[Method of evaluation of the right atrial function following complete right atrial bypass in tricuspid valve stenosis--ejection fraction of the right atrium].
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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.
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.
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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.
Sinus node recovery times and the premature atrial stimulus test were studied in 36 patients, seven with gross sinus node disease, 25 with possible sinus node disease and four with no clinical evidence of sinus node disease. The corrected sinus node recovery time proved of most value in predicting which patients needed and would benefit from permanent pacemaker implantation, though there was one false negative diagnosis and two patients with abnormal corrected sinus node recovery times were asymptomatic. The premature atrial stimulus test usually proved to be of no practical value once severe sinus node disease was present and, in the group of patients with suspected sino-atrial disease, only 13 of 25 graphs could be analysed due to gross "scatter" in the others. When patients with symptoms have unequivocal evidence of sino-atrial dysfunction, invasive study seems unnecessary. With lesser degrees of sino-atrial disease, premature atrial stimulation may provide confirmatory evidence; but when sinus arrhythmia, atrial escape beats, or more marked dysfunction are present, one is likely to encounter useless "scatter" graphs. In the absence of regular sinus rhythm on the ECG, overdrive sinus node suppression in the only invasive study worth attempting.
The native atria remains intact after total artificial heart (TAH) implantation. The electrical activity of the recipient's atria can be recorded from wires placed during TAH implantation. Regulating TAH heart rate by coupling it with native atrial activity has the potential for a more physiologically responsive TAH. The reactivity of the atrial impulse rate is a critical component of this link, but little is known about atrial responsiveness after TAH placement. Two human and three animal TAH recipients had recordable atrial electrical activity. Human atrial impulse rate after TAH was relatively constant at rest but unresponsive to physiologic stimuli. Analysis of human atrial contraction provided no discernable effect on ventricular filling. Animal atrial impulse rate at rest was more rapid than calves without a TAH. The bovine TAH recipients had an atrial impulse rate that responded to catecholamine stimulation and blockade. Isoproterenol caused a significant rise in atrial impulse rate (152 +/- 16 impulses per minute to 216 +/- 24 impulses per minute; p < 0.05) and propranolol caused a decrease in atrial impulse rate (142 +/- 20 impulses per minute to 122 +/- 19 impulses per minute; p > 0.05). Despite beta blockade, the atrial impulse rate remained abnormally elevated secondary to unknown factors. Animal atrial contraction did appear to intermittently augment TAH ventricular filling. These data indicate that the atria remains electrically intact after TAH implantation. The human atrial impulse rate was unresponsive to physiologic stimuli although the animal atrial impulse rate was affected by exogenous catecholamine administration, but the rate remained abnormally rapid.(ABSTRACT TRUNCATED AT 250 WORDS)
The total immediate sino-atrial conduction time (SACT) as calculated by constant relative pacing, 40 or 50% of the immediate sinus cycle (SC), normally varies inversely with the SC. 50 patients were investigated by this method. In 38 patients without sino-atrial block (SAB) on the surface ECG, it was found that the mean slope of correlation between SACT and SC varied with the shape of the curve of Strauss and with the presence or absence of a post-pacing depression. The smallest slope was found in the group in which the curve of Strauss was horizontal in zone II, and in which there was no depression. In the groups with a rising zone II, comparative use of pacing with a fixed relationship in milliseconds suggested a phenomenon of decreasing retrograde conduction. In cases with sinus arrhythmia and a Strauss curve with scattered coordinates, the relationship between SACT and SC was maintained. 1st degree right-sided SAB should therefore be defined as a function of the immediate SC. In 12 other patients with SAB on the surface ECG, the immediate SACT was greatly lengthened so as to be immeasurable, and bore no relationship to the SC.
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A 18-year-old female with unusual type of parchment-like right ventricle died of intractable congestive heart failure was reported. A catheter study revealed the absence of systolic contraction of the right ventricle. The pressure tracing curve in the right ventricle was virtually the same as in the right atrium. At autopsy, there was an extensive myocardial fibrosis of the left ventricle in addition to the almost total absence of the myocardium of the right ventricle. The case was considered to be a unique type of idiopathic cardiomyopathy.
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Atrial and ventricular pacemaker function was studied in 20 patients with idiopathic chronic complete heart block using the rate response to an intravenous bolus dose of isoprenaline (5 mug/70 kg bodyweight). Pacemaker responses were compared with those of 16 normal control subjects. None of the patients was having syncopal attacks at the time of admission and they were therefore selected in that none required immediate pacing. Ten of the patients had His bundle electrograms; all were shown to have a pre-His type of atrioventricular block. Two major groups emerge from the responses to isoprenaline. (a) High risk group: 11 of the 14 patients with reduced ventricular pacemaker responses had frequent syncopal attacks; 8 of the patients with Adams-Stokes syncope had a bundle-branch block pattern, while 3 had a narrow QRS. These patients require pacing. (b) Low risk group: a low risk asymptomatic group (5 patients) was identified with atrial and ventricular responses to isoprenaline within normal range. One of these patients had a bundle-branch block pattern, while 4 had a narrow QRS. These patients might be managed without pacing. The atrial response to isoprenaline was reduced in 12 of the 20 cases, 10 of whom also had reduced ventricular responses. All 9 patients with bundle-branch block had reduced ventricular responses, while 7 had reduced atrial responses. This evidence indicates that cardiac conducting tissue pathophysiology is widespread in complete heart bolck. The present work suggests that consideration of the ventricular pacemaker function is important in assessing liability to syncope in complete heart block. While patients with Adams-Stokes attacks require pacing it is suggested that all asymptomatic patients with complete heart block and those with minor symptoms are assessed using studies of both ventricular pacemaker function and site. A low risk group not requiring a pacemaker may emerge after sufficient follow-up assessment.
The effect of pericardial constraint on atrial systolic function was investigated in nine acutely instrumented anesthetized dogs. Left and right atrial pressures were recorded by high-fidelity catheters; auricular diameters and free wall segment lengths were measured by sonomicrometry. Atrial function curves were constructed by relating atrial systolic dimensional shortening to atrial end-diastolic pressure during progressive volume loading. With the pericardium closed, the function curves were shifted markedly downward and rightward, such that atrial systolic shortening was reduced at any given pressure. There was a concomitant leftward and upward shift of the atrial end-diastolic pressure-dimension relationship. The relationship between atrial systolic shortening and atrial end-diastolic dimension was not shifted. These results suggest that the apparent depression of atrial systolic function with the pericardium closed is due to a restrictive effect of the pericardium on atrial filling. In conclusion, in the acutely dilated heart, the pericardium restricts atrial filling and thus causes a reduction in atrial systolic contribution to ventricular filling.
OBJECTIVE: To measure exercise duration (which frequently is diminished by atrial fibrillation) and to compare the gain in exercise duration achieved by heart rate control with the gain after cardioversion. METHODS AND RESULTS: Eighteen patients (10 with structural heart condition and eight with lone atrial fibrillation) did the treadmill exercise stress test using the Bruce protocol. Resting supine heart rate was lowered below 100 beats/min by verapamil (initial exercise stress test). An exercise stress test was then repeated as often as needed to achieve 'heart rate control' (less than 130 beats/min at the end of a 3 min walk at 10 degrees elevation and 2.74 km/h speed). This heart rate control was obtained by gradual increases in verapamil dose. Subsequently, the patients were converted to normal sinus rhythm chemically (seven patients) or electrically (11 patients) and an exercise stress test was repeated. At cardioversion, patients were on antiarrhythmic therapy and verapamil was discontinued in most. All patients had left atrial size measured by echocardiogram before and after cardioversion, and all were followed for four months. Upon achieving controlled heart rate, exercise duration increased in 16 patients (average gain was 164 s). After cardioversion to normal sinus rhythm, exercise duration further increased in 13 cases with an average additional gain of 90 s. The total increase in exercise duration after cardioversion was 254 s. Post cardioversion, all patients with lone atrial fibrillation improved. A decline in exercise performance occurred in four patients with fixed cardiac output. Average gain in exercise duration was independent of drugs used. Left atrial size remained increased post cardioversion (50.4 mm before and 52 mm after). During four months of follow-up, only eight patients could continue on the same medication given for cardioversion. Three patients did not maintain normal sinus rhythm. CONCLUSIONS: Conversion to normal sinus rhythm in patients with atrial fibrillation is associated with improved exercise tolerance except in cases with fixed cardiac output. Restoration of mechanical atrial function appears to be responsible for improved exercise performance following cardioversion.
Atrial stretch causes the release of atriopeptin (AP, ANF) from preformed vesicular storage sites. The circulating hormone acts on unique receptor sites (containing guanylate cyclase) to release guanosine 3',5'-cyclic monophosphate (cGMP) that mediates the natriuresis and vasodilation and probably the suppression of renin, aldosterone, and vasopressin. The biological effects of atriopeptin are transient because of the rapid inactivation of the circulating hormone (by neutral endopeptidase or clearance receptors) or the second messenger (by cGMP-phosphodiesterase). Heart failure due to chronic cardiac volume overload [aortovenocaval (A-V) fistula] exhibits markedly elevated circulating AP blood levels and urinary cGMP levels, accompanied by induction of ventricular AP gene and protein expression and release. Pharmacological manipulation of endogenous AP, either by inhibiting cGMP phosphodiesterase (i.e., mediator prolongation) or neutral endopeptidase (i.e., prolongation of hormone half-life) in A-V fistula animals results in profound natriuresis and diuresis without hypotension. These pharmacological maneuvers bypass the suppressed renal response to exogenous AP seen in heart failure and provide a rational therapeutic strategy based on our understanding of the underlying physiological and pathological mechanisms.
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.
Excursions of the left-atrial myocardium were recorded by tensiometric transducers in patients with mitral valvular disease. The structural features of myocardial excursions were evaluated as symptoms. Myocardial shortening in P-Q interval was considered a negative symptom in relation to heart weakness, shortening in T-Q interval as an indefinite symptom, and shortening in Q-T interval as a positive symptom. Appraisal of the sensitivity and specificity of these symptoms revealed their high diagnostic efficacy.
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.