A new approach for evaluation of left ventricular diastolic function: spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography

OBJECTIVES: To evaluate left ventricular diastolic function and differentiate the pseudonormalized transmitral flow pattern from the normal pattern, the propagation of left ventricular early filling flow was assessed quantitatively using color M-mode Doppler echocardiography. BACKGROUND: Because the propagation of left ventricular early filling flow is disturbed in the left ventricle with impaired relaxation, quantification of such alterations should provide useful indexes for the evaluation of left ventricular diastolic function. METHODS: Study subjects were classified into three groups according to the ratio of early to late transmitral flow velocity (E/A ratio) and left ventricular ejection fraction: 29 subjects with an ejection fraction > or = 60% (control group); 34 with an ejection fraction < 60% and E/A ratio < 1 (group I); and 25 with ejection fraction < 60% and E/A ratio > or = 1 (group II). The propagation of peak early filling flow was visualized by changing the first aliasing limit of the color Doppler signals. The rate of propagation of peak early filling flow velocity was defined as the distance/time ratio between two sampling points: the point of the maximal velocity around the mitral orifice and the point in the mid-left ventricle at which the velocity decreased to 70% of its initial value. High fidelity manometer-tipped measurement was performed in 40 randomly selected subjects. RESULTS: The rate of propagation decreased in groups I and II compared with that in the control group (33.8 +/- 13.8 [mean +/- SD] and 30.0 +/- 8.6 vs. 74.3 +/- 17.4 cm/s, p < 0.001, respectively) and correlated inversely with the time constant of left ventricular isovolumetric relaxation and the minimal first derivative of left ventricular pressure (peak negative dP/dt) (r = 0.82 and r = 0.72, respectively). CONCLUSIONS: Spatial and temporal analysis of filling flow propagation by color M-mode Doppler echocardiography was free of pseudonormalization and correlated well with the invasive variables of left ventricular relaxation.     

Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction

OBJECTIVES: The purpose of this study was to determine whether left atrial size and ejection fraction are related to left ventricular filling pressures in patients with coronary artery disease. BACKGROUND: In patients with coronary artery disease, left ventricular filling pressures can be estimated by using Doppler mitral and pulmonary venous flow velocity variables. However, because these flow velocities are age dependent, additional variables that indicate elevated left ventricular filling pressures are needed to increase diagnostic accuracy. METHODS: Echocardiographic left atrial and Doppler mitral and pulmonary venous flow velocity variables were correlated with left ventricular filling pressures in 70 patients undergoing cardiac catheterization. RESULTS: Left atrial size and volumes were larger and left atrial ejection fractions were lower in patients with elevated left ventricular filling pressures. Mean pulmonary wedge pressure was related to mitral E/A wave velocity ratio (r = 0.72), left atrial minimal volume (r = 0.70), left atrial ejection fraction (r = -0.66) and atrial filling fraction (r = -0.66). Left ventricular end-diastolic and A wave pressures were related to the difference in pulmonary venous and mitral A wave duration (both r = 0.77). By stepwise multilinear regression analysis, the ratio of mitral E to A wave velocity was the most important determinant of pulmonary wedge (r = 0.63) and left ventricular pre-A wave (r = 0.75) pressures, whereas the difference in pulmonary venous and mitral A wave duration was the most important variable for both left ventricular A wave (r = 0.75) and left ventricular end-diastolic (r = 0.80) pressures. The sensitivity of a left atrial minimal volume > 40 cm3 for identifying a mean pulmonary wedge pressure > 12 mm Hg was 82%, with a specificity of 98%. CONCLUSIONS: Left atrial size, left atrial ejection fraction and the difference between mitral and pulmonary venous flow duration at atrial contraction are independent determinants of left ventricular filling pressures in patients with coronary artery disease. The additive value of left atrial size and Doppler variables in estimating filling pressures and the possibility that left atrial size may be less age dependent than other mitral and pulmonary venous flow velocity variables merit further investigation.     

Doppler echocardiographic evaluation of mitral flow velocity and prognosis of cardiac insufficiency

The aim of this study was to determine the role of Doppler echocardiography in establishing the prognosis of Stages to 4 cardiac failure. The echocardiographic indices of left ventricular filling were correlated with catheter data and the 2 year out come of patients. The study population included 54 patients examined prospectively in the context of an evaluation of their cardiac failure. Two years after the initial examination, 19 patients were dead or transplanted. Of the remaining 35 patients, 18 were reevaluated at 6 months. Of the echocardiographic parameters, "hyper normal" mitral flow with a high E/A ration indicated poor prognosis; when E/A > 2, the one year survival was 50% and the 2 year survival 42%. There was overlap between the groups of dead or transplanted and surviving patients only when the E/A ratio was between 2 and 3. The patients with E/A < 2 were all alive without any major events at 2 years. All patients with E/A > 3 had a poor prognosis. The E/A ratio was closely correlated with pulmonary capillary pressure levels (p < 0.001, r = 0.55) and lees closely with cardiac index (p < 0.05, r = 0.4) and radionuclide ejection fraction (p < 0.05, r = 0.28). After 6 months' vasodilator treatment with an angiotensin converting enzyme inhibitor (captopril) the E/A ratio decreased significantly from 1.85 +/- 0.78 to 1.0 0.55 (p < 0.02). A "hyper-normal" mitral flow is related to many factors, including high left ventricular filling pressures, mitral regurgitation and reduced left ventricular compliance. This appearance of mitral flow is a poor prognosis factor in severe cardiac failure.     

Reduced periinfarction mortality as a result of long-term therapy with captopril but not hydralazine or propranolol in spontaneously hypertensive rats

Hypertension and left ventricular hypertrophy (LVH) are known to increase susceptibility to ventricular arrhythmias during and before myocardial ischemia and to increase the risk of periinfarction mortality. Although regression of LVH has been advocated as a therapeutic goal, little evidence exists to suggest that it can reduce periinfarction mortality, and if it does, by which mechanisms it may do this. In this study, we evaluated the effects of control of systemic arterial blood pressure, of regression of myocardial hypertrophy, and of cardiac fibrosis on the susceptibility to ventricular arrhythmias and periinfarction mortality in the spontaneously hypertensive rat (SHR) model of hypertension and LVH. After 12 weeks of treatment, captopril and hydralazine reduced systolic blood pressure to 93 +/- 14 and 126 +/- 13 mm Hg, respectively, as compared with 193 +/- 12 mm Hg, p < 0.05, in the untreated control SHR group. The decrease with propranolol (to 185 +/- 12 mm Hg) was of borderline significance. There was a significant decrease in inducibility of ventricular arrhythmias by programmed electrical stimulation with captopril (5%; p < 0.05). One hour after infarction, there was a trend toward reduced mortality in the rats treated with hydralazine, 9.5% (p = 0.20 vs. control; p = 0.10 vs. propranolol), and captopril, 5% (p = 0.08 vs. control; p = 0.010 vs. propranolol). However, only captopril reduced 3-h postinfarction mortality (40%; p = 0.022) compared with 72% in the control group. The results showed a significant decrease of the left ventricular weight/body weight ratio in the rats treated with hydralazine (2.6 +/- 0.2 mg/g; p < 0.05) and captopril (2.2 +/- 0.2 mg/g; p < 0.05) compared with the control group (2.8 +/- 0.2 mg/g). An assessment of cardiac fibrosis indicated that captopril decreased the volume percentage of collagen the most (2.01 +/- 0.53; p < 0.05), followed by propranolol (2.29 +/- 0.64; p < 0.05) and hydralazine (2.92 +/- 0.58; p < 0.05) versus controls (3.23 +/- 0.61). This study suggests that regression of myocardial hypertrophy or long-term normalization of arterial systolic blood pressure or both are the major determinants of very early mortality (within 1 h after infarction) and that later mortality (3 h after infarction) may be the result of a more complex interplay of regression of myocardial hypertrophy and fibrosis and of control of blood pressure.     

Evaluation of left atrial contribution to left ventricular filling in aortic stenosis by velocity-encoded cine MRI

Velocity-encoded cine MRI (VEC-MRI) can measure volume flow at specified site in the heart. This study used VEC-MRI to measure flow across the mitral valve to compare the contribution of atrial systole to left atrial filling in normal subjects and patients with left ventricular hypertrophy. The study population consisted of 12 normal subjects (mean age 34.5 years) and nine patients with various degrees of left ventricular hypertrophy resulting from aortic stenosis (mean age 70 years). VEC-MRI was performed in double-oblique planes through the heart to measure both the mitral inflow velocity pattern (E/A ratio) and the volumetric flow across the mitral valve. The left atrial contribution to left ventricular filling (AC%) was calculated. The results were compared with Doppler echocardiographic parameters. The VEC-MRI-derived mitral E/A ratios showed a significant linear correlation with E/A ratios calculated from Doppler echocardiography (r = 0.94), and the VEC-MRI-derived E/A ratios (2.1 +/- 0.5 vs 1.0 +/- 0.4) and AC% values (24.9 +/- 7.2 vs 45.7 +/- 16.4) were significantly different between normal subjects and patients with aortic stenosis (p < 0.01 in both groups). The same differences were seen in the Doppler echocardiographic parameters. The VEC-MRI-derived E/A ratio and AC% showed significant hyperbolic and linear correlations with left ventricular mass indexes (r = 0.95 and 0.86). In addition, the VEC-MRI-determined E/A ratio and the volumetric AC% displayed a highly significant hyperbolic correlation (r = 0.95). Thus VEC-MRI can be used to evaluate left ventricular diastolic filling characteristics in normal subjects and patients with abnormalities of diastolic filling.     

Scatter rejection in modular gamma cameras for use in dynamic 3D spect brain imaging system

This study examined the effects of Albunex (sonicated 5% human serum albumin) infusion on left ventricular inflow velocity by Doppler echocardiography. Left ventricular pressure and left ventricular inflow velocity were recorded simultaneously under eight different conditions in dogs: 1) baseline 1 (control), 2) Albunex 0.2 ml/kg, 3) baseline 2, 4) Albunex 0.5 ml/kg, infusion of dextran 100 ml, 5) baseline 3, 6) Albunex 0.2 ml/kg, 7) baseline 4, and 8) Albunex 0.5 ml/kg. In the normal state (no dextran), Albunex (0.2 ml/kg) caused no hemodynamic changes or inflow velocity changes. In contrast, infusion of Albunex (0.5 ml/kg) caused time velocity integrals of early filling to increase from the baseline (5.51 +/- 1.13 vs 7.19 +/- 1.14 cm, p < 0.05). After dextran infusion (100 ml), Albunex (0.2 ml/kg) caused peak early filling velocity to increase (62.4 +/- 6.9 vs 67.3 +/- 9.4 cm/sec, p < 0.05), and infusion of Albunex (0.5 ml/kg) also caused peak early filling velocity to increase from baseline (64.6 +/- 8.5 vs 73.7 +/- 14.5 cm/sec, p < 0.05). Infusion of Albunex (0.5 ml/kg) after dextran infusion caused increases in left ventricular pressure at the mitral valve opening (12.7 +/- 3.1 vs 15.2 +/- 3.3 mmHg, p < 0.05) and in left atrial driving force (13.5 +/- 3.6 vs 16.7 +/- 5.9 mmHg, p < 0.05). Clinicians should be cautious about using Albunex at doses of greater than 0.2 ml/kg when evaluating the pressure gradient of the left ventricle in patients with elevated left ventricular diastolic pressure. In patients with normal hemodynamics, Albunex infusion at doses of less than 0.2 ml/kg apparently did not affect the velocity measurement.     

Effects of exercise on plasma level of brain natriuretic peptide in congestive heart failure with and without left ventricular dysfunction

This study was designed to determine whether plasma brain natriuretic peptide (BNP) increases in response to exercise in patients with congestive heart failure and to show what kind of hemodynamic abnormalities induce increased secretion of BNP during exercise. Plasma levels of atrial natriuretic peptide (ANP) and BNP and hemodynamic parameters were measured during upright bicycle exercise tests in seven patients with dilated cardiomyopathy and nine with mitral stenosis. At rest, there were no intergroup differences in cardiac output or pulmonary capillary wedge pressure; however, the group with dilated cardiomyopathy had higher left ventricular end-diastolic pressures and lower left ventricular ejection fractions than did the group with mitral stenosis. Plasma ANP levels were comparable between the dilated cardiomyopathy group (170 +/- 77 [SE] pg/ml) and the mitral stenosis group (106 +/- 33 pg/ml) (p, not significant), whereas BNP was significantly higher in the dilated cardiomyopathy group (221 +/- 80 pg/ml) than in the other group (37 +/- 10 pg/ml) (p < 0.05). The plasma concentration of BNP but not of ANP significantly correlated with left ventricular end-diastolic pressure and volume. Exercise increased plasma ANP and BNP in the two groups. The dilated cardiomyopathy group had a larger increment in BNP (+157 +/- 79 pg/ml) than did the mitral stenosis group (+17 +/- 5 pg/ml) (p < 0.05), although the increase in pulmonary capillary wedge pressure was greater in the mitral stenosis group. Thus exercise increases plasma levels of BNP, and impaired left ventricular function may be a main factor in the greater increment in BNP during exercise in patients with congestive heart failure.     

Congestive heart failure in patients with valvular aortic stenosis. A clinical and echocardiographic Doppler study

The aim of this study was to evaluate echographically anatomic and functional features of the left ventricle in adult patients with valvular aortic stenosis according to the presence or absence of congestive heart failure and the level of ventricular performance. Fifty-six adult patients with moderate-to-severe aortic stenosis underwent echocardiographic Doppler examination in order to evaluate left ventricular mass and dimensions, systolic function and filling dynamics. Twenty-seven patients had no heart failure and were symptomatic for angina (5), syncope (4) or were symptom-free (group I); the other 29 had heart failure (group II): 16 with normal left ventricular systolic performance (fractional shortening > 25%, group IIa) and 13 with systolic dysfunction (fractional shortening < or = 25%, group IIb). Despite a similar left ventricular mass, compared to group IIa, group IIb showed a significant left ventricular dilatation (end-diastolic diameter: 61 +/- 6.5 vs. 45.5 +/- 6.1 mm, p < 0.001) and mild or no increase in wall thickness (11.5 +/- 1.6 vs. 14.9 +/- 2 mm, p < 0.001). Indices of left ventricular filling on Doppler transmitral flow were also significantly different between the two groups, with a higher early-to-late filling ratio and a shorter deceleration time of early filling in group IIb (2.8 +/- 1.9 vs. 1.2 +/- 0.85, p < 0.01, and 122 +/- 66 vs. 190 +/- 87 ms, p < 0.05, respectively), both indirectly indicating higher left atrial pressure. Finally, heart failure was generally more severe in group IIb patients. In some patients with aortic stenosis, symptoms of heart failure may be present despite a normal left ventricular systolic function and seem to depend on abnormalities of diastolic function. The presence of systolic or isolated diastolic dysfunction appears to be related to a different geometric adaptation of the left ventricle to chronic pressure overload.     

Determinants of myocardial performance after blunt chest trauma

OBJECTIVE: This study investigates whether factors that determine myocardial performance (preload, afterload, heart rate, and contractility) are altered after isolated unilateral pulmonary contusion. METHODS: Catheters were placed in the carotid arteries, left ventricles, and pulmonary arteries of anesthetized, ventilated (FiO2=0.5) pigs (31.2+/-0.6 kg; n=26). A unilateral, blunt injury to the right chest was delivered with a captive bolt gun (n=17) followed by tube thoracostomy. To control for anesthesia and instrumentation at FiO2 of 0.5, one group received tube thoracostomy only (sham injury; n=6). To control for effects of hypoxia without chest injury, an additional sham-injury group (n=3) was ventilated with FiO2 of 0.12. To generate cardiac function (i.e., Starling) curves, lactated Ringer's solution was administered in three bolus infusions at serial time points; the slope of stroke index versus ventricular filling pressure defines cardiac contractility. RESULTS: By 4 hours after pulmonary contusion, pulmonary vascular resistance, airway resistance, and dead space ventilation were increased, whereas PaO2 (72+/-6 mm Hg at FiO2=0.5) and dynamic compliance were decreased (all p < 0.05). Despite profound lung injury, arterial blood pressure, heart rate, cardiac filling pressures, and output remained within the normal range, which is inconsistent with direct myocardial contusion. The slope of pulmonary capillary wedge pressure versus left ventricular end-diastolic pressure (LVEDP) regression was reduced by more than 50% from baseline (p < 0.05), but there was no significant change in the slope of the central venous pressure versus LVEDP regression. By 4 hours after contusion, the slope of the stroke index versus LVEDP curve was reduced by more than 80% from baseline (p < 0.05). By the same time after sham injury with FiO2 of 0.12 (PaO2 < 50 mm Hg), the regression had decayed a similar amount, but there was no change in the slope after sham injury with FiO2 of 0.5 (PaO2 > 200 mm Hg). CONCLUSION: After right-side pulmonary contusion, the most often used estimate of cardiac preload (pulmonary capillary wedge pressure) does not accurately estimate LVEDP, probably because of changes in the pulmonary circulation or mechanics. Central venous pressure is a better estimate of filling pressure, at least in these conditions, probably because it is not directly influenced by the pulmonary dysfunction. Also, ventricular performance can be impaired by depressed myocardial contractility and increased right ventricular afterload even with normal left ventricular afterload and preload. It is thus conceivable that occult myocardial dysfunction after pulmonary contusion could have a role in the progression to cardiorespiratory failure even without direct cardiac contusion.     

Left ventricular systolic torsion and early diastolic filling by echocardiography in normal humans

This study describes a novel 2-dimensional echocardiographic technique to measure left ventricular (LV) systolic twist in humans and relates this measure to early ventricular filling. LV twist is the counterclockwise rotation of the left ventricle during systole when viewed from the apex. The effect of ventricular twist has been postulated to store potential energy, which ultimately aids in diastolic recoil, leading to ventricular suction. The generated negative early diastolic pressures may augment early ventricular filling. We measured ventricular twist in 40 patients with normal transthoracic echocardiograms. End-systolic twist was determined by measuring rotation of the anterolateral papillary muscle about the center of the ventricle. LV filling was assessed by analysis of transmitral Doppler flow velocities. The mean value obtained was 9 +/- 7 degrees of rotation. Twist measurements were highly reproducible with an intraobserver correlation coefficient of r = 0.881, p <0.001. The magnitude of ventricular twist was strongly correlated positively with acceleration of the mitral E-wave (r = 0.75; p <0.0001) and negatively with the mitral E-wave acceleration time (r = -0.83; p <0.0001).     

Mortality and platelet depletion occur independently of fibrinogen consumption in murine models of tumour necrosis factor-mediated systemic inflammatory responses

The link between left ventricular dysfunction and arrhythmogenesis is commonly known. However, so far, only the systolic left ventricular dysfunction has been evaluated. Because of the controversial results of those studies, we decided to assess if is there a link between late potentials (LP) and left ventricular diastolic dysfunction. Our material consisted of 56 patients: 11 women and 45 men, mean age was 61.12 +/- 10.07 years. Signal averaged ECG and ECHO were performed in each patient, 2-3 months after myocardial infarction. For high pass filter of 40 Hz, LP were defined as 2 or 3 abnormal SAECG variables (the averaged QRS > 114 ms, the low amplitude signal duration LAS > 38 ms and root mean square voltage of the terminal 40 ms RMS40 < 20 microV). During ECHO study, we assessed E and A waves E/A ratio, left ventricular end-diastolic volume (LVEDV), ejection fraction (EF), acceleration (AT) and deceleration times (DT). The patients were divided into 2 groups: group I-30 patients LP positive and group II-26 patients LP negative. There were no significant differences between the groups in terms of age, EF, and heart rate. We presented significant differences between group I and II in terms of E wave velocity (0.75 +/- 0.19 vs 0.64 +/- 0.19 p < 0.03) E/A ratio (2.13 +/- 1.56 vs 1.0 +/- 0.5 p < 0.05) respectively. We did not confirm significant differences as regards A wave velocity, AT, isovolumetric time (IVRT) and LVEDV between both tested groups. In group I we revealed a significant correlation between E wave (r = 0.45), E/A ratio (r = 0.62), AT (r = -0.42) E/A ratio (r = 0.56), DT (r = 0.55) and QRS, as well as DT and LPD (r = 0.40) and between IVRT and RMS40 (r = -0.43). The results of our study suggest that in patients after myocardial infarction: 1/incidence of LP depends on the degree of left ventricular filling pattern like in impaired relaxion, quite well correlated with filtered QRS time 3/in LP positive patients there was predominance of restrictive left ventricular filling pattern, quite well correlation with RMS40 amplitude.     

Pulmonary metastasectomy for soft tissue sarcomas: is it justified?

beta-blocker therapy for mitral stenosis is controversial. This study compares right and left heart hemodynamics at rest and supine submaximal exercise in patients (n = 7) receiving chronic beta-antagonists with untreated patients (n = 17) matched for age (mean +/- SD = 51 +/- 12 years) and valve area (0.7 +/- 0.2 cm2/m2). Little benefit was observed with treatment at rest. Although pulmonary capillary wedge pressures (PCWP) were lower during exercise in the beta-blocker group (22 +/- 4 vs. 31 +/- 9 mmHg; P < 0.05), exercise performance was not enhanced and cardiac output response during exercise was reduced (control = 41% increase vs. 12% for beta-blockade). PCWP rose rapidly when diastolic filling periods were < 300 msec in both groups. Pulmonary capillary wedge pressure was found to be a nonlinear functions (P < 0.001) of diastolic filling period (PCWP = 15.9 + 5.84 x 10(5)/dfp2). These data suggest that there is a critical heart rate in patients with mitral stenosis above which hemodynamic compromise rapidly occurs.     

Prognostic value of Doppler transmitral flow velocity patterns in acute myocardial infarction

Doppler transmitral flow patterns are partially dependent on age. We investigated the correlations between the age-adjusted transmitral flow patterns, hemodynamic indexes, and the coronary and clinical outcome in 206 patients with acute myocardial infarction (AMI) and 102 normal control subjects. The peak flow velocity at atrial contraction was significantly lower in 50 of the 206 patients (24%) (low-A group) than in the 102 normal controls. Pulmonary capillary wedge pressure was significantly higher in the low-A group than in the remaining 156 patients with AMI (20 +/- 7 vs 11 +/- 5 mm Hg, p <0.001), and the cardiac index and left ventricular ejection fraction were significantly lower (2.2 +/- 0.6 vs 2.9 +/- 0.7 L/min/m2, p <0.001; 38 +/- 15% vs 52 +/- 13%, p <0.001). The incidence of cardiogenic shock was significantly higher in the low-A group than in the other patients with AMI (42% vs 19%, p <0.001). Regression analysis demonstrated a significant association between decreased atrial filling velocity and increased in-hospital mortality as well as the incidence of heart failure in AMI (p <0.001). The 5-year mortality rate was also significantly higher in the low-A group (p <0.001). The age-adjusted transmitral flow pattern in AMI can identify patients with left ventricular dysfunction, which can lead to a poor prognosis.     

Structural basis for changes in left ventricular function and geometry because of chronic mitral regurgitation and after correction of volume overload

Left ventricular function and myocyte structure were examined in three groups of dogs: (1) 3 months of mitral regurgitation caused by chordal rupture (n = 7); (2) chronic mitral regurgitation followed by mitral valve replacement and a 3-month recovery period (n = 7), and (3) sham controls (n = 8). The left ventricular end-systolic stiffness constant (Kess) was measured as an index of left ventricular contractile function with stress-strain relationships obtained by cinecatheterization. Isolated myocyte structure and composition were examined with computer-assisted morphometry and nuclear area computed with deoxyribonucleic acid fluorescence. Left ventricular contractile function was significantly depressed with chronic mitral regurgitation compared with control values (Kess, 2.1 +/- 0.1 versus 3.6 +/- 0.2; p < 0.05) and returned to control values with mitral valve replacement (3.8 +/- 0.2). Left ventricular mass significantly increased in both the mitral regurgitation and mitral valve replacement groups compared with control values (121 +/- 10, 120 +/- 5 versus 95 +/- 9 gm, respectively; p < 0.05). Myocyte length increased with mitral regurgitation beyond control values (194 +/- 4 versus 218 +/- 8 microns; p < 0.05) and increased beyond mitral regurgitation values after mitral valve replacement (231 +/- 7 microns; p < 0.05). Myocyte volume with mitral regurgitation increased slightly beyond control values (33.5 +/- 0.7 versus 37.6 +/- 1.3 microns3; p = 0.15) and significantly increased with mitral valve replacement (40.1 +/- 1.2 microns3; p < 0.05). Myocyte myofibril volume significantly declined with mitral regurgitation compared with control values (14.8 +/- 1.5 versus 22.2 +/- 0.7 microns3; p < 0.05) and significantly increased beyond both mitral regurgitation and control values with mitral valve replacement (27.1 +/- 1.1 microns3; p < 0.05). Myocyte nuclear area with mitral regurgitation remained unchanged from control values (1430 +/- 122 versus 1163 +/- 89 microns2) but increased significantly with mitral valve replacement (2209 +/- 250 microns2; p < 0.05). In summary, the left ventricular contractile dysfunction with chronic mitral regurgitation is accompanied by increased myocyte length and reduced myofibril content. In contrast, the left ventricular hypertrophy and improved left ventricular pump function with mitral valve replacement were due to increased myocyte volume and increased contractile protein content.     

Left ventricular diastolic function in young men with high normal blood pressure

OBJECTIVE: Abnormalities in left ventricular (LV) diastolic filling have been reported in hypertensive patients. This study was designed to compare LV diastolic filling between individuals with high normal blood pressure (HNBP) and optimal blood pressure (OBP). SUBJECTS AND DESIGN: From a survey of 219 young male individuals (age 21 +/- 0.1 years), two groups were selected according to their BP (group A: systolic BP [SBP] 120 mmHg and diastolic BP [DBP] 80 mmHg, n = 23 and group B: SBP 130 to 139 mmHg and/or DBP 85 to 89 mmHg, n = 21). Subjects habits, anthropometric characteristics, LV structure and systolic and diastolic function were compared. RESULTS: No differences were detected between the two groups in habits, systolic function or early diastole. LV mass index (LVMI) was higher in group B (103.6 +/- 4.58 g/m2 versus 90.49 +/- 3.27 g/m2 in group A, P < 0.05), though the values were not high enough to indicate LV hypertrophy. The pattern of LV late filling was different between the two groups. The peak late diastolic flow velocity (A) was 0.45 +/- 0.02 m/s in group B and 0.52 +/- 0.03 m/s in group A (P < 0.05). The early peak velocity (E):A ratio was 1.82 +/- 0.08 in group A and 1.59 +/- 0.08 in group B (P < 0.05). The early filling fraction also demonstrated a significant shift to more prominent late diastolic filling in group B (0.68 +/- 0.01% versus 0.73 +/- 0.01% in group A, P < 0.05). This pattern in LV filling did not correlate to inheritance, age, sex, heart rate, habits or body mass index. CONCLUSIONS: This shift in filling pattern to a late flow in young men with HNBP seemed to be an early indicator of an increased dependence of LV filling on atrial contraction and may reflect an impairment in LV relaxation.     

Using the World Wide Web--a new approach to risk identification of diabetes mellitus

We evaluated 30 consecutive patients and 48 age- and sex-matched controls to explore the possibility of a pathogenic contribution by plasma endothelin-1 in the cardiac expression of systemic sclerosis. Venous plasma endothelin-1 was measured by radio-immunoassay and left ventricular function by echocardiography. The patient group had elevated plasma endothelin-1 (2.6 +/- 0.2 vs. 1.8 +/- 0.1 pmol/1, P < 0.001), but endothelin-1 was not related to age, heart rate, blood pressure, total peripheral resistance, disease duration or systemic sclerosis score. Endothelin-1 was related to left ventricular hypertrophy in terms of septal thickness (r = 0.33, P < 0.01) and left ventricular mass index (r = 0.32, P < 0.01). Plasma endothelin-1 was further related to measures indicating reduced left ventricular filling; left atrial emptying index (r = -0.50, P < 0.0005), the first third filling fraction (r = -0.31, P < 0.05) and the time velocity integral of Doppler early/late filling velocity (r = -0.40, P < 0.001). Furthermore, circulating endothelin-1 was related to impaired left ventricular contractility as estimated by pre-ejection period/left ventricular ejection time (r = 0.32, P < 0.01) and end-systolic wall stress/volume index (r = -0.30, P < 0.05). We conclude that plasma endothelin-1 is elevated in relation to the degree of left ventricular hypertrophy, diastolic dysfunction and impaired contractility in systemic sclerosis. It may be of pathogenic importance to the cardiac involvement in systemic sclerosis which is not mediated via an increase in systemic blood pressure. It is not yet clear whether our findings are exclusive to systemic sclerosis patients or represent a generalized phenomenon in patients with impaired left ventricular function.     

Effect of chronotropic and inotropic stimulation on the coronary pressure-flow relation in left ventricular hypertrophy

Left ventricular hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during increased cardiac work. The present study was performed to study the effects of chronotropic and inotropic stimulation on the coronary pressure-flow relation of the hypertrophied left ventricle of dogs and to determine the individual contributions of increases in heart rate and contractility to the exaggerated exercise-induced increases in effective back pressure (pressure at zero flow; Pzf). Ascending aortic banding in seven dogs increased the LV to body weight ratio to 7.7 +/- 0.3 g/kg compared to 4.8 +/- 0.2 g/kg in 10 normal dogs (p < or = 0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. During resting conditions maximum coronary blood flow in the pressure overloaded hypertrophied left ventricle was impaired by both an increase in Pzf (25.1 +/- 2.6 vs 13.8 +/- 1.2 mmHg in hypertrophied vs normal ventricles, respectively, p < or = 0.01) and a decrease in maximum coronary conductance (slope of the linear part of the pressure-flow relation, slopep > or = linear) (8.6 +/- 1.1 vs 12.7 +/- 0.9 ml/min/mmHg, p < or = 0.01). Right atrial pacing at 200 and 250 beats/min resulted in similar rightward shifts of the pressure-flow relation in hypertrophied and normal hearts with 3.1 +/- 0.8 and 4.7 +/- 0.8 mmHg increases in Pzf in LVH and normal dogs, respectively; stepwise multivariate regression analysis indicated that the exaggerated decrease in filling pressure (10 +/- 2 vs 6 +/-2 mmHg) and decrease in left ventricular systolic pressure (45 +/- 5 vs 3 +/- 3 mmHg, p < or = 0.01) may have blunted a greater rightward shift of the pressure-flow relation produced by atrial pacing in the hypertrophied hearts. Inotropic stimulation with dobutamine (10-20 micrograms/kg/min, i.v.) resulted in minimal flow changes in normal hearts but produced a 4.4 +/- 1.5 mmHg (p < or = 0.05) rightward shift of the pressure-flow relation in hypertrophied hearts. which correlated with a greater increase in left ventricular systolic pressure (83 +/- 16 vs 18 +/- 4 mmHg. p < or = 0.05). Exercise resulted in a rightward shift in both normal and hypertrophied left ventricles, but the increase in Pzf was significantly greater in the hypertrophied hearts (15.2 +/- 0.9 vs 10.3 +/- 0.9 mmHg. p < or = 0.05). Stepwise multivariate regression analysis indicated that not only increases in left ventricular filling pressure, but also increases in heart rate and LV systolic pressure contributed to the abnormally great increase in effective coronary back pressure which results in limitation of myocardial perfusion during exercise in the pressure overloaded hypertrophied left ventricle.     

Determinants of the pulmonary artery pressure rise in left ventricular dysfunction

Pulmonary artery hypertension in patients with left ventricular dysfunction is related to poor outcome but the role of cardiac functional abnormalities in the genesis of pulmonary hypertension remains unknown. The aim of this prospective study was to identify the determinants of pulmonary hypertension in 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%). Systolic pulmonary artery pressure was measured by continuous wave Doppler. Left ventricular systolic and diastolic function, severity of functional mitral regurgitation, cardiac output, and left atrial volume were assessed using Doppler echocardiography. In patients with left ventricular dysfunction, systolic pulmonary artery pressure was increased (51 +/- 14 mmHg, range 23 to 87 mmHg). Mitral deceleration time (r = -0.61; p = 0.0001) and mitral effective regurgitant orifice (r = 0.50; p = 0.0001) were the strongest parameters related to systolic pulmonary artery pressure. Multivariate analysis identified these two variables as the strongest predictors of systolic pulmonary artery pressure in association with the mitral E/A ratio (p = 0.006) and age (p = 0.005). In conclusion, pulmonary hypertension is common and variable in patients with left ventricular dysfunction. It is closely related to diastolic dysfunction and severity of functional mitral regurgitation but not independently to the degree of left ventricular systolic dysfunction. These findings underline the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.     

Left ventricular concentric remodelling and carotid structural changes in essential hypertension

AIM: Left ventricular concentric remodelling defines a modified left ventricular geometry in the presence of a normal left ventricular mass; it is an early and frequent adaptation in arterial hypertension. The present study was designed to evaluate the extent of carotid structural changes in essential hypertensives with left ventricular remodelling. PATIENTS AND METHODS: Two groups of hypertensive patients, who had never previously received anti-hypertensive treatment, 14 with left ventricular concentric remodelling (group I, relative wall thickness 0.48 +/- 0.02) and 48 with normal left ventricular geometry (group II, relative wall thickness 0.37 +/- 0.04) underwent clinical and laboratory examination, echocardiography, carotid artery ultrasonography and 24 h ambulatory blood pressure monitoring (ABPM). The left ventricular dimensions and mass were obtained according to the Penn convention. The intima-media thickness (IMT) of the posterior wall of both common carotid arteries was measured 5, 10 and 20 mm caudally to the bulb and the average value was used for analysis. RESULTS: In both groups age (group I 44 +/- 9 years; group II 40 +/- 9 years), body surface area (group I 1.85 +/- 0.2 m2; group II 1.80 +/- 0.2 m2), duration of hypertension (group I 4.4 +/- 4; group II 3.8 +/- 3.9 years), metabolic parameters and smoking habits were similar. Both clinic and 24 h ABPM values were higher in group I (clinic 157 +/- 12/102 +/- 5; 24 h ABPM 145 +/- 10/95 +/- 7 mmHg) than they were in group II (clinic 146 +/- 11/97 +/- 5; 24 h ABPM = 134 +/- 10/87 +/- 8 mmHg, P < 0.01). The left ventricular mass index (LVMI) and IMT were found to be slightly but significantly greater in group I than they were in group II (LVMI 106 +/- 7 versus 98 +/- 12 g/m2, P < 0.05; IMT 0.68 +/- 0.13 versus 0.61 +/- 0.10 mm, P < 0.05). A significant correlation was found between LVMI and common carotid IMT in the whole group of hypertensive patients (r = 0.43, P < 0.01). CONCLUSIONS: Our results indicate that left ventricular concentric remodelling does not represent the only early cardiovascular change in arterial hypertension but rather is associated often with carotid intima-media thickening.     

Doppler analysis of pulmonary venous flow profiles in orthotopic heart transplant recipients: a comparison with mitral flow profiles and atrial function

Previous Doppler studies of transmitral flow profiles in heart transplant recipients suggested left ventricular (LV) diastolic dysfunction. The influence of left atrial filling and emptying on mitral Doppler profiles in heart transplant recipients has not been studied systematically. In the present study, pulmonary venous flow profiles, mitral flow profiles, left atrial area change and mitral annulus motion were analyzed in 20 orthotopic heart transplant recipient and 20 control subjects by transthoracic and transesophageal echocardiography and Doppler. Mitral flow profiles revealed a "restrictive" pattern with a high early-to-late diastolic flow velocity ratio in transplant patients (2.16 +/- 0.52 vs. 1.30 +/- 0.25, p < 0.0001), which was mainly due to a reduced late diastolic maximum mitral flow velocity (32.6 +/- 8.3 vs. 51.6 +/- 12.4 cm/s, p < 0.0001). Left atrial area change (35.9 +/- 13.9 vs. 58.1 +/- 17.0%, p < 0.0006) and mitral annulus motion (9.2 +/- 3.3 vs. 12.2 +/- 2.0%, p < 0.05) were reduced in transplant recipients, compared to controls. Pulmonary venous flow parameters in transplant recipients were markedly altered during systole, when pulmonary venous flow parameters are influenced primarily by atrial function rather than by diastolic LV properties: peak systolic flow velocity (45.5 +/- 8.2 vs. 62.3 +/- 14.0 cm/s, p < 0.001), maximum flow velocity ratio (0.87 +/- 0.19 vs. 1.45 +/- 0.33), time velocity integral of pulmonary venous flow during systole (9.3 +/- 2.3 vs. 17.1 +/- 4.0 cm, p < 0.001) and the systolic fraction of the time velocity integral (52.6 +/- 10.8 vs. 68.5 +/- 6.8%, p < 0.001) were lower in heart transplant recipients than in controls. These findings are compatible with atrial dysfunction and reduced mitral annulus motion. The results of this study indicate that LV diastolic dysfunction is not the only possible cause of altered transmitral Doppler profiles in heart transplant recipients. Atrial abnormalities represent a major contributing factor to altered mitral and pulmonary venous flow patterns. Analysis of transmitral Doppler profiles alone are therefore not adequate for analysis of diastolic LV function in heart transplant recipients.