Search

The purpose of this study was to assess the effect of heart rate on left ventricular (LV)-arterial coupling and LV mechanical efficiency before and after heart failure (CHF). The production of LV stroke work (SW) and mechanical efficiency depends on the coupling of the LV and arterial system. The response of LV-arterial coupling to tachycardia may be altered in heart failure. We compared the response of LV-arterial coupling to increased heart rate (HR) in six conscious, instrumented dogs before and after pacing-induced CHF. Coupling was quantified as E(ES)/ E(A), where E(ES) is the slope of end-systolic pressure ( P)-volume ( V) relation, and E(A) is arterial elastance. Mechanical efficiency was determined as the ratio of SW to a total P-V area (PVA). Before CHF, E(ES) and E(A) increased similarly with increased heart rate to 180 min(-1). Thus, E(ES)/ E(A) remained unaltered (0.96 +/- 0.08 vs 0.94 +/- 0.35), and SW/PVA was unchanged (0.62 +/- 0.03 vs 0.59 +/- 0.06). Compared with the results prior to CHF and after CHF the resting E(ES) was decreased, thus both E(ES)/ E(A) (0.58 +/- 0.09) and SW/PVA (0.48 +/- 0.06) were less ( P << 0.05) than baseline. After CHF, an increase in HR to 180 min(-1) increased E(A) but not E(ES), thus E(ES)/ E(A) fell to 0.44 +/- 0.06 ( P << 0.05) and SW/PVA fell to 0.41 +/- 0.05 ( P << 0.05). Under normal conditions, LV-arterial coupling remains optimal during increases in HR. After CHF, tachycardia exacerbates the suboptimal baseline LV-arterial coupling, reducing the efficiency of producing SW.

Wave intensity (WI) is a novel hemodynamic index, which is defined as (d P/d t) x (d U/d t) at any site of the circulation, where d P/d t and d U/d t are the derivatives of blood pressure and velocity with respect to time, respectively. However, the pathophysiological meanings of this index have not been fully elucidated in the clinical setting. Accordingly, we investigated this issue in 64 patients who underwent invasive evaluation of left ventricular (LV) function. WI was obtained at the right carotid artery using a color Doppler system for blood velocity measurement combined with an echo-tracking method for detecting vessel diameter changes. The vessel diameter changes were automatically converted to pressure waveforms by calibrating its peak and minimum values by systolic and diastolic brachial blood pressures. The WI of the patients showed two sharp positive peaks. The first peak was found at the very early phase of LV ejection, while the second peak was observed near end-ejection. The magnitude of the first peak of WI significantly correlated with the maximum rate of LV pressure rise (LV max. d P/d t) (r = 0.74, P << 0.001). The amplitude of the second peak of WI significantly correlated with the time constant of LV relaxation (r = -0.77, P << 0.001). The amplitude of the second peak was significantly greater in patients with the inertia force of late systolic aortic flow than in those without the inertia force (3,080 +/- 1,741 vs 1,890 +/- 1,291 mmHg m s(-3), P << 0.01). These findings demonstrate that the magnitude of the first peak of WI reflects LV contractile performance, and the amplitude of the second peak of WI is determined by LV behavior during the period from late systole to isovolumic relaxation. WI is a noninvasively obtained, clinically useful parameter for the evaluation of LV systolic and early diastolic performance at the same time.

Background: Although decreased heart rate variability (HRV) is an independent predictor of death in various populations, its prognostic value in patients with end-stage renal disease on chronic haemodialysis is unknown., Methods: We prospectively studied 120 chronic haemodialysis patients (age 61+/-11 years; males 51%; diabetics 38%; duration of haemodialysis therapy 50+/-114 months) who underwent 24 h electrocardiography at baseline for analysis of time- and frequency-domain HRV., Results: All HRV measures in the patients were significantly reduced compared with those obtained from 62 age-matched healthy subjects. During a follow-up period of 26+/-10 months, 21 patients died (17.5%); 10 from cardiac causes and 11 from non-cardiac causes (seven fatal strokes and four other causes). A Cox proportional hazards model revealed that, of the HRV measures, decreases in the triangular index (TI), very-low-frequency (0.0033-0.04 Hz) power, ultra-low-frequency (<0.0033 Hz) power (ULF) and the ratio of low-frequency (0.04-0.15 Hz) power to high-frequency (0.15-0.4 Hz) power had significant predictive value for cardiac death. None of the HRV measures, however, had predictive value for non-cardiac death, including stroke death. Even after adjustment for other univariate predictors including age, diabetes, serum albumin and coronary artery disease, the predictive value of decreased TI and ULF remained significant-adjusted relative risk (95% confidence interval) per 1 SD decrement of TI and ULF, 3.28 (1.08-9.95) and 1.92 (1.01-3.67), respectively., Conclusions: Decreases in some HRV measures, particularly those reflecting long-term variability, are independent predictors of cardiac death in chronic haemodialysis patients.

The objective of the present study was to establish that HDL3 has a greater antiperoxidative effect on the peroxidative modification of LDL than HDL2 has. The protective influence of HDL subfractions on this form of LDL modification was examined in samples by measuring the concentration of thiobarbituric acid-reactive substance (TBARS), as well as the electrophoretic mobility of LDL. LDL was incubated for 96 hours in phosphate-buffered saline (PBS) alone, without the addition of transition-metal ions or in the presence of PBS and HDL2 or HDL3. All samples were subjected to agarose gel electrophoresis. Both HDL2 and HDL3 significantly inhibited peroxidative modification of LDL, as assessed by electrophoretic mobility, but this effect was much more pronounced with HDL3. HDL3 may play a more important role than HDL2 in the prevention of atherosclerosis in vivo by more effectively inhibiting LDL peroxidation.

The mechanism of emergence and the clinical significance of apically directed intraventricular flow during isovolumic relaxation were investigated. The relation between the spatial distribution of the flow and left ventricular (LV) apical wall motion abnormality, as well as LV performance, was studied in 97 patients who underwent cardiac catheterization for evaluation of chest pain. According to the distribution of the flow, the patients were classified into the following 3 groups: flow observed in the whole area between the tip of the papillary muscle and the apex (spread flow) (n = 38), flow observed in the same area that did not fill the whole area (localized flow) (n = 15), and no apparent flow observed in the area (without flow) (n = 44). An absence of flow disclosed apical asynergy with a sensitivity of 97% and specificity of 87%. The time constant of LV relaxation was significantly shorter in patients with spread flow than in those without flow. A significant difference was also observed in end-systolic volume index (18.8 +/- 6.8 vs 30.9 +/- 7.7 vs 42.3 +/- 20.2 mL/m(2), spread flow < localized flow < without flow, P <.05) among the 3 groups. The propagation velocity of LV early diastolic filling flow was significantly greater in patients with spread flow (47.0 +/- 8.3 cm/s) than in those with localized flow (30.7 +/- 7.8 cm/s) or without flow (28.6 +/- 7.8 cm/s) (P <.001). These findings indicate that the greater magnitude of LV elastic recoil and the faster LV relaxation in patients without LV apical asynergy produce apically directed intraventricular flow during isovolumic relaxation, enhancing the speed of LV early diastolic filling. Apically directed intraventricular flow during isovolumic relaxation may play an important role as a mediator of better LV systolic performance and LV relaxation to LV early diastolic filling. Absence of apically directed intraventricular flow during isovolumic relaxation is a manifestation of LV apical asynergy and global LV dysfunction from end systole to early diastole.

Unlabelled: In patients with myocardial infarction (MI), an expansion of the remote normal regions of the left ventricle is often observed. However, the characteristics of such regions are not fully understood. Thus, we investigated this issue from the standpoint of myocardial oxidative metabolism using (11)C-acetate PET., Methods: In 33 patients with recent MI (24 not receiving beta-blockers, 9 receiving beta-blockers) and 12 age-matched normal control subjects, (11)C-acetate dynamic myocardial PET scanning was performed at rest. Time-activity curves of (11)C-acetate in 5-7 regions of interest (ROIs) on the midventricular transaxial image in each subject were generated, and the clearance rate constant (K(mono)) in each ROI was calculated by monoexponential fitting as an index of myocardial oxidative metabolism. The left ventricular (LV) end-diastolic volume index as an index of LV remodeling and the heart rate. pressure product were obtained in all subjects., Results: The LV end-diastolic volume index was significantly larger in patients with MI without beta-blockers than in normal control subjects (101 +/- 22.5 vs. 61.6 +/- 12.8 mL x m(-2); P < 0.001). There was no significant difference in the heart rate x pressure product between the patients with MI without beta-blockers and the normal control subjects (8,229 +/- 1,503 vs. 8,311 +/- 1,311 mm Hg x min(-1)). The K(mono) in remote normal regions was significantly greater in patients with MI without beta-blockers even when compared with the highest K(mono) on the anteroseptal wall of the left ventricle in normal control subjects (0.078 +/- 0.022 vs. 0.065 +/- 0.007 min(-1); P < 0.01). In contrast, the heart rate. pressure product (6,911 +/- 1,135 mm Hg x min(-1)) and the K(mono) (0.054 +/- 0.009 min(-1)) in remote normal regions were significantly less in patients with beta-blockers than in those without beta-blockers (P < 0.001). No significant difference in the LV end-diastolic volume index was found between the MI patients with and without beta-blockers. Multivariate regression analysis showed that beta-blockers significantly and directly decreased the K(mono) in remote normal regions after adjusting the effect of the heart rate x pressure product, although the prime determinant of the K(mono) in such regions was the heart rate x pressure product., Conclusion: Myocardial oxidative metabolism in remote normal regions is accelerated in the left ventricles with remodeling after acute MI. Therapy using beta-blockers normalizes the myocardial oxidative metabolism in such regions through the reduction of the heart rate x pressure product and their direct effect on the myocardium.

The R-R interval of the electrocardiogram during atrial fibrillation (AF) appears absolutely irregular. However, the Poincaré plot of the R-R interval reveals a sector shape of distribution that is unique to AF. Furthermore, the height of lower envelope (LE1.0) of the distribution and the degree of scatter above the envelope (scattering index) may reflect the refractoriness and concealment of atrioventricular (AV) conduction, respectively. We previously observed that both the LE1.0 and scattering index show clear circadian rhythms in patients with chronic AF and that the rhythms are blunted in those with congestive heart failure and chronic AF. In the present study, we examined if the blunted circadian rhythm of the AV conduction has prognostic value in patients with chronic AF. We studied a retrospective cohort of 120 patients who underwent 24h Holter monitoring at baseline. During an observation period of 33 +/- 16 mon, there were 25 deaths (21%) including 13 cardiac and 8 stroke deaths. All patients showed significant circadian rhythms in both LE1.0 and scattering index with acrophases occurring at night; however, patients dying subsequently from cardiac causes, but not those from fatal stroke were blunted in the circadian rhythms (the amplitudes were < 55% of those in surviving patients). Furthermore, the reduced circadian amplitude of scattering index was an increased risk for cardiac death even after adjustment of coexisting cardiovascular risks [adjusted relative risk (95% confidence interval) per 1-SD decrement, 4.24 (1.54-11.6)]. When patients were divided by the circadian amplitude of the scattering index of 36.5 msec (mean minus 1-SD), the 5yr cardiac mortality below and above the cutoff was 57 and 6%, respectively (log-rank test, p < 0.001). We conclude that the blunted circadian rhythm of AV conduction is an independent risk for cardiac death in patients with chronic AF.

Aims: To evaluate the effect of considerably high left ventricular filling pressure with mitral regurgitation on mitral annular velocity during early diastole., Subjects: Two hundred and forty-three patients who underwent cardiac catheterization for evaluation of chest pain., Methods: Mitral annular velocity during early diastole was measured by colour M-mode tissue Doppler imaging. Patients were divided into the following three groups according to the cardiac catheterization data. Group A (n=147): patients having left ventricular relaxation time constant tau<46 ms and left ventricular end-systolic volume index <38 ml m(-2); group B (n=88): patients having tau>or=46 ms and/or end-systolic volume index >or=38 ml m(-2); group C (n=8): patients having mean pulmonary capillary wedge pressure >or=16 mmHg in addition to tau>or=46 ms and end-systolic volume index >or=38 ml m(-2)., Results: Mitral annular velocity during early diastole was significantly less in group B (4.8+/-1.4 cm s(-1)) than in group A (7.7+/-1.9 cm s(-1)). However, there was no significant difference between groups A and C (8.3+/-0.8 cm s(-1)). A transmitral E/A >1.0 was observed in 12/147 patients of group A, 10/88 of group B, and 8/8 of group C. The incidence of >or=Sellers' grade II mitral regurgitation was higher in group C than the others., Conclusions: A paradoxically faster mitral annular velocity during early diastole is found in patients having left ventricular dysfunction with moderate to severe mitral regurgitation and considerably high left ventricular filling pressure. Attention should be paid to an interpretation of mitral annular velocity during early diastole regarding left ventricular early diastolic performance in patients having mitral regurgitation with an E/A >1.0 in their transmitral flow., (Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.)

Study Objectives: We examined whether autonomic functions assessed by heart rate variability (HRV) during standardized head-up tilt testing (HUTT) predict risk for death in stable patients with coronary artery disease (CAD)., Design and Setting: Retrospective cohort study in medium-sized university general hospital., Measurements and Results: In a cohort of 250 patients with CAD who were undergoing elective coronary angiography, we analyzed HRV during standardized HUTT under paced breathing with discontinuation of treatment with all medications. During a subsequent mean follow-up period of 99 months, there were 13 cardiac deaths and 12 noncardiac deaths. Cox regression analysis adjusted for cardiovascular risks revealed that increased postural change (supine to upright) in the power of low-frequency component (LF) power predicted an increased risk for cardiac death (relative risk [per 1-ln ms(2) increment], 4.36; 95% confidence interval, 1.64 to 11.6), while neither the high-frequency component nor its response to HUTT predicted any form of death. When the patients were trichotomized by the level of postural LF change (large drop, < or = - 0.6 ln[ms(2)]; small drop and rise, > 0 ln[ms(2)]), the three groups did not differ in terms of clinical features or CAD severity at baseline or coronary interventions during the follow-up period; however, the 8-year cardiac mortality rates were 0%, 6%, and 12%, respectively (p = 0.008 [log rank test]). Additionally, the difference was enhanced when analyzed excluding 64 patients who had been treated with a beta-blocker during the follow-up period (0%, 7%, and 15%, respectively; p = 0.006 [log rank test])., Conclusions: The postural response of HRV predicts the risk for death in patients with CAD. Postural LF increase (LF rise), in particular, is an independent risk factor for cardiac death.

Propagation velocity of left ventricular (LV) early diastolic filling flow (PVE) has been acknowledged as a useful parameter for LV early diastolic performance; however, the effect of LV systolic performance on PVE is not fully understood. Thus the purpose of this study was to investigate such an effect. Propagation of LV early diastolic filling flow was visualized by M-mode color Doppler imaging, and the slopes of the peak velocity tracings were measured as PVE in 150 patients who underwent coronary angiography. In cardiac catheterization, mean pulmonary capillary wedge pressure, time constant tau of LV pressure decay, LV end-systolic volume index, and LV ejection fraction were obtained. In univariate regression analysis, PVE significantly correlated with LV end-systolic volume index (r = -0.68, P <.001), LV ejection fraction (r = 0.66, P <.001), and time constant tau (r = -0.52, P <.001). In multivariate regression analysis, PVE was regressed by the LV end-systolic volume index, tau, and mean pulmonary capillary wedge pressure. The contribution of each parameter to the variance of the PVE was 46%, 3%, and 2%, respectively. A break-point linear regression analysis showed that the relation between the LV end-systolic volume index and PVE was much better characterized by a broken line than a straight line. The broken line had a steeper slope in patients with LV end-systolic volume index < or =41 mL/m(2) than in those with >41 mL/m(2). These findings suggest that PVE is determined mainly by LV systolic performance and partly by both LV relaxation and LV filling pressure. Left ventricular systolic performance may play a key role in generating a much faster PVE, especially in patients with relatively better LV systolic performance.

The diastolic dysfunction present at rest in congestive heart failure (CHF) is exacerbated during exercise (Ex). Increases in circulating ANG II and endothelin-1 (ET-1) during Ex may contribute to this response. We assessed the effect of Ex on circulating plasma levels of ANG II and ET-1 and left ventricular (LV) dynamics before and after pacing-induced CHF at rest and during Ex in nine conscious, instrumented dogs. Before CHF, there were modest increases in circulating levels of ANG II (but not ET-1) during Ex. LV diastolic performance was enhanced during Ex with decreases in the time constant of LV relaxation (tau), LV end-systolic volume (V(ES)), and LV minimum pressure with a downward shift of the LV early diastolic portion of the pressure-volume (P-V) loop. This produced an increase in peak LV filling rate without an increase in mean left atrial (LA) pressure. After CHF, the resting values of ANG II and ET-1 were elevated and increased to very high levels during Ex. After CHF, mean LA pressure, tau, and LV minimum pressure were elevated at rest and increased further during Ex. Treatment with L-754,142, a potent ET-1 antagonist, or losartan, an ANG II AT(1)-receptor blocker, decreased these abnormal Ex responses in CHF more effectively than an equally vasodilatory dose of sodium nitroprusside. Combined treatment with both ANG II- and ET-1-receptor blockers was more effective than either agent alone. We conclude that in CHF, circulating ANG II and ET-1 increase to very high levels during Ex and exacerbate the diastolic dysfunction present at rest.

Peroxidatively modified low-density lipoprotein (LDL) may contribute to atherosclerotic processes; therefore, protecting LDL against peroxidation may thus reduce or retard the progression of atherosclerosis. We have evaluated the protective effects of ascorbic acid on copper-catalyzed LDL peroxidative modification. The protective effects of ascorbic acid on copper-catalyzed LDL peroxidative modification were examined by measurement of concentration of lipid hydroperoxides in LDL and by the provision of LDL cholesterol to lymphocytes via LDL receptor-mediated pathway. The measurement of concentration of lipid hydroperoxides in LDL showed that ascorbic acid inhibited peroxidative modification of LDL. Also, ascorbic acid preserved the ability of LDL to be recognized by LDL receptors in peripheral blood lymphocytes to the same extent as native LDL. These findings indicate that ascorbic acid may protect LDL against peroxidative modification, maintaining its ability to act as a ligand for LDL receptors in vivo.

BACKGROUND-Variations in the ventricular response interval (VRI) during atrial fibrillation (AF) may be reduced in patients with adverse clinical outcomes. The properties of VRI dynamics associated with prognosis remain undetermined. METHODS AND RESULTS-In 107 patients with chronic AF (age, 64+/-9 years), we analyzed a 24-hour ambulatory ECG for VRI variability (SD, SD of successive differences, and SD of 5-minute averages) and VRI irregularity (Shannon entropy of histogram, symbolic dynamics, and approximate entropy of beat-to-beat and minute-to-minute fluctuations [ApEn(b-b) and ApEn(m-m)]). During a follow-up period of 33+/-16 months, 18 patients died (17%), 9 from cardiac causes, 7 from fatal strokes, and 2 from malignancies. Reductions in all VRI variability and irregularity measures were associated with an increased risk for cardiac death but not for fatal stroke. A significant association with cardiac death was also found for ejection fraction (relative risk, 1.10; 95% confidence interval [CI], 1.04 to 1.17, per 1% decrement) and ischemic AF (relative risk, 6.52; 95% CI, 1.62 to 26. 3). After adjustment for these clinical variables, all irregularity measures except symbolic dynamics had predictive value (relative risks [95% CIs] per 1SD decrement: Shannon entropy of histogram, 2. 03 [1.14 to 3.61]; ApEn(b-b), 1.72 [1.14 to 2.60]; and ApEn(m-m), 1. 90 [1.03 to 3.52]); however, the predictive power of variability measures was no longer significant. When the patients were stratified with the 33rd and 67th percentile values of ApEn(b-b) (1. 83 and 1.94, respectively), the 5-year cardiac mortality rates for the upper, middle, and lower tertiles were 0%, 13%, and 43%, respectively (log-rank test, P=0.04). CONCLUSIONS-Reduced VRI irregularity in a 24-hour ambulatory ECG has an independent prognostic value for cardiac mortality during long-term follow-up in patients with chronic AF.

Atrial natriuretic peptide (ANP) has potent vasodilatory and natriuretic actions and may have therapeutic benefit in congestive heart failure (CHF). These benefits may be offset by a negative inotropic effect of ANP seen in isolated preparations. However, ANP's integrated effect on left ventricular (LV) contraction and relaxation, independent of loading conditions, both under normal conditions and after CHF, is not known. We studied six conscious dogs, instrumented to measure LV and left atrial pressures and to determine LV volume from three dimensions. ANP produced significant (P<.05) decreases in LV end-systolic pressure (101.2+/-11.8 versus 91.7+/-11.2 mm Hg, P<.05) in normal dogs and in dogs with CHF (93.1+/-6.4 versus 87.1+/- 4.4 mm Hg, P<.05). ANP also caused significant reductions of the slope of end-systolic pressure-end-systolic volume relation both before (7.0 +/-1.5 versus 6.3+/-1.5 mm Hg/ml) and after CHF (4.8+/-1.3 versus 4.4+/-1.2 mm Hg/ml, P<.05). Both before and after CHF, ANP slowed LV relaxation at matched end-systolic pressure. Before CHF, steady-state stroke volume and peak LV filling rate (dV/dt(max)) were reduced. However, after CHF, the fall in end-systolic pressure more than offset the load-independent LV depression, as stroke volume, the rate LV relaxation, and dV/dt(max) were increased and minimum LV pressure reduced. ANP has negative effects on LV contractility and relaxation both before and after CHF. However, after CHF, afterload reduction with ANP overcomes its negative effects, resulting in net improvement of LV ejection and relaxation. Thus, the direct cardiodepressant effects of ANP should not limit its usefulness in CHF.

An abnormal relaxation pattern in transmitral flow velocity waveforms has been observed in older healthy subjects as well as in patients with heart disease. Accordingly, we investigated whether the hemodynamic differences between patients with coronary artery disease (CAD) with an abnormal relaxation pattern in transmitral flow (ratio of E-wave to A-wave velocities < 1.0) and healthy older subjects with an abnormal relaxation pattern can be distinguished with the use of mitral annular velocity (MAV) during early diastole. We measured MAV in the longitudinal direction of the heart during early diastole by M-mode color tissue Doppler imaging in 24 patients with atypical chest pain (defined as healthy subjects in this study) and 70 patients with CAD who underwent cardiac catheterization. In all patients a time constant of left ventricular pressure decay (tau) and the left ventricular (LV) end-systolic volume index were also measured. Twenty-one healthy subjects and 59 patients with CAD had an abnormal relaxation pattern in their transmitral flow. The age, heart rate, mean blood pressure, and ratio of E-wave to A-wave velocities were not different between the two groups. However, the tau was longer and the LV end-systolic volume index was greater in patients who had an abnormal relaxation pattern with CAD than in healthy subjects with an abnormal relaxation pattern. The MAV during early diastole was lower in the former than in the latter (5.8 +/- 1. 9 vs 9.8 +/- 1.9 cm/s, P <.001). Mitral annular velocity during early diastole by M-mode color tissue Doppler imaging can detect the differences in LV relaxation and LV systolic performance between the abnormal relaxation pattern with CAD and the physiologically abnormal relaxation pattern with aging, providing further information regarding the meaning of an LV abnormal relaxation pattern.

Background: Mortality is high in chronic haemodialysis patients with cardiovascular disease, and many of them die suddenly. Reduced heart rate variability (HRV) is an increased risk for death in various populations, but its prognostic value in haemodialysis patients remains uninvestigated., Methods: We analysed the associations between 24-h HRV measures and long-term mortality through a prospective follow-up of 31 chronic haemodialysis patients who underwent diagnostic coronary angiography., Results: Of the 31 patients, at baseline, seven had a previous myocardial infarction, five had a history of congestive heart failure and 14 had significant (> or =75%) coronary stenosis (four had multi-vessel stenosis). During follow-up for 60+/-5 months, 14 patients died, 11 of them suddenly. A left ventricular ejection fraction of <0.45, multi-vessel coronary stenosis, ventricular tachycardia on 24-h ECG and decreased/abnormal 24-h HRV (triangular index <22 and abnormal Poincaré plot) carried a univariate risk of all-cause death, while the risk of sudden death was only correlated with decreased HRV (standard deviation of normal-normal R-R interval <50 ms, triangular index <22 and ultra-low frequency power <8.7 ln(ms2)). Multivariate analysis revealed that a triangular index <22 was the best predictor of increased risk for both all-cause and sudden death (hazards ratio (95% CI); 8.1 (1.3-48.6) and 12.6 (1.3-126.4), respectively) and that the association was independent of cardiac function, macrovascular diseases, ventricular arrhythmias and cardiovascular risk factors. The 5-year mortality when the triangular index was > or =22 or <22 was 33 or 88% for patients with coronary artery disease and 0 or 50% for those without., Conclusions: These results indicate that HRV has an independent prognostic value in chronic haemodialysis patients and identifies an increased risk for all-cause and sudden death.

A 40-year-old woman who had been treated for Takayasu's arteritis was admitted to the hospital with fever, fatigue, malaise, and severe chest pain. Computed tomography of the chest demonstrated massive pericardial effusion and bilateral pleural effusion. In laboratory data, the C-reactive protein was high at 22.0 mg/dL, and erythrocyte sedimentation rate was also high at 80 mm/hr. The diagnosis was pericarditis with a recurrence of the systemic inflammatory process of Takayasu's arteritis. The patient was treated with methylprednisolone pulse therapy. Her massive pericardial effusion disappeared without pericardiocentesis.

Left ventricular (LV) early diastolic performance is determined by LV behavior in the late systole to early diastole and may relate to the physical potential of patients. Isovolumic relaxation flow (IRF) velocity was obtained by continuous Doppler echocardiography in the left ventricle from the apex in 26 patients with atypical chest pain and 63 patients with coronary artery disease (CAD) with or without prior myocardial infarction (MI) who underwent cardiac catheterization. In each patient, a time constant of LV relaxation (tau) was calculated from the LV pressure waves obtained by a catheter-tipped micromanometer. The LV end-systolic volume index was measured using contrast left ventriculography. IRF velocity in patients having CAD with prior MI (24.8 +/- 5.4 cm/s) was significantly less than in those with atypical chest pain (41.2 +/- 9.6 cm/s). It was also significantly less than in patients having CAD without prior MI (37.3 +/- 6.8 cm/s). IRF velocity significantly correlated with the time constant tau (r = -0.42, p < 0.001) and LV end-systolic volume index (r = -0.84, p < 0.001). This study indicates that IRF velocity obtained by continuous Doppler echocardiography in the left ventricle provides important information regarding LV systolic performance and early diastolic performance.

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.

Reverse redistribution (RRD) of 201Tl is often observed in patients with recent myocardial infarction. However, the difference in the extent of myocardial damage between regions with 3-h RRD and those with 24-h RRD remains unknown. Accordingly, we investigated RRD from the standpoint of myocardial oxidative metabolism. Carbon-11 (11C) acetate dynamic myocardial PET scanning was performed at rest in 14 patients with recent myocardial infarction, and the clearance rate constant (Kmono) of 11C-acetate was calculated in 6-7 ROIs on the transaxial image in each patient using a monoexponential fit as an index of myocardial oxidative metabolism. Exercise 201Tl myocardial SPET was also performed. Ninety-two regions corresponding to the PET study were then classified based on the findings of transaxial 201Tl SPET imaging; that is, regions with reverse redistribution, regions with severely decreased 201Tl activity or no 201Tl activity on the 24-h delayed images, and regions with normal 201Tl activity throughout the study. Kmono in regions with reverse redistribution (0.051 +/- 0.009 min-1) was significantly lower than that in regions with normal 201Tl activity throughout the study (0.066 +/- 0.011 min-1) (P < 0.001) but significantly higher than that in regions with severely decreased or no 201Tl activity on the 24-h delayed images (0.037 +/- 0.003 min-1) (P < 0.001). Percent Kmono (i.e. Kmono in region with RRD/the mean of Kmono in all regions with a normal 201Tl SPET result) was significantly lower in the 3-h RRD regions (81.3 +/- 6.3%) than in the 24-h RRD regions (87.6 +/- 6.1%) (P < 0.05). Impairment of myocardial oxidative metabolism is observed in regions with RRD, suggesting that RRD corresponds to mild myocardial damage. Reverse redistribution on 24-h delayed images may indicate much milder myocardial damage compared with RRD on 3-h delayed images.

Objective: The positive inotropic effect of endothelin-1 (ET-1) on normal myocardial contraction may be altered in pathological states. The purpose of this study was to assess the direct effect of ET-1 on cardiomyocyte performance and its cellular mechanism in congestive heart failure (CHF)., Methods: We measured the plasma levels of ET-1 and compared the effects of ET-1 (10(-10)-10(-8) M) on contractile performance and the [Ca2+]i transient in the myocytes of left ventricles (LV) from 15 age-matched normal adult rats and 15 rats with isoproterenol (ISO)-induced CHF., Results: With CHF, the plasma levels of ET-1 (19.7 +/- 6.3 vs. 4.1 +/- 0.5 fmol/ml, p < 0.05) were markedly elevated. In normal myocytes, superfusion of ET-1 caused significant increases in the systolic amplitude (SA, 8-16%) and the peak velocity of shortening (dL/dtmax, 20-35%; p < 0.01) without causing a change in the peak [Ca2+]i transient. In contrast, in myocytes from CHF rats, ET-1 produced significant reductions in SA (9-13%) and in the velocity of relengthening, dR/dtmax (10-14%; p < 0.05). The myocytes' dR/dtmax also decreased by 8-10% (p < 0.05). These changes were associated with a significant decrease in the peak [Ca2+]i transient (20-23%, p < 0.01). These responses to ET-1 were abolished by the incubation of myocytes with an ETA receptor antagonist (BQ123) or a protein kinase C (PKC) inhibitor (H-7 or staurosporine)., Conclusion: ISO-induced CHF is associated with elevated plasma ET-1 and an altered cardiomyocyte response to ET-1. After CHF, ET-1 produces a direct depression of cardiomyocyte contractile performance that is associated with a significant decrease in the peak [Ca2+]i transient. These effects are likely to be mediated through ETA receptors and involve the PKC pathway.

Objectives: The purpose of this study was to determine the level and functional effects of endogenous bradykinin in congestive heart failure (CHF)., Background: There is experimental evidence that bradykinin is increased in several cardiac disease states. However, it is unknown whether plasma levels of bradykinin are elevated in CHF. Further, the cardiac and vascular responses to bradykinin in CHF are unclear., Methods: The circulating levels of bradykinin and the effects of endogenous bradykinin were assessed in eight instrumented, conscious dogs both before and after pacing-induced CHF., Results: Before CHF, the plasma bradykinin level was 53.1 +/- 12.4 pg/ml. Blocking endogenous bradykinin with HOE-140 (0.3 mg/kg), a specific bradykinin B2-receptor antagonist, produced no significant alterations in heart rate, left ventricular (LV) end-systolic pressure (Pes), total systemic resistance (TSR), the time constant of LV relaxation (tau) or the maximal rate of LV filling (dV/dt(max)). However, coronary blood flow was significantly reduced (p < 0.05). LV contractile performance measured by the slopes of pressure-volume relations was unaffected. After induction of CHF, the plasma bradykinin level increased to 234.2 +/- 19.4 pg/ml (p < 0.05). Blocking endogenous bradykinin with HOE-140 reduced coronary blood flow and produced significant increases in Pes and TSR, prolonged tau, decreased dV/dt(max) and elevated minimal LV pressure and mean left atrial pressure. Furthermore, the slopes of pressure-volume relations (p < 0.05) were decreased, indicating depressed contractility with HOE-140 after CHF., Conclusions: Before CHF, endogenous bradykinin results in coronary dilation but has no effect on systemic arterial vasodilation or cardiac performance. After CHF, endogenous bradykinin is significantly increased and, acting through B2-receptors, produces coronary and arterial vasodilation and improves LV relaxation and contractile performance. Thus, endogenous bradykinin may play an important role in preserving cardiovascular function in CHF.

Left ventricular (LV) short- and long-axis contractile function and LV structural changes were serially measured in eight instrumented dogs during the development of congestive heart failure (CHF) induced by rapid right ventricular (RV) pacing. After 10 days of pacing, LV end-diastolic volume (VED) had not increased; however, the slope of LV end-systolic pressure-volume relation had decreased from 7.4 +/- 2.6 to 4.9 +/- 1.1 mmHg/ml (P < 0.05), and the slope of LV stroke work-VED relation had fallen from 78.4 +/- 9.1 to 64.2 +/- 7.2 mmHg (P < 0.05). The slopes of end-systolic pressure-dimension relation and the stroke work area-end-diastolic dimension relation in the short axes (i.e., anteroposterior and septal-lateral) had decreased by 30% (P < 0.05), whereas the slopes of the long-axis (i.e., apical-basal) relations were unchanged (not significant). After 20 days of pacing, VED had significantly increased by 14% due to selective dilation of the short axes by 7%, and LV global contractility had further declined with a 40% contractile depression in the short axes and a 25% contractile depression in the long axis. After 30 days, the long-axis dimension at end diastole was also significantly increased with a further increase in the short-axis dimensions. In contrast to the spherical dilation occurring during CHF, acute volume loading of normal animals produced symmetrical LV dilation. These observations suggest that heterogeneous contractile depression initiates the spherical end-diastolic chamber dilation in pacing-induced CHF.

We compared the effects of pimobendan (0.25 mg/kg i.v.), a Ca++ sensitizer, with some phosphodiesterase-III inhibition effects, and amrinone (1 mg/kg plus 10 microg/kg/min i.v.), a PDE-III inhibitor, on left ventricular (LV) systolic and diastolic performance, both at rest and during exercise, in seven conscious dogs before and after pacing-induced congestive heart failure (CHF). Before CHF, under resting conditions, both pimobendan and amrinone caused a similar significant decrease in left ventricle size and end-systolic pressure, arterial elastance, and the time constant of LV relaxation. Similar results were obtained during exercise. Both agents also produced a similar increase in E(ES), the slope of the LV end-systolic pressure-volume relation (3.4 +/- 1.5 vs. 4.2 +/- 1.1 mm Hg/ml; amrinone vs. pimobendan). After CHF, the vasodilatory effects of amrinone and pimobendan were preserved both at rest and during exercise; however, the inotropic actions were different. After CHF, pimobendan increased E(ES) (3.9 +/- 0.5 vs. 5.7 +/- 0.4 mm Hg/ml, P < .05), decreased the time constant of LV relaxation, increased the maximum rate of LV filling (37 +/- 19 ml/sec) (P < .05) and produced a downward shift of the early diastolic portion of LV pressure-volume loop. Pimobendan also augmented LV contractile performance during CHF exercise. In contrast, after CHF, amrinone no longer produced a positive inotropic effect. Amrinone improved LV relaxation and filling, both at rest and during exercise after CHF, but significantly less than pimobendan. We conclude that after CHF, the cardiac response to a PDE-III inhibitor is attenuated, but the response to Ca++ sensitizer is preserved. Thus, after CHF, pimobendan is more effective than amrinone in enhancing LV contractile state, LV relaxation and LV filling both at rest and during exercise.

We investigated whether the isovolumic relaxation time (IRT) and an interval from the start of opening to the maximal amplitude of the anterior mitral leaflet in early diastole (D-E interval) would be useful predictors of the pulmonary capillary wedge pressure (PCWP). We recorded M-mode mitral echograms and phonocardiograms in 33 patients (aged 38-70 years) with acute myocardial infarction (AMI) in the coronary care unit and in 34 patients (aged 40-75 years) with prior myocardial infarction (OMI) during cardiac catheterization. All patients underwent the insertion of a flow-directed pulmonary artery catheter to obtain the PCWP. We measured the IRT and the D-E interval from the phonocardiograms and the M-mode echograms. There was no significant correlation between the IRT and the mean PCWP (mPCWP) in patients with AMI and in patients with OMI. The D-E interval was significantly and inversely correlated with the mPCWP (r = -0.91, p <0.0001) in all patients. The regression equation was mPCWP = -0.42 x (D-E) +47.9. The D-E interval of < or = 75 ms indicated a high mPCWP (mPCWP > or = 18 mm Hg) with high sensitivity (96%) and specificity (88%). The derived equation was tested in a prospective group of 32 additional patients (aged 43-75 years). A significant correlation was observed between the predicted and measured mPCWP (r = 0.91, p <0.0001). Thus, the PCWP can be estimated by using the D-E interval derived from M-mode mitral echograms in patients in the coronary care unit and in patients with chronic heart disease.

The influences of cardiac loading conditions and left ventricular performance on pulmonary venous flow are poorly understood. The authors studied the effects of volume loading on the pattern of pulmonary venous flow in normal and ischemic hearts. Thirteen anesthetized dogs were equipped with a transit-time ultrasonic flow probe around the left upper pulmonary vein. In 6 of the dogs, the left anterior descending artery was ligated to induce myocardial ischemia. The remaining 7 dogs had normal hearts. Heart rate was fixed at 110 beats/minute by right atrial pacing. Dextran was infused from the femoral vein until mean left atrial pressure increased 3 mm Hg above the baseline value in both groups. In normal heart, systolic pulmonary venous flow volume (SI) increased significantly, but early diastolic flow volume (DI) did not show a significant change during volume loading. The ratio of SI/DI increased significantly (1.12 +/- 0.34 vs 2.11 +/- 0.49, P < 0.05). After ligation of the left anterior descending artery, the SI and DI decreased significantly. The ratio of SI/DI did not show a significant change (0.88 +/- 0.32 vs 0.87 +/- 0.30, ns). In dogs with myocardial ischemia, volume loading caused increases in the SI and DI. However, no significant change was observed in the ratio of SI/DI (0.87 +/- 0.30 vs 0.97 +/- 0.36, ns). These findings demonstrate that left ventricular performance influences the alteration in pulmonary venous flow pattern that is caused by systemic volume loading.

We studied the usefulness of simultaneous evaluation of the Doppler-derived transmitral flow velocity waveform and left ventricular isovolumic relaxation time (IRT) in patients with coronary artery disease (CAD). Subjects consisted of 26 healthy volunteers, 54 patients with prior myocardial infarction (MI), and 27 patients with CAD but without prior MI. IRT was measured as the time from the beginning of the aortic valve closure sound to the onset of transmitral flow. Peak filling velocity during early diastole (E-wave velocity), peak filling velocity during atrial contraction (A-wave velocity), and IRT were compared among the three groups. No significant difference in A-wave velocity was found among these groups. Whereas E-wave velocity was significantly lower and IRT was significantly longer in patients with CAD but without prior MI than in healthy subjects, no significant differences in E-wave velocity or IRT were observed between patients with prior MI and healthy subjects. We then divided the patients with prior MI into two subgroups, one consisting of 45 patients with mean pulmonary capillary wedge pressure (mPCWP) < 16 mm Hg and the other consisting of 9 patients with mPCWP > or = 16 mm Hg. There was no significant difference in A-wave velocity between the two subgroups and healthy subjects. E-wave velocity was significantly lower in patients with MI and lower mPCWP than in healthy subjects, however, no significant difference in E-wave velocity was found between the patients with MI and higher mPCWP and the healthy subjects. On the other hand, IRT was significantly longer in those with lower mPCWP and significantly shorter in those with higher mPCWP than in healthy subjects. In conclusion, normal transmitral flow velocity waveform with short IRT suggests a 'pseudonormal' pattern due to elevated mPCWP in patients with CAD.

Lp(a) is considered to be an independent risk factor for the development of cardiovascular disease. A case of myocardial infarction with elevated serum Lp(a) concentration and the rare apo(a) phenotype and its successful recanalization using tissue plasminogen activator is reported.

Alterations in the cardiac response to angiotensin II (Ang II) may contribute to the functional impairment in tachycardia-induced heart failure (congestive heart failure [CHF]). Accordingly, we studied the response to Ang II in eight conscious instrumented dogs before and after inducing CHF. Left ventricular (LV) performance was assessed by measuring LV pressure and LV volume. Isolated myocyte function was evaluated using computer-assessed videomicroscopy. In conscious animals before CHF, Ang II produced a load-dependent slowing of the time constant of LV relaxation (tau) and did not depress intact LV contractile function. After CHF, although Ang II produced a similar increase in LV systolic pressure, the increases in LV diastolic pressure and time constant tau were much greater, and contractile performance was depressed. These changes persisted when the elevation of end-systolic pressure was prevented by nitroprusside. Similar changes were also present after autonomic blockade. In isolated myocytes, before CHF, Ang II (10(-6) mol/L) produced a slight positive inotropic effect. In contrast, after CHF, Ang II produced a negative inotropic effect and slowed the rate of relengthening. The effects in the intact LV and myocytes were reversed by an Ang II AT1 receptor blocker (losartan). We conclude that pacing-induced CHF alters the LV and myocyte response to Ang II, so that Ang II produces direct depressions in intact LV contraction, relaxation, and filling and exacerbates myocyte contractile dysfunction. These effects are mediated through the activation of AT1 receptors.

A fifty-four-year-old woman was evaluated at the authors' hospital for symptoms of repeated chest and back pain. The symptoms had recurred for five months prior to admission. A dynamic computed tomographic scan was performed on admission and demonstrated an enlarged ascending aorta with four barrels secondary to split intimal flaps. This case is an extremely rare example of a patient with a four-barrel aortic dissection involving the ascending aorta.

We investigated isovolumic relaxation flow in patients with coronary artery disease (CAD) and evaluated the relationship between its velocity and left ventricular performance in 23 patients with atypical chest pain, 30 patients with CAD without prior myocardial infarction (MI), and 57 patients with prior MI, in whom cardiac catheterization was performed. The isovolumic relaxation flow velocity was measured at the basal portion of the left ventricle with pulsed Doppler echocardiography. The isovolumic relaxation flow ( > 15 cm/sec) was detected in 98 of 110 patients. The isovolumic relaxation flow velocity was significantly lower in patients with prior MI than in patients with atypical chest pain (p < 0.001) and in those with CAD without prior MI (P < 0.05). It was significantly lower in patients with CAD without prior MI than in those with atypical chest pain (p < 0.05). The isovolumic relaxation flow velocity showed a significant positive correlation with left ventricular ejection fraction. It also showed a significant negative correlation with left ventricular end-systolic volume index. These findings suggest that the isovolumic relaxation flow velocity is decreased in patients with CAD and is influenced by left ventricular systolic performance. Isovolumic relaxation flow may be a clinical manifestation of elastic recoil of the left ventricle.

The purpose of this study was to evaluate the characteristics of mitral annular motion during diastole in 28 normal subjects, 40 patients with prior myocardial infarction (MI), and 23 patients with coronary artery disease but without prior MI. Mitral annular motion during diastole was obtained from the apex by M-mode echocardiography at the posterior wall of the left ventricle. Determinants of mitral annular excursion during early (MAE-E) and late diastole (MAE-L) were investigated in all subjects. Differences in the MAE-E, MAE-L, and the MAE-L:MAE-E ratio were compared among the three patient groups. The Doppler-derived transmitral flow velocity-time integral during early (EI) and late (AI) diastole and mitral annular excursions during diastole were obtained in 55 other patients with a prior MI and in 29 healthy volunteers. The relationships between the MAE-L:MAE-E ratio and AI:EI ratio in these two groups were studied. The MAE-E was determined mainly by heart rate and left ventricular ejection fraction (LVEF). The MAE-L was determined only by age. The magnitude of MAE-E was significantly less in patients with a prior MI than in normal subjects (P < 0.01). However, the MAE-L did not differ among the three groups. The MAE-L:MAE-E was higher in patients with a prior MI than in normal subjects (P < 0.05), and was significantly correlated with AI:EI in healthy volunteers (r = 0.65, P < 0.001) and in patients with a prior MI (r = 0.50, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of altered loading conditions on the pattern of pulmonary venous flow are poorly understood. The authors investigated such effects, therefore, by using volume loading in 6 open-chest dogs. The pulmonary venous flow volume rate curve was obtained with a transit-time ultrasonic flowmeter at a fixed heart rate. Measurements were performed in the control and several states during the intravenous infusion of dextran. The influences of volume loading on hemodynamic and pulmonary venous flow variables were compared between the control state and three interventional states in which mean left atrial pressure was approximately 1, 2, and 3 mm Hg above the control value. The systolic flow volume (SI), which corresponds to left atrial reservoir volume, significantly increased, but the early diastolic flow volume (DI), which corresponds to left atrial conduit volume, did not show significant change with volume loading. The flow volume during left atrial contraction significantly increased with volume loading. The flow volume during one cardiac cycle (PVF) significantly increased with volume loading. Approximately 73% of increased PVF was distributed to the systolic flow. The rest was distributed to the early diastolic flow (14%) and to the flow during left atrial contraction (12%). The change in the ratio of SI/DI significantly and positively correlated with the change in mean left atrial pressure (r = 0.87, P < 0.001). These findings indicate that increased pulmonary venous flow induced by volume loading in dogs with normal left ventricular function is mainly distributed to the left atrial reservoir volume.

A 39-year-old man presented with type III hyperlipoproteinemia in association with heterozygous familial hypercholesterolemia (FH). He had extensive tuberous xanthomas over the knees and elbows and xanthomas in the Achilles tendons. He also had palmar xanthomas. He exhibited severe hypercholesterolemia and hypertriglyceridemia. This patient was heterozygous for FH, as evidenced by low low-density lipoprotein (LDL) receptor function on lymphocytes, and had type III hyperlipoproteinemia, as determined by apolipoprotein (apo) E phenotype 2/2 in isoelectric focusing of the E isoproteins and the presence of a broad beta band on electrophoresis. Because therapy consisting of diet restrictions and lipid-lowering agents such as clinofibrate and niceritrol did not decrease serum total cholesterol ([TC] 15.26 mmol/L) and triglyceride ([TG] 10.79 mmol/L) levels effectively, the patient underwent plasmapheresis once every 2 weeks using a dextran sulfate-cellulose column. Repeated plasmapheresis markedly reduced serum TC and TG and induced complete regression of the palmar xanthoma after 6 months. The severity of tuberous xanthomas on the knees and elbows was reduced after 2.5 years. After plasmapheresis, TC decreased to 1.94 mmol/L from 10.40 mmol/L and TG decreased to 0.33 mmol/L from 7.90 mmol/L. Plasmapheresis performed with a dextran sulfate-cellulose column was highly effective in removing the lipoprotein-remnant particles in this patient, leading to generalized improvement in the lipoprotein profile.

Unlabelled: Clinical significance of reverse redistribution on 24-hr delayed images after exercise 201Tl myocardial SPECT was investigated in 16 patients with recent myocardial infarction., Methods: Findings of 24-hr delayed 201Tl SPECT imaging were compared with those of glucose-loaded 18F-fluorodeoxyglucose (FDG) imaging by myocardial PET and with left ventricular wall motion obtained by bi-plane contrast left ventriculography. In each patient, transaxial thallium images and corresponding 18F-FDG images were divided into five ROIs., Results: Reverse redistribution was found in 15 of 80 regions. The mean FDG activity score in regions with reverse redistribution was significantly lower than that in regions having normal or slightly decreased thallium activity on 24-hr delayed imaging; it was significantly higher than that in regions having severely decreased or no thallium activity on 24-hr delayed imaging. The mean wall motion score in regions with reverse redistribution was significantly lower than in regions with normal or slightly decreased thallium activity, however, it was significantly higher than that in regions with moderately or more decreased thallium activity., Conclusion: These findings demonstrate that in regions showing reverse redistribution on 24-hr delayed 201Tl imaging, myocardial exogenous glucose utilization and left ventricular wall motion had deteriorated, but were not on a level with the scar.

A seventy-one-year-old woman suffering from angina pectoris had a superdominant left anterior descending artery with a 95% stenosis just after it extended the apex. This superdominant artery was demonstrated angiographically by the findings that it ran in the posterior interventricular sulcus and reached the crux of the heart. Percutaneous transluminal coronary angioplasty for the stenosis beyond the apex was successfully performed. After the procedure, she was relieved from chest pain.

We assessed the usefulness of dipyridamole radionuclide ventriculography for detecting significant coronary artery stenosis in 89 patients who were undergoing cardiac catheterization. Radionuclide ventriculography was performed before and after the infusion of dipyridamole (0.56 mg/kg). The end-diastolic regions of interest of the left ventricle were divided into 5 sectors for calculation of the regional ejection fractions. Results were considered to be positive when the regional ejection fraction decreased by more than 5% after the infusion of dipyridamole. The presence of significant coronary artery stenosis (> 75%) was demonstrated by arteriography in 49 patients and was absent in 40 patients. A decrease in the regional ejection fraction greater than 5% was observed in 41 (84%) of the 49 patients with significant coronary artery stenosis and in 2 of the 40 without significant coronary stenosis. The sensitivity and specificity of this method for detecting significant coronary artery stenosis were 84% and 95%, respectively. We conclude that a decrease in the radionuclide-determined regional ejection fraction after the infusion of dipyridamole reflects left ventricular dysfunction and is a sensitive and specific indicator of significant coronary artery stenosis.

We attempted to evaluate left ventricular performance from the shortest distance between the mitral leaflets coaptation and the interventricular septum at end-systole (MVC-IVS distance). The subjects were 37 patients with coronary artery disease (CAD) with prior myocardial infarction (MI), 8 with CAD without prior MI, 22 with atypical chest pain, and 4 with aortic regurgitation. The MVC-IVS distance was measured on a two-dimensional echocardiogram obtained from the parasternal or apical long-axis view and frozen at end-systole. Left ventricular end-systolic volume and end-diastolic volume were obtained by left ventriculography, and the left ventricular ejection fraction was calculated. A significant positive correlation was observed between the MVC-IVS distance and the end-systolic volume (r = 0.83, p less than 0.001); a close correlation was observed between the MVC-IVS distance end-systolic volume and ejection fraction by monoexponential fitting (r = -0.91, p less than 0.001). Thus, a significant negative correlation was observed between the MVC-IVS distance and the left ventricular ejection fraction (LVEF) (r = -0.83, p less than 0.001). An MVC-IVS distance of greater than or equal to 30 mm suggests diagnosis of left ventricular dysfunction (LVEF less than 50%) with high sensitivity (94.4%) and specificity (90.6%), while a value less than 30 mm suggests that the left ventricular performance is likely to be normal. Thus one can easily evaluate the left ventricular performance noninvasively using this new index.

The authors investigated the effects of alterations in heart rate, contractility, and loading conditions on a newly defined systolic time interval, the Q-V peak, in 46 anesthetized dogs. The Q-V peak was measured as the time from the beginning of the electrocardiographic Q wave to the moment at which the blood flow rate reached its peak in the ascending aorta as determined with an electromagnetic flowmeter. The Q-V peak did not change significantly as the heart rate was varied by atrial pacing between 70 and 110 beats/minute. The Q-V peak shortened when the contractility was augmented with dobutamine (p = 0.0001) and was prolonged when it was depressed with propranolol (p = 0.0001). However, the Q-V peak did not change significantly when the left ventricular end-diastolic pressure or the mean aortic blood pressure was increased to 130% or decreased to 70% of the baseline values. These findings suggest that one may also evaluate left ventricular performance by measuring the time to systole, which the authors define as the Q-V peak.

We tried to differentiate "pseudonormal" from normal transmitral flow velocity waveforms by evaluating isovolumic relaxation times (IRT) in patients with old myocardial infarction. Forty-three healthy volunteers and 54 patients with old myocardial infarction were studied. Transmitral flow velocity waveforms were obtained by pulsed Doppler echocardiography with a phonocardiogram. Early peak filling velocity (E) and late peak filling velocity (A) were measured, and the E/A ratio was calculated. The time from the beginning of the IIA sound to the onset of transmitral flow was defined as IRT. We observed a significantly positive correlation between IRT and age in the healthy volunteers (r = 0.56, p < 0.01). Based on these results, we selected age-matched healthy subjects (control group, n = 23) older than 35 years from the healthy volunteers. We divided the patients into 2 groups; those with a mean pulmonary capillary wedge pressure (mPCWP) of > or = 16 mmHg (H group, n = 9) and those with an mPCWP of < 16 mmHg (L group, n = 45). E, E/A, IRT, mean blood pressure (mBP), and heart rate were compared among the H, L, and control groups. There was no significant difference in mBP or heart rate between these 3 groups. Both E and E/A were significantly lower in the L group than in the control group (p < 0.05), however, no significant difference was observed in E and E/A between the H and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular performance was evaluated in 51 patients with acute myocardial infarction and angina pectoris using parameters derived from the flow velocity waveform at the ascending aorta. Flow velocity waveforms were obtained from the suprasternal notch by continuous-wave Doppler echocardiography and were recorded on a line-scan recorder at a paper speed of 100 mm/sec with lead II ECG. The peak flow velocity and the systolic time interval from the beginning of ECG Q wave to the peak flow velocity (Q-V peak interval) were measured. Relationships were investigated between these parameters and the left ventricular ejection fraction (LVEF) obtained from multigated equilibrium blood pool imaging with 99mTc-pertechnetate. The peak flow velocity did not correlate with LVEF (r = 0.27). However, a highly significant negative correlation was observed between the systolic time interval Q-V peak and LVEF (r = -0.84, p less than 0.001). The regression equation was LVEF = -0.46 X (Q-V peak) + 142. We conclude that left ventricular performance can be evaluated in patients with coronary artery disease at the bedside using the Q-V peak interval measured from simultaneous recording of the velocity waveform at the ascending aorta and the ECG.

Decreased vagal activity is frequently observed in coronary artery disease, but the mechanism of this association is unknown. We investigated cardiac autonomic function by relating heart rate spectral components to clinical and angiographic findings in 80 patients who were undergoing coronary angiography. The age- and sex-adjusted magnitude of the respiratory spectral component, which is an index of cardiac vagal tone, showed a significant negative correlation with the extent of coronary atheromatosis (r = -0.43, p less than 0.0001) and a less significant negative correlation with the severity of coronary stenosis (r = -0.30, p = 0.0070). These relationships were independent of previous myocardial infarction and of left ventricular function. Stepwise regression analysis showed that the respiratory spectral component contributed to atheromatosis independently of established coronary risk factors (partial R2 = 9.4%, p = 0.002), but not to stenosis. Our results support the hypothesis that decreased cardiac vagal activity is associated with an increased risk of coronary atherosclerosis.

We evaluated relationships between pulsed Doppler echocardiographic (PDE) parameters of flow velocity profiles across the mitral orifice and left ventriculographic (LVG) parameters of left ventricular volume changes. Subjects consisted of 19 patients with coronary artery disease and 12 patients with chest pain syndrome. Peak flow velocities at the rapid filling (E) and atrial contraction (A) were measured by PDE. Time constant of left ventricular relaxation (T), left ventricular minimum pressure (LVPmin), LV end-diastolic pressure (LVEDP) and pulmonary capillary wedge V wave pressure (PCW-V) were measured during cardiac catheterization. From the analysis of LVG, the rapid filling fraction (RFF), and the atrial filling fraction (AFF) were obtained. The left ventricular chamber stiffness (K) was identified by the analysis of the pressure-volume relationship of the left ventricle. We investigated the relationship between A/E and AFF/RFF by univariate linear regression analysis. We then performed stepwise multivariate linear regression analysis to predict E, A, A/E, RFF, AFF and AFF/RFF by the variables of left ventricular filling, i.e., T, LVPmin, LVEDP, PCW-V, K, heart rate (at the examination of PDE or LVG), mean arterial blood pressure (at PDE or LVG) and age. The A/E correlated significantly with AFF/RFF (r = 0.50, p < 0.01). The results of the multivariate linear regression analyses were as follows: [sequence: see text] The correlation of A/E and AFF/RFF were explained by some variables, except the variable T. The results of uni- and multivariate linear regression analyses showed that factors affecting the flow velocity profile across the mitral orifice did not account for the left ventricular volume changes. We also observed that, even in subjects with coronary heart disease, aging is a main factor that influences peak flow velocity at atrial contraction (A).

Coronary risk factors were assessed in 186 consecutive patients who received coronary angiography. The severity of coronary luminal narrowing was scored as the coronary sclerosis index (CSI). Patients were divided into normal coronary arteries (N, n = 72), coronary sclerosis without infarction (C, n = 73) and previous myocardial infarction (MI, n = 41). The CSI increased with age. A significant difference in serum triglycerides, HDL cholesterol and atherogenic index was observed between Groups C or MI and N. Multivariate analysis revealed that CSI had correlated with total- and HDL-cholesterol, uric acid and age in subjects under 55 years; and with age, blood sugar, factor H and HDL cholesterol in those of 55 years or over. When patients were classified by their total and LDL cholesterol level, a significantly different CSI was found between the desirable and high cholesterol levels in subjects under the age of 55, but it was not significant in those over 55. Therefore, disorders in lipid metabolism should be corrected in early middle age.

A case report of chronic recurrent pulmonary embolism treated by embolectomy and Günther vena caval filter. A 62-year-old man had suffered from dyspnea on effort for 4 years, and his feeling of dyspnea had gradually increased during the past 3 months. On the day of admission he was in a preshock state, and his pulmonary artery pressure was very high at 90/30 mmHg. Pulmonary blood perfusion scintigraphy showed multiple defects of isotope uptake. Immediately after the scintigraphy, pulmonary embolectomy was performed while using extracorporeal circulation. The operation was successful and his physical activity was markedly improved. After the operation, anti-coagulant and anti-platelet therapies were continued, but recurrence of pulmonary emboli was detected by scintigraphy, and some thrombi were found by venography in deep veins of the lower parts of both legs. To prevent recurrent pulmonary embolism, a Günther vena caval filter was inserted into the inferior vena cava. We considered this case as an acute worsening of chronic recurrent pulmonary embolism and we had the impression that pulmonary embolectomy is a very effective therapeutic method for serious pulmonary embolism, and that insertion of the Günther vena caval filter is a very easy and safe procedure.

We analyzed the spectral components of RR interval variability under controlled respiration (15 breaths/min) in 56 patients (age range, 35-73 years) referred for coronary angiography; 14 patients had multivessel disease (group M), 21 had one-vessel disease (group S), and 21 had nonsignificant disease or normal coronary artery (group N). There were 43 healthy controls (age range, 36-71 years) (group C). The patients had no clinical evidence of heart failure, hypertension, diabetes mellitus, or acute stage of infarction and had taken no medication for 3 days. The autoregressive power spectral density of RR interval variability contains two major components, respiratory sinus arrhythmia (RSA) (0.25 Hz) and Mayer wave-like sinus arrhythmia (MWSA) (0.04-0.15 Hz), which have magnitudes that are quantitative markers of cardiac vagal activity and sympathetic activity with vagal modulation, respectively. We represented the magnitudes by the coefficient of component variance (CCV), which provided the amplitude relative to the mean RR interval. The age- and sex-adjusted mean of CCVRSA significantly decreased with advancing angiographic severity (1.64 +/- 0.09%, 1.66 +/- 0.12%, 1.22 +/- 0.13%, and 0.81 +/- 0.16% for groups C, N, S, and M, respectively) (p = 0.0001). The CCVRSA was unrelated to left ventricular function, previous myocardial infarction, or stenosis of any specific artery including the sinoatrial and atrioventricular node arteries. The CCVMWSA decreased only in group M (p = 0.0462). These results indicate that coronary artery disease is associated with vagal dominant impairment in autonomic cardiac function and that reduction in the vagal cardiac function correlates with the angiographic severity.

Left ventricular function was evaluated using parameters derived from the flow velocity waveforms at the ascending aorta as obtained at the suprasternal notch by continuous-wave Doppler echocardiography in 39 patients; 12 with chest pain but without coronary stenosis, eight with angina pectoris; and 19 with myocardial infarction. Peak flow velocity and the time interval from the beginning of the Q wave of lead II of the ECG to peak flow velocity (Q-V peak) correlated with specific invasive hemodynamic parameters, such as max dp/dt and (max dp/dt)/IP (IP: total left ventricular pressure at the same instant) during isometric contraction of the left ventricle measured with a catheter tip manometer, and left ventricular ejection fraction (LVEF) obtained by bi-plane cineangiography (using the area-length method). There was no correlation between the peak flow velocity and the invasive hemodynamic parameters. However, significant negative correlations were observed between the Q-V peak time and max dp/dt, with r = 0.40 (p less than 0.05), and between the Q-V peak time and (max dp/dt)/IP with r = -0.61 (p less than 0.01). A negative correlation was obtained between the Q-V peak time and LVEF (r = -0.75, p less than 0.01). The regression equation was LVEF = -0.67 x (Q-V peak) + 176. To compare the effectiveness for predicting LVEF between the Q-V peak and the established systolic time intervals as PEP and PEP/ET, these time intervals were measured from flow velocity waveforms invasively obtained with a catheter-type electromagnetic flowmeter inserted into the ascending aorta in 14 patients selected from the original subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular end-diastolic pressure (LVEDP) was estimated noninvasively using cardiac parameters obtained from simultaneous recordings of the echocardiograms, electrocardiograms and phonocardiograms in 30 patients who underwent diagnostic left cardiac catheterization. Special attention was paid to the mitral valve motion which reflects global left ventricular function. The interval from the onset of the Q wave of the ECG to the echocardiographic C point of mitral valve closure (Q-C), the interval from the aortic component of the second heart sound to the E point of the mitral echogram (IIa-E), and the time from the opening of the mitral valve (D point) to the E point (D-E) were measured. A good correlation with LVEDP was observed with Q-C/IIa-E (r = 0.87, p less than 0.001), and inversely with D-E time (r = -0.81, p less than 0.001). The correlation of Q-C/D-E and LVEDP was most significant (r = 0.89, p less than 0.001). The regression equations were LVEDP = 36.6 X (Q-C/IIa-E) -10.9 and LVEDP = 4.49 X (Q-C/D-E) +5.56. This noninvasive and easily repeated method for predicting LVEDP is very useful clinically.