Author + information
- Alejandro Cruz-Utrilla, MDa,∗ (, )
- Eduardo Pozo, MD, PhDa,
- Gina LaRocca, MDb,
- Marcos Ferrández-Escarabajal, MDa and
- David Filgueiras-Rama, MD, PhDa
- aDepartment of Cardiology, Hospital Clínico San Carlos, Madrid, SpainDepartment of Cardiology, Hospital Clinico San Carlos, Madrid, Spain
- bCardiovascular Institute and Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, Mount Sinai School of Medicine, New York, New YorkCardiovascular Institute and Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, Mount Sinai School of Medicine, New York, New York
- ↵∗Address for correspondence:
Dr. Alejandro Cruz-Utrilla, Department of Cardiology, Hospital Clínico San Carlos, Calle Profesor Martín Lagos, S/N, 28040, Madrid, Spain.
This paper reports the case of an 88-year-old male with a history of chronic abdominal aortic aneurysm admitted to the emergency department with resting chest pain consistent with angina. Beta-blockade therapy triggered a cardiogenic shock, which motivated an urgent computed tomography scan and echocardiogram that confirmed high-output-related heart failure secondary to aortocaval fistula. (Level of Difficulty: Beginner.)
An 88-year-old male with a history of chronic abdominal aortic aneurysm (AAA) of 5.5-cm maximum diameter. The patient was admitted to the emergency department due to recurrent self-limited episodes of resting chest pain consistent with angina, without a history of coronary artery disease. Electrocardiography showed diffuse ST-segment depression on 4 of the precordial leads (V2 to V5) and blood testing demonstrated mild elevation of cardiac biomarkers (peak troponin I level at 24 h of 2.1 ng/ml; and a laboratory cutoff value of 0.05 ng/ml), which confirmed the diagnosis of non-ST-segment elevation myocardial infarction. Upon admission, serum N-terminal pro–B-type natriuretic peptide (NT-proBNP) levels were 869 pg/ml (laboratory cutoff value: 450 pg/ml) without overt exploratory signs of congestive heart failure. The patient refused any invasive treatment, consequently, initial management included aspirin, clopidogrel, and bisoprolol (2.5 mg once daily). After the first dose of bisoprolol, the patient suffered sudden deterioration of his overall status with onset of hypotension, diaphoresis, and systemic lactic acidosis. An urgent transthoracic echocardiography showed a severely dilated right ventricle, hyperdynamic left and right ventricular function at 105 beats/min (Video 1) and a high cardiac output of 20.2 l/min (cardiac index: 9.6 l/min/m2), based on Doppler measurements. Further physical examination identified a faint abdominal murmur without overt abdominal mass, although ultrasonography imaging was consistent with progression of the AAA up to >7 cm of maximum diameter. A computed tomography scan confirmed a 7.7-cm (maximum-diameter) AAA and an aortocaval fistula (Figure 1) with a massive contrast reflux into the inferior vena cava, reaching the diaphragm (Figure 1). The patient was admitted to the acute cardiac care unit for inotropic and noninvasive respiratory support, which were initiated immediately. Despite receiving immediate treatment, the patient rapidly went into heart failure (NT-proBNP levels increased to 30.503 pg/ml), and he died 72 h after the beginning of symptoms.
This case shows an acute coronary syndrome after increased cardiac output caused by a high-flow aortocaval fistula. The clinical presentation without previous angina and rapid progression of acute heart failure suggested an acute or subacute development of left-to-right extracardiac shunt. An acute oxygen supply-demand imbalance rather than a coronary-related event was the most likely pathophysiological mechanism. Although invasive measurements were not obtained, the lack of left ventricular dilation or hypertrophy and the hyperdynamic status of both ventricles also support acute or subacute development of the fistula (1). Rapid deterioration after β-blockade therapy highlights the negative effect of an acute decrease of cardiac performance in a low systemic vascular resistance condition requiring a very high cardiac output (1). Although other authors have previously reported high-output heart failure that resulted from chronic aortocaval fistula (2), this report shows that the initial clinical presentation may be a coronary syndrome due to an oxygen supply-demand imbalance. Our report also highlights the difficulty of an early diagnosis to avoid β-blockade therapy in cases presenting with angina, which in this case, triggered a fatal cardiogenic shock. Although definitive diagnosis of aortocaval fistula has been described as challenging (3) even after meticulous physical examination, an echocardiography test upon admission could have identified the increase in cardiac output and signaled suspicion for a coronary event related to high cardiac output in a patient with a history of AAA.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 21, 2019.
- Revision received April 30, 2019.
- Accepted May 2, 2019.
- 2019 The Authors
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