Relationship between systolic and diastolic function of the left ventricle in patients with impaired relaxation of the left ventricle without symptoms of heart failure. Attempt at quantitative estimation of diastolic function in the impaired relaxation stage

Diastolic dysfunction of left ventricle appears very often in patients with coronary artery disease (CAD) and hypertension (HT) and is a main cause of heart failure in 30-40% of all cases. Relation between systolic and diastolic function of left ventricle (LV) is commonly known but not documented well enough. Moreover, no quantitative classification of diastolic dysfunction is still available. AIM OF THE STUDY: To find out the relations between the parameters of systolic and diastolic function of LV in patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure and to make up the quantitative classification of diastolic dysfunction in the stage of impaired relaxation of LV. METHODS: Investigations were carried out in 57 patients (mean age 55.5 +/- 11.5) with angiographically proven CAD and in 91 patients (mean age 56.3 +/- 10.6) with HT and angiographically excluded CAD, all without regional myocardial contractility abnormalities and valvular heart diseases. Control group consisted of 54 healthy subjects (mean age 55.4 +/- 11.4). During 2D echocardiography examination left ventricular end-diastolic (LVEDD) and end-systolic diameters (LVESD) and left atrial dimension (LA) were obtained. Using Doppler method transmitral inflow indices: E velocity (E), A velocity (A), E velocity integral (E-VTI), A velocity integral (A-VTI), total velocity integral (T-VTI), E deceleration time (DT), isovolumic relaxation time (IVRT) and aortic flow velocity integral (Ao-VTI) were measured. Only patients with E/A < or = 1 and--to exclude pseudonormalization of mitral inflow--with DT > or = 140 ms were qualified to the study. We proposed diastolic dysfunction ratio (DDR) calculated from formula: DDR = E/A x E-VTI/T-VTI. Using AFVI, LV outflow diameter, heart rate (HR) and body surface area cardiac index (CI) was calculated. RESULTS: In studied group there were significantly higher values of LA, A, IVRT, DT and lower values of E, E/A, E-VTI and DDR compared to controls. There were no significant differences between these groups in HR, LVEDD, LVESD, T-VTI and CI. No significant differences in any of studied parameters were found between subgroups with CAD and HT. Among healthy subjects in subgroup with abnormal mitral inflow pattern (E/A < or = 1) there were significantly higher values of LA, IVRT, DT and lower values of DDR than in sugroup with normal one. Both subgroups did not differ in LVEDD, LVESD, CI. In the studied group there was positive correlation between DDR and CI (r = 0.69, p < 0.001), DDR and IVRT (r = 0.71, p < 0.001), DDR and DT (r = 0.61, p < 0.001), CI and E (r = 0.34, p < 0.01), CI and IVRT (r = 0.52, p < 0.001), CI and DT (r = 0.42, p < 0.001), CI and E/A (r = 0.54, p < 0.001), CI and E-VTI (r = 0.43, p < 0.001). In the control group significant correlation was found only between DDR and IVRT (r = 0.64, p < 0.02) and between DDR and DT (r = 0.52, p < 0.02) but not between DDR and CI. Using DDR DD was divided into 3 classes: class I with DDR > 0.47, class II with 0.47 > or = 0.30, and class III with DDR < 0.30. Applying of such intervals of values of DDR determined the groups which significantly differed between themselves in CI, IVRT and DT. CONCLUSIONS: (1) In patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure there is relation between parameters of systolic and diastolic function of LV: the more advanced diastolic dysfunction, the more impaired systolic function. (2) In healthy subjects there is no relation between parameters of systolic and diastolic function of LV. (3) DDR is a good indicator of quantitative estimation of diastolic dysfunction in the stage of impaired relaxation of LV.     

Comparison of the effects of potential parenteral vehicles for poorly water soluble anticancer drugs (organic cosolvents and cyclodextrin solutions) on cultured endothelial cells (HUV-EC)

Left atrial (LA) adaptation during the development of left ventricular (LV) dysfunction is not fully understood. We performed echocardiographic assessment of LA volumes simultaneously with recordings of pulmonary wedge pressures in 60 patients. Twenty patients had no structural or functional LV abnormalities, 20 had a recent myocardial infarction with LV dysfunction, and 20 suffered from congestive heart failure (CHF). Pressure-volume loops were obtained at baseline and during increases in LA pressure produced by normal saline infusion. LA afterload was estimated by the effective LV elastance (E(LV)). Atrioventricular coupling was calculated by the E(LV)/E(es) ratio (where E(es) is the end-systolic elastance). E(es) increased in patients with myocardial infarction (0.80 +/- 0.09 mm Hg/ml, p <0.001), whereas it decreased in patients with CHF (0.22 +/- 0.05 mm Hg/ml, p <0.001) compared with controls (0.61 +/- 0.07 mm Hg/ml). Similarly, stroke workload increased in patients with myocardial infarction (60.7 +/- 7.3 mm Hg x ml, p <0.001), whereas it decreased in patients with CHF (25.4 +/- 2.2 mm Hg x ml, p <0.001) compared with controls (44.8 +/- 5.5 mm Hg x ml). In all patients LA stiffness (slope of the relation of the filling portion of the pressure-volume loop) was increased compared with controls (controls: 0.13 +/- 0.04, patients with myocardial infarction: 0.22 +/- 0.05, and patients with CHF: 0.27 +/- 0.05 mm Hg/ml, p <0.001 for both comparisons). Moreover, the E(LV)/E(es) ratio increased gradually as LV function deteriorated (controls: 1.06 +/- 0.10, patients with myocardial infarction: 1.35 +/- 0.16, and patients with CHF: 6.90 +/- 0.84, p <0.001). Thus, early in heart failure, LA pump function is augmented but LA stiffness increases and work mismatch occurs. With further progression of LV dysfunction, LA pump function decreases as a result of increased afterload imposed on the LA myocardium.     

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.     

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.     

Reversibility of changes in left and right ventricular geometry and hemodynamics in pulmonary hypertension. Echocardiographic characteristics before and after pulmonary thromboendarterectomy

Pulmonary thromboendarterectomy (PTE) leads to an acute decrease of right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension. We investigated the changes in right and left ventricular (LV) geometry and hemodynamics by means of transthoracic echocardiography. The prospective study was performed in 14 patients (8 female, 6 male; age 55 +/- 20 years) before and 18 +/- 12 days after PTE. Total pulmonary vascular resistance and systolic pulmonary artery pressure were significantly decreased (PVR: preoperative 986 +/- 318, postoperative 323 +/- 280 dyn x s/cm5, p < 0.05; PAP preoperative 71 +/- 40, postoperative 41 +/- 40 mm Hg + right atrial pressure, p < 0.05). End diastolic and end systolic RV area decreased from 33 +/- 12 to 23 +/- 8 cm2, respectively, from 26 +/- 10 to 16 +/- 6 cm2, p < 0.05. There was an increase in systolic RV fractional area change from 20 +/- 12 to 30 +/- 16%, p < 0.05. RV systolic pressure rise remained unchanged (516 +/- 166 vs. 556 +/- 128 mm Hg/sec). LV ejection fraction remained within normal ranges (64 +/- 16 vs. 62 +/- 12%). Echocardiographically determined cardiac index increased from 2.8 +/- 0.74 to 4.1 +/- 1.74 l/min/m2. A decrease in LV excentricity indices (end diastolic: 1.9 +/- 1 vs. 1.1 +/- 0.3, end systolic: 1.7 +/- 0.6 vs. 1.1 +/- 0.4, p < 0.05) proved a normalization of preoperatively altered septum motion. LV diastolic filling returned to normal limits: (E/A ratio: 0.62 +/- 0.34 vs. 1.3 +/- 0.8; p < 0.05); Peak E velocity: 0.51 +/- 0.34 vs. 0.88 +/- 0.28 m/sec, p < 0.05; Peak A velocity: 0.81 +/- 0.36 vs. 0.72 +/- 0.42 m/sec, ns; E deceleration velocity: 299 +/- 328 vs. 582 +/- 294 cm/sec2, p < 0.05; Isovolumic relaxation time: 134 +/- 40 vs. 83 +/- 38 m/sec, p < 0.05). We could show a marked decrease in RV afterload shortly after PTE with a profound recovery of right ventricular systolic function--even in case of severe pulmonary hypertension. A decrease in paradoxic motion of the interventricular septum and normalization of LV diastolic filling pattern resulted in a significant increase of cardiac index.     

Effects of postural changes on left atrial function in patients with hypertrophic cardiomyopathy

BACKGROUND: We assessed left atrial function in normal subjects and in patients with hypertrophic cardiomyopathy (HCM) by using Doppler echocardiography at the supine position and after sudden standing. METHODS AND RESULTS: Twenty-seven patients with hypertrophic obstructive cardiomyopathy (HOCM), 17 patients with HCM, and 35 normal subjects were studied. From the transmitral Doppler flow velocities, peak early and late (E and A) waves, E/A ratio, and time velocity integrals (Ei and Ai) were calculated. Left atrial active contribution (LAAC) was assessed as the ratio Ei/(Ei + Ai). Furthermore, isovolumetric relaxation time (IVRT) was estimated by means of Doppler echocardiography. In the supine position, the E/A ratio was similar in the 3 groups. Conversely, LAAC was significantly higher in patients with HOCM (24.4 +/- 2.0) and in patients with HCM (23.3 +/- 3.3) compared with normal subjects (20.3 +/- 2.3, P <.001 and P <.05, respectively). After sudden standing, LAAC increased significantly in normal subjects by 11%, in patients with HOCM by 24%, and in patients with HCM by 13% (P <.001). Similarly, IVRT increased significantly in all study groups (P <. 001). By using stepwise forward multiple linear regression analysis, we found that LAAC was associated with age, IVRT, and body mass index in the supine position and with diastolic blood pressure and IVRT in the standing position. CONCLUSIONS: Left atrial contribution to left ventricular filling was increased after sudden changes of posture in normal subjects and in patients with HOCM or HCM.     

Increased intraventricular velocities: an unrecognized cause of systolic murmur in adults

OBJECTIVES: The purpose of this study was to determine the frequency, clinical features and echocardiographic characteristics of increased intraventricular velocities (IIVs) in patients referred to the echocardiography laboratory for systolic murmur. BACKGROUND: A subset of patients referred to the echocardiography laboratory for evaluation of a systolic murmur have IIVs in the absence of other recognized causes of systolic murmur. METHODS: We prospectively studied echocardiograms from 108 consecutive patients referred for evaluation of a systolic murmur. Clinical data were obtained from patient examinations and medical records. RESULTS: The sole explanation for systolic murmur was IIVs in 16.7% of referred patients. Compared with those without IIVs, patients with IIVs had a higher ejection fraction (EF) (58.7+/-7.8% vs. 51.1+/-12.5%, p < 0.001), percent fractional shortening (42.3+/-9.7% vs. 31.0+/-11.4%, p < 0.0001), left ventricular (LV) mass index (181+/-70 vs. 152+/-48 g/m2, p=0.046) and prevalence of hypertension (73.3% vs. 51.7%, p=0.043) and a lower prevalence of segmental wall motion abnormalities (2.2% vs. 39.3%, p < 0.001). CONCLUSIONS: Increased intraventricular velocities are a common cause of systolic murmur in this group of patients and should be included in the differential diagnosis of systolic murmurs in adults. The association of IIVs with LV hypertrophy should be a clinical consideration when these murmurs are identified.     

Preclinical cardiac dysfunction in transfusion-dependent children and young adults detected with low-dose dobutamine stress echocardiography

Transfusion-dependent (TD) patients develop cardiac iron overload that will eventually lead to cardiac pump failure. Low-dose dobutamine stress echocardiography may complement resting echocardiography and identify preclinical myocardial dysfunction caused by early cardiac hemosiderosis. Twenty-six iron-overloaded TD patients had stress echocardiography with 5 microg/kg per minute of dobutamine. Indexed left ventricular (LV) mass, LV dimensions, meridional wall stress, and cardiac index were significantly increased. TD patients had similar LV shortening fraction by M-mode (40.5% +/- 5.6% vs 39.4% +/- 4.5%) but had a lower mean LV ejection fraction (53.3% +/- 3.9% vs 46.8% +/- 6.9%, P < .002) and a subnormal increase in cardiac index during dobutamine stress (35% +/- 20% vs 11% +/- 16%, P < .0001). Impairment in LV relaxation was demonstrated by a prolonged isovolumetric relaxation time (0.060 +/- 0.005 vs 0.088 +/- 0.019 seconds, P < .0001), increased peak mitral E wave, and abnormal E/A ratio. Asymptomatic TD patients demonstrate decreased systolic functional reserve and abnormal left ventricular relaxation that may be caused by cardiac hemosiderosis. Low-dose dobutamine stress echocardiography may be useful for detecting and following cardiac dysfunction in patients at risk for cardiac hemosiderosis.     

Short deceleration time of mitral inflow E velocity: prognostic implication with atrial fibrillation versus sinus rhythm

The present study retrospectively identified 367 patients who had restrictive physiology as defined by deceleration time < or = 130 msec; 293 were in sinus rhythm (SR) (194 men and 99 women; mean age 64 +/- 14 years) and 74 were in atrial fibrillation (AF) (51 men and 23 women; mean age 72 +/- 11 years; p < 0.001). Both groups had similar underlying diagnoses and no significant difference in Doppler indices (E wave, 96 +/- 23 vs 99 +/- 22 cm/sec in SR and AF, respectively; deceleration time, 116 +/- 12 vs 116 +/- 13 msec; and left ventricular outflow tract time velocity integral, 14.8 +/- 4.8 vs 14.5 +/- 4.4 cm). Left ventricular ejection fraction was significantly lower in SR patients (29% +/- 16% vs 39% +/- 20%; p = 0.0003). There were 120 deaths (41%) in the SR group and 35 (47%) in the AF group (median follow-up for both groups, 2.2 years). Restrictive physiology as defined by Doppler echocardiography (deceleration time < or = 130 msec) appears to predict a similar poor prognosis with AF as with SR.     

Midwall fractional shortening is an independent predictor of left ventricular diastolic dysfunction in asymptomatic patients with systemic hypertension

Conventional measures of left ventricular (LV) systolic performance suggest that diastolic dysfunction precedes the development of systolic dysfunction in hypertension. Midwall fractional shortening is a new measure of systolic function that identifies hypertensive patients who have evidence of target-organ damage, impaired contractile reserve, and increased mortality. We therefore sought to determine whether depressed midwall fiber shortening is associated with abnormal diastolic function. Echocardiograms were obtained in 102 otherwise healthy hypertensive patients without treatment with normal conventional measures of systolic function. Of these, 15 had depressed midwall shortening based on previously described normative relations. Patients with depressed midwall shortening had slightly higher blood pressure. Abnormal diastolic function, defined as late (A) LV inflow velocity greater than early (E) velocity, was observed in 33% of those with normal midwall shortening but in 60% of those with depressed shortening (p <0.05). Patients with A/E >1 had lower absolute midwall fiber shortening (15 +/- 3% vs 18 +/- 3%, p <0.0001) but similar endocardial shortening. Patients with abnormal midwall shortening had higher A/E and longer isovolumic relaxation times (both p <0.05). In multivariate analysis, midwall fractional shortening, age, and heart rate were independent predictors (p <0.01) of A/E in a model including blood pressure, LV mass, and endocardial shortening. We conclude that subnormal midwall shortening predicts LV diastolic abnormalities in this population of hypertensive patients with otherwise normal measures of LV systolic function. Contrary to our previous understanding, depressed LV systolic performance, when identified with this newer method, occurs coincidentally with impaired diastolic function.     

Exercise hemodynamics in small (< or = 21 mm) aortic valve prostheses assessed by Doppler echocardiography

Exercise Doppler echocardiography was used to assess hemodynamics in 25 patients with a < or = 21 mm aortic valve prosthesis (14 with a Medtronic-Hall 21 mm valve, three with a Medtronic-Hall 20 mm valve, three with a Sorin 21 mm valve, one with a Duromedics 21 mm valve, and four with a Carpentier-Edwards 21 mm valve). A symptom-limited upright bicycle exercise test was performed, and Doppler gradients were recorded during exercise. Gradients increased with exercise from 30 +/- 8/16 +/- 4 mm Hg (peak/mean) at rest to 46 +/- 12/24 +/- 7 mm Hg during exercise; both p < 0.001. Mean exercise gradient exceeded 30 mm Hg in five patients, and the highest mean gradient recorded was 37 mm Hg. Within the group of mechanical valves, gradients at exercise were similar for different types of valves. A linear relationship was found between gradients at rest and during exercise (peak r = 0.75, mean r = 0.77; both p < 0.001). Additional findings were midventricular velocities exceeding 1.5 m/sec in late systole in 10 patients (40%) and intraventricular flow (> or = 0.2 m/sec) toward the apex during isovolumic relaxation in 11 patients (44%). The patients with these velocity patterns had significantly smaller left ventricular cavities (end-diastolic diameter 39.8 +/- 4.8 vs 46.5 +/- 4.2 mm, p < 0.01; end-systolic diameter 24.2 +/- 3.0 vs 28.5 +/- 4.5 mm, p = 0.013).(ABSTRACT TRUNCATED AT 250 WORDS)     

Limb salvage and survival rates among elderly patients with advanced limb ischemia

Beta-Thalassemia hemoglobin E (beta-thal/Hb E) is the commonest form of hemoglobinopathy in Thailand. Shortened red cell life span, rapid iron turnover and tissue deposition of excess iron are major factors responsible for functional and physiological abnormalities found in various forms of thalassemia. Increased deposition of iron had been found in renal parenchyma of thalassemic patients, but no systematic study of the effect of the deposits on renal functions has been available. The purpose of this study is to describe the functional abnormalities of the kidney in patients with beta-thal/Hb E and provide evidence that increased oxidative stress might be one of the factors responsible for the damage. Urine and serum samples from 95 patients with beta-thal/Hb E were studied comparing with 27 age-matched healthy controls. No difference in the creatinine clearance was observed. beta-thal/Hb E patients excreted significantly more urinary protein (0.8+/-0.5 vs. 0.3+/-0.1 g/day, p < 0.001). Aminoaciduria was found in 16 % of the patients. Analysis of urinary protein by SDS-PAGE electrophoresis and silver staining revealed abnormal pattern of protein with increased small molecular weight (<45 kD) bands. Morning urine analysis showed significant lower urine osmolality (578.3+/-164.6 vs. 762.4+/-169.9 mosm/kg, p < 0.001) in patients. Patients excreted more NAG (N-acetyl beta-D-glucosaminidase, 26.3+/-41.3 vs. 8.4+/-3.9 U/g Cr, p < 0.0001) and beta2-microglobulin, 124.3+/-167 vs. 71+/-65.5 microg/g Cr, p = 0.001. Plasma and urine MDA (malonyldialdehyde) levels were both raised (p < 0.0001). Nine patients were selected for renal acidification study. All were found to be normal, but showed poor response to DDAVP challenge (urine osmolality 533+/-71). This is the first report of renal tubular defects found associated with beta-thal/Hb E disease. The mechanism leading to the damage is not known but it might be related to increased oxidative stress secondary to tissue deposition of iron, as indicated by the raised levels of serum and urine MDA. It is not known whether these functional defects would have any long-term effects on the patients. Further studies are warranted and means of prevention of these defects should urgently be sought.     

Evaluation of left ventricular early diastolic performance by color tissue Doppler imaging of the mitral annulus

A noninvasive assessment of left ventricular (LV) diastolic performance by tissue Doppler imaging was performed in 56 patients (8 patients with atypical chest pain, 42 with coronary artery disease with a previous myocardial infarction, and 6 without a previous myocardial infarction) who underwent cardiac catheterization. Mitral annular velocity (MAV) during early ventricular diastole was obtained by M-mode color tissue Doppler imaging at the posterior corner of the mitral annulus. In each patient, the negative peak of the first derivative of LV pressure decay (peak -dP/dt) and a time constant of LV relaxation (tau) were calculated from the LV pressure waves obtained by a catheter-tip micromanometer. LV end-systolic volume index was measured from contrast left ventriculography. MAV during early diastole was significantly correlated with tau (r = -0.73, p <0.001), peak -dP/dt (r = 0.58, p <0.001), and LV end-systolic volume index (r = -0.63, p <0.001). On multivariate regression analysis with MAV during early diastole, tau and LV end-systolic volume index were selected as prime determinants (r = 0.80, p <0.001). These findings suggest that MAV during early diastole has a direct relation to LV elastic recoil as well as to LV relaxation. MAV during early diastole gives important information regarding LV behavior in late systole to early diastole where LV early diastolic performance is determined.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

Hypothesis of the compression of morbidity: an example of theoretical development in epidemiology]

To assess the usefulness of the tissue Doppler imaging variables for the evaluation of left ventricular (LV) systolic function, we compared variables obtained by the pulsed Doppler method with the LV ejection fraction (%EF) and the maximum value for the first derivative of LV pressure (peak dP/dt). We examined 65 patients, including 15 patients with noncardiac chest pain, 15 with ischemic heart disease, 15 with dilated cardiomyopathy, 10 with hypertensive heart disease, and 10 with asymmetric septal hypertrophic cardiomyopathy. The subendocardial systolic wall motion velocity patterns were recorded for LV posterior wall and ventricular septum in the parasternal LV long-axis view. The peak dP/dt was significantly lower in the hypertensive heart disease, hypertrophic cardiomyopathy, and dilated cardiomyopathy groups. The peak systolic velocity was lower and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall was longer in the hypertensive heart disease (5.9 +/- 0.5 cm/sec and 215 +/- 21 msec, respectively), hypertrophic cardiomyopathy (6.2 +/- 0.9 cm/sec and 217 +/- 17 msec, respectively), and dilated cardiomyopathy (5.2 +/- 0.8 cm/sec and 235 +/- 26 msec, respectively) groups than in the noncardiac chest pain (7.7 +/- 0.9 cm/sec and 187 +/- 24 msec, respectively) and the ischemic heart disease (7.6 +/- 0.8 cm/sec and 184 +/- 22 msec, respectively) groups. In all groups, the peak systolic velocity and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall correlated directly and inversely, respectively, with the %EF (r = 0.59, p < 0.0001; r = -0.59, p < 0.0001) and the peak dP/dt (r = 0.75, p < 0.0001; r = -0.68, p < 0.0001). Both tissue Doppler variables for the ventricular septum did not correlate with the %EF but roughly correlated with peak dP/dt. We conclude that the systolic LV wall motion velocity parameters obtained by pulsed tissue Doppler imaging may be useful for noninvasive evaluation of global LV systolic function in patients with no regional asynergy.     

Changes in left ventricular diastolic function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy

BACKGROUND: Nonsurgical septal reduction therapy (NSRT) decreases left ventricular outflow tract (LVOT) gradient and improves symptoms in patients with hypertrophic obstructive cardiomyopathy (HOCM). NSRT effects on LV/left ventricular diastolic function are currently unknown. METHODS AND RESULTS: HOCM patients (n=29) had Doppler echocardiography at baseline and 6 months after NSRT to evaluate changes in LV volume, pre-A-wave pressure, early diastolic mitral annulus velocity (Ea) by tissue Doppler, and tau. At 6 months, a significant reduction in LVOT gradient (from 53.6+/-15 to 6+/-5 mm Hg; P<0.001) was accompanied by improvement in exercise duration (from 284+/-147 to 408+/-178 seconds; P=0.04) and New York Health Association class (from III to I; P<0.001). Pre-A pressure (18+/-6 to 14+/-5 mm Hg; P<0.01) and tau (62+/-8 to 51+/-8 ms; P<0.01) decreased, whereas Ea (5.8+/-1.8 to 8+/-1.8 cml/s; P<0.01) and LV end-diastolic volume (117+/-16 to 130+/-22 mL; P<0.01) increased. CONCLUSIONS: NSRT improves LV relaxation and compliance, which contributes to the symptomatic relief seen at 6 months.     

A novel monoclonal antibody permitting recognition of NKT cells in various mouse strains

OBJECTIVES: The purpose of this study was to determine whether restrictive left ventricular (LV) filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. BACKGROUND: We recently demonstrated a diastolic ventricular interaction in approximately 50% of a series of patients with chronic heart failure, as evidenced by paradoxic increases in LV end-diastolic volume despite reductions in right ventricular end-diastolic volume during volume unloading achieved by lower body negative pressure (LBNP). We reasoned that such an interaction would impede LV filling in mid and late diastole, but would be minimal in early diastole, resulting in a restrictive LV filling pattern. METHODS: Transmitral flow was assessed using pulsed wave Doppler echocardiography in 30 patients with chronic heart failure and an LV ejection fraction < or = 35%. Peak early (E) and atrial (A) filling velocities and E wave deceleration time were measured. Left ventricular end-diastolic volume was measured using radionuclide ventriculography before and during -30-mm Hg LBNP. RESULTS: Nine of the 11 patients with and 2 of the 16 patients without restrictive LV filling patterns (E/A > 2 or E/A 1 to 2 and E wave deceleration time < or = 140 ms) increased LV end-diastolic volume during LBNP (p = 0.001). The change in LV end-diastolic volume during LBNP was correlated with the baseline A wave velocity (r = -0.52, p = 0.005) and E/A ratio (r = 0.50, p = 0.01). CONCLUSIONS: Restrictive LV filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. Volume unloading in the setting of diastolic ventricular interaction allows for increased LV filling. Identifying patients with chronic heart failure and restrictive filling patterns may therefore indicate a group likely to benefit from additional vasodilator therapy.     

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.     

Cardiac pacing following surgery for acquired heart disease

BACKGROUND: This study is comprised of 3493 consecutive patients who underwent open heart surgery at our institution. Data on all patients were collected prospectively. METHODS: In 45 patients (Group P) (1.3%), a permanent pacemaker (PP) was inserted postoperatively. For the purpose of the study, these patients were compared to 3448 patients (Group NP) who did not require insertion of a PP after surgery. Mean follow-up was 33 months (range 1.5 to 66). RESULTS: We found Group P patients were older (64.8 +/- 11.0 vs 61.0 +/- 11.0 years, p < 0.05), had a higher proportion of elderly (> 70 years) 36% vs 19%, p = 0.01), and of female patients (48.8% vs 22.7%, p < 0.001) compared to Group NP. Group P also had a higher incidence of preoperative rhythm abnormalities (26.6% vs 5.7%, p < 0.0001), redo surgery (13.3% vs 4.6%, p = 0.02), aortic valve surgery (48.8% vs 10.8%, p < 0.001), and tricuspid valve surgery (repair 3, replacement 1) (8.8% vs 0.5%, p < 0.001), in addition to a higher proportion of patients in whom cold (vs warm) blood cardioplegia was used (68.8% vs 52.3%, p = 0.03). Indication for postoperative PP was sick sinus syndrome (SSS) in nine patients; atrial fibrillation in eight patients; atrioventricular block (AVB) in 27 patients; and combined AVB/SSS in 1 patient. There were no operative deaths in Group P. Necessity for PP after heart surgery had a significant impact on resource utilization resulting in prolonged ventilation (3.1 +/- 7.5 vs 1.4 +/- 3.3 days, p < 0.01), intensive care unit (5.1 +/- 10.2 vs 2.5 +/- 4.0 days, p < 0.01), and postoperative hospital stay (18.0 +/- 13.4 vs 8.1 +/- 9.4 days, p < 0.01). CONCLUSIONS: By multivariate logistic regression (odds ratio and p value in parentheses), aortic valve surgery (8.23, p = 0.001), the absence of preoperative sinus rhythm (5.60, p = 0.001), postoperative myocardial infarction (3.46, p = 0.024), and female gender (2.52, p = 0.003), were found to be independent predictors for PP requirement post surgery.     

Diastolic function parameters and atrial arrhythmias in patients with arterial hypertension

OBJECTIVE: To investigate in patients with arterial hypertension (HT) the extent of left ventricular (LV) hypertrophy and diastolic function in relation to atrial arrhythmias. PATIENTS AND METHODS: In 112 hypertensive patients (40 women, 72 men; mean age 50 +/- 6.6 years) with a mean systolic blood pressure for the cohort of 170 +/- 5 mmHg, their first invasive coronary angiography was performed between July 1995 and October 1997 because of angina pectoris and/or an abnormal stress electrocardiogram. After excluding coronary heart disease LV dimensions and diastolic function were measured by echocardiography; in 59 of the 112 patients LV hypertrophy was demonstrated. In addition, long-term blood pressure monitoring, exercise and long-term electrocardiography, late-potential analysis and measurement of heart rate variability were undertaken. The control group consisted of 51 patients without arterial hypertension after exclusion of coronary heart disease. RESULTS: Even in the hypertensive patients without LV hypertrophy diastolic LV function and ergometric exercise capacity were reduced. The risk of LV arrhythmias was significantly higher in patients with LV hypertrophy than those without and in the control group, as measured by the complexity of atrial arrhythmias (P < 0.001), the incidence of abnormal late potentials (P < 0.001) and reduction in heart rate variability (29.3 +/- 5.3 ms vs 47.8 +/- 12.1 ms vs 60.7 +/- 6.6 ms; P < 0.001). There were similar results regarding severe complex atrial arrhythmias (38.5 vs 15.0 vs 0%; P < 0.001). The incidence of atrial arrhythmias correlated with the LV diameter (r = 0.68, P < 0.001), LV morphological dimensions and diastolic function (isovolumetric relaxation time r = 0.44, P < 0.001) and the ratio of early to late diastolic inflow (r = 0.46; P < 0.001). CONCLUSIONS: Hypertensive patients have a higher risk of atrial and ventricular arrhythmias, depending on the degree of LV hypertrophy. But atrial arrhythmias, in contrary to ventricular arrhythmias, are also closely related to abnormalities in LV diastolic function.