[Cardiac function using ultrafast computed tomography].
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Studies were performed in anesthetized control dogs (n = 6) and in dogs (n = 6) with acute low-output heart failure produced by inflation of a balloon in the thoracic inferior vena cava. Studies were designed to determine the effects of synthetic atrial natriuretic peptide on renal function and renin release in this acute high-renin, sodium-retaining preparation. Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 micrograms X kg-1 X min-1) resulted in decreases in arterial pressure and renal blood flow in both groups. Glomerular filtration rate increased in both low-output (delta + 10.7 +/- 3.1 ml/min) and control (delta + 8.7 +/- 2.9 ml/min) groups. Fractional lithium excretion, a marker of proximal tubule reabsorption, also increased in both low-output (delta + 12.0 +/- 4.6%) and control (delta + 14.3 +/- 5.0%) groups. Renin secretory rate decreased in the low-output group from 852.8 +/- 183.0 to 149.5 +/- 73.7 ng/min and in the control group from 308.5 +/- 84.5 to 44.5 +/- 27.5 ng/ml. Intrarenal infusion of atrial natriuretic peptide resulted in an attenuated increase in both urinary sodium excretion (delta + 42.3 +/- 10.7 vs delta + 201.2 +/- 37.9 mueq/min) and fractional excretion of sodium (delta + 0.48 +/- 0.13% vs delta + 2.85 +/- 0.45%) in the low-output as compared with the control group. Our studies demonstrate that administration of synthetic atrial natriuretic peptide results in an increase in glomerular filtration rate and a decrease in proximal tubule reabsorption, as estimated by lithium excretion, in both control dogs and those with acute low-output heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: We tested the hypothesis that double potentials recorded during atrial flutter in a functionally determined reentrant circuit reflect activation of the reentrant wave front around an area of functional conduction block. BACKGROUND: The center of the atrial flutter reentrant circuit in the sterile pericarditis canine model is characterized by double potentials. METHODS: We studied 11 episodes of atrial flutter in eight dogs during interruption of atrial flutter while pacing the atria. A multielectrode mapping system was used to record simultaneously from 190 electrodes on the right atrium (location of reentry). RESULTS: Interruption of atrial flutter occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction in the reentrant circuit. The response of the double potential with interruption of atrial flutter depended on the location of the recording site relative to this area of block. Two types of response were seen. When the double potential was recorded orthodromically distal to this area of block, interruption of atrial flutter was associated with disappearance of the second deflection, and continued pacing after interruption of atrial flutter was not associated with reappearance of the second potential. When the double potential was recorded at a site orthodromically proximal to the area of block, interruption of atrial flutter was not associated with disappearance of the second potential, and when rapid atrial pacing was continued, the double potential remained despite disappearance of the atrial flutter reentrant circuit. CONCLUSIONS: Double potentials represent functional conduction block in the center of the reentrant circuit, with each deflection of the double potential reflecting activation on either side of the area of functional block. The data also demonstrate that double potentials are not limited to a reentrant circuit, as they were recorded on either side of an area of block in the absence of such a circuit.
Ten patients with coronary artery disease and stable angina (mean age fifty-seven) were included in the study. Five of the patients had normal left ventricular function, 5 had local hypokinesia or akinesia; 8 had one-stem and 2 had two-stem disease, but all had left anterior descending (LAD) lesions ranging from 75% to 100%. Ejection fraction varied between 35% and 75% (mean 59%). Immunoreactive atrial natriuretic polypeptide (ANP) levels in the femoral vein (FV) and the coronary sinus (CS) were measured before, immediately after, and up to twenty-four hours after percutaneous transluminal coronary angioplasty (PTCA) of the LAD. ANP secretion increased by 83% (FV) and 11% (CS) within minutes after PTCA and reached control levels after thirty to sixty minutes. In patients with hypokinesia of the anterior wall, ANP secretion was significantly lower, 48% (FV) and 11% (CS) respectively. ANP secretion during PTCA was higher in patients with concomitant increase in pulmonary capillary pressure (PCP) but was also observed without an increase of PCP, suggesting ventricular ANP secretion. IN conclusion, transient myocardial ischemia leads to immediate ANP secretion even in the absence of significant pressure elevation in the left atrium. As a part of the continuous medical education program of the American College of Angiology the second part of the paper reviews the mechanisms that allow the ischemic heart to counteract the ischemic condition and thus to escape from myocardial infarction. A review of this subject is presently not available in the literature.
In patients with depressed left ventricular function, the normal precautions during transesophageal atrial pacing may not be sufficient to prevent life threatening arrhythmias. In this article two cases of ventricular fibrillation induced during this technique, aimed at treating atrial flutter, are described.
Internal atrial defibrillation (IAD) has been extensively evaluated for clinical efficacy but the need for concomitant demand pacing and the effect of IAD shocks on pacemaker function is not well studied. We prospectively evaluated: (1) the incidence of bradycardia as a result of IAD shocks; and (2) effect of these shocks on functioning of implanted cardiac pacemakers. Consecutive consenting patients with atrial fibrillation (AF) requiring cardioversion or undergoing electrophysiological study were selected for IAD. IAD shocks were delivered using the right ventricle to right atrium (RV-RA), right ventricle to superior vena cava (RV-SVC), right atrium to axillary patch (RA-AX), and right atrium to left pulmonary artery or coronary sinus (RA-LPA/CS) lead configurations. Mean RR interval before and after the shocks and the time interval from shock delivery to first QRS complex were analyzed for unsuccessful and successful shocks. Pacing and sensing function was analyzed in patients with previously implanted pacemakers. Twenty-five patients, 18 men, mean age 67.9 +/- 10 years were included in the study. A total of 305 shocks (264 unsuccessful, 41 successful) were analyzed. For unsuccessful shocks the mean post-IAD shock RR interval (795 +/- 205 ms) and the time to first post-IAD shock QRS complex (970 +/- 438 ms) were both significantly greater than the pre-IAD shock RR interval (685 +/- 131 ms, P < 0.001). The increase in post-IAD shock RR interval and time to first post-IAD shock QRS complex was seen with all four lead configurations used. With successful shocks the mean post-IAD shock sinus cycle length (1,105 +/- 450 ms) and time to first post-IAD shock QRS complex (1,126 +/- 443 ms) were both also significantly greater than the pre-IAD shock RR interval (766 +/- 172 ms). Nine patients (36%) had episodes of significant bradycardia after shock delivery. Shocks of up to 20 J using the RA-LPA/CS lead configuration did not affect pacemaker function. IAD can result in transient bradycardia related to sinus and atrioventricular nodal effects requiring backup ventricular pacing. Shocks can be safely delivered using RA-LPA or RA-CS lead configurations in patients with implanted bipolar cardiac pacemakers.
OBJECTIVE: The incidence of stroke associated with atrial fibrillation, even in high-risk patients, can be reduced significantly by adequate anticoagulation. However, anticoagulation does not abolish the stroke rate, and unfortunately only 40% of patients with atrial fibrillation actually receive anticoagulant therapy, even in areas where adequate health care is available. METHODS: During the past 11.5 years, we have performed the maze procedure for the treatment of medically refractory atrial fibrillation in 306 patients, 58 of whom presented with a history of having had a stroke (n = 40) or transient ischemic attack (n = 18) before surgery. All patients with atrial fibrillation are at an increased risk for these complications, but they are especially prevalent in those patients with previous thromboembolic events and those with other recognized risk factors. RESULTS: Among the 306 patients who had surgery, there were only 2 perioperative strokes (0. 7%), and in the 265 patients followed for up to 11.5 years after the maze procedure, there has been only 1 late minor stroke that has now completely resolved. CONCLUSIONS: The ability of the maze procedure to decrease the risk of stroke associated with atrial fibrillation so dramatically is likely due to the restoring of sinus rhythm and atrial transport function in combination with surgical removal or obliteration of the left atrial appendage, where most thrombi associated with atrial fibrillation develop.
The effects of shen xian sheng mai ye (SXSMY) on experimental sick sinus syndrome (SSS) were observed. By applying 20% formaldehyde to the rabbits' sino-atrial node area, we got the acute animal model of SSS. By observing the rabbits' heart rate (HR), arrhythmia and cardioelectric physiologic index in different periods, the results were as follows: (1) Increasing heart rate: SXSMY could increase rabbits' HR 10-30 times per minute by observing electrocardiogram within 2 hours (P less than 0.05-0.001). (2) Correcting arrhythmia: SXSMY could reduce arrhythmia of sinus nodal arrest and nodal rhythm remarkably. (3) Improving sinus atrial node function: SXSMY could improve sinus node recovery time (SNRT) and sinus atrial conducting time (SACT) with the method of atrial pacing (AP) (P less than 0.01-0.001). But the above results did not appear in atropine and glucose groups.
Transmitral flow was studied using Doppler echocardiography with the A/E ratio as a parameter of left ventricular diastolic function in 21 patients (ages 2.5-30.0 years) who had undergone early surgical correction of an isolated secundum type atrial septal defect (ASD) compared to a healthy cohort of 21 subjects. Pre- and postoperative M-mode recordings were compared in 12 of the 21 patients to evaluate the effect of operation on interventricular septal motion (IVS) and left ventricular (LV) and right ventricular (RV) end-diastolic diameter ratio (LVDD/RVDD) as parameters of right ventricular volume overload. No significant difference in A/E ratio was found between the patient and control groups. IVS was shown to normalize in 11 of 12 patients postoperatively and to improve from paradox to flattened in 1 of 12. LVDD/RVDD increased from 1.26 +/- 0.31 to 2.10 +/- 0.51 (p = 0.0008), with no significant difference remaining between the control and patient groups postoperatively. These findings support the conclusion that an intrinsic abnormality of the left ventricle is not responsible for its diastolic dysfunction in patients with ASD who develop left ventricular failure, thereby implicating an acquired abnormality. Mechanical sequelae of right ventricular volume overload were shown to normalize in all patients subsequent to operation in the present study, and therefore cannot be excluded as a cause of left ventricular failure in ASD.
By means of transoesophageal atrial stimulation of higher frequency in patients with sinus node syndromes (n = 78) in about 60% of the cases a prolonged sinus node recovery time could be proved. After the end of the stimulation secondary stops appeared in about half of the patients, so that in 81% of the cases at least one pathological result was established. By means of premature individual transoesophageal stimulation (n = 99) in 2/3 of the patients with sinus node syndrome we contrived to perform a calculation of the sinuatrial conduction time. Half of all calculable values were above the normal. In 1/3 of the examined persons pathological stimulation patterns were found. Altogether 90% of the patients showed at least one pathological result, when apart from prolonged sinus node recovery times and sinuatrial conduction times at the same time secondary stops after serial stimulation with higher frequency and abnormal behaviour patterns of the post-extrasystolic stops after individual stimulation were taken into consideration. In patients with different cardiovascular diseases without clinical or electrocardiographic reference to a sinus node dysfunction in 25% of the cases at least one pathological result was found, in which case cannot be clarified, whether latent functional sinus node disturbances or falsely positive results are in question or not. Altogether the non-invasive transoesophageal stimulation technique leads to on principle diagnostic evidences of the same value as the up to now usual stimulation of the right atrium. Methodical problems which arise from the stimulation of the righ atrium in transoesophageal approach are to be taken into consideration in the interpretation of the results.
The susceptibilities of atria and ventricles to cold preservation were studied in rat hearts. Rat hearts were stored in Collins' solution at 4 degrees C for 0, 12, or 24 hours, and the atrial and ventricular function was measured in a working heart model and in isolated atrial and papillary muscle preparations. In working heart preparations, cardiac output decreased to 0 ml/min and other parameters of ventricular function (systolic and end-diastolic pressure and dP/dt of the left ventricle) markedly deteriorated after 12 hours of preservation. After 24 hours, no contraction of the left ventricle was observed despite the presence of atrial contraction. In isolated atrial muscle preparations, the rate of spontaneous beating of the right atrium was not affected by cold preservation. The twitch contractions of right and left atria were attenuated but elicited after 24 hours. In electrically driven papillary muscles, twitch contractions were also markedly attenuated by 12 hours of preservation and were abolished after 24 hours. The positive inotropic effect of isoproterenol was also markedly attenuated in the atrial preparations by cold preservation. However, the positive chronotropic response to isoproterenol and the negative chronotropic and inotropic responses to carbachol were little affected by cold preservation. Intramural cholinergic and adrenergic nerve stimulation produced first negative and then positive effects on the beating rate and twitch contraction in the isolated right atria. Cold preservation selectively attenuated and finally abolished the adrenergic responses. In the ventricles, the adenosine triphosphate and creatine phosphate content significantly decreased and the lactate content increased with an increase in the preservation period. On the other hand, changes of such metabolites in the atria were either not observed or were much smaller. These results suggest that atrial function is maintained better than ventricular function in the cold-preserved heart.
This study was designed to evaluate the renal effects of atrial natriuretic factor [ANF(8-33)] in rats with aminonucleoside (AMN)-induced nephrotic syndrome. AMN (100 mg/kg iv) was administered to adult female rats either 2 (AMN 2, n = 7), 4 (AMN 4, n = 7), 6 (AMN 6, n = 7), or 14 (AMN 14, n = 6) days before clearance experiments; untreated (UNT, n = 7) animals served as controls. During clearance experiments, rats were anesthetized with pentobarbital sodium. Protein excretion rates were similar between UNT and AMN 2 but increased stepwise in AMN 4, AMN 6, and AMN 14 rats. The glomerular filtration rate (GFR) was similar in UNT and AMN 2, lower in AMN 4 and AMN 14, and lowest in AMN 6 rats. Basal sodium excretion (UNaV) was not different among the five groups. An ANF primer (1.0 micrograms/kg iv) plus a constant infusion (0.1 micrograms.kg-1.min-1) for 1 h produced a significantly lower increase in UNaV in AMN 2 and AMN 14 than in UNT and was not natriuretic or diuretic in AMN 4 or AMN 6 rats. The ANF-induced increase in UNaV was similar between AMN 2 and AMN 14 rats. ANF had no effect on the GFR in any group. A higher ANF bolus (5.0 micrograms/kg iv) was then infused. This ANF bolus increased UNaV only in UNT and AMN 2 rats. Finally, a bolus of furosemide (4.0 mg/kg iv) was given; UNaV increased similarly in UNT, AMN 2, and AMN 14, and to a lesser extent in AMN 4 and AMN 6 rats. Thus, there is an attenuated natriuretic and diuretic response to ANF in rats with AMN-induced nephrotic syndrome. This altered responsiveness to ANF may contribute to the sodium and water retention characteristic of this disorder.
The function of atrial natriuretic peptide (ANP) is claimed to be control of salt and water homeostasis, and thus, the hormone may be involved in the pathogenesis of certain diseases with impaired volume regulation. We, therefore, studied plasma ANP concentration in dogs with chronic renal failure, congestive heart failure, and hyperadrenocorticism. Dogs with chronic renal failure had twofold higher plasma ANP concentration (16.2 +/- 5.8 fmol/ml), compared with healthy dogs (8.3 +/- 3.5 fmol/ml). An even more distinct increase (sixfold) of plasma ANP concentration was found in dogs with congestive heart failure (52.9 +/- 29.7 fmol/ml). In contrast, dogs with hyperadrenocorticism did not have high ANP plasma concentration (5.5 +/- 2.0 fmol/ml). High-performance liquid chromatographic analysis of plasma from dogs with congestive heart failure indicated that, in addition to the normal circulating form of ANP (99-126), the unprocessed precursor ANP (1-126) is detectable in the circulation. These qualitative and quantitative alterations of plasma ANP concentration in dogs further suggest involvement of this peptide in the development and/or maintenance of diseases associated with impaired volume regulation.
To study the functional role of the atriorenal reflex in the nonhuman primate, we chronically instrumented six Macaca fascicularis with left atrial snares and left atrial and aortic catheters. After inserting a bladder catheter, we determined hemodynamic and renal responses of the conscious chair-restrained monkey to increased left atrial pressure. In 23 snare experiments, no significant changes in renal or cardiovascular function were observed even though left atrial pressure increased from 6.5 +/- 3.3 to 16.2 +/- 3.4 mmHg. The animals were subjected also to blood volume expansion with isoncotic isotonic dextran solutions (+15% of calculated blood volume). They responded normally to this volume stimulus. Conscious dogs prepared in the same manner as the nonhuman primate exhibited diuresis in response to elevations of atrial pressure. We conclude that left atrial stretch receptors are not importantly involved in volume homeostasis in the nonhuman primate.
The determination of the sino-atrial conduction time by means of premature individual atrial stimulation is an important partial function in the intracardial sino-atrial functional test and a reasonable parameter in selected diagnostic questions for the clarification of syncopic conditions under suspicion of a sick-sinus syndrome. In order to alleviate the clinical use and to reduce the considerable expenditure of time in the calculation of the results for the determination of the sino-atrial conduction time by about 60% a computerized evaluation method was elaborated. This methodology resulted in an exoneration from the manual graphic-calculatory expenditure and in comparison to the traditional calculation method it did not show any statistically significant differences.
To determine the precise contributory role of neural and humoral factors in the efferent mechanism of the atrial receptor-renal reflex, we have examined the effects of prolonged (45 min) stimulation of left atrial receptors on renal haemodynamics and function simultaneously in both kidneys (right kidney intact and left kidney denervated) of anaesthetized dogs. Aortic pressure in these dogs was held constant by means of an arterial reservoir connected to the aorta; heart rate changes were prevented by blocking beta 1-adrenoceptor activity with atenolol (2 mg kg-1 i.v.). Localized stimulation of atrial receptors in six dogs increased renal blood flow (6 +/- 2%), creatinine clearance (11 +/- 4%), urine flow (9 +/- 3%), sodium excretion (14 +/- 7%) and osmolal excretion (10 +/- 4%), and decreased free water clearance (14 +/- 7%) in intact kidneys, but led to no changes in denervated kidneys. In an additional four dogs, cooling the vagus nerves to 6-7 degrees C or cutting them in the neck abolished the renal responses to stimulation of atrial receptors in these stabilized preparations. These data clearly demonstrate that the renal responses to prolonged stimulation of atrial receptors are primarily mediated via myelinated vagal afferents and renal sympathetic efferents.
Progress achieved during the last three decades in medical and surgical treatment of infants and children with congenital heart disease has resulted in a significant number of patients surviving to adulthood. The complexity of the basic malformations in addition to the superimposed surgical interventions makes accurate diagnostic imaging essential. The scope of information obtainable from high-quality TEE supports its use in the follow-up of operated and unoperated adult patients, as well as in surgical and interventional procedures. Application of the segmental analysis of anatomy is as important during TEE as it is during TTE. Supplemental transthoracic 2-D and spectral Doppler flow measurements may be needed when poor beam alignment during TEE precludes accurate gradient determinations. Although, to date, most reports of TEE in patients with congenital heart disease have involved children and adolescents, the informational advantage is potentially greater in older adolescents and adults in whom transthoracic windows are frequently limited. In our experience with 125 TEE studies in adult patients with congenital heart disease (the majority using a biplane probe), horizontal plane TEE imaging provided important additional information concerning pulmonary venous connections, atrial baffle function, atrioventricular anatomy and function, left ventricular outflow tract lesions, and great artery positional relationships. Vertical plane TEE enhances imaging of systemic and pulmonary venous connections, atrial situs, venosus atrial septal defects, atrioventricular anatomy and function, and the ventricular septum and outflow tracts and is essential for complete assessment of complex right ventricular outflow tract anatomy, ventriculoarterial alignment, and the sizing of all aortic segments in coarctation of the aorta.
Respiratory function after repair of atrial septal defect (ASD) was analysed in 44 adults (> 40 years), 21 of whom had preoperative respiratory dysfunction, 14 of restrictive type, defined as % vital capacity (% VC) less than 80% of predicted value, 3 with an obstructive pattern, defined as % forced expiratory volume/1 s (% FEV1) less than 70% of predicted value, and 4 patients with a mixed pattern. Increased % VC was found postoperatively in all 14 patients with restrictive respiratory dysfunction, with normal values in 8 out of the 14. Although the three patients with obstructive, and the four with mixed-pattern respiratory dysfunction improved preoperatively in % VC or % FEV1, or both, none had normalized values. We conclude that preoperative restrictive respiratory dysfunction in ASD patients frequently normalizes postoperatively, but not dysfunction of obstructive or mixed restrictive-obstructive type.