Arterial hypertension is the most common cardiovascular disease in older than middle-aged patients. The prevalence of resistant hypertension is around 10% of all hypertensive population [1],[2], and clinicians should always consider possible secondary causes of hypertension in this clinical setting, especially in young adults. Hypertension caused by vascular origin is usually caused by renal artery stenosis and infrequently aortic coarctation. As for stenosis of the aorta, coarctation of the thoracic aorta at the level of the ligamentum arteriosum is considered as congenital vascular lesion. Infrequently, stenosis in distal thoracic or abdominal aorta may cause hypertension, and the pathophysiology of this vascular lesion is considered as vasculitis such as Takayasu arteritis. We report secondary hypertension caused by stenosis of the aorta, probably due to Takayasu arteritis, in three female patients in their early sixties. Diagnosis of aortic stenosis was delayed, and its presence was suggested by detection of high abdominal aortic flow velocity during transthoracic echocardiography.

We described three cases of resistant hypertension caused by stenosis of aorta that was diagnosed in persons who are in their early 60’s. Unfortunately, the detection of aorta stenosis as a cause of hypertension was delayed until early 60’s, and it was incidentally detected by imaging of the abdominal aorta during echocardiographic examination. Takayasu arteritis was diagnosed by typical imaging findings and by exclusion of other causes of stenosis of aorta. Their laboratory findings, which indicated secondary hypertension, especially renin, aldosterone, and VDRL, are unremarkable. The three patients are old and have hypertension; therefore, the atherosclerotic change of the aorta could be possible. But angiographic and ultrasonographic findings of these patients were compatible for Takayasu arteritis, rather than diffuse and multiple atherosclerosis.

Takayasu arteritis is a chronic inflammatory disease, which usually involves the aorta and its main branches [3]. The onset of Takayasu arteritis is usually insidious with nonspecific symptoms such as fever or night sweat and thus remains easily unrecognized until late (sclerotic) stage, but it is usually diagnosed before the patient enters his 50’s [4]. After acute inflammatory period, the development of arterial impairment may cause symptoms that vary according to the involved vasculature. The common complaints of patients with Takayasu arteritis are claudication (upper extremities are involved more often than lower extremities), bruits, and asymmetrical pulses in the right and left extremities. Aneurysm involving ascending aorta can also be a complication of the disease. The development of hypertension in Takayasu arteritis occurs in more than one-half of the patients and is usually a consequence of renal artery stenosis. In rare cases, hypertension can also be induced by suprarenal aortic coarctation.

Suspicion of secondary hypertension caused by vascular stenosis of renal artery or suprarenal aorta usually begins when the examiner notices audible bruits or blood pressure differences between extremities. All the hypertension guidelines recommend measurement of blood pressure in both arms and careful auscultation of the carotid, renal, and heart sounds and murmur [5]. In the cases presented here, systolic bruit was not clearly evident in the first and second cases, and bruit was probably missed due to concomitant loud to-and-fro aortic regurgitation murmur in the third case. However, if at the initial stage, blood pressure was measured in the upper and lower extremities, aortic stenosis as a cause of resistant hypertension could have been detected earlier in our three cases. It is important to note that early diagnosis is critical to prevent vascular complications as the progression of Takayasu arteritis could be stopped by administration of glucocorticoid treatment [6].

Another interesting point in our cases is that aortic stenosis was diagnosed during transthoracic echocardiographic examination. Generally, echocardiographic evaluation for hypertensive patients was helpful to develop a diagnosis and treatment strategy and to estimate a prognosis. Echocardiographic examination provides the information about left ventricular geometry and function, and left atrial volume and function. Therefore, clinicians could evaluate the presence of target organ damage and the changes of cardiac structure and function by resistant or secondary hypertension. During echocardiographic examination, cardiac subcostal four-chamber view showed venous connection to the right atrium and abdominal aorta. The examiner usually concentrates to get good images of cardiac structures and intracardiac blood flow characteristics. In addition, careful abdominal aortic imaging during echocardiographic examination can provide valuable information such as size of aorta, intimal flap, and atherosclerotic plaque along the aorta wall. In all three cases, high velocity jet by Doppler examination inside the abdominal aorta and decreased size of the aorta seen by echocardiographic examination prompted clinicians to search for the stenosis of the middle aorta. Blood pressure measurement in the four extremities after observing high flow velocity in the abdominal aorta could diagnose aorta stenosis immediately.

Our cases had several instructive points. First, even in elderly patients, secondary cause of hypertension needs to be considered when there is uncontrolled blood pressure despite use of multiple drugs. The medical history of the three cases revealed that blood pressure was left uncontrolled for at least 5 years. Second, during echocardiography examination, it is important to get a good image of the abdominal aorta and its flow velocity. Third, a complete and thorough physical examination is always important. Even in presumably primary hypertension cases, an initial examination should be included. Lastly, blood pressure measurement of the extremities should be performed, especially when a patient presents with resistant hypertension.

Written informed consent was obtained from the patients for publication of this Case Report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.