[Proceedings: Left atrial function--a study with special emphasis on left atrial volume].
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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.
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.
75 patients with isolated mitral stenosis were studied. Particular attention was paid to the integration of the parametres VTD, FE, mitral area, pulmonary artery pressure and dynamic systolic and diastolic geometry of the left ventricle. The existence of isolated MS with alteration of the left ventricular function not depending on the alterations of the preload and the forms with raised FE, was demonstrated. A classification into 6 groups was made, each characterized by special geometric modalities of contraction and relaxation. A significant compensation of several of the parametres of systolic mecanism (hyperkinesia) and diastolic (SERP) dynamic geometry was observed. It was therefore concluded that a more precise definition of the interaction of ventricular function with left atrial function is necessary.
In patients with hypertrophic cardiomyopathy (HCM) and essential hypertension (HT), left ventricular dysfunction in early diastole which is associated with left atrial contraction plays an important role in left ventricular filling. To evaluate left atrial booster pump function, we analyzed left atrial preload (left atrial pressure at the end of diastasis; LAPd, left atrial volume index at the end of diastasis; LAVd), left atrial afterload (left ventricular end-diastolic pressure; LVEDP, left ventricular chamber stiffness constant; K), and left atrial ejection indices (left atrial ejection fraction during atrial contraction; LAEF, left atrial ejection volume index during atrial contraction; ACVI). The study subjects consisted of control subjects (n = 5), HT patients (n = 6), and HCM patients (n = 11). The left ventricular wall was significantly thicker in the HT and HCM groups. The left ventricular rapid filling volume index was less in the HT group, and significantly less in the HCM than in the control group. LAPd and LAVd were greater in the HT group than in the control group, and greater in the HCM group than in the HT group. LVEDP and K were greater in the HT group than in the control group, and significantly greater in the HCM group than in the other 2 groups. ACVI was greater in the HT group than in the control group, but in the HCM group, ACVI was significantly less than in the HT group and did not differ significantly from that in the control group. LAEF was significantly less in the HCM group than in the other 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac performance was evaluated in 12 infants with isolated total anomalous pulmonary venous return. Four had significant pulmonary venous obstruction and severe pulmonary hypertension (group A). Eight had no obvious venous obstruction, and the pulmonary pressures were lower (group B). In all subjects, right ventricular end-diastolic volume was increased (197% of predicted normal) and its ejection fraction was normal. Left ventricular volume was, generally speaking, still in the normal range (87% of predicted normal); however, its ejection fraction was reduced (0.57 vs normal of 0.73) and left ventricular output was low (3.08 L/min/m2 vs normal of 3.98). Left atrial volume was consistently small (53% of predicted normal) with an appendage of normal size. The infants in group A had smaller chamber volumes/m2 BSA than those in group B. Left atrial function was abnormal, characterized by reduced reservoir function and a greater role as "conduit" from right atrium to left ventricle. Left atrial size was not found to be critical in the surgical repair of TAPVR. Cardiac function is restored to normal following surgery.
Computer analysis of the M-mode echocardiogram in 50 normal newborns provided measurements of wall thicknesses and chamber size and, in addition, assessment of right and left ventricular wall, septal, and cavity dynamics throughout the cardiac cycle. Data obtained with this new technique indicated that (1) right and left ventricular cavity functions are similar in the normal newborn, (2) right and left ventricular cavity filling and emptying vary directly with peak rates of septal and ventricular wall thinning and thickening, respectively, and (3) there is a close time relationship among maximum left atrial dimension, minimum left ventricular dimension, and mitral valve opening. This analysis, which is the first complete analysis of the echocardiogram in the newborn, provides a normal range of septal and ventricular wall dynamics as well as right and left ventricular and left atrial function and has clinical implications in that it may allow early recognition of both congenital and perinatal myocardial disease.
Previous in vitro studies showed that epinephrine stimulation can induce atrial natriuretic factor (ANF) release only form the right atrium but not from the left. In addition, sinus node has been shown to play an important role in the release of ANF. In vitro studies were done in isolated left and right rat atria to determine if pacing can induce the left atria to release ANF during epinephrine stimulation. ANF concentrations in the perfusate were measured by a radioimmunoassay method. Epinephrine increased ANF release in the right atria (from 6.3 +/- 0.8 to 10.8 +/- 0.9 pg/min/mg), but not in the unpaced left atria (4.2 +/- 0.4 and 4.2 +/- 0.3 pg/min/mg). However, when the atria were paced, ANF release rose in both the left (from 6.2 +/- 0.5 to 11.5 +/- 1.4 pg/min/mg) and right (from 8.4 +/- 1.15 to 16.6 +/- 1.8 pg/min/mg) atria with epinephrine addition. These results suggest that atrial contraction and tension play an important role in epinephrine-stimulated ANF release.
Left ventricular function in 53 patients with secundum atrial septal defect was assessed by computer-assisted analysis of the left ventricular echocardiogram and by cardiac catheterization. The patients were divided into two groups, those younger and those older than 60 years, to investigate the effect of aging on left ventricular function. Cavity size was significantly smaller than normal (p less than 0.01) and septal motion was abnormal in 86%, but values for cardiac index, left ventricular end-diastolic pressure, velocity of circumferential fiber shortening, left ventricular filling rate, and duration of rapid filling were normal in both groups. Regional dynamics assessed in terms of peak rates of systolic thickening and diastolic thinning of the septum and posterior wall were also normal in both groups. We concluded that, although left ventricular minor dimensions are small, and septal motion is reversed in the majority of patients with atrial septal defect, left ventricular function is normal, and it does not appear to deteriorate with increased age, pulmonary hypertension, or the presence of right ventricular failure. The abnormal septal motion appears to be compensated for by enhanced septal and posterior wall percentage thickening.
To investigate the left atrial ejection performance in heart failure, we observed both the transmitral (TMF) and pulmonary venous flow waves (PVF) by transesophageal Doppler echocardiography in 20 patients with heart failure (16 males, 4 females, 56 +/- 13 years old). In 7 of 20 patients, pulmonary capillary wedge pressures (PC) were also obtained within 72 hours after the transesophageal Doppler echocardiographic examinations. A reversal flow on PVF during atrial systole (atrial backward ejection flow) was observed in all of the 20 patients. Corrected atrial pre-ejection period correlated significantly with PC (r = -0.76, p < 0.05), indicating that the period was shortened in accordance with left atrial Starling's law. This period correlated significantly with both the duration and the time velocity integral of atrial backward flow (r = -0.72, p < 0.005; r = -0.55, p < 0.05, respectively), but not with the atrial ejection time nor with the time velocity integral of atrial systole. These results suggest that in some cases of heart failure, left atrial contractile function is preserved despite the marked augmentation of left atrial afterload, resulting in a decrease of the left atrial forward ejection and an increase of the left atrial backward ejection. Thus, the observations of TMF and PVF by transesophageal Doppler echocardiography are useful for assessing the left atrial ejection performance in patients with heart failure.
Left ventricular function and volume data from 17 control subjects and 27 young patients with secundum atrial septal defect (ASD) without overt left or right ventricular failure were compared. ASD patients were subdivided in low shunt (Qp/Qs less than 2.0) and high shunt (Qp/Qs larger than or equal to 2.0) groups. Mean left ventricular (LV) stroke volume was significantly less in ASD patients (46 +/- 16 ml/m2 in the low shunt and 44 +/- 9 ml/m2 in high shunt group) compared with control patients (51 +/- 13 ml/m2, P less than 0.01 and P less than 0.02, respectively). There was no significant difference in mean left ventricular end-diastolic volume (LVEDV) between any group of patients (control subjects 67 +/- 17 ml/m2; low shunt ASD 66 +/- 17 Ml/m2, and high shunt ASD 62 +/- 12 ml/m2). High shunt ASD had a significantly lower cardiac index compared with control patients (5.0 liters/min/m2 vs. 5.9 liters/min/m2, P less than 0.02). Both low shunt and high shunt ASD showed significantly lower stroke work indices than control subjects (42 +/- 13 GmM/m2 and 37 +/- 8 GmM/m2 compared with 51 +/- 14 GmM/M2 , P less than 0.05 and P less than 0.001, respectively) but only the high shunt group had a significantly lower peak systolic pressure (94 +/- 12 mm Hg vs. 109 +/- 11 mm Hg for control patients, P less than 0.01). There was no significant difference between the control and ASD groups in LV end-diastolic, mean right atrial, right ventricular end-diastolic, and pulmonary pressures. External systolic time intervals were compared in 5 control and 12 ASD patients. There was no significant difference between the two groups of patients in absolute values or indices for pre-ejection period, ejection time, or electromechanical systole. However, the ratio of the pre-ejection period index to left ventricular ejection time index (PEPI/LVETI) was significantly higher in ASD patients (P less than 0.05). In young subjects with large shunt ASD, certain indicators of left ventricular function are depressed. Evaluation of PEPI/LVETI may allow noninvasive determination of LV function.
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.
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.
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.
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.
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.
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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.