Heart Failure ― Under-Recognized Link to Post-Stroke Functional Status ―
論文ID: CJ-22-0284
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論文ID: CJ-22-0284
Heart failure (HF) is more prevalent in older people, and its prevalence increases with aging.1 In patients with HF, functional abilities are impaired, and functional disability progresses over time.2 Consequently, HF potentially causes functional decline and eventually results in a long-term adverse prognosis.
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Stroke is not uncommon in patients with HF, because stroke also affects the older population; HF and stroke share similar cardiovascular risk factors, and HF increases the short- and long-term risks of ischemic stroke. Stroke is also a major cause of functional disability and has a significant effect on activities of daily living after disease onset. Thus, the coexistence of these diseases further exerts adverse effects on functional status and activities of daily living (Figure 1). Nevertheless, cardiologists and stroke physicians may not be fully aware of the comorbidity’s serious consequences.
Time course changes in functional status after (A) heart failure, (B) ischemic stroke, (C) and both heart failure and ischemic stroke.
In this issue of the Journal, Takahashi et al3 demonstrate that HF is independently associated with increased risk of poor functional outcome 1 year after ischemic stroke. Their finding highlights the close link between HF and stroke, with respect to long-term functional outcome after the onset of the diseases. The potential effect of stroke on functional status should be recognized in clinical practice, particularly when managing and treating patients with HF.
In patients with HF, the risk of stroke is higher especially in the short term, but also in the long term than in the general population.4 A number of pathological pathways are proposed to explain the causal mechanisms underlying the condition, such as increased thrombosis and coagulation, reduced fibrinolysis, and increased endothelial dysfunction.5 In cases of atrial fibrillation concomitant with HF, the risk of cardioembolic stroke increases remarkably after the formation of thrombus in the left atrial appendage. Thrombus originating from the left atrium tends to lodge in the main trunk, particularly at the bifurcation, where the arterial diameter suddenly narrows, which often causes a large territorial infarct involving cortical lesions.6 In patients with low cardiac output and systemic hypoxia, the ischemic penumbra is at an increased risk of irreversible damage due to reduced perfusion and oxygenation. Moreover, HF can be complicated by endothelial dysfunction,7 which contributes to parenchymal damage and, subsequently, neurological deficits after brain ischemia.8 Thus, HF may have harmful effects on the ischemic brain and hamper recovery from brain ischemic insult.
In acute stroke care, HF may hinder optimal treatment of brain ischemia. In the hyperacute stage of ischemic stroke, high blood pressure is generally untreated unless it is exceedingly high (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg in general; systolic blood pressure >185 mmHg or diastolic blood pressure >110 mmHg in patients receiving reperfusion therapy), to preserve perfusion pressure in the brain.9 However, in patients with HF, blood pressure is controlled to below optimal levels, and intravenous fluid is restricted to avoid exacerbating heart dysfunction due to excess fluid, which is disadvantageous to brain ischemia in terms of cerebral perfusion. Furthermore, HF reduces exercise tolerance and limits functional capacity, potentially leading to prolonged hospital stay and delay of aggressive rehabilitation.
Muscle wasting and cachexia may be also associated with functional decline after stroke in patients with HF.10 Various hypothetical pathways, involving hormonal imbalance, appetite and satiety, metabolic imbalance, and testosterone, have been proposed to explain the development of sarcopenia in patients with HF.11 If stroke develops in a patient with HF, sarcopenia will be unfavorable for functional improvement after disease onset, and reduced adiposity is unlikely to act as a reserve during recovery. Moreover, social and economic factors, such as prolonged hospital stay, malnutrition, low physical activity, and insufficient rehabilitation, may contribute to the poor post-stroke functional status of patients with HF. In the long run, limited exercise capacity after stroke reduces physical activity, accelerating muscle weakness. Overall, patients with HF are likely to be functionally dependent or bedridden or even die after stroke, compared with patients without HF (Figure 2).
Unfavorable interactions between heart failure and ischemic stroke in terms of functional status. BP, blood pressure.
To prevent further progression of functional decline, new treatment strategies need to be urgently established for patients with HF and stroke. Firstly, frailty should be excluded using well-validated assessment tools, because it also leads to poor functional outcome in older patients.12 Exercise, nutrition, and rehabilitation require more attention in high-risk patients (e.g., patients with stroke, HF, and sarcopenia). Currently, cardiac rehabilitation, exercise training, and self-care counselling have been shown to improve clinical outcomes in patients with chronic HF.13 Therefore, stroke rehabilitation should be integrated into cardiac rehabilitation programs for patients with HF. Sufficient, appropriate, and integrated rehabilitation may be crucial in improving the functional outcome of patients with HF and stroke. Further study is warranted to elucidate the mechanisms of the functional decline after stroke and to determine the effectiveness of a comprehensive approach involving multidisciplinary treatments for patients with HF.
