Comprehensive validation of early diagnostic algorithms for myocardial infarction in the emergency department.

OBJECTIVE: To comprehensively evaluate diagnostic algorithms for myocardial infarction using a high-sensitivity cardiac troponin I (hs-cTnI) assay. PATIENTS AND METHODS: We prospectively enrolled patients with suspected myocardial infarction without ST-segment elevation from nine emergency departments in Japan. The diagnostic algorithms evaluated: (i) based on hs-cTnI alone, such as the European Society of Cardiology (ESC) 0/1-h or 0/2-h and High-STEACS pathways; or (ii) used medical history and physical findings, such as the ADAPT, EDACS, HEART, and GRACE pathways. We evaluated the negative predictive value (NPV), sensitivity as safety measures, and proportion of patients classified as low or high-risk as an efficiency measure for a primary outcome of type 1 myocardial infarction or cardiac death within 30 days. RESULTS: We included 437 patients, and the hs-cTnI was collected at 0 and 1 hours in 407 patients and at 0 and 2 hours in 394. The primary outcome occurred in 8.1% (33/407) and 6.9% (27/394) of patients, respectively. All the algorithms classified low-risk patients without missing those with the primary outcome, except for the GRACE pathway. The hs-cTnI-based algorithms classified more patients as low-risk: the ESC 0/1-h 45.7%; the ESC 0/2-h 50.5%; the High-STEACS pathway 68.5%, than those using history and physical findings (15-30%). The High-STEACS pathway ruled out more patients (20.5%) by hs-cTnI measurement at 0 hours than the ESC 0/1-h and 0/2-h algorithms (7.4%). CONCLUSIONS: The hs-cTnI algorithms, especially the High-STEACS pathway, had excellent safety performance for the early diagnosis of myocardial infarction and offered the greatest improvement in efficiency.

Contribution of atmospheric nitrate to stream-water nitrate in Japanese coniferous forests revealed by the oxygen isotope ratio of nitrate.

Evaluation of the openness of the nitrogen (N) cycle in forest ecosystems is important in efforts to improve forest management because the N supply often limits primary production. The use of the oxygen isotope ratio (delta(18)O) of nitrate is a promising approach to determine how effectively atmospheric nitrate can be retained in a forest ecosystem. We investigated the delta(18)O of nitrate in stream water in order to estimate the contribution of atmospheric NO(3) (-) in stream-water NO(3) (-) (f(atm)) from 26 watersheds with different stand ages (1-87 years) in Japan. The stream-water nitrate concentrations were high in young forests whereas, in contrast, old forests discharged low-nitrate stream water. These results implied a low f(atm) and a closed N cycle in older forests. However, the delta(18)O values of nitrate in stream water revealed that f(atm) values were higher in older forests than in younger forests. These results indicated that even in old forests, where the discharged N loss was small, atmospheric nitrate was not retained effectively. The steep slopes of the studied watersheds (>40 degrees ) which hinder the capturing of atmospheric nitrate by plants and microbes might be responsible for the inefficient utilization of atmospheric nitrate. Moreover, the unprocessed fraction of atmospheric nitrate in the stream-water nitrate in the forest (f(unprocessed)) was high in the young forest (78%), although f(unprocessed) was stable and low for other forests (5-13%). This high f(unprocessed) of the young forest indicated that the young forest retained neither atmospheric NO(3) (-) nor soil NO(3) (-) effectively, engendering high stream-water NO(3) (-) concentrations.

Reduced ventricular response irregularity is associated with increased mortality in patients with chronic atrial fibrillation.

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.

Functional effects of endogenous bradykinin in congestive heart failure.

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.

Altered inotropic response of endothelin-1 in cardiomyocytes from rats with isoproterenol-induced cardiomyopathy.

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.

Clinical significance of reverse redistribution on 24-hour delayed imaging of exercise thallium-201 myocardial SPECT: comparison with myocardial fluorine-18-FDG-PET imaging and left ventricular wall motion.

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.

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.

Postural response of low-frequency component of heart rate variability is an increased risk for mortality in patients with coronary artery disease.

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.

Coexisting type III hyperlipoproteinemia and familial hypercholesterolemia: a case report.

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.

Striking effect of left ventricular systolic performance on propagation velocity of left ventricular early diastolic filling flow.

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.

Differentiation of abnormal relaxation pattern with aging from abnormal relaxation pattern with coronary artery disease in transmitral flow with the use of tissue Doppler imaging of the mitral annulus.

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.

Left ventricular isovolumic relaxation flow and left ventricular systolic performance.

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.

Extent of myocardial damage in regions with reverse redistribution at 3 h and at 24 h on 201Tl SPET: evaluation based on regional myocardial oxidative metabolism.

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.

Detection of impaired left ventricular function in coronary artery disease with acceleration index in the first derivative of the transthoracic impedance change.

In order to detect impaired left ventricular (LV) function in coronary artery disease (CAD) patients using acceleration index (Ac) of impedance cardiography (ICG), exercise ICG was performed in 29 patients with chest pain but without CAD (Group 1) and 21 patients with CAD (Group 2), and their resting values were compared with 30 healthy controls (Group 3). The acceleration index, which reflects indirectly aortic blood flow acceleration, was calculated as the ratio of dZ/dtmax to its accelerating time (AT). At rest, the values for Ac in Groups 1, 2, and 3 were 23 +/- 10, 15 +/- 6, and 36 +/- 13 omega/s2, respectively. There were significant differences between Group 1 versus 3, 2 versus 3, and 1 versus 2 (all p less than 0.001). At maximal exercise, Ac showed the largest percent change among the various indices used in this study. An increase of 198% for Group 2 was markedly lower than that of 250% in Group 1 (40 +/- 14 vs. 68 +/- 24 omega/s2, p less than 0.001). With a value of less than or equal to 40 omega/s2, Ac can detect the CAD patients, with a sensitivity of 62% and specificity of 90%, superior to stress ECG using CM5 lead. It is concluded that: (1) Ac is the sole index capable of distinguishing not only between the normals and diseased groups, but also between CAD patients and suspected CAD cases at rest. (2) Ac is a remarkably sensitive index for detecting impaired LV function at maximal exercise. (3) Exercise ICG is useful for predicting CAD from the population predisposing to CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive evaluation of left ventricular performance by the shortest distance between mitral leaflets coaptation and interventricular septum at end-systole.

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.

Elevated serum Lp(a) concentration and the rare apo(a) phenotype in a patient with myocardial infarction.

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.

Percutaneous transluminal coronary angioplasty of "superdominant" left anterior descending artery. A case report.

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.

Evaluation of a new systolic time interval, the Q-V peak: effects of heart rate, contractile state, and loading conditions in dogs.

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.

Effects of volume loading on pulmonary venous flow pattern in dogs with normal left ventricular function.

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.

Comparative effects of volume loading on pulmonary venous flow in dogs with normal heart and with myocardial ischemia.

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.