Diastolic Stress Test Research Articles

Diastolic Stress Test for the Evaluation of Exertional Dyspnea

Recent studies have highlighted that dyspneic patients comprise a high-risk subgroup of patients referred for cardiac stress testing. Even after adjusting for the presence and degree of coronary artery disease the risk of cardiac and all-cause mortality is at least three- to fivefold higher in dyspneic patients compared to asymptomatic or those with chest pain. Stress echocardiography is uniquely positioned to characterize all potential cardiovascular etiologies of dyspnea from global and regional systolic dysfunction, myocardial ischemia to valvular heart disease, pulmonary hypertension and diastolic dysfunction. Various data point to diastolic dysfunction and associated heart failure as the major potential etiology for dyspnea as well as the likely cause of the heightened mortality risk. Doppler echocardiography at rest and with stress can now characterize the hemodynamics of diastolic dysfunction and close the loop on the comprehensive assessment of the patient who has exertional shortness of breath. This review discusses the role of the Doppler echocardiographic diastolic stress test in the evaluation of patients with cardiac dyspnea.

The diastolic stress test: a new approach to an old problem

The evaluation of ischemic heart disease is the cornerstone of clinical Cardiology. Although there are many means of ischemic evaluation, all are with their own limitations. While perfusion-based studies are highly sensitive, they lack specificity. Conversely, systolic wall motion analysis with echocardiography tends to have high specificity; however, the sensitivity may be limited by short duration of systolic abnormalities when present. With the advent of Doppler echocardiography, and more specifically tissue Doppler imaging, and strain and strain rate imaging, a more comprehensive evaluation of the left ventricular function is available, including diastole. Diastolic abnormalities in the setting of ischemia are now being studied using these new parameters and have been suggested as a reliable marker of ischemia. Exercise-induced abnormalities in diastolic parameters have improved sensitivities and specificities over traditional stress testing and persist longer than systolic abnormalities. A review of the medical literature regarding the subject will be discussed here.

Abstract 2570: Effects Of Exercise On Left Ventricular Diastolic Function Depend On Homogenous Increase In Diastolic Strain Rates

Objectives: It has been speculated that early diastolic left ventricular (LV) suction depends on LV apex relaxing more promptly than LV base, and that these relationships are accentuated during exercise. In this study, we sought to determine impact of exercise on the relationship between parameters of LV diastolic mechanics (peak early longitudinal (E SrL), circumferential (E SrC) and radial (E SrR) strain rate, and peak LV untwisting velocity) and intraventricular pressure gradient (IVPG) as marker of diastolic suction. Methods: We studied 23 healthy volunteers (age 38 ± 10 years, 13 females) by Vivid 7 ultrasound machine (GE) during supine bicycle stress. Segmental diastolic strain rates and untwisting velocity were obtained by speckle tracking software (EchoPac, GE Medical) while IVPG was measured by applying the Euler equation to the transmitral color Doppler M mode of the LV inflow. Segmental diastolic strain rates were averaged over basal, mid, and apical levels. Results: Absolute values of E SrL, E SrC and E SrR homogenously increased during exercise (P<0.001 for all) by the same degree at all LV three levels (p=NS for the difference between levels). (see table ) Untwisting velocity during exercise increased from -1.54 ± 0.69 to -3.40 ± 1.54 rad/s while IVPG increased from 1.41 ± 0.67 to 3.90 ± 1.69 mmHg (p<0.001 for both). Out of strain parameters, average E SrL increase during exercise showed strongest correlation with IVPG (r=0.64, p<0.001) and untwisting velocity (r=0.62, p<0.001). Higher untwisting velocity was associated with the greater IVPG (r=0.70, p<0.001). Conclusions: Increase of suction during exercise is related to homogeneous augmentation of relaxation throughout left ventricle. Longitudinal strain rate was the best predictor of the increase of untwisting velocity and IVPG. These data could serve as a reference for diastolic stress testing.

1111 Development of the diastolic stress test: non-invasive assessment of left ventricular filling pressure post-exercise

1111 Development of the diastolic stress test: non-invasive assessment of left ventricular filling pressure post-exercise

Echocardiography as a Noninvasive Swan-Ganz Catheter

Diwan and co-investigators report in this issue of Circulation that the interval between onset of mitral E and annular early diastolic velocity (Ea) by tissue Doppler, TE−Ea, can be used to estimate left ventricular (LV) filling pressure in patients with mitral valve disease.1 Garcia and colleagues were the first to report that the onset of Ea occurred 7.5±3.5 ms after peak mitral inflow velocity in 7 patients with restrictive cardiomyopathy, whereas Ea started 22±19 ms earlier than did E in the normal group.2 Subsequently, TE−Ea has been shown to correlate with the time constant of LV relaxation (τ) demonstrated by Hasegawa and associates in their elegant animal experiment.3 With worsening of heart failure by rapid pacing, Ea progressively decreased in velocity and delayed in onset. Mitral E occurred coincidently with the termination of the early diastolic left arterial (LA) and LV pressure gradient at baseline and all stages of heart failure. In contrast, with increasing heart failure, Ea was progressively delayed after LA to LV pressure crossover, and TE−Ea was related to τ. Rivas-Gotz, Nagueh, and their associates also demonstrated that TE−Ea was prolonged after constriction of the circumflex coronary artery in dogs.4 In patients with heart failure, LV myocardial relaxation and compliance are decreased. See p 3281 Although LV filling is initiated and enhanced by augmentable myocardial relaxation in healthy individuals, it is driven by high filling pressure in patients with heart failure because myocardial relaxation remains reduced, not being sensitive to preload. Myocardial relaxation also affects the isovolumic relaxation time (IVRT). As relaxation becomes abnormal, LV pressure falls more slowly and the opening of the mitral valve is delayed, resulting in a longer IVRT. IVRT, however, becomes shorter as LA pressure increases; hence, IVRT∝τ/LA pressure. Because TE−Ea∝τ, …