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CommentaryRecurrent Syncope: An Unusual Complication of Hypertensive Heart Disease

Recurrent Syncope: An Unusual Complication of Hypertensive Heart Disease

Resting gradient 60 mm Hg increasing to 87 mm Hg with Valsalva maneuver.
Resting gradient 60 mm Hg increasing to 87 mm Hg with Valsalva maneuver.

To the Editor:

Syncope accompanied by outflow tract obstruction most commonly is associated with obstructive forms of hypertrophic cardiomyopathy. Outflow tract obstruction also may be seen in select diseases that cause ventricular hypertrophy, including aortic valve replacement for aortic valve stenosis, myocardial infarction, and pheochromocytoma. Initially described by Brock, there have been several reports of hypertension implicated in outflow tract obstruction. Although Brock later concluded that hypertension may not be a chief factor, we describe a patient with isolated hypertensive heart disease who developed marked outflow tract obstruction.

Case Report

A 62-year-old hypertensive woman presented with a syncopal episode of 15 minutes duration after voiding on the toilet. The patient denied any presyncopal symptoms, postictal confusion, urinary, or bowel incontinence but reported several previous episodes of syncope. On examination, she had a grade III/VI systolic murmur and appeared hypovolemic with flat neck veins and orthostatic hypotension. Relevant laboratory results revealed hyponatremia, acute kidney injury, hypomagnesemia, elevated transaminase, and leukocytosis, all of which normalized after serial monitoring.

Serial cardiac biomarkers and electrocardiograms were normal. An echocardiogram demonstrated an ejection fraction of 65% to 70% with no valvular abnormalities; however, it was notable for mild left ventricular hypertrophy and substantial outflow tract resting gradient of 60 mm Hg increasing to 87 mm Hg with Valsalva maneuver. These findings were interpreted as evidence of hypertrophic cardiomyopathy (Figure). Cardiac magnetic resonance revealed asymmetric left ventricular basal septal hypertrophy but no characteristic features of hypertrophic cardiomyopathy.

Ultimately, the patient’s septal hypertrophy was attributed to hypertensive heart disease. Her outflow tract gradient improved substantially after the administration of intravenous fluids, indicating a dynamic obstructive lesion provoked by reduced preload. During the Valsalva maneuver, the patient was particularly prone to syncope. The patient was treated with aggressive oral hydration and titration of afterload reducing agents.

 

To read this article in its entirety please visit our website.

-Syed I. Rahman, MD, Paul A. Bergl, MD

This article originally appeared in the November 2016 issue of The American Journal of Medicine.

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