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At least 289 records · Page 16Linked to original sources
PubMed1994

Haemodynamic actions of a novel sino-atrial node function modulator, ZENECA ZD7288, in the anaesthetized dog: a comparison with zatebradine, atenolol and nitrendipine.

1. ZENECA ZD7288 (4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyrimidinium chloride, formerly ICI D7288) is a novel sino-atrial node function modulator which selectively slows sinus node rate. Its effects on haemodynamic function have been studied in pentobarbitone anaesthetized dogs, in comparison with zatebradine, atenolol and nitrendipine. 2. ZD7288 lowered heart rate in the dose-range 0.02 to 1.0 mg kg-1 i.v. from 152 to 77 beats min-1. Myocardial contractile function (measured as both dPLV/dtmax and right ventricular free wall developed force) decreased along with rate. Stroke volume increased as rate decreased. Cardiac output decreased at doses in excess of 0.2 mg kg-1, i.v. 3. These haemodynamic changes were reversed when heart rate reduction was reversed by atrial pacing and are, therefore, considered to be indirect consequences of heart rate changes induced by ZD7288. 4. The effects of zatebradine paralleled those of ZD7288 (heart rate reduced from 149 to 60.5 beats min-1 over the dose-range 0.02 to 1.0 mg kg-1, i.v.), except that dPLV/dtmax did not decrease with heart rate and increased during arial pacing. 5. Neither ZD7288 nor zatebradine had significant effects on atrio-ventricular conduction at intrinsic heart rates, but both significantly and dose-dependently prolonged the atrio-ventricular conduction interval during atrial pacing at 180 beats min-1. 6. The observed effects of atenolol were commensurate with removal of beta-sympathetic cardiac drive. Atrial pacing was found not to restore the pre-atenolol heamodynamic state completely. 7. Nitrendipine up to 0.2 mg kg- i.v. induced changes indicative of direct vasodilatation accompanied by reflex compensation, followed by cardiac depression at higher doses. Atrial pacing failed to compensate for the effects of vasodilatation, but caused atrio-ventricular conduction block at doses above 0.5mgkg-1, i.v.8.data show ZD7288 has marked heart rate slowing properties and that accompanying haemodynamic changes appear to be secondary to the rate changes, being reversed by atrial pacing even in the continued presence of the drug. Heart rate slowing without depression of contractile function should prove to be of benefit in the treatment of myocardial ischaemia, particularly in the presence of myocardial dysfunction.

Animals↗
PubMed1993

An alternative surgical technique in orthotopic cardiac transplantation.

Forty patients underwent orthotopic cardiac transplantation at Wythenshawe Hospital between May 1991 and November 1992. Twenty patients had transplantation using an alternative technique that preserves the shape of the left atrium and leaves the right atrium intact (group A). The remaining twenty had conventional transplantation using the technique described by Lower and Shumway (group B). The patients were randomized to either the new or the conventional technique on an alternate basis. There was no mortality in group A, but two patients in group B developed right ventricular failure and died. Two patients in each group developed nodal rhythm and all four recovered sinus rhythm. Echocardiography and Doppler velocimetry at the transvalvular level confirmed normal atrial function in group A with erratic atrial contraction wave in group B. There was also slightly lower incidence of mitral and tricuspid valve regurgitation in group A than in group B. The improved atrial function in group A may play a part in the prevention of right sided failure following cardiac transplantation.

Echocardiography↗
PubMed1994

The haemodynamic actions of ZENECA ZD7288, a novel sino-atrial node function modulator, in the exercising beagle: a comparison with zatebradine and propranolol.

1. ZENECA ZD7288 (4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyrimidinium chloride, formerly ICI D7288) is a novel sino-atrial node function modulator which selectively slows heart rate. 2. The haemodynamic effects of ZD7288 (0.1, 0.3 and 1.0 mg kg-1, i.v.) have been evaluated and compared with those of placebo (physiological saline), zatebradine (ULFS 49, 0.1, 0.3 and 1.0 mg kg-1, i.v.) and propanolol (0.03, 0.1, and 0.3 mg kg-1, i.v.) in beagles chronically instrumented for measurement of heart rate, aortic pressure, aortic flow and dPLV/dtmax. The dogs were trained to run at 6.5 k h-1 on a level treadmill for 5 min at half hourly intervals over a period of 4 h. Drugs were dosed cumulatively after the second, fourth and sixth exercise periods. 3. Control experiments demonstrated a degree of accommodation to repeated exercise over a period of 4 h. Resting heart rate decreased by 21 beats min-1, but heart rate response to exercise was maintained, whereas dPLV/dtmax at rest remained steady while the response to exercise decreased significantly (by 25% after 2 h, P < 0.05). 4. ZD7288 and zatebradine both decreased heart rate during exercise in a dose-dependent manner, whilst heart rate at rest did not differ from resting heart rates in saline dosed control animals. In contrast, heart rate at rest and during exercise were lowered equally by the lowest doses of propranolol (approximately by 30 beats min-1), and additional doses caused only minor additional decreases. The exercise-induced tachycardia was maintained within 12% of pre-dose levels, presumably by withdrawal of vagal tone.5. Cardiac inotropism, as indicated by dPLv/dt max, was not affected by ZD7288 or zatebradine at rest,although the inotropic response to exercise decreased in proportion to the decreases in exercise-induced tachycardia. Propranolol caused a marked dose-dependent decrease in the exercise-induced inotropic response (by 85% at 0.3mg kg-1).6. Whilst the sino-atrial node modulators increased stroke volume at rest, and augmented increases in response to exercise, propranolol did not affect resting stroke volume and decreased the responses to exercise.7. Cardiac output at rest and cardiac output increases during exercise were well maintained in the presence of ZD7288 and zatebradine in contrast to propranolol which induced a significant depression of cardiac output, both at rest and during exercise. Propranolol also caused significant systemic vasoconstriction.8. In conclusion, ZD7288 has haemodynamic actions comparable to those of zatebradine despite their chemical dissimilarity. ZD7288 may be of benefit in the treatment of ischaemic heart disease by reducing heart rate without impairing cardiac function.

Animals↗
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↗
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↗