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Meandering and unstable reentrant wave fronts induced by acetylcholine in isolated canine right atrium.

The mechanism(s) by which acetylcholine (ACh) increases atrial vulnerability to reentry and maintains its activity for longer durations remains poorly defined. In the present study we used high-resolution activation maps to test the hypothesis that ACh promotes meandering of atrial reentrant wave fronts, resulting in breakup and the generation of new wave fronts that sustain the activity. Reentry was induced in 11 isolated canine right atrial tissues (3.8 x 3.2 cm) by a premature point stimulus (S2) before and after superfusion with ACh (15 x 10(-6) M). Endocardial isochronal activation maps were constructed with the use of 509 bipolar electrodes (1.6-mm spatial resolution), and the dynamics of the activation wave fronts were visualized with animation. A vulnerable period was found during which an S2 current strength > 4.4 +/- 2.5 mA [lower limit of vulnerability (LLV)] and < 26 +/- 13 mA [upper limit of vulnerability (ULV)] induced a single stationary reentrant wave front that lasted 3 +/- 2.5 s with a period of 159 +/- 17 ms (16 episodes). AC shortened the refractory period from 100 +/- 12 to 59 +/- 9 ms (P < 0.001) and increased vulnerability to reentry induction by simultaneous decrease in the LLV (0.7 +/- 0.2 mA, P < 0.001) and an increase in the ULV (82 +/- 24 mA, P < 0.01). ACh accelerated the rate (period of 110 +/- 16 ms, P < 0.001) and converted the stationary reentrant wave front to a nonstationary (meandering) reentrant wave front showing polymorphic electrograms, i.e., "fibrillation-like" activity (22 episodes). Rapid meandering of the reentry tip led to wave front breakup (18 episodes) and the generation of new wave fronts (19 episodes). These wave front dynamics also led to sustained (76 +/- 224 s, P < 0.001) fibrillation-like electrograms. We conclude that ACh increases the ULV and promotes meandering of a single reentrant wave front, leading to breakup and the generation of new wave fronts. Single meandering and complex wave front dynamics cause fibrillation-like activity and sustain the activity for longer duration.

Acetylcholine↗

Potential ionic mechanism for repolarization differences between canine right and left atrium.

Experimental and clinical evidence suggests a critical role for the left atrium (LA) in atrial fibrillation (AF). In animal models, repolarization is faster in the LA than in the right atrium (RA), leading to more stable reentry circuits with a shorter intrinsic period in the LA. The ionic mechanisms underlying LA-RA repolarization differences are unknown. Therefore, we evaluated ionic currents and action potentials (APs) with the whole-cell patch clamp in isolated canine atrial myocytes. The density of the rapid delayed rectifier current (I(Kr)) was greater in the LA (eg, 1.83+/-0.10 pA/pF at +20 mV) than in the RA (1.15+/-0.07 pA/pF, P<0.01; n=16 cells per group). The slow and ultrarapid delayed rectifier, the inward rectifier, L-type Ca(2+), and transient outward K(+) currents were all comparable in the LA and RA. There were no differences in kinetic or voltage-dependent properties of currents in LA versus RA. Western blots of ether-a-go-go-related gene (ERG) protein in three RA and corresponding LA regions showed significantly greater ERG expression in LA. AP duration (APD) was shorter in the LA versus RA in both isolated cells and multicellular preparations, and the effective refractory period (ERP) was shorter in the LA compared with the RA in vivo. Dofetilide had significantly larger APD- and ERP-increasing effects in the LA compared with RA, and LA-RA repolarization differences were eliminated by exposure to dofetilide. We conclude that LA myocytes have larger I(Kr) than do RA myocytes, contributing importantly to the shorter APD and ERP in LA. The larger LA I(Kr) may participate in the ability of the LA to act as a "driver region" for AF, with potentially important implications for understanding AF mechanisms and antiarrhythmic therapy.

Action Potentials↗

Electrophysiological characteristics and catheter ablation in patients with paroxysmal right atrial fibrillation.

BACKGROUND: Catheter ablation of the right atrial (RA) substrate has had variable efficacy in curing paroxysmal atrial fibrillation (PAF), suggesting that RA substrate ablation can play an important role in the treatment of atrial fibrillation (AF) in some patients. The aim of this study was to investigate the electrophysiological characteristics and ablation strategy and its results in a specific group of patients with paroxysmal RA-AF. METHODS AND RESULTS: The study population consisted of 13 patients (8 men; age, 64+/-15 years) with drug-refractory (2+/-1 drugs), frequent episodes of PAF. Provocation maneuvers did not reveal any ectopic beat-initiating AF. However, rapid atrial pacing easily induced AF. Activation mapping during sinus rhythm, atrial pacing, and AF was visualized by using a noncontact mapping system. Noncontact mapping revealed RA reentry (6 patients with single-loop circuits and 7 with double-loop circuits) with conduction through channels between lines of block, crista terminalis gaps, and the cavotricuspid isthmus, which could be identified during sinus rhythm and atrial pacing, resulting in fibrillatory conduction in other parts of the RA. The consistency of wavefront activation was confirmed by frequency analysis from equally distributed mapping sites in the RA. Short lines of ablation lesions were aimed at the conduction channels between the lines of block, crista terminalis gaps, and the cavotricuspid isthmus, resulting in bidirectional block. AF was eliminated in 11 (85%) of 13 patients, and those 11 patients with acute success were free of AF without any antiarrhythmic drugs during the long-term follow-up period (16+/-6 months). CONCLUSIONS: RA ablation still can cure selected patients with PAF. Linear ablation of the RA substrate guided by the electrophysiological characteristics of RA-AF is an effective approach for treating this specific group of patients with AF.

Aged↗

Structural atrial remodeling alters the substrate and spatiotemporal organization of atrial fibrillation: a comparison in canine models of structural and electrical atrial remodeling.

Several animal models of atrial fibrillation (AF) have been developed that demonstrate either atrial structural remodeling or atrial electrical remodeling, but the characteristics and spatiotemporal organization of the AF between the models have not been compared. Thirty-nine dogs were divided into five groups: rapid atrial pacing (RAP), chronic mitral regurgitation (MR), congestive heart failure (CHF), methylcholine (Meth), and control. Right and left atria (RA and LA, respectively) were simultaneously mapped during episodes of AF in each animal using high-density (240 electrodes) epicardial arrays. Multiple 30-s AF epochs were recorded in each dog. Fast Fourier transform was calculated every 1 s over a sliding 2-s window, and dominant frequency (DF) was determined. Stable, discrete, high-frequency areas were seen in none of the RAP or control dogs, four of nine MR dogs, four of six CHF dogs, and seven of nine Meth dogs in either the RA or LA or both. Average DFs in the Meth model were significantly greater than in all other models in both LA and RA except LA DFs in the RAP model. The RAP model was the only one with a consistent LA-to-RA DF gradient (9.5 +/- 0.2 vs. 8.3 +/- 0.3 Hz, P < 0.00005). The Meth model had a higher spatial and temporal variance of DFs and lower measured organization levels compared with the other AF models, and it was the only model to show a linear relationship between the highest DF and dispersion (R(2) = 0.86). These data indicate that structural remodeling of atria (models known to have predominantly altered conduction) leads to an AF characterized by a stable high-frequency area, whereas electrical remodeling of atria (models known to have predominantly shortened refractoriness without significant conduction abnormalities) leads to an AF characterized by multiple high-frequency areas and multiple wavelets.

Animals↗

A preliminary study of cardiopulmonary resuscitation by circumferential compression of the chest with use of a pneumatic vest.

BACKGROUND: More than 300,000 people die each year of cardiac arrest. Studies have shown that raising vascular pressures during cardiopulmonary resuscitation (CPR) can improve survival and that vascular pressures can be raised by increasing intrathoracic pressure. METHODS: To produce periodic increases in intrathoracic pressure, we developed a pneumatically cycled circumferential thoracic vest system and compared the results of the use of this system in CPR (vest CPR) with those of manual CPR. In phase 1 of the study, aortic and right-atrial pressures were measured during both vest CPR (60 inflations per minute) and manual CPR in 15 patients in whom a mean (+/- SD) of 42 +/- 16 minutes of initial manual CPR had been unsuccessful. Vest CPR was also carried out on 14 other patients in whom pressure measurements were not made. In phase 2 of the study, short-term survival was assessed in 34 additional patients randomly assigned to undergo vest CPR (17 patients) or continued manual CPR (17 patients) after initial manual CPR (duration, 11 +/- 4 minutes) had been unsuccessful. RESULTS: In phase 1 of the study, vest CPR increased the peak aortic pressure from 78 +/- 26 mm Hg to 138 +/- 28 mm Hg (P < 0.001) and the coronary perfusion pressure from 15 +/- 8 mm Hg to 23 +/- 11 mm Hg (P < 0.003). Despite prolonged unsuccessful manual CPR, spontaneous circulation returned with vest CPR in 4 of the 29 patients. In phase 2 of the study, spontaneous circulation returned in 8 of the 17 patients who underwent vest CPR as compared with only 3 of the 17 patients who received continued manual CPR (P = 0.14). More patients in the vest-CPR group than in the manual-CPR group were alive 6 hours after attempted resuscitation (6 of 17 vs. 1 of 17) and 24 hours after attempted resuscitation (3 of 17 vs. 1 of 17), but none survived to leave the hospital. CONCLUSIONS: In this preliminary study, vest CPR, despite its late application, successfully increased aortic pressure and coronary perfusion pressure, and there was an insignificant trend toward a greater likelihood of the return of spontaneous circulation with vest CPR than with continued manual CPR. The effect of vest CPR on survival, however, is currently unknown and will require further study.

Aorta↗

Effects of age and physiologic variables on right ventricular filling dynamics in normal subjects.

The reference values for right ventricular (RV) filling of normal persons and the effects of physiologic variables in a large series have not been described. The objective of this study was to characterize superior vena cava, hepatic vein, and RV inflow Doppler measurements in a large normal reference group to reflect the aging process, gender, heart rate, and effects of respiration. We prospectively performed pulsed-wave Doppler echocardiography of the superior vena cava, hepatic vein, and RV inflow during inspiration, expiration, and apnea in 115 healthy volunteers (62 women and 53 men) ranging in age from 21 to 84 years (mean +/- SEM 48 +/- 17). For analysis, the study subjects were classified by age into 2 groups: those < 50 years of age (group 1; n = 60) and those > or = 50 years of age (group 2; n = 55). Multiregression models were used to assess the influence of age, gender, and heart rate on Doppler variables. There were important differences in superior vena cava and RV inflow between the 2 groups. Group 2 had a greater superior vena cava peak atrial flow velocity (16 +/- 3 vs 13 +/- 3 cm/s), flow integrals (1.5 +/- 0.4 vs 1.1 +/- 0.3 cm), and reverse flow as a percentage of forward flow (17 +/- 6% vs 14 +/- 6%) than group 1. In group 2, peak RV inflow early filling velocity (41 +/- 8 vs 51 +/- 7 cm/s) and ratio of early filling-to-atrial filling (1.3 +/- 0.4 vs 2 +/- 0.5) were lower than that of group 1. Likewise, peak atrial filling velocity was higher (33 +/- 8 vs 27 +/- 8 cm/s) and deceleration time was longer (198 +/- 23 vs 188 +/- 22 ms) in group 2. The superior vena cava and hepatic vein peak forward flow velocities were significantly higher during inspiration than during expiration and apnea. Similarly, RV inflow velocities were significantly higher during inspiration than in expiration and apnea. Multiregression analysis showed that age, gender, and heart rate had important effects on Doppler variables. Thus, this study demonstrates the effects of aging and normal physiologic variable flow velocities in the superior vena cava, hepatic veins, and RV inflow in a large series of normal subjects.

Adult↗

Right atrial and right ventricular transmural pressures in dogs and humans. Effects of the pericardium.

BACKGROUND: To determine the transmural pressure-dimension relations of the right atrium (RA) and right ventricle (RV) before and after pericardiectomy, six open-chest dogs were instrumented with pericardial balloons placed over the RA and RV free walls. METHODS AND RESULTS: PA appendage dimensions and RV free-wall segment lengths were measured using sonomicrometry. Intact-pericardium RA and RV transmural pressures were calculated by subtracting the pericardial pressures (measured using balloons) from the cavitary pressures. Pooled data from six animals with pericardium intact indicate that at RA and RV cavitary pressures of 5, 10, and 15 mm Hg, RV pericardial pressure was 4.3 +/- 0.3, 8.6 +/- 1.0, and 13.3 +/- 1.5 mm Hg, respectively, and RA pericardial pressure was 4.8 +/- 0.3, 9.6 +/- 0.6, and 14.6 +/- 0.6 mm Hg, respectively (mean +/- SD). With calculated unstressed dimensions, the cavity dimension data were normalized to strain (in percent). We determined that in the dog, RV strain would increase by 14% and RA by 68% to maintain cavitary pressure at 10 mm Hg on pericardiectomy. To compare these results with clinical data, RV (n = 7) and RA (n = 6) transmural pressures were measured using balloons in patients (age, 19 to 76 years) undergoing cardiac surgery. RA transmural pressure of six patients was 1.0 +/- 1.5 mm Hg when central venous pressures (CVPs) ranged from 3 to 16 mm Hg. RV transmural pressure equaled 1.2 +/- 1.9, 2.3 +/- 1.9, and 3.4 +/- 2.0 mm Hg when CVP was 5, 10, and 15 mm Hg, respectively. CONCLUSIONS: Pericardial constraint (as evaluated by the ratio of pericardial to intracavitary pressures when CVP is 10 mm Hg) accounted for 96% of RA cavitary pressure in the dog and 89% in humans and at least 86% of RV cavitary pressure in the dog and 77% in humans.

Adult↗

Action potential remodeling in the human right atrium with chronic lone atrial fibrillation.

It has been shown in animal experiments that recurrent induction of atrial fibrillation (AF) or long-lasting atrial pacing causes a shortening of the atrial effective refractory period (ERP) and action potential duration (APD) and a loss of their physiological adaptation to rate. Much remains to be clarified as to the electrical remodeling in human patients with chronic AF. We recorded monophasic action potentials (MAPs) from the right atrium at pacing cycle lengths (CLs) of 300, 333, 400, 500, 600, and 750 ms after external cardioversion in 13 patients with chronic lone AF. Their configuration was compared with those obtained from 13 control patients. APDs at 50% and 90% repolarization (APD50, APD90) at the shortest CL (300 ms) in control and AF patients were 131 +/- 14, 211 +/- 19 ms and 136 +/- 12, 210 +/- 22 ms, respectively (mean +/- SD). APDs in control patients increased linearly with increases of CL, reaching maximal values of 174 +/- 30 ms (APD50) and 277 +/- 38 ms (APD90) at a CL of 750 ms. In AF patients, the steady-state CL-APD relation was shifted downward and flattened at CLs > 500 ms; APD50 and APD90 at a CL of 750 ms were 158 +/- 19 ms, 232 +/- 28 ms, respectively. APD90s at CLs of 600 and 750 ms were significantly shorter in AF than in control patients. No statistically significant difference was obtained in APD50 between the two groups at any CL tested. MAP configuration in AF patients was characterized by an acceleration of the late repolarization. The difference between APD90 and APD50 (APD90-50) in control patients was increased with increases of CL, reaching a plateau at a CL of 600 ms. This CL dependent slowing of the late repolarization of MAPs was abolished in AF patients. The atrial ERP, measured at CLs of 400 and 600 ms, showed changes parallel to those of APD90. ERP at a CL of 600 ms in AF patients (224 +/- 13 ms) was significantly shorter than that in control patients (247 +/- 25 ms). We conclude that chronic lone AF leads to electrical remodeling in the human atrium, which causes a loss of rate response of the late repolarization of action potential, leading to a shortening of APD and ERP at slower heart rates.

Action Potentials↗

Rate-dependent conduction block of the crista terminalis in patients with typical atrial flutter: influence on evaluation of cavotricuspid isthmus conduction block.

BACKGROUND: The crista terminalis (CT) has been identified as the posterior boundary of typical atrial flutter (AFL) in the lateral wall (LW) of the right atrium (RA). To study conduction properties across the CT, rapid pacing was performed at both sides of the CT after bidirectional conduction block was achieved in the cavotricuspid isthmus by radiofrequency catheter ablation. METHODS AND RESULTS: In 22 patients (aged 61+/-7 years) with AFL (cycle length, 234+/-23 ms), CT was identified during AFL by double electrograms recorded between the LW and posterior wall (PW). After the ablation procedure, decremental pacing trains were delivered from 600 ms to 2-to-1 local capture at the LW and PW or coronary sinus ostium (CSO). At least 5 bipolar electrograms were recorded along the CT from the high to the low atrium next to the inferior vena cava. No double electrograms were recorded during sinus rhythm in that area. Complete transversal conduction block all along the CT (detected by the appearance of double electrograms at all recording sites and craniocaudal activation sequence on the side opposite to the pacing site) was observed in all patients during pacing from the PW or CSO (cycle length, 334+/-136 ms), but it was fixed in only 4 patients. During pacing from the LW, complete block appeared at a shorter pacing cycle length (281+/-125 ms; P<0.01) and was fixed in 2 patients. In 3 patients, complete block was not achieved. CONCLUSIONS: These data suggest the presence of rate-dependent transversal conduction block at the crista terminalis in patients with typical AFL. Block is usually observed at longer pacing cycle lengths with PW pacing than with LW pacing. This difference may be a critical determinant of the counterclockwise rotation of typical AFL.

Aged↗

Characterization of the 5-HT4 receptor mediating tachycardia in piglet isolated right atrium.

1. In order to explore whether 5-HT4 receptor subtypes exist, we have characterized further the 5-HT4 receptor that mediates tachycardia in the piglet isolated right atrium. All experiments were carried out in the presence of propranolol (400 nM) and cocaine (6 microM). We used tryptamine derivatives, substituted benzamides and benzimidazolone derivatives as pharmacological tools. 2. Tachycardia responses to 5-hydroxytryptamine (5-HT) were mimicked by other tryptamine derivatives with the following order of potency: 5-HT > 5-methoxytryptamine alpha-methyl-5-HT = bufotenine bufotenine > 5-carboxamidotryptamine = tryptamine (after treatment with pargyline) > 5-methoxy-N,N-dimethyltryptamine > 2-methyl-5-HT. 3. The substituted benzamides were all partial agonists relative to 5-HT except (-)-zacopride which was a full agonist. The stimulant potency order was renzapride > cisapride = (-)-zacopride > metoclopramide > (+)-zacopride. 4. The benzimidazolone derivatives had contrasting effects. BIMU 8 (endo-N-(8-methyl-8-azabicyclo[3.2.1]oct-3-yl)-2,3-dihydro-(1-methyl(eth yl- 2-oxo-1H-benzimidazole-1-carboxamide hydrochloride) was a full agonist relative to 5-HT whilst BIMU 1 (endo-N-(8-methyl-8-azabicyclo[3.2.1]oct-3-yl)-2,3-dihydro-3-ethyl-2-oxo - 1H-benzimidazole-1-carboxamide hydrochloride) was a partial agonist with low intrinsic activity compared to 5-HT but had similar potency. We estimated a pKB of 7.9 for BIMU 1 antagonism of 5-HT-induced tachycardia. DAU 6215 (N-endo-8-methyl-8-azabicyclo[3.2.1]-oct-3-yl)-2,3-dihydro-2-oxo-lH-benzimidazole-l-carboxamide, hydrochloride) had no chronotropic activity and was found to be a simple competitive antagonist with a pKB of 7.15.SB 203186 (1-piperidinyl)ethyl lH-indole 3-carboxylate) was a potent antagonist with a pKB of 8.3.The affinity of SB 203186 was approximately 20 times higher than that of tropisetron (ICS 205-930;pKB= 6.9) and DAU 6215 (pKB= 7.0). GR1 13808 (([1-[2-[methylsulphonyl amino]ethyl]-4-piperidinyl]methyl 1-methyl-1H-indole-3-carboxylate) and SDZ 205-557 ((2-diethylaminoethyl)2-methoxy-4-amino-5-chloro-benzoate) also antagonized 5-HT-induced tachycardia but not by simple competitive blockade.6. The sinoatrial 5-HT4 receptor in the piglet has a pharmacological profile that correlates well with 5-HT4 receptors characterized in rat oesophagus, guinea-pig ileum and colon, mouse embryonic colliculi neurones and human atrium.

Animals↗

Acute and chronic effects of nitrendipine in patients with precapillary pulmonary hypertension due to pulmonary fibrosis.

Eleven patients with histologically confirmed fibrosis of the lung were investigated for the effects of the dihydropyridine calcium antagonist nitrendipine on pulmonary hemodynamics. After 5 mg of acute sublingual nitrendipine, mean pulmonary artery pressure was significantly lowered (p less than or equal to 0.05) from 32 +/- 3 to 29 +/- 3 mmHg at rest, and significantly lowered (p less than or equal to 0.05) during exercise from 55 +/- 4 to 49 +/- 4 mmHg. Short-term oxygen application at rest significantly reduced this parameter to 28 +/- 3 mmHg (p less than or equal to 0.001). Nitrendipine lowered total pulmonary vascular resistance during both rest (from 412 +/- 50 to 351 +/- 49 dyn.s.cm-5; p less than or equal to 0.05), although it did not affect pulmonary arteriolar resistance. Also, oxygen treatment at rest influenced only total pulmonary vascular resistance (reduction from 412 +/- 50 to 373 +/- 48 dyn.s.cm-5; p less than or equal to 0.01), but not pulmonary arteriolar resistance. Pressure-flow curves, which were derived from cardiac output at rest and during exercise and from the corresponding gradient between mean pulmonary artery pressure and pulmonary capillary wedge pressure, remained unchanged by acute medication. Since a change in arterial oxygen partial pressure was not noticed after nitrendipine, arteriovenous shunting or a worsening of ventilation perfusion relationships can be excluded. Long-term (3 weeks) treatment (double-blind parallel design) with 10 mg of nitrendipine (4 patients) once daily showed no advantage in comparison to placebo (6 patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Changes in pulmonary hemodynamics predict benefits in exercise capacity after ACE inhibition in patients with mild to moderate congestive heart failure.

Several causes may affect the efficacy of angiotensin-converting enzyme (ACE) inhibitors in congestive heart failure (CHF). The present study was undertaken to identify what factors might predict benefits in exercise capacity after ACE inhibition in 22 patients with mild to moderate CHF. All patients underwent hemodynamic evaluation before and following an oral dose of quinapril (20 mg). They were then treated daily with 20 mg of quinapril and underwent exercise stress test off-drugs 1 day and 6 months later. Patients were grouped according to their relative changes in vascular resistances after quinapril: Group A (n = 15) showed a greater decrease in pulmonary vascular resistance (PVR) than in systemic vascular resistance (SVR) (% delta PVR/% delta SVR > 1). The opposite occurred in Group B (n = 7). Comparison of pretreatment baseline features revealed that the two groups had similar biochemical and hormonal variables, cardiac index, and SVR. Conversely, Group A patients had higher (p < 0.05) pulmonary artery pressure and PVR compared with Group B patients. Following quinapril, Group A patients showed a greater (p < 0.05) increase in cardiac index than Group B patients, despite a similar reduction in SVR. Accordingly, 1-day drug treatment significantly (p < 0.001) increased exercise duration in Group A (+29%), but not in Group B patients (+7%). Benefits in exercise capacity were still significant (p < 0.001) 6 months later.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Left ventricular diastolic collapse in low-pressure cardiac tamponade.

A case of systemic hypotension with volume depletion not responding to intravenous fluids was found to have features of cardiac tamponade on two-dimensional (2-D) echocardiography. Intracardiac pressures were normal on cardiac catheterization. An interesting observation was the presence of left ventricular (LV) collapse on 2-D echocardiography. To the authors' best knowledge, such a case of low pressure cardiac tamponade with LV collapse has not been reported earlier.

Adolescent↗

The effect of transient balloon occlusion of the mitral valve on left atrial appendage blood flow velocity and spontaneous echo contrast.

BACKGROUND: Spontaneous echo contrast (SEC) is a phenomenon that is commonly seen in areas of blood stasis. It is a slowly moving, cloud-like swirling pattern of "smoke" or increased echogenicity recorded on echocardiography. SEC is commonly seen in the left atrium of patients with mitral stenosis or atrial fibrillation. The presence of SEC has been shown to be a marker of increased thromboembolic risk. HYPOTHESIS: By using transesophageal echocardiography during percutaneous balloon mitral valvotomy (PBMV), the study investigated the relationship between SEC and varying left atrial appendage (LAA) blood flow velocity in the human heart. METHODS: Thirty-five patients with rheumatic mitral stenosis underwent percutaneous balloon mitral valvotomy with intraoperative transesophageal echocardiography monitoring. We alternatively measured LAA velocities and observed the left atrium for various grades of SEC (0 = none to 4 = severe) before and after each balloon inflation. RESULTS: Left atrial appendage maximal ejection velocity was reduced from 35 +/- 14 to 6 +/- 2 mm/s at peak balloon inflation and increased to 40 +/- 16 mm/s after balloon deflation. In comparison with the values before balloon inflation and after balloon deflation, LAA velocities were significantly lower (p < 0.001). New or increased SEC grade was observed during 54 of 61 (88%) inflations and unchanged in 7 (12%) inflations at peak balloon inflation. Spontaneous echo contrast became lower in grade after 55 balloon deflations (90%), completely disappeared after 18 deflations (30%), and remained unchanged after 6 deflations (10%). The mean time to achieve maximal SEC grade (2.5 +/- 1.2 s) coincided with the mean time to trough LAA velocities (2.3 +/- 1.1 s) after balloon inflation. Upon deflation, the mean time to lowest SEC grade (2.9 +/- 1.8 s) coincided with mean time to achieve maximal LAA velocities (2.7 +/- 1.6 s). CONCLUSION: During balloon inflation, the severity of SEC was enhanced with corresponding reduction in LAA flow velocity. Upon balloon deflation, SEC lightens or disappears with increase in LAA flow velocity.

Adolescent↗

Atrial electrophysiologic abnormalities in patients with Wolff-Parkinson-White syndrome but without paroxysmal atrial fibrillation.

BACKGROUND: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. HYPOTHESIS: The purpose of this study was to analyze the atrial electrophysiologic abnormalities and vulnerability to develop atrial fibrillation (AF) in patients with WPW syndrome but with no previous history of PAF. METHODS: We investigated atrial electrophysiologic abnormalities and vulnerability to AF in patients with WPW syndrome but without PAF. An electrophysiologic study was performed in 28 patients with WPW syndrome, 23 with atrioventricular nodal reentrant tachycardia (AVNRT) and 25 with other arrhythmias (control), all of whom had no history of PAF. The following atrial excitability parameters were assessed: effective refractory period (ERP), spontaneous or paced (A1) and extrastimulated (A2) atrial electrogram widths, percent maximum atrial fragmentation (%MAF; A2/A1 x 100), wavelength index (WLI; ERP/A2), and inducibility of AF. RESULTS: The ERP tended to be shorter in patients with WPW syndrome and in those with AVNRT than in the control group. The %MAF increased (154 +/- 33 vs. 137 +/- 23%, p < 0.05) and WLI decreased (2.7 +/- 0.8 vs. 3.4 +/- 1.0, p < 0.05) significantly in patients with WPW syndrome compared with the control group; however, these parameters in patients with AVNRT showed intermediate values. Atrial fibrillation was more inducible in patients with WPW syndrome (4/28 [14.3%]) than in those with AVNRT (4.3% [1/23]) and the control group (0/25 [0%]). With respect to patients with WPW syndrome and with and without inducible AF, the %MAF increased (195 +/- 23 vs. 148 +/- 30%, p < 0.01) and the WLI decreased (2.2 +/- 0.3 vs. 2.9 +/- 0.9, p < 0.05) in subjects with inducible AF. CONCLUSIONS: Atrial electrophysiologic abnormalities, especially atrial conduction delays, are more prominent in patients with WPW syndrome, even if they had no previous history of PAF. These abnormalities may play an important role in determining the vulnerability to AF.

Adolescent↗

Accuracy of four indirect methods of blood pressure measurement, with hemodynamic correlations.

In 38 adults undergoing cardiac surgery, 4 indirect blood pressure techniques were compared with brachial arterial blood pressure at predetermined intervals before and after cardiopulmonary bypass. Indirect blood pressure measurement techniques included automated oscillometry, manual auscultation, visual onset of oscillation (flicker) and return-to-flow methods. Hemodynamic measurements or calculations included heart rate, cardiac index, stroke volume index, and systemic vascular resistance index. Indirect and intraarterial blood pressure values were compared by simple linear regression by patient and measurement period. Measurement errors (arterial minus indirect blood pressure) were calculated, and stepwise regression assessed the relationship between measurement error and heart rate, cardiac index, stroke volume index, and systemic vascular resistance index. Indirect to intraarterial blood pressure correlation coefficients varied over time, with the strongest correlations often occurring at the first and last measurement periods (preinduction and 60 minutes after cardiopulmonary bypass), particularly for systolic blood pressure. Within-patient correlations between indirect and arterial blood pressure varied widely--they were consistently high or low in some patients. In other patients, correlations were especially weak with a particular indirect blood pressure method for systolic, mean, or diastolic blood pressure; in some cases indirect blood pressure was inadequate for clinical diagnosis of acute blood pressure changes or trends. The mean correlations between indirect and direct blood pressure values were, for systolic blood pressure: 0.69 for oscillometry, 0.77 for auscultation, 0.73 for flicker, and 0.74 for return-to-flow; for mean blood pressure: 0.70 for oscillometry and 0.73 for auscultation; and for diastolic blood pressure: 0.73 for oscillometry and 0.69 for auscultation. The mean measurement errors (arterial minus indirect values) for the individual indirect blood pressure methods were, for systolic: 0 mm Hg for oscillometry, 9 mm Hg for auscultation, -5 mm Hg for flicker, 7 mm Hg for return-to-flow; for mean: -6 mm Hg for oscillometry, and -3 mm Hg for auscultation; and for diastolic: -9 mm Hg for oscillometry and -8 mm Hg for auscultation. Mean measurement error for systolic blood pressure was thus least with automated oscillometry and greatest with manual auscultation, while standard deviations ranging from 9 to 15 mm Hg confirmed the highly variable nature of single indirect blood pressure measurements. Except for oscillometric diastolic blood pressure, a combination of systemic hemodynamics (heart rate, stroke volume index, systemic vascular resistance index, and cardiac index) correlated with each indirect blood pressure measurement error, which suggests that particular numeric ranges of these variables minimize measurement error.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Haemodynamic responses to tracheal intubation following etomidate and fentanyl for anaesthetic induction.

The haemodynamic response to anaesthetic induction and tracheal intubation was studied in 29 patients undergoing elective myocardial revascularization surgery. All patients included in the study were anaesthetized with etomidate, 0.3 mg.kg-1. The patients were randomized to three groups: Group I received fentanyl, 2.5 micrograms.kg-1; Group II received fentanyl, 5 micrograms.kg-1; and Group III received fentanyl, 10 micrograms.kg-1. Haemodynamic variables were measured at baseline (awake), after anaesthetic induction, and at one, three, five, and ten minutes after tracheal intubation. The number of patients with haemodynamic responses to intubation (> 20% increase in heart rate or mean arterial pressure) was greater (P < 0.05) in Group I than in Groups II and III. Statistically significant, but clinically minor, decreases in mean arterial pressure and cardiac output occurred in all groups at the last three study times. The frequency of involuntary muscle movements was 14%, and all of these events occurred in patients in Group I. In conclusion, the authors recommend using fentanyl, 5-10 micrograms.kg-1 to blunt the haemodynamic response to tracheal intubation following anaesthetic induction with etomidate, 0.3 mg.kg-1.

Aged↗

Alfentanil-midazolam anaesthesia has no electrophysiological effects upon the normal conduction system or accessory pathways in patients with Wolff-Parkinson-White syndrome.

The effects of alfentanil-midazolam anaesthesia upon the electrophysiologic (EP) properties of normal atrioventricular (A-V) and accessory pathway (AP) conduction were studied in eight patients with Wolff-Parkinson-White syndrome during accessory pathway surgical ablation. The presence of an AP was confirmed by preoperative EP studies. Anaesthesia was induced with alfentanil (50 micrograms.kg-1) and midazolam (0.15 mg.kg-1) and maintained with an alfentanil infusion (2 micrograms.kg-1.min-1) and intermittent boluses of midazolam (1-2 mg q 15 min, PRN). Following sternotomy, a baseline EP study was performed which consisted of effective refractory period (ERP) and shortest cycle length (SCC) measurement during antegrade conduction in the AV and AP, as well as during retrograde conduction in the AP. Comparison with preoperative EP studies indicated that the administration of alfentanil-midazolam anaesthesia had no effect upon conduction or ERP in either pathway. Haemodynamic stability occurred throughout the surgical procedure with no tachyarrhythmias. We conclude that a combination of alfentanil-midazolam is suitable for general anaesthesia in patients undergoing ablative procedures for accessory pathways.

Adult↗