Left ventricular and left atrial function in patients with borderline and established hypertension.
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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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In normoalbuminuric patients with insulin-dependent diabetes mellitus, plasma atrial natriuretic factor (ANF), cyclic GMP and active renin and the renal clearances of [99Tcm]-diethylenetriaminepentaacetic acid (DTPA) lithium and sodium were studied on a hyperglycaemia day and a euglycaemia day. Baseline euglycaemia was achieved by an overnight variable insulin infusion, which during study days was fixed at the rate necessary to maintain euglycaemia in the morning. After a baseline euglycaemic clearance period of 90 min, measurements were repeated in a new 90-min period beginning 150 min later. On the hyperglycaemia day i.v. infusion of 20% glucose was started at the end of the euglycaemic baseline period, increasing blood glucose (5.3 +/- 1.3 vs 12.1 +/- 1.2 mmol l-1, p less than 0.01). On the euglycaemia day blood glucose declined (5.1 +/- 1.0 vs 4.2 +/- 1.0 mmol l-1, p less than 0.02). Glomerular filtration rate (GFR) was unchanged by acute hyperglycaemia (127 +/- 16 vs 129 +/- 24 ml min-1, NS), but nearly normalized during maintained euglycaemia on the euglycaemia day (124 +/- 17 vs 105 +/- 16 ml min-1, p less than 0.01). When comparing the hyperglycaemic study period with the similarly timed period on the euglycaemia day, GFR was elevated by hyperglycaemia (129 +/- 24 vs 105 +/- 16 ml min-1, p less than 0.01), while the renal clearances of lithium and sodium were similar. Consequently, the calculated absolute proximal reabsorption rate of sodium and water was elevated during hyperglycaemia. Hyperglycaemia reduced the slight decline in plasma concentrations of ANF and cyclic GMP observed on the euglycaemia day. Active renin, glucagon and plasma osmolality were unchanged. In conclusion, marked changes in glomerular filtration rate are induced by changes in blood glucose concentration, but the effect is delayed and thus not directly related to renal tubular transport of glucose. Hyperglycaemia does not affect renal clearances of lithium and sodium, while proximal tubular reabsorption is markedly stimulated. These changes are not related to changes in ANF, renin, glucagon or plasma osmolality.
The effects of synthetic human atrial natriuretic peptide (ANP) on the release of catecholamines, aldosterone, or cortisol were observed in human adrenal tumors obtained surgically from patients with pheochromocytoma, primary aldosteronism, or Cushing's syndrome, respectively. Each tumor tissue or adjacent normal cortical tissue was sectioned into slices, which were incubated in medium-199 in the presence or absence of adrenocorticotrophin (ACTH) and ANP. The amounts of epinephrine, norepinephrine, aldosterone, or cortisol released into the medium were measured. Existence of ANP receptors on the adrenal tissues was examined by binding assays, affinity labeling, and immunohistochemistry. Release of catecholamines from pheochromocytoma tissues was inhibited by ANP, and the presence of the ANP receptor on pheochromocytoma was further demonstrated by both binding assays and affinity labeling; Scatchard analysis revealed a single class of binding sites for ANP with a Kd of 1.0 nM and a Bmax of 0.4 pmol/mg of protein and the molecular size was estimated as 140 and a 70 kDa under nonreducing and reducing conditions, respectively. The presence of ANP receptors in pheochromocytoma was demonstrated by immunohistochemistry. ANP inhibited both basal and ACTH-stimulated aldosterone secretion in the slices of normal cortex, and localization of ANP receptors in zona glomerulosa cells was also demonstrated. However, ANP did not inhibit basal and ACTH-stimulated aldosterone and cortisol secretion in both tissue slices from aldosteronoma and Cushing's adenoma. Consistent with these observations, the absence of ANP receptors in adenoma tissues was determined by binding assays, affinity labeling, and immunohistochemistry.(ABSTRACT TRUNCATED AT 250 WORDS)
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OBJECTIVES: We sought to evaluate the effect of clinical factors on recovery of atrial function after cardioversion for atrial fibrillation. BACKGROUND: Lack of effective mechanical atrial function (EMAF) after cardioversion of atrial fibrillation predisposes to thromboembolic complications and delays improvement in functional capacity. METHODS: Fifty-two patients underwent cardioversion (group I, electrical cardioversion, n = 40; group II, pharmacologic or spontaneous cardioversion, n = 12) for atrial fibrillation. Serial transmitral inflow Doppler variables were recorded after cardioversion until EMAF (atrial filling velocity > 0.50 m/s) was seen. Clinical variables (age, duration of atrial fibrillation, left ventricular ejection fraction, left atrial diameter, underlying cardiovascular disease, antiarrhythmic drug therapy and mode of cardioversion) were tested for an association with the outcomes of recovery of atrial function by day 3 and day 7. RESULTS: Effective mechanical atrial function recovered in 68% of patients by day 3 and in 76% by day 7 after cardioversion. The mode of cardioversion was significantly associated with recovery of atrial function by day 3 in bivariate and multivariate analyses (odds ratio 0.12, 95% confidence interval 0.01 to 1.0, for electrical cardioversion). None of the variables had an association with recovery of atrial function by day 7. Group I patients took a longer time to recover atrial function than group II patients (p = 0.012). In addition, group I patients had a significantly lower peak atrial filling velocity (mean [+/-SD] 0.39 +/- 0.19 m/s vs. 0.56 +/- 0.16 m/s) and a higher early filling to atrial filling velocity ratio (2.5 +/- 1.2 vs. 1.5 +/- 0.5) after cardioversion. CONCLUSIONS: A high proportion of patients recover EMAF within 1 week after cardioversion. Patients who undergo electrical cardioversion display a greater degree and a longer duration of mechanical atrial dysfunction than those who convert pharmacologically or spontaneously.
Although several flow patterns in the left atrial appendage have been described, mechanical determinants of its function have not been elucidated in human beings. We attempted to investigate changes in left atrial appendage function after cardioversion of atrial fibrillation and examine the potential relation between appendage function and left atrial mechanical function. Twenty patients without mitral valvular disease underwent transesophageal and transthoracic echocardiography at 24 hours and 1 week after cardioversion of atrial fibrillation. Left atrial appendage function was assessed by the pulsed Doppler measurements of left atrial appendage emptying and filling velocities corresponding to early and late ventricular diastole, respectively. Left atrial mechanical function was evaluated by the transmitral A-wave velocity, percent atrial contribution of the total left ventricular filling (percent atrial filling), and the pulmonary venous A-wave velocity. Left ventricular function was also estimated with conventional M-mode echocardiography. The late appendage emptying and filling velocities markedly increased during 1 week after cardioversion (p < 0.0001, respectively). This finding was associated with an increase in left atrial mechanical function. Changes in the late emptying and filling velocities significantly correlated with changes in the transmitral A-wave velocity (r = 0.59, p < 0.01), percent atrial filling (r = 0.61, p < 0.005), and the pulmonary venous A-wave velocity (r = 0.56, p < 0.05). In contrast, little change was observed in the early emptying and filling velocities. There was no relation between the indexes of left ventricular function and those of appendage function. In conclusion, unless there was an alteration of the loading conditions, left atrial appendage function improved over several days after cardioversion, and its function was related to left atrial mechanical function.
Seventy-eight patients with chronic nonrheumatic atrial fibrillation were studied by transesophageal echocardiography with regard to the left atrial appendage function and its relation to the coarseness of atrial fibrillation on electrocardiogram. These 78 patients (52 men and 26 women; mean age, 66 +/- 10 years; range, 40 to 94 years) were classified into two groups according to the presence of coarse (group 1, n = 46; those with the greatest amplitude of fibrillatory wave in lead V1 > or = 1 mm) or fine (group 2, n = 32; those without the coarse fibrillatory wave in lead V1) atrial fibrillation on a standard 12-lead electrocardiogram within 1 month of echocardiographic studies. There were no significant differences in age, sex, mean duration of atrial fibrillation, left ventricular end-diastolic dimension, left ventricular end-systolic dimension, left ventricular ejection fraction, and left atrial dimension between the two groups. In group 1, however, the left atrial appendage ejection fraction (24.4 +/- 14.2% vs 32.6 +/- 14.8%; p < 0.05) and the peak emptying velocity (21.7 +/- 12.6 cm/s vs 30.4 +/- 14.3 cm/s; p < 0.01) were lower than those in group 2. There were higher incidences of left atrial appendage spontaneous echo contrast (26/46 vs 7/32; p < 0.005) and thrombus (8/46 vs 0/32; p < 0.05) in group 1 patients. The coarse atrial fibrillation revealed a sensitivity of 80.0%, a specificity of 58.1%, a positive predictive value of 60.9%, and a negative predictive value of 78.1% for the presence of left atrial appendage spontaneous echo contrast and/or thrombus formation. In conclusion, in patients with coarse nonrheumatic atrial fibrillation, the left atrial appendage function is usually poor and the incidence of spontaneous echo contrast and thrombus formation appears to be higher in these patients.
In patients with conventional indication for ICD implantation, atrial fibrillation may occur in more than 50% during the life-span of the device and may lead to severe adverse events. Dual chamber defibrillators with atrial antitachycardia functions, including prevention algorithms, arrhythmia detection capability and atrial therapy options (antitachy pacing and cardioversion) have been recently introduced. The aim of this review is to examine the effectiveness of these new devices and to identify patients who may benefit. We recently studied 112 patients who received the device because of life-threatening ventricular arrhythmias. Fifty-five percent of them had atrial fibrillation prior to implantation. During the follow-up (one year on average), 27% had at least one episode of sustained atrial tachyarrhythmia. Effectiveness of atrial antitachy pacing was 71% on regular atrial tachycardia and 36% on irregular atrial tachyarrhythmias. Atrial shock efficacy was over 90% when adequately programmed. Interestingly, near half of the episodes started as regular atrial tachycardia and accelerated and became less organized in few minutes. Early delivery of antitachy pacing may increase success rate and decrease the need for atrial shock. Furthermore, it may prevent atrial remodeling and reduce atrial fibrillation burden. Based on our experience, we recommend that all patients with a class I indication for defibrillator implantation (related to risk of ventricular arrhythmias) who have a history of or are at risk of developing atrial tachyarrhythmias should receive a dual chamber defibrillator equipped with atrial antitachycardia functions. Furthermore, patients either with a history of heart failure, with poor functional capacity (functional class III or IV), depressed left ventricular ejection fraction, a need for monitoring of atrial rhythm, or in whom there is some concern about appropriate detection of ventricular arrhythmias, may benefit from a single device capable of managing ventricular and supraventricular arrhythmias.
Previous methods used to assess atrial baffle function after correction of transposition of the great arteries have included precordial echocardiography and cardiac catheterization. To evaluate whether single plane transesophageal echocardiography might provide additional information, its findings were correlated with information derived from both precordial echocardiography and cardiac catheterization in 15 patients (14 Mustard procedures, 1 Senning procedure) aged 4.2 to 33 years (mean 16.3). Precordial ultrasound with combined imaging, color flow mapping and pulsed Doppler ultrasound visualized the supramitral portion of the common systemic venous atrium in every case but could identify only superior limb obstruction in three of six patients, mid-baffle obstruction in zero of two and inferior limb obstruction in zero of two patients. Transesophageal studies with use of the same range of ultrasound methods demonstrated superior limb obstruction (severe in four, mild in two) in six of six patients, mid-baffle obstruction in two of two and inferior limb obstruction in two of two patients. The entire pulmonary venous atrium was equally well interrogated by either ultrasound approach, with both identifying three cases (two mild, one moderate) of mid-pulmonary venous atrium obstruction. However, individual pulmonary vein velocity profiles could only be recorded by transesophageal pulsed Doppler ultrasound. Precordial studies identified baffle leaks (1 large, 2 small) in only three patients, whereas transesophageal studies identified 11 such baffle leaks (1 large, 10 small), which were multiple in two patients. It is concluded that transesophageal echocardiography provides a more detailed and accurate assessment of atrial baffle morphology and function than is provided by either precordial ultrasound or cardiac catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)
The relationship between the left atrial appendage (LAA) function, as assessed by transesophageal echocardiography, and the incidence of left atrial thrombus was evaluated in 62 patients with nonvalvular chronic atrial fibrillation (AF; n=50) and atrial flutter (AFL; n=12). It was hypothesized that in both AF and AFL not only the LAA flow velocity (LAAFV), but also the frequency of the LAA movement (the LAA flow time, LAAFT) is a major contributing factor to thrombus formation. LAAFT was defined as the average duration of LAA flow with emptying and filling waves. The patients with AF were divided into 2 groups: lone AF (n=14) and non-lone AF (n=36). LAA thrombus was found in 6 patients with none-lone AF. LAAFV was lower and LAAFT was shorter in patients with thrombus as compared with patients without thrombus (12.0+/-2.2 cm/s vs 24.1+/-10.6 cm/s, 68.7+/-1.5 ms vs 72.9+/-3.3 ms, p<0.01, respectively). Patients with AFL had higher LAAFV and longer LAAFT than those with chronic AF. The present data suggest that, in addition to LAAFV, LAAFT characterized LAA function and might serve as a predictor of thrombus formation in chronic AF. With respect to LAA function, patients with lone AF or AFL are at low risk for thrombus formation.
To determine the value of echocardiographic parameters for predicting maintenance of sinus rhythm after internal atrial defibrillation (IAD), transthoracic and transesophageal echocardiography were performed in 38 patients with atrial fibrillation (AF) before IAD. In addition, serial echocardiographic examinations were performed at 1, 7, and 28 days after IAD in 20 patients to assess the effect of IAD on echocardiographic markers of thromboembolic risk. AF had recurred in 49% of patients within 6 months following IAD. Left atrial chamber and appendage size and ejection fraction were not predictive of recurrence of atrial fibrillation. However, peak emptying velocities of the left atrial appendage were significantly lower in patients with recurrence of atrial fibrillation as compared with patients who had maintained sinus rhythm (0.26 +/- 0.1 m/sec vs 0.49 +/- 0.17 m/sec; P = 0.001). A peak emptying velocity < 0.36 m/sec had a sensitivity of 82% and specificity of 83% for predicting the recurrence of AF. Peak A wave velocities increased gradually after cardioversion from 0.47 +/- 0.16 m/sec at 24 hours to 0.61 +/- 0.13 m/sec after 7 days (P < 0.05). One patient developed a new thrombus in the left atrial appendage and another patient suffered a thromboembolic event after IAD. Assessment of left atrial appendage function adds information regarding the probability of maintaining sinus rhythm after the procedure and the need for anticoagulation therapy with IAD.
BACKGROUND: A high incidence of embolic phenomena is associated with atrial fibrillation (AF) and the left atrial appendage (LAA) is frequently the source of the emboli. Thrombus formation may be due to stasis within the fibrillating and inadequately emptying LAA. Because LAA emptying in AF may be the result of mechanical compression by the adjacent left ventricle, it is possible that left ventricular diastolic filling duration will importantly influence passive emptying of the LAA. We hypothesized that the magnitude of emptying of the LAA in AF is related to the duration of left ventricular diastolic filling which is determined by the ventricular response rate in AF. OBJECTIVE: The objective of our study was to determine the relationship of ventricular response rate in AF to LAA emptying and to assess the influence of sinus rhythm and heart rate on LAA emptying immediately after direct current cardioversion to sinus rhythm. METHODS: To study this, we used transesophageal echocardiography to measure LAA ejection fraction ([LAAmax-LAAmin]/LAAmax x 100%) and evaluated its relationship to left ventricular response rate (VRR) in 26 patients with AF (mean age, 65 +/- 7 [1 SD] years). RESULTS: There was a strong inverse relationship between LAA ejection fraction and VRR in AF (r = -0.73; p < 0.001). LAA ejection fraction during AF was 26 +/- 10%, and immediately after successful cardioversion, it increased to 46 +/- 12% (p < 0.001). However, during sinus rhythm there was no relationship between LAA ejection fraction and VRR (r = 0.06; p = NS) in the subgroup of patients who were successfully converted to sinus rhythm. There were poor relationships between LAA ejection fraction and peak transmitral flow velocity (r = -0.41; p = NS) or pulmonary venous flow velocity (r = -0.03; p = NS) in AF. CONCLUSION: These results indicate that the magnitude of LAA emptying in AF is strongly and inversely influenced by ventricular rate. Direct current cardioversion to sinus rhythm is associated with an increase in the magnitude of LAA emptying that is not influenced by heart rate. The magnitude of LAA emptying may be an important factor in the formation of thromboemboli in AF. The extent to which controlling the VRR in chronic AF will prevent stasis and LAA thrombus formation remains to be determined.
BACKGROUND: It has been shown that cardioversion of atrial fibrillation may result in left atrial chamber and appendage dysfunction and cause new thrombi in the left atrium. The aim of this prospective study was to investigate right atrial appendage function and assess the incidence of new right atrial thrombi after electrical cardioversion. METHODS: Transthoracic echocardiography was performed in 25 patients 4 h before and at 24 h and 7 days after electrical cardioversion to determine right and left atrial mechanical function (internal atrial defibrillation, n = 16; external electrical cardioversion, n = 9), as assessed by peak A wave velocities derived from the transtricuspid and transmitral velocity profiles. In addition, transesophageal echocardiography was performed 4 h before and 24 h after cardioversion to evaluate postcardioversion thrombus formation in the right and left atrial chambers and to assess right and left atrial appendage function. The degree of spontaneous echo contrast was noted, and peak emptying velocities of the appendages were measured before and after cardioversion. RESULTS: Peak emptying velocities of both the right atrial appendage (mean +/- SD, 0.23 +/- 0.1 vs 0.32 +/- 0.11 m/sec; P = 0.02) and the left atrial appendage (0.3 +/- 0.15 vs 0.4 +/- 0.15 m/sec; P = 0.01) were significantly lower 24 h after cardioversion compared with 4 h before cardioversion, respectively. The degree of spontaneous echo contrast increased in the left atrium after cardioversion from 1.0 +/- 1.2 to 1.9 +/- 2.1 (P = 0.02), and in the right atrium, it increased from 0.8 +/- 1.1 to 1.2 +/- 1.1 (P = 0.1) after cardioversion. Peak A wave transtricuspid velocity increased from 0.26 +/- 0.05 m/sec at 24 h to 0.38 +/- 0.06 m/sec (P = 0.001) after 7 days; respective values for transmitral peak A wave velocity were 0.39 +/- 0.15 and 0.54 +/- 0.16 m/sec (P = 0.009). No thrombi were found in either the right or left atrium before cardioversion. In two patients, new thrombi in the right atrium were detected 24 h after internal atrial defibrillation. Thrombi were located at the superior rim of the fossa ovalis in both patients with patent foramen ovale. Another patient had developed a thrombus in the left atrial appendage. CONCLUSIONS: Electrical cardioversion may not only cause left atrial chamber and appendage dysfunction and left atrial thrombi but also lead to depressed right atrial appendage function and the generation of new thrombi in the body of the right atrium.