Late-gestation prediction of outcome in tricuspid valve dysplasia and Ebstein's anomaly using fetal tricuspid regurgitation waveform analysis.

OBJECTIVE: To investigate the criteria, based on fetal TR waveforms in late gestation, to predict biventricular circulation (BV) after birth in cases of tricuspid valve dysplasia (TVD) or Ebstein's anomaly diagnosed during the fetal period. METHODS: We included 35 consecutive cases diagnosed with TVD or Ebstein's anomaly during the fetal period between January 2008 and December 2021 at Kanagawa Children's Medical Center, Kanagawa, Japan. The maximum velocity and change in pressure over time of tricuspid regurgitation (TR) jet (dP/dt), estimated using TR waveforms obtained during the late-gestation period (gestational age ≥ 28 weeks), were collected from patient records. dP/dt was calculated by dividing the change in estimated right ventricular pressure obtained using Bernoulli's principle by the time taken for the TR maximum velocity to change from one-third to two-thirds of its peak value. The outcome was divided into four categories: BV, single ventricular circulation, neonatal death and fetal death. Patients with BV were included in the BV group, while patients with single ventricular circulation, neonatal death or fetal death were included in the non-BV (NBV) group. RESULTS: Overall, 19 and 16 patients were included in the BV and NBV groups, respectively. The median TR maximum velocity was 3.3 (range, 2.4-3.6) m/s in the BV group and 1.9 (range, 1.0-3.3) m/s in the NBV group. There were no cases of postnatal BV in fetuses with TR maximum velocity < 2.4 m/s; cases with TR maximum velocity of 2.4-3.3 m/s were observed in both BV and NBV groups. Receiver-operating-characteristics-curve analysis was performed on the 11 patients in the BV group and five patients in the NBV group with a TR maximum velocity of 2.4-3.3 m/s. dP/dt ≥ 350 mmHg/s and TR maximum velocity ≥ 2.9 m/s were identified as criteria for predicting the outcome in such cases. The performance of dP/dt ≥ 350 mmHg/s in predicting BV after birth in fetuses with TVD or Ebstein's anomaly was higher compared to that of TR maximum velocity ≥ 2.9 m/s (sensitivity, 90.9% vs 72.3% and specificity, 80.0% vs 80.0%, respectively). CONCLUSIONS: In fetuses with TVD or Ebstein's anomaly, the postnatal outcome may be BV or NBV when the TR maximum velocity is 2.4-3.3 m/s. In such cases, by combining the TR maximum velocity with dP/dt ≥ 350 mmHg/s, BV after birth may be predicted with greater accuracy. © 2022 International Society of Ultrasound in Obstetrics and Gynecology.

Inhibition of P-glycoprotein by orange juice components, polymethoxyflavones in adriamycin-resistant human myelogenous leukemia (K562/ADM) cells.

We investigated the effects of the ethyl acetate extract of grapefruit juice (GFJ), that of orange juice (OJ) and their components on the uptake of [(3)H]vincristine into adriamycin-resistant human myelogenous leukemia cells. Its uptake was increased by the extracts of GFJ and OJ up to 7- and 3-fold, respectively, as well as verapamil and cyclosporin A. OJ components, i.e. 3,3',4',5,6,7,8-heptamethoxyflavone, nobiletin and tangeretin, also increased the uptake of [(3)H]vincristine in a concentration-dependent manner. Although GFJ components, dihydroxybergamottin and bergamottin, significantly increased the uptake, their potencies were considerably weaker than those of OJ components. These data suggest that OJ components inhibit P-gp-mediated efflux of [(3)H]vincristine, resulting in the intracellular accumulation of chemotherapeutic drugs. These components may become candidates of multi-drug resistance reversing agents in cancer chemotherapy.

Prognostic significance of 24-hour ambulatory electrocardiographic monitoring in patients with dilative cardiomyopathy: a prospective study.

We studied 33 patients with dilative cardiomyopathy to evaluate the predicting factors for sudden death occurring within one year. The information on each of the patients included history, physical examinations, two-dimensional echocardiograms, 24-h ambulatory electrocardiograms, and cardiac catheterization or autopsy. Patients were followed up for one year. Univariate analysis showed maximum number of premature ventricular complexes per hour (PVCs/h) (p = .0012), maximum beats per episode of ventricular tachycardia (VTmax) (p = .0012), and left ventricular end-diastolic pressure (p = .046) to be significant prognostic risk indicators of sudden death within one year. To select the best combination of factors that predict sudden death, multivariate stepwise logistic regression analysis was performed. By this method, only PVCs/h and VTmax were selected as the best combination. Probability of sudden cardiac death within 1 year = 1/(1 + exp[6.65-1.78 (log PVCs/h)-0.71 (VTmax)]). The equation showed 85.7% sensitivity and 69.2% specificity at a probability cutoff point of p = .124, with accuracy of 72.7%. The incidence of sudden death was 80% in patients showing both frequent (greater than 100/h) PVCs and presence of VT (VTmax greater than or equal to 3), and 6% in patients with neither or both. We concluded that PVCs/h and VTmax are independent and significant prognostic factors in patients with dilative cardiomyopathy.

[Studies on the bottles of mineral water and the foreign plastic like substances].

The containers of mineral water and the foreign plastic substances which were found in the mineral water were investigated. Most of plastic bottles were made of polyethylene terephthalate (PET) and the caps were made of polypropylene (PP), polyethylene (PE) or aluminum. PE liners were attached to some caps. Most of the foreign plastic substances were PET while others were PE, PP, Teflon and rubber. Some bottles had a scratch on the top inside. The origin of most PET fragments was presumed to be scraped off the bottles by the lowering of the injection nozzle during the water filling process. The sources of the other substances were also determined.

Coronary angiography after myocardial infarction. A comparison between a Japanese community hospital and Western countries.

The purpose of our study was to determine differences in coronary lesions after myocardial infarction between Japan and Western countries. One hundred ninety-two patients under 69 years of age admitted to our CCU were diagnosed as having an acute myocardial infarction. One hundred thirty of 153 surviving patients received coronary arteriography, and 12% had zero-vessel, 42% single-vessel, 25% two-vessel and 12% three-vessel coronary artery disease. Of 113 patients without a previous history of myocardial infarction, 12% had zero-vessel, 44% single-vessel, 27% two-vessel and 17% three-vessel disease. We compared these results with the reports of three similar studies from Western countries. The percentage of multivessel patients in our study was the lowest among the four studies (p less than 0.05). Coronary lesions in patients without a previous history of myocardial infarction differ from reports in the United States (p less than 0.05). These results may suggest that we should carefully evaluate the reports of secondary prevention for chronic myocardial infarction, considering the different severity of coronary lesions in each country.

Variations in myocardial contraction sequence under various hypoxic conditions.

Hypokinetic myocardial segment motion is observed in various pathophysiologic conditions. The aim of this study was to clarify the mechanisms involved in differences in segment motion of hypokinesis. Nineteen open-chest dogs were studied with regard to myocardial segment length, left ventricular pressure, and internal minor-axis diameter. Sequential instantaneous myocardial elastance [alpha(t) curve] was calculated under 4 different hypoxic conditions: complete coronary occlusion and reperfusion, partial coronary occlusion, coronary microembolization, and anoxic perfusion. The alpha(t) curve peaked at end-systole in the case of normal contraction; but it was almost totally flat when complete bulging occurred. The hypokinesis which occurred during development of the complete systolic bulge immediately after complete coronary occlusion had an earlier alpha(t) peak curve than the hypokinesis resulting from partial coronary stenosis (209.5 +/- 35.6 ms after end-diastole vs. 261.9 +/- 18.2 ms; p less than 0.02), microsphere injection into the coronary artery (243.2 +/- 24.5 ms vs. 289.3 +/- 15.4 ms; p less than 0.05), or anoxic perfusion (213.4 +/- 40.2 vs. 275.6 +/- 28.3 ms; p less than 0.05). The early alpha(t) peak resulted in a late-systolic bulge in segment length motion. In conclusion, hypokinetic segment motion differed depending on whether the coronary blood flow was present or not. A late-systolic bulge only developed immediately after complete coronary occlusion, and resulted from an abrupt decrease in myocardial stiffness during the cardiac cycle, which is closely related to the abrupt cessation of coronary blood flow.

Calcium concentration during anoxic perfusion modifies post-ischemic hypercontraction in the canine heart.

The purpose of this study was to clarify the role of calcium flux in the pathogenesis of transient overshoot in regional myocardial contractile function after brief ischemia (post-ischemic hypercontraction). Six open-chest anesthetized dogs were examined. The left anterior descending coronary artery (LAD) was cannulated with a bypass system from the left carotid artery. Two minutes of total coronary occlusion of the LAD resulted in a post-ischemic hypercontraction 1 minute after reperfusion. Post-ischemic hypercontraction was abolished after reperfusion following 2 minutes of perfusion with anoxic Krebs-Henseleit solution containing 2.5 mM calcium. Post-ischemic hypercontraction occurred after calcium-free anoxic perfusion. The regional myocardial contractile function remained depressed 1 minute after reperfusion following anoxic perfusion with 5.0 mM calcium solution. Thus, post-ischemic hypercontraction was modified by the calcium concentration during anoxia. Alteration in transsarcolemmal calcium influx during reperfusion, which was modified by alterations in the calcium environment during anoxia, could be responsible for this phenomenon.

[Left atrial booster pump function in left ventricular blood filling: clinical and experimental analyses].

Left atrial booster pump function produces variable effects on cardiac output. Generally, cardiac output decreases by only 15-20% when atrial fibrillation occurs, however, in some cases, hemodynamic collapse occurs through loss of left atrial contraction. We evaluated the relative significance of left atrial booster pump function in acute or chronic load and in myocardial ischemia using the left ventricular volume curve. Blood entering into the left ventricle during the left atrial contraction phase (FVLA) represents the left atrial volume work, and the ratio of FVLA to the left ventricular filling volume during one cardiac cycle (%FVLA) represents the relative significance of left atrial booster pump function in cardiac output. In dog experiments, we calculated the change in FVLA and %FVLA by measuring the the left ventricular internal minor axis diameter and using Pombo's method. We also measured the change of the left atrial segment length as a direct indicator of left atrial contraction. In the acute change in preload, FVLA changed with stroke volume, but %FVLA remained unchanged. The change in FVLA correlated with the direct indicator of the left atrial excursion; the extent of the left atrial segment length (LASL). During acute change of left ventricular afterload, both FVLA and %FVLA were unchanged. In regional myocardial ischemia, both FVLA and %FVLA were increased, suggesting an increase in the left atrial booster pump function. In clinical study, we calculated FVLA and %FVLA from the left ventricular diameter using M-mode echocardiography. In chronic volume overloading (aortic regurgitation), FVLA increased while %FVLA was maintained unchanged. The same FVLA-%FVLA relationship was observed in acute volume loading. In cases of left ventricular hypertrophy (LVH) and old myocardial infarction (MI), both FVLA and %FVLA were increased, suggesting the increased left atrial booster pump function. In these cases, the left ventricular rapid filling velocity decreased, suggesting that impairment of rapid filling caused the increase of left atrial preload and hence increased left atrial volume work. The results of this study show that in old MI and in LVH, both left atrial volume work and the relative significance of left atrial booster pump function increase. We concluded that prevention of atrial fibrillation may be very important in these diseases.

Observations on rapid ventricular pacing during reentrant ventricular tachycardia in canine myocardial infarction--the use of epicardial mapping in demonstrating the modes of resetting, concealed perpetuation and termination of reentry.

The changes in activation sequences in and around the epicardial reentrant circuit were analyzed during rapid pacing against ventricular tachycardia by using a canine infarction model. In 13 episodes of sustained ventricular tachycardia induced by a premature stimulation technique in eight dogs, reentry circuits were located in the superficial subepicardial myocardium in eight. Pacing stimuli were clearly demonstrated to enter the reentrant circuit in two directions: one wavefront collided with the orthodromic reentrant wavefront and the other entered prematurely into the reentrant circuit to reset the tachycardia (resetting phenomenon). With a faster pacing rate, stimuli failed to reset the tachycardia due to slower entry into the circuit despite the fact that most epicardial recording sites were activated by pacing wavefronts (concealed perpetuation). Termination of tachycardia was achieved by a local conduction block in the center of the reentrant circuit. A pacing impulse which encountered the local block was also shown to reinitiate the tachycardia using a different reentrant pathway. These different phenomena could be observed in consecutive pacing beats. These epicardial mapping data provided a direct electrophysiological basis for the mechanisms of reentrant ventricular tachycardia and the mode of its termination.