Radionuclide determination of the relationship between left ventricular contractile state and ejection fraction

To determine whether the relationship between various measures of left ventricular (LV) contractile state and ejection fraction (EF) is linear in man, we studied 30 patients during right atrial pacing over a range of loading conditions. With the use of micromanometer LV pressures and radionuclide LV volumes, pressure-volume (P-V) loops were generated for each loading condition. Then isochronal, instantaneous P-V data points were obtained by linear regression analysis to attain the maximum slope (Emax) of these time-varying isochrones. Other measures of LV end systole were also used to calculate end-systolic P-V relations in a similar fashion, and indirect P-V relations were obtained from the linear regression analysis of brachial artery peak pressure vs minimum LV volume data points. When the slopes of these LV contractile measures were compared to the radionuclide LV EFs, the linear correlation coefficients ranged from 0.53 to 0.67. After natural log transformation of the LV contractile state and EF data, the correlation coefficients for the polynomial curve fits ranged from 0.80 to 0.88. When the correlation coefficients for the polynomial curve fits of the natural log transformed data were compared to those for the linear regression analyses of the raw data, significant improvements were evident (p less than 0.05). Thus the relationship between various measures of LV contractile state and EF obtained with radionuclide angiography is best approximated by a complex, curvilinear relationship that is due, in part, to the wide range of LV contractile states within the relatively narrow normal range of LV ejection fractions.     

The Relationship Between Aortic Stiffness and Left Ventricular Dyssynchrony in Hypertensive Patients with Preserved Left Ventricular Systolic Function

Left ventricular (LV) dyssynchrony is often seen in patients with hypertension, even without heart failure. Arterial stiffness is well accepted as an important factor of increasing blood pressure and influencing ventricular function. The purpose of this study was to determine the relationship between aortic stiffness and LV dyssynchrony in hypertensive patients with preserved LV systolic function. Eighty hypertensive patients with preserved LV systolic function (LV ejection fraction > 50%) and 30 controls were studied. The LV systolic and diastolic dyssynchrony indices were determined as the standard deviation of the time interval from onset of the QRS complex to peak myocardial systolic velocity (Ts-SD) and to early diastolic velocity (Te-SD) and the maximal differences in Ts (Ts-Max) and Te (Te-Max) in 12 LV segments. Aortic stiffness index was calculated from aortic diameters in the systolic and diastolic phases, as measured by echocardiography and blood pressure. No relationship was observed between LV systolic and diastolic dyssynchrony indices (r = 0.057, P = .61). In simple regression, aortic stiffness parameter was related to left ventricular mass index (LVMI), E/A ratio, and LV diastolic dyssynchrony index. But using multiple linear regression, Te-Max remained as a single variable related to aortic strain and aortic stiffness index (r = ?0.271, P = .008 and r = 0.269, P = .008). LVMI was related to aortic distensibility using multiple linear regression (r = ?0.239, P = .02). Aortic stiffness index was related to LV diastolic dyssynchrony index and LVMI. These findings suggest that LV diastolic dyssynchronous changes may be caused by increased LV mass and arterial stiffness.     

The relationship of various measures of end-systole to left ventricular maximum time-varying elastance in man

This investigation was designed to calculate left ventricular maximum time-varying elastance (Emax), to define the relationship between Emax and pressure-volume (P-V) relations at other, more easily defined measured of end-systole, and to determine whether these measures of left ventricular contractile function can be normalized in man. Accordingly, we studied 10 subjects with simultaneous high-fidelity micromanometer left ventricular and ascending aortic pressure recordings and biplane contrast cineangiograms at control conditions and during infusion of methoxamine and nitroprusside. Emax was defined as the maximum slope of the linear relation of isochronal, instantaneous P-V data points obtained from each of the three loading conditions. Left ventricular end-systole was also defined for each loading condition as: the time of the maximum P-V ratio (maxPV), minimum ventricular volume (minPV), (-)dP/dtmin [(-)dP/dtPV], and zero systolic flow approximated by the central aortic dicrotic notch (AodiPV). The mean heart rates and LV (+)dP/dtmax were insignificantly altered during the three loading conditions. Isochronal Emax ranged from 3.38 to 6.73 mm Hg/ml (mean 5.48 +/- 1.23 [SD] mm Hg/ml) and the volume-axis intercepts at zero pressure ranged from -2 to 51 ml (mean 18 +/- 16 ml). The isochronal slope calculations were reproducible (r = .97 to .99). The end-systolic P-V slope values for the maxPV, minPV, (-)dP/dtPV, and AodiPV relations correlated with isochronal Emax (r = .90, .88, .69, and .74, respectively). The average slope values for these end-systolic P-V relations, however, underestimated the mean Emax (p less than .01 to p less than .001). The mean extrapolated volume-axis intercepts for these end-systolic P-V relations also underestimated that for Emax. Finally, the isochronal Emax and other end-systolic P-V relation slope values demonstrated inverse linear relationships with left ventricular mass (r = -.68 to -.91, p less than .05 to p less than .001). Only the Emax volume-axis intercepts showed a linear relationship with left ventricular end-diastolic volume (r = .75). Thus we conclude that the time-varying elastic properties of the left ventricle can be calculated in man, that commonly used end-systolic P-V relations significantly underestimate isochronal Emax, and that normalization of isochronal Emax and other end-systolic P-V relation slope values might be performed in man with left ventricular mass; no obvious relationship between volume-axis intercepts and measures of left ventricular or body size was apparent.     

Passive properties of canine left ventricle: diastolic stiffness and restoring forces

Left ventricular (LV) diastolic pressure-volume (P-V) relations arise from a complex interplay of active decay of force (i.e., relaxation), passive elastic myocardial properties, and time-varying inflow across the mitral orifice. This study was designed to quantify the passive properties of the intact ventricle and the effects of elastic recoil by separating filling from relaxation with a method of LV volume clamping with a remote-controlled mitral valve. Eleven open-chest fentanyl-anesthetized dogs were instrumented with aortic and mitral flow probes, LV and left atrium micromanometers, and a remote-controlled mitral valve. We prevented complete (end-systolic volume clamping) or partial filling at different times in diastole. The ventricle thus relaxed completely at different volumes, and we generated P-V coordinates for the passive ventricle that included negative, as well as positive, values of pressure. We then estimated ventricular volumes from ventricular weight in eight dogs, using regression equations based on data in the literature, to determine the equilibrium volume (V0), that is, volume at zero transmural pressure, in the working ventricle. We abandoned the traditional exponential approach and characterized by the P-V relation with a logarithmic approach that included maximum LV volume (Vm), minimum volume (Vd), and stiffness parameters (Sp and Sn) for the positive (p) and negative (n) phases: Pp = -Sp In[(Vm - V)/(Vm - V0)] and Pn = Sn In[(V - Vd)/(V0 - Vd)]. With this formulation, the chamber compliance, dP/dV, is normalized by the LV operating volume, and Sp and Sn are size-independent chamber stiffness parameters with the units of stress. In eight ventricles with LV weight = 131 +/- 20 g, Vm = 116 +/- 18 ml, V0 = 37 +/- 6 ml, and Vd = 13 +/- 2 ml, stiffness Sp = 14.6 mm Hg and Sn = 5.1 mm Hg were determined from the slopes of the log-linearized equations. Also, the duration of LV relaxation is increased by the process of ventricular filling (161 +/- 31 msec, filling versus 108 +/- 36 msec, nonfilling, measured from dP/dtmin, p less than 0.0001). We conclude that volume clamping is a useful method of studying restoring forces and that the logarithmic approach is conceptually and quantitatively useful in characterizing the passive properties of the intact ventricle.     

Assessment of interaction between the left and right ventricles using pressure-volume loops in various heart diseases

To assess the interaction and interdependence of left and right ventricular function, ECG-gated radionuclide angiocardiography was performed immediately after cardiac catheterization during right atrial pacing for 11 patients with old myocardial infarction (MI), two with non-obstructive hypertrophic cardiomyopathy, one with aortic stenosis (AS), two with pulmonary infarction (PI), and one with neurocirculatory asthenia (NCA). Absolute left ventricular (LV) volume curves were obtained by the count-based method with attenuation factor corrections. Biventricular pressure and volume curves were digitized and synchronized to end-diastole, and pressure-volume (P-V) loops were constructed throughout a cardiac cycle. The stroke work index (SWI), the work index per min (WI/M) and the contractility index (CNTI) were calculated from the P-V loops. In a patient with NCA, LV end-diastolic volume decreased during rapid pacing, but no significant change in the LV end-systolic P-V relation was recognized. However, the entire right ventricular (RV) P-V loop was shifted toward the left during rapid pacing. In a patient with AS, the LV P-V loop was markedly enlarged and every parameter of LV function was much greater than that of the right ventricle due to increased LV afterload. The areas of RV P-V loops in two patients with PI were larger than those of other patients, because RV pressure was relatively high, and RV volume was increased. It is suggested that RV pressure and volume overloads prevail in patients with PI. In four MI patients with three vessel disease and having collateral circulation, the LV end-systolic P-V relationship was shifted toward the lower right, and every parameter (SWI, WI/M, CNTI) of LV function decreased by rapid pacing. Myocardial ischemia may be induced by rapid pacing stress, causing decreased LV contractility. It was concluded that the P-V loops obtained by RNA and catheterization are clinically useful for estimating the interaction and interdependence between right and left ventricular hemodynamics.     

Cardiac consequences of prolonged exposure to an isolated increase in aortic stiffness.

In elderly patients, aortic stiffness is a major determinant of increased end-systolic stress leading to left ventricular (LV) hypertrophy with impaired cardiac performance. However, in a rat model of aortic elastocalcinosis (induced by vitamin D(3)-nicotine [VDN] treatment), brief exposure (1 month) to increased aortic stiffness modified neither cardiac function nor cardiac structure. Here we report the impact of longer exposure (3 months) to aortic stiffness. Three months after induction of aortic stiffness, aortic characteristic impedance was measured in awake rats, 8 control and 10 VDN. Stroke volume was measured (electromagnetic probe) at baseline and after acute volume overload. LV weight/body weight ratio, collagen, and myosin heavy chain (MHC) contents were determined. Although aortic characteristic impedance increased (controls, 32+/-2; VDN rats, 50+/-8 10(3) dyne. s/cm(5); P=0.0248), stroke volume was maintained in VDN rats at baseline (controls, 223+/-18; VDN, 211+/-13 microL) and after volume overload (controls, 378+/-14; VDN, 338+/-15 microL). However, LV weight/body weight ratio (controls, 1.54+/-0.07; VDN, 1.73+/-0.05 g/kg; P=0.0397) and LV collagen content (controls, 31+/-4; VDN, 52+/-4 microgram/g dry wt; P=0.0192) increased. A shift from alpha-MHC (controls, 82+/-2%; VDN, 69+/-3%; P=0.0056) to beta-MHC (controls, 18+/-2%; VDN, 31+/-3%; P=0. 0056) was also observed. Three months' exposure to increased aortic stiffness in VDN rats induced LV hypertrophy with moderate interstitial fibrosis and a shift in the MHC-isoform pattern. Such structural adaptation maintains LV performance.     

Mitral valve compensation for annular dilatation: in vitro study into the mechanisms of functional mitral regurgitation with an adjustable annulus model.

BACKGROUND AND AIM OF THE STUDY: Mitral annulus dilatation has been identified as an important factor in functional mitral regurgitation (FMR). However, the pathophysiologic interaction of annular dilatation and papillary muscle (PM) displacement in FMR, which occurs clinically in left ventricular (LV) dilatation, is still not well understood. It is difficult to separate these competing factors in vivo, leading to confusion in identifying the real role of the annular dilatation in FMR and its interaction with PM displacement. METHODS: To better understand the competing factors, an in vitro model was developed with a D-shaped adjustable mitral annulus that could be changed from 5.5 cm2 to 13.0 cm2 during experiments, independent of varying PM positions. Six excised normal porcine mitral valves were mounted in a left ventricular model with the adjustable annulus device and tested in a physiologic pulsatile flow system under normal cardiac output and left ventricular pressure (5.0 l/min, 120 mmHg). Papillary muscles were placed in normal and then displaced to an apical posterolateral position, to simulate pathological conditions seen clinically. Regurgitation was measured directly by a flow probe and the mitral valve geometry and leaflet coaptation were recorded by video camera through the model's atrium window. In addition, 2D echocardiography was used to evaluate leaflet coaptation and color Doppler flow mapping to detect the regurgitant flow field. RESULTS: The results showed that in normal PM position, the mitral regurgitant was consistently at low level until the annulus was enlarged to 1.75 times the normal size, at which time it increased sharply. Papillary muscle apical posterolateral displacement, which simulates a dilated LV, caused regurgitation to occur earlier (1.5 times the normal annulus size), and had an increased regurgitant volume (p < 0.05). The leaflet gaps were first observed at the commissural areas of the valves, consistent with the location of regurgitant jets detected by color Doppler flow mapping. Asymmetric PM displacement created more regurgitation than both the symmetric PM tethering (p = 0.063) and normal PM position (p < 0.01). The regurgitant jets were observed at the same commissural side as the PM displacement, even without significant enlargement of the annulus. CONCLUSIONS: This in vitro study provides insight into the interaction between annular dilatation and PM displacement on FMR. The resulting effects and their overall similarity to clinical observation could help further understand the mechanism of FMR and provide additional information to improve future therapeutic strategies.     

Reduced Bone Mineral Density in Hypertensive Patients Is Associated with Left Ventricular Diastolic Dysfunction,Not Left Ventricular Hypertrophy

Left ventricular (LV) hypertrophy and diastolic dysfunction are commonly observed in hypertensive patients, and have been demonstrated to be risk factors of chronic heart failure due to LV diastolic dysfunction. Recently, reduced bone mineral density has been found in hypertensive patients compared with healthy controls. However, relationships between bone mineral density and LV hypertrophy and diastolic dysfunction have not been fully assessed. We examined relationships between bone mineral density and both LV hypertrophy and diastolic dysfunction in 38 hypertensive patients (23 males, 15 females; mean age 71 ± 8 y) who had been treated with antihypertensive drugs for at least 1 year. The bone mineral density of the calcaneus was measured with a quantitative ultrasound measurement device (A-1000 EXPRESS/InSight, GE Healthcare, Horten, Norway), and the stiffness index was determined as a parameter of bone mineral density. Echocardiography was performed to measure the left ventricular mass index as a parameter of LV hypertrophy. Left ventricular diastolic dysfunction was also assessed by early diastolic mitral annular velocity (e′), and the ratio of early transmitral flow velocity (E) to e′ (E/e′). The bone mineral density did not correlate with left ventricular mass index, but did correlate with e′ (r = 0.453, P < .01) and E/e′ (r = ?0.359, P < .05). Thus, reduced bone mineral density in hypertensive patients is not associated with LV hypertrophy but with LV diastolic dysfunction. Hypertensive patients with reduced bone mineral density may have a high risk of chronic heart failure due to LV diastolic dysfunction as well as bone fractures due to osteoporosis.     

Independent and incremental prognostic value of early mitral annulus velocity in patients with impaired left ventricular systolic function

OBJECTIVES: This study sought to investigate the incremental prognostic value of non-invasive measures of early myocardial relaxation and left ventricular diastolic pressure (LVDP) in patients with impaired left ventricular (LV) systolic function. BACKGROUND: The early diastolic mitral annulus velocity (Em) reflects myocardial relaxation, and the combined ratio of the early transmitral flow velocity (E) to Em (E/Em) >15 correlates well with elevated mean LVDP. It is unknown if these new indexes will predict poorer survival in patients with LV systolic dysfunction. METHODS: Echocardiograms were prospectively obtained in 182 patients with impaired LV systolic function, defined as an LV ejection fraction <0.50. The end point was cardiac mortality. The majority of this patient sample (80%) has been reported on in a previous publication. RESULTS: After a median 48 months' follow-up, Em emerged as an independent predictor of survival (hazard ratio 0.61, 95% confidence interval 0.45 to 0.82). An Em <3 cm/s was associated with a significantly excess mortality (log-rank statistic 9.36, p = 0.002), and this measurement added incremental prognostic value to standard indexes of systolic or diastolic function, including a deceleration time <140 ms and an E/Em >15 (p = 0.038). CONCLUSIONS: Early diastolic mitral annulus velocity is a powerful predictor of cardiac mortality in patients with LV systolic impairment; Em <3 cm/s emerged as the best prognosticator in long-term follow-up, incremental to other clinical or echocardiographic variables, including the ratio E/Em.     

Effect of Left Ventricular Function on Long-Term Left Ventricular Pacing and Sensing Threshold

Background: The effect of left ventricular (LV) systolic function on the long-term left ventricular pacing and sensing threshold is unclear. Methods and Results: We studied the effect of LV ejection fraction (LVEF) on the LV pacing and sensing threshold in 56 patients (mean age: 70.2 ± 10.5 years) underwent permanent LV pacing using a self-retaining coronary sinus lead (Model 1055 K, St Jude Medical, USA). In 49 patients, the LV lead was implanted for conventional pacemaker indication (sick sinus syndrome = 14, heart block = 26 or slow atrial fibrillation = 9). The remaining 7 patients were implanted for congestive heart failure. The LV pacing and sensing threshold, and lead impedance were compared between patients with LVEF <40% (Group 1, n = 28) and LVEF >40% (Group 2, n = 28) during implant and at 3-month follow up. The LV pacing lead was successfully implanted in all patients without any lead dislodgement on follow-up. At implant, Group 1 patients had a significant lower R wave amplitude, but similar LV pacing threshold and lead impedance as compared to Group 2. However, at 3-month follow-up, Group 1 patients had a significantly higher LV pacing threshold compared to Group 2 patients. There were no significant differences in the sensing threshold and lead impedance between the two groups. Furthermore, there was also a significant interval increase in LV pacing threshold in Group 1 patients (0.94 ± 0.12 V) after 3 months, but not in Group 2 patients (0.16 ± 0.08 V, p < 0.01). Conclusions: The results of this study suggest that the LV systolic function has a significant impact on the long-term LV pacing threshold. The long-term left ventricular pacing threshold in patients with left ventricular systolic dysfunction increased after implant and was higher than patients with normal left ventricular systolic function.     

Ventricular long-axis contraction as an earlier predictor of outcome in asymptomatic aortic regurgitation

The long-term prognostic significance of left ventricular (LV) long-axis contraction was investigated prospectively in 65 consecutive patients aged 58+/-15 years with asymptomatic aortic regurgitation, normal LV ejection fraction at rest, and no coronary artery or aortic root disease. A complete transthoracic echocardiographic study was performed at baseline and 12 months later. In 24 of 65 patients with peak systolic wave velocity at the lateral mitral annulus (LatS)<9 cm/s, LV diameter (p<0.01), volume (por=9 cm/s, none of these parameters was significantly affected during follow-up. Aortic valve replacement was performed in 6 of 24 patients (25%) with peak systolic wave velocity at the lateral mitral annulus<9 cm/s and none with peak systolic wave velocity at the lateral mitral annulus>or=9 cm/s. In patients with peak systolic wave velocity at the lateral mitral annulus<9 cm/s, a cut-off value of 6.25 cm/s predicted aortic valve replacement within the next year with 97% sensitivity and 83% specificity. In conclusion, ventricular long-axis contraction seems to be a reliable indicator for outcome prediction in patients with asymptomatic aortic regurgitation.     

心肌梗死大鼠左心室收缩与舒张功能的改变及其影响因素

目的 探讨心肌梗死大鼠左心室收缩和舒张功能的改变、以及心室重构对心室舒缩功能的影响.材料和方法结扎Wistar大鼠左冠状动脉、制成心肌梗死模型,6周后测定左室心肌力学指标,心肌胶原含量、血浆及心肌的血管紧张素Ⅱ(Aug Ⅱ)浓度.结果 心肌梗死组与对照组比较,LVPSP、+dp/dt_(max)、dp/dt_(max)绝对值及V_(max)明显降低(P<0.01),LVEDP增加(P<0.01),T值延长(P<0.01),MAP无差异.心肌梗死组与对照组比较、心肌羟脯氨酸和心肌胶原含量明显增高(P均0.01),心肌AngⅡ含量明显升高(P<0.01)、血浆AngⅡ浓度无显著差异.结论 心肌梗死后左室收缩与舒张　功能明显降低,同时出现心肌细胞的肥大和纤维细胞的增生以及间质纤维化、后者可进一步导致和加重心脏泵血功能的异常.     

Cardiovascular Effects of the Converting Enzyme Inhibitor Ramipril (HOE 498) In Anesthetized Dogs with Acute Ischemic Left Ventricular Failure

The non-sulfhydryl converting enzyme inhibitor Ramipril (HOE 498) is characterized by long lasting antihypertensive activity in man. To examine its cardiovascular potential in heart failure, ramipril was administered during acute ischemic left ventricular failure in pentobarbital anesthetized dogs, induced by repeated injections of plastic microspheres into the left main coronary artery.

Repeated embolizations produced stable left ventricular (LV) pump failure characterized by LV enddiastolic pressure of 22 mmHg, reductions in LV dp/dt max and cardiac output. Blood pressure and heart rate were not changed while total peripheral resistance increased. After a stabilization period ramipril was administered in two doses at 30 or 100 μg/kg as an intravenous bolus followed by continuous infusion of 3 or 10 μg/kg/min for 150 min. Ramipril in the lower dose decreased LV enddiastolic pressure by 8 mmHg, mean pulmonary artery pressure by 4 mmHg, systemic blood pressure by 40 mmHg and total peripheral resistance by 1280 dyn × sec × cm^?5. LV dp/dt max, heart rate and cardiac output remained unchanged during ramipril administration. More pronounced effects were obtained with the higher dose.

In conclusion, the improvements of hemodynamics produced by ramipril during acute ischemic left ventricular failure in anesthetized dogs are best explained by a reduction in both preload and afterload.     

Acute Effects of Single‐site Pacing from the Left and Right Ventricle on Ventricular Function and Ventricular–Ventricular Interactions in Children with Normal Hearts

Objective. We studied, as a physiological benchmark, acute effects of right ventricular (RV) apical, RV outflow, and left ventricular (LV) pacing in children with normal cardiac function on LV and RV function and ventricular–ventricular interactions. Design. The design of the study was a prospective, acute intervention. Setting. The study was conducted in a tertiary care electrophysiology laboratory. Population and Methods. Seven children (mean ± SD, 12 ± 4 years) were paced after accessory pathway ablation, at baseline (AOO), and with atrioventricular pacing (DOO) from the RV apex, RV outflow, and left ventricle. Outcome Measures. Right ventricular dP/dT_max and RV dP/dT_neg (high‐fidelity transducer‐tipped catheters, Millar Instruments, Houston, TX, USA), cardiac index (Fick), blood pressure, and QRS duration were measured at each pacing condition. Intra‐ and interventricular mechanical dyssynchrony, systolic‐ and diastolic peak tissue velocities, and isovolumic acceleration were recorded by tissue Doppler imaging at the lateral mitral, septal, and tricuspid annuli at each condition. Results at each pacing condition were compared by repeated‐measures analysis of variance. Results. Pacing prolonged QRS duration, causing electrical dyssynchrony (86 ± 19 ms [baseline], 141 ± 44 ms [RV apex], 121 ± 18 ms [RV outflow], and 136 ± 34 ms [LV], P < .01). Right ventricular outflow pacing caused LV intraventricular delay (63 ± 52 vs. 12 ± 7 ms, P < .05). Right ventricular apical pacing caused interventricular delay (61 ± 29 vs. 25 ± 18 ms, P < .05). There were no significant changes in blood pressure, cardiac index, RV dp/dT_max, RV dP/dT_neg, regional tissue velocities, or isovolumic acceleration during any of the pacing conditions, indicating preserved ventricular function and hemodynamics. No important ventricular–ventricular interactions were seen. Conclusions. In children with normal cardiac anatomy and function, single‐site RV apical, RV outflow, and LV pacing induce electromechanical dyssynchrony without significantly changing ventricular function or hemodynamics, or adversely affecting ventricular–ventricular interactions.     

Tissue Doppler imaging provides incremental prognostic value in patients with systemic hypertension and left ventricular hypertrophy

OBJECTIVES: We sought to determine the prognostic value of left ventricular (LV) mitral annular velocities measured by tissue Doppler imaging (TDI) in hypertensive patients with echocardiographic evidence of LV hypertrophy. BACKGROUND: Echo LV hypertrophy and LV geometry provide additional predictive value of all-cause mortality beyond traditional cardiovascular risk factors. Limited data exist regarding the predictive value of TDI velocities for cardiovascular risk stratification in treated hypertensive patients. METHODS: Two-dimensional and Doppler echocardiograms were obtained in 252 consecutive subjects, including 174 subjects with systemic hypertension and 78 age-matched normal subjects. The end point was cardiac death in subsequent median follow-up of 19 months. RESULTS: Nineteen patients (7.54%) died of cardiac causes. The TDI mitral annulus systolic velocity and the early diastolic mitral annular velocity (Em) were significantly lower in the non-survivors (all P < 0.001). The pseudonormal (PN) or restrictive filling pattern (RFP) was associated with cardiac mortality. The other parameters associated with cardiac mortality were LV ejection fraction, LV mass index, inter-ventricular septal wall thickness in diastole and the ratio of early mitral inflow to early myocardial velocity. In multivariate analysis, Em, inter-ventricular septal wall thickness in diastole and either PN or RFP were the strongest predictors. The addition of Em < 3.5 cm/s significantly improved the outcome of a model that contained clinical risk factors, inter-ventricular septal wall thickness in diastole > 1.4 cm and either PN or RFP (P = 0.043). CONCLUSIONS: Early diastolic mitral annulus velocity measured by TDI provides prognostic information, incremental to clinical data and standard echocardiographic variables, for risk stratification of hypertensive patients under treatment.     

Left Ventricular Assist Device Implantation Combined with Surgical Ventricular Reconstruction

Nine months after sustaining a transmural anteroseptal myocardial infarction, a 45-year-old man presented with ischemic heart disease, severe mitral valve insufficiency, New York Heart Association functional class IV congestive heart failure, and a left ventricular aneurysm. Coronary angiography revealed 3-vessel disease. Echocardiography showed severe left ventricular impairment, pronounced thrombosis in the left ventricular apex, and low myocardial reserve. To reduce the high risk of performing left ventricular and mitral valve reconstruction concurrently with revascularization, we decided to perform ventricular reconstruction and to implant a Berlin Heart INCOR left ventricular assist device as a bridge to heart transplantation. The patient had an uncomplicated recovery, was discharged from the hospital with symptomatic improvement after 20 days, and was placed on the list for heart transplantation. We describe the patient''s case, the surgical procedure, and the reasoning behind the chosen course of treatment.Key words: Cardiac surgical procedures/methods, cardiac volume/physiology, heart aneurysm/surgery, heart failure/complications, heart-assist devices, prosthesis implantation/methods, reconstructive surgical procedures, treatment outcome, ventricular dysfunction, left/surgeryLeft ventricular (LV) reconstructive surgery is one method of treatment for patients who have ischemic heart disease with LV aneurysm and concomitant congestive heart failure.^1–3 However, preoperative deterioration of hemodynamic status is associated with high risk in such patients, who are candidates for heart transplantation. We present the case of a man who underwent LV reconstructive surgery combined with LV bypass with use of the Berlin Heart INCOR® LV assist device (LVAD) (Berlin Heart GmbH; Berlin, Germany).     

Specific tissue Doppler predictors of preserved systolic and diastolic left ventricular function after an acute anterior myocardial infarction

The degree of left ventricular (LV) dysfunction determines the outcome of patients suffering an acute anterior myocardial infarction (AAMI). Many recent studies have utilized tissue Doppler echocardiography (TDE) parameters in the assessment of LV function. We sought to investigate whether some variables easily obtained from TDE profiles of mitral annulus corners would predict a relatively preserved LV global function traditionally assessed with ejection fraction (EF) and deceleration time (DT), within the acute phase of AAMI. Included were 50 consecutive patients with a first AAMI. Standard echocardiography and TDE of mitral annulus were performed within 36 hours of admission. Pulsed wave sample volumes were set at the septal, lateral, anterior, and inferior corners of the mitral annulus. Preserved LV function was defined as an EF > 40% together with a DT > or = 140 ms and < 220 ms. An inferior annular systolic velocity of > 7.5 cm/s predicts preserved global left ventricular function with a sensitivity of 81% and specificity of 71%. An anterior mitral annular early diastolic velocity of > 8cm/s had a sensitivity of 69% and specificity of 85%. When these two velocities both exceed the limits above, such a combined index yielded a sensitivity of 69%, specificity of 94%, and an overall diagnostic accuracy of 86% for the estimation of preserved LV global function. The parameters derived from TDE profiles of inferior and anterior mitral annulus comers provide valuable information to predict preserved global left ventricular function during the early period of AAMI.     

Electrical Delay in Apically Positioned Left Ventricular Leads and Clinical Outcome After Cardiac Resynchronization Therapy

Electrical Delay in Apically Positioned LV Leads. Introduction: In recent studies, an anatomical apical left ventricular (LV) lead pacing location has been associated with deleterious outcome after cardiac resynchronization therapy (CRT). The differential impact of the LV lead electrical location in these patients remains unknown. Methods and Results: Thirty‐one consecutive CRT patients (mean age 71.7 ± 12.7 years, 55% left bundle‐branch block [LBBB] morphology) with an apical LV lead and LV lead electrical delay (LVLED) were studied. Anatomical LV lead location was determined via review of coronary venography and chest radiographs. Electrical location was assessed through intraprocedural LVLED measurement. Patients were dichotomized into either “long” LVLED (LVLED ≥ 50% of QRS) or “short” LVLED groups (LVLED < 50%). Patients in the long LVLED group demonstrated significantly greater freedom from a primary composite endpoint of all‐cause death, heart failure hospitalization, and cardiac transplantation at 2 years (81% vs 30%, P = 0.007 vs short LVLED patients). Longer LVLED was also associated with more favorable LV remodeling (LV end‐systolic volume –41.9 ± 10.3 mL vs –4.3 ± 17.2 mL; P = 0.05), and greater improvement in LV ejection fraction (+9.4 ± 2.9% vs +2.3 ± 7.5%; P = 0.04). Even after multivariate adjustment, LVLED remained an independent predictor of the primary composite endpoint (HR 0.47, P = 0.031). Conclusions: Electrical lead localization, as estimated by LVLED ≥ 50%, is associated with improved long‐term clinical outcome and measures of LV remodeling in patients with apical LV leads. Intraprocedural LVLED assessment may provide incremental utility in targeting lead placement even in conventionally unfavorable anatomical segments. (J Cardiovasc Electrophysiol, Vol. 24, pp. 182‐187, February 2013)     

Impaired Left Ventricular Filling in Young Female Diabetics

ABSTRACT To assess left ventricular (LV) function in diabetes mellitus, M-mode echocardiograms were recorded in 36 insulin-treated diabetic women, mean age 25±6 (SD) years, and 13 healthy women of the same age. Echocardiographic tracings of the septum and LV posterior wall were digitized and continuous plots were made of LV dimension and its rate of change. The pattern of LV filling was abnormal in 19 diabetics, when the mean value ±2 SD in the healthy women was taken as the normal range of the indices. The most common abnormality was a prolonged rapid filling period. The LV systolic function was normal in all diabetics. Diabetics with severe microvascular complications had thicker LV walls (p<0.05) and smaller LV end-diastolic diameters and stroke volumes (p<0.01) than the healthy women. The electrocardiographic voltage was lower in the diabetic group (p<0.05). These studies suggest that minor abnormalities in LV function reflecting stiffness of the myocardium are common in young female diabetics, a patient group with a relatively low prevalence of coronary artery disease.     

Ventricular interdependence in patients with dual-chamber pacing: a Doppler tissue imaging study

PURPOSE: To analyze pulsed-Doppler tissue imaging (DTI) of the right ventricular (RV) tricuspid annulus and left ventricular (LV) mitral annulus in patients paced in the DDD mode at three different pacing modes as compared with healthy subjects, and to investigate possible physiologic interaction between the RV and LV in this subgroup of patients. METHODS: We selected a population of 22 subjects with pacemakers (PM) for atrioventricular (AV) block and/or sick sinus syndrome and compared them to 20 healthy subjects. Standard echo Doppler and DTI parameters were measured at baseline (heart rate [HR] 70 beats/min; AV delay 125 msec) and after at least 5 minutes of constant stimulation at two different pacing modes: (1) HR 70 beats/min, AV delay 188 msec, and (2) HR 89 beats/min, AV delay 125 msec. LV stroke volume was obtained by LV outflow Doppler method. RESULTS: In the PM group, RV and LV annulus exhibited significantly higher peak systolic (S(m)) and early (E(m)) diastolic wall velocities than controls. In the PM population, LV stroke volume was strongly associated to RV E(m) peak velocity (r = 0.83; P < 0.00001) and RV S(m) peak velocity (r = 0.81; P < 0.0001). These associations between LV stroke volume and RV DTI parameters remained significant even after increase of HR and AV delay in the pacing modalities. Moreover, univariate relations were found in the PM group between DTI indexes of RV tricuspid annulus and the homologous indexes of LV mitral annulus. In a multiple linear regression analysis, both RV E(m) (P < 0.001) and RV S(m) (P < 0.001) were related independently to LV stroke volume (cumulative R(2) = 0.85, P < 0.00001). CONCLUSIONS: Our findings suggest the usefulness of pulsed-DTI to display physiologic ventricular interaction in patients with PM. Therefore, DTI may be taken into account as a valuable supporting tool to predict LV systolic performance and to select the most appropriate pacing mode in individual PM patients.