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PubMed1995

Effects of heart rate on left atrial contractile performance and left ventricular filling during atrial systole in dogs.

Left ventricular (LV) diastolic filling and left atrial (LA) contribution have been investigated in patients with heart disease. However, many of these studies were not conducted at a constant heart rate, and the effects of heart rate remain unclear. The purpose of this study was to clarify the effects of the heart rate on left atrial contractile performance and left ventricular filling during atrial systole. The changes in LA and LV dimensions and pulmonary venous (PV) flow were determined in 9 open-chest dogs by a sonomicrometer and an electromagnetic flowmeter. With a stepwise decrease in the pacing rate from 110 beats/minute to 70 beats/minute, the LA dimension just before atrial contraction increased from 21.4 +/- 0.6 mm to 23.1 +/- 0.7 mm (p < 0.01), and the LA systolic shortening increased from 1.6 +/- 0.1 mm to 2.1 +/- 0.1 mm (p < 0.01). However, the calculated LV filling volume during atrial systole decreased from 1.9 +/- 0.3 ml to 1.4 +/- 0.2 ml (p < 0.01). The PV flow during atrial systole was directed toward the LA, and the LA influx volume from PV decreased from 0.6 +/- 0.1 ml to 0.2 +/- 0.04 ml (p < 0.01). With a decrease in the pacing rate, the LA Frank-Starling mechanism operated. However, LV filling during atrial systole decreased because of the decrease in PV flow to the LV via the LA. Thus, LA contractile performance cannot always be evaluated from LV filling.

Animals↗
PubMed2004

Genome-wide expression profiling of a cardiac pressure overload model identifies major metabolic and signaling pathway responses.

Cardiac hypertrophy is a predictor of cardiovascular morbidity and mortality independent of other risk factors. Pressure overload induces the development of left ventricular hypertrophy (LVH) and left atrial enlargement (LAE) in the mammalian heart. To systematically investigate the transcriptional changes, which mediate these processes, we have performed a genome-wide transcriptional profiling of each of the four heart chambers from mice subjected to transverse aortic constriction (TAC). A major new finding of this analysis is that during enlargement the left atrium undergoes radical changes in gene transcription that may play a significant role in pathophysiology. Structural changes in the LA and LV are correlated with significant changes in the transcriptional profile of these chambers, with thousands of differentially expressed known and novel factors. Statistical analysis of the results identified Gene Ontology biological process groups with significant group-wide changes, including angiogenesis, energy pathways, fatty acid oxidation, oxidative phosphorylation, cytoskeletal and matrix reorganization, and G-protein coupled receptor (GPCR) signaling. To facilitate future research, a searchable annotated Internet database has been constructed that allows access to the expression data presented here. Further study of these genes and processes will lead to better understanding of pathways involved in the pathophysiology of the cardiac response to pressure overload.

Animals↗
PubMed1995

Adverse pacemaker hemodynamics evaluated by pulmonary venous flow monitoring.

The pacemaker syndrome refers to symptoms and signs in the pacemaker patient caused by an inadequate timing of atrial and ventricular contractions. The lack of normal atrioventricular synchrony may result in a decreased cardiac output and venous cannon A waves. The objective of this study was to define the left atrial and pulmonary venous flow response to ventricular pacing in a group of 14 unselected consecutive patients with total heart block and sinus rhythm. Pulmonary venous flow was assessed by transesophageal pulsed Doppler echocardiography in the VVI and DDD pacing modes. An inappropriate atrial timing caused a marked augmentation of the normally small pulmonary venous z wave in all patients ("negative atrial kick," peak z wave in DDD pacing 14.5 +/- 4.6 cm/s, VVI pacing 51.8 +/- 15.0 cm/s). Restoration of AV synchrony (DDD pacing, AV interval 100 ms) abolished these "cannon z waves" in all patients, and a normal pattern of pulmonary venous flow was achieved. Abnormal pulmonary venous flow characteristics were observed in 2 of 14 patients during DDD pacing with short AV intervals (100 ms). The Doppler pattern was similar to the findings seen in VVI pacing. Assessment of pulmonary venous flow by transesophageal pulsed Doppler echocardiography may provide a simple, sensitive, and relatively noninvasive technique to evaluate patients with suspected pacing induced adverse hemodynamics.

Aged↗
PubMedDate not supplied

Pulmonary venous flow: its relationship to left atrial and mitral valve motion.

The factors affecting pulmonary venous flow were studied in a group of 50 patients divided into four groups. Group 1 consisted of 14 normal subjects. Group 2 consisted of 10 patients with pure mitral stenosis and normal sinus rhythm. Group 3 consisted of 15 patients with pure mitral stenosis and atrial fibrillation. Group 4 consisted of 11 patients with atrial fibrillation alone. Pulmonary venous flow, atrial septal motion, and mitral valve flow were obtained by transesophageal echocardiography. Pulmonary wedge pressure or left atrial pressure was measured invasively in all patients. We observed that pulmonary venous flow had a reversed flow during atrial contraction and a biphasic flow in the ventricular phase. The first phase of flow occurred during ventricular systole, corresponding to the beginning of atrial relaxation. The second phase of flow, during ventricular diastole, occurred consistently after the rapid filling wave of mitral flow. The beginning of the second phase, corresponding to maximal relaxation of the atrial septum, reached a maximum corresponding to the beginning of atrial contraction. Results of the present study also indicate that decrease or absence of reversed atrial flow and decrease in the first phase of ventricular flow were noticeable in patients in Groups 2, 3, and 4. The second phase of pulmonary venous flow was significantly decreased in patients with mitral obstruction (Groups 2 and 3), but was maintained when the mitral valve was normal (Group 4). In six patients undergoing percutaneous mitral valvuloplasty, the ventricular phase of pulmonary venous flow increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed2006

Changes in P-wave after percutaneous mitral valvuloplasty in patients with mitral stenosis and left atrial enlargement.

OBJECTIVE: To investigate potential clinical, echocardiographic and/or hemodynamic predictors of the regression of electrocardiographic (ECG) signs of left atrial enlargement (LAE) after successful percutaneous mitral valvuloplasty (PMV). METHODS: We studied 24 patients (75% female, mean age =37.1 +/- 11.9 years) with moderate to severe mitral stenosis (MS), sinus rhythm (SR) and ECG signs of LAE who underwent successful PMV between 2002 and 2004. At least 6 months after the procedure (388.2 +/- 192.9 days), the patients returned for clinical, ECG and echocardiographic follow-up. They were then divided in 2 groups: patients of group 1 (n = 8; 33.3%) still had ECG signs of LAE, and patients of group 2 (n = 16; 66.6%), had normal P wave. A multivariate analysis of clinical, ECG, echocardiographic and hemodynamic variables was performed. RESULTS: The mitral valve area (MVA) increased from 1.12 +/- 0.15 cm2 to 1.9 +/- 0.35 cm2 immediately after the procedure (p < 0.0001) and decreased to 1.89 +/- 0.41 cm2 at follow-up (p = NS). Left atrium diameter decreased from 48 +/- 2.9 mm pre-procedure to 43 +/- 4.8 mm at follow-up (p = 0.0001). P-wave duration decreased from 0.12 +/- 0.01 sec pre-PMV to 0.09 +/- 0.02 sec at follow-up (p = 0.0001). An MVA > or = 1.7 cm2 at follow-up was the only independent predictor of a normal P-wave after PMV (p=0.02). CONCLUSION: ECG changes suggestive of LAE regress in the majority of patients with MS and sinus rhythm that undergo a successful PMV. An MVA > or = 1.7 cm2 at late follow-up was found to be an independent predictor of such normalization.

Adult↗
PubMed2000

P wave dispersion in hypertensive patients with paroxysmal atrial fibrillation.

It is important to assess the risk of developing paroxysmal atrial fibrillation (PAF) in hypertensive patients since hypertension is a common disorder predisposing to PAF. We sought to determine if patients with hypertension at risk of PAF can be identified while in sinus rhythm by measurements of P wave dispersion. Twelve-lead surface electrocardiograms were recorded in 44 hypertensive patients with history of PAF (group I, mean age = 60) and in 50 hypertensive patients without history of AF (group II, mean age = 57). The maximum P wave duration, the minimum P wave duration, and P wave dispersion (Pd = Pmax - Pmin) were calculated from 12-lead surface ECGs. Left atrial dimension (LAD) and left ventricular ejection fraction (LVEF) were measured by echocardiography. P wave dispersion was significantly greater in group I than group II (50 +/- 12 vs 38 +/- 8 ms, P = 0.001). P minimum (75 +/- 13 vs 87 +/- 11 ms, P = 0.001) and LVEF (0.63 +/- 0.05 vs 0.67 +/- 0.04, P = 0.03) were significantly lower in group I than group II. However P maximum and LAD were not significantly different in group I than group II (P > 0.05). In univariate analysis, P minimum, P wave dispersion, and LVEF were significant predictors of PAF, whereas only P wave dispersion remained a significant independent predictor of PAF in a multivariate analysis. Measurement of P wave dispersion in sinus rhythm may be a useful noninvasive clinical tool to identify patients with hypertension at risk of developing atrial electrical instability and atrial fibrillation.

Adult↗
PubMed1999

Electrophysiological effects of homocysteine in isolated rat right ventricular papillary muscles and left atria.

There is clinical and epidemiological evidence that elevated plasma homocysteine (Hcy) levels are associated with increased myocardial infarction mortality; however, very little is known about Hcy's direct cardiac effects. Thus, we aimed to characterize the cellular electrophysiologic effects of Hcy, a sulfur-containing amino acid in isolated rat hearts. A conventional microelectrode technique was used in left atria and right ventricular papillary muscles. At concentrations higher than 10(6) M, Hcy significantly decreased the maximum rate of rise of the depolarization phase (Vmax) in both cardiac preparations in a dose-dependent manner. Hcy at 10(-4)-5 x 10(-4) M concentrations increased the action potential duration (APD) at late stages of repolarization (at 75% and 90% of APD) both in atria and in ventricles. There was a slight decrease in action potential amplitude in ventricular papillary muscles and atria at concentrations higher that 10(-5) M. The resting membrane potential and the early repolarization phase (APD25 and APD50) remained unchanged in every preparation studied at all concentrations of Hcy administered. The present data suggest that homocysteine may decrease the Na+ channel activity in in vitro cardiac preparations. reserved.

Action Potentials↗
PubMed2003

Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis.

Pressure waves are thought to travel from the left atrium (LA) to the pulmonary artery (PA) only retrogradely, via the vasculature. In seven anesthetized open-chest dogs, a balloon was placed in the LA, which was rapidly inflated and deflated during diastole, early systole, and late systole. High-fidelity pressures were measured within and around the heart. Measurements were made at low volume [LoV; left ventricular end-diastolic pressure (LVEDP) = 5-9 mmHg], high volume (HiV; LVEDP = 16-19 mmHg), and HiV with the pericardium removed. Wave-intensity analysis demonstrated that, except during late systole, balloon inflation created forward-going PA compression waves that were transmitted directly through the heart without measurable delay; backward PA compression waves were transmitted in-series through the pulmonary vasculature and arrived after delays of 90 +/- 3 ms (HiV) and 103 +/- 5 ms (LoV; P < 0.05). Direct transmission was greater during diastole, and both direct and series transmission increased with volume loading. Pressure waves from the LA arrive in the PA by two distinct routes: rapidly and directly through the heart and delayed and in-series through the pulmonary vasculature.

Animals↗
PubMedDate not supplied

Efficacy of amikacin, ofloxacin, pefloxacin, ciprofloxacin, enoxacin and fleroxacin in experimental left-sided Pseudomonas aeruginosa endocarditis.

The efficacies of amikacin, ofloxacin, pefloxacin, ciprofloxacin, enoxacin and fleroxacin, each as monotherapy, were evaluated in a rabbit model of induced left-sided Pseudomonas aeruginosa endocarditis. Therapy started 48 h after infection and lasted 5 days. All agents were given intramuscularly; amikacin at 7 mg/kg/12 h, and each quinolone at 35 mg/kg/12 h. All animals survived except for 1 of the group that received amikacin, and 2 of the untreated control group. No sterile vegetations were found in the untreated group and the group of fleroxacin, while 3 animals from the amikacin, ofloxacin, and enoxacin groups, and 2 from the ciprofloxacin and pefloxacin groups had sterile vegetations. All agents used significantly reduced the number of CFU per gram of vegetation versus untreated controls. Enoxacin and ciprofloxacin were equipotent and more effective than pefloxacin, ofloxacin and amikacin. Fleroxacin had a weaker activity.

Amikacin↗
PubMed1997

Left atrial distension and antiorthostatic decrease in arterial pressure and heart rate in humans.

It was investigated to what degree left atrial distension augments the hypotensive effects of a 15-min moderate antiorthostatic maneuver in humans. Ten healthy males underwent a posture change from upright seated (Seat, legs horizontal) to supine (Sup) or to supine with simultaneous lower body negative pressure (Sup + LBNP) to keep left atrial diameter (LAD) unchanged. After 2.5 min of Sup, mean arterial pressure (MAP) decreased from 94 +/- 3 to 86 +/- 3 mmHg (P < 0.05), whereas a similar decrease was delayed 7.5 min into Sup + LBNP. Heart rate (HR) decreased within 2.5 min of Sup from 68 +/- 2 to 60 +/- 3 beats/min (P < 0.05) and remained significantly decreased for at least 2.5 min longer than during Sup + LBNP. Aortic systolic distension (ASD) increased by 59 +/- 17% during Sup (P < 0.05) but was unchanged during Sup + LBNP. The 29 +/- 4% decrease in plasma norepinephrine (NE) during Sup (P < 0.05) was abolished during Sup + LBNP. In conclusion, the increases in LAD and ASD seem important stimuli for the prompt decrease in MAP, the 2.5-min longer-lasting decrease in HR, and the sustained decrease in NE during a 15-min moderate antiorthostatic posture change in humans.

Adult↗
PubMed2003

Functional anatomy of the normal mitral apparatus: a transthoracic, two-dimensional echocardiographic study.

BACKGROUND AND AIM OF THE STUDY: Normal mitral valve function relies on integrity of the leaflets, annulus, subvalvular apparatus, and the left ventricle. Echocardiography has contributed significantly to the understanding of normal and abnormal mitral valve function. Thus, plausible pathophysiologic mechanisms have been proposed for various etiologies of mitral regurgitation, based on echocardiographic measurement of a limited number of parameters. This study provides quantitative echocardiographic assessment of various components of the mitral valve-left ventricular (LV) complex. METHODS: Mitral annulus, leaflets, papillary muscles and basal LV posterior wall length were measured at end-systole and end-diastole in 10 adults (7 females, 3 males; mean age 61 +/- 15 years) with structurally and functionally normal hearts. In addition, LV size and function and left atrial and aortic root sizes were measured. RESULTS: Mitral valve competence in these normal hearts was achieved by systolic reduction in LV volume, diameter and length of 66%, 31% and 18%, respectively. The LV posterior wall (from mitral annulus to origin of the posteromedial papillary muscle) was shortened by 32%. The mitral annulus likewise showed a reduction in diameter of 6% in anteroposterior and 13% in mediolateral planes. Anterior mitral valve leaflet apposed with posterior leaflet by 23% in length in systole, whereas the papillary muscle shortened by 34%. The interpapillary muscle distance decreased by 51% in systole. CONCLUSION: These data provide echocardiographic reference values for various components of the mitral valve-LV complex in normal adults. Further studies are needed to identify the relative significance of each of these components in the pathogenesis of mitral regurgitation of various etiologies.

Adult↗
PubMed1994

In vitro evaluation of the influence of pulsatile intraventricular pumping on ventricular pressure patterns.

The Pulsatile catheter (PUCA) pump consists of a single port membrane pump connected to an indwelling valved catheter. This so-called transarterial blood pump was originally designed to be introduced through a superficial artery into the left ventricular cavity to pump blood from the left ventricle into the ascending aorta. By introducing the catheter directly into the thoracic aorta or the pulmonary artery, the possibility is created of applying large-diameter catheter PUCA pumps as left, right, or biventricular assist devices (LVAD, RVAD, or BIVAD) without damaging any of the structures of the heart. The pump performance of an 8 mm PUCA pump prototype (internal diameter catheter, 8 mm; catheter length, 40 cm; stroke volume, 80 ml) was studied in a mock circulation to investigate the influence of pulsatile intraventricular pumping on ventricular pressure patterns. The pumping mode of the PUCA pump was changed from approximately 1:1 ([n + 1]:n) to 1:2 ([1/2n + 1]:n) and 1:3 ([1/3n + 1]:n) in relation to the frequency of a ventricle-simulating membrane pump. Apart from the pumping mode, timing of the PUCA pump driving system (ejection phase) seems to be crucial in obtaining optimal unloading of the ventricle.

Aorta↗
PubMed1995

Left atrial appendage flow velocity and spontaneous echo contrast in patients with rheumatic mitral stenosis: a multiplane transesophageal echocardiographic study.

BACKGROUND: Left atrial spontaneous echo contrast (LASEC), a putative marker of thrombo-embolic risk, is commonly located in the left atrial appendage (LAA). The aims of this work were to evaluate, using multiplane transesophageal echography, the echocardiographic determinants, specifically LAA outflow Doppler velocity, in the presence of SEC in patients with rheumatic MS. METHODS: Transthoracic and transesophageal echocardiographic tests were performed on 61 patients. The patients were divided into 3 groups based on the presence and type of valvular disease. Patients in group I (n = 28) presented with rheumatic mitral stenosis (MS). Patients in group II (n = 18) presented with valvular heart disease other than MS, and patients in group III (n = 15) had no history of valvular heart disease. The left atrium and appendage were examined for the presence of spontaneous echocontrast and thrombus, using multiplane echo scopy with transducer rotation. Minimal and maximal appendage areas were measured, on a computer-assisted bablet, by tracing a line from the top of the limbus of the left upper pulmonary vein to the appendage endocardial border. The LAA ejection fraction was calculated according to the formula: (maximal area-minimal area)/maximal area. Mitral valvular condition was evaluated with transthoracic and transesophageal echocardiography. Left atrial appendage blood flow velocity profiles were obtained with pulsed-wave Doppler at the orifice of the LAA. RESULTS: LASEC was present in 18 of 28 patients with mitral stenosis (64.3%). Patients with LASEC showed a greater incidence of atrial fibrillation (14/18 vs 12/43, p < 0.005), larger LAD (53.67 +/- 8.74 vs 40.54 +/- 14.85, p < 0.005), smaller LAAEF (38.7 +/- 1.53 vs 69.5 +/- 24.0, p < 0.05), smaller LAAMEV (20.28 +/- 10.07 vs 2.95 +/- 25.11, p < 0.005) and smaller LAAMFV (24.6 +/- 12.23 vs 36.00 +/- 11.01, p < 0.01), when compared with patients without LASEC. For group I, LAAEF, LAAMEV and LAAFV were smaller in patients with SEC than in patients without SEC (p < 0.005, p < 0.05, p < 0.01). However LAD values were similar for patients with and without SEC (53.67 +/- 8.75 vs 54.20 +/- 18.81, p = NS). Both LAAMEV and LAAMFV were related to SEC in patients with atrial fibrillation. However, LAD did not show the same trend. CONCLUSIONS: LASEC is more commonly observed in patients with rheumatic mitral stenosis or atrial fibrillation. Both LAAMEV and LAAMFV are associated with SEC in these patients.

Adult↗
PubMedDate not supplied

Pulsed Doppler characterization of left atrial appendage flow.

Recent evidence suggests that left atrial (LA) appendage velocities may provide clues to the thrombogenic potential of this structure. Pulsed Doppler evaluation of LA appendage flow during transesophageal echocardiography was performed in 109 patients to evaluate the effects of rhythm, mitral regurgitation, and spontaneous contrast. During sinus rhythm, there was a forward LA appendage contraction wave of 46 +/- 18 cm/sec followed by a retrograde filling wave of 46 +/- 17 cm/sec. In 40% of the patients in sinus rhythm, additional forward and retrograde velocities of 23 +/- 10 and 22 +/- 11 cm/sec, respectively, were seen. In contrast, atrial fibrillation was associated with reduced forward and retrograde flows in an irregularly irregular pattern. In sinus rhythm moderate to severe mitral regurgitation did not appear to affect the LA appendage velocities. Last, although forward LA appendage velocities were found to be significantly reduced in patients with spontaneous contrast by univariate analysis, multivariate analysis demonstrated that only the presence of atrial fibrillation was a significant predictor for spontaneous contrast.

Atrial Fibrillation↗
PubMed2000

Efficacy of anticoagulation in resolving left atrial and left atrial appendage thrombi: A transesophageal echocardiographic study.

BACKGROUND: Transesophageal echocardiography (TEE) is the gold standard for evaluation of the left atrium and the left atrial appendage (LAA) for the presence of thrombi. Anticoagulation is conventionally used for patients with atrial fibrillation to prevent embolization of atrial thrombi. The mechanism of benefit and effectiveness of thrombi resolution with anticoagulation is not well defined. METHODS AND RESULTS: We used a TEE database of 9058 consecutive studies performed between January 1996 and November 1998 to identify all patients with thrombi reported in the left atrium and/or LAA. One hundred seventy-four patients with thrombi in the left atrial cavity (LAC) and LAA were identified (1.9% of transesophageal studies performed). The incidence of LAA thrombi was 6.6 times higher than LAC thrombi (151 vs 23, respectively). Almost all LAC thrombi were visualized on transthoracic echocardiography (90.5%). Mitral valve pathology was associated with LAC location of thrombi (P <.0001), whereas atrial fibrillation or flutter was present in most patients with LAA location of thrombi. Anticoagulation of 47 +/- 18 days was associated with thrombus resolution in 80.1% of the patients on follow-up TEE. Further anticoagulation resulted in limited additional benefit. CONCLUSIONS: LAC thrombi are rare and are usually associated with mitral valve pathology. Transthoracic echocardiography is effective in identifying these thrombi. LAA thrombi occur predominantly in patients with atrial fibrillation or flutter. Short-term anticoagulation achieves a high rate of resolution of LAA and LAC thrombi but does not obviate the need for follow-up TEE.

Adult↗
PubMed2005

Automated drug delivery system to control systemic arterial pressure, cardiac output, and left heart filling pressure in acute decompensated heart failure.

Pharmacological support with inotropes and vasodilators to control decompensated hemodynamics requires strict monitoring of patient condition and frequent adjustments of drug infusion rates, which is difficult and time-consuming, especially in hemodynamically unstable patients. To overcome this difficulty, we have developed a novel automated drug delivery system for simultaneous control of systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (Pla). Previous systems attempted to directly control AP and CO by estimating their responses to drug infusions. This approach is inapplicable because of the difficulties to estimate simultaneous AP, CO, and Pla responses to the infusion of multiple drugs. The circulatory equilibrium framework developed previously (Uemura K, Sugimachi M, Kawada T, Kamiya A, Jin Y, Kashihara K, and Sunagawa K. Am J Physiol Heart Circ Physiol 286: H2376-H2385, 2004) indicates that AP, CO, and Pla are determined by an equilibrium of the pumping ability of the left heart (SL), stressed blood volume (V), and systemic arterial resistance (R). Our system directly controls SL with dobutamine, V with dextran/furosemide, and R with nitroprusside, thereby controlling the three variables. We evaluated the efficacy of our system in 12 anesthetized dogs with acute decompensated heart failure. Once activated, the system restored SL, V, and R within 30 min, resulting in the restoration of normal AP, CO, and Pla. Steady-state deviations from target values were small for AP [4.4 mmHg (SD 2.6)], CO [5.4 ml x min(-1) x kg(-1) (SD 2.4)] and Pla [0.8 mmHg (SD 0.6)]. In conclusion, by directly controlling the mechanical determinants of circulation, our system has enabled simultaneous control of AP, CO, and Pla with good accuracy and stability.

Animals↗
PubMed1998

Left atrial energy in normal subjects, in patients with symptomatic mitral stenosis, and in patients with advanced heart failure.

In a population consisting of 45 subjects (15 patients with mitral stenosis, 15 patients with heart failure, and 15 normal subjects), the left atrial (LA) pressure-area relation was assessed and the correlations between LA stroke work, LA kinetic energy, and LA ejection force were studied. The area of the counterclockwise A loop expressing the LA external work was measured. LA kinetic energy was obtained from the formula: 1/2 x stroke volume x 1.06 x v2, where v = transmitral Doppler A velocity. An excellent correlation was found between LA stroke work index and LA kinetic energy when data from all patients were plotted together (r = 0.95, p <0.001). The Pearson's correlation similarity coefficient between LA ejection force and kinetic energy as well as between LA ejection force and stroke work index was r = 0.54 (p <0.001). The r value of 0.54 was significantly lower than r = 0.95 (p <0.03). LA kinetic energy extends the use of transmitral flow Doppler data to include assessment of LA work. LA work can be obtained noninvasively with a high degree of accuracy.

Atrial Function↗
PubMed1998

Postoperative junctional ectopic tachycardia.

PURPOSE: To report the management of junctional ectopic tachycardia after cardiac surgery in an infant. Postoperatively, the patient suffered profound cardiac decompensation secondary to the accelerated rhythm and required extracorporeal membrane oxygenation (ECMO) for haemodynamic support. CLINICAL FEATURES: A 14-day-old, 3.5 kg boy exhibited junctional ectopic tachycardia after cardiopulmonary bypass. Left atrial pressure was 25-28 mmHg. No impact on the tachycardia was seen after rapid overdrive atrial pacing or after 20 micrograms fentanyl i.v., 45 micrograms digitalis, 100 mg magnesium or procainamide (loading dose 15 mg, then 30 mg.kg-1.min-1). Active cooling decreased the nasopharyngeal temperature to 35.2 degrees C, when the heart rate decreased below 180 bpm with a left atrial pressure of 8-10 mmHg. Dopamine (2 micrograms.kg-1.min-1) and dobutamine (5 micrograms.kg-1.min-1) were added to improve the cardiac output. Sodium nitroprusside (0.25 to 1 microgram.kg-1.min) maintained the systolic pressure < 100 mmHg. On arrival in ICU, heart rate increased to 200 bpm. The patient received cardiac massage for severe hypotension 75 min after surgery. Emergency ECMO was instituted for circulatory support. Procainamide, digoxin, dopamine, dobutamine, sodium nitroprusside and hypothermia were continued. Sinus rhythm resumed on the first postoperative day, but procainamide and induced hypothermia at 34 degrees C were maintained for 36 hr after normalization of the rhythm to prevent recurrence of the tachycardia. Total duration of ECMO was three and a half days. Recovery was uneventful. CONCLUSION: The use of ECMO, as a first line of defence, is suitable for the emergency support of patients with JET because of the ease of support of circulation and precise control of hypothermia.

Anesthetics, Intravenous↗