Lam Carolyn S P, Roger Véronique L, Rodeheffer Richard J, Bursi Francesca, Borlaug Barry A, Ommen Steve R, Kass David A, Redfield Margaret M
Division of Cardiovascular Diseases, Mayo Clinic and Foundation, 200 First St SW, Rochester, MN 55905, USA.
Circulation. 2007 Apr 17;115(15):1982-90. doi: 10.1161/CIRCULATIONAHA.106.659763. Epub 2007 Apr 2.
Mechanisms purported to contribute to the pathophysiology of heart failure with normal ejection fraction (HFnlEF) include diastolic dysfunction, vascular and left ventricular systolic stiffening, and volume expansion. We characterized left ventricular volume, effective arterial elastance, left ventricular end-systolic elastance, and left ventricular diastolic elastance and relaxation noninvasively in consecutive HFnlEF patients and appropriate controls in the community.
Olmsted County (Minn) residents without cardiovascular disease (n=617), with hypertension but no heart failure (n=719), or with HFnlEF (n=244) were prospectively enrolled. End-diastolic volume index was determined by echo Doppler. End-systolic elastance was determined using blood pressure, stroke volume, ejection fraction, timing intervals, and estimated normalized ventricular elastance at end diastole. Tissue Doppler e' velocity was used to estimate the time constant of relaxation. End-diastolic volume (EDV) and Doppler-derived end-diastolic pressure (EDP) were used to derive the diastolic curve fitting (alpha) and stiffness (beta) constants (EDP=alphaEDVbeta). Comparisons were adjusted for age, sex, and body size. HFnlEF patients had more severe renal dysfunction, yet smaller end-diastolic volume index and cardiac output and increased EDP compared with both hypertensive and healthy controls. Arterial elastance and ventricular end-systolic elastance were similarly increased in hypertensive controls and HFnlEF patients compared with healthy controls. In contrast, HFnlEF patients had more impaired relaxation and increased diastolic stiffness compared with either control group.
From these cross-sectional observations, we speculate that the progression of diastolic dysfunction plays a key role in the development of heart failure symptoms in persons with hypertensive heart disease.
据称,射血分数正常的心力衰竭(HFnlEF)病理生理学的促成机制包括舒张功能障碍、血管和左心室收缩期僵硬以及容量扩张。我们对社区中连续的HFnlEF患者和合适的对照进行了无创性左心室容积、有效动脉弹性、左心室收缩末期弹性和左心室舒张弹性及舒张功能的特征分析。
前瞻性纳入了明尼苏达州奥姆斯特德县无心血管疾病的居民(n = 617)、患有高血压但无心力衰竭的居民(n = 719)或患有HFnlEF的居民(n = 244)。舒张末期容积指数通过超声多普勒测定。收缩末期弹性通过血压、每搏输出量、射血分数、时间间期以及舒张末期估计的标准化心室弹性来确定。组织多普勒e'速度用于估计舒张时间常数。舒张末期容积(EDV)和多普勒衍生的舒张末期压力(EDP)用于推导舒张曲线拟合(α)和刚度(β)常数(EDP = αEDVβ)。比较时对年龄、性别和体型进行了校正。与高血压和健康对照相比,HFnlEF患者有更严重的肾功能不全,但舒张末期容积指数和心输出量更小,EDP更高。与健康对照相比,高血压对照和HFnlEF患者的动脉弹性和心室收缩末期弹性同样增加。相比之下,与任一对照组相比,HFnlEF患者的舒张功能受损更严重,舒张期刚度增加。
从这些横断面观察结果来看,我们推测舒张功能障碍的进展在高血压性心脏病患者心力衰竭症状的发展中起关键作用。