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PubMed1992

Effect of left atrial plication for the giant left atrium on left ventricular function.

Left atrial plication (LAP) following Kawazoe's method was performed on eight patients with mitral valve stenosis associated with a giant left atrium. To investigate the effect of LAP particularly on left ventricular function, the preoperative and postoperative left ventricular function in these patients were compared. The data were also compared to that of the non-left atrial plication (non-LAP) group with left atrial dimension of 60 mm or over. In the LAP group, there were significant differences between preoperative and postoperative data in the following parameters; New York Heart Association (NYHA) class, cardiothoracic ratio, mean pulmonary arterial pressure (PAP), left ventricular end-diastolic pressure (LVEDP), left atrial dimension, stroke volume index, ejection fraction and cardiac index. On the contrary, in the non-LAP group, there were significant differences between preoperative and post-operative data in the following two factors; NYHA class and PAP. The size of the left atrium in the non-LAP group remained unchanged over the course of long-term follow-up. Despite severe clinical symptoms and severely reduced cardiac function of the patients in the LAP group, cardiac function in all patients improved satisfactorily. This suggests that left atrial plication has a considerably beneficial effect on left ventricular function, and therefore, may be recommended for patients with a giant left atrium.

Adult↗
PubMed1988

Effect of sodium intake on gene expression and plasma levels of ANF in rats.

The effect of short- and long-term sodium loading and sodium restriction on the gene expression as well as on circulating plasma levels of atrial natriuretic factor (ANF) was evaluated in normotensive Wistar rats. These rats were fed either a low-, a regular-, or a high-sodium diet (regular diet and 1% saline as drinking fluid) and studied after 1 and 3 wk. The ANF mRNA was determined in pooled atria and ventricles of the different groups of rats, using the dot-blot technique. Plasma ANF levels were measured with a radioimmunoassay. After 1 wk on the high-sodium diet, ANF mRNA was increased in right atria and ventricles together with circulating ANF levels when compared with animals maintained for the same period on a low-sodium diet. After 3 wk on the various diets, the differences in cardiac ANF mRNA and in plasma ANF levels had disappeared. Gene expression of ANF was also looked for in different areas of the brain, lung, thyroid, adrenals, and the kidney; no hybridization was detected in any of these organs. These data suggest that in rats, the transcription of the ANF gene and peptide release in enhanced only during short-term adaptation to dietary sodium loading.

Animals↗
PubMed1994

Space sickness and fluid shifts: a hypothesis.

In a sample of 64 first-time Space Shuttle crew members, 9 preflight variables related to fluid, electrolyte, and cardiovascular status were previously found to be significantly related to space sickness. The nine variables are serum uric acid, red cell count, environmental temperature at the launch site, serum phosphate, urine osmolality, serum thyroxine, sitting systolic blood pressure, calculated blood volume, and serum chloride. Using discriminant analysis, these preflight variables were used to correctly classify the 64 astronauts according to their space sickness incidence (NOTSICK or SICK) with 80% success, using two methods of pseudo-crossvalidation. Symptoms of motion sickness may be induced on Earth, either with a sufficiently high level of vestibular stimulation or with less vestibular stimulation after reducing the threshold for motion sickness induction. Some of the nine predictor variables support a fluid shift hypothesis of space sickness etiology by which central volume expansion in weightlessness may lower the threshold required for novel vestibular stimulation to cause space sickness. According to this hypothesis, some astronauts suffer a greater central volume expansion than do others, causing them to have greater physiologic responses to fluid shifts, which, in turn, proportionally reduces their threshold for induction of space sickness. The hypothesis is supported by preflight and postflight echocardiographic comparisons of heart volumes in 19 shuttle astronauts. The postflight left ventricular diastolic volume index was decreased by 34 +/- 3% in the astronauts with MODERATE or SEVERE space sickness, but only 9 +/- 5% (P < .05) in the NONE or MILD group, indicating that an exaggerated physiologic adaptation to fluid shifts is associated with space sickness.

Atrial Function↗
PubMedDate not supplied

Atrial natriuretic peptide concentrations in children with pulmonary hypertension: correlation with hemodynamic measurements.

To define the relation between atrial natriuretic peptide (ANP) and hemodynamic parameters in children with pulmonary artery hypertension, we measured the ANP concentrations of the femoral vein, right atrium, pulmonary artery, left atrium and left ventricle, or femoral artery in 32 patients during right or left heart catheterization. There is a strong correlation among the ANP levels obtained from different locations (p < 0.001), and these ANP levels are positively correlated with pulmonary arterial pressures and pulmonary resistance. Patients were divided into two groups according to their pulmonary arterial pressure. The group with pulmonary arterial systolic pressure higher than 31 mmHg had higher ANP levels than the group with pulmonary arterial systolic pressure lower than 31 mmHg. When patients were grouped according to their pulmonary resistance, ANP levels in the group with pulmonary resistance over 2 U/m2 were higher than those in the group with pulmonary resistance lower than 2 U/m2. In this study ANP levels showed a correlation with the right ventricular systolic pressure. A correlation was not seen between ANP levels and the flow ratios or the presence of shunt. The results of our study suggest that ANP should be considered an important factor in pulmonary hypertension, independent of other factors.

Adolescent↗
PubMed1986

Cardiovascular effects of atrial natriuretic extract in the whole animal.

Atrial tissue extract (AE) and ventricular tissue extract cause identical decreases in total peripheral resistance when they are injected i.v. into anesthetized rats. However, only AE causes significant hypotension because of cardiac inhibition. This involves both bradycardia and failure of stroke volume to increase appropriately. The observations cannot be explained by direct action of AE on myocytes, but are more likely to be the result of interactions with cardiovascular reflex mechanisms. Excitation of chemosensitive cardiac receptors with vagal afferents appears to be an important afferent mechanism. The efferent limb for the negative chronotropic response resides partly in the vagus nerves and partly in cardiac sympathetic nerves. The negative inotropic response of AE was not altered by vagotomy, spinal section, atropine, or propranolol. These results suggest that atrial peptides may cause the release of a negatively inotropic substance from a site that is not yet identified.

Afferent Pathways↗
PubMed2001

Left atrial appendage flow in nonrheumatic atrial fibrillation : relationship with pulmonary venous flow and ECG fibrillatory wave amplitude.

OBJECTIVE: This study was conducted (1) to examine the relationship between left atrial appendage (LAA) flow velocity and pulmonary venous flow (PVF) variables during nonrheumatic atrial fibrillation (AF), and (2) to determine whether a reduction in LAA flow is reflected by the fibrillatory wave amplitude on the surface ECG. BACKGROUND: Although LAA Doppler echocardiographic signals provide information regarding the velocity and direction of flow only for a localized narrow sample, systolic PVF represents in part the global left atrial function, mainly relaxation. Controversy exists about whether the amplitude of fibrillatory waves recorded on the surface ECG correlates with LAA flow velocity during AF. MEASUREMENTS AND RESULTS: Thirty-three patients (20 men, 13 women; mean [+/- SD] age, 61 +/- 11 years) with nonrheumatic AF undergoing transthoracic and transesophageal echocardiography were studied. A correlation between LAA flow velocity and systolic PVF variables (peak systolic velocity, R: = 0.450, p = 0.009; velocity-time integral of systolic flow, R = 0.491, p = 0.004; systolic fraction of PVF, R: = 0.627, p < 0.0001) was observed. Patients with a low LAA flow profile (< 25 cm/s) had a reduced systolic PVF. Longer AF duration and the occurrence of moderate mitral regurgitation were related to reduced LAA flow. AF was subdivided into coarse (peak-to-peak fibrillatory amplitude > or = 1 mm) or fine (< 1 mm) in standard ECG lead V1. There was no association between the coarseness of AF and the LAA flow profile. CONCLUSION: In patients with nonrheumatic AF, a reduction in LAA flow velocity correlates with a reduction in systolic PVF. These hemodynamic changes are not reflected by the ECG fibrillatory wave amplitude.

Aged↗
PubMed2000

Dobutamine-induced increase of right ventricular contractility without increased stroke volume in adolescent patients with transposition of the great arteries: evaluation with magnetic resonance imaging.

OBJECTIVE: Prognosis in patients with surgically corrected (Senning or Mustard) transposition of the great arteries (TGA) depends mainly on right ventricular (RV) function and RV functional reserve. We examined the role of dobutamine stress in the early detection of RV dysfunction in asymptomatic or slightly symptomatic patients with TGA using magnetic resonance imaging (MRI). DESIGN AND PATIENTS: Twelve asymptomatic or slightly symptomatic patients with chronic RV pressure overload, surgically corrected (Mustard or Senning) TGA (age 22.8 (+/- 3.4) years; New York Heart Association (NYHA) class I/II) and nine age matched healthy volunteers (age 27.3 (+/- 4.4) years) were included. MRI was applied both at baseline and during dobutamine stress (start dose 5 microg/kg/min to maximum dose 15 microg/kg/min) to determine RV and left ventricular (LV) stroke volumes (SV) and ejection fraction (EF). RESULTS: At baseline only RVEF was significantly higher in controls than in patients (71 (+/- 9) vs. 57 (+/- 10)%, p < 0.001), other RV parameters were not significantly different between the two examined groups: RVSV (86 (+/- 21) vs. 72 (+/- 27) ml, p = ns), RV end-diastolic volume (EDV) (123 (+/- 37) vs. 123 (+/- 33) ml, p = ns), and heart rate (61 (+/- 10) vs. 69 (+/- 14) bpm, p = ns), respectively. During dobutamine stress RVEF increased significantly both in controls and patients (20 (+/- 16) vs. 17 (+/- 18)%, p < 0.01 and p < 0.02 vs. rest, respectively), but stress RVEF was significantly higher in controls than in patients (85 (+/- 3) vs. 66 (+/- 7)%, p < 0.0001). RVSV increased significantly in controls (22 (+/- 19)%, p < 0.02), and there was no significant increase in RVSV in patients (-10 (+/- 28)%, p = ns). The controls showed no change in RVEDV (2 (+/- 17)%, p = ns), but in patients a significant decrease in RVEDV (-24 (+/- 15)%, p < 0.001) was observed. Maximal heart rate was significantly higher in patients than in controls (122 (+/- 20) vs. 101 (+/- 14) bpm, p < 0.02). CONCLUSION: In asymptomatic or slightly symptomatic patients with surgically corrected TGA dobutamine had a positive inotropic effect on RV, but the increased contractility was not accompanied by an appropriate increase in SV. Our data suggest inadequate RV filling in this category of patients, possibly due to rigid atrial baffles and compromised atrial function or decreased compliance due to RV hypertrophy.

Adolescent↗
PubMed1997

Effects of left ventricular chamber size and left ventricular diastolic pressure on left atrial booster pump function in patients with old myocardial infarction.

We characterized the influence of the size of the left ventricular (LV) chamber (LV diastolic diameter, LVDD) and LV end-diastolic pressure (LVEDP) on left atrial active stroke index (LAASI) in patients with old myocardial infarction (OMI) (n = 118) and controls (n = 25). Patients with OMI were classified into four groups according to the grade of LVDD (> or = 55 or < 55 mm) and LVEDP (> or = 18 or < 18 mmHg). LAASI was determined by multiplying the LV stroke index by the fraction of left atrial active contraction of the velocity-time integral on the pulsed-wave Doppler echocardiogram. LAASI in the "LVDD > or = 55 & LVEDP > or = 18" group was less than that in the groups with normal LVEDP. LAASI did not differ among the normal LV dimension groups. The combination of LV enlargement and high LVEDP was related to the decrease in LAASI in patients with OMI.

Aged↗
PubMed1990

Atrial-specific granule number and plasma atrial natriuretic peptide in rats: effects of beta-adrenoceptor blockade and sodium intake.

An interrelationship between atrial natriuretic peptide (ANP) and the renin-angiotensin system has been established. Both of these hormonal systems are modulated by sodium balance. The role of the beta-adrenoceptor in the regulation of release of ANP is not clear. We therefore undertook a study to examine changes in atrial-specific granule number and plasma ANP level following beta-adrenoceptor blockade in rats on low and high sodium intakes. A low-sodium diet, as compared with a high-sodium diet, elevated right and left atrial-specific granule number (right atria 54.6 +/- 8.7 vs. 42.3 +/- 5.7; left atria 47.7 +/- 7.7 vs. 30.6 +/- 3.4 granules/unit area) and plasma renin activity (28 +/- 3.7 vs. 5.4 +/- 0.8 ng AI/ml/hr). Plasma ANP levels were lower in the low-sodium animals (98 +/- 34 vs. 345 +/- 38 pg/ml). When treated with the nonspecific beta-adrenoceptor blocker propranolol, the elevated plasma renin activity and atrial-specific granule number in rats on a low sodium intake were significantly less. Neither of these parameters changed in rats on a high sodium intake. Conversely, propranolol treatment resulted in lower plasma ANP levels in rats with high sodium intake. The already-suppressed plasma ANP level in rats on a low-sodium diet was unaltered with beta-adrenoceptor blockade. The results suggest that dietary sodium intake is an important determinant of the response of atrial-specific granule number and plasma ANP levels following beta-adrenoceptor blockade with propranolol.

Adrenergic beta-Antagonists↗
PubMed1993

Hormonal control of atrial natriuretic peptide synthesis and secretion from cultured atrial myocytes.

We have established optimal culture conditions for growing well-differentiated atrial myocytes from newborn rats. These myocytes show the morphological features of myocytes in intact atria; including perinuclear endocrine storage granules, contractile apparatus and numerous mitochondria. The cells synthesise, store and secrete immunoreactive ANP. Stored ANP is of similar molecular weight to pro-ANP (1-126); secreted ANP is the active form ANP (99-126) but processing appears to take place slowly after secretion. ANP secretion is stimulated by endothelin. Synthesis and secretion of ANP are markedly reduced by the beta-adrenergic agonist isoproterenol, and by forskolin.

Animals↗
PubMed1996

Atrial natriuretic factor secretion: a role for atrial systolic ejection force?

The increase in plasma concentration of atrial natriuretic factor in heart transplant patients has not been fully elucidated. Besides an eventual pressure or volume overload leading to passive atrial distension, the atrial tension developed during atrial systole, or atrial ejection force, which may be increased by the transplantation procedure, is an important determinant of atrial natriuretic factor release. We therefore determined the plasma concentration of atrial natriuretic factor and the maximal atrial ejection force in 15 heart transplant patients and 8 controls, matched for age and body mass. Atrial ejection force, as defined as the force exerted by the left atrium to accelerate blood into the left ventricle during atrial systole, was obtained using combined two-dimensional imaging and doppler echocardiography. Serum creatinin concentrations, heart rate [91.9 (SD 13.2) vs 71.8 (SD 10.9) beats.min-1], mean arterial blood pressure [103.9 (SD 9.8) vs 87.4 (SD 5.8) mmHg, 13.85 (SD 1.31) vs 11.65 (SD 0.77) kPa], left ventricular posterior wall thickness and interventricular septum thickness were higher in heart transplant patients compared to controls. Plasma concentration of atrial natriuretic factor was also elevated in heart transplant patients [63.9 (SD 18.1) vs 34.0 (SD 3.2) pg.ml-1; P < 0.001]. In contrast, although the left atrial area was greater in heart transplant patients [28.2 (SD 4.8) vs 15.8 (SD 2.5) cm2; P < 0.001], mitral area, transmitral Doppler A-wave maximal velocity and atrial ejection force were similar in transplant and in control patients [7.7 (SD 3.5) vs 8.9 (SD 2.8) kdyn, 77 (SD 35) vs 89 (SD 28)mN]. No significant correlation was observed between concentration of atrial natriuretic factor and atrial ejection force, either in heart transplant patients or in controls. Thus, the elevated plasma concentration of atrial natriuretic factor observed in these heart transplant patients was multifactorial in origin, and was considered to depend upon an hypersecretion rather than upon a decreased clearance rate. Moreover, it is suggested that the atrial ejection force was unlikely to have participated in this enhanced release of atrial natriuretic factor.

Adult↗
PubMed1993

Beta-adrenoceptor blockade potentiates acute exercise-induced release of atrial natriuretic peptide by increasing atrial diameter in normotensive healthy subjects.

The role of atrial distension and/or adrenergic mechanisms in the regulation of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP, norepinephrine (NE), epinephrine (E) and left atrial diameter at rest, during and after graded bicycle exercise has been studies in 8 healthy male subjects after single doses of placebo, tertatolol 5 mg (a non-selective beta-adrenoceptor blocker), prazosin 1 mg (an alpha 1-adrenoceptor antagonist) and their combination. Systolic and diastolic left atrial diameters were measured before, during and just after exercise by bidimensional echocardiography. Exercise caused an increase in plasma ANP, which was greater after tertatolol alone, and tertatolol plus prazosin, than after placebo or prazosin alone; the mean area under the plasma ANP concentration curve was increased by 35% after tertatolol alone, by 45% after tertatolol and prazosin compared to placebo, and by 82% and 94%, respectively when compared to prazosin alone. The rise in plasma ANP was more marked during the post-exercise period: 80% after tertatolol alone, 67% after tertatolol and prazosin compared to placebo, and 133% and 115%, respectively, compared to prazosin alone. The rise in plasma ANP was accompanied by an increase in both the systolic and diastolic atrial diameter, which was also significantly greater after tertatolol alone and the combination than placebo, or after prazosin alone. beta-Adrenoceptor blockade alone did not affect the plasma catecholamine concentrations, but the exercise-induced increase in plasma norepinephrine was significantly potentiated by prazosin and by prazosin plus tertatolol, and that of plasma epinephrine by the drug combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Increase in atrial pressure releases atrial natriuretic peptide from isolated perfused rat hearts.

To elucidate the mechanism involved in the release of atrial natriuretic peptide, we modified the isolated perfused rat heart preparation to permit a step-wise increase in right atrial tension. Perfusate was introduced into the right atrium through the superior vena cava and was collected via the pulmonary artery. Right atrial pressure was manipulated by changing the perfusion rate. Perfusate from the pulmonary artery was collected in 1-min-fractions, extracted, and assayed for atrial natriuretic peptide like immunoreactivity (ANP-li). The basal rate of ANP-li release at an atrial pressure of 1.41 +/- 0.31 mm Hg was 964 +/- 144 pg/min (n = 11). As right atrial pressure was increased (range 0.4-4.5 mm Hg), a linear correlation (r = 0.85, P less than 0.001) was observed between the change in ANP-li release and the change in atrial pressure. High pressure liquid chromatography revealed that the major fraction in the perfusate had the same elution time than alpha-rANP. This peak fraction, as well as synthetic atriopeptin III, caused a dose-dependent relaxation in rat aortic strips that had been subjected to contraction with norepinephrine. Further, it corresponded exactly to the material we previously identified in rat plasma. These results suggest that atrial distension is involved in the release of ANP. In addition, ANP is released per se, as the active peptide.

Animals↗
PubMed1987

Plasma atrial natriuretic peptide and blood pressure during chronic salt loading in spontaneously hypertensive rats with right atrial appendectomy.

Spontaneously hypertensive rats (SHR) were subjected to right atrial appendectomy (ATRX) or sham operated. Five days after this procedure the rats were put on tap water or 1.5% NaCl as drinking water for 1 week. The blood pressure (carotid artery), 24 hours urinary sodium and kalium excretion, plasma levels of immunoreactive atrial natriuretic peptide (ir-ANP) and the rise in plasma ir-ANP concentrations after an acute volume expansion by homologous whole blood (10%) were evaluated after 1 week on the different diets. At the start of the dietary period the rise in plasma ir-ANP values was blunted in ATRX rats. After 1 week the salt loaded animals excreted tenfold more sodium than control rats. At this time basal ir-ANP values in plasma were not significantly influenced by the ATRX and/or the high salt diet but the rise in plasma ir-ANP concentrations to acute volume expansion was blunted in the salt loaded rats. However, the basal blood pressure was not influenced by the salt diet and/or the ATRX. These data do not support the notion that an alleged deficiency in ANP release mechanisms in the SHR is a major determinant for the blood pressure development in this rat strain.

Animals↗
PubMed1985

[The heart as an endocrine organ: the discovery of a new hormone].

Ever since the early work of Henry and Gauer (1956) it has been clear that a link exists between the atria of mammals and diuresis. In 1981, De Bold et al. described that atrial extracts, injected intravenously into rats, caused diuresis. The hormone responsible for this diuresis has quickly been identified. The peptide hormone, atrial natriuretic factor (ANF), which is also known as atrial natriuretic peptide(s) (ANP), cardionatrin, cardiodilatin, atrin or auriculin, has been sequenced and synthetically produced. Its genomic DNA has been cloned. ANF raises cyclic GMP in target cells and activates particulate guanylate cyclase but not soluble guanylate cyclase. So far, no other hormone has conclusively been shown to activate particulate guanylate cyclase. ANF is formed and secreted in the atria but not in the ventricles of mammals, including man. The action of ANF involves natriuresis, vasorelaxation and inhibition of aldosterone secretion. ANF or ANF derivatives may represent a therapeutically useful new class of agents.

Adrenal Glands↗
PubMed2006

Role of the simultaneous sequential strategy for failed acute sinus restoration after modified left maze procedure for persistent atrial fibrillation with concomitant mitral surgery.

BACKGROUND: We assessed whether the simultaneous sequential strategy could (1) achieve additional sinus restoration for those patients who were not in sinus rhythm while coming off bypass after modified left maze procedure and (2) attain the same long-term success rates as the bi-atrial maze procedure in patients with persistent atrial fibrillation (AF) and mitral valve disease. MATERIALS AND METHODS: Twenty-seven consecutive patients - ten men and 17 women with a mean age of 52 +/- 13 years, all with persistent AF and mitral valve disease - underwent the modified maze procedure with the simultaneous sequential strategy. In the first phase, the modified left atrial maze operation was carried out with concomitant valvular surgery; the right side maze operation was subsequently carried out as a second phase of the sequential strategy only if AF re-appeared following the spontaneous restoration of heart beats during the operation. RESULTS: Twenty patients (74.1%) underwent the left atrial maze procedure only, and seven patients (25.9%) required the subsequent right atrial maze procedure as part of the sequential strategy. At a mean follow-up of 15.1 +/- 7.7 months, six of the 27 patients (22.2%) who underwent additional right atrial maze procedure had restored sinus rhythm. At a mean follow-up of 17.8 +/- 7.3 months, 24 of the 27 patients (88.9%) had restored sinus rhythm and 22 patients (81.5%) had restored bi-atrial transport function (right atrial filling fraction: 40.8 +/- 11.7%; left atrial filling fraction: 22.9 +/- 8.1%) after application of the sequential strategy. CONCLUSIONS: Compared with modified left atrial maze procedure, the application of the simultaneous sequential strategy successfully restored sinus rhythm in an additional 22.2% of patients with persistent AF. The overall sinus conversion rate of 88.9% was comparable with that of the standard bi-atrial maze procedure.

Adult↗
PubMed1988

Atrial natriuretic peptide in congestive heart failure: postural changes and reset with chronic captopril therapy.

The response of atrial natriuretic peptide (ANP) to standing and the acute and chronic administration of the vasodilator, captopril, were examined in 15 patients with chronic congestive heart failure. In the supine position, ANP was increased (361 +/- 202 pg/ml); however, only a loose correlation existed between atrial pressures and ANP (right atrial vs ANP, r = 0.03, p = N.S., and pulmonary capillary wedge pressures vs ANP, r = 0.4, p = N.S.). Standing and acute captopril therapy decreased atrial pressures and ANP but did not significantly improve the correlation between atrial pressures and ANP. With chronic captopril therapy, atrial pressures remained decreased; however, ANP had returned to control values (370 +/- 254 pg/ml vs 361 +/- 202 pg/ml) and failed to decrease with standing (370 +/- 259 pg/ml lying vs 351 +/- 194 pg/ml standing). These changes in ANP (with chronic captopril therapy) persisted even once the hemodynamic effects of captopril had dissipated (3 hours post dose). This study indicates that in patients with severe chronic congestive heart failure (1) only a poor correlation exists between ANP and atrial pressures and (2) with chronic captopril therapy ANP increases to higher levels for a given atrial pressure and fails to decrease with standing despite a decrease in atrial pressures.

Atrial Function↗
PubMed1988

Increased circulating atrial natriuretic factor (ANF) release during induced ventricular tachycardia.

During sustained ventricular tachycardia (VT), there is usually a rise in mean atrial pressure. Atrial natriuretic factor (ANF) is a peptide released by the atria in response to increased atrial pressure or distension. ANF causes arterial vasodilation and natriuresis in man, and may contribute to the polyuria noted during tachycardia. We hypothesized that induction of sustained VT would cause elevation of right atrial pressure and lead to increased release of ANF. We measured mean arterial pressure, right atrial pressure, VT cycle length, atrial cycle length, plasma norepinephrine, and central ANF in 11 patients during 20 episodes of VT. The mean cycle length of induced tachycardia was 335 +/- 15 msec, with a mean atrial cycle length of 547 +/- 43 msec. Baseline plasma ANF was 70 +/- 11 femtomoles per milliliter and increased to 133 +/- 22 fmol/ml (p less than 0.001) after 4 minutes of VT. There was a decrease in mean arterial pressure from 87 +/- 3 to 66 +/- 3 mm Hg, and a rise in mean right atrial pressure from 4.0 +/- 0.8 to 11 +/- 1 mm Hg (p less than 0.001). The change in plasma ANF was quite variable among individual patients and was correlated with changes in mean right atrial pressure but poorly correlated with changes in mean arterial pressure, plasma norepinephrine, and atrial cycle length. Our data demonstrate that significant increased in ANF levels occur during sustained VT and are associated with increased right atrial pressure.

Atrial Function↗