Pulsed Tissue Doppler and left ventricular filling in acute coronary syndromes

Abstract: Pulsed tissue Doppler is a new technique, which can investigate longitudinal left ventricular(LV) function, by measuring tissue velocities and timings. Patients with acute coronarysyndromes (ACS) frequently display a reduced longitudinal function. They also developglobal LV filling impairment. This pathology involves an elevated LV filling pressure (FP),left atrial (LA) enlargement and elevation of right ventricular pressure (RVp). We aimed toinvestigate the relative timing of the onsets of the LV early diastolic longitudinal wall motionand blood flow, and further, to evaluate clinical tools to assess global LV filling.We studied 160 ACS patients and 60 controls with echocardiography, including pulsed tissueDoppler. Using pulsed blood pool Doppler, we semi-quantitatively classified the patients withrespect to LV filling: normal (group 0); delayed relaxation (group 1); isolated pathologicalmitral-pulmonary venous-A-wave-duration difference (group 2); pseudo normal (group 3); ora restrictive (group 4) filling pattern. The temporal onset relationship of the LV early diastolicwall lengthening (e) and the mitral inflow (E) was explored, for a regional wall analysis(paper I). In order to evaluate a recent application, suggested to predict pulmonary capillarywedge pressure (PCWP) through the formulas tau=32+0.7x (e-E) and PCWP = LV endsystolicpressure x e-IVRT/ tau (IVRT=the isovolumic relaxation time), we tested these formulasin normal individuals, at rest and during non-pharmacological preload alterations (Paper IV).The sensitivity of a new LV filling variable, the E/e (=E/E ) filling index was investigatedby comparing E/e to RVp in their identification of a Doppler-assumed elevated LVFP, i.e. apseudo normal or a restrictive filling pattern (Paper II). We compared the intraindividual atrialsize difference and absolute LA size, as detectors of LA enlargement (Paper III).In the patients, e started later than E (12±30 vs. 2±19 ms later, p<0.0001) and the intraindividualtime range was wider (43±27 vs. 30±18 ms, p<0.0001). In normal individuals atrest (n=50), the formula-calculated PCWP was 9±9 mmHg, exceeding 12 mmHg in 28 %.During altered preload (n=14), it showed an intraindividual fluctuation of up to 40 mmHg.An E/e filling index >15 and an RVp >30 mmHg had the following (%) sensitivity (32/94),specificity (95/76), positive (68/59), and negative (80/97) predictive value of a diagnosedgroup 3 or 4. Absolute LA area , LA area/body height and LA-right atrial area indicated aLA enlargement in; for controls: 2%, 2% and 4%; and for patients: group 0 and 1: 15%, 17%and 46%; group 2: 26%, 29% and 52%; and group 3 and 4: 42%, 38% and 54%.In ACS patients, the early diastolic LV tissue- to blood temporal relationship may reveal anasynchronous, and in relation to the mitral inflow delayed, initial LV wall lengthening.The formulas to predict PCWP failed to render plausible values in normal individuals. TheE/e filling index >15, as a single variable, may have a limited sensitivity of an elevated LVFP.An RVp of !30 mmHg could exclude a currently elevated LVFP. Atrial size inequality cansensitively detect LA enlargement, especially in only mildly impaired LV filling.