Daytime blood pressure surges following hypoxic episodes in a case of pneumoconiosis with lacunar stroke recurrences
A 71-year-old Japanese man diagnosed with pneumoconiosis, hypertension, and three lacunar strokes was referred to us the day after his third stroke for a hypertension evaluation. He had been under antihypertensive (daily evening 8 mg candesartan) and antiplatelet (daily morning 100 mg aspirin) medication since his first lacunar midbrain infarction at 70 years. However, his condition was then complicated by two more lacunar strokes: the right-side pons (8 months after the first stroke) and left-side pons (3 months after the second stroke). He had worked for 35 years at a limestone mine and was diagnosed with pneumoconiosis because of this. He had no history of smoking or excess alcohol consumption. His activities of daily living were obtained. Physical examination indicated high BP (179/98 mmHg), low BMI (18.3 kg/m2), and some dysarthria; other results were normal. There was no evidence of atrial fibrillation. Endocrinologic data were normal. There was no carotid artery plaque and no significant stenosis on magnetic resonance angiography (Fig. 1). Spirometry data showed decreased percentage vital capacity (48%) and decreased forced expiratory volume (%) in 1 s (65.6%), indicating both restrictive and obstructive respiratory impairment. We added daily morning 5 mg amlodipine. Forty-six days after the third stroke, we performed ambulatory blood pressure monitoring (ABPM) simultaneously with 24 h oxygen saturation monitored by pulse oximetry to evaluate ambulatory BP and hypoxia-related BP surges (Fig. 2). Daytime BP surges were observed following hypoxic episodes. Although his BP control status was poor, we did not add antihypertensive medication as he reported dizziness on standing and developed orthostatic hypotension (94/70 mmHg). We prescribed respiratory rehabilitation and nutrition education, and he was discharged. Eighty-one days after the third stroke, he experienced his fourth lacunar stroke of the pons. Sixty-one days after the fourth stroke, we re-evaluated ABPM simultaneously with 24 h oxygen saturation monitoring. BP control had improved compared with the first ABPM, but daytime BP surges remained following hypoxic episodes (Fig. 2).
Our patient experienced multiple lacunar strokes; however, there were no atherosclerotic changes in large arteries. Lacunar strokes result from the occlusion of the strain vessels, which are susceptible to hemodynamic stress. There are two major vascular pathologies underlying lacunar strokes 4: (a) thickening of the arterial media because of lipohyalinosis and fibrinoid necrosis, and (b) obstruction of the origins of penetrating arteries by parent artery intimal plaques, which is also called branch atheromatous disease. Lipohyalinosis and fibrinoid necrosis are more strongly associated with elevated BP, and lacunar stroke recurrences are more frequent compared with branch atheromatous disease 5. The rapid-fire sequence of lacunar infarctions in the present patient may be because of fibrinoid necrosis owing to the exaggerated hemodynamic stress.
In CRD patients, cardiovascular disease risk is increased independent of smoking or age. The underlying mechanism is not fully understood, but increased BPV because of hypoxia may play a major role. We proposed a novel disease entity, systemic hemodynamic atherothrombotic syndrome (SHATS) 6,7, characterized by a synergistic risk of exaggerated hemodynamic stress and vascular disease, which advances hypertensive organ damage and also triggers cardiovascular events. SHATS targets are strain vessels such as small arteries in the brain, heart, kidney, and eyes. The exaggerated hemodynamic stress in CRD patients because of hypoxic episodes supports the SHATS concept.