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Expression of angiotensin II receptors in human left and right atrial tissue in atrial fibrillation with and without underlying mitral valve disease.

UNLABELLED: TIVES: We postulated a change of angiotensin II receptor subtype expression in patients with lone atrial fibrillation (AF) and AF with underlying mitral valve disease (MVD) both compared with sinus rhythm (SR). BACKGROUND: Atrial fibrillation is a progressive disease associated with electrical and structural remodeling. Angiotensin II (ANGII) is involved in the process of myocardial remodeling. Actions of ANGII are mediated by ANGII receptor subtypes 1 and 2 (AT(1) and AT(2)). METHODS: Left atrial (LA) and right atrial (RA) tissue samples were obtained from patients with AF or SR with or without underlying MVD. The AT(1) and AT(2) protein levels were measured by quantitative Western blotting techniques. RESULTS: The AT(1) protein level in the LA was significantly increased in patients with AF (all forms) compared with SR (p < 0.05), whereas AT(2) expression was not significantly altered. Comparison of the subgroups revealed a similar increase of AT(1) in both paroxysmal AF and chronic AF with or without MVD. Additionally, investigations of ANGII receptor subtypes in the RA did not exhibit any significant changes either in AT(1) or in AT(2) in patients with AF versus SR. Underlying MVD did not significantly affect AT(2) receptor subtype expression in LA. CONCLUSIONS: Atrial fibrillation is associated with an up-regulation of AT(1) in LA, but not in RA, and did not appear to influence the AT(2) expression in the atrium. Because we found an enhanced expression of AT(1)in the LA, we conclude that AT(1) might be involved in the pathogenesis of AF in the LA.

Adult↗

Reduction in atrial defibrillation threshold by a single linear ablation lesion.

INTRODUCTION: This study investigated a hybrid approach to reduce the atrial defibrillation threshold (ADFT) by determining the effect of a single linear radiofrequency ablation (RFA) lesion on both the ADFT and activation patterns during atrial fibrillation (AF). METHODS AND RESULTS: In 18 open chest sheep (45 to 57 kg), coil defibrillation electrodes were placed in a superior vena cava/right ventricular configuration. AF was induced by burst pacing and maintained with acetyl beta-methylcholine (2 to 42 microL/min). ADFTs were obtained before and after a linear RFA lesion was created in the left atrium (LAL; n = 6), right atrium (RAL; n = 6), or neither atrium as a control (n = 6). In animals receiving an LAL, a 504-unipolar-electrode plaque was sutured to the LA. For animals receiving an RAL, two 504-electrode plaques were placed, one each on the LA and RA. From each plaque, activations were recorded before and after ADFT shocks, and organizational characteristics of activations were analyzed using algorithms that track individual wavefronts. In sham-treated controls, the ADFT did not change. In contrast, LAL reduced ADFT energy 29%, from 4.5 +/- 2.3 J to 3.2 +/- 2.0 J (P < 0.05). RAL reduced ADFT energy 25%, from 2.0 +/- 0.9 J to 1.5 +/- 0.7 J (P < 0.05). AF activation was substantially more organized after RFA than before RFA for both the RAL- and LAL-treated animals. CONCLUSION: A single RFA lesion in either the RA or LA reduces the ADFT in this sheep model. This decrease is associated with an increase in fibrillatory organization.

Animals↗

The effect of intravenous magnesium administration on aortic, right atrial and coronary perfusion pressures during CPR in swine.

OBJECTIVE: To determine the effect of magnesium administration on aortic, right atrial and coronary perfusion pressure (CPP) during cardiopulmonary resuscitation (CPR). DESIGN: Twelve swine weighing 23.2 +/- 3.1 kg were instrumented for CPP, aortic systolic (AOSP) and aortic diastolic (AODP) pressures. INTERVENTION: Ventricular fibrillation was induced and after 20 min of CPR the animals were allocated to receive epinephrine 0.2 mg/kg, or epinephrine 0.2 mg/kg plus magnesium 0.14 g/kg. Epinephrine was repeated every 5 min. Arterial blood gases were determined during normal sinus rhythm and prior to drug administration. RESULTS: Pressures were recorded and averaged over four consecutive 5-min intervals following initial drug administration. AOSP, AODP and CPP were compared using an analysis of covariance. AOSP was statistically lower in the group receiving magnesium. There was a trend toward lower AODP and CPP in the group receiving magnesium as well. These statistical differences and trends were absent after adjusting for pressures during normal sinus rhythm and serum bicarbonate prior to drug administration. CONCLUSIONS: In this model of prolonged cardiac arrest, the administration of magnesium with epinephrine appeared to have a negative effect on aortic pressures during CPR. Further study is needed to determine the confounding effect of serum bicarbonate on the response to epinephrine and magnesium during CPR.

Animals↗

[Value of the study of electrocardiographic P wave in pheochromocytoma].

The diagnostic value of electrocardiographic P wave analysis in the frontal plane was assessed with respect to previously reported abnormalities: right atrial hypertrophy-dilatation; an enlarged, crenalleted summit without criteria of right atrial hypertrophy. Two observers studied the ECG recordings of 20 hypertensive patients with pheochromocytomas: 10 men and 10 women, aged 45.5 +/- 16 years, and in 30 patients with essential hypertension, 15 men and 15 women, aged 48.9 +/- 9 years (NS). The duration of hypertension was 2.6 +/- 2 years versus 4.7 +/- 4 years (p = 0.02). Right atrial hypertrophy-dilatation was observed in 5 patients in the pheochromocytoma group and in none of the essential hypertensive patients: an isolated abnormality of the summit of the P wave was observed in 5 other cases of pheochromocytoma and by 1 observer in 1 of the essential hypertension. These abnormalities disappeared after ablation of the tumour. These changes were not recorded in 3 patients who had predominant noradrenaline hypersecretion; nevertheless, comparison of the urinary adrenaline, noradrenaline, normeta- and metanephrine levels were inconclusive. No relationship was established between these concentrations, global urinary catecholamines and meta block, the duration of hypertension, the frequency and level of hypertensive crises, or the presence of "ischaemic" ST-T wave changes. P wave changes are thought to be related to high plasma catecholamine levels irrespective of the clinical impact; the sensitivity of these changes is modest (10/20) but the specificity is better within a group of hypertensive patients. An experienced observer can orient the diagnostic investigations to the search for a pheochromocytoma or to a secondary recurrence of the tumour from the surface ECG. The role of marker of a very high noradrenaline or adrenaline secretion cannot be confirmed from a series limited in separated plasma concentration measurements.

Adrenal Gland Neoplasms↗

Test of dynamic closed-loop baroreflex and autoregulatory control of total peripheral resistance in intact and conscious sheep.

This is the first study able to examine and delineate the actual actions of the physiological mechanisms responsible for the dynamic couplings between cardiac output (CO), arterial pressure (Pa), right atrial pressure (PRA), and total peripheral resistance (TPR) in an individual subject without altering the underlying regulatory mechanisms. Eight conscious male sheep were used, where both types of baroreceptors were independently exposed to simultaneous beat-to-beat pressure perturbations under intact closed-loop conditions while CO, Pa, PRA, and TPR were measured. We applied the cardiovascular system identification method proposed in a companion paper (4) to quantitatively characterize the dynamic closed-loop transfer relations CO-->Pa, PRA-->Pa, Pa-->TPR, and PRA-->TPR from the measured signals. To validate the dynamic properties of the estimated transfer relations, the essential parts of the linear dynamics of the model were independently and comprehensively evaluated via error model cross-validation, and the overall model's steady-state behavior was compared with a separate random effects regression approach. In addition to numerous physiological findings, we found that the cardiovascular system identification results were exceptionally consistent with the analytically derived solutions previously discussed in Ref. 4. In conclusion, this study presents the first time validation of a cardiovascular system identification method by means of experimentally acquired animal data in the intact and conscious animal and offers a set of powerful quantitative tools essential to advancing our knowledge of cardiovascular regulatory physiology.

Animals↗

Quantification and comparison of pulmonary emboli formation after pneumatic tourniquet release in patients undergoing reconstruction of anterior cruciate ligament and total knee arthroplasty.

UNLABELLED: The amount of emboli formed (percentage of total emboli area to the right atrial area [%Ae]) after tourniquet release in invasive procedures of the medullary cavity is empirically much larger than that in noninvasive procedures, even if the tourniquet duration is similar. Thus, we compared %Ae between arthroscopic reconstruction of the anterior cruciate ligament (ACL, n = 20) and total knee arthroplasty (TKA, n = 20). The right atrium was continuously monitored by transesophageal echocardiography to assess %Ae. Peak %Ae +/- SD (ACL, 4.1% +/- 3.4%; TKA, 20.7% +/- 16.7%) appeared 30-40 s after tourniquet release in both groups. However, %Ae in the TKA group was always larger than the peak %Ae in the ACL group. In addition, although the ET(CO(2)) significantly increased after tourniquet release in both groups, increase of ET(CO(2)) (1.1% +/- 0.3%) in the ACL group was significantly larger than that in the TKA group (0.5% +/- 0.2%). An increase in ET(CO(2)) was inversely proportional to peak %Ae (P < 0.01; r = 0.703). Therefore, the present data suggest that the risk of acute pulmonary embolism after tourniquet release may be more frequent during TKA than ACL. IMPLICATIONS: We compared emboli formation after tourniquet release in patients undergoing arthroscopic reconstruction of the anterior cruciate ligament (ACL, n = 20) and total knee arthroplasty (TKA, n = 20) using transesophageal echocardiography. The present data suggest that the risk of acute pulmonary embolism after tourniquet release could be more frequent during TKA than ACL.

Acute Disease↗

Assessment of the effects of various maneuvers on both atrial pressure changes.

The aim of the present study was to determine which maneuver causes the greatest pressure difference between both atria by measuring right and left atrial pressures simultaneously after certain maneuvers. Thirty-two coronary care unit patients, whom a Swan-Ganz catheter was inserted because of acute left ventricular dysfunction, hypotension, sinus tachycardia with unknown cause, were included in this study. The basal values of peak right atrium (RA) pressure and corresponding pulmonary capillary wedge pressure (PCWP) were measured via two separated transducers. Patients were tutored with several trials to perform breath holding, successive three strong coughs, Valsalva maneuver, 20 degrees head down, respectively. In the end of these maneuvers, the peak RA pressure and corresponding PCWP were measured simultaneously. All maneuvers caused an increase in RA pressure. The highest peak RA pressure was obtained by means of the Valsalva maneuver (7.6 +/- 5 versus 20.4 +/- 7.6 mmHg before and after Valsalva, respectively; P<0.001). PCWP (18.8 +/- 5.9 mmHg) increased only with coughing (21.2 +/- 6.7 mmHg, P<0.01) and 20 degrees head down maneuver (20 +/- 5.7 mmHg, P<0.05). The highest increase in pressure gradient between peak RA pressure and corresponding PCWP was observed during Valsalva maneuver (-11 +/- 6.6 vs. 2.3 +/- 5.9 mmHg, P<0.001). The lowest increase was obtained in 20 degrees head down maneuver (-11 +/- 6.6 vs. -8.5 +/- 5.8 mmHg, P<0.001). When measuring the pressure of both atria invasively and simultaneously, Valsalva maneuver was the most effective maneuver consistent with pressure difference in favour of RA among all the other maneuvers.

Atrial Function, Left↗

Correlation between measured inferior vena cava diameter and right atrial pressure depends on the echocardiographic method used in patients who are mechanically ventilated.

In patients who are mechanically ventilated, the correlation between inferior vena cava diameter (IVCD) measurements and mean right atrial pressure (RAP) varies in the literature. The purpose of this study was to test if the correlation between IVCD and RAP measurement in patients who are critically ill depends on the transthoracic echocardiography (TTE) methodology used. Twenty patients who were critically ill, sedated, and required respiratory support were prospectively studied by TTE during mechanical ventilation in a controlled mode. The TTE measures of IVCD were made, using methods previously cited. First, IVCD was measured at end-expiration and end-diastole, with ECG synchronization, using the M-mode, on short-axis view 2 cm below the right atrium. Second, IVCD was assessed at end-expiration, without ECG synchronization, using the 2-dimensional long-axis view at the same location. RAP was measured simultaneously by using a central venous catheter positioned in the superior vena cava. All measurements were taken in the supine position. IVCD at end-expiration and end-diastole, with ECG synchronization, using the M-mode, and IVCD at end-expiration, without ECG synchronization, using the 2-dimensional long-axis view, correlate linearly with RAP (0.81, P <.0001 and 0.71, P =.0004). Mean bias between the 2 TTE methods (Bland-Altman analysis) was 1.6 mm (SD +/- 2.03 mm). In conclusion, this study confirms that variation of correlation between TTE IVCD measurement and RAP depends on the ultrasonographic methodology used and the timing of measurement during the cardiac cycle. IVCD at end-expiration and end-diastole, with ECG synchronization, using the M-mode (IVCD-MM) correlates more satisfactory with RAP than with IVCD at end-expiration, without ECG synchronization, using the 2-dimensional long-axis view, in patients during mechanical ventilation.

Adult↗

Site-dependent intra-atrial conduction delay. Relationship to initiation of atrial fibrillation.

BACKGROUND: Atrial dysrhythmia patients have exaggerated intra-atrial conduction delays and prolonged relative refractoriness in response to atrial premature depolarizations (APDs). Furthermore, atrial fibrillation (AF) is more readily inducible by APDs from the high right atrium (HRA) than the coronary sinus (CS). In this study, we postulated that site-specific intra-atrial conduction delays can explain why AF is initiated more from the HRA than from the CS. METHODS AND RESULTS: We examined 17 patients (age, 49 +/- 22 years) without a history of atrial flutter, AF, or structural heart disease. Programmed stimulation was carried out from the HRA and distal CS, and bipolar recordings were made at the HRA, His bundle, posterior triangle of Koch, and CS. More prolongations in conduction and relative refractoriness in all intra-atrial sites were observed during HRA than CS APDs. AF was induced in 8 patients after HRA and not CS stimulation. During HRA stimulation, patients with AF inducibility exhibited significant prolongation of conduction to the posterior triangle of Koch and marked broadening of the posterior triangle of Koch electrogram compared with CS stimulation. In patients without AF inducibility, the posterior triangle of Koch electrogram width was the same during HRA and CS stimulation. CONCLUSIONS: The existence of site-dependent intra-atrial conduction delays and site-dependent dispersion of refractoriness appears to be a common property of the atrial myocardium and does not necessarily forecast AF inducibility. However, the presence of nonuniform anisotropic characteristics of the posterior triangle of Koch may be critical for AF induction.

Adult↗

Pronounced effect of procainamide on clockwise right atrial isthmus conduction compared with counterclockwise conduction: possible mechanism of the greater incidence of common atrial flutter during antiarrhythmic therapy.

INTRODUCTION: It has been shown that the induction rates of common and reversed common atrial flutter are comparable during baseline control study, whereas the rate is significantly greater for common flutter than reversed common flutter during administration of antiarrhythmic agents. The mechanism of this discrepancy is not known. METHODS AND RESULTS: The study consisted of 15 patients (group 1) with clinically documented common atrial flutter either with (n = 10) or without (n = 5) Class I antiarrhythmic therapy, and 15 patients with paroxysmal supraventricular tachycardia (group 2). Bidirectional conduction velocity and minimal pacing cycle length of 1:1 conduction during incremental pacing from both the low lateral right atrium and coronary sinus were assessed. The response of these variables to procainamide was analyzed in correlation with the induction rate of each type of flutter during the pacing protocol. Conduction velocity in the clockwise (CW) direction was significantly slower for all pacing cycle lengths than conduction velocity in the counterclockwise (CCW) direction in group 1 but was similar in group 2. Minimal pacing cycle length of 1:1 conduction did not differ between CW and CCW conduction in either group. However, in group 1, minimal pacing cycle length of 1:1 conduction of CW conduction was prolonged to a greater degree after procainamide than that of CCW conduction. There also was a significant increase in the induction rate of common flutter. This preferential effect of procainamide on CW conduction was not observed in group 2. CONCLUSION: CW conduction over the isthmus is preferentially influenced by procainamide compared with CCW conduction, which may explain the greater incidence and induction probability of common flutter during antiarrhythmic therapy.

Adult↗

The beta1-adrenoceptor site activated by CGP12177 varies in behavior according to the estrous cycle phase and stress.

The aim of this work was to assess whether stress and estrous cycle phases affected the beta1-adrenoceptor (beta1-AR) site activated by CGP12177 in the right atria of rats. The chronotropic response to CGP12177 in the absence or presence of antagonists was determined in atria from rats submitted to one daily foot-shock session for 3 consecutive days. Blood was collected for hormonal assays. The pD2 for CGP12177 in atria from females was lower than in atria from males and was unaltered by stress or the estrous cycle. Propranolol (200 nM) or CGP20712A (3 microM) shifted the concentration-response curves to CGP12177 to the right in control and stressed estrus or control diestrus rats. Atria from stressed diestrus rats were resistant to blockade by propranolol or CGP20712A, indicating that the effect of beta-adrenoceptor antagonists on the response to CGP12177 is influenced by estrous cycle phases. The stress-induced increase in serum corticosterone levels was independent of the estrous cycle or gender, but the estradiol/progesterone ratio was affected differently in the two groups of female rats. In the diestrus group, serum estradiol levels decreased after the first foot-shock session and remained low until the day of sacrifice, whereas in the estrus group the serum levels of estradiol did not decrease after stress and peaked on the second day, which corresponded to proestrus. These data do not indicate whether there is a direct or indirect effect of stress hormones and (or) sex steroids on cardiac beta1-AR sensitivity. However, they do show that the classic and low-affinity binding sites of the beta1-AR are independently regulated and that the beta1-AR atypical site affinity for antagonists depends on the estrous cycle.

Adrenergic beta-1 Receptor Agonists↗

Free-floating thrombi in the right heart: diagnosis, management, and prognostic indexes in 38 consecutive patients.

BACKGROUND: Floating right heart thrombi (FRHTS) are a rare phenomenon, encountered almost exclusively in patients with suspected or proven pulmonary embolism and diagnosed by transthoracic echocardiography. Their management remains controversial. METHODS AND RESULTS: We report on a series of 38 consecutive patients encountered over the past 12 years. Thirty-two patients were in NYHA class IV, 20 in cardiogenic shock. Echocardiography usually demonstrated signs of cor pulmonale: right ventricular overload (91.7% of the population), paradoxical interventricular septal motion (75%), and pulmonary hypertension (86. 1%). The thrombus was typically wormlike (36 of 38 patients). It extended from the left atrium through a patent foramen ovale in 4 patients. Pulmonary embolism was confirmed in all but 1. Mortality was high (17 of 38 patients) irrespective of the therapeutic option chosen: surgery (8 of 17), thrombolytics (2 of 9), heparin (5 of 8), or interventional percutaneous techniques (2 of 4). The in-hospital mortality rate was significantly linked with the occurrence of cardiac arrest. Conversely, the outcome after discharge was usually good, because 18 of 21 patients were still alive 47.2 months later (range, 1 to 70 months). CONCLUSIONS: Severe pulmonary embolism was the rule in our series of FRHTS (mortality rate, 44.7%). The choice of therapy had no effect on mortality. Emergency surgery is usually advocated. However, thrombolysis is a faster, readily available treatment and seems promising either as the only treatment or as a bridge to surgery. In patients with contraindications to surgery or lytic therapy, interventional techniques may be proposed.

Adult↗

Nonuniformity of AH intervals during stimulation at different left atrial sites.

Studies in humans have found left atrial stimulation via the coronary sinus (CS) to elicit significantly shorter atrium-His (AH) intervals as compared to right atrial stimulation, but whether pacing at different left atrial sites (anterior vs posterior left atrium, i.e., far distal vs proximal CS) affects the AH interval has not been studied. Hence, in 22 patients, we compared the effects of stimulation from various atrial sites, including anterior high right atrium (HRA), distal CS, mid-CS, and proximal CS, on: stimulus-atrium (SA), AH, and stimulus-His intervals on the His bundle electrogram. Paced cycle length differed for each patient (range 900-350 msec, mean 532 +/- 140 msec), but conduction intervals from different atrial sites were compared using identical cycle length in each patient. The mean SA intervals were 34 +/- 10 msec, 57 +/- 10 msec, 44 +/- 11 msec, and 32 +/- 8 msec with stimulation, respectively, from HRA, distal CS, mid-CS, and proximal CS (each significantly different except for HRA vs proximal CS). The mean AH intervals were 123 +/- 23 msec, 104 +/- 28 msec, 95 +/- 15 msec, and 90 +/- 18 msec with stimulation, respectively, from HRA, distal CS, mid-CS, and proximal CS (each significantly different except for mid-CS vs proximal CS). In 13 patients, the discrepancy in AH intervals during distal versus proximal CS stimulation was > or = 15 msec; in 9 patients this difference was only < or = 10 msec, considered within the range of measurement error. Thus, in a significant portion of patients, discrepant AH intervals were demonstrated during stimulation from the distal versus proximal CS. These previously undescribed observations suggest that electrophysiological studies on atrioventricular nodal conduction that involve left atrial stimulation must take into account actual location of the stimulation site (anterior or posterior) in order to properly interpret the findings.

Adolescent↗

Mechanisms of entrainment of human common flutter studied with multiple endocardial recordings.

BACKGROUND: The mechanisms of common atrial flutter entrainment have not been directly studied in humans. METHODS AND RESULTS: Endocardial mapping in six cases of common flutter showed large right atrial (RA) reentry circuits. Activation was craniocaudal in the anterolateral right atrium and caudocranial in the septum. The inferior vena cava-tricuspid isthmus (IVC-TV) closed the circuit. The high right atrium was paced at progressively shorter cycle lengths (CLs) in all, and the IVC-TV was paced in three cases. We recorded six to eight simultaneous RA electrograms from septum and anterior wall. Transient entrainment was recognized from all sites by capture of all electrograms at two or more paced CLs, with total or partial preservation of baseline flutter sequence and return to baseline after pacing. Antidromic circuit penetration was documented in five cases during high RA pacing and in one with IVC-TV pacing. Short CLs induced orthodromic conduction delays that resulted in a postpacing pause longer than basal flutter CL. ECG fusion with high RA pacing correlated poorly with antidromic septal penetration. This was related to overlap of orthodromic septal activation with anterior wall activation of the following cycle. Pacing disorganized flutter into a brief irregular rapid rhythm in two cases and atrial fibrillation in one case. In two cases, complete antidromic septal penetration led to sudden flutter interruption, and in another case it led to circuit inversion. CONCLUSIONS: Direct recordings confirm orthodromic and antidromic penetration of flutter circuits by high and low RA pacing. Short CLs modify the circuit. Disorganization is the most common mode of flutter interruption.

Aged↗

Atrial electrical remodeling by rapid pacing in the isolated rabbit heart: effects of Ca++ and K+ channel blockade.

INTRODUCTION: Electrical remodeling describes atrial electrophysiologic changes that occur following atrial fibrillation. The mechanism(s) responsible for this phenomenon is not well understood. The purpose of this study was to examine the effects of rapid atrial pacing on atrial action potential duration, conduction time and refractoriness in the isolated rabbit heart. The effects of Ca++ and K+ blockade in this model were also studied. METHODS AND RESULTS: Monophasic action potential recordings were made from 12 epicardial atrial sites in 50 isolated perfused rabbit heart preparations. These recordings were analyzed for activation time (AT), 90% action potential duration (APD) and conduction times (CT) measured at a 250 msec cycle length. Atrial effective refractory periods (ERP) were determined at a 200 msec cycle length. All measurements were made at baseline and repeated after 2 hours of biatrial pacing at 250 msec (control group, n = 10) or 2 hours of rapid biatrial pacing (approximately 80 msec) in 4 groups: rapid pacing alone (rapid pacing group); rapid pacing in the presence of 0.1 mM verapamil (verapamil group) for L-type Ca++ channel blockade; rapid pacing with 1 mM 4-aminopyridine (4-AP group) for K+ channel blockade; and rapid pacing with 50 microM nickel chloride (Ni++ group) for T-type Ca++ channel blockade (n = 10 each group). All baseline and post pacing measurements were taken in the presence of Ca++ or K+ blockers for the respective groups. After rapid atrial pacing alone the average APD shortened by 8.2 +/- 10.4 msec compared to 3.6 +/- 12.5 msec shortening for control group (p = 0.002). The shortening of APD was uniform at all recording sites. For the rapid pacing group, CT was unchanged for right to left atrial conduction but shortened significantly for left to right atrial conduction (26.8 +/- 1.9 msec at baseline to 22.3 +/- 4.1 msec post pacing, p = 0.005). Conduction times were unchanged in the control group. The dispersion of repolarization was unchanged by rapid pacing alone. The decrease in APD from baseline to post rapid pacing was similar to the control group for those hearts treated with verapamil and 4-AP (1.5 +/- 12.3 and 4.7 +/- 10.4 msec, respectively, both p > or = 0.18 vs control group). The decrease in APD was significantly greater for the Ni++ group (11.8 +/- 14.3 msec) than for either the control group or rapid pacing group (both p < or = 0.023). The dispersion of repolarization was increased only in the 4-AP group post rapid pacing (41.7 +/- 6.2 msec at baseline to 53.5 +/- 9.6 msec post pacing, p = 0.01). ERPs were unchanged in any of the 5 groups except for a decrease in left atrial ERP in the Ni++ group after rapid pacing (98 +/- 14 msec at baseline to 88 +/- 8 msec post rapid pacing, p = 0.005). CONCLUSIONS: In the isolated rabbit heart model: 1) atrial APD is shortened after rapid pacing; 2) the shortening of APD is attenuated by verapamil and 4-AP but exaggerated by Ni++; 3) atrial conduction times are shortened in a direction specific manner after rapid pacing; and 4) shortening of ERP in this model is measured only in the presence of Ni++. These findings suggest that both L-type Ca++ and 4-AP sensitive channels may participate in atrial electrical remodeling.

4-Aminopyridine↗

Variable electrocardiographic characteristics of isthmus-dependent atrial flutter.

OBJECTIVES: The purpose of this study was to characterize variations in flutter-wave (F-wave) morphology among patients with clockwise isthmus-dependent (CWID) and counterclockwise isthmus-dependent (CCWID) right atrial flutter (AFL) and to attempt to correlate F-wave morphology with echocardiographic data and clinical patient characteristics. BACKGROUND: Variations in F-wave morphology on surface electrocardiogram (ECG) during CCWID and CWID flutter have been reported but never systematically characterized. METHODS: Over a four-year period, 139 patients with AFL on ECG underwent electrophysiologic study and echocardiography at our institution. Electrocardiographic data, intracardiac recordings, echocardiographic data, and patient characteristics were reviewed retrospectively. RESULTS: Of 156 AFLs evaluated, 130 were CCWID, 26 were CWID. Three types of CCWID flutter were observed: type 1 had purely negative F-waves inferiorly, types 2 and 3 had F-waves inferiorly with small (type 2) or broad (type 3) positive terminal deflections; CCWID flutter types 2 and 3 were associated with higher incidence of left atrial (LA) enlargement, heart disease, and atrial fibrillation (Afib) than type 1. Two types of CWID flutter were observed: type 1 had notched positive F-waves with a distinct isoelectric segment inferiorly. Type 2 had broader F-waves inferiorly with positive and negative components and a short isoelectric segment. CONCLUSIONS: Variable ECG patterns for CCWID and CWID AFL exist. A positive component of the F-wave in the inferior leads during CCWID flutter is associated with an increased likelihood of heart disease, Afib, and LA enlargement.

Adult↗

Reduced collateral perfusion is a direct consequence of elevated right atrial pressure.

In the present study we determined quantitatively the effects of increased right atrial pressure (RAP) on coronary and collateral flows. In an isolated, blood-perfused, maximally vasodilated dog heart preparation in which the left ventricle was vented, we used the retrograde flow method to assess collateral flow. When RAP was elevated from 5 +/- 1 (control) to 13 +/- 1 and 23 +/- 1 mmHg, retrograde flow from the left circumflex coronary artery (which was open to atmospheric pressure) increased 29 +/- 8 and 97 +/- 21% relative to control while left anterior descending flow decreased 5 +/- 1 and 14 +/- 2%, respectively (P < 0.01; n = 7). The increase in retrograde flow could be due to 1) an increase in collateral flow due to increased pressure at the origin of the collaterals or 2) the elevated RAP (venous outflow pressure), which forces the antegrade collateral flow component in the retrograde direction. To distinguish between these possibilities we embolized the circumflex with 30-microns spheres to eliminate the antegrade flow component. After embolization there was no significant change in retrograde flow with elevated RAP, indicating that the second supposition was correct. We conclude that increased RAP 1) results in a reduction of flow to the collateral-dependent myocardium and 2) reduces perfusion of the unoccluded coronary vessel. Furthermore, we found that under conditions of varying venous outflow pressure, retrograde flow may not serve as a reliable index of collateral flow.

Animals↗

Effect of positive pressure on venous return in volume-loaded cardiac surgical patients.

The hemodynamic effects of increases in airway pressure (Paw) are related in part to Paw-induced increases in right atrial pressure (Pra), the downstream pressure for venous return, thus decreasing the pressure gradient for venous return. However, numerous animal and clinical studies have shown that venous return is often sustained during ventilation with positive end-expiratory pressure (PEEP). Potentially, PEEP-induced diaphragmatic descent increases abdominal pressure (Pabd). We hypothesized that an increase in Paw induced by PEEP would minimally alter venous return because the associated increase in Pra would be partially offset by a concomitant increase in Pabd. Thus we studied the acute effects of graded increases of Paw on Pra, Pabd, and cardiac output by application of inspiratory-hold maneuvers in sedated and paralyzed humans. Forty-two patients were studied in the intensive care unit after coronary artery bypass surgery during hemodynamically stable, fluid-resuscitated conditions. Paw was progressively increased in steps of 2 to 4 cmH(2)O from 0 to 20 cmH(2)O in sequential 25-s inspiratory-hold maneuvers. Right ventricular (RV) cardiac output (CO(td)) and RV ejection fraction (EF(rv)) were measured at 5 s into the inspiratory-hold maneuver by the thermodilution technique. RV end-diastolic volume and stroke volume were calculated from EF(rv) and heart rate data, and Pra was measured from the pulmonary artery catheter. Pabd was estimated as bladder pressure. We found that, although increasing Paw progressively increased Pra, neither CO(td) nor RV end-diastolic volume changed. The ratio of change (Delta) in Paw to Delta Pra was 0.32 +/- 0.20. The ratio of Delta Pra to Delta CO(td) was 0.05 +/- 00.15 l x min(-1) x mmHg(-1). However, Pabd increased such that the ratio of Delta Pra to Delta Pabd was 0.73 +/- 0.36, meaning that most of the increase in Pra was reflected in increases in Pabd. We conclude that, in hemodynamically stable fluid-resuscitated postoperative surgical patients, inspiratory-hold maneuvers with increases in Paw of up to 20 cmH(2)O have minimal effects on cardiac output, primarily because of an in-phase-associated pressurization of the abdominal compartment associated with compression of the liver and squeezing of the lungs.

Abdomen↗