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Le calme après la tempête ? Les vaisseaux rétiniens après une crise hypertensive

Malignant hypertension (MH) is a life- and organ-threatening condition. Retinal microcirculation is the only vascular network directly observable and measurable. Following MH, there may be a spectrum of retinal lesions, the evolution of which has received little attention despite its interest as a surrogate of the cerebral circulation.

Patients with a recent episode of MH were followed by serial retinal imaging sessions comprising adaptive optics ophthalmoscopy (AOO), optical coherence tomography (OCT) and OCT angiography (OCTA). Qualitative and quantitative changes in the vessels and neural structures of the retina were analyzed.

Sixteen patients recently discharged from ICU for MH (81% male; mean age ±SD 43±10 years; initial systolic blood pressure (SBP) 185±26 mmHg) were followed-up over a mean period of 11.6±8 months. At initial examination (mean SBP 136±16 mmHg; mean delay after diagnosis of MH 4±3.5 days), the mean wall-to-lumen ratio (WLR) of retinal arterioles was 0.354±0.069 (range, 0.270– 0.530). Evidence of focal retinal ischemia on OCT was found in 47% of eyes. During follow-up, divergent evolutions of arteriolar diameters were observed, with 31% of patients showing additional reduction of arterial diameter, while 25% increasing their diameter. While the four cases of focal arteriolar narrowings (FANs) identified at first examination resolved during follow-up, new FANs were observed in 8 other eyes (25%). At last examination, the mean WLR was not significantly different from first examination (0.351±0.053; range, 0.250–0.430; p=0.17). The evolution of WLR was positively correlated to evolution of FANs, that is, new FANS appeared in constricting retinal vessels, and resolving FANs in dilating vessels. A post-critical new focal ischemic episode happened in one patient consisting in a arteriolar occlusion. BP level, age, kidney or brain damage or pharmacologic therapeutic classes were not correlated with microvascular changes.

Following an episode of malignant hypertension, variations of retinal vascular diameters may persist during several months. Hypertensive retinopathy may progress despite blood pressure control. 

We hypothesize that malignant hypertension causes long-term dysfunctional vasomotricity that may potentially cause additional neurovascular damage. Retinal vascular metrics may provide useful biomarkers for the management of patients following acute hypertension.