a new steady state. The incompetent cardiovascular control of the vulnerable infant fails to stabilize SVR which decreases in an uncontrolled manner. Accordingly CO increases above the needs to hyper-dynamic state, high output heart failure and hyper-dynamic shock. Conclusions The proposed hypothesis provides an appropriate alternative to either respiratory crises or arrhythmia though both speculations cannot be entirely excluded.

Graphical abstract, Highlights • Arteriovenous fistula for hemodialysis occasionally causes heart failure. • Noninvasive assessment of arteriovenous fistula hemodynamics is not established. • Refractory heart failure developed in a patient with an arteriovenous fistula. • Echocardiography can monitor hemodynamics, directing arteriovenous fistula occlusion.

Introduction The differential for cardiomyopathy in a young patient is challenging. While there has been published research into genetic cardiomyopathy and lymphocytic myocarditis, there is still much to be studied. Case Report A 27 year old male with significant family history of heart disease and no drug/steroid use, initially presented following cardiac arrest while exercising. Patient was found to be apneic and pulseless upon arrival of EMS. ACLS was performed. In the ED, he was found to have an EF of 10% and global hypokinesis. Lab work showed an elevated troponin which peaked at 20. Angiogram showed no significant obstructions. Patient developed evidence of cardiogenic shock, ultimately requiring pressors, IABP, and VA ECMO. Genetic testing was obtained which showed variance in FLNC and RBM40. Cardiac MRI demonstrated no late gadolinium enhancement. Right heart catherization and myocardial biopsy demonstrated evidence of high output heart failure and borderline lymphocytic myocarditis. Repeat ECHO demonstrated an improved ejection fraction of 43%. Patient was later decannulated and IABP was removed. Patient ultimately underwent AICD placement, and later interrogation noted episodes of VTach of unclear etiology. Patient was optimized on beta blockers, ARNI, and antiarrhythmics. Ejection fraction one year after admission remained 43%. Summary This case highlights the differential for cardiomyopathy in a 27 year old. While the diagnosis at this time is unclear, two main diagnoses become prominent: lymphocytic myocarditis versus underlying genetic disorder. Lymphocytic myocarditis accounts for 54% of all myocarditis, with viral illness the most common identified cause. Workup includes exclusion of other etiologies, as well as endomyocardial biopsy. While the role of medical therapy, such as immunosuppression or antivirals is unclear, the most effective treatment is supportive care. Genetic cardiomyopathies, however are more insidious. While there is still much to know about genetic cardiomyopathies, there have been advances in the recognition of genetic mutations that lead to earlier recognition and treatment. Also, patients with underlying genetic cardiomyopathies can be predisposed to lymphocytic myocarditis. This case is interesting in that it allows us to explore the differential for cardiomyopathy in a young healthy patient, and how the field of cardiomyopathy is evolving.

Background High-output heart failure (HF) is an unusual cause of cardiac failure that has not been well-characterized. Objectives This study sought to characterize the etiologies, pathophysiology, clinical and hemodynamic characteristics, and outcomes of high-output HF in the modern era. Methods We performed a retrospective analysis of all consecutive patients referred to the Mayo Clinic catheterization laboratory for hemodynamic assessment between 2000 and 2014. Subjects with definite HF, as defined by the Framingham criteria, were compared to controls of similar age and sex. Results The most common etiologies of high-output HF (n = 120) were obesity (31%), liver disease (23%), arteriovenous shunts (23%), lung disease (16%), and myeloproliferative disorders (8%). Compared with controls (n = 24), subjects with high-output HF displayed eccentric left ventricular remodeling, greater natriuretic peptide activation, higher filling pressures, pulmonary hypertension, and increased cardiac output, despite similar ejection fraction. Elevated cardiac output in high-output HF patients was related to both lower arterial afterload (decreased systemic vascular resistance) and higher metabolic rate. Mortality was increased in high-output HF as compared with controls (hazard ratio: 3.4; 95% confidence interval: 1.6 to 7.6). Hemodynamics and outcomes were poorest amongst patients with the lowest systemic vascular resistance. Conclusions High-output HF is an important cause of clinical HF in the modern era that is related to excessive vasodilation, and most frequently caused by obesity, arteriovenous shunts, and liver disease. Given the high mortality and increasing prevalence of these comorbidities in Western countries, high-output HF must be considered in the differential diagnosis of patients presenting with dyspnea, congestion, and a normal ejection fraction.

Introduction Acute injury to the large vessels is the most feared of diagnoses for a spinal surgeon, but far more common is the delayed presentation of arteriovenous fistula (AVF) formation. The mean time to diagnosis of an AV fistula in this scenario is just over 1 month. Treatment can include both open and endovascular repair. Report This study presents a case of an otherwise healthy 39-year-old woman who initially presented with orthopnea, leg edema, and a presumptive diagnosis of post-partum cardiomyopathy. Cardiac investigations revealed high output cardiac failure and an abdominal CT scan confirmed an arterial venous fistula from the left common iliac artery to left common iliac vein. The patient maintained a cardiac output three times normal prior to her definitive treatment. This high flow physiology caused unique challenges for the endovascular procedure as the stent graft collapsed and distorted toward the iliac side wall. The AV fistula was eventually covered successfully and post-operative studies show no further fistula and normal cardiac function. This case demonstrates an unanticipated effect of very high flows of stent graft deployment. Discussion Extreme high flow AV fistulas can present as unexpected challenges to endovascular repair. These issues may be ameliorated by techniques such as controlled hypotension, adenosine, ventricular pacing, or proximal balloon occlusion., Highlights • This chronic AV fistula was diagnosed 12 years after lumbar discectomy. • Only after the normal physiological state of pregnancy, and its elevated high cardiac output requirements did the patient decompensate with orthopnea and edema. • This otherwise healthy 39-year-old woman had three times the cardiac output expected which was caused by her iliac artery to iliac vein fistula. • Endovascular treatment is a viable option to cover the fistula, but the high flows can collapse and distort the stent graft during deployment. • Controlled hypotension, adenosine, ventricular pacing or proximal balloon occlusion may be appropriate if extreme flows are anticipated.

Recently, the zebrafish has gained attention as an innovative experimental model to decipher molecular and cellular mechanisms involved in cardiovascular development and diseases. Nevertheless, the use of zebrafish models has been challenged because the transparency of these fish, which allows for accurate cardiac evaluation, disappears in adulthood. In this study, the epicardial outline method was performed to investigate the feasibility of echocardiography in assessing cardiac function in pathological adult zebrafish.We attempted to estimate heart failure in adult zebrafish treated with three distinct regulators of cardiac function: phenylhydrazine hydrochloride (PHZ), doxorubicin (DOX), and ethanol. B-mode and Doppler images were evaluated at frequencies of up to 50 MHz and 40 MHz, respectively. The correlation between alterations in cardiac function, haemoglobin concentration, and myocardial histopathology were assessed.Cardiac output (CO) in PHZ-treated zebrafish was significantly higher than that in control zebrafish (151 ± 67 vs. 84 ± 37 μl/min, P = 0.004), whereas ejection fraction (EF) was lower (36.3 ± 10.9 vs. 50.9 ± 8.7%, P 0.001), indicating typical high output heart failure derived from anaemia. Additionally, ventricular dysfunction in DOX-treated zebrafish was characterised by low CO (57 ± 38 μl/min) and EF (28.8 ± 10.4%), accompanied by an enlarged ventricle in diastole and systole, representing low output heart failure. For ethanol-treated zebrafish, EF was markedly reduced (39.6 ± 7.2%) indicating a dilated heart, while CO remained unchanged (90 ± 40 μl/min).The epicardial outline method is an effective way of using echocardiography to assess cardiac dysfunction in pathological adult zebrafish, unlocking a major bottleneck in this research field with limited cardiac functional assays.

Patients with severe thiamine deficiency leading to wet beriberi typically present with high output heart failure and predominately right sided symptoms, but a rare and acute form of beriberi known as Shoshin Beriberi can lead to acute cardiovascular collapse. A 52-year-old woman with a history of

High output heart failure is a less frequent cause of heart failure and numerous etiologies should be considered in order to evaluate and treat these patients. A 32-year-old female presented with dyspnea for 1 week. Physical exam revealed bilateral lung crackles, normal S1, S2, and a faint S3, and

Congestive heart failure (CHF) with high cardiac output is an uncommon, yet potentially hemodynamically significant result of arteriovenous malformations. 64-year-old male presented in acute renal and liver failure, with suspected cardiogenic shock. Cardiac catheterization identified an elevated

High output heart failure is an infrequently encountered entity characterized by normal cardiac function with low systemic vascular resistance. It's defined as cardiac output more that 8L/min of cardiac index more than 4.0/min/m2. It is due to an underlying disease process leading to increased

High-output heart failure is not seen as commonly as low-output heart failure and some of the typical guideline recommendations may not benefit patients with high-output failure. High-output failure is caused by several diseases, including thyrotoxicosis and beriberi, highlighted in this article. Thyrotoxicosis, caused by excessive thyroid hormone production, has profound hemodynamic effects. Wet beriberi, affecting predominately the cardiovascular system, is caused by severe thiamine deficiency, most commonly seen in patients with chronic alcoholism or poor nutrition from other causes. Prompt recognition of these infrequently seen syndromes is essential. This article outlines the medical treatment and nursing care needed to return these patients to a normal state.

We present the case of a 63-year-old woman presenting with a huge pelvic and retroperitoneal high flow arteriovenous malformation (AVM) causing high-output heart failure, who was treated with combined therapies, including transarterial embolization with n-butyl cyanoacrylate–iodized oil mixture (NBCA–lip) and coils for the right ovarian, both internal iliac, 3rd and 4th lumber arteries, venous sclerotherapy using coils and ethanolamine oleate (EO) for the right ovarian and both internal iliac veins with balloon-occluded retrograde transvenous obliteration technique, and direct percutaneous sclerotherapy using the NBCA–lip and EO for the large nidus of AVM under outflow control using occlusion balloon catheters.

La Presse Medicale - In Press.Proof corrected by the author Available online since samedi 20 decembre 2014

Background & Aims Though hepatic involvement is common in patients with hereditary haemorrhagic telangiectasia (HHT), symptomatic liver disease is rare but potentially fatal without liver transplantation. Factors associated with clinically significant liver disease in patients with HHT are unknown. Methods In this prospective cohort study, we included consecutive patients from 2001 to 2011 with definite HHT, who underwent systematic protocol screening including contrast-enhanced hepatic CT and/or abdominal ultrasound. Using a multivariable logistic regression model, we developed a simple clinical scoring index to identify the presence of symptomatic liver disease (cardiac failure, portal hypertension, or biliary disease) or ‘at-risk' liver disease (asymptomatic patients, with hepatic bruit, abnormal liver biochemistry, or elevated cardiac index). Results Of 316 patients with definite HHT, 171 patients (54.1%; age 53.4±15.2y, 101 females) had hepatic involvement on imaging. Twenty-nine patients had symptomatic liver disease (22 patients with high-output heart failure); 45 patients were ‘at-risk' for liver disease. Using multivariable logistic regression analysis, we derived a score using age, gender, hemoglobin and alkaline phosphatase at presentation which could accurately distinguish patients with clinically significant liver involvement from patients with no or incidental liver lesions (c-statistic=0.80). A score 6 indicated high risk (>80%) of harboring clinically significant liver disease in HHT. Conclusions A simple scoring system can distinguish patients at low, moderate, and high risk of harboring clinically significant liver disease. With validation, this score may be used to identify patients for individualized screening and enrollment in clinical trials.

High-output heart failure from arteriovenous fistula (AVF) is an often overlooked cause of pulmonary hypertension. A 63 year-old male with hepatitis C, cirrhosis, and chronic atrial fibrillation presents with worsening exertional dyspnea since a nail gun injury 7 years ago. Vitals are normal. He

High output heart failure is characterized by elevated cardiac index (CI) and decreased systemic vascular resistance (SVR). Obesity, liver disease and arteriovenous (AV) shunting are common etiologies. A 58-year-old male with history of end-stage renal disease on dialysis, alcoholic cirrhosis

Although hemodialysis patients who initiate and maintain a permanent form of dialysis vascular access have improved all-cause and cardiovascular survival compared with those who use catheters, the presence of an arteriovenous fistula has been shown to have a short-term, adverse effect on cardiac function. Through its effect as a left-to-right extracardiac shunt, the arteriovenous fistula can increase cardiac workload substantially, and, in certain patients, result in a high-output state and resultant heart failure over time. Here we review the mechanisms by which dialysis arteriovenous access may promote the development of high-output cardiac failure in end-stage renal disease patients, describe risk factors for and the diagnosis of high-output heart failure, and suggest management strategies for patients who develop high-output heart failure.

We thank Dr. Cerit and colleagues for their interest in our paper describing the pathophysiology and outcomes of high-output heart failure (HF) [(1)][1]. We demonstrated that obesity-related high-output HF, the most common etiology, is caused by excessive vasodilation, plasma volume expansion

We have read the paper by Martin-Perez et al. [(1)][1] with great interest. The investigators reported that high-output heart failure (HF) is an important cause of cardiac failure that is associated with increased mortality. Despite the wide variety of underlying etiologies, the causes share a

SummaryA 68-year-old woman was admitted with dyspnea. The patient had been treated with hemodialysis for renal failure for 11 years. On admission, chest X-ray showed pulmonary edema. Right-heart catheterization revealed high cardiac output (11.8l/min) and elevated pulmonary capillary wedge pressure (PCWP). Doppler ultrasonography showed high-flow of an arteriovenous fistula (AVF) for hemodialysis. The patient was diagnosed as having high-output heart failure due to a high-flow AVF. Inflow reduction of the AVF was performed by proximal radial artery ligation. Right-heart catheterization performed 2 weeks after the operation revealed that cardiac output had decreased from 11.8 to 9.5l/min and PCWP was also reduced from 21 to 9mmHg. Furthermore, flow of the AVF measured by Doppler ultrasonography was also decreased. To our knowledge, this is the first report that assessed hemodynamics of high-output heart failure before and after inflow reduction of the AVF by repeated right-heart catheterization.

Anomalous coronary arteriovenous fistulas (CAVF) are rare and usually do not require intervention. A 75 year old female with hypertension, type 2 diabetes, chronic kidney disease, atrial fibrillation, and heart failure with preserved ejection fraction presents with three months of progressive

A 57 year-old male with Klippel-Trenaunay Syndrome (KTS) presented with four weeks of dyspnea on exertion with unilateral right lower extremity swelling and pain. Vital signs were unremarkable though exam demonstrated elevated jugular venous distension and unilateral pitting edema in the right

Hereditary hemorrhagic telangiectasia (HHT) is characterized by mucocutaneous telangiectasias and arteriovenous malformations (AVMs) leading to pulmonary and liver shunting. Liver shunts from the hepatic artery (HA) to hepatic vein (HV) cause high output heart failure, from portal vein (PV) to HV

A 26-year-old man presented with high output heart failure and severe systolic left ventricular dysfunction. The underlying cause was determined to be thyrotoxicosis. With aggressive treatment of the hyperthyroid state, near-normalization of the patient's left ventricular systolic function was achieved. Unfortunately, he succumbed to pancreatitis, followed by multiple ICU complications. A brief review of the literature is provided.

Patients with hepatic hemangiomas have been known to have high-output heart failure as a result of left-to-right arteriovenous shunting. We report a patient with a hepatic hemangioma that presented with high-output heart failure with hypoxia on exertion. After embolization of the hemangioma, the patient's hypoxia resolved and ejection fraction improved. In the absence of cardiopulmonary pathophysiology, we presume that our patient's hemangioma was causing a right-to-left shunt as opposed to an expected left-to-right shunt.

After more than two decades of experimental and clinical work, fetal surgery has become an accepted treatment modality for selected fetuses with life-threatening anomalies. Color Doppler ultrasound and ultrafast fetal magnetic resonance imaging have enhanced the accuracy of prenatal evaluation traditionally made by ultrasound alone. Fetal lung masses associated with hydrops are nearly 100% fatal. These lesions can be resected in utero if they are predominantly solid or multicystic. Thoracoamniotic shunting may be effective in the setting of a single large predominant cyst. Fetuses diagnosed with left congenital diaphragmatic hernia before 26 weeks' gestation with liver herniation and a sonographic right lung to head circumference ratio (LHR) of less than one may benefit from fetal tracheal occlusion. Fetal sacrococcygeal teratoma complicated with placentomegaly, hydrops, or progressive high output heart failure may benefit from in utero resection of the tumor. Although preterm labor still remains the Achilles heel of open fetal surgery, effective tocolysis may, in the future, expand the scope of fetal surgery.

Traumatic arteriovenous fistula (AVF) is not an uncommon disorder, but late discovery and the presentation of high-output heart failure is very rare. This patient did not know that he had traumatic AVF after a gunshot injury in the left thigh 14 years ago. The major presentation of the AVF was signs of heart failure. We performed surgical repair after making the diagnosis. The patient recovered with an uneventful course. This report stresses the importance of history-taking and physical examination in making the diagnosis of traumatic AVF.

Renal arteriovenous fistula is a rare condition. The clinical presentations include gross hematuria, hypertension, high output heart failure and flank bruit. Interventional therapy includes observational treatment, partial or total nephrectomy, endovascular embolization and insertion of a covered stent. We present the case of a 70-year-old woman who presented with heart failure symptoms of 2 years' duration prior to admission. On presentation, she had evidence of congestive heart failure, pulmonary hypertension and increased cardiac output. Subsequent investigations led to the diagnosis of left renal arteriovenous fistula. While she opted for conservative treatment, the various therapeutic options of this uncommon condition are addressed.

Background : Hepatic involvement in hereditary hemorrhagic telangiectasia (HHT) is infrequent and poorly studied. The aim of this study was to describe the clinical, radiological, and hemodynamic patterns of this involvement. Methods : Eleven consecutive patients with HHT and hepatic involvement observed within 12 years were retrospectively studied. They were 8 females and 3 males, mean age, 47. Results : The patients presented with heart failure (4 cases), hepatomegaly and murmur of the right hypochondrium (7 cases), and digestive hemorrhage (6 cases). Eight patients had anicteric cholestasis. Celiac angiography showed a dilated hepatic artery in 8 cases, disseminated intrahepatic telangiectasias in 10, and early opacification of the hepatic veins in 7. Liver dynamic computed tomography (CT) scan performed in 7 patients allowed the diagnosis of liver involvement in each case. Hemodynamic studies were performed in 5 patients. A lef-tto-right intrahepatic shunt was proven in the 5 patients. Shunt output was estimated between 25% and 58% of cardiac output. Mild pulmonary hypertension was observed in the 5 cases. Conclusions : Diagnosis of liver involvement in HHT can be made by dynamic CT scan or celiac angiography. The main feature of this involvement is high output heart failure due to left-to-right intrahepatic shunt. Thus, right-heart catheterization is necessary in these patients to confirm and evaluate the shunt.

Plasma immunoreactive endothelin (irET) concentration and renal glomerular ET receptors were investigated in rats with chronic high-output heart failure. Plasma irET was higher ( 0.67 ± 0.03 fmol/ml vs. 0.52 ± 0.04 fmol/ml ) and the density of glomerular ET receptors lower ( B max : 420 ± 20 fmol/mg protein vs. 510 ± 12 fmol/mg protein ) in rats with heart failure than in controls. Our results indicate that circulating ET levels are responsive to changes in cardiovascular hemodynamics and suggest a potential role for ET as a vasoactive regulatory peptide during heart failure.

During a period of 13 years 11 patients were operated on because of a spontaneous aortocaval fistula caused by a ruptured abdominal aortic aneurysm. The classic diagnostic signs of an aortocaval fistula (pulsatile abdominal mass with bruit and high output heart failure) were present in approximately half of the patients, whereas hematuria was a constant finding in all patients. Six patients had macrohematuria, and five had microhematuria. Seven patients (64% survived, and four had postoperative complications: 1 ileus, 2 postoperative pneumonias, 2 deep venous thrombosis, 1 postoperative hemorrhage. The mean operative blood loss was 7 L. After operation the average follow-up time was 4 years. In four patients who died the perioperative (within 30 days) causes of death were renal failure, a bleeding duodenal carcinoma, myocardial infarction, and operative bleeding. It is concluded that hematuria is a more frequent finding than earlier assumed among patients whose abdominal aortic aneurysm has ruptured into the vena cava. The presence of hematuria in a patient suffering from an abdominal aortic aneurysm is an indication for aortography to rule out an aortocaval fistula.

A 58-year-old man who received a gunshot wound to the left thigh 40 years previously was admitted to the hospital for investigation of heart failure. At the time of the accident, he had received conservative treatment.Onphysical examination, the patient had fremitus in the left popliteal fossa. Computed tomography showed a significant increase in tortuosity and diameter of the left iliac, femoral, and popliteal arteries due to a large arteriovenous fistula (AVF) located in the popliteal fossa,which also caused increased diameters of the left iliac and femoral veins (A) and an aneurysm of the iliac vein (B; Cover). Through an S-shaped incision in the popliteal fossa, the artery and vein were exposed, separated, and the fistula was closed with 5-0 Prolene sutures. Oral anticoagulationwasmaintained after surgery, and the patient was discharged on the fourth postoperative day in good clinical condition.

A 55-year-old man who received a gunshot wound to the right buttock 30 years previously was admitted to the hospital with complaints of progressive exertional dyspnea, nausea, vomiting and right flank pain. On admission, his physical examination demonstrated a blood pressure of 106/73 mmHg, an irregular heart rate of 170 beats/min and an oxygen saturation of 99% on room air. Auscultation revealed bibasilar pulmonary rales and a bruit in the right lower quadrant of the abdomen where palpation demonstrated a tender, pulsatile abdominal mass. Atrial fibrillation with a rapid ventricular response was evident on an electrocardiogram, and an echocardiogram demonstrated new marked biventricular dilation with signs of right ventricular volume overload and a left ventricular ejection fraction of 50%. Subsequent contrast-enhanced computed tomography (CT) scanning revealed cardiomegaly, bilateral pleural effusions, a dilated inferior vena cava and hepatic veins as well as an arteriovenous fistula arising from the right internal iliac artery (RIIA) and communicating with the right common iliac vein (RCIV). There was also evidence of a 12.4 cm × 10.1 cm × 12.3 cm aneurysmal dilation of the RCIV (Figures 1 and ​and2).2). Numerous gunshot pellets were noted throughout the abdomen. Figure 1) Abdominopelvic computed tomography scan demonstrating a 12.4 cm × 10.1 cm × 12.3 cm aneurysmal dilation of the right common iliac vein (RCIV). IVC Inferior vena cava; LCIV Left common iliac vein Figure 2) Abdominopelvic computed tomography scan with three-dimensional reconstruction. IVC Inferior vena cava; RIIA Right internal iliac artery The patient underwent catheterization, at which point, his cardiac output was measured, by the thermodilution method, to be 13.3 L/min. Several percutaneous attempts at exclusion of the RIIA using an Amplatzer vascular plug device (AGA Medical Corporation, USA) as well as several Nester coils (Cook Medical Inc, USA) were unsuccessful. Eventually, the fistula was occluded using a 16 mm Amplatzer atrial septal defect occluder (AGA Medical, USA). Nevertheless, persistent flow from the RIIA into the right internal iliac vein was demonstrated; however, this was expected to diminish as anticoagulation was withdrawn. The patient’s hospital course was further complicated by thrombosis of the venous aneurysm with resultant thrombocytopenia, hematuria and obstructive jaundice. A follow-up angiogram revealed persistent opacification of the fistula from the RIIA. Together with a vascular surgical team, the patient subsequently underwent placement of an endovascular graft converter (Zenith Flex, Cook Medical Inc) in the RIIA (Figure 3) and a permanent inferior vena cava filter (Trapease; Johnson & Johnson, USA) in the RCIV (Figure 4). Although minimal residual flow into the RCIV remained postintervention, it had been reduced significantly by the described interventions. Figure 3) Abdominopelvic computed tomography scan with three-dimensional reconstruction postendovascular graft implantation in the right internal iliac artery Figure 4) Sagittal cut of an abdominopelvic computed tomography scan demonstrating a Trapease filter (Johnson & Johnson, USA) in the inferior vena cava (IVC), the endovascular graft in cross-section and an Amplatzer closure device (AGA Medical Corporation, ... Three weeks after endovascular graft placement, collateral flow from the right L4 lumbar artery into the RIIA was demonstrated by CT angiography with continued opacification of the RCIV from the RIIA. Percutaneous coiling (Diamond Vortex coils; Boston Scientific, USA) of the L4 lumbar artery was then attempted, which resulted in successful exclusion of the RIIA. No further flow into the RIIA could be demonstrated on fluoroscopy. Two weeks later, the patient was pain free and ambulating without complaints of dyspnea. At that time, an echocardiogram demonstrated reduced left and right ventricular dimensions as well as normal biventricular systolic function. A follow-up CT of the patient’s abdomen and pelvis showed a reduction in the size of the aneurysm (9.3 cm × 9.0 cm) as well as absent flow within the fistula and into the RIIA from the L4 lumbar artery. The present case highlights two important points. Previously healthy, young men presenting with high-output congestive heart failure and a history of penetrating injuries to the abdomen and/or pelvis should undergo thorough testing for arteriovenous fistulas. In addition, chronic arteriovenous fistulas often involve complex arteriovenous anatomy, as did our patient, often complicating percutaneous closure. For this reason, meticulous preprocedural evaluation is of the utmost importance. As well, close collaboration between vascular surgery and interventional cardiology/radiology is necessary to facilitate the selection of the most appropriate intervention on a case-by-case basis.