Dobutamine stress echocardiography Doppler estimation of cardiac diastolic function: a simultaneous catheterization correlation study.

BACKGROUND: Doppler echocardiography using the ratio of early diastolic transmitral velocity to early diastolic mitral annular tissue velocity (E/E') is routinely used to evaluate left ventricular (LV) filling pressures at rest. We tested the hypothesis that measurement of E/E' in patients undergoing dobutamine stress echocardiography (DSE) will detect changes in LV filling pressures. METHODS: In this prospective study, 16 patients with normal LV ejection fraction and normal coronary arteries by angiography underwent a standard DSE protocol with simultaneous LV filling pressure monitoring with a fluid filled pigtail catheter. Doppler echocardiographic assessment of LV diastolic function was performed using E/E' at rest and during DSE. RESULTS: The average age of the study participants was 57 ± 8 years. Average heart rate was 61 ± 11 bpm at baseline and 141 ± 12 bpm at peak stress. LV mean diastolic pressure decreased from 12.3 ± 2.6 mmHg at baseline to 9.0 ± 2.3 mmHg at peak stress (P = 0.0001). Baseline E/E' at the septum and lateral annulus were 8.7 ± 2.2 and 7.5 ± 1.9 and during peak stress were 8.3 ± 3.1 and 7.9 ± 3.5, respectively. There was no significant change in E/E' at either the septum or the lateral annulus (P = 0.55, P = 0.66). There was no significant correlation between LV mean diastolic pressure and E/E' with dobutamine stress. CONCLUSIONS: In patients with normal LV ejection fraction and no significant coronary artery disease undergoing DSE, the ratio of early diastolic transmitral velocity to early diastolic tissue velocity (E/E') at peak stress with dobutamine does not predict changes in LV filling pressures.

The role of the renin-angiotensin system in the pathophysiology, prevention, and treatment of renal impairment in patients with the cardiometabolic syndrome or its components.

Chronic kidney disease and cardiovascular disease share many risk factors, including hypertension, obesity, and insulin resistance. All of these are components of the cardiometabolic syndrome and are associated with increased risk of morbidity and mortality. One mechanism that links renal injury with the cardiometabolic syndrome is activation of the renin-angiotensin system. Chronic angiotensin II activation promotes development of renal disease through hemodynamic effects and up-regulation of inflammatory cytokines and growth factors. Inhibition of the renin-angiotensin system delays progression of renal disease and improves measures of renal function independent of blood pressure lowering in patients with the cardiometabolic syndrome or its components. Higher doses of renin-angiotensin system inhibitors may provide greater renoprotection in both normotensive and hypertensive patients with the cardiometabolic syndrome. Inhibition of the renin-angiotensin system in patients with risk factors or vascular disease with or without recognized glycemic abnormalities may be a useful strategy for preventing the progression of chronic kidney disease in patients with vascular disease and in those with the cardiometabolic syndrome or its components.