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At least 73 records · Page 4Linked to original sources

Failure of left atrial distension to alter renal function in the nonhuman primate.

Experiments were undertaken to determine the influence of increasing left atrial pressure on renal function in the nonhuman primate. Significant elevations of left atrial pressure, produced by using an intra-atrial balloon, had no effect on salt or water excretion, renal plasma flow, or glomerular filtration rate. There were no significant changes in heart rate or blood pressure. We conclude that, unlike those in the dog, atrial receptors in the nonhuman primate play little or no role in modulating salt and water excretion.

Animals

[Effects of atrial natriuretic peptide on left ventricular function in man].

The effects of atrial natriuretic peptide (ANP) infusion were determined in 9 subjects undergoing cardiac catheterization which did not disclose heart disease. Data were obtained at rest and during the steady-state phase of alpha-human-(1-28)-atrial natriuretic peptide infusion (0.5 microgram/Kg bolus dose, 0.05 microgram Kg/min iv for 20 min). Mean blood pressure decreased from 105 +/- 3 to 98 +/- 4 mmHg (p less than 0.05); pressure measurements and left ventricular (LV) angiograms suitable for analysis were available in 7 of 9 subjects at matched heart rate. The infusion of ANP reduced LV end-diastolic and end-systolic volume indices from 93 +/- 6 to 80 +/- 6 ml/m2 (p less than 0.01) and from 25 +/- 3 to 17 +/- 1 ml/m2 (p less than 0.05), respectively. Left ventricular ejection fraction insignificantly increased from 72 +/- 5 to 77 +/- 4%. End-systolic pressure/volume ratio showed a slight but not significant rise (from 3 +/- 0.4 to 4 +/- 0.8). Initial plasma levels of ANP (48 +/- 12 pg/ml) rose to 1890 +/- 423 pg/ml (p less than 0.001) during the infusion and individual hemodynamic responses were not related to plasma concentrations of the peptide. These data suggest that the administration of ANP has no negative effects on LV function and the ANP-induced changes on cardiac performance are related to the reduced cardiac load.

Adult

Effect of dexmedetomidine, an alpha 2-adrenergic agonist, in the isolated heart.

Dexmedetomidine (DM) was studied in the isolated dog heart in the form of a Starling heart-lung preparation, (HLP). Hearts were subjected to increased loading by (a) increasing cardiac output, and (b) increasing systemic resistance. Results are depicted by cardiac function curves, prepared by plotting left atrial pressure against either systemic cardiac output or mean arterial pressure. DM, given in divided doses up to 44 micrograms, had no effect on heart rate or cardiac function, nor did injection of 0.5 mg of atipamezole, a selective alpha 2-antagonist. Additional injections of very large doses of DM, up to 4,444 micrograms, caused an increase in heart rate and a leftward shift of the function curves, ie, positive chronotropic and inotropic effects. Plasma catecholamine levels increased markedly between the 444 micrograms and the 4,444 micrograms cumulative doses of DM. Administration of 1 mg of prazosin had no effect, but 1 mg of propranolol returned the rate to baseline and markedly shifted function curves to the right and depressed their slopes. Thus, whereas low doses (corresponding to between 1 and 30 micrograms/kg in intact animals) of DM, given acutely IV, have been shown to depress cardiac function in intact and denervated dogs, this effect is not due to a direct effect on the myocardium. High doses, far beyond doses maximally effective in intact animals and man, release catecholamines from cardiac stores. Plasma DM levels after low doses in the HLP were between 1 to 10 times those seen in intact animals and human volunteers after the usual doses given clinically for their central effects. Because DM caused no myocardial depressant effect in the isolated, blood-perfused canine HLP, decreases in cardiac function seen after this drug is given to intact and autonomically denervated dogs must be due to factor(s) other than a direct action on the myocardium.

Adrenergic alpha-Agonists

[The effects of atrial natriuretic peptide on left ventricular function in subjects with heart failure].

The effects of atrial natriuretic peptide (ANP) infusion was evaluated in 11 patients with congestive heart failure undergoing cardiac catheterization. Data were obtained at rest and during steady-state phase of alpha-human (1-28) ANP infusion (1 microgram/kg bolus dose, 0.1 microgram/kg/min iv for 30 min). Mean blood pressure decreased from 104 +/- 20 to 89 +/- 21 mmHg (p less than 0.05) 15 min after ANP infusion, as well as left ventricular end-diastolic pressure (from 27 +/- 6 to 14 +/- 11 mmHg, p less than 0.05) and wedge pressure (from 22 +/- 5 to 13 +/- 7 mmHg, p less than 0.05). Left ventricular ejection fraction increased significantly after ANP infusion from 39 +/- 7 to 47 +/- 2%, p less than 0.01. The ANP infusion significantly increased cardiac output from 4.9 +/- 0.8 to 5.8 +/- 1.41/min, p less than 0.05, and decreased the relaxation constant from 69 +/- 17 to 48 +/- 18, p less than 0.05. These results demonstrate that in patients with congestive heart failure ANP infusion decreased wedge pulmonary pressure, left ventricular end-diastolic pressure and increased cardiac output and left ventricular ejection fraction.

Adult

Histological Determinants of Atrial Dysfunction in Patients With Atrial Fibrillation.

BACKGROUND: Atrial fibrillation (AF) is associated with diverse histological abnormalities, but their contributions to atrial dysfunction and functional recovery remain unclear. METHODS: In a discovery cohort of 375 patients with nonvalvular AF undergoing catheter ablation, atrial biopsy samples were quantitatively analyzed for fibrosis, intercellular space expansion, myofibrillar loss, myocardial nuclear density, and amyloid deposition. Left atrial reservoir strain (LASr) was assessed as a measure of atrial function during sinus rhythm (Group 1) or AF (Group 2) at the time of echocardiography. Functional recovery was defined as the change in LASr 12 months after ablation. Findings were validated in an independent cohort of 191 patients with AF. A subset of samples was additionally analyzed for DNA damage markers, poly(ADP-ribose), and phosphorylated histone H2A.X. RESULTS: LASr improved significantly after ablation in Group 2 but not in Group 1. Multivariable analyses identified greater fibrosis, reduced myocardial nuclear density, and advanced amyloid deposition as significant determinants of impaired atrial function in both groups and of limited postablation functional recovery in Group 2 (all P<0.01). Amyloid deposition was also significantly associated with adverse clinical outcomes. Decision-tree models incorporating LASr accurately identified advanced amyloid deposition in both cohorts (accuracy, 94%-96%). DNA damage markers were inversely associated with myocardial nuclear density and positively associated with cardiomyocyte hypertrophy. CONCLUSIONS: Fibrosis, DNA damage-associated reduction in myocardial nuclear density, and advanced atrial amyloidosis are key determinants of atrial dysfunction and impaired postablation functional recovery in patients with AF. LASr enables noninvasive identification of advanced atrial amyloidosis.

Humans

Cardiac effects of atrial natriuretic peptide in subjects with normal left ventricular function.

The effects of atrial natriuretic peptide (ANP) infusion were determined in 9 subjects undergoing cardiac catheterization that did not disclose heart disease. Data were obtained at rest and during the steady-state phase of alpha-human-(1-28)-atrial natriuretic peptide infusion (0.5 micrograms/kg bolus, 0.05 micrograms/kg/min intravenously for 10 minutes). Mean blood pressure decreased from 105 +/- 3 to 98 +/- 4 mm Hg (p less than 0.05); pressure measurements and left ventricular (LV) angiograms suitable for analysis were available in 7 of 9 subjects at matched heart rate. The ANP infusion reduced LV end-diastolic and end-systolic volume indexes from 93 +/- 6 to 80 +/- 6 ml/m2 (p less than 0.01) and from 25 +/- 3 to 17 +/- 1 ml/m2 (p less than 0.05), respectively. The LV ejection fraction increased insignificantly from 72 +/- 5 to 77 +/- 4%. End-systolic pressure/volume ratio showed a slight but not significant increase (from 3 +/- 0.4 to 4 +/- 0.8). Initial plasma levels of ANP (48 +/- 12 pg/ml) increased to 1,890 +/- 423 pg/ml (p less than 0.001) during the infusion and individual hemodynamic responses were not related to plasma ANP concentrations. These data suggest that the administration of ANP has no negative effects on LV function and the ANP-induced changes on cardiac performance are related to the reduced cardiac load.

Adult

Effect of therapeutic-dose irradiation on left ventricular function in conscious dogs.

Every week, 8 conscious, chronically instrumented dogs underwent left ventricular (LV) function studies before, during, and after cardiac irradiation with cobalt 60 (myocardial dose of 5,000 rads at 200 rads per day through a 5 X 5 cm port). During the weekly LV function studies, left atrial pressures were raised by rapid infusion of balanced saline solution. Heart rate, aortic pressures, left and right atrial pressures, LV pressure, left ventricular end-diastolic pressure (LVEDP), and maximum rate of rise of LV pressure were recorded. Electrocardiograms were made. Cardiac outputs were obtained by thermodilution. Stroke volume, LV stroke work, and LV minute work were calculated. LV function curves were constructed each week. All dogs lost weight and became irritable after approximately 800 rads. The electrocardiograms showed signs of myocardial injury after 1,200 rads. All variables were slightly depressed during the first 8 weeks following irradiation. At the eleventh week, both left atrial pressure and LVEDP increased significantly and LV function declined. There was also clinical evidence of LV failure at rest and after volume loading. This study documents that external cardiac irradiation, in a therapeutic dose and schedule range, causes depression of LV function. These functional changes were partially reversed when the follow-up study was continued to six months after irradiation.

Animals

[Functional status of the left side of the heart in patients with ischemic heart disease during isometric exercise].

Hemodynamic parameters of left-ventricular and left-atrial contractility and pumping function were examined in 47 males with postinfarction cardiosclerosis and no clinical signs of circulatory insufficiency and in 30 normal male subjects, exposed to isometric leg exercise with the highest possible compression force. At the height of exercise, normal subjects showed increased left-ventricular myocardial contractility along with the initiation of the Frank-Starling mechanism, spreading to the left atrium as well, while coronary patients responded to increased stress by growing left-atrial reservoir function during the first minutes of exercise, and activated left-atrial transport and pumping functions afterwards. Isometric leg exercise is capable of detecting left-atrial and left-ventricular pumping and contractility disorders in coronary patients.

Adult

Influence of loading conditions and contractile state on pulmonary venous flow. Validation of Doppler velocimetry.

BACKGROUND: Although recent studies suggest that pulmonary venous flow velocities may be used to evaluate left ventricular diastolic function, the influence of loading conditions and contractile state on the magnitude and pattern of pulmonary venous flow are poorly understood. METHODS AND RESULTS: Fourteen anesthetized open-chest mongrel dogs were instrumented with pulmonary venous flow probes, atrial sonomicrometer crystal paris, and high-fidelity micromanometers; transesophageal Doppler echocardiography was used to obtain simultaneous pulmonary venous flow velocities. Measurements were made over a wide range of left atrial pressure obtained by either intravascular volume infusion and inferior vena caval balloon inflation (n = 8), halothane inhalation (n = 6), or phenylephrine infusion (n = 5). There was an excellent correlation for pulmonary venous systolic (J) to diastolic (K) time integral between the Doppler and flow probe signal (r = 0.94; SEE, 0.18). When left atrial pressure was increased by volume infusion, there was a significant linear relation between mean left atrial pressure and the Doppler J/K peak (r = 0.64; SEE, 3.4 mm Hg) and flow velocity-time integral ratio (r = 0.75; SEE, 2.9 mm Hg). By contrast, when left atrial pressure was elevated by halothane-induced cardiac depression, there was no correlation. The independent determinants of the pattern of pulmonary venous flow (stepwise multiple linear regression analysis) under all conditions were atrial systolic shortening, aortic systolic pressure, heart rate, and left ventricular end-systolic dimension (cumulative r = 0.80). CONCLUSIONS: The pattern of pulmonary venous flow can be measured accurately with Doppler velocities and is differentially influenced by loading conditions and myocardial contractile state; in the absence of myocardial contractile dysfunction, the pattern of pulmonary venous flow may provide an estimate of left atrial pressure; and pulmonary venous flow is determined largely by atrial systolic function.

Animals

Echocardiographic evaluation of left ventricular filling in mitral stenosis. Role of atrial contraction.

Echocardiographic evaluation of left ventricular volume change during rapid and atrial filling periods was made in patients with mital stenosis. The significant reduction of rapid filling volume was observed and the rate of rapid filling was approximately the half of normal in mitral stenosis. The rapid filling period showed a good correlation to the mitral valve area measured at operation. After surgical treatment, the rate of rapid filling was significantly increased but was still significantly smaller than normal. It was suggested that the remained structural abnormality of mitral apparatus depressed the inflow through the mitral valve in early diastole despite successful mitral valvotomy. Left ventricular filling during atrial contraction (atrial filling) was augmented twice as much as normal in patients with milder mitral stenosis, compensating the decreased early diastolic filling. In contrast, the atrial filling did not increase in severe mitral stenosis, resulting in the decreased cardiac output. Following mitral commissurotomy, the atrial filling in milder mitral stenosis was reduced but remained significantly larger than normal. There was no change of atrial filling in severe mitral stenosis postoperatively. This fact suggested the existence of impaired contraction of left atrium in cases with severe mitral stenosis. Our results show that the altered left atrial transport function plays an important role in the left ventricular filling in mitral stenosis.

Adult

[A case of tricuspid pouch associated with ventricular septal defect and functional left ventricular-right atrial communication].

We reported a 60-year-old woman with tricuspid pouch associated with ventricular septal defect and subsequent left ventricular-right atrial communication. Preoperative angiographic findings suggested the presence of membranous septal aneurysm, ventricular and atrial septal defects, and tricuspid insufficiency. However, at operation, besides perimembranous inlet type ventricular septal defect, a pouch, 1.5 cm in diameter was found in the adjacent part to the septal leaflet within the anterior one of the tricuspid valve. The ventricular septal defect was closed with a patch. From these findings, it is speculated that the tricuspid pouch was formed by the effect of jet stream through the ventricular septal defect.

Diagnosis, Differential