Carotid artery stiffness mechanisms, heart failure events, and atrial fibrillation in MESA: the Multi-Ethnic Study of Atherosclerosis.

IF 4.1 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Ryan Pewowaruk, Claudia E Korcarz, David A Bluemke, Mohamed H Hamdan, Susan R Heckbert, Joao A C Lima, Yacob Tedla, Adam D Gepner
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引用次数: 0

Abstract

Arterial stiffness can be separated into two main mechanisms: 1) load-dependent stiffening from higher blood pressure and 2) structural stiffening due to remodeling of the vessel wall. The relationship of stiffness mechanisms with heart failure (HF) and atrial fibrillation (AF) is unknown. MESA (multi-ethnic study of atherosclerosis) participants with baseline carotid ultrasound images were included in this study (HF n = 6,278; AF n = 5,292). Carotid pulse wave velocity (cPWV) was calculated from B-mode carotid ultrasound to represent total stiffness. Structural stiffness was calculated by adjusting cPWV to a 120/80 mmHg blood pressure with participant-specific models. Load-dependent stiffness was the difference between total and structural stiffness. Associations with incident heart failure events and atrial fibrillation diagnosis were assessed with adjusted Cox hazard models. Four hundred-seven HF events and 1,157 AF diagnoses occurred during a median 17.7 and 16.8 years of follow-up. The associations of carotid artery stiffness mechanisms with HF events were: total cPWV adjusted HR per 1 SD 1.09 [0.98-1.22], P = 0.11; structural cPWV adjusted HR 1.06 [0.94-1.18], P = 0.33; and load-dependent PWV adjusted HR 1.23 [1.05-1.44] per 1 m/s, P = 0.009. The associations of carotid artery stiffness mechanisms with AF diagnoses were: total cPWV adjusted HR 1.11 (1.04-1.20), P = 0.004; structural cPWV adjusted HR 1.10 [1.02-1.16], P = 0.017; load-dependent cPWV adjusted HR 1.12 [1.02-1.23], P = 0.020. Both structural and load-dependent cPWV were associated with the development of AF, and load-dependent cPWV was associated with HF events. These findings indicate that load-dependent cPWV may be a potential treatment target to reduce the incidence of both HF and AF.NEW & NOTEWORTHY We evaluated associations between novel components of arterial stiffness: 1) load-dependent stiffening from higher blood pressure and 2) structural stiffening due to remodeling of the vessel wall and their associations with incident heart failure (n = 6,278) and atrial fibrillation (n = 5,292) over ∼17 years of follow-up. We found that both baseline structural and load-dependent stiffness were associated with the development of atrial fibrillation and load-dependent stiffness was associated with heart failure events.

MESA地区颈动脉僵硬机制、心力衰竭事件和心房颤动:动脉粥样硬化的多民族研究。
动脉硬化可分为两种主要机制:(1)由高血压引起的负荷依赖性硬化;(2)由血管壁重塑引起的结构性硬化。僵硬机制与心力衰竭(HF)和心房颤动(AF)的关系尚不清楚。方法与结果MESA (Multi-Ethnic Study of Atherosclerosis,多民族动脉粥样硬化研究)参与者均有基线颈动脉超声图像(HF n=6278;房颤n = 5292)。颈动脉脉冲波速度(cPWV)由b型颈动脉超声计算,代表总刚度。通过参与者特定模型将cPWV调整为120/80 mm Hg血压来计算结构刚度。荷载相关刚度为总刚度与结构刚度之差。用调整后的Cox风险模型评估与心力衰竭事件和房颤诊断的关系。在平均17.7年和16.8年的随访期间,407例心衰事件和1157例房颤诊断。颈动脉僵硬机制与HF事件的关联如下:总cPWV(每1SD调整HR 1.09 [0.98-1.22], p=0.11;结构性cPWV调整后的HR为1.06 [0.94-1.18],p=0.33;负载相关PWV调整HR为1.23 [1.05-1.44]/ m/s, p=0.009。颈动脉僵硬机制与房颤诊断的相关性为:总cPWV校正HR 1.11 [1.04-1.20], p=0.004;结构性cPWV调整后的HR为1.10 [1.02-1.16],p=0.017;负荷相关cPWV调整后的HR为1.12 [1.02-1.23],p=0.020。结论结构型和负荷依赖型cPWV与房颤的发生有关,负荷依赖型cPWV与心衰事件有关。这些发现表明,负荷依赖性cPWV可能是降低心衰和房颤发生率的潜在治疗靶点。
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来源期刊
CiteScore
9.60
自引率
10.40%
发文量
202
审稿时长
2-4 weeks
期刊介绍: The American Journal of Physiology-Heart and Circulatory Physiology publishes original investigations, reviews and perspectives on the physiology of the heart, vasculature, and lymphatics. These articles include experimental and theoretical studies of cardiovascular function at all levels of organization ranging from the intact and integrative animal and organ function to the cellular, subcellular, and molecular levels. The journal embraces new descriptions of these functions and their control systems, as well as their basis in biochemistry, biophysics, genetics, and cell biology. Preference is given to research that provides significant new mechanistic physiological insights that determine the performance of the normal and abnormal heart and circulation.
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