Loss Of Atrial Contraction Research Articles

Is the automatic atrial defibrillator a promising approach?

Atrial fibrillation is a common arrhythmia, accounting for more consumption of medical resources than any other arrhythmia. The impact of the disease results from the combination of a loss of atrial contraction, and atrial control over cardiac rate. Studies in animals demonstrated the basic feasibility of atrial defibrillation using electrodes passed intravenously. Subsequent studies in patients confirmed that low-energy shocks were effective in converting atrial fibrillation and were safe if delivered synchronous to the R wave in the absence of a short preceding RR interval. Preliminary experience suggests that a small implanted device might provide beneficial therapy for patients with recurring episodes of persistent, drug-refractory, atrial fibrillation.

Atrial contribution to ventricular filling in mitral stenosis.

The importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both. We studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean +/- SD atrial contribution to left ventricular filling volume was 18 +/- 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 +/- 0.7 cm2) and severe mitral stenosis (MVA, 0.9 +/- 0.2 cm2) had atrial contributions of 29 +/- 4% and 9 +/- 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase. The atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect of increasing heart rate as the cause of decompensation during atrial fibrillation.

Importance of the “atrial kick” in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 ± 0.9 vs 5.2 ± 0.8 liters/min at 110 beats/min, 4.2 ± 0.9 vs 5.1 ± 0.9 liters/min at 140 beats/min; p < 0.05) and LV end-diastolic volume (77 ± 27 vs 93 ± 29 ml at 110 beats/min, 54 ± 17 vs 65 ± 19 ml at 140 beats/min; p < 0.05), an increase in left atrial pressure (28 ± 3 vs 20 ± 5 mm Hg at 110 beats/min, 30 ± 4 vs 25 ± 5 mm Hg at 140 beats/min; p < 0.05), and a decrease in mitral valve area (1.2 ± 0.4 vs 1.4 ± 0.5 cm 2 at 110 beats/min, 1.2 ± 0.4 vs 1.4 ± 0.4 cm 2 at 140 beats/min; p < 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.

Beneficial effects of atrioventricular sequential pacing on cardiac output and left ventricular filling assessed with pulsed doppler echocardiography.

There has been increased interest in the beneficial effects of atrio-ventricular (AV) pacing over ventricular (V) pacing. This study attempted to evaluate the changes in cardiac output and left ventricular filling dynamics when the pacing mode was switched from V pacing to AV pacing. Study population consisted of 26 patients with multiprogrammable AV pacemakers. Cardiac output was determined as a product of echocardiographically determined cross sectional area of the aortic annulus and Doppler-determined velocity integral of left ventricular outflow over systole. Left ventricular peak rapid filling rate (PFR) and peak atrial filling velocity to peak rapid filling velocity ratio (A/R) were determined from measurements at the mitral annulus. Cardiac output showed a significant improvement when the pacing mode was switched from V to AV pacing, and the percent change ranged from 3 to 73% (average 26%). The improvement in cardiac output brought about by AV synchrony was greater in patients with smaller PFR (r = -0.71, p less than 0.01) and larger A/R ratio (r = 0.77, p less than 0.01). On the other hand, PFR was greater with V pacing than with AV pacing. Greater increment of the PFR was produced by the loss of atrial contraction in patients with smaller PFR (r = -0.82, p less than 0.01) and larger A/R ratio (r = 0.76, p less than 0.01). Thus, AV pacing provides a great improvement in left ventricular filling, i.e., cardiac output, which cannot be obtained with V pacing even with the compensatory enhancement of left ventricular rapid filling. These beneficial effects of AV pacing seemed to be greater in patients with impaired left ventricular rapid filling.

The effects of glycerol treatment on the isolated rat heart.

Isolated rat hearts were perfused with a balanced electrolyte solution containing 1000mM glycerol for 15min and then perfused with normal electrolyte solution for up to 32 min. The perfusion with hypertonic glycerol solution and subsequent washout is termed “glycerol treatment”. Initially, glycerol removal causes swelling and rupture of the T-system in ventricular myocardial cells which correlates temporally with a period of cardiac arrest. Contractility returns during further glycerol removal and concomitant recovery of the T-system is observed. Atomic absorption spectometry and neutron activation analysis were used to measure ventricular sodium, potassium and calcium ion content. There is no apparent correlation between changes in ion content and cardiac arrest or recovery. The water movements were calculated from wet weight, dry weight and inulin space, and confirmed by morphometric analysis of extracellular and intracellular space. It is suggested that the swelling and rupture of the T-system is due to the rapid water movements that were observed during the onset of glycerol removal. Ultrastructural analysis of glycerol-treated atrium from the same hearts shows damage of mitochondria and of the L-system and intracellular edema. The structural changes are correlated with a loss of atrial contraction. As in ventricular myocardium, resumption of contraction is associated with an almost complete recovery from ultrastructural damage.

The contribution of atrial contraction to right heart function before and after right ventriculotomy: Experimental and clinical observations

Effective atrial contraction was abolished by simultaneous atrial and ventricular (A-V) pacing in an acute canine preparation. At constant cardiac output, aortic pressure, and heart rate, only a small rise (1.4 mm. Hg) in mean right atrial pressure was observed before vertical right ventriculotomy, but a larger rise (9.5 mm Hg) occurred after ventriculotomy (p less than 0.01). Right heart failure with tricuspid regurgitation was induced after ventriculotomy by volume overload and A-V pacing. Restoration of atrial contraction (sequential A-V pacing) eliminated regurgitation and lowered average mean right atrial pressure from 22 to 4 mm. Hg (p less than 0.001). After right ventriculotomy, loss of atrial contraction at a constant right atrial pressure resulted in a 42 per cent reduction in cardiac output. In 8 patients who had had right ventriculotomies, abolition of effective atrial contraction by A-V pacing caused an average reduction in cardiac output of 22 per cent, whereas cardiac output fell only 5 per cent in 5 control patients (p less than 0.01).

The hemodynamic response to the i.v. administration of Cedilanid in patients with rheumatic heart disease.

Pulmonary venous flow (PVF) pattern can be easily recorded by using transesophageal Doppler echocardiography. Recent reports suggest that the analysis of PVF pattern could be useful to better understand the role of atrial contraction on left ventricular filling. In order to evaluate the effect of loss of atrial contraction, we studied 50 consecutive patients with atrial fibrillation. We then compared the PVF pattern of atrial fibrillation with the normal pattern obtained from 20 healthy subjects. The reversal flow (A wave) resulting from atrial contraction was lost in patients with atrial fibrillation. The systolic flow was composed by 1 wave in almost all the patients and the peak velocity was reduced compared to normal sinus rhythm. On the contrary, the diastolic flow was increased comparing to normal subjects. In atrial fibrillation the flow shifted from systolic to diastolic filling. The restore of sinus rhythm induced a normalization of PVF pattern.