Arteriovenous fistula presented with right ventricular failure, Farveh Vakilan, Fereshte Ghaderi, Hoorak Poorzand, Mahmood Mohammadzadeh Shabestari, Arash Gholobi Archives of Cardiovascular Imaging 2017 5(2):37-40 Arteriovenous fistula could be traumatic with one manifestation as high-output heart failure. We present a 29-year-old male, referred for unexplained right-sided enlargement and the symptoms of right ventricular failure for 8 months ago. Considering right-sided dilatation, marked inferior vena cava plethora, and increased pulmonary passage of flow in the absence of intracardiac shunts, arteriovenous shunt was suspected. He had a history of penetrating abdominal trauma which raised the suspicion for further evaluation. Abdominal sonography and contrast-enhanced computed tomography revealed a large arteriovenous fistula between the left common iliac artery and vein. The patient underwent successful percutaneous repair with a stent graft and dramatic improvement in symptoms and resolution of flushing and edema.

Introduction

High-output heart failure (HF) is an important and unusual cause of clinical HF that has not been well characterized. It is related to excessive vasodilation and most frequently caused by morbid obesity (31%), arteriovenous shunts (23%), liver disease (23%), lung disease (16%), and myeloproliferative disorders (8%).^[1] Traumatic arteriovenous fistula (AVF) could result in HF, in which high cardiac output, low-normal systemic vascular resistance, and pulmonary hypertension with normal pulmonary vascular resistance are the characteristic findings.^[2]

We report the case of an AVF with a history of penetrating abdominal trauma who was referred due to intractable symptoms of right-sided failure and unexplained RV enlargement in echocardiographic study with no previous cardiac disease.

Case Report

A 29-year-old male referred to the HF clinic with exertional dyspnea, facial and leg edema, and ascites (4 months ago) and also unexplained right ventricular (RV) failure, detected in echocardiography. He had orthopnea, but denied chest pain or any other cardiovascular complaints or any known heart, lung, or other systemic disorders. A 4 cm scar was noted in his left upper quadrant due to a penetrating (knife) abdominal trauma and was repaired surgically, and he had no symptoms or further evaluation in the past year. His blood pressure was 120/65 mmHg (pulse pressure: 55) and heart rate 85/min with normal respiratory rate. There was no gallop, cardiac murmur, or precordial heave. The lung sound was clear. Increased liver span and ascites were detected. Electrocardiogram showed sinus tachycardia with small R wave in V1. Transthoracic echocardiography (TTE) revealed RV enlargement (mid daimeter 51 mm) with mild systolic dysfunction and right atrial enlargement with bulging of interatrial septum toward the left atrium [Video 1]. Diastolic d-shaped configuration of the left ventricle (LV) was seen, assumed to be due to RV volume overload [Video 2]. There was tricuspid annulus dilation with severe functional tricuspid regurgitation with 25 mmHg gradient [Video 3]. Inferior vena cava (IVC) was markedly dilated (diameter in TTE 35 mm) and had reduced collapsibility [Video 4]. Mild circumferential pericardial and left-sided pleural effusions were also seen. Intracardiac shunts were not found in TTE (including contrast study) [Figure 1]. As we did not find any reasonable structural abnormality for right heart enlargement and failure, high output state and extracardiac shunt was proposed. Abdominal sonography was done which implied severe dilatation of IVC and hepatic vein, ascites, normal diameter of the aorta, and suspicious abdominal aortocaval fistula. Multidetector three-dimensional thoracic and abdominal CT angiography was recommended, which revealed a markedly dilated IVC (diameters: 4.6 cm × 4.2 cm) with large (12 mm) fistulous arterio venous, high flow connection between left iliac artery and vein at 23 mm distance from the aortic bifurcation [Figure 2]. There was simultaneous opacification of both arterial and venous circulation at this region which was compatible with the presence of this fistula.

Figure 1: Transthoracic echocardiography showed (a) right heart dilation, tricuspid annulus dilation with shifting of the septum toward the left ventricle in the diastolic phase with marked dilation of inferior vena cava (b) Click here to view

Figure 2: Computed tomography showed (a) marked dilation of the right ventricle and atrium; interatrial septum seems to be intact. In (b and c), arrow denotes the fistulous connection between the left common iliac artery and the dilated vein. In (d), reconstructed computed tomography image denoting the arteriovenous connection and severe dilation of the left common iliac vein and inferior vena cava Click here to view

The patient was scheduled for corrective interventional repair of the fistula. After bilateral femoral access and performing adequate angiographic views [Figure 3], we implanted a 12 × 61 mm Advanta V12 covered stent (Atrium Medical Corporation) at the left common iliac artery. However, there was a significant residual leakage which was sealed off by postdilating the stent using a 16 × 40 mm Zelos balloon (Optimed) several times.

Figure 3: Abdominal aortography revealed simultaneous visualization of abdominal aorta and inferior vena cava denoting a large arteriovenous fistulae; inferior vena cava was apparently dilated. (a) Abdominal aortography showed exact location of the exit point of arteriovenous fistula from the left common iliac artery. (b) Stenting and postdilation of the left common iliac artery using a covered stent. (c) Abdominal aortography after right iliac artery stenting revealed complete sealing of the arteriovenous fistula Click here to view

The patient was discharged after uneventful inhospital course and was completely asymptomatic 6 months later; repeated TTE showed normalization in the size and function of RV and IVC diameter [Figure 4].

Figure 4: (a and b) Transthoracic images denoting to the restoration of inferior vena cava and right ventricle/atrial size Click here to view

Discussion

High-output HF is known to occur in a number of systemic illnesses such as severe anemia, chronic renal disease, and arteriovenous fistulas (AVFs). It must be considered in the differential diagnosis of patients presenting with dyspnea, congestion, and a normal ejection fraction.

Standard therapies for HF, such as vasodilators and inotropes, are potentially detrimental in high-output HF, and there is no proven treatment. It seems diuretic could be the cornerstone of medical treatment.^[1] The incidence of aortocaval fistula has been described from 0.22% to 10% of all atherosclerotic aortic aneurysm (AAA). The etiology would be the spontaneous rupture of an atherosclerotic plaque in an existing AAA with trauma or iatrogenic after lumbar disc surgery or after penetrating abdominal trauma.^[3] In another study, trauma is the cause in approximately 80% of all iliac AVFs.^[4]

After the creation of an AVF, blood is shunted from the high-pressure arterial side to the low-pressure venous side. This diversion of blood back to the right-sided circulation reduces overall systemic arterial blood flow. The counterregulatory response is an increase in cardiac output mediated by the sympathetic nervous system and circulating catecholamines. Initially, the heart increases cardiac output via an increase in heart rate and stroke volume. With time, excess cardiac stimulation leads to left ventricular hypertrophy, reduction in LV ejection fraction, and eventual HF.^[5]

Classic signs of such fistula include high-output cardiac failure, audible bruit, a palpable abdominal mass, and low back pain, but a definitive diagnosis can be difficult because these classic signs are present in only 20%–50% of all such cases.^[6]

According to the size and location of the fistula, multiple clinical scenarios could happen. The must signs and symptoms used to be high-output cardiac failure, abdominal bruit and thrill, palpable abdominal aneurysm, oliguria, evidence of regional venous hypertension (limb edema with/without cyanosis, hematuria, and rectal bleeding). Once the diagnosis of HF has been made, the clinician must prove that it is a consequence of increased blood flow through the fistula.

The history and physical examination, in particular, palpitation and auscultation, should be carried out over the scars and far from them, in search of characteristic bruit and thrill, irrespective of the interval duration from traumatic or surgical events. In this case, abdominal bruits were not heard, but noninvasive imaging strategies were selected as abdominal ultrasonography with subsequent contrast-enhanced CT (for better delineation of the fistulous tract and its connections). Physical examination, though important, should not be considered as the final stage in suspicious cases.

Early diagnosis is, hence, the key to improve the patient outcome in this condition, which is dependent on the physicians to be aware of it.^[3]

Endovascular techniques, including the use of stent grafts and coil embolization, has a promising role to reduce the morbidity and mortality associated with an open approach to traumatic arterial injuries and AVFs.^[7] The first recorded repair of an AVF using an endovascular stent occurred in 1992 by Parodi et al.^[8] Some advantages of endovascular repair for traumatic AVFs compared with open surgical repair include diminished pain, rapid recovery with decreased disability, and lower cost. Although data do not exist for a direct comparison of open and endovascular approaches to iliac AVFs, it would seem reasonable to assume the endovascular approach lowers the expected morbidity and mortality.^[7]

This rare case emphasizes that patients with RVF must be closely examined (with particular attention to palpation and auscultation) and noninvasive imaging modalities can be very helpful in diagnosis.

Conclusion

It is well accepted that AVFs may be a cause of high-output HF. The size and location of the shunt is very important with resultant wide spectrum of manifestations. In a young man with RVF and echocardiographic evidence of RV enlargement, we should carefully look for related causes, especially extracardiac shunts. Timely diagnosis and treatment of this patient can reverse the cavity enlargement and prevent further damage. Endovascular techniques are an effective and possibly a preferred alternative to open surgical approaches for traumatic chronic AVFs.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 

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