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The effects of cardioplegic arrest on right atrial function.

Atrial electrical and mechanical activity persists during cardioplegic arrest. It has been postulated that atrial ischemia may occur and cause deterioration in atrial function. This study was designed to assess the effect of cardioplegic arrest on right atrial function. Twenty-one pigs were placed on cardiopulmonary bypass (CPB), and the right atrium was isolated from the circulation by snaring both venae cavae and incising the coronary sinus. The tricuspid valve was closed through a small right ventriculotomy, and baseline atrial function was assessed using a compliant balloon in the atrium. Fourteen pigs underwent one hour of cardioplegic arrest (7 with cardioplegia alone [CCA group] and 7 with the addition of topical hypothermia [CCA + TH group]) followed by one hour of normothermic reperfusion. Seven other pigs were placed on CPB for the same period of time (CPB group). Atrial electrical and mechanical activity persisted at 45 beats per minute in the CCA group but was virtually abolished in the CCA + TH group. Cardioplegic arrest caused considerable deterioration in right atrial function (developed pressure, 18.9 +/- 0.8 [baseline] versus 14.1 +/- 0.7 mm Hg; p less than 0.05; first derivative of atrial pressure [dP/dt], 187 +/- 19 versus 134 +/- 25 mm Hg per second; p less than 0.05; 60 minutes of reperfusion and balloon volume of 20 ml). It was not affected by topical cooling. Right atrial developed pressure was maintained, but dP/dt was significantly reduced in the CPB group. This study suggests that cardioplegic arrest does not protect the atrium.

Animals

[Effects of oxyfedrine on sino-atrial function and on conduction in patients with sinus node and/or atrial dysrhythmias (author's transl)].

The electrophysiological effects of Oxyfedrine on sino-atrial function and on A-V junctional and subjunctional conduction have been studied in 16 patients with sinus node and/or atrial dysrhythmias. The following effects have been observed: --a positive chronotropic effect on the sinus node; --an essentially indirect (rate-dependent) shortening of the Functional and Effective Refractory Periods (FRP and ERP) of the atria without variation of the Intra-Atrial Conduction Time (HRA-LRA). There was no significant shortening of the Maximal Atrial Latency (max AL), of the Corrected Sinus Node Recovery Time (CSNRT) and of the Sino-Atrial Conduction Time (SACT). The limits of Zones I, II, III of the sinus node response to atrial extra-stimuli were reduced with no significant change in their duration, expressed as percentage of the Sinus Cycle Length (SCL); --an improvement in the A-V junctional conduction (shortening of the A-H interval for comparable cycle lengths) due to a relatively shortened A-V junctional ERP. The use of the drug in patients with sinus bradycardia and/or atrial dysrhythmias and conduction disturbances, is proposed.

Adult

[Evaluation of left atrial function by 99mTc gated blood pool scan].

99mTc gated blood pool scans were studied to assess the left atrial function. Relationship between filling time and rapid emptying time was y = 0.695 x + 109 (r = 0.761, p less than 0.05, n = 14) in LAO and LPO projections. On the other hand, relationship between slow filling and rapid emptying time was good closely (y = 0.846 x + 16.9 (p less than 0.01, r = 0.975, n = 8] in standard and retrograde acquisition. To assess the left atrial function by standard acquisition in LAO projection should be available for clinical use.

Aged

Assessment of left atrial function in patients with hypertensive heart disease.

Left atrial function in patients with hypertensive heart disease was compared with that in control subjects. In patients with hypertensive heart disease, the time constant of left ventricular relaxation was significantly greater than that in controls (54 +/- 18 vs 31 +/- 16 msec; p less than 0.01). The ratio of left ventricular filling volume before atrial contraction (left atrial reservoir volume/left atrial emptying volume before atrial contraction, and conduit volume/flow volume from the pulmonary vein into the left ventricle) to left ventricular stroke volume was significantly smaller than that in controls (65 +/- 13 vs 76 +/- 7%; p less than 0.05). In patients with hypertensive heart disease, the ratio of reservoir volume to stroke volume was not significantly different from that in controls, while the ratio of conduit volume to stroke volume was significantly smaller than that in controls (43 +/- 13 vs 57 +/- 9%; p less than 0.05). The latter ratio was inversely correlated with the time constant of left ventricular relaxation (r = -0.05, p less than 0.05). In patients with hypertensive heart disease, the ratio of left ventricular filling volume during atrial contraction to stroke volume was significantly larger than that in controls (35 +/- 13 vs 24 +/- 7%; p less than 0.05). The ratio of left ventricular filling volume during atrial contraction to stroke volume had a significant inverse correlation with the ratio of conduit volume to stroke volume (r = -0.84, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

[Modifications in left atrial function in response to changes in left ventricular filling].

In order to investigate the effects of increasing degrees of left ventricular filling impairment on left atrial function, in 9 A-fillers (E/A ratio less than 1, E wave deceleration time greater than 170 ms) and 9 E-fillers (E/A ratio greater than 1, E wave deceleration time less than 150 ms) we constructed the left ventricular and the left atrial volume curves according to a previously validated Doppler 2-dimensional echo method which combines mitral and pulmonary venous flow. Eight normals served as control. The left atrial reservoir (defined as maximum-minimum atrial volume), pump (defined by the volume of blood that enters the left ventricle with the atrial contraction) and conduit functions (defined as left ventricular filling volume--the reservoir and the pump volume) expressed as % of the left ventricular filling volumes, varied significantly between normals (37 +/- 9%, 25 +/- 3%, 37 +/- 11%), A-fillers (48 +/- 9% p less than 0.05, 39 +/- 5% p less than 0.05, 14 +/- 10% p less than 0.001) and E-fillers (27 +/- 6% p less than 0.05, 19 +/- 7% p less than 0.05, 54 +/- 10% p less than 0.01). Also maximum left ventricular and left atrial volumes differed significantly (normals 165 +/- 31 ml, 76 +/- 20 ml; A-fillers 174 +/- 33 ml, 100 +/- 20 ml p less than 0.05; E-fillers 322 +/- 34 ml p less than 0.001, 136 +/- 41 ml p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris

Is atrial function affected by conventional cardioplegic arrest?

Conventional cardioplegic arrest results in persistent atrial electrical and mechanical activity. This activity has been postulated to result in atrial ischemia which can induce postoperative arrhythmias and impair the transport function of the atrium. In this study, the effects of simple cardiopulmonary bypass (CPB) (seven pigs) and conventional cardioplegic arrest (CCA) (seven pigs) on right atrial function were evaluated. Function was assessed in an isolated right atrial preparation with a compliant balloon inserted via the superior vena cava. CCA for 1 hr produced significant deterioration in right atrial function (developed pressure 14.1 +/- 0.7 vs 18.9 +/- 0.8 mm Hg, P less than 0.05, diastolic pressure 10.0 +/- 1 vs 4.5 +/- 1.4 mm Hg, P less than 0.05, dP/dt 134 +/- 25 vs 187 +/- 19 mm Hg/sec, P less than 0.05 at a balloon volume of 20 ml after 1 hr of reperfusion). CPB alone caused no alteration in pressures in the right atrium but was associated with a late decrease in dP/dt (developed pressure 19.3 +/- 1.8 vs 18.9 +/- 0.8 mm Hg, diastolic pressure 4.0 +/- 1.2 vs 4.5 +/- 1.4 mm Hg, dP/dt 148 +/- 18 vs 187 +/- 19, P less than 0.05 at a balloon volume of 20 ml at a time corresponding to 1 hr of reperfusion in the CCA group). These results are consistent with the postulate that conventional techniques of cardioplegic arrest are associated with ischemic dysfunction of the right atrium.

Animals

[Evaluation of sino-atrial function using the method of extrasystole induced by constant-relative premature impulses. 1. Method and normal results].

Atrial pacemaking under conditions of relative constancy (40 or 50% of the preceding cycle) enables us to calculate the immediate sino-atrial conduction time (retrograde and antegrade) (SACT). 17 patients were chosen for their normal sino-atrial function under spontaneous changes of the sinus cycle (SC). In each case, a significant inverse linear relationship was found between SACT and the corresponding SC. The mean correlation slope was -0.36 in 10 patients with no post-pacing depression (PPD). The slope was greater in 7 patients with a PPD (-0.89); if this depression is taken into account when the SACT is calculated, the slope decreases. In 5 patients, atropine (1 mg I.V. reduced the mean value of SC, and shortened (constant relative value) the SACT. The mechanisms for the spontaneous and induced variations in the sinus output are discussed; it may be that there are substitute pacemakers within the cells of the sino-artrial node, which are affected by variations in sympathetic or parasympathetic activity or by pacing. In clinical practice, automatism and conduction with the sinus node should be interpreted as inter-related functions, both under normal conditions and after vagal block.

Adult

Recovery of isolated rat atrial function related to ATP under different anoxic conditions.

Spontaneously beating isolated rat atria were subjected to 1 h of anoxia at 37 degrees C in various cardioplegic solutions. Contraction continued for different times upon initiation of anoxia, depending on the nature of the cardioplegic solution. Two hundred micromolar P1,P5-di(adenosine-5')pentaphosphate (Ap5A) stopped atrial function in less than 30 s of anoxia in contrast to 50 s in the case of Hearse's cardioplegic solution (16 mM MgCl2, 16 mM KCl, 1 mM Procaine), and 20 min in the case of controls. The stopping time was also prolonged from 30 to approximately 50-55 seconds if a lower concentration of Ap5A (100 microM) was used. Function, adenine nucleotides (AN), and phosphocreatine (PCr) were then measured 20 min after reoxygenation. The recovery of both function and AN was most rapid and complete with 200 microM Ap5A (97% recovery in ATP and 100% in function) and least complete in control (50% recovery in ATP and 78% in function). A positive correlation between recovery of ATP, or total adenine nucleotides, and recovery of function was observed in all cases. The higher the level of ATP remaining at the end of 1 h of anoxia and the more recovered after 20 min of reoxygenation, the more complete the recovery of function. The PCr returned to normal or even higher than normal values in all cases, even though function returned only in proportion to ATP. Since PCr is mitochondrial in origin, it appears that loss of a portion of the AN localized at the energy-utilizing sites occurred before serious mitochondrial damage and was responsible for the incomplete postanoxic functional recovery.

Adenine Nucleotides

Left atrial function in acute transient left ventricular ischemia produced during percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery.

Left atrial (LA) function was studied in 32 patients during percutaneous transluminal coronary angioplasty of the proximal left anterior descending artery with a dual micromanometer positioned transseptally in the left atrium and in the left ventricle. In 10 patients LA and left ventricular (LV) cineangiography was performed 30 minutes before percutaneous transluminal coronary angioplasty and 30 seconds after the occlusion of the left anterior descending coronary artery. Thirty seconds after left anterior descending occlusion, LV peak systolic pressure decreased from 135 +/- 12 to 106 +/- 9 mm Hg (p less than 0.05) and LV maximum dP/dt decreased from 1,634 +/- 136 to 1,137 +/- 127 mm Hg/s (p less than 0.01). Simultaneously, LA mean pressure increased from 11 +/- 2 to 29 +/- 1 mm Hg (p 177 +/- 13 to 381 +/- 21 mm Hg (p less than 0.001). There was a difference between LV end-diastolic pressure and LA mean pressure of 1.5 mm Hg at rest and 7.8 mm Hg during ischemia and LA pulse pressure increased from 16 +/- 3 to 26 +/- 3 mm Hg (p less than 0.05) together with increase of LA A and V waves peak pressure. LV stroke volume index decreased from 46 +/- 5 to 43 +/- 3 ml/m2 (difference not significant). The LA maximal volume increased from 18 +/- 2 to 29 +/- 3 ml/m2 (p less than 0.001). LA volume before LA contraction increased from 29 +/- 2 to 54 +/- 3 ml/m2 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Left atrial function in ischemic heart disease assessed by intravenous digital subtraction angiography.

To investigate changes in left atrial morphology and dimensions during the cardiac cycle, the atrium was visualized by intravenous digital subtraction angiography (DSA). The study subjects consisted of 22 male patients whose average age was 54.5 +/- 8.6 years. They had ischemic heart disease without mitral valve disease and were in sinus rhythm. They were 11 patients with old myocardial infarction (OMI group) and 11 who had chest pain without evidence of infarction (AP group). DSA was performed in the continuous mode. Contrast material (35 ml) was injected at a rate of 18 ml/sec via a catheter in the superior vena cava and subtraction images were obtained at a speed of 30 frames/sec in the right anterior oblique projection. The left atrial and left ventricular margins were traced manually, their areas were calculated, and fractional changes in area were analyzed. The left ventricular ejection fraction (LVEF) was calculated by densitometry. Cardiac catheterization was performed in 16 patients and the left ventricular end-diastolic pressure (LVEDP) and mean pulmonary arterial wedge pressure (PAWP) were measured. The entire left atrium was clearly imaged using DSA. Phase analysis of the time-area curves in the right anterior oblique projection revealed that the left atrial area was maximal during left ventricular end-systole (%LA1 = 100%), it decreased during early left ventricular diastole (%LA2), and then increased slightly again during mid-diastole (%LA3). After left atrial contraction, the minimum area was obtained (%LA4). The left atrium showed a two-stage decrease in the area due to passive emptying and active contraction during left ventricular diastole. Passive emptying (%LA1-%LA2) was significantly less in the OMI group than in the AP group (6.3 +/- 3.6 vs 13.3 +/- 4.8%, p < 0.01, respectively). In all 22 subjects, passive emptying correlated with LVEF (r = 0.70, p < 0.001) and LVEDP (r = -0.58, p < 0.05). There was no difference in active contraction (%LA3-%LA4) between the 2 groups (26.0 +/- 5.7% in the OMI group, 28.2 +/- 8.4% in the AP group), and it did not correlate with LVEF or LVEDP. The ratio of passive emptying to active contraction [(%LA1-%LA2)/(%LA3-%LA4)] correlated with LVEF (r = 0.63, p < 0.01). These findings suggested that impaired left ventricular diastolic function and a relative increase in atrial contraction were present in patients with a lower LVEF. The %LA4 correlated with LVEDP and PAWP (r = 0.65, r = 0.63, p < 0.01, respectively). In conclusion, DSA proved to be a useful method for investigating left atrial morphology and function.

Aged