Guest Editor: H. Ralph Schumacher, Jr, MD Professor of Medicine University of Pennsylvania School of Medicine, Philadelphia Exacerbations of Congestive

Exacerbation of congestive heart failure (CHF) is the most common admitting diagnosis in elderly patients, but the exacerbating factors are often missed. A thorough history and physical examination are key to identifying the cause. The following case is a good example of a patient with CHF who had frequent hospital admissions, in whom the presence of femoral arteriovenous fistulae (AVF) related to a cardiac catheterization he had had more than 10 years earlier was undiagnosed all those years.

Case Presentation
A 59-year-old black man was referred to the cardiology clinic with progressive congestive symptoms and angina pectoris. His medical history was significant for chronic arterial hypertension and an ischemic stroke without permanent focal neurologic deficit. Twelve years earlier (in 1990) he had a normal coronary angiogram after several episodes of chest discomfort. He had no history of surgeries or allergies. His mother had a myocardial infarction (MI) when she was in her 50s, and his sister died from an MI at age 61. The patient was a 40-pack-year smoker until 3 months ago; he denied alcohol and drug abuse. Since 1990 he had been hospitalized frequently with exacerbations of congestive symptoms as well as exacerbations of hypertension while taking diuretics and other antihypertension medications.

Physical examination showed a well-developed and well-nourished patient, with pulse rate, 83 beats/min; blood pressure (BP), 158/89 mm Hg; respiratory rate, 18 breaths/min; temperature, 97°F.

Jugular venous pressure and carotid pulses were normal. The apical pulse was deviated to the left, with a sustained left ventricular (LV) heave. The first and second heart sounds were normal. A fourth heart sound and a 2/6 ejection systolic murmur were observed at the left upper sternal border. His lungs were clear, and the abdominal examination was normal. Peripheral pulses were full and symmetric, but a palpable thrill with a systolic bruit on the right femoral pulse was noted.

The electrocardiogram showed sinus rhythm with left atrial enlargement and LV hypertrophy, without acute ST–T-wave changes. Echocardiography revealed an ejection fraction of 30% to 35%, with inferior wall hypokinesis and LV hypertrophy but no significant valvular regurgitation or stenosis. Given his progressive angina and congestive symptoms, a cardiac catheterization, with access through his left femoral artery, was performed. LV pressures were 140/6/12 mm Hg, and aortic pressure was 145/95 mm Hg. The ejection fraction was estimated at about 35%. The left coronary system was normal, and the right coronary system was dominant, with obstructions at the proximal right coronary artery (80%) and midright coronary artery (50%) and 70% stenosis of the bifurcation.

The right coronary artery was stented. During the procedure, the interventional cardiologist noticed a rocking movement of the catheter tip in the ascending aorta. The possibility of aortic regurgitation was ruled out. When the catheter was pulled back and the aortogram repeated, a significant shunt flow between the right femoral artery and vein was evident (Figure). Subsequently, the patient underwent vascular surgery for ligation and division of a right-groin AVF. He had an impressive thrill, bruits, and a positive Branham’s sign at the right groin. During surgery it was noted that he actually had 2 fistulae, 0.5 and 1.5 cm in diameter, located between the common femoral vein and artery.

At 6 months after coronary stenting and ligation of the AVF, the patient was no longer complaining of angina or congestive symptoms. Physical examination showed: pulse rate, 75 beats/min; BP, 150/85 mm Hg; temperature, 97.5°F; respiratory rate, 18 breaths/min. Jugular venous pressure was normal, and other findings had not changed from 6 months earlier, except for the disappearance of the right femoral bruits and thrill. A new echocardiogram showed improved inferior wall motion and an increase in ejection fraction to 45%.

Discussion
The reported incidence of vascular complications of cardiac catheterization range from 1% to 9%; the incidence of AVF varies from 0.006% to 0.14%.^1-5 However, all the data are based on retrospective studies.

A 2002 prospective study of 10,271 consecutive patients with cardiac catheterization who were followed for 3 years reported an AVF incidence of 0.86%.⁶ Significant and independent risk factors for AVF in that study were high heparin dosage, warfarin sodium (Coumadin) therapy, left-groin puncture, arterial hypertension, and female gender (Table).⁶ Within 1 year, 38% of the fistulae had closed spontaneously; no signs of cardiac volume overload or limb damage were observed in patients with persistent AVF.

In contrast, an earlier retrospective review of 23,291 cardiac catheterizations identified 7 patients with iatrogenic AVF, for an incidence of 0.017%.⁵ CHF and lower limb ischemia, the most common presenting features, developed from 2 to 10 months after catheterization. There are also sporadic case reports of CHF in patients with posttraumatic femoral AVF who presented with refractory congestive symptoms at 15,⁷ 39,⁸ and 50⁹ years posttrauma.

Persistence of iatrogenic AVF 12 years after right femoral artery catheterization and refractory congestive symptoms secondary to high-output failure are 2 very rare and interesting findings in our patient. Although the shunt fraction was not measured, the patient’s apparent clinical and echocardiographic improvements favor the contributing role of AVF in his high-output failure in addition to his hypertensive and ischemic heart disease.

One may suggest that the patient’s low ejection fraction argues against high-output heart failure and that the enhanced right ventricular perfusion after right coronary artery stenting could explain his improvement. In addition, different loading states can affect the measurement of ejection fraction. Although high-output states are usually associated with a normal or high ejection fraction, it has been suggested that they rarely cause heart failure in patients without underlying heart disease.¹⁰ When high-output states superimpose on underlying heart disease that is associated with decreased contractility, a low ejection fraction does not exclude the role of a concomitant high-output state in the pathogenesis of the patient’s symptoms. Because ejection fraction is a volume parameter, patients with high-output states and congestive symptoms can pre­sent with low ejection fraction if the LV end-diastolic volume and heart rate are increased to maintain the high output. The different loading conditions did not seem to affect the ejection fraction estimation in our patient, because he had the same BP (afterload) and body weight (preload) and was taking the same medications before and after surgery. Given his normal left coronary system and LV hypertrophy, however, it is unlikely that enhanced right ventricular perfusion increased the ejection fraction from 35% to 45% after right coronary stenting alone.

Conclusion
This case emphasizes the importance of thorough history taking and physical examination in patients with heart failure. These are needed for reviewing the broad list of etiologic and exacerbating factors, especially in patients with frequent and refractory congestive symptoms.

References
1. McCann RL, Schwartz LB, Pieper KS. Vascular complications of cardiac catheterization. J Vasc Surg. 1991;14:375-381.

2. Ricci MA, Trevisani GT, Pilcher DB. Vascular complications of cardiac catheterization. Am J Surg. 1994;167:375-378.

3. Messina LM, Brothers TE, Wakefield TW, et al. Clinical characteristics and surgical management of vascular complications in patients undergoing cardiac catheterization: interventional versus diagnostic procedures. J Vasc Surg. 1991;13:593-600.

4. Oweida SW, Roubin GS, Smith RB III, et al. Postcatheterization vascular complications associated with percutaneous transluminal coronary angioplasty. J Vasc Surg. 1990;12:310-315.

5. Glaser RL, McKellar D, Scher KS. Arteriovenous fistulas after cardiac catheterization. Arch Surg. 1989;124:1313-1315.

6. Kelm M, Perings SM, Jax T, et al. Incidence and clinical outcome of iatrogenic femoral arteriovenous fistulas: implications for risk stratification and treatment. J Am Coll Cardiol. 2002;40:291-297.

7. Erdol C, Baykan M, Gokce M, et al. Congestive heart failure associated with chronic venous insufficiency and leg ulcers secondary to an arteriovenous fistula caused by a shotgun wound 15 years ago. Vasa. 2002;31:125-128.

8. Turgeman Y, Rosenfeld T. Severe left heart failure long after acquired arteriovenous fistula [in Hebrew]. Harefuah. 1989;116:41-43.

9. Schneider M, Creutzig A, Alexander K. Untreated arteriovenous fistula after World War II trauma. Vasa. 1996;25:174-179.

10. Givertz MM, Colucci WS, Braunwald E. Clinical aspects of heart failure: high-output failure, pulmonary edema. In: Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A Textbook of Cardiovascular Medicine. 6th ed. Philadelphia, Pa: WB Saunders; 2001:534-561.

Commentary

Arteriovenous fistula (AVF) is a rare but serious complication of cardiac catheterization. It occurs when the needle used to access the femoral artery perforates the posterior wall, creating a fistula tract to the adjacent femoral vein. Initially only minimal flow occurs, but over time the fistula can enlarge substantially. Although local hematoma or hemorrhage can also occur and are usually detected early (because of local pain, anemia, or hypotension), an AVF may not become evident for several days or weeks. A fistula is usually suspected by the finding of a continuous bruit or thrill over the femoral artery and is confirmed by ultrasound. Surgical repair is generally required.

Vascular complications occur more frequently in the setting of antithrombotic or antiplatelet therapy, which are used with increasing frequency in patients with coronary artery disease (CAD), especially in those undergoing percutaneous interventions (angioplasty or stent placement). In addition, the routine practice of outpatient catheterization, with the shorter postprocedure observation time, can delay the detection of an AVF. Obesity may also play a role, because it makes obtaining arterial access more difficult, and it can mask complications.

High-output cardiac failure can occur when an AVF is associated with a high flow rate and low vascular resistance. The degree of heart failure can be worsened by concomitant heart disease, such as hypertension or ischemic heart disease, as in this patient. Hypertensive heart disease and/or CAD probably accounted for this patient’s reduced ejection fraction, although the high-output failure from the AVF was an important cause of his symptoms, especially the worsening angina caused by increased myocardial oxygen demand. The patient’s clinical improvement resulted from stenting of the right coronary artery and repair of the AVF.

The most important lesson to be learned from this case is the value of the physical examination. This man’s AVF developed at the time of his 1990 catheterization procedure but was only detected when the right groin was examined as an access site for the second catheterization more than 10 years later. Because he had normal coronary arteries in 1990, there was no need for repeat angiography (and thus no groin examination subsequently). Had the right groin been a source of pain or bleeding, the AVF would have been detected much earlier.

The message we should take home from this case is the need for a careful groin examination subsequent to a seemingly uncomplicated catheterization procedure.