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PubMed1992

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↗
PubMed2026

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↗
PubMed1979

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↗
PubMed1978

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↗
PubMed1975

Hemodynamic and clinical significances of atrial fibrillation, pulmonary vascular resistance and left ventricular function in rheumatic mitral stenosis.

Seventy-four patients with rheumatic mitral stenosis were catheterized and hemodynamic and clinical significances of atrial fibrillation, pulmonary vascular resistance and left ventricular function were studied. These data were also compared to those in the 6 control cases. In addition to the correlation of mitral valve area to the functional classification of patients, significance of atrial fibrillation was also demonstrated. Patients with this arrhythmia had lower cardiac index than those with regular sinus rhythm by approximately 20%, throughout the range of mitral valve area observed. The lower average cardiac index was associated with a higher average left ventricular end-diastolic pressure in cases with atrial fibrillation than in cases without the arrhythmia, in the face of similar average heart rate and average mitral valve area; Average pulmonary vascular resistance correlated to the functional classification, but its systematic influence on the relation between mitral valve area and cardiac index was not observed. Abnormalities of left ventricular function were suggested frequently by various combinations of abnormal values in end-diastolic pressure, end-diastolic volume, ejection fraction, angiographically-measured circumferential fiber shortening velocity (Vcf), and pressure-derived maximal contractile element velocity (Vmax). Patients with enlarged left ventricle had significantly lower average cardiac index than those with normal ventricular size.

Adult↗
PubMed1992

High levels of plasma atrial natriuretic factor and impaired left ventricular diastolic function in hypertensives without left ventricular hypertrophy.

OBJECTIVE: To seek possible correlations between plasma atrial natriuretic factor (ANF) and left ventricular diastolic function (LVDF) in hypertensive patients. DESIGN: Since LVDF abnormalities can be detected in patients with normal left ventricular mass, we studied a group of hypertensive patients without left ventricular hypertrophy. METHODS: Untreated hypertensive patients (n = 23) and normotensive control subjects (n = 19) were studied. LVDF indices were obtained by M-mode and pulsed Doppler echocardiography. Blood samples for plasma ANF were taken in the recumbent position from subjects on normal-sodium intake. RESULTS: Plasma ANF levels were significantly higher in hypertensive patients than in normotensive subjects. All indices for systolic function were normal in both normotensive subjects and hypertensive patients. Left atrial diameter was significantly higher for hypertensive patients than for normotensive subjects. Considering LVDF, all indices for ventricular filling were found to be altered, on average, in hypertensive patients, the only exception being peak early velocity. In addition, significant correlations were found between plasma ANF and the pulsed Doppler parameters of left ventricular filling, peak atrial velocity and the peak early:peak atrial velocity ratio. Overall correlations between plasma ANF and left atrial diameter, and between left atrial diameter and left ventricular mass index were also observed. CONCLUSIONS: The high levels of plasma ANF observed in our hypertensive patients and their correlation with the LVDF indices (which mainly reflect the atrial contribution to ventricular filling) could be the result of an increased atrial stretch due to diastolic ventricular dysfunction. This may exist in hypertensive patients before the development of ventricular hypertrophy.

Adult↗
PubMed1992

Effects of androgens and antiandrogens on the inotropism induced by ouabain and isoproterenol on the left atrium of the rat in vitro.

1. The effect of androgens 5 beta- and 5 alpha-dihydrotestosterone (DHT, 10(-9) M), and the antiandrogens cyproterone acetate (CPA, 10(-8)-10(-6) M), chlormadinone acetate (CMA, 10(-8)-10(-6) M), medroxyprogesterone acetate (MPA, 10(-8)-10(-6) M), spironolactone (SPI, 10(-5) M), flutamide (F, 10(-5) M) and cimetidine (C, 10(-5) M), on inotropic positive effect induced by ouabain (10(-8)-10(-5) M) and isoproterenol (10(-8)-10(-6) M), on electrically stimulated left atria of rat, has been assayed. 2. Ouabain (10(-6) M) did not modify the inotropic effect of isoproterenol (10(-8)-10(-6) M). 3. The androgens 5 beta- and 5 alpha-DHT (10(-9) M) and the antiandrogens SPI (10(-6) M), F (10(-5) M) and C (10(-5) M) inhibit the inotropic effect of ouabain and isoproterenol on electrically stimulated left atria of the rat. 4. The antiandrogens CPA, MPA and CMA to 10(-7) M, inhibit the inotropic effect of ouabain. The CPA (10(-8)-10(-6) M) inhibit, in a dose-dependent way the positive inotropic effect of isoproterenol. MPA and CMA (10(-8)-10(-6) M) also inhibit the inotropic effect isoproterenol but the inhibitory effect is greater with 10(-8) M than 10(-6) M of both drugs. 5. Taken together, our results suggest that steroidal hormones could modulate the cardiac contractility through interference with Na-pump in a non-digitalic site and/or with intracellular mediators in left atrium.

Androgen Antagonists↗
PubMed1975

Intra-aortic balloon counterpulsation: potential for therapy in hemorrhagic shock with associated myocardial failure.

After attaching appropriate monitoring devices enabling the measurement of the slope of the left ventricular function curve, left atrial pressure, mean aortic pressure, peak left ventricular pressure, and tension time index, three groups of ten dogs were subjected to varying periods of hemorrhagic shock until a slope of their ventricular function curve was reduced to either 75% (Group I), 50% (Group II), or 25% (Group III) of their baseline value. Resuscitation was attempted in all dogs by the intravenous infusion of shed blood plus additional balanced salt solution. This infusate was administered to maintain either the mean aortic pressure within 15 mm Hg of the baseline value or a left atrial pressure of 15 mm Hg, whichever occurred forst. One half of the dogs received, in addition, intra-aortic balloon counterpulsation. All dogs not receiving counterpulsation expired within two hours. There was no apparent effect of counterpulsation on Group I animals. Three of five animals (Group II) and four of five animals (Group III) receiving counterpulsation survived to the end of the experiment with significant (p smaller than .01) improvement in the parameters monitored. The utilization of counterpulsation as an adjunct to treatment in hemorrhagic shock is suggested.

Animals↗
PubMed1992

[Rhythmogenic cardiomyopathies of atrial origin in children. Myth or reality?].

Incessant, rapid, supraventricular tachycardia may be complicated by cardiac failure with ventricular dilatation and hypokinetic wall motion on echocardiography: so-called tachycardia-induced cardiomyopathy. The diagnosis is simple when the cardiac rhythm is not sinus rhythm. The authors report the cases of 4 children aged 7 months to 12 years, referred for diagnosis and treatment of apparently primary cardiomyopathy. The findings of spontaneous or vagally-induced atrioventricular conduction defects, a permanently rapid atrial rhythm though influenced by 24 hour variations, or periodic abnormal rate increases, suggested myocardial dysfunction due to an ectopic atrial tachycardia. This was an essential step in management as the control of the tachycardia by amiodarone or betablocker therapy resulted in regression of symptoms and normalisation of left ventricular function. However, some atrial tachycardias are very resistant to medical treatment and, in such cases, there should be no hesitation in using more radical approaches, surgery or ablation, even and especially in patients with severe cardiac failure. In conclusion, apparently primary dilated cardiomyopathy in children may be due to chronic atrial arrhythmia and it is essential to perform at least Holter monitoring in order not to miss this diagnosis.

Adrenergic beta-Antagonists↗
PubMed1979

Spinal cord ischemia and left atrial myxoma.

A 62-year-old man had an acute, transient, flaccid paraplegia. Examination showed a primary cardiac tumor with emboli to major branches of the aorta. A myxoma was removed from the left atrium, and normal function returned. Left atrial myxoma should be suspected as a cause for embolism to the CNS.

Embolism↗
PubMed1992

Left atrial contribution to ventricular filling during the course of evolving heart failure.

BACKGROUND: Abnormal left ventricular (LV) filling has been observed in patients with heart failure and is characterized by marked heterogeneity of mitral inflow velocity. In the present study, the contribution of the left atrium to LV filling was examined in eight dogs during the course of evolving heart failure. METHODS AND RESULTS: Heart failure was produced by multiple sequential intracoronary embolizations with microspheres. Pulsed Doppler echocardiography was used to measure mitral inflow velocity at baseline, before embolization, and at 3, 8, 15, 23, and 33 weeks after initiation of microembolization. The early rapid LV filling (Ei) and late left atrial filling (Ai) components were quantitated based on the time-velocity integral of the early and late mitral inflow velocity waveforms, respectively. Ei decreased progressively from 7.6 +/- 1.5 cm at baseline to 4.0 +/- 0.4 cm at 33 weeks (p less than 0.01). In contrast, Ai initially increased from 1.8 +/- 0.9 cm at baseline to 2.7 +/- 0.4 cm at 3 weeks (p less than 0.01) and subsequently decreased gradually to below baseline values reaching 0.8 +/- 0.4 cm at 33 weeks (p less than 0.01). These temporal changes of Ei and Ai were accompanied by a gradual reduction of LV ejection fraction (56 +/- 5% versus 22 +/- 2%) (p less than 0.01) (baseline versus 33 weeks) and by a gradual increase of LV end-diastolic wall stress (24 +/- 7 versus 92 +/- 8 g/cm2) (p less than 0.01), left atrial dimension (2.4 +/- 0.2 cm to 3.3 +/- 0.3 cm) (p less than 0.01), and left atrial fractional shortening (22 +/- 3% versus 15 +/- 2%) (p less than 0.01). CONCLUSIONS: The initial rise in left atrium contribution to LV filling may represent a compensatory response to the diminution of the rapid early component of LV filling. With further progression of LV dysfunction, the left atrium contribution to LV filling gradually decreased. This reduction may be mediated by increased workload imposed on the left atrial myocardium due to increased LV diastolic wall stress, which, over time, may have lead to intrinsic left atrium dysfunction.

Animals↗
PubMed1992

Simultaneous measurement of left atrial pressure by Doppler echocardiography and catheterization.

Simultaneous, continuous wave Doppler echocardiography, left ventricular systolic and mean pulmonary capillary wedge pressure measurements were performed during cardiac catheterization in 54 patients with mitral regurgitation. Doppler-derived left atrial pressure, which was calculated by subtracting mitral regurgitant gradient from brachial artery systolic pressure, correlated well with mean pulmonary capillary wedge pressure by catheter (r = 0.933, SEE = 2.9 mmHg, P < 0.001); a comparison between non-invasive and invasive systolic gradients across the mitral valve yielded a high correlation (r = 0.91, SEE = 6.0 mmHg, P < 0.001); and there was also a high correlation between brachial artery and left ventricular systolic pressures (r = 0.93, SEE = 4.9 mmHg, P < 0.01). It is concluded that Doppler echocardiography provides a reliable and accurate method for complete non-invasive assessment of left atrial pressure in patients with mitral regurgitation.

Adolescent↗
PubMed1992

The indirect negative inotropic effects of the P1-receptor agonist, L-phenylisopropyladenosine, in guinea-pig isolated cardiac preparations: comparison with cromakalim.

The possible mechanisms of the indirect negative inotropic responses to the P1-receptor agonist, L-phenylisopropyladenosine (L-PIA) were evaluated in electrically paced (2 Hz, 5 ms pulse width, voltage 50% above threshold) left atria and papillary muscles of guinea pigs. The responses were compared in naive tissues (direct effects) or after prestimulation with submaximal concentrations of either cAMP-dependent positive inotropes (isoprenaline or forskolin) or the cAMP-independent inotrope Bay K 8644. Cumulative concentration-response curves were obtained in naive or prestimulated preparations for L-PIA or the potassium channel activator, cromakalim, for comparison. L-PIA and cromakalim exerted negative inotropy in naive atrial tissues, whereas only cromakalim was active in naive papillary muscles. In atria prestimulated with isoprenaline (31 nM) or forskolin (1.4 microM), the negative inotropy of L-PIA was enhanced compared with naive tissues. In contrast, prestimulation with Bay K 8644 (1 microM) exerted a significant functional antagonism of the response to L-PIA. In the case of cromakalim, prestimulation with isoprenaline exerted a functional antagonistic effect. In papillary muscles, an indirect negative inotropic effect of L-PIA was only seen in tissues prestimulated with the cAMP-dependent inotropes isoprenaline (31 nM) or forskolin (2.4 microM), and not in naive tissues or those prestimulated by Bay K 8644 (333 nM). As with atria, prestimulation with isoprenaline exerted a functional antagonistic effect on the response to cromakalim. These results suggest that the P1-receptor agonist, L-PIA, exerts its indirect negative inotropic effects in left atria by two mechanisms.2+ with cAMP-dependent positive inotropes.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Pulmonary venous flow dynamics before and after balloon mitral valvuloplasty as determined by transesophageal Doppler echocardiography.

The pattern of left atrial filling was studied in 14 patients with severe mitral stenosis in sinus rhythm before and immediately after successful balloon mitral valvuloplasty by transesophageal pulsed Doppler echocardiography of the left superior pulmonary vein. Mean mitral valve orifice area increased from 0.8 +/- 0.1 to 2.2 +/- 0.3 cm2 (p less than 0.0001), and left atrial mean pressure decreased from 30 +/- 5 to 12 +/- 4 mm Hg (p less than 0.0001) after the procedure. After balloon mitral valvuloplasty, significant increases in peak systolic pulmonary velocity (35 +/- 16 to 44 +/- 10 cm/s; p less than 0.01), systolic flow velocity time integral (3.3 +/- 1.5 to 5.9 +/- 2.0 cm; p less than 0.001) and the ratio of systolic/diastolic pulmonary venous flow velocity time integrals (0.8 +/- 0.4 to 1.4 +/- 0.5; p less than 0.001) were observed. An acute increase in mitral valve orifice area caused no significant changes in peak diastolic forward flow velocity (40 +/- 7 to 41 +/- 9 cm/s; p = not significant [NS]), diastolic forward flow velocity time integral (4.3 +/- 1.7 to 4.6 +/- 1.8 cm; p = NS) and atrial flow reversal velocity (30 +/- 3 to 35 +/- 3 cm/s; p = NS) compared with at baseline. The results suggest that in patients with severe mitral stenosis and sinus rhythm, left atrial filling is biphasic with a diastolic preponderance, and successful mitral valvuloplasty is associated with an immediate increase in pulmonary venous systolic forward flow.

Adult↗
PubMedDate not supplied

Decreased and abnormal left ventricular filling in acute heart failure: role of pericardial constraint and its mechanism.

Pericardial constraining force is minimal in normal hearts; however, it is considered to be prominent in moderate to severe heart failure. Thus, effects of the pericardium on pulsed Doppler transmitral flow velocity pattern were examined in 17 dogs with acute left ventricular dysfunction. Left ventricular dysfunction with left ventricular end-diastolic pressure > or = 15 mm Hg was produced by injection of microspheres into the left coronary artery. Transmitral flow velocity pattern, left atrial and left ventricular diameters, and high-fidelity left atrial and left ventricular pressures were recorded before and after pericardiectomy. In five of the 17 dogs, mitral regurgitation with giant "v" wave of left atrial pressure occurred with reductions of left ventricular systolic pressure and peak rate of the left ventricular pressure fall (dP/dt) after pericardiectomy. In the other 12 dogs, peak early and late diastolic filling velocities increased with a decrease in left ventricular minimal pressure and increases in left arterial and left ventricular diameters and left atrial and left ventricular compliance after pericardiectomy. In these 12 dogs, left atrial to left ventricular crossover pressure, left ventricular end-diastolic pressure, and references for left ventricular relaxation did not change after pericardiectomy. Thus the release from pericardial constraining force in severe heart failure may increase chamber compliance of the left ventricle and left atrium and, in turn, increase peak early and late diastolic filling velocities through an increment in forward transmitral pressure gradient. Increased pericardial constraining force is a possible cause limiting left ventricular filling and hence cardiac output in heart failure.

Acute Disease↗