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PubMed1985

Dose-related cardiac electrophysiologic effects of sulfinpyrazone.

To test the hypothesis that sulfinpyrazone exerts cardiac electrophysiologic effects, the drug was intravenously injected into 20 subjects during invasive electrophysiologic testing. Sulfinpyrazone was given intravenously as a bolus and by infusion to achieve two different and stable serum levels. The 20 subjects who were treated with drug were assigned to either a low- (N = 10) or high- (N = 10) dose regimen. The resultant four serum levels of sulfinpyrazone were 102 +/- 45, 199 +/- 75, 278 +/- 57, and 352 +/- 77 X 10(-3) mumol (means +/- SD). Electrophysiologic measurements were made during a baseline electrophysiologic study and at each of the sulfinpyrazone levels and at equivalent times in an untreated control group (N = 11). Two electrophysiologic measurements differed when measured at the highest level of sulfinpyrazone and in control subjects: increased HV interval in sinus rhythm and shortened atrial functional refractory period in sinus rhythm (only for those values below the median). Serum levels of sulfinpyrazone correlated with increased sinoatrial conduction time (only for those values above the median; r = 0.64) and with shortened atrial functional refractory periods (r = 0.37). The latter was stronger (r = 0.67) when only values below the median were included in analysis. Shortening of atrial functional refractory period correlated with serum sulfinpyrazone levels during atrial pacing at fixed cycle lengths of 600 and 500 msec. Serum levels of sulfinpyrazone did not correlate with changes in HV interval. HV intervals did not increase in subjects receiving sulfinpyrazone during atrial pacing and, therefore, the effect on HV interval in sinus rhythm is felt to be spurious.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Metoclopramide does not affect renal function and atrial natriuretic peptide release in response to acute saline loading in conscious rats.

It was previously shown in man that metoclopramide (MCP), a dopamine (DA)-2 receptor blocker, attenuates the natriuresis of water immersion. In the present study, we therefore investigated the effects of MCP on renal function and atrial natriuretic peptide (ANP) release in conscious rats. Under basal conditions MCP did not affect glomerular filtration rate (GFR) (7.4 +/- 1.7 ml/min/kg without and 7.8 +/- 0.6 ml/min/kg with MCP), urinary fractional excretion of Na (FENa) (0.3 +/- 0.1% without and 0.3 +/- 0.1% with MCP) and K (FEK) (20.6 +/- 1.4% without and 28.0 +/- 6.2% with MCP) or plasma ANP (37 +/- 5 pmol/l without and 31 +/- 6 pmol/l with MCP). During acute saline loading equal to a 10% rise in body weight, which significantly (p < 0.05) increased GFR, MCP again had no effects on GFR (8.8 +/- 1.8 ml/min/kg with vs. 9.7 +/- 2.5 ml/min/kg without MCP), FENa (24.5 +/- 6.9% with vs. 20.4 +/- 5.1% without MCP), FEK (52.5 +/- 6.9% with vs. 52.5 +/- 9.5% without MCP) and plasma ANP (89 +/- 8 pmol/l with vs. 91 +/- 9 pmol/l without MCP). These results indicate that DA does not modulate renal function or ANP release via DA-2 receptors under basal conditions nor in response to acute saline loading in conscious rats.

Animals↗
PubMed2005

New parameters for left ventricular function in atrial fibrillation: based on the relationship between RR interval and performance.

This study was designed to obtain new parameters representing left ventricular (LV) function independent of irregular RR intervals in atrial fibrillation (AF). AF patients were divided into Normal (n=9) and LV Dysfunction (n=9) groups. The relations between LV outflow peak ejection velocity (Vpe) and preceding (RR-1) or prepreceding RR intervals (RR-2) were obtained using logarithmic equations, from which the squared correlation coefficient (r2), slope, Vpe at RR-1 or RR-2=1 sec (Vpe-1), and the ratio of slope to Vpe-1 (Slope/Vpe-1) were calculated. Among the parameters between RR-1 and Vpe, Slope/Vpe-1 was higher in LV Dysfunction group than in Normal group (p=0.05). When only coordinates with RR-1 from 0.6 to 1 sec were included, Slope/Vpe-1 (p=0.001) was higher in LV Dysfunction group than in Normal group. Among the parameters between RR-2 and Vpe, Slope/Vpe-1, slope, and r2 were different between the two groups. In multivariate analysis, Slope/Vpe-1 between RR-2 and Vpe was only independent parameter. However, Slope/Vpe-1 between RR-1 and Vpe in the coordinates with RR-1 from 0.6 to 1 sec had the highest discriminating power. New parameters derived from the relations between RR intervals and LV performance might be useful to evaluate LV function quantitatively in AF.

Age Factors↗
PubMed1999

Radial approach: a new concept in surgical treatment for atrial fibrillation I. Concept, anatomic and physiologic bases and development of a procedure.

BACKGROUND: The maze procedure cures atrial fibrillation; however, it isolates the pulmonary vein area and results in discordant activation in certain adjacent left atrial segments, which affects left atrial function. To preserve a more physiologic atrial transport function, we developed a new concept of surgical treatment for atrial fibrillation-the radial approach. The atrial incisions radiate from the sinus node toward the atrioventricular annular margins to allow a more physiologic atrial activation sequence and parallel the atrial coronary arteries to preserve blood supply to most atrial segments. METHODS: We examined the atrial coronary arteries and the activation sequence during sinus rhythm in normal canine hearts to design the atrial incisions according to the concept of a radial approach. RESULTS: The pattern of coronary artery distribution was centripetal, branching from the right coronary or left circumflex coronary artery at the right or left atrioventricular groove and spreading toward the sinus node. The endocardial mapping of the atria disclosed some important findings in designing the atrial incisions of the radial approach: the activation sequence at the left atrial septum and at the posterior left atrium between the pulmonary vein orifices. The atrial incisions were designed according to these findings. CONCLUSIONS: The radial approach may represent a more physiologic atrial transport function.

Animals↗
PubMed1991

Assessment of left atrial appendage function by transesophageal echocardiography. Implications for the development of thrombus.

BACKGROUND: The predilection of the left atrial appendage (LAA) for thrombus formation has long been known. METHODS AND RESULTS: We prospectively studied the two-dimensional echocardiographic and Doppler patterns of LAA function in 82 patients by transesophageal echocardiography. In the 63 patients in sinus rhythm, LAA area was measured during LAA diastole at the onset of the electrocardiographic (ECG) P wave (LAAmax) and after LAA systole at the ECG R wave (LAAmin) and LAA ejection fraction was calculated as (LAAmax-LAAmin)/LAAmax; peak Doppler velocity was recorded from the LAA outlet. The 58 patients in sinus rhythm without LAA thrombus were grouped according to left atrial size on transthoracic echocardiography; 39 patients had a left atrial size of less than 40 mm (group 1) and 19 had a left atrial size of 40 mm or greater (group 2). Five patients in sinus rhythm had LAA thrombus. In the 19 patients with atrial fibrillation or flutter LAAmax was measured independent of the ECG; three of these patients had LAA spontaneous contrast, four had thrombus, and one had both. Patients in sinus rhythm without LAA thrombus demonstrated a characteristic pattern of a contractile LAA apex and a noncontractile base with color flow and pulsed Doppler evidence of LAA emptying that coincided with the P wave. Patients in sinus rhythm with LAA thrombus had a mean +/- SD LAAmax (8.0 +/- 1.5 cm2) larger than that in group 1 (5.0 +/- 1.9 cm2) (p less than 0.01) but not group 2 (6.7 +/- 3.1 cm2), LAAmin (6.5 +/- 1.0 cm2) larger than that in both group 1 (2.3 +/- 1.5 cm2) and group 2 (4.2 +/- 2.7 cm2) (p less than 0.01), and LAA ejection fraction (17 +/- 11%) and LAA velocity (0.24 +/- 0.10 m/sec) less than those in both group 1 (55 +/- 21% and 0.48 +/- 0.24 m/sec, respectively) and group 2 (45 +/- 27% and 0.46 +/- 0.24 m/sec, respectively) (p less than 0.01). Patients with atrial fibrillation or flutter with LAA spontaneous contrast and/or thrombus had LAAmax (10.4 +/- 6.6 cm2) greater than that in patients with atrial fibrillation or flutter without LAA contrast and/or thrombus (6.8 +/- 3.0 cm2) (p less than 0.05). The LAA appeared as a static pouch in seven of eight of the former compared with in two of 11 of the latter. When attempted, Doppler demonstrated a recognizable fibrillatory LAA outflow velocity pattern in none of three in the former versus four of seven in the latter group. CONCLUSIONS: We conclude that the LAA has a characteristic pattern of emptying in sinus rhythm. LAA thrombus formation in sinus rhythm and atrial fibrillation is associated with both poor LAA contraction and LAA dilation.

Adult↗
PubMed1993

Atrial natriuretic peptide and left atrial systolic function in normal subjects.

The purpose of this study is to elucidate factors determining the release of atrial natriuretic peptide (ANP) in normal volunteers at rest. Ten normal volunteers were included in this study. Ages ranged between twenty-seven and thirty-three years (mean twenty-seven). The authors measured plasma levels of ANP, and four cardiac chamber volumes, and their functions by cine magnetic resonance imaging using the rephased gradient-echo method. Plasma levels of ANP in 10 normal subjects were 15.0-37.1 pg/mL (mean 23.6 pg/mL). No significant relationship was seen between ANP level and heart rate or blood pressure. The level of ANP was positively correlated with left atrial (LA) emptying fraction and negatively correlated with LA minimal volume (r = 0.85, P < 0.01; r = 0.64, P < 0.05, respectively). No significant relationship was observed between plasma ANP level and left ventricular, right ventricular, or right atrial parameters. These results suggest that LA systolic function is one of the major determinants for ANP release in normal subjects at rest.

Adult↗
PubMed2001

Effect of blood pressure reduction on abnormal left atrial appendage function in untreated systemic hypertensive patients with sinus rhythm.

To investigate whether reduction in blood pressure has a beneficial effect on left atrial appendage (LAA) function, the authors evaluated 24 untreated systemic hypertensive patients with normal left ventricular systolic function in sinus rhythm at baseline and at 3 months after initiation of antihypertensive therapy. They performed transthoracic and transesophageal echocardiographic examinations in hypertensive patients before and after treatment of hypertension. Three of the 24 patients had blood pressure that failed to respond to the regimen of antihypertensive therapy and were removed from the analysis. Of the remaining 21 patients, mean systolic and diastolic blood pressures at baseline were 170 +/- 18 and 104 +/- 6 mm Hg, respectively, and fell significantly at 3 months to 141 +/- 10 and 90 +/- 5 mm Hg, respectively, (p<0.001) after initiation of antihypertensive therapy. There was no significant change in heart rate with treatment (baseline 81 +/- 8 and at 3 months 84 +/- 9 beats/min). There was no significant change in left ventricular end-diastolic diameter, left ventricular ejection fraction, left ventricular wall thickness, or left atrial diameter from baseline (49 +/- 4 mm, 58 +/- 5%, 12 +/- 1 mm, and 41 +/- 4 mm, respectively) at 3 months (48 +/- 5 mm, 59 +/- 4%, 12 +/- 1 mm, and 40 +/- 3 mm). The treatment caused a significant reduction in maximal LAA areas (6.3 +/- 1.3 cm2 at baseline, 4.6 +/- 0.7 cm2 at 3 months, p<0.001), with a concomitant increase in LAA emptying velocity (44 +/- 7 cm/sec at baseline, 60 +/- 9 cm/sec at 3 months, p<0.001). In conclusion, these findings suggest that reduction in blood pressure with antihypertensive therapy could improve LAA function in hypertensive patients with normal left ventricular systolic function in sinus rhythm.

Adult↗
PubMed1975

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.

Adolescent↗
PubMed2000

Left atrial appendage function in patients with different pacing modes.

Many studies suggest that patients who receive a ventricular pacemaker have a higher incidence of systemic thromboembolism compared to patients receiving a physiological pacemaker. However, the exact mechanism regarding the etiology of thromboembolism remains unclear. We evaluated the left atrial appendage (LAA) functions, using multiplane transesophageal echocardiography (TEE), in patients with different pacing modes. In order to evaluate the ejection fraction (EF), peak emptying (V(E)) and filling (V(F)) flow velocities of the LAA by TEE, we studied 31 patients (mean age 63+/-18.5 years) who had been paced for 5.0+/-2.9 years. Patients with atrial fibrillation, left ventricular dysfunction and mitral valve disease were excluded. The pacing indications were complete atrioventricular block (AVB) in 19 patients (9 VVI, 10 VDD or DDD) and sick sinus syndrome (SSS) in 12 patients (5 VVI, 7 DDD). Mean EF, V(E) and V(F) of the LAA were significantly lower in all patients with ventricular pacing (25.5+/-15.6%, 30.4+/-15.6 cm/s and 29. 1+/-19.2 cm/s, respectively) compared to those with physiologic pacing (48.5+/-16.9%, 59.6+/-16.3 cm/s, 57.9+/-18.5 cm/s, respectively) (P<0.01 in all). When patients were further classified with respect to underlying heart disease whether they had SSS or AVB, all measurements of the LAA (EF, V(E) and V(F)) in both subgroup of patients with SSS and AVB were found significantly lower in those with ventricular pacing than in those with physiologic pacing (Tables 3 and 4). This decrease, especially in LAA flow, was much greater in those with SSS (Mean V(E) and V(F) <20 cm/s). In a patient paced with VVI for SSS, a thrombus was detected within the LAA cavity. In conclusion, these results suggest that the pacing modality appeared to influence the LAA functions in paced patients. Patients with asynchronous ventricular pacing modes had a significantly higher incidence of depressed LAA functions than did patients with physiological pacing, especially more marked in patients with sick sinus syndrome. This may be a factor responsible for increased risk of thrombus formation and thromboembolic events in this patient population.

Adult↗
PubMed1989

Left atrial conduit function for left ventricular filling dynamics in patient with myocardial infarction.

This study observed the left function in determining filling dynamics of the left ventricle in patients with myocardial infarction. The study consisted of eight control subjects and ten patients with myocardial infarction. The left ventricular filling volume is considered to be composed of the left atrial passive emptying, active emptying, and conduit volumes. The change of left ventricular filling volume was correlated with that of conduit volume (r = .87, P less than .01). However, the change of left ventricular filling volume did not have any correlation to those of left atrial passive emptying and active emptying volumes. These results suggested that the left atrial conduit function was important in determining filling dynamics of the left ventricle.

Adult↗
PubMed2006

Evaluation of atrial thrombus formation and atrial appendage function in patients with pacemaker by transesophageal echocardiography.

BACKGROUND: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. METHODS: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity. RESULTS: A total 72 patients (mean age, 65 +/- 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean +/- SD; %) was 53.3 +/- 6.2% in ventricular pacing mode and 52.2 +/- 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 +/- 18 cm/s vs 40.94 +/- 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 +/- 2.3 mm vs 37.79 +/- 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. CONCLUSION: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm.

Aged↗
PubMed1989

Right ventricular myocardial function after atrial switch operation for transposition of the great arteries.

Postoperative right ventricular (RV) myocardial function was evaluated in 6 patients who underwent atrial switching for simple transposition of the great arteries (TGA). The average age at study was 5.5 years. RV function was evaluated at rest and during administration of methoxamine by cardiac catheterization and RV angiography. The data were compared with left ventricular function in a control group, which consisted of 6 patients, 3 with functional murmur and 3 with pulmonary valvar stenosis. During stress, the TGA group showed a significant increase in end-diastolic pressure, minute work index and end-diastolic and end-systolic volume indexes, along with a significant decrease in ejection fraction. The control group also showed an increase in these variables except for ejection fraction during stress, which did not change. The slope of the work-function curve for the TGA group was lower than that for the control group (p = 0.02). The TGA group had a lower slope of the peak systolic pressure-volume relation than the control group (p = 0.005). There was no significant correlation between the slope of the peak systolic pressure-volume relation and age at repair or study. This study shows that RV pump dysfunction observed in postoperative TGA patients may be caused by depressed myocardial function.

Cardiac Catheterization↗
PubMed1991

[Modified Fontan procedure, is the right atrial pump function necessary or not? Experimental approach using simulation model].

The effect of pulsatile pulmonary flow and the characteristics of pulmonary arterial pressure (PAP) trace were examined using a model simulating the right heart following the modified Fontan procedure. An inlet overflow tank (preload), valveless axial pulsatile pump, Windkessel model (afterload), and an outlet overflow tank (left atrium) were connected in series. Standard conditions were: flow 2.00 l/m, with 12 mmHg preload, 3.0 wood units resistance and left atrial pressure at 6 mmHg. The pump rate was set at 80 bpm. Simulated PAP and pulmonary flow (PF) waves produced by this model closely resembled those obtained from patients who had undergone the modified Fontan procedure. Parameters except preload were fixed and changes in PF were examined at varying preload of 8, 12, 15 and 17 mmHg. At the various preload levels, PF increased to values greater than the PF for the same conditions in the non-pulsatile state. With a preload value of 8 mmHg, PF increased from 1.10 l/m (non-pulsatile) to a maximum of 1.55 l/m at a peak PAP of 14 mmHg. With a preload of 12 mmHg, the PF increased from 2.00 l/m (non-pulsatile) to 2.65 l/m at 19 mmHg peak PAP. A preload of 15 mmHg resulted in an increase in PF from 2.65 l/m (non-pulsatile) to 3.30 l/m at 22 mmHg peak PAP, and when the preload was 17 mmHg the PF increased from 3.15 l/m (non-pulsatile) to 3.80 l/m at 25 mmHg peak PAP. The afterload of this model was fixed so the increase in PF with pulsation suggests a decrease in resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Function, Right↗