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PubMed2003

Effective long-term left atrial pacing using regular screw-in leads implanted within the coronary sinus.

Passive-fixation leads positioned inside the coronary sinus (CS) have been found to be effective in LA pacing and sensing, but their use is limited by a high incidence of early and late dislodgment. Since anatomic studies have shown that the proximal part of the CS is surrounded by a relatively thick musculature, the feasibility, safety, and efficacy of acute and chronic coronary sinus pacing via regular screw-in leads positioned within the first centimeters of the CS were evaluated as compared to passive-fixation leads. Thirty-three patients (21 men, age 62 +/- 10 years) underwent dual chamber pacemaker implantation with LA pacing obtained via passive-fixation leads (7 patients) or regular screw-in leads (26 patients). The former approach was prematurely abandoned because of a high rate of acute and late lead dislodgment (42%). The chronic pacing threshold was 1.7 +/- 1.0 V at 0.67-ms pulse width and 1.47 +/- 1.3 V at 0.5-ms pulse width for passive- and active-fixation leads, respectively. In the CS active-fixation lead group, no postoperative pericardial effusion, CS lead dislodgment, nor diaphragmatic stimulation were observed. In this last group, steroid eluting leads (14 patients) have a statistically lower pacing threshold than noneluting steroid leads (12 patients) (0.88 +/- 0.23 vs 2.29 +/- 1.68 V, P = 0.011) at long-term follow-up. The use of regular screw-in leads implanted within the CS allows effective and safe long-term LA pacing without risk of dislodgment.

Atrial Function, Left↗
PubMed2001

Effects of left atrial compliance on left atrial pressure in pure mitral stenosis.

In mitral stenosis (MS), left atrial (LA) pressure is commonly elevated because of increased LA afterload. There is a wide spectrum of LA pressure in patients with MS, however, despite a similar mitral valve orifice area. LA compliance is an important determinant of both cardiovascular performance and pathological physiology. Few data are available, however, regarding the effects of LA compliance on LA pressure. We hypothesized that LA pressure may be higher in patients with decreased LA compliance. We analyzed the right heart and transseptal catheterization data in 47 patients (41 female, mean age 40 +/- 10 years) with pure MS and sinus rhythm. The magnitude of LA a and v waves was measured from transseptal catheterization. Fick's method was used to determine cardiac output. LA compliance was calculated by dividing the systolic rise in LA pressure (DeltaP(LA) = P(LA(v)) - P(LA(x))) into the stroke volume. LA size, mitral valve area (MVA), mean diastolic pressure gradient (MG), left ventricular (LV) end-diastolic and end-systolic dimensions were obtained by using two-dimensional and Doppler echocardiography. Multiple regression analysis was performed to identify independent factors determining LA pressure. The mean MVA was 0.95 +/- 0.22 cm(2). MG and LA dimension were 11.2 +/- 5.2 mm Hg and 50.6 +/- 5.2 mm, respectively. The mean LA pressure and cardiac output obtained by cardiac catheterization were 23.4 +/- 8.4 mm Hg and 4.3 +/- 1.5 L/min, respectively. The calculated LA compliance was 4.9 +/- 2.8 cm(3)/mm Hg. Univariate analysis showed that factors associated with increased LA pressure were smaller MVA (r = -0.33, P < 0.05), higher MG (r = 0.69, P < 0.01) and lower LA compliance (r = -0.55, P < 0.01); among them, MG (beta coefficient 0.59, SE 0.19, P < 0.01) and LA compliance (beta coefficient -0.26, standard error 0.34, P < 0.05) were the strongest predictors of LA pressure. In conclusion, LA compliance, along with MG that reflects the severity of MS, is an important contributing factor determining LA pressure in patients with pure MS and sinus rhythm.

Adult↗
PubMed1994

Increased left atrial pressure inhibits hypoxic pulmonary vasoconstriction.

An increase in left atrial pressure (Pla) has been reported to either inhibit or not affect hypoxic pulmonary vasoconstriction in intact dogs. We investigated mean pulmonary arterial pressure (Ppa)-flow (Q) relationships at low and high fixed Pla and Ppa-Pla relationships at fixed Q in piglets, which are known to present with a stronger hypoxic pulmonary pressor response than dogs. Seven piglets were anesthetized; equipped with balloon catheters in inferior vena cava and left atrium to control Q and Pla, respectively; and ventilated alternatively in hyperoxia [fractional concn of O2 in inspired air (FIO2) 0.4] and hypoxia (FIO2 0.12). In all experimental conditions, Ppa-Q plots were best described by a linear approximation with extrapolated pressure intercepts (Pi) not different from Pla. Hypoxia increased slope but not Pi of Ppa-Q plots. An increase in Pla from 8 to 17 mmHg induced a parallel shift of Ppa-Q plots to higher Ppa in hyperoxia but did not affect Ppa-Q plots in hypoxia. In hyperoxia, an increase in Pla at constant Q induced an approximately equal increase in Ppa, whereas in hypoxia there was no effect. The hypoxia-induced increase in Ppa was blunted by increased Pla at all levels of Q studied. We conclude that in anesthetized piglets at fixed Pla hypoxia increases the slope of Ppa-Q plots without affecting Pi and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. The results suggest that no closing pressure higher than normal Pla contributes to hyperoxic or hypoxic Ppa in the intact porcine pulmonary circulation.

Animals↗
PubMed2005

Deceleration time of systolic pulmonary venous flow: a new clinical marker of left atrial pressure and compliance.

The curvilinearity of the atrial pressure-volume curve implies that atrial compliance decreases progressively with increasing left atrial (LA) pressure (LAP). We predicted that reduced LA compliance leads to more rapid deceleration of systolic pulmonary venous (PV) flow. With this rationale, we investigated whether the deceleration time (t dec) of PV systolic flow velocity reflects mean LAP. In eight patients during coronary surgery, before extracorporeal circulation, PV flow by ultrasonic transit time and invasive LAP were recorded during stepwise volume loading. The t dec was calculated using two methods: by drawing a tangent through peak deceleration and by drawing a line from peak systolic flow through the nadir between the systolic and early diastolic flow waves. LA compliance was calculated as the systolic PV flow integral divided by LAP increment. Volume loading increased mean LAP from 11 +/- 3 to 20 +/- 5 mmHg (P < 0.001) (n = 40), reduced LA compliance from 1.16 +/- 0.42 to 0.72 +/- 0.40 ml/mmHg (P < 0.004) (n = 40), and reduced t dec from 320 +/- 50 to 170 +/- 40 ms (P < 0.0005) (n = 40). Mean LAP correlated well with t dec (r = 0.84, P < 0.0005) (n = 40) and LA compliance (r = 0.79, P < 0.0005) (n = 40). Elevated LAP caused a decrease in LA compliance and therefore more rapid deceleration of systolic PV flow. The t dec has potential to become a semiquantitative marker of LAP and an index of LA passive elastic properties.

Atrial Function, Left↗
PubMed1999

Optimal pulse pressure of pulmonary circulation under bi-ventricular assist after cardiogenic shock.

In order to evaluate an appropriate pulse pressure of pulmonary circulation during bi-ventricular assist, an experimental study was carried out in swine. The cardiogenic shock model was made by the left anterior descending (LAD) ligation method. When the hear fibrillated due to acute myocardial infarction, both left and right hearts were supported by ventricular assist devices (VADs) for two hours. The left heart assist was operated with a pneumatic pulsatile ventricular assist device (VAD) and the right was operated with a pneumatic VAD or centrifugal pump. According to the pulse pressure of the pulmonary artery these models were divided into three groups: Low-P group (n = 3), in which a low pulse pressure (less than 20 mmHg) was made by VAD, High-P group (n = 5), in which over 20 mmHg of pulse pressure was initiated. NP group (n = 10), in which nonpulsatile assist was done with a centrifugal pump. In pulmonary gas exchange, the Low-P group was superior to the other two groups. The average PaO2 was 214+/-57 mmHg in the Low-p group, and 117+/-41 mmHg and 148+/-81 mmHg in the NP group and High-P group respectively. In the pathological study, a remarkable extension of pulmonary lymphoducts was found in the High-P group. On the other hand, this change was not recognized in other groups. These results suggested that pulmonary microcirculation might deteriorate due to high pulse pressure of the pulmonary artery. We consider the most suitable pulmonary pulse pressure to be around 20 mmHg to maintain normal pulmonary circulation.

Animals↗
PubMed2005

Acute hemodynamic benefits of bi-atrial atrioventricular sequential pacing with the optimal atrioventricular delay.

OBJECTIVES: We evaluate the acute effects on hemodynamics of bi-atrial (BiA) pacing with the optimal atrioventricular (AV) delays, in comparison with high right atrial (HRA) pacing and coronary sinus (CS) pacing. BACKGROUND: Bi-atrial pacing has been suggested as one of the alternative therapy for preventing the recurrence of atrial fibrillation (AF). There are, however, few reports on the hemodynamic effects of BiA pacing, and the results that exist are controversial. METHODS: Twenty patients were paced from HRA, left lateral site of CS, and both sites with the optimal AV delays at 80 and 100 beats/min, in random order. After 5-min pacing, maximal P-wave duration in a 12-lead electrocardiogram, cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and the transmitral flow pattern by transthoracic echocardiography were measured. RESULTS: Compared with HRA and CS pacing, BiA pacing delivered the shortest P-wave duration (HRA: 130 +/- 14 ms, CS: 132 +/- 19 ms, and BiA: 94 +/- 8 ms, respectively, p < 0.001) and the most improvement in CO and PCWP (HRA: 3.63 +/- 0.67 l/min and 9.2 +/- 4.3 mm Hg, CS: 3.71 +/- 0.70 l/min and 8.8 +/- 3.4 mmHg, and BiA: 3.88 +/- 0.63 l/min and 8.0 +/- 3.1 mmHg, respectively, p < 0.01). Bi-atrial pacing also significantly increased the mitral flow time velocity integral and peak A-wave velocity by transthoracic echocardiography, compared with HRA and CS pacing (HRA: 7.6 +/- 1.4 cm and 68.8 +/- 12.2 cm/s, CS: 7.8 +/- 1.4 cm and 70.5 +/- 14.5 cm/s, and BiA: 8.2 +/- 1.2 cm and 76.3 +/- 14.2 cm/s, respectively, p < 0.01). Bi-atrial pacing most significantly decreased the intervals between the atrial pacing spike and the peak of A-wave (HRA: 180 +/- 28 ms, CS: 165 +/- 21 ms, and BiA: 157 +/- 19 ms, respectively, p < 0.01). These improvements in hemodynamics significantly correlated with interatrial conduction delay. CONCLUSIONS: Bi-atrial pacing made the most significant improvements of hemodynamics. These benefits may be due to the improvements in interatrial conduction delay and atrial dyssynchrony.

Aged↗
PubMed1991

Modifications of cardiac contractility by redox cycling alkylating and mixed redox cycling/alkylating quinones.

The effects of redox cycling, alkylating and mixed redox cycling/alkylating benzo- and naphthoquinones were examined in electrically driven guinea pig left atria. Cardiac microsomal and mitochondrial NAD(P)H-dependent metabolism of the quinones and consequent generation of superoxide anion (O2.-) were also measured. Mixed redox cycling/alkylating 2-methyl-1,4-naphthoquinone, redox cycling 2,3-dimethoxy-1,4-naphthoquinone and alkylating p-benzoquinone determined concentration-dependent positive inotropic responses, whereas redox cycling 2,3,5,6-tetramethyl-p-benzoquinone had no effect. The positive inotropic effect of 2,3-dimethoxy-1,4-naphthoquinone was completely catecholamine-mediated, that of 2-methyl-1,4-naphthoquinone was approximately 70% adrenergic and 30% direct. p-Benzoquinone acted directly on heart muscle. In time, quinones with alkylating properties caused increases in the resting force of atria, whereas redox cycling quinones did not produce toxic effects. Mitochondrial NADH-oxidoreductase accounted for 90 to 95% of the metabolism of all quinones, whereas the contribution of the microsomal pathway was negligible. Considerable amounts of O2.- were produced by mitochondrial biotransformation of 2-methyl-1,4-naphthoquinone and 2,3-dimethoxy-1,4-naphthoquinone but not of 2,3,5,6-tetramethyl-p-benzoquinone and p-benzoquinone, suggesting a kind of relation between O2.- generation and the release of catecholamines.

Alkylating Agents↗
PubMed2002

[Infectious endocarditis of the left heart atrium in injection drug addicts].

AIM: To study etiology, clinical picture, course and prognosis of left heart infection endocarditis (LHIE) in drug addicts. MATERIAL AND METHODS: 61 drug addicts entered the study. 14 of them had lesions of the left heart valves (group 1), 11--of the right and left heart valves (group 2), 36--of the tricuspid valve (group 3), 39 control patients with LHIE had no addiction. Mean age in group 1 was 25.9 +/- 8.8 years, in group 4--48.3 +/- 12.6 years, p < 0.001. RESULTS: Females prevailed in group 3, males--in group 4. Splenomegaly was more frequent in the addicts. Lung lesions (abscesses and infarction) prevailed in groups 2 and 3. Cardiac failure was found more frequently in groups 1 and 4, edema--in group 3, brain affections--in groups 1 and 4. Renal damage was encountered with equal frequency in the addicts and non-addicts. The addicts had, largely, infarctions, non-addicts--glomerulonephritis. Viral hepatitis C was associated with drug addiction. Blood seedings were on the whole positive in 54%, in drug addicts--in 69%. St. aureus predominated (44%). In group 3 it was detected in 72%. It was higher than in groups 4 and 1 (p < 0.001, p < 0.01, respectively). Lethality in group 1 (57%) was higher than in group 3 (22%, p < 0.05) and group 2 (18%, p < 0.01). The leading cause of death in group 1 was cerebral thromboembolism with development of meningoencephalitis. Other causes--progressive cardiac and renal failure.

Adult↗
PubMed2005

Successful radiofrequency ablation in patients with previous atrial fibrillation results in a significant decrease in left atrial size.

BACKGROUND: The objective of the present study was to evaluate the relation between freedom from atrial fibrillation (AF) and left atrial (LA) size in patients who underwent circumferential pulmonary vein (PV) isolation and LA ablation. METHODS AND RESULTS: One hundred five consecutive patients with symptomatic and drug-refractory paroxysmal or persistent AF were included in the present study. The mean age was 52+/-9.5 years (range, 27 to 75 years); 74 patients (70%) were male. Paroxysmal AF was present in 52 (49.5%) and persistent AF in 53 (50.5%) patients. Mean AF duration was 6.0+/-5.1 years in the paroxysmal AF group and 7.6+/-6.0 years in the persistent AF group. A 3D electroanatomic map of the LA including the PV ostia was constructed with a nonfluoroscopic navigation system (Carto, Biosense Webster). Left- and right-sided PVs were encircled by continuous radiofrequency ablation lines. We performed 128 ablation procedures in 105 patients, ie, 23 redo procedures. The mean long-term follow-up duration was 14.6+/-4.9 months (range, 6 to 24 months). Sinus rhythm was present in 45 patients (86.5%) in the paroxysmal AF group and in 41 patients (77.3%) in the persistent AF group at the latest follow-up. Six months after ablation, LA dimension in the persistent AF subjects who remained in sinus rhythm decreased from 44.0+/-5.8 to 40+/-4.5 mm (range, 31 to 51 mm). In contrast, in patients with recurrences of AF, LA dimension increased from 45+/-6.5 to 49+/-5.4 mm (range, 32 to 59 mm). In the successfully treated paroxysmal AF group, LA dimension decreased from 40.5+/-4.4 to 37.5+/-3.5 mm (P<0.01). CONCLUSIONS: In radiofrequency ablation of AF using an electroanatomic approach, there is a statistically significant relationship between medium-term procedural success and LA size: persistent sinus rhythm is associated with reduced and recurrent AF with increased LA dimensions.

Adult↗
PubMed2005

Left atrial systolic force and cardiovascular outcome. The Strong Heart Study.

BACKGROUND: The force needed to fill the left ventricle (LV) in late diastole (left atrial systolic force [LASF]) is abnormal in diseased hearts. The goal of this study was to determine whether LASF adds to prognostic prediction of other markers of preclinical cardiovascular disease in a population with a high prevalence of hypertension and diabetes. METHODS: Doppler echocardiography was performed on 2808 participants of the Strong Heart Study (age 59.3 +/- 8.0 years, 62.5% women, 43.0% hypertensive, 46.7% diabetic, and 54.1% obese) without valvular abnormalities or previous cardiovascular events. The LASF was estimated from mitral orifice area and mitral peak A velocity. RESULTS: The LASF was correlated with older age, higher BP, body mass index, creatinine, serum glucose, insulin levels, and heart rate. After controlling for clinical covariates, LASF was independently associated with higher LV dimensions, LV mass, stroke volume, and cardiac output (all P < .01). In Cox regression analysis, greater LASF was associated with a higher rate of CV events (HR = 1.033, 95% CI = 1.005 to 1.061; P = .021), independently of demographic characteristics, risk factors, LV geometry, and transmitral diastolic pattern. CONCLUSIONS: In a population-based sample of middle-aged and elderly adults with a high prevalence of hypertension and diabetes and without prevalent cardiovascular disease, LASF was associated with geometric changes of the heart and with increased rate of combined fatal and nonfatal cardiovascular events.

Atrial Function, Left↗
PubMed2001

Dissociation between coronary sinus and left atrial conduction in patients with atrial fibrillation and flutter.

INTRODUCTION: Coronary sinus (CS) recordings are routinely used during electrophysiologic studies for various supraventricular and ventricular arrhythmias with the understanding that they represent left atrial (LA) activity. However, the behavior of CS electrical activity during atrial arrhythmias has not drawn any special attention beyond standard considerations. METHODS AND RESULTS: The study population consisted of 9 patients (3 women; mean age 59 +/- 11 years) with atrial fibrillation (AF) and atrial flutter (AFL) who developed dissociation of conduction between the CS and posterior LA during spontaneous AF and AFL. In all patients, the LA and the CS were mapped using a 64-electrode basket catheter and a multipolar electrode catheter, respectively. The right atrium (RA) was mapped simultaneously using a 24-polar electrode catheter (7 patients) or a 64-electrode basket catheter (2 patients). Eight patients showed stable double potentials in CS recordings during AF (9 episodes) and AFL (3 episodes). During ongoing arrhythmias, the first row of potentials maintained a constant relationship with the RA activity, whereas the second row of potentials was discordant with the posterior wall of the LA in 7 patients and concordant in 2 patients. In 1 patient with counterclockwise AFL, CS activation was isolated from the posterior wall of the RA until it reached the distal portion of the CS, after which it entered the lateral region of the LA. In 1 patient, a macroreentrant LA tachycardia involving CS muscle was observed. Rapid atrial pacing from the proximal CS and extrastimuli produced longitudinal dissociation of CS activation in all patients. CONCLUSION: Conduction between the CS and posterior LA can be dissociated during spontaneous atrial arrhythmias and provocative proximal CS pacing.

Arrhythmias, Cardiac↗
PubMed2004

Left atrial dilatation resulting from chronic mitral regurgitation decreases spatiotemporal organization of atrial fibrillation in left atrium.

Atrial conduction properties have been shown to differ among animal atrial fibrillation (AF) models of rapid atrial pacing (RAP), chronic mitral regurgitation (MR), and control. We hypothesized that these conduction differences would continue with the onset of AF, which would affect AF spatiotemporal organization, resulting in model-specific characteristics of AF. With frequency domain analysis of electrograms acquired from high-density optical mapping, AF from the right (RA) and left (LA) atrium in animals with RAP and MR were compared with control animals. At follow-up, the hearts were excised and perfused, and optical action potentials were recorded from a 2 x 2-cm area each of the RA and LA free wall with a 16 x 16 photodiode array. AF was induced with extra stimuli, several 2.4-s AF episodes were recorded in each dog, and a fast Fourier transform was calculated. The dominant frequency (DF) was determined, and the organization (organization index, OI) was calculated as the ratio of the area under the dominant peak and its harmonics to the total area of the spectrum. All possible pairs of electrograms for each episode were cross-correlated. LA AF in the chronic MR model showed an increase in the highest DF, the number of DF domains, and in frequency gradient compared with AF in control or RAP models. In addition, there was a decrease in OI and in the correlation coefficients in the LA of the MR model. These results suggest that the AF substrate in the MR model may be different from that of control or RAP models.

Animals↗
PubMed2001

Alveolar fluid reabsorption is impaired by increased left atrial pressures in rats.

Cardiogenic pulmonary edema results from increased hydrostatic pressures across the pulmonary circulation. We studied active Na(+) transport and alveolar fluid reabsorption in isolated perfused rat lungs exposed to increasing levels of left atrial pressure (LAP; 0--20 cmH(2)O) for 60 min. Active Na(+) transport and fluid reabsorption did not change when LAP was increased to 5 and 10 cmH(2)O compared with that in the control group (0 cmH(2)O; 0.50 +/- 0.02 ml/h). However, alveolar fluid reabsorption decreased by approximately 50% in rat lungs in which the LAP was raised to 15 cmH(2)O (0.25 +/- 0.03 ml/h). The passive movement of small solutes ((22)Na(+) and [(3)H]mannitol) and large solutes (FITC-albumin) increased progressively in rats exposed to higher LAP. There was no significant edema in lungs with a LAP of 15 cmH(2)O when all active Na(+) transport was inhibited by hypothermia or amiloride (10(-4) M) and ouabain (5 x 10(-4) M). However, when LAP was increased to 20 cmH(2)O, there was a significant influx of fluid (-0.69 +/- 0.10 ml/h), precluding the ability to assess the rate of fluid reabsorption. In additional studies, LAP was decreased from 15 to 0 cmH(2)O in the second and third hours of the experimental protocol, which resulted in normalization of lung permeability to solutes and alveolar fluid reabsorption. These data suggest that in an increased LAP model, the changes in clearance and permeability are transient, reversible, and directly related to high pulmonary circulation pressures.

Absorption↗
PubMedDate not supplied

An echocardiographic study of net atrioventricular compliance in juvenile and adult mitral stenosis.

BACKGROUND: Left atrial compliance is an important determinant of symptoms in mitral stenosis. About one-third of patients with mitral stenosis have reduced left ventricular compliance. We measured the net atrioventricular compliance in rheumatic mitral stenosis patients noninvasively and analyzed if there were any clinical, electrocardiographic, roentgenographic or echocardiographic correlates of net atrioventricular compliance. METHODS AND RESULTS: Seventy-six patients with mitral stenosis were analyzed and as many normal subjects were taken as control group. Patients were divided into two groups--those 20 years and below were grouped as juvenile mitral stenosis and those above 20 years as adult mitral stenosis patients. The net atrioventricular compliance in patients with mitral stenosis was significantly impaired compared to normal population. Mean compliance in juvenile group was 4.66+/-2.18 ml/mmHg (range 2.17-9.6) and in adult group it was 4.79+/-1.99 ml/mmHg (range 2.04-8.9) (p = ns). There was no difference in net atrioventricular compliance between the juvenile and adult patients with mitral stenosis. Mitral valve area showed an independent positive correlation with net atrioventricular compliance. CONCLUSIONS: The net atrioventricular compliance was significantly reduced in patients with rheumatic mitral stenosis; however, there was essentially no difference in the net atrioventricular compliance between the juvenile and adult patients with mitral stenosis. The net atrioventricular compliance may not be responsible for the more severe symptoms observed in juvenile mitral stenosis.

Adolescent↗
PubMed1994

Effect of amiloride on inotropic and toxic actions of ouabain in guinea-pig left atria.

The effect of amiloride on the positive inotropic and toxic effects of ouabain in guinea-pig left atria has been studied. In atria driven at 1 Hz, amiloride (0.3 and 0.5 mM) decreased the EC50 but did not affect the maximal tension developed by ouabain. At 0.1 Hz, amiloride did not change either the EC50 or the maximal tension developed by ouabain. Ouabain toxicity (onset of arrhythmias) was not changed by amiloride at either frequency of stimulation. Therefore, amiloride did not antagonize either the positive inotropic or the toxic effect of ouabain. The positive inotropic effect of amiloride has been ascribed to the inhibition of the Na+/Ca2+ exchanger. Since amiloride inhibits also the Na+/H+ exchanger, 5-(N-ethyl-N-isopropyl)amiloride (EIPA), an amiloride derivative which selectively inhibits the Na+/H+ exchange, has been tested to evaluate the role of the Na+/H+ exchange in the amiloride-ouabain interaction. EIPA increased the EC50 values of ouabain and decreased the maximal developed tension by the glycoside in atria driven at 0.1 and 1 Hz, but did not antagonize the toxic response (arrhythmias) of atria to ouabain. It is suggested that the inhibition of Ca2+ exit through the Na+/Ca2+ exchange by amiloride and ouabain may explain the observation that the positive inotropic effects of amiloride and ouabain are additive.

Amiloride↗
PubMed2001

Catecholamines increase lung edema clearance in rats with increased left atrial pressure.

During hydrostatic pulmonary edema, active Na(+) transport and alveolar fluid reabsorption are decreased. Dopamine (DA) and isoproterenol (ISO) have been shown to increase active Na(+) transport in rat lungs by upregulating Na(+)-K(+)-ATPase in the alveolar epithelium. We studied the effects of DA and ISO in isolated rat lungs with increased left atrial pressure (Pla = 15 cmH(2)O) compared with control rats with normal Pla (Pla = 0). Alveolar fluid reabsorption decreased from control value of 0.51 +/- 0.02 to 0.27 +/- 0.02 ml/h when Pla was increased to 15 cmH(2)O (P < 0.001). DA and ISO increased the alveolar fluid reabsorption back to control levels. Treatment with the D(1) antagonist SCH-23390 inhibited the stimulatory effects of DA (0.30 +/- 0.02 ml/h), whereas fenoldopam, a specific D(1)-receptor agonist, increased alveolar fluid reabsorption in rats exposed to Pla of 15 cmH(2)O (0.47 +/- 0.04 ml/h). Propranolol, a beta-adrenergic-receptor antagonist, blocked the stimulatory effects of ISO; however, it did not affect alveolar fluid reabsorption in control or DA-treated rats. Amiloride (a Na(+) channel blocker) and ouabain (a Na(+)-K(+)-ATPase inhibitor), either alone or together, inhibited the stimulatory effects of DA. Colchicine, which disrupts the cellular microtubular transport of ion-transporting proteins to the plasma membrane, inhibited the stimulatory effects of DA, whereas the isomer beta-lumicolchicine did not block the stimulatory effects of DA. These data suggest that DA and ISO increase alveolar fluid reabsorption in a model of increased Pla by regulating active Na(+) transport in rat alveolar epithelium. The effects of DA and ISO are mediated by the activation of dopaminergic D(1) receptors and the beta-adrenergic receptors, respectively.

Amiloride↗
PubMed1997

Influence of inhaled nitric oxide on systemic flow and ventricular filling pressure in patients receiving mechanical circulatory assistance.

BACKGROUND: In patients with left ventricular (LV) dysfunction, inhaled nitric oxide (NO) decreases pulmonary vascular resistance (PVR) but causes a potentially clinically significant increase in left atrial pressure (LAP). This has led to the suggestion that inhaled NO may reach the coronary circulation and have a negative inotropic effect. This study tested an alternative hypothesis that LAP increases because of volume shifts to the pulmonary venous compartment caused by NO-induced selective pulmonary vasodilation. METHODS AND RESULTS: The Thermo Cardiosystems Heartmate is an LV assist device (LVAD) that can be set (by controlling pump rate) to deliver fixed or variable systemic blood flow. Eight patients (between 1 and 11 days after LVAD implantation) were administered inhaled NO (20 and 40 ppm for 10 minutes), and LAP, systemic flow, and pulmonary arterial pressure were measured in both fixed and variable pump flow modes. In both modes, inhaled NO lowered PVR (by 25 +/- 6% in the fixed mode, P < .001, and by 21 +/- 5% in the variable mode, P < .003). With fixed pump flow, LAP rose from 12.5 +/- 1.2 to 15.1 +/- 1.4 mm Hg (P < .008). In the variable flow mode, LAP did not increase and the assist device output rose from 5.3 +/- 0.3 to 5.7 +/- 0.3 L/min (P < .008). CONCLUSIONS: A selective reduction in PVR by inhaled NO can increase LAP if systemic flow cannot increase. These data support the hypothesis that with LV failure, inhaled NO increases LAP by increasing pulmonary venous volume and demonstrate that inhaled NO has beneficial hemodynamic effects in LVAD patients.

Administration, Inhalation↗
PubMed1998

Assessment of abnormal left atrial relaxation by transesophageal pulsed Doppler echocardiography of pulmonary venous flow velocity.

BACKGROUND: Several studies on left ventricular relaxation have been undertaken in the past; however, left atrial (LA) relaxation has not been fully evaluated. HYPOTHESIS: The purpose of this study was to assess abnormalities in LA relaxation by evaluating pulmonary venous flow velocity and interatrial septal motion using transesophageal echocardiography. METHODS: The subjects were 56 untreated patients in sinus rhythm, including 25 with previous myocardial infarction, 9 with hypertrophic cardiomyopathy, 11 with dilated cardiomyopathy, as well as 11 with chest pain syndrome as controls. Peak first systolic velocity (PVS1), peak atrial systolic velocity (PVA), and their time-velocity integrals (PVS1-I and PVA-I, respectively) were calculated from the pulmonary venous flow velocity. RESULTS: The PVS1 and PVS1-I correlated negatively with the maximum LA dimension and mean pulmonary capillary wedge pressure, and correlated positively with the amplitude of the interatrial septal motion during LA relaxation and percent fractional LA relaxation. The PVA and PVA-I did not correlate with the mean pulmonary capillary wedge pressure. There was a weak positive correlation between PVA and PVS1, and a close positive correlation between the ratio of PVA to PVS1 and mean pulmonary capillary wedge pressure. Multiple regression analysis indicated that the PVS1 was most closely related to percent fractional LA relaxation, followed by mean pulmonary capillary wedge pressure. CONCLUSION: The PVS1 determined from the pulmonary venous flow velocity is closely related to parameters of LA relaxation which may be determined by transesophageal M-mode echocardiography, and the ratio of PVA to PVS1 is useful for noninvasive evaluation of LA pressure.

Adult↗