Mechanism of left a trial enlargement related to ventricular diastolic impairment in hypertension

Background and hypothesis: Systemic hypertension is the leading cause of left ventricular (LV) hypertrophy. The present study aimed to investigate the mechanism of left atrial (LA) enlargement in patients with hypertensive heart disease during cardiac catheterization. Methods: Data were obtained from eight control subjects and seven patients with hypertensive heart disease. Left atrial and LV pressures from catheter-tip micromanometer, and LA and LV volumes from biplane cineangiograms were analyzed during the same cardiac cycle. Results: Left atrial maximal volume were 93 ± 26 ml in patients with hypertensive heart disease and 63 ± 12 ml in control subjects (p<0.05). In patients with hypertensive heart disease, time constant of LV relaxation was significantly greater than that in controls (54 ± 18 vs. 31 ± 16 ms, respectively p<0.01). Left atrial maximal volume correlated with time constant of LV relaxation (r = 0.86, p<0.01). The ratio of LV filling volume before LA contraction to LV stroke volume in patients with hypertensive heart disease was significantly lower than that in control subjects (65 ± 13 vs. 76 ± 7%, respectively p<0.05). On the other hand, the ratio of LV filling volume during LA contraction to stroke volume in patients with hypertensive heart disease was significantly higher than that in controls (35 ± 13 vs. 24± 7%, respectively p<0.05). Left atrial volume before LA contraction in patients with hypertensive heart disease was significantly larger than that in controls (74 ± 22 vs. 47 ± 10 ml, respectively, p<0.01). During LA contraction, LA work was significantly increased in patients with hypertensive heart disease compared with that in controls (274 ± 101 vs. 94 ± 42 mmHg. ml, respectively p<0.001). Left atrial work showed significant correlation with LA volume before LA contraction (r = 0.75, p <0.01). Conclusion: Left ventricular diastolic filling was impaired in patients with hypertensive heart disease. Enlargement of left atrium might be attributed to the impairment of blood flow from left atrium to left ventricle due to the increased LV stiffness.     

Characterization of left ventricular chamber distortion: alterations in cavity shape and orientation in mitral stenosis

Distortion of the left ventricular (LV) chamber silhouette was identified in 28 patients with mitral stenosis (MS) by disparity between normally identical chamber volumes calculated independently from the frontal (AP) and lateral (LAT) views of biplane cineangiograms (AP end diastolic volume 157.8 +/- 10.0 ml, LAT end diastolic volume 115.6 +/- 7.2 ml, p less than .001). Similar systematic disparity was observed in estimates of end systolic volume in these views. While no directional difference in ejection fraction was found, identical (+/- 10%) AP and LAT measurements were obtained in only 36% of patients, indicating poor reproducibility of the estimate of LV function between single radiographic views. A technique was also devised for determining the spatial orientation of the LV long axis (mid mitral valve to apex) from biplane cineangiograms; this axis was shown to intercept the frontal plane at an angle of 50.9 +/- 2.4 degrees in 12 subjects with normal LV anatomy and 36.1 +/- 4.5 degrees in seven patients with MS, indicating that the long axis was rotated posteriorly toward alignment with the frontal plane in the latter group. The presence and magnitude of LV chamber distortion was clearly related to the degree of angiographically estimated right ventricular dilatation. Implications of these observations, particularly with reference to the estimation of single plane LV volume characteristics in patients with MS, are discussed.     

Myocyte contractile function is intact in the post-infarct remodeled rat heart despite molecular alterations

OBJECTIVE: To investigate the cellular mechanisms underlying global and regional LV dysfunction in the post-infarct (MI) remodeled rat hearts. METHODS: LV remodeling and function were quantified by echocardiography, morphometry, in vivo hemodynamics, and isolated perfused heart studies in 6 weeks post-MI and sham-operated rats. LV myocytes from sham and MI hearts were used for morphometric and functional studies. Myocyte contractile function and intracellular calcium kinetics were measured at different stimulation frequencies (0.2-2 Hz), temperatures (30 and 37 degrees C), and external viscous load (1, 15, 200 and 300 centipoise). Myocyte apoptosis was measured by DNA laddering; BCL-2, BAX, Na(+)-Ca(2+) exchanger, and SERCA-2 proteins by western blot; and brain natriuretic peptide (BNP), SERCA-2 mRNA by RT-PCR. RESULTS: MI hearts were remodeled (Echo LV diameter 7.3+/-0.38 vs. 5.9+/-0.16 mm, P<0.03), and showed global (Echo % fractional shortening 30+/-2.4 vs. 58+/-3, P<0.001), and regional contractile dysfunction of non-infarcted myocardium (Echo % systolic posterior wall thickening 36+/-2 vs. 57+/-1.7, P<0.001). In vivo hemodynamic and isolated heart function studies confirmed depressed LV systolic and diastolic function and increased volumes. Whereas, myocytes isolated from infarcted hearts were remodeled (40% longer and 10% wider), their contractile function and calcium kinetics under basal conditions and at high stimulation frequency, temperature and viscous load were similar to sham myocytes. The mRNA for BNP was increased whereas that for SERCA-2 decreased, but the SERCA-2 protein was normal. Despite myocyte hypertrophy, ventricular septal thickness was reduced in infarcted hearts (2.2+/-0.1 vs. 2. 6+/-0.07 mm, P<0.01), and showed increased apoptosis. CONCLUSIONS: Myocytes from remote non-infarcted myocardium of the remodeled hearts have normal contractile function, despite structural remodeling and altered gene expression. Non-myocyte factors may be more important in genesis of contractile dysfunction in the remodeled heart, for up to 6 weeks after MI.     

Compensatory changes in atrial volumes with normal aging: is atrial enlargement inevitable?

OBJECTIVES: The aim of this study was to evaluate left atrial volume and its changes with the phases (active and passive) of atrial filling, and to examine the effect of normal aging on these parameters and pulmonary vein (PV) flow patterns. BACKGROUND: Atrial volume change with normal aging has not been adequately described. Pulmonary vein flow patterns have not been volumetrically evaluated in normal aging. Combining atrial volumes and PV flow patterns obtained using transthoracic echocardiography could estimate shifts in left atrial mechanical function with normal aging. METHODS: A total of 92 healthy subjects, divided into two groups: Group Y (young <50 years) and Group O (old > or =50 years), were prospectively studied. Maximal (Vol(max)) and minimal (Vol(min)) left atrial volumes were measured using the biplane method of discs and by three-dimensional echocardiographic reconstruction using the cubic spline interpolation algorithm. The passive filling, conduit, and active emptying volumes were also estimated. Traditional measures of atrial function, mitral peak A-wave velocity, velocity time integral (VTI), atrial emptying fraction, and atrial ejection force were measured. RESULTS: As age increased, Vol(max), Vol(min), and total atrial contribution to left ventricle (LV) stroke volume were not significantly altered. However, the passive emptying volume was significantly higher (14.2 +/- 6.4 ml vs. 11.6 +/- 5.7 ml; p = 0.03) whereas the active emptying volume was lower (8.6 +/- 3.7 ml vs. 10.2 +/- 3.8 ml; p = 0.04) in Group Y versus Group O. Pulmonary vein flow demonstrated an increase in peak diastolic velocity (Group Y vs. Group O) with no corresponding change in diastolic VTI or systolic fraction. CONCLUSIONS: Normal aging does not increase maximum (end-systolic) atrial size. The atrium compensates for changes in LV diastolic properties by augmenting active atrial contraction. Pulmonary vein flow patterns, although diastolic dominant using peak velocity, demonstrated no volumetric change with aging.     

Effects of aging on left atrioventricular coupling and left ventricular filling assessed using cardiac magnetic resonance imaging in healthy subjects

Left ventricular (LV) filling results from diastolic suction of the left ventricle and passive left atrial (LA) emptying at early diastole and LA contraction at end-diastole. Effects of aging on LA and LV geometric characteristics and function and its consequences for LV filling are incompletely understood. Insight into these effects may increase the understanding of diastolic function. Cardiac magnetic resonance imaging was used to study effects of aging on left atrioventricular coupling and LV filling. Forty healthy volunteers underwent cardiac magnetic resonance imaging and were subdivided into 2 age groups of 20 to 40 (younger group) and 40 to 65 years (older group). For the older group, LA volumes were larger (p <0.05) and LV volumes, including stroke volumes, were smaller (p <0.05), whereas ejection fraction remained constant. LA/LV volume ratios were larger (0.27 +/- 0.06 vs 0.19 +/- 0.03; p <0.001) and correlated with LV mass-volume ratio (r = 0.42, p <0.01). The older group also had lower LA passive emptying (15 +/- 3.0 vs 19 +/- 4.8 ml/m(2); p <0.05) and higher LA active emptying volumes (13 +/- 3.1 vs 11 +/- 3.9 ml/m(2); p <0.05). For both groups, conduit volume contributed most to LV filling, but was lower in the older group (21 +/- 5.1 vs 27 +/- 9.0 ml; p <0.05). In conclusion, changes in LA volume and function were age dependent and related to changes in LV mass-volume ratio. Conduit volume contributed most to LV filling and decreased with age, suggesting it to be an indicator of diastolic function.     

Abnormalities of left ventricular function and geometry in adults with an atrial septal defect. Ventriculographic, hemodynamic and echocardiographic studies.

Left ventricular function and motion in 12 adults with an ostium secundum atrial septal defect were analyzed utilizing biplane cineangiography. Values for left ventricular end-diastolic volume index, stroke volume index, ejection fraction, left ventricular end-diastolic pressure and mean rate of circumferential fiber shortening were compared with values in an age-matched group of 11 normal subjects. Comparisons of ventriculographic and echocardiographic data were also made in 5 patients and 10 control subjects. Cardiac index was smaller in patients than in the normal subjects (3.6 vs. 4.5 liters/min per m2, P less than 0.01). Although left ventricular end-diastolic pressure was similar (8 mm Hg in both groups), the end-diastolic volume index was significantly smaller in patients than in normal subjects (56 vs. 76 ml/m2, P less than 0.05). Stroke volume index was also significantly smaller in patients (40 vs. 52 ml/m2, P less than 0.01). The two groups had similar values for ejection fraction (65 +/- 2 percent [standard error of the mean] in patients vs. 68 +/- 2 percent in normal subjects), circumferential fiber shortening velocity (1.67 +/- 0.13 vs. 1.81 +/- 0.15 circumferences/sec.), heart rate (91 +/- 7 vs. 90 +/- 5 beats/min) and mean systemic arterial pressure (92 +/- 5 vs. 87 +/- 3 mm Hg). Early systolic bulging of the upper ventricular septum toward the right ventricle was seen in 10 of 12 patients with an atrial septal defect but in no normal subject. Echocardiographic data supported these findings. No other abnormalities of motion were consistently noted. It is concluded that the left ventricle of patients with an atrial septal defect is subnormal in volume and abnormal in sequence of contraction of the septum and is characterized by apparent decreased distensibility.     

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.     

Right ventricular performance in patients with coronary artery disease.

While left ventricular (LV) performance in patients with coronary artery disease (CAD) has been extensively investigated, little attention has been given to right ventricular (RV) function in this disease. For this purpose, a new geometric model for RV volume has been developed and RV end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI) and ejection fraction (EF) have been determined from biplane RV cineangiograms in 26 patients. Eight patients served as normal (control) subjects (group I). Eighteen patients with obstructive CAD comprised two other groups: six who had no significant disease of the right coronary artery (RCA) (group II) and 12 who had a high grade RCA lesion (group III). The mean values for EDVI, SVI and EF in group I were 76 +/- 11 ml/m2, 50 +/- 6 ml/m2, and 66 +/- 6%. The only significant difference between groups I and II was that SVI was lower in group II than in group I (P less than 0.01). No measurements in groups II and III were statistically different from each other. However, markedly subnormal values were found in group III (EDVI: 61 +/- 16 ml/m2, SVI: 33 +/- ml/m2 and ef: 52 +/- 7%); all values being significantly lower (SVI and EF: P less than 0.001; EDVI: P less than 0.05) than in group I. RV end-diastolic pressure was normal in all patients. These findings may related to 1) reduced RV compliance, 2) distorted LV geometry, 31 possible RV ischemia or 4) reduced Frank-Starling effect.     

Global and regional diastolic filling dynamics in compensated dilated cardiomyopathy

To assess the left ventricular (LV) global and regional (anterior, apical, inferior) diastolic filling dynamics in compensated dilated cardiomyopathy (DCM), we measured left ventricular pressure and instantaneous volume from angiography in 7 normal controls (CTL) and 6 DCM patients with sinus rhythm. Global and regional peak filling rate (PER), time constant of LV pressure decline (T; Weiss's method) and LV chamber stiffness (k; Gaasch's method) were calculated. In DCM, left ventricular end-diastolic volume (ml/m2) was larger than in CTL (137 +/- 29 vs. 74 +/- 6, p less than 0.001), and stroke index (ml/m2) was not different from CTL (46 +/- 14 vs. 46 +/- 8, NS), indicating a compensated state of LV. Mitral valve opening pressure (mmHg) tended to increase in DCM compared with CTL (12 +/- 6 vs. 8 +/- 4). Global PFR (ml/sec/m2) (CTL = 216 +/- 47 vs. DCM = 201 +/- 36) and k (CTL = 0.044 +/- 0.023 vs. DCM = 0.029 +/- 0.016) were not different between 2 groups. However, T (msec) was markedly prolonged in DCM compared with CTL (61 +/- 10 vs. 35 +/- 5, p less than 0.001). In CTL, regional PFR (1/sec) showed almost the same values in each region, but in DCM, apical region showed higher PFR than in other regions. Thus, early diastolic filling might play an important role in maintaining the total transmitral flow in DCM despite severe impairment of LV relaxation. This compensation could be related mainly to accelerated regional lengthening of the LV apical region.     

Importance of the "atrial kick" in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 +/- 0.9 vs 5.2 +/- 0.8 liters/min at 110 beats/min, 4.2 +/- 0.9 vs 5.1 +/- 0.9 liters/min at 140 beats/min; p less than 0.05) and LV end-diastolic volume (77 +/- 27 vs 93 +/- 29 ml at 110 beats/min, 54 +/- 17 vs 65 +/- 19 ml at 140 beats/min; p less than 0.05), an increase in left atrial pressure (28 +/- 3 vs 20 +/- 5 mm Hg at 110 beats/min, 30 +/- 4 vs 25 +/- 5 mm Hg at 140 beats/min; p less than 0.05), and a decrease in mitral valve area (1.2 +/- 0.4 vs 1.4 +/- 0.5 cm2 at 110 beats/min, 1.2 +/- 0.4 vs 1.4 +/- 0.4 cm2 at 140 beats/min; p less than 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.     

Left ventricular inotropic effect of atrial pacing after coronary artery bypass grafting

The effect of atrial pacing on left ventricular (LV) performance was studied in 19 patients, 24 hours after coronary artery bypass grafting (CABG). LV volumes were calculated from simultaneous radionuclide-thermodilution measurements at rest (heart rate 82 +/- 12 beats/min), 10 minutes after the start of atrial pacing (100 beats/min), and with atrial pacing plus volume loading to return preload toward baseline. Atrial pacing reduced preload as reflected by LV end-diastolic volume index (69 +/- 14 vs 60 +/- 14 ml/m2, mean +/- standard deviation) (p less than 0.0001), but returned to baseline with volume loading. Afterload, as reflected by arterial end-systolic pressure, did not change with atrial pacing (63 +/- 9 at baseline vs 64 +/- 8 mm Hg with pacing, difference not significant). Afterload increased with volume loading (68 +/- 10 mm Hg, p less than 0.025 vs baseline and pacing). LV stroke volume decreased with atrial pacing due to reduced preload, but returned to baseline with volume loading. Cardiac index increased with atrial pacing and increased further with volume loading. Compared with baseline, LV end-systolic volume index was reduced during atrial pacing both before and after volume loading, despite unchanged or augmented afterload. The combination of atrial pacing and volume loading resulted in augmentation of LV stroke work, despite no increase in preload compared with baseline. Thus, after CABG, increased (paced) heart rate augments inotropic state, as indicated by reduced LV end-systolic volume under conditions of unchanged or increased afterload, and elevated LV stroke work without an increase in preload or a decrease in afterload.     

Accuracy of biplane axial oblique and oblique cineangiographic left ventricular cast volume determinations using a modification of Simpson''s rule algorithm

In order to compare biplane left ventricular cast volume determinations from orthogonal and nonorthogonal axial oblique and standard orthogonal oblique cineangiograms to those that were obtained by water (H2O) displacement, we evaluated 14 human heart specimens in the following projections: 30-degree right anterior oblique and 60-degree left anterior oblique/20-degree cranial (LVa), 45-degree left posterior oblique and 60-degree left anterior oblique/30-degree cranial (LVb), and 30-degree right anterior oblique and 60-degree left anterior oblique (LVc). The correlation coefficients and standard errors of the estimate (SEEs) for the biplane orthogonal and nonorthogonal axial oblique (LVa and LVb, respectively) and standard orthogonal oblique (LVc) cineangiographic left ventricular volume determinations compared with the left ventricular cast volumes obtained by H2O displacement were similar (each r = 0.99 with SEEs = 5 to 7 milliliters (ml)). However, the mean biplane cineangiographic cast volume of 69 +/- 43 ml (SD) by LVa exceeded the average left ventricular cast volume of 60 +/- 35 ml by H2O displacement (p less than 0.01), while the average left ventricular cast volumes obtained with LVb and LVc (63 +/- 35, and 60 +/- 34 ml, respectively) did not differ significantly from the mean left ventricular cast volume obtained by H2O displacement. We concluded that the biplane orthogonal and nonorthogonal axial oblique cineangiographic views of the left ventricle, which have been reported to improve the delineation of cardiac anatomy, left ventricular regional wall motion, and the assessment of mitral regurgitation, also provide accurate determinations of left ventricular volume that are similar to those calculated from standard biplane orthogonal oblique cineangiograms.     

Pattern of left ventricular diastolic filling associated with right ventricular enlargement

Right ventricular (RV) dilatation associated with pressure overload may alter left ventricular (LV) geometry resulting in abnormal diastolic function as demonstrated by a smaller LV diastolic volume for a given LV diastolic pressure. To determine whether abnormalities in LV geometry due to RV dilatation result in abnormalities in the LV diastolic filling pattern, we obtained pulsed Doppler transmitral recordings from 23 patients with RV dilatation with RV systolic pressure estimated to be less than 40 mm Hg (group 1), 18 patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg (group 2) and 33 normal patients. RV systolic pressures were estimated from continuous wave Doppler peak tricuspid regurgitation velocities using the modified Bernoulli equation. Diastolic filling parameters in group 1 patients were similar to normals. In group 2 patient, increased peak atrial filling velocity (76 +/- 14 vs 57 +/- 12 cm/s, p less than 0.001), decreased peak rapid filling velocity/peak atrial filling velocity (1.1 +/- 0.4 vs 1.5 +/- 0.4, p less than 0.01), increased atrial filling fraction (41 +/- 14 vs 30 +/- 10%, p less than 0.01) and prolongation of the atrial filling period (171 +/- 47 vs 152 +/- 39 ms, p less than 0.05) were noted compared with the normal group. RV end-diastolic size and LV end-systolic shape were significantly correlated with the atrial filling fraction in group 2 patients. In patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg, there is increased reliance on atrial systolic contribution to the LV filling volume.     

Left atrial function in acute transient left ventricular ischemia produced during percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery

Left atrial (LA) function was studied in 32 patients during percutaneous transluminal coronary angioplasty of the proximal left anterior descending artery with a dual micromanometer positioned transseptally in the left atrium and in the left ventricle. In 10 patients LA and left ventricular (LV) cineangiography was performed 30 minutes before percutaneous transluminal coronary angioplasty and 30 seconds after the occlusion of the left anterior descending coronary artery. Thirty seconds after left anterior descending occlusion, LV peak systolic pressure decreased from 135 +/- 12 to 106 +/- 9 mm Hg (p less than 0.05) and LV maximum dP/dt decreased from 1,634 +/- 136 to 1,137 +/- 127 mm Hg/s (p less than 0.01). Simultaneously, LA mean pressure increased from 11 +/- 2 to 29 +/- 1 mm Hg (p 177 +/- 13 to 381 +/- 21 mm Hg (p less than 0.001). There was a difference between LV end-diastolic pressure and LA mean pressure of 1.5 mm Hg at rest and 7.8 mm Hg during ischemia and LA pulse pressure increased from 16 +/- 3 to 26 +/- 3 mm Hg (p less than 0.05) together with increase of LA A and V waves peak pressure. LV stroke volume index decreased from 46 +/- 5 to 43 +/- 3 ml/m2 (difference not significant). The LA maximal volume increased from 18 +/- 2 to 29 +/- 3 ml/m2 (p less than 0.001). LA volume before LA contraction increased from 29 +/- 2 to 54 +/- 3 ml/m2 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation of optimal lead positioning as defined by three-dimensional echocardiography to long-term benefit of cardiac resynchronization

We sought to define the impact of echocardiographically defined left ventricular (LV) lead position on the efficacy of cardiac resynchronization therapy (CRT) in a serial study using 3-dimensional echocardiography. Fifty-eight consecutive patients (53+/-9 years of age; 37 men) with heart failure were included in the study. Echocardiograms were obtained before CRT, within 7 days after implantation, and at 12+/-2 months of follow-up using a 3-dimensional digital ultrasound scanner (iE33, Philips, Andover, Massachusetts). Analysis of the temporal course of contraction in 16 LV segments was performed offline using a semiautomatic contour tracing software (LV Analysis, TomTec, Unterschleissheim, Germany). Based on the resulting volume/time curves the segment with the latest minimum of systolic volume in each patient was identified preoperatively (segment A). In addition, the temporal difference between the pre- and postoperative (within 7 days) minimum of systolic volume was determined for each segment. The segment with the longest temporal difference was defined to show the greatest effect of CRT. Location of the LV lead tip was assumed to be within this segment (segment B). LV lead position was defined as optimal when segments A and B were equal and as nonoptimal when they were far from each other. Using this definition, 26 patients had a nonoptimal and 32 patients an optimal LV lead position. Before CRT ejection fraction (32+/-4% vs 31+/-6%), LV end-systolic and end-diastolic volumes (242+/-92 vs 246+/-88 ml, 315+/-82 vs 323+/-90 ml), and peak oxygen consumption (14.3+/-1.4 vs 14.6+/-1.5 ml/min/kg) were equal in the 2 groups. At 12+/-2 months of follow-up, patients with an assumed optimal LV lead position showed greater increases of ejection fraction (10+/-2% vs 6+/-3%) and peak oxygen consumption (2.4+/-0.3 vs 1.5+/-0.4 ml/min/kg) and greater decreases of LV end-systolic (32+/-7 vs 21+/-5 ml) and end-diastolic (20+/-7 vs 13+/-6 ml) volumes. In conclusion, correspondence of the segment with the latest preoperative LV contraction with the segment with the greatest effect based on CRT results in a significantly greater benefit of ejection fraction and peak oxygen consumption and a greater improvement in LV remodeling. Thus, there is an optimal LV lead position that should be obtained.     

Relation of aneurysmectomy in patients with advanced left ventricular remodeling to postoperative left ventricular filling pressure, redilatation with ischemic mitral regurgitation

Left ventricular (LV) volume, mitral E deceleration time, and mitral regurgitation (MR) fraction were measured by echocardiography in 14 patients with surgical LV aneurysmectomy. Late MR developed 3 to 6 months after surgery in 5 of the 14 patients (36%). Compared with patients without late MR, those with late MR had a significantly greater preoperative LV end-diastolic volume index (LVEDVI) (134 +/- 21 vs 93 +/- 19 ml/m(2), p <0.01), surgical reduction in LVEDVI (-51 +/- 14 vs -20 +/- 16 ml/m(2), p <0.01), early postoperative LV diastolic dysfunction with shortened mitral E deceleration time (106 +/- 23 vs 141 +/- 24 ms, p <0.01), and a late postoperative reincrease in LVEDVI (+28 +/- 4 vs +3 +/- 8 ml/m(2), p <0.01), suggesting that surgical LV aneurysmectomy in patients with advanced preoperative LV remodeling may result in postoperative LV diastolic dysfunction, promoting later LV redilation with ischemic MR.     

Estimation of left ventricular function in right ventricular volume and pressure overload. Detection of early left ventricular dysfunction by Tei index.

Although the effects of right ventricular (RV) volume and pressure overload (RVVO and RVPO) on ventricular septal motion are different, the differential effect on left ventricular (LV) function is still controversial. The Doppler-derived index (Tei index) combining systolic and diastolic ventricular function, defined as the sum of isovolumetric contraction time (ICT) and isovolumetric relaxation time (IRT) divided by ejection time (ET), has been demonstrated to be a useful index to estimate LV function and to predict the prognosis of patients with congestive heart failure. This study was designed to evaluate the differential effects of RVVO and RVPO on LV function using the Tei index. Study patients consisted of 26 age-matched normal subjects, 22 patients with atrial septal defect (ASD) with normal or borderline RV pressure and 25 with primary pulmonary hypertension (PPH). All subjects had normal LV ejection fractions measured with 2-dimensional echocardiogram using biplane Simpson's method (61 +/- 4 vs 61 +/- 4 vs 63 +/- 8%, normal vs ASD vs PPH). Tei index was easily obtained in all subjects from transthoracic Doppler echocardiogram of LV inflow and outflow. Patients with ASD had normal ICT, IRT and ET, resulting in normal Tei index, however, patients with PPH had significantly prolonged ICT and IRT with shortened ET, resulting in a significant increase in Tei index (0.38 +/- 0.04 vs 0.36 +/- 0.03 vs 0.61 +/- 0.22, p < 0.001). Although RVVO due to ASD has no significant effects on LV function, RVPO due to PPH can adversely affect LV function. The Tei index is a simple and sensitive measure to assess LV function caused by RVVO or RVPO.     

Left ventricular emptying dynamics in patients with asymmetric septal hypertrophy and concentric hypertrophic cardiomyopathy

We studied the dynamics of left ventricular (LV) emptying in 8 patients with asymmetric septal hypertrophy (ASH), 6 patients with concentric hypertrophic cardiomyopathy (CHC), and 6 normal controls. Four patients with ASH had resting systolic gradients >20 mmHg, all had significant post premature ventricular contraction (PVC) systolic pressure gradients. LV volume (V) was obtained by frame-by-frame analysis of cineangiograms. End-diastolic volume was similar for all groups; end-systolic volume was significantly less in ASH and CHC patients than in normals. Maximum dV/dt was similar in ASH and CHC, and significantly greater than normals. Total systolic contraction time (SCT), i.e., time from peak volume to last cine frame at minimum volume, was similar for all groups, but the time required to eject 90% of stroke volume (90%T), as a fraction of SCT, was shorter for ASH (0.52±0.07) and CHC patients (0.51 ±0.05) than normals (0.67±0.07) (p < 0.05 vs myopathy groups). In the sinus beat following a PVC, however, this ratio decreased significantly in normals and CHC patients, but did not change in ASH patients. We conclude that ASH and CHC have similar exaggerated systolic LV ejection dynamics in the basal state; the failure of ASH patients with post-PVC systolic outflow gradient to reduce 90% T/SCT post PVC may reflect obstruction to LV emptying.     

Influence of age on left atrial appendage function in patients with nonvalvular atrial fibrillation

BACKGROUND: Age is an independent risk factor for thromboembolism in nonvalvular atrial fibrillation (NVAF). An association between low left atrial appendage (LAA) Doppler velocities and thromboembolic risk in NVAF has been reported. Hypothesis: The study was undertaken to identify age-related differences in LAA function that may explain the higher thromboembolic rates in older patients with NVAF. METHODS: Forty-two consecutive patients (age 69+/-2 years [range 42-92], 24 [57%] men) with NVAF underwent transthoracic and transesophageal echocardiography. The following were compared in 22 patients younger and 20 older than 70 years: left ventricular (LV) diameter, mass and ejection fraction, left atrial (LA) diameter and volume, LAA area and volume, LAA peak emptying (PE) and peak filling (PF) velocities, presence and severity of spontaneous echo contrast (SEC) and mitral regurgitation (MR). RESULTS: Left atrial diameter (4.6+/-0.1 vs. 4.5+/-0.2 cm), LA volume (105+/-10 vs. 92+/-8 ml), LAA area (6.8+/-0.6 vs. 5.2+/-0.8 cm2), and LAA volume (5.6+/-0.9 vs. 3.9+/-1.0 ml) were similar (p>0.05) in both groups. Older patients had lower LAA PE (26+/-2 vs. 34+/-3 cm/s, p = 0.02) and PF (32+/-2 vs. 41+/-4 cm/s, p = 0.04) velocities, lower LV mass (175+/-13 vs. 234+/-21 gm, p = 0.02), higher relative wall thickness (0.52+/-0.02 vs. 0.43+/-0.03, p = 0.02), smaller LV diastolic diameter (4.3+/-0.1 vs. 5.2+/-0.2 cm, p < 0.001), and higher LV ejection fraction (62+/-2 vs. 55+/-2%, p = 0.025). Frequency and severity of SEC and MR were similar in both groups. Multivariate analysis identified older age as the only significant predictor of reduced LAA velocities. CONCLUSION: Compared with younger patients, older patients with NVAF have lower LAA velocities despite higher LV ejection fraction, smaller LV size, and similar LA and LAA volumes. These findings may explain the higher thromboembolic rates in older patients with NVAF.     

Topographic changes in the left ventricle after experimentally induced myocardial infarction in the rat

The factors that determine the thickness of transmural myocardial infarcts are unknown. Therefore, the relation between the size and thickness of transmural infarcts in 67 rats 21 days after occlusion of the left main coronary artery was studied. On examination of histologic sections, infarct size was determined by planimetry and expressed as a percentage of the left ventricular (LV) area, and thickness was expressed as a percentage of noninfarcted ventricular septal wall thickness. The circumferential length of the infarcted ventricle was measured in millimeters, as well as the circumferential length of the noninfarcted ventricular septum. Septal wall thickness was similar in rats with transmural infarcts and in sham-operated rats. No significant correlation was observed between infarct size and thickness (r = 0.10) or between circumferential length of the infarct and infarct thickness (r = 0.17). However, large (greater than or equal to 20% of the left ventricle, n = 37) and small (less than 20% of the left ventricle, n = 30) infarcts which were similarly thin (37 +/- 1% and 34 +/- 2% of septal wall thickness, respectively) affected LV topography differently. Large infarcts resulted in a 23% greater loss of myocardium (p less than 0.001), greater expansion of the LV cavity (18 +/- 9 mm2 compared with 14 +/- 1 mm2 in small infarcts, p less than 0.005), and lengthening of the septal wall (7.2 +/- 1.1 mm and 6.7 +/- 1.0 mm in large and small infarcts, respectively [p less than 0.05], and 6.3 +/- 0.1 mm in shams). Increase in cavity area and septal length in infarcted ventricles suggested a volume overload hypertrophy, which at 3 weeks was nonetheless inadequate to provide as much normal muscle as was present in sham-operated rats. In an additional 9 rats with subendocardial infarctions (involving less than 75% of the LV wall from endocardium to epicardium), the LV walls were thicker (94 +/- 5% of septal wall thickness, compared with 35 +/- 1% for transmural infarcts, p less than 0.001) and an inverse correlation was observed between infarct size and thickness. In conclusion, neither the size of a transmural infarct in rat nor the circumferential length of infarction determines the thickness of the infarct; however, infarct size does affect LV topography by increasing LV cavity area and the length of the noninfarcted septal wall. Subendocardial infarcts result in less myocardial thinning than do transmural infarcts.