Noninvasive estimation of impaired hemodynamics for patients with acute myocardial infarction by Tei index.

BACKGROUND: Tei index, defined as the sum of isovolumic contraction and relaxation times divided by ejection time, has been proposed to express global left ventricular function. For patients with acute myocardial infarction (AMI), left ventricular function can potentially be a major determinant of hemodynamics with limited time for compensation, such as increased brain natriuretic peptide to attenuate congestion, and usually without any intervention to modify cardiac loading on arrival at the hospital during the acute phase. We, therefore, hypothesized that left ventricular function, expressed by the Tei index, allows noninvasive estimation of impaired hemodynamics for patients with AMI. METHODS: We studied 86 consecutive patients with first AMI (34 inferoposterior and 52 anteroseptal). Tei index was obtained as: (a - b)/b, where a is the interval between the cessation and onset of mitral flow and b is the ejection time by aortic flow by pulsed Doppler echocardiography. By using pulmonary capillary wedge pressure (PCWP) > or = 18 mm Hg or <18 mm Hg and cardiac index (CI) < or = 2.2 L/min/m(2) or > 2.2 L/min/m(2) by consecutive catheterization, patients were classified into 4 subsets: subset I with normal hemodynamics; subset II with elevated PCWP; subset III with reduced CI; and subset IV with both elevated PCWP and reduced CI. RESULTS: For patients with inferoposterior AMI, there was no significant correlation between the Tei index and PCWP or CI. For patients with anteroseptal AMI, however, the Tei index showed significant correlation both with PCWP (r = 0.59, P <.0001) and CI (r = -0.42, P <.01). Diagnosis of impaired hemodynamics (subset II-IV) by a Tei index > or = 0.60 showed a sensitivity, specificity, and accuracy of 86%, 82%, and 83%, respectively. CONCLUSIONS: Although the Tei index has limitations to evaluate hemodynamics in patients with inferoposterior AMI, the index allows approximate but quick and practical noninvasive estimation of impaired hemodynamics in patients with anteroseptal AMI.

Mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior myocardial infarction: quantitative analysis of left ventricular and mitral valve geometry in 103 patients with prior myocardial infarction.

OBJECTIVE: The mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction despite less global left ventricular remodeling and dysfunction is controversial. We hypothesized that inferior myocardial infarction causes left ventricular remodeling, which displaces posterior papillary muscle away from its normal position, leading to ischemic mitral regurgitation. METHODS: In 103 patients with prior myocardial infarction (61 anterior and 42 inferior) and 20 normal control subjects, we evaluated the grade of ischemic mitral regurgitation on the basis of the percentage of Doppler jet area, left ventricular end-diastolic and end-systolic volumes, midsystolic mitral annular area, and midsystolic leaflet-tethering distance between papillary muscle tips and the contralateral anterior mitral annulus, which were determined by means of quantitative echocardiography. RESULTS: Global left ventricular dilatation and dysfunction were significantly less pronounced in patients with inferior myocardial infarction (left ventricular end-systolic volume: 52 +/- 18 vs 60 +/- 24 mL, inferior vs anterior infarction, P<.05; left ventricular ejection fraction: 51% +/- 9% vs 42% +/- 7%, P <.0001). However, the percentage of mitral regurgitation jet area and the incidence of significant regurgitation (percentage of jet area of 10% or greater) was greater in inferior infarction (percentage of jet area: 10.1% +/- 7.5% vs 4.4% +/- 7.0%, P =.0002; incidence: 16/42 (38%) vs 6/61 (10%), P <.0001). The mitral annulus (area = 8.2 +/- 1.2 cm2 in control subjects) was similarly dilated in both inferior and anterior myocardial infarction (9.7 +/- 1.7 vs. 9.5 +/- 2.3 cm2, no significant difference), and the anterior papillary muscle-tethering distance (33.8 +/- 2.6 mm in control subjects) was also similarly and mildly increased in both groups (35.2 +/- 2.4 vs 35.2 +/- 2.8 mm, no significant difference). However, the posterior papillary muscle-tethering distance (33.3 +/- 2.3 mm in control subjects) was significantly greater in inferior compared with anterior myocardial infarction (38.3 +/- 4.1 vs 34.7 +/- 2.9 mm, P =.0001). Multiple stepwise regression analysis identified the increase in posterior papillary muscle-tethering distance divided by body surface area as an independent contributing factor to the percentage of mitral regurgitation jet area (r2 = 0.70, P <.0001). CONCLUSIONS: It is suggested that the higher incidence and greater severity of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction can be related to more severe geometric changes in the mitral valve apparatus with greater displacement of posterior papillary muscle caused by localized inferior basal left ventricular remodeling, which results in therapeutic implications for potential benefit of procedures, such as infarct plication and leaflet or chordal elongation, to reduce leaflet tethering.

Impact of atrial fibrillation on tricuspid and mitral annular dilatation and valvular regurgitation.

To investigate the effects of atrial fibrillation (AF) on the mitral and tricuspid valves, the corresponding annular dilatation and valvular regurgitation were compared with 2-dimensional and Doppler echocardiography in 31 consecutive patients with lone AF and 28 normal controls. Mid-systolic mitral and tricuspid annular areas were measured from 2 diameters in 2 orthogonal apical echocardiograms. Percent (%) mitral regurgitant (MR) or tricuspid regurgitant (TR) jet area to the left or right atrial area was evaluated and % MR or TR jet area >20% was considered moderate or significant. Both the mitral and tricuspid annular areas in patients with lone AF were significantly larger compared with the controls (mitral: 9.5 +/- 1.2 vs 6.6 +/- 0.9 cm2, lone AF vs control, p < 0.01) (tricuspid: 12.0 +/- 2.0 vs 7.5 +/- 0.9 cm2, p < 0.01). The % increase in the annular area relative to the mean normal value was significantly greater in the tricuspid valve (44 +/- 18 vs 60 +/- 28%, p < 0.01). Moderate or severe MR was not observed and the incidence of moderate or severe valve regurgitation (% jet area >20%) was significantly higher in the tricuspid valve (0/31 vs 11/31, MR vs TR, p < 0.01) in patients with lone AF. The % TR jet area showed significant correlation with tricuspid annular area (r2 = 0.65, p < 0.001). Lone AF is associated with annular dilatation of both mitral and tricuspid valves, but the annular dilatation and valvular regurgitation are significantly greater in the tricuspid valve.

Noninvasive differentiation of normal from pseudonormal/restrictive mitral flow using TEI index combining systolic and diastolic function.

Differentiation of normal from pseudonorma/restrictive mitral flow is not necessarily easy. Pseudonormal/restrictive flow is usually associated with left ventricular (LV) dysfunction, which can be detected using the TEI index, combining systolic and diastolic function. The purpose of this study was to test the feasibility of using the TEI index to differentiate pseudonormal/restrictive from normal mitral flow. In 33 patients with mitral flow E/A > or = 1 and LV mid-diastolic pressure measured by catheterization, the LV volumes, mitral E and A velocity, deceleration time of the E velocity, and the TEI index, defined as the sum of the isovolumic contraction and relaxation time divided by ejection time, were evaluated using Doppler echocardiography. Pseudonormal/restrictive mitral flow was defined as mitral flow E/A > or = 1 associated with LV mid-diastolic pressure > 12 mmHg. There were 22 and 11 patients with normal and pseudonorma/restrictive mitral flow, respectively. Among the indices of LV function, the TEI index achieved the best correlation with LV mid-diastolic pressures (r2 = 0.63, p < 0.0001). By setting the TEI index > or = 0.65 as the criteria for pseudonormal/restrictive mitral flow, this diagnosis had sensitivity, specificity, and accuracy of 82%, 96%, and 91%, respectively. TEI index allows noninvasive differentiation of pseudonormal /restrictive from normal mitral flow.

Isolated annular dilation does not usually cause important functional mitral regurgitation: comparison between patients with lone atrial fibrillation and those with idiopathic or ischemic cardiomyopathy.

OBJECTIVES: We sought to test whether isolated mitral annular (MA) dilation can cause important functional mitral regurgitation (MR). BACKGROUND: Mitral annular dilation has been considered a primary cause of functional MR. Patients with functional MR, however, usually have both MA dilation and left ventricular (LV) dilation and dysfunction. Lone atrial fibrillation (AF) can potentially cause isolated MA dilation, offering a unique opportunity to relate MA dilation to leaflet function. METHODS: Mid-systolic MA area, MR fraction, LV volumes and papillary muscle (PM) leaflet tethering length were compared by echocardiography among 18 control subjects, 25 patients with lone AF and 24 patients with idiopathic or ischemic cardiomyopathy (ICM). RESULTS: Patients with lone AF had a normal LV size and function but MA dilation (isolated MA dialtion) significant and comparable to that of patients with ICM (MA AREA: 8.0 +/- 1.2 vs. 11.6 +/- 2.3 vs. 12.5 +/- 2.9 cm(2) [control vs. lone AF vs. ICM]; p < 0.001 for both lone AF and ICM). However, patients with lone AF had only modest MR, compared with that of patients with ICM (MR fraction: -3 +/- 8% vs. 3 +/- 9% vs. 36 +/- 25%; p < 0.001 for patients with ICM). Multivariate analysis identified PM tethering length, not MA dilation, as an independent primary contributor to MR. CONCLUSIONS: Isolated annular dilation does not usually cause moderate or severe MR. Important functional MR also depends on LV dilation and dysfunction, leading to an altered force balance on the leaflets, which impairs coaptation.