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Two patients, who were receiving therapy with mianserin for depressive disorders, developed signs of disturbed cardiac function which resolved after mianserin therapy was discontinued. One of the patients also developed hypokalaemia which was probably caused by the drug. It is felt that these side effects warrant further research.
The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
To define normal criteria of size and dynamics of the inferior vena cava (IVC) and its clinical value in assessing right-sided cardiac function, 2-dimensional (2-D) and M-mode echocardiography (echo) were performed in 175 subjects, who were classified into 3 groups: group 1-80 normal subjects; group IIA--65 patients with documented right-sided cardiac disease, and group IIB--30 patients with cardiac disease but no right-sided abnormality. The IVC was adequately imaged in 175 of 185 subjects (95%). There was good correlation between M-mode and 2-D echo (r = 0.84) and long- and short-axis (r = 0.88) measurements. The IVC diameter during expiration was: group 1-9 to 28 mm (mean 18.2 +/- 4.6); group IIA--15 to 40 mm (mean 23.1 +/- 4.8) and group IIB-8-24 mm (mean 15.6 +/- 3.7). Collapsibility index (inspiratory decrease in diameter) was: group I-37 to 100% (mean 55.8 +/- 15.9); group IIA--0 to 39% (mean 13.5 +/- 10.5); and group IIB--44 to 100% (mean 60.4 +/- 13.1). A and V waves could be measured in 120 of 151 cases (79%). Both A and V waves were less than 125% of its diameter in group I. The A wave was absent in 34 patients; 30 (88%) were in atrial fibrillation. Among 8 patients with tricuspid regurgitation, 5 (63%) had V waves greater than 125%. There was no correlation between diameter or collapsibility index and age, sex, rhythm or body surface area.(ABSTRACT TRUNCATED AT 250 WORDS)
We studied the cardiovascular effects of increasing intrathoracic pressure in an acute pentobarbital-anesthetized canine model of acute ventricular failure induced by large doses of propranolol. Left ventricular (LV) function curves were generated by volume loading from LV filling pressures of 5-20 Torr. The animals were ventilated by using intermittent positive-pressure ventilation with large tidal volumes (30 ml/kg). Chest and abdominal pneumatic binders were used to increase intrathoracic pressure. When compared with the control state, acute ventricular failure was associated with a decrease in the slope of the LV function curves (P less than 0.01). After binding the increase in intrathoracic pressure (1.1 +/- 1.6 to 12.1 +/- 2.4 Torr, P less than 0.01) was associated with an improvement in both right ventricular and LV function. Our study demonstrates that in this model of acute ventricular failure, increasing intrathoracic pressure improves cardiac function. We postulate that this observed improvement with increased intrathoracic pressure is due to reduced LV wall stress in a manner analogous to that seen with arterial vasodilator therapy in congestive heart failure.
Magnetic resonance (MR) imaging of the heart has, to date, been limited in its ability to evaluate cardiac function. The authors have implemented a technique for functional assessment of the heart using shorter echo times than those generally used for conventional spin-echo imaging. With these short echo times, multiple images can be obtained in a multisection mode approximately within the isovolumetric phases of the cardiac cycle. This permits a pair of image stacks to be obtained, one in end systole and the other in end diastole. With the use of a modified Simpson rule, left ventricular volume and ejection fraction were calculated and compared with results obtained from contrast material-enhanced ventriculography. Preliminary results indicate that this method has promise for the evaluation of a variety of functional parameters in the heart. The short acquisition times for this functional study permit it to be combined with a tissue characterization study within the time constraints of a clinical MR imaging session.
OBJECTIVES: This study sought to evaluate the effect of adenosine receptor blockade by aminophylline on cardiac functional reserve in patients with syndrome X. BACKGROUND: Aminophylline may have a potentially antiischemic effect through the inhibition of adenosine and, thus, the coronary steal phenomenon in patients with syndrome X. METHODS: A single-blind, placebo-controlled study of an intravenous infusion of aminophylline (6 mg/kg body weight over 15 min) or placebo (20 ml of saline solution over 15 min) was performed during continuous radionuclide monitoring of left ventricular ejection fraction in 12 patients performing supine bicycle ergometric exercise. RESULTS: Aminophylline increased exercise time (aminophylline 400 s vs. placebo 355 s, p < 0.01), decreased degree of ST segment depression (aminophylline 1.6 mm vs. placebo 2.4 mm, p < 0.01) and either abolished (seven patients) or diminished (five patients) chest pain during exercise. Aminophylline also increased left ventricular ejection fraction at rest (aminophylline 66.5% vs. placebo 62.3%, p < 0.05) but did not improve its deterioration at peak exercise (aminophylline 60.1% vs. placebo 56.6%, p = NS) or shorten the abnormally prolonged interval between the end of exercise and the overshoot (aminophylline 115 s vs. placebo 130 s, p = NS). CONCLUSIONS: Aminophylline infusion increases ischemic threshold and prolongs exercise duration in patients with syndrome X. It is hypothesized that aminophylline acts by inhibiting the coronary steal phenomenon through adenosine receptor blockade. It does not improve the deterioration in left ventricular function at peak exercise or the delayed response in ejection fraction in the recovery period, presumably because the beneficial effects of aminophylline that result from the redistribution of coronary blood flow are limited.
To study the assessment of cardiac function in acute myocardial infarction (AMI), we measured left atrial diameter, left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), ejection fraction (EF) in 20 patients with acute myocardial infarction. Left atrial diameter was measured using echocardiography and was expressed as left atrial index (LAI, mm/m2) dividing by body surface area. LAI in AMI was 21.3 +/- 2.7 mm/m2 and significantly larger than LAI in normal subject (19.9 +/- 2.0 mm/m2) (p less than 0.05), In AMI, LVEDP was 13.3 +/- 3.4 mmHg, PCWP was 9.0 +/- 2.8 mmHg and EF was 52.3 +/- 14.8%, Relationship (r value) between LAI and LVEDP (r = 0.70, p less than 0.001, y = 0.87 x-5.4 x; LAI, y; LVEDP) was greater than PCWP and LVEDP (r = 0.60, p less than 0.01). LVEDP calculated from LAI using this method was directly measured LVEDP directly measured +/- 2.4 mmHg. In 9 patients, LAI was larger than 20.9 mm/m2, in 8 patients of them LVEDP was higher than 13 mmHg. In 11 patients LAI was smaller than 20.9 mmHg, only in 2 of them LVEDP was lower than 13 mmHg. It concluded that sensitivity was 88.9%, specificity was 81.8%, accuracy was 85.0%. Relationship between LAI and PCWP (r = 0.30), LAI and EF (r = -0.36) were not significant. We can measure LAI repeatedly in AMI non-invasively, and predict LVEDP. Thus, the measurement of LAI is useful in treatment of AMI.
Effects of 5-([2-(diethylamino)-ethyl]amino)-3-phenyl-1,2,4-oxadiazole (DEPO) on cardiac functions and myocardial metabolism were examined using the heart in vivo and the isolated perfused heart of dogs. In the heart in vivo DEPO i.v. produced dose-dependent decreases in coronary perfusion pressure (PP), heart rate (HR), left ventricular pressure (LVP), dP/dt max of LVP and coronary vascular resistance (VR). DEPO i.c. dose-dependently increased left circumflex coronary flow (LCCF) and decreased PP, LVP and dP/dt max of LVP, but did not change HR. In the isolated perfused heart, DEPO induced a marked increase in coronary blood flow (CBF) and depressed HR and myocardial contractile force. Myocardial oxygen consumption and myocardial redox potential were not significantly changed. DEPO could not modify the effects of isoproterenol, adenosine and reactive hyperaemia on the heart. The results suggest that DEPO may have a coronary vasodilating action and some direct inhibitory actions on the heart.
In order to test the hypothesis that clinical and biochemical features of liver disease due to cardiac failure regress upon relief of cardiac decompensation, 38 patients with constrictive pericarditis were studied before and after pericardiectomy for periods ranging from 1 week to 25 years. All patients were judged to be free of clinical evidence of heart failure. Hepatomegaly was present in 10 of the 38 patients studied. Of the patients studied 1-25 years after operation, 96% had elevated serum levels of total and conjugated bilirubin. The percentage Bromsulphalein (BSP) retention at 45 minutes was abnormal in all 29 patients studied 1 year or more after surgery. There was no significant correlation between the level of bilirubin or the percentage BSP retained when these were compared with the pre-operative height of jugular venous pressure, degree of pulsus paradoxus, duration of symptoms or degree of hepatic congestion. Our study reveals that the liver lesion of cardiac failure persists for up to 25 years after restoration of normal cardiac function.
The use of miniature swine in biomedical research is increasing; however, a comparison of cardiac function and morphology between strains has yet to be characterized. The purpose of this project was to examine comprehensive hemodynamics and cardiac morphology of three groups of ten normal, 4 months old, age-matched Yucatan miniature (MINI) pigs, Yucatan micropigs (MICRO) and Hanford (HAN) miniature pigs, 5 males and five females per group. Closed chest cardiac catheterization under equivalent conditions was performed followed by post mortem cardiac morphometry. Mean arterial pressure was significantly greater in the Hanford group when compared to both the minipig and micropig pigs (HAN: 89 +/- 4; MINI: 48 +/- 3; MICRO: 53 +/- 2 mmHg). Pulmonary vascular resistance was significantly different between the three groups (HAN: 9 +/- 1; MINI: 60 +/- 12; MICRO: 111 +/- 29 dyne x sec/cm x m2). The Hanford strain had a significantly smaller heart weight to body weight ratio than the other two groups (HAN: 4.6 +/- 1.0; MINI: 5.7 +/- 0.1; MICRO: 5.5 +/- 1.0). Variations in cardiovascular parameters occur among these strains and should be considered when constructing experimental designs.
This study tests the hypothesis that the administration of cyclocreatine prior to global ischemia enhances recovery of cardiac function during reperfusion. Two models were used. First, in a Langendorff-working heart model of normothermic cardioplegic arrest, rats (n = 6 per group) were injected intravenously with saline or cyclocreatine (600, 300, or 150 mg/kg). After 30 min or 2 h, hearts were excised and perfused in the Langendorff mode for 5 min and then in the working heart mode for 20 min. Normothermic arrest was induced by infusing warm St. Thomas solution once; then hearts were kept at 37 degrees C for 40 min. Following arrest, hearts were reperfused in the Langendorff mode for 15 min and then in the working mode for 30 min. Cyclocreatine consistently produced significantly better recovery of aortic flow and cardiac output compared to that of saline hearts. Second, in an intact canine model of cold cardioplegic arrest, adult mongrel dogs (n = 3 to 6 per group) underwent aortic cross-clamping for 1 h, followed by reperfusion on bypass for 45 min and off bypass for 4 h. Dogs were injected intravenously with saline or cyclocreatine (500 mg/kg) for 1 h before experiment. Post-bypass segmental contractility and cardiac output were significantly better in cyclocreatine hearts compared to that of controls. In a limited study, after a 3 h aortic cross-clamp time, cyclocreatine hearts achieved 91% baseline function while control hearts failed after 2 h. Results of this study suggest that cyclocreatine, without inotropic or chronotropic effect, protects the heart from global ischemic injury.
The effects of regression of left ventricular hypertrophy following atenolol and bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats (SHR) were studied. Atenolol (50 mg/kg/day) and bunazosin (5 mg/kg/day) were administered to SHR from 19 to 26 weeks of age, whereas tap water was given to control SHR and normotensive Wistar-Kyoto rats (WKY). Both atenolol and bunazosin significantly decreased arterial blood pressure and significantly decelerated the increase in left ventricular weight in SHR. At the end of the long-term treatment, hearts were removed and perfused by the working heart technique for 15 min, and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The pressure-rate product and the extent of recovery of the coronary flow after reperfusion following 30 min of ischemia in the bunazosin-treated SHR were significantly higher than those in the control SHR and the atenolol-treated SHR. The levels of adenosine triphosphate (ATP), creatine phosphate (CrP), and energy charge potential in the SHR heart reperfused after 30 min of ischemia were significantly lower than those in the reperfused WKY. Both atenolol and bunazosin improved the restoration of ATP and CrP in SHR after reperfusion following 30 min of ischemia. In conclusion, antihypertensive therapy with either atenolol or bunazosin was effective in preventing cardiac hypertrophy and ischemic damage caused by different mechanisms. Factors resulting from stimulation of the cardiac alpha 1 adrenoceptor may play an important role in the development of hypertensive cardiac hypertrophy, just as factors resulting from stimulation of the beta 1-adrenoceptor do.
A new cardiotonic agent, (R)-[[4-(1,4,5,6-tetrahydro-4-methyl-6-oxo-3-pyridazinyl)-phenyl] hydrazono]propanedinitrile (Levosimendan), has been developed and screened for its ability to bind to cardiac troponin C. In perfused hearts, low concentrations of 0.03 or 0.1 mumol/L Levosimendan increased +dP/dt, but did not affect the speed of relaxation and produced only a slight increase in spontaneous heart rate in the hearts perfused with 0.1 mumol/L of the drug. In these same hearts, perfusion with 0.03 mumol/L Levosimendan did not alter the 32P incorporation into troponin I or C protein, whereas a slight but significant increase was noted for phospholamban, with no detectable change in tissue cAMP levels. Administration of 0.1 or 0.3 mumol/L Levosimendan significantly increased myocardial cAMP levels as well as the phosphorylation of phospholamban, troponin I, and C protein. Levosimendan (0.03 to 10 mumol/L) reversibly increased force generated by detergent-extracted fiber bundles over a range of submaximally activating free Ca2+ concentrations with no significant effect on maximum force or on Ca2+ binding to myofilament troponin C. There was no direct effect of Levosimendan on Ca2+ uptake by vesicles of sarcoplasmic reticulum (SR). In contrast, under conditions optimal for cAMP-dependent phosphorylation, Levosimendan slightly but significantly lowered the concentration of Ca2+, yielding half-maximal uptake rates by the SR vesicles. Our results indicate that at low concentrations Levosimendan acts preferably as a Ca2+ sensitizer, whereas at higher concentrations its action as a phosphodiesterase inhibitor contributes to the positive inotropic effect.
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The general objective of this study was to develop a noninvasive method for efficiently and reproducibly determining relative cardiac function parameters in the chick embryo. The specific objectives of the study were 1) to develop several methods for computer-assisted image processing and quantitation of relative intraventricular blood volumes in the 3-day-old embryonic chick heart and 2) to compare methods for precision and with a previously established manual processing method. Images of the embryonic chick heart in ovo were recorded on videocassette tape, digitized, and enhanced by computer-aided histogram equalization. The area occupied by blood within the common ventricle was extracted by region-growing and spurious region removal algorithms and defined by the determination of edge-pixel coordinates. Edge-pixel coordinates of the longitudinal and transverse axes of the common ventricular blood region were located by three different methods, the lengths of the axes calculated, and volumes computed from the equation for determining volume of a prolate spheroid. Twenty-five images of the embryonic heart were randomly selected and processed. Volumes were calculated with each of the three methods on six different occasions. A coefficient of variation was calculated for each method. The intraobserver mean coefficient of variation for each method was 7.4%. When a 2-way ANOVA was conducted, mean coefficients of variation did not differ significantly for the three methods. However, computer processing (in addition to significantly reducing the time required to generate data) reduced the coefficient of variation observed in manual processing by 56.5%.
This article describes the application and limitations of noninvasive techniques to assess cardiac function and to diagnose pulmonary hypertension in newborn infants in whom PPHN is suspected.
A study was undertaken to examine the effects of autologous bone marrow transplantation (BMT) on cardiac function at rest (n = 111) and pulmonary gas exchange during exercise (n = 110). Left ventricular cardiac ejection fraction (LVEF) was measured by radionuclide ventriculography before autologous BMT and after 6 months and 1, 3 and 5 years. Expired gas volume per oxygen consumption (VE/VO2) and transcutaneous PO2 were measured at rest and during submaximal exercise before and 6 and 12 months after autologous BMT, and the alveolar-arterial oxygen difference was calculated after 12 months. In lymphoma patients conditioned with BCNU, cyclophosphamide, etoposide and cytarabine, a long-lasting reduction in LVEF of 11 +/- 14% mean (+/- SD) was noted. The risk of cardiac deterioration was not increased by a subnormal LVEF before autologous BMT or total body irradiation (TBI). Impaired gas exchange during exercise was a common feature, but severe disturbances were uncommon. During exercise transcutaneous PO2 fell pathologically in 15% and 20% of the patients examined after 6 and 12 months, respectively, and the alveolar-arterial oxygen difference increased pathologically in 50% after 12 months. The VE/VO2 ratio increased significantly during exercise 6 months after autologous BMT in TBI-treated patients.
A large body of evidence has accumulated to substantiate the accuracy of functional MR measurements of both ventricles. Because of good accuracy and superior reproducibility, MR imaging may be considered the gold standard for in vivo quantification of left and right ventricular ejection fraction, myocardial mass, and wall stress. New prospects for functional MR imaging include determination of the end-systolic volume-pressure relation as an index of myocardial contractility. The ability of MR imaging to detect wall motion disturbances may be enhanced further by combining myocardial tagging techniques with finite element analysis. Conventional MR imaging is limited by long examination times, but recent ultrafast modifications of echo-planar imaging allow completion of a functional heart study within seconds. Implementation of ultrafast MR imaging will greatly increase the usefulness of MR imaging for routine evaluation of cardiac function.