Acute pulmonary edema secondary to a hidden hypertensive emergency

Abstract

Severe stenosis of the subclavian artery is a rare clinical finding, even more so for bilateral existence of the condition. Subclavian artery stenosis leads to erroneously normal or even low blood pressure values when measured at the brachial artery on the ipsilateral side. The poor control of blood pressure may cause cardiovascular complications such as heart failure and acute pulmonary edema without the patient having high blood pressure in the arms. Widespread clinical reliance on a sole brachial measurement of blood pressure, particularly in the emergency room setting, may result in inappropriate clinical management in patients with conditions that alter brachial blood pressure. We report a case of acute diastolic heart failure secondary to hypertensive emergency hidden due to bilateral stenosis of both subclavian arteries in a patient with severe atherosclerosis, cerebrovascular disease, and symptoms of subclavian steal syndrome.

<Learning objective: We present a case of acute pulmonary edema with hidden hypertensive emergency in the measures at upper limbs made in the emergency department due to severe bilateral subclavian stenosis. Knowledge of this entity and suspicion in patients at high cardiovascular risk is important in patients who often have complications from poorly controlled hypertension. The measurement of blood pressure in all four limbs is a useful measure in patients at high cardiovascular risk.>

Introduction

Severe stenosis of the subclavian artery is a rare clinical finding, even more so for bilateral existence of the condition. Subclavian artery stenosis leads to erroneously normal or even low blood pressure values when measured at the brachial artery on the ipsilateral side. We report a case of acute diastolic heart failure secondary to hypertensive emergency hidden due to bilateral stenosis of both subclavian arteries in a patient with severe atherosclerosis, cerebrovascular disease, and symptoms of subclavian steal syndrome.

Case Report

We present a 69-year-old patient with essential hypertension, dyslipidemia, former smoker, with thromboangeitis obliterans (Buerger disease), and chronic lower limb ischemia grade IIa of Fontaine classification (clinical characteristics are shown in Table 1). Two years previously, he complained about effort angina and percutaneous coronary revascularization by femoral access was performed with two drug-eluting stents at the right coronary artery and at the first obtuse marginal branch.

Table 1.

Clinical characteristics of the patient.

Baseline characteristics
Height (m)	1.68
Body weight (kg)	72
Body mass index	25.5
Basal plasma glucose (mg/dl)	89
Total serum cholesterol (mg/dl)	204
Serum LDL cholesterol (mg/dl)	124
Serum HDL cholesterol (mg/dl)	47
Serum triglycerides (mg/dl)	162
Blood test in Emergency Department
Hemoglobin (g/dl)	12.9
Creatinine (mg/dl)	1.2
Sodium (mmol/L)	140
Potassium (mmol/L)	5.7

HDL, high-density lipoprotein; LDL, low-density lipoprotein.

He currently presented with progressive severe dyspnea and chest pain. He also complained about dizziness and presyncope since several months before. At admission, non-invasive right brachial arterial pressure was 100/65 mmHg, heart rate 100 bpm and initial oxygen saturation was 80%. The thorax X-ray showed signs of acute pulmonary edema (Fig. 1A). The electrocardiogram showed signs of left ventricular hypertrophy and secondary repolarization abnormalities without dynamic changes (Fig. 1B). Blood tests and serum biochemistry showed no abnormalities (Table 1). Cardiac biomarkers increased mildly with peak troponin I of 2.1 ng/ml (N < 0.05 ng/dl). An echocardiogram demonstrated moderate left ventricular hypertrophy with mass ventricular index of 135 g/m² (N 49–115 g/m²), left ventricular ejection fraction of 55%, diastolic dysfunction with pseudonormal filling pattern, E/E′ ratio of 18 and systolic pressure of pulmonary artery of 45 mmHg.

Fig. 1.

(A) Thorax X-ray showing signs of acute pulmonary edema. The cardiothoracic ratio was not increased. (B) The electrocardiogram showed sinus rhythm, enlargement of left atrium, left ventricular hypertrophy criteria by Cornell and Sokolow with secondary repolarization abnormalities.

In order to rule out an acute coronary syndrome as the cause of the pulmonary edema, a coronary angiography was performed. Radial access was chosen, however the guide did not progress toward the ascending aorta due to an obstruction of the brachiocephalic trunk with severe calcification of the aortic arch and the proximal portion of supra-aortic vessels (Fig. 2A). By femoral access, the coronary angiography could be performed, showing no significant de novo coronary lesions nor restenosis or thrombosis of previous stents (Fig. 2B,C). The non-invasive arterial pressure in both brachial arteries was 138/91 mmHg, however the invasive arterial pressure with the diagnostic catheter at the aorta and at the femoral artery was 219/76 mmHg (Fig. 1D).

Fig. 2.

(A) Angiography showing obstruction of the brachiocephalic trunk (white arrow head); (B and C) Right coronary artery and first obtuse marginal branch without restenosis or thrombosis of previous stents nor de novo coronary lesions; (D) Blood pressure registry on coronary angiography. Top left of image the intra-aortic blood pressure (219/76 mmHg). The non invasive blood pressure in arm bottom left of image (138/91 mmHg); (E) Tridimensional reconstruction of supra-aortic trunks: severe calcification and stenosis at both subclavian arteries (white arrow heads) and severe calcification at internal carotid arteries (white arrows); (F) Severe calcification of the aortic arch and calcification and obstruction of brachiocephalic trunk, stenosis at left subclavian artery and severe stenosis of the left and right internal carotid arteries (white arrows).

A computed tomography and a Doppler echography of supra-aortic vessels confirmed a severe stenosis of both internal carotids and both subclavian arteries (Fig. 2E,F).

After ruling out any possible cause of the acute pulmonary edema we concluded that a hypertensive emergency could be the cause of it. The hypertensive crisis was not suspected at admission because it was hidden by the stenosis of supra-aortic trunks, with a severe pressure gradient between inferior and superior limbs as an “inverted” aortic coarctation.

We intensified the antihypertensive treatment and blood pressure control was successfully achieved. We recommended blood pressure monitoring on lower limbs during follow-up as it corresponded to the real arterial pressure. Endarterectomy of both right and left internal carotids was performed. Given the severity of the subclavian arteries stenosis and symptoms consistent with subclavian steal syndrome, percutaneous treatment was offered to the patient but at the time that the present manuscript was written it had not yet been performed.

Discussion

Hidden arterial hypertension, when only brachial blood pressure is measured, is a rare condition and may be caused by bilateral subclavian stenosis (BSS). Unilateral subclavian stenosis can be suspected comparing bilateral brachial systolic blood pressures (>15 mmHg difference), however BSS is a diagnostic challenge as this finding is absent. Most often it is due to atherosclerosis, and although it is usually asymptomatic, neurological symptoms (vertebrobasilar system dysfunction) are three times more frequent if the stenosis is bilateral, as in our patient [1]. In addition to atherosclerosis, other causes of BSS are inflammation due to radiation exposure, fibromuscular dysplasia, compression syndromes, neurofibromatosis, and arteritis or aortitis syndrome [2]. In our patient, the two main possible causes of BSS were atherosclerosis and Buerger's disease. The age of the patient, the absence of necrotic skin ulcers and other inflammatory phenomena in the upper limbs (arthritis or Raynaud's syndrome), and the angiographic findings (deformed arteries with severe calcification and tortuosity, with irregular internal diameter) support the atherosclerosis as the origin of the patient's disease [3]. Furthermore, in patients with Buerger's disease, the involvement of distal vascular territories is characteristic rather than proximal territories.

BSS can cause chronic poor blood pressure control because the measure of blood pressure in the arms may show falsely normal or even low values and therefore, it is an independent cardiovascular mortality factor [4]. As it happened in our patient, it may also cause acute cardiovascular complications such as diastolic heart failure due to hypertensive emergency [5] that can be unrecognized in the setting of falsely normal brachial blood pressure. Although, common clinical practice relies much more frequently on blood pressure measurement from upper extremities, and even only in one side, this case underscores the importance of blood pressure measurement in all extremities, especially in patients with multiple cardiovascular risk factors [6] and when subclavian stenosis is suspected, because in them brachial blood pressure may be inaccurate, and ankle blood pressure could be a more precise reflection of the patient's true blood pressure.

Conflict of interest

The authors do not have any conflict of interest.