Hemodynamic insufficiency in association with severe unilateral occlusive carotid disease (OCD) is a rare cause of stroke. Most cases of stroke due to hemodynamic insufficiency are related to low-output cardiac states and hypotension. Carotid intraplaque haemorrhage is a known complicating factor of OCD and has been associated with higher rates of thromboembolic ischaemic events. We present a case of documented acute symptomatic left middle cerebral artery (MCA) territory perfusion deficit without intracranial atherosclerosis/stenosis/thrombus and associated with plaque haemorrhage, completely reversed by carotid angioplasty and stenting.

A 70-year-old male was admitted with sudden onset of right-hand weakness and aphasia lasting for about an hour. He had improved completely by the time of arrival. Medical history was negative for diabetes and hyperlipidemia. He denied a history but presented to the ER with very high blood pressure (220/120 mmHg). Attempts to lower it resulted in repeated deficits.

Head computerized tomography (CT) showed an early small stroke in the left fronto-parietal region, suggesting a watershed infarct (Figure 1A: arrowheads). CT angiography (CTA) showed severe (measured at 77% by NASCET criteria) left cervical carotid stenosis (Figure 1B), mild right cervical carotid stenosis at the bifurcation and no evidence of intracranial stenosis or clot (Figure 1C). CT perfusion showed an increased mean transit time (MTT), decreased blood flow (CBF) and normal blood volume (CBV) in the left MCA territory (Figure 1E). MRI with MRA angiography (MRA) of the brain and craniocervical vessels confirmed the small ischaemic areas in the high left frontal and parietal regions without other areas of restricted diffusion. It also showed evidence of acute haemorrhage in the left carotid plaque (Figure 1D).

Figure 1

Plain CT head showing a small stroke in the left fronto-parietal region, suggesting an watershed infarct (A - arrowheads). CT angiogram: severe left cervical carotid stenosis (B), and no evidence of intracranial stenosis or clot (C). CT perfusion with an increased mean transit time (MTT), decreased blood flow (CBF) and normal blood volume (CBV) in the left MCA territory (E). Acute hemorrhage in left carotid plaque (D) on MRI. Carotid angioplasty and stenting (F) followed by improvement of CTP parameters and total resolution of the perfusion mismatch (G).

An urgent carotid angioplasty and stenting were performed approximately 10 hours after the initial presentation, with good radiological results (Figure 1F). A CT/CTA/CTP less than 6 hours after this procedure showed total resolution of the perfusion mismatch (Figure 1G).

Thromboembolic events related to carotid atherosclerotic disease are the underlying cause of a large percentage of strokes.Reference Lanzino, Tallarita and Rabinstein ¹ Intraplaque haemorrhage (IPH) has been described as a risk factor for recurrent emboli and strokeReference Altaf, Beech, Goode, Gladman, Moody and Auer ^{2 -} Reference Hosseini, Kandiyil, MacSweeney, Altaf and Auer ⁷ due to recurrent thromboembolic phenomena.Reference Spagnoli, Mauriello, Sangiorgi, Fratoni, Bonanno, Schwartz and Piepgras ^{8 ,} Reference Redgrave, Lovett, Gallagher and Rothwell ⁹ Hemodynamic cerebral events may result from low cardiac output (orthostatic ischaemia, myocardial ischemia, cardiac arrhythmias) or severe carotid stenosis or occlusion, and they have been implicated as the underlying mechanism in roughly 10% of all strokes.Reference Bladin and Chambers ¹⁰ Approximately two-thirds of cases are associated with severe carotid stenosis, often bilateral, or carotid occlusion.

In the absence of any evidence of intracranial thrombus and a large area of mismatch in the MCA territory, we speculate that plaque rupture and haemorrhage lead to acute hemodynamic insufficiency.Reference Derdeyn, Grubb and Powers ^{11 ,} Reference Nemoto, Yonas, Kuwabara, Pindzola, Sashin and Meltzer ¹² The likely compensatory increase in blood pressure and the recurrent deficits with attempts to lower it support this hypothesis. Also, the patient had a carotid ultrasound at another institution two weeks before, due to arm weakness, that showed no hemodynamically significant carotid stenosis. A computerized tomography done at the same time also showed no stroke.

Another possibility was that a clot occluding the MCA resolved rapidly enough not to be picked up in the first imaging. This is unlikely due to the short time elapsed between the beginning of his symptoms and the CT scan (40 minutes to conclusion of the scan), and it would not explain the complete resolution of his recurrent symptoms and perfusion mismatch after carotid revascularization.

This case illustrates what seems to be a rare association of intraplaque haemorrhage and acute hemodynamic insufficiency in the absence of contralateral craniocervical vascular occlusive disease oripsilateral intracranial occlusive disease.