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PubMed1994

[Effect of alpha 1-adrenoceptor subtypes on beta-adrenoceptor mediated positive inotropic response in rat left atria].

The distribution of the alpha 1-adrenoceptor (alpha 1-AR) subtypes and the effects of activation of alpha 1-AR subtypes on the beta-adrenoceptor (beta-AR) mediated positive inotropic response were investigated. The radioligand binding assays indicated that the Bmax and Kd values were 11.7 +/- 18 fmol/mg.protein and 86.0 +/- 9.6 pmol/L respectively. Pretreatment of the preparations with 20 mumol/L chloroethylclonidine (CEC) which inactivated alpha 1B subtype, decreased the Bmax to 45.7 +/- 5.2 fmol/mg.protein (P < 0.01). The inhibition curves of 5-methyl-urapidil were best fitted to two site model and indicated that alpha 1A subtype took 28.5% of total 125IBE specific binding sites. In the functional experiments, norepinephrine (NE) induced a positive inotropic response in a concentration dependent manner by activation of both beta- and alpha 1-AR. The concentration-response curves (CRC) for NE were shifted rightward after the pretreatment of the preparations with 20 mumol/L CEC, but leftward in the presence of 1 nmol/L WB4101. In the presence of 10 mumol/L phentolamine which inactivated both alpha 1-AR subtypes, the CRC for NE were shifted leftward. When alpha 1-AR was activated by phenylephrine the CRC for isoproterenol (selective beta-AR agonist) were shifted rightward. The results suggested that the alpha 1B subtype enhanced while the alpha 1A subtype inhibited the beta-AR mediated positive inotropic response. When both alpha 1A and alpha 1B subtypes were activated simultaneously the alpha 1A subtype showed a dominate role.

Animals↗
PubMed1991

Nitrous oxide does not worsen myocardial ischaemia following beta-receptor blockade in isoflurane anaesthetized dogs.

The effect of nitrous oxide (N2O) on ischaemic myocardium was investigated in the presence of beta-receptor blockade. Three anaesthetics were compared in each of six dogs: isoflurane 1.8% alone, isoflurane 1.4% with 50% N2O, and isoflurane 1.8% with 50% N2O. Heart rate (HR), systolic aortic blood pressure (SBP), and left atrial pressure (LAP) were held constant during the three treatments. The left anterior descending coronary artery (LAD) was cannulated and perfused with an autoperfusion circuit. Systolic segment length was measured with a sonomicrometer in the LAD and circumflex regions. Regional myocardial blood flow was measured using radioactive microspheres. Propranolol was administered intravenously and then measurements were made during imposition of a stenosis on the perfusion circuit sufficient to decrease systolic shortening by 30%. The substitution of 50% N2O for 0.4% isoflurane had no effect on systolic shortening or transmural myocardial blood flow in the ischaemic or normal region. When N2O was added to 1.8% isoflurane, systolic shortening decreased by 34.6% in the ischaemic and 57.3% in the normally perfused region, while transmural myocardial blood flow distribution did not change significantly. The decrease in shortening was therefore not due to increased ischaemia. These results were similar to those of a previous experiment which was identical except that beta-blockade was absent. It is concluded that beta-receptor blockade does not markedly alter the response of normal or ischaemic myocardium to N2O.

Anesthesia, Inhalation↗
PubMed2006

Wave intensity analysis of left atrial mechanics and energetics in anesthetized dogs.

The left atrium (LA) acts as a booster pump during late diastole, generating the Doppler transmitral A wave and contributing incrementally to left ventricular (LV) filling. However, after volume loading and in certain disease states, LA contraction fills the LV less effectively, and retrograde flow (i.e., the Doppler Ar wave) into the pulmonary veins increases. The purpose of this study was to provide an energetic analysis of LA contraction to clarify the mechanisms responsible for changes in forward and backward flow. Wave intensity analysis was performed at the mitral valve and a pulmonary vein orifice. As operative LV stiffness increased with progressive volume loading, the reflection coefficient (i.e., energy of reflected wave/energy of incident wave) also increased. This reflected wave decelerated the forward movement of blood through the mitral valve and was transmitted through the LA, accelerating retrograde blood flow in the pulmonary veins. Although total LA work increased with volume loading, the forward hydraulic work decreased and backward hydraulic work increased. Thus wave reflection due to increased LV stiffness accounts for the decrease in the A wave and the increase in the Ar wave measured by Doppler.

Animals↗
PubMed2001

Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans.

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 +/- 1 mmHg, P < 0.05) and less during WI + NS (4 +/- 1 mmHg) and NS (3 +/- 1 mmHg). The decrease in heart rate (HR) by 13 +/- 1 beats/min (P < 0.05) and the increase in arterial pulse pressure (PP) by 17 +/- 4 mmHg (P < 0.05) during supine was more pronounced (P < 0.05) than during WI + NS (10 +/- 2 beats/min and 7 +/- 2 mmHg, respectively) and WI (8 +/- 2 beats/min and 6 +/- 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS (P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change.

Adult↗
PubMed2005

Techniques, evaluation, and consequences of linear block at the left atrial roof in paroxysmal atrial fibrillation: a prospective randomized study.

BACKGROUND: There are no reports describing the technique, electrophysiological evaluation, and clinical consequences of complete linear block at roofline joining the superior pulmonary veins (PVs) in patients with paroxysmal atrial fibrillation (AF). METHODS AND RESULTS: Ninety patients with drug-refractory paroxysmal AF undergoing radiofrequency ablation were prospectively randomized into 2 ablation strategies: (1) PV isolation (n=45) or (2) PV isolation in combination with linear ablation joining the 2 superior PVs (roofline; n=45). In both groups, the cavotricuspid isthmus, fragmented peri-PV-ostial electrograms, and spontaneous non-PV foci were ablated. Roofline ablation was performed at the most cranial part of the left atrium (LA) with complete conduction block demonstrated during LA appendage pacing by the online mapping of continuous double potential and an activation detour propagating around the PVs to activate caudocranially the posterior wall of the LA. The effect of ablation at the LA roof was evaluated by the change in fibrillatory cycle length, termination and noninducibility of AF, and clinical outcome. PV isolation was achieved in all patients with no significant differences in the radiofrequency duration, fluoroscopy, or procedural time between the groups. Roofline ablation required 12+/-6 (median 11, range 3 to 25) minutes of radiofrequency energy delivery with a fluoroscopic duration of 7+/-2 minutes and was performed in 19+/-7 minutes. Complete block was confirmed in 43 patients (96%) and resulted in an activation delay that was shorter circumventing the left than the right PVs during LA appendage pacing (138+/-15 versus 146+/-25 ms, respectively; P=0.01). Roofline ablation resulted in a significant increase in the fibrillatory cycle length (198+/-38 to 217+/-44 ms; P=0.0005), termination of arrhythmia in 47% (8/17), and subsequent noninducibility of AF in 59% (10/17) of the patients inducible after PV isolation. However, LA flutter, predominantly perimitral, could be induced in 10 patients (22%) after roofline ablation. At 15+/-4 months, 87% of the roofline group and 69% with PV isolation alone are arrhythmia free without antiarrhythmics (P=0.04). CONCLUSIONS: This prospective randomized study demonstrates the feasibility of achieving complete linear block at the LA roof. Such ablation resulted in the prolongation of the fibrillatory cycle, termination of AF, and subsequent noninducibility and is associated with an improved clinical outcome compared with PV isolation alone.

Adult↗
PubMed2003

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling.

Acute myocardial ischemia has been associated with abnormal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to postsystolic shortening of ischemic apical segments, which leads to reversal of early diastolic apical flow. Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and left atrium and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by strain Doppler echocardiography (SDE) were assessed from an apical view. Measurements were taken before and after 5 min of left anterior descending coronary artery (LAD) occlusion. In four dogs, we measured the pressure difference between the LV apex and outflow tract. At baseline, peak early diastolic flow velocities in the distal one-third of the LV were directed toward apex (9.2 +/- 1.6 cm/s). After LAD occlusion, the velocities reversed (-2.3 +/- 0.4 cm/s, P < 0.01), indicating that blood was ejected from the apex toward the base during early filling. This interpretation was confirmed by wall motion analysis, which showed postsystolic shortening of apical myocardial segments. The postsystolic shortening represented 9.7 +/- 1.7% (P < 0.01) and 14.2 +/- 2.4% (P < 0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. In the present model, acute LAD occlusion resulted in reversal of early diastolic apical flow, and this was attributed to postsystolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined.

Animals↗
PubMed1995

Pulmonary venous congestion augments respiratory motoneuronal responses to cigarette smoke in rabbit.

We examined the effects of cigarette smoke inhaled during subthreshold pulmonary venous congestion (sPVC) on phrenic nerve (PN) and unit activity in the ventral respiratory group in rabbits. sPVC was achieved by inflating a balloon in the left atrium. Inhalation of low-nicotine cigarette smoke produced initial prolonged bursts in 34 (19 bulbospinal) out of 43 inspiratory (I) cells and in PN. Smoke decreased the activity of 29 out of 36 expiratory (E) cells (27 of 32 early E and 2 of 4 late E). The prolonged PN bursts occasionally progressed to doublets superimposed over regularly occurring PN bursts. sPVC augmented the smoke effects: I cells displayed greater increases in spikes/burst (27 vs. 12%; P = 0.02) and burst duration (42 vs. 20%; P = 0.02) and greater decreases in interburst interval (34 vs. 10%; P < 0.02); PN displayed greater increases in I time (40 vs. 27%; P < 0.05), greater decreases in E time (18 vs. 26%; P < 0.05), and a greater incidence and duration of time of PN doublets (29 +/- 9 vs. 9 +/- 4 s; P < 0.03); E cells displayed greater decreases in spikes/burst (43 vs. 29%; P = 0.01) and burst durations (35 vs. 18%; P < 0.01). Smoke-induced respiratory changes may be exaggerated during sPVC.

Animals↗
PubMed2002

Comparison of left atrial dimensions by transesophageal and transthoracic echocardiography.

Left atrial (LA) size, as determined by transthoracic echocardiography (TTE), predicts the risk of atrial fibrillation and stroke and the success of cardioversion. Transesophageal echocardiography (TEE) is increasingly used in these clinical situations. However, unlike TTE, measurement of LA size by TEE has not been standardized. To validate TEE measurement, we determined LA dimensions in 4 standard views by TTE at the same time in 121 patients undergoing TEE. The mid-esophageal basal short-axis view at the level of the aortic valve (TEE 30-60) was the only view in which complete visualization of a LA axis of measurement could be obtained with an acceptably high yield (97.2%). The measurement from this view provided a value that had the highest correlation between TTE and TEE (r = 0.758, P <.0001, 95% confidence interval 0.68-0.86; bias 0.37 +/- 1 cm). Overall, TEE underestimated the LA dimension by 9% compared with TTE. These results suggest that the short-axis view at the level of the aortic valve is the preferred site for measuring the LA dimension by TEE.

Adult↗
PubMed2006

Wedging the pulmonary artery catheter: changes in left atrial and pulmonary artery pressures and risk for perforation.

OBJECTIVE: Clinical and experimental data indicate that when there is lung disease, wedging the pulmonary artery catheter (PAC) could cause decreases in cardiac output and systemic arterial blood pressure and an increase in mean pulmonary artery pressure (PAP). The authors studied whether wedging would alter mean left atrial pressure (LAP), and report perforations with PACs in their unit since 1975. DESIGN: Observational study. SETTING: University hospital operating room and intensive care unit. PARTICIPANTS: Ten adult patients undergoing cardiac surgery. INTERVENTIONS: Placement of epidural catheters in the left atrium and pulmonary artery, and a PAC. MEASUREMENTS AND MAIN RESULTS: After weaning from cardiopulmonary bypass, mean LAP, mean PAP, and cardiac output were measured before and during wedging with the chest open and closed. Mean LAP decreased during wedging, from 13.5 +/- 2.8 (SD) mmHg to 13.0 +/- 3.0 mmHg (open chest) and from 15.8 +/- 3.2 mmHg to 15.3 +/- 3.1 mmHg (closed chest; p < 0.001), and mean PAP increased, from 18.8 +/- 3.5 mmHg to 19.7 +/- 3.5 mmHg (open chest) and from 21.3 +/- 4.3 mmHg to 21.9 +/- 4.2 mmHg (closed chest; p < 0.001). Mean PAP-mean LAP increased by 20% to 25%. Wedge pressure did not differ from mean LAP. Cardiac output and systemic arterial pressure did not change. Four perforations due to PACs occurred since 1975. CONCLUSIONS: In adult patients undergoing cardiac surgery, wedging of a PAC resulted in a small decrease in mean LAP and a small increase in mean PAP. The wedging maneuver carries a small risk. How wedging is performed could influence the risk for perforation.

Adult↗
PubMedDate not supplied

Echocardiographic estimation of mean left atrial pressure in a canine model of acute mitral valve insufficiency.

High mean left atrial pressure (MLAP) due to canine degenerative mitral valve disease is associated with clinically relevant morbidity and mortality. The ability to noninvasively measure MLAP would assist in the diagnosis and treatment of disease. Doppler echocardiography allows measurement of early transmitral blood flow (E) and the velocity of the mitral valve annulus (Ea). The ratio of early mitral inflow velocity to early mitral annular velocity (E: Ea) correlates well with MLAP in human subjects. We sought to determine the ability of E: Ea to predict MLAP in dogs with experimentally induced mitral regurgitation. Nine anesthetized purpose-bred dogs underwent placement of a Swan-Ganz catheter into the left atrium and recording of MLAP. Simultaneous transthoracic echocardiographic and hemodynamic studies were performed after acute chordae tendineae rupture and during IV infusion with nitroprusside (2.5-5.0 microg x kg(-1) x min(-1)) or hydralazine (1-1.5 mg/kg). Mitral regurgitant fraction, measured by single-plane angiography and thermodilution, ranged from 17% to 81%. MLAP increased from 5.4 +/- 2.5 mm Hg to 17.4 +/- 9.4 mm Hg after creation of mitral valve regurgitation (MR; P = .018). Forty sets of echocardiographic measurements were obtained from 7 dogs, and E, as well as E: Ea, were linearly related to MLAP. The R2 value for the linear regression equation containing E: Ea as the dependent variable (0.83) was greater than that for E (0.73). The 95% confidence intervals were calculated for predicting MLAP = 20 mm Hg from E:Ea, and E:Ea >9.1 or <6.0 indicated a 95% probability that MLAP was >20 mm Hg or <20 mm Hg, respectively. Echocardiography can be used to predict MLAP in isoflurane-anesthetized dogs with experimentally induced acute mitral valve insufficiency.

Animals↗
PubMed1991

Diagnostic accuracy of the resting electrocardiogram in detection and estimation of left atrial enlargement: an echocardiographic correlation in 551 patients.

The identification of LA enlargement may have important clinical implications. Previous correlations of ECG P wave morphologies associated with LA enlargement and echocardiography have been limited by the use of small numbers of patients and by the employment of M-mode echocardiography without the benefit of two-dimensional guidance. The purpose of this study was to further examine the sensitivity and specificity of various P wave morphologies (P wave greater than or equal to 110 msec, notched P greater than or equal to 40 msec, and PTFV1 greater than or equal to 40 msec.mm) for the diagnosis of LA enlargement and to determine if these waveforms may be predictive of LA size. ECGs and surface echocardiograms obtained within 1 week of each other were evaluated in 551 patients (140 normal and 411 study subjects). The various P wave morphologies were found to be poorly sensitive (30% to 60%) but very specific (90%) for LA enlargement. Combinations of P wave morphologies did not improve sensitivity or specificity. ECG features did give an estimate of the degree of LA enlargement. When PTFV1 is greater than or equal to 40 msec.mm, 95% of patients had LA size greater than or equal to 40 mm; and when this parameter was greater than or equal to 60 msec.mm, 75% had LA size greater than or equal to 60 mm. These criteria for LA enlargement on the ECG are specific and predictive of the degree of LA enlargement measured by echocardiography.

Atrial Function, Left↗
PubMed2004

Early mitral deceleration and left atrial stiffness.

Left ventricular (LV) filling deceleration time (DT) is determined by the sum of atrial and ventricular stiffnesses (KLA + KLV). If KLA, however, is close to zero, then DT would reflect KLV only. The purpose of this study was to quantify KLA during DT. In 15 patients, KLV was assessed, immediately after cardiopulmonary bypass, from E wave DT as derived from mitral tracings obtained by transesophageal echocardiography and computed according to a validated formula. In each patient, a left atrial (LA) volume curve was also obtained combining mitral and pulmonary vein (PV) cumulative flow plus LA volume measured at end diastole. Time-adjusted LA pressure was measured simultaneously with Doppler data in all patients. KLA was then calculated during the ascending limb of the V loop and during DT. LA volume decreased by 7.3 +/- 6.5 ml/m2 during the first of mitral DT, whereas LV volume increased 9.4 +/- 8.4 ml/m2 (both P < 0.001). There was a small amount of blood coming from the PV during the same time interval, with the cumulative flow averaging 3.2 +/- 2.4 ml/m(2) (P < 0.001). Mean LA pressure was 10.0 +/- 5.1 mmHg, and it did not change during DT [from 7.8 +/- 4.3 to 8.0 +/- 4.3 mmHg, not significant (NS)], making KLA, which averaged 0.46 +/- 0.39 mmHg/ml during the V loop, close to zero during DT [KLA(DT): from -0.002 +/- 0.08 to -0.001 +/- 0.031 mmHg/ml, NS]. KLV, as assessed noninvasively from DT, averaged 0.25 +/- 0.32 mmHg/ml. In conclusion, notwithstanding the significant decrement in LA volume, KLA does not change and can be considered not different from zero during DT. Thus KLA does not affect the estimation of KLV from Doppler parameters.

Acceleration↗
PubMed1995

Magnetic resonance velocity mapping of normal human transmitral velocity profiles.

We used magnetic resonance imaging (MRI) velocity mapping to assess the velocity profile of early diastolic mitral inflow in 11 normal subjects. Velocity maps of left ventricular inflow were obtained in the horizontal long axis of the left ventricle at the time of peak early diastolic filling. Velocity profile curves across the mitral inflow were obtained at 1-cm intervals from the mitral ring to 4 cm into the cavity. The jet width was 3.06 +/- 0.64 cm at the mitral ring level, increasing to 3.6 +/- 0.61 cm at 4 cm. The peak/mean velocity was 1.2 +/- 0.07 at the mitral ring and increased to around 1.4 at 3-4 cm from the mitral ring. The point at which the peak velocity was recorded at each level was skewed towards the septal side by 10%-13% of jet width from the center at the mitral ring and 2-4 cm from the ring. However, at a depth of 1 cm, corresponding to the mitral tip level, the peak velocity was at the center of the jet. The ratio of vertical and horizontal dimensions of the jet cross section was 1.11 +/- 0.05. Thus, the mitral inflow velocity profile is relatively flat at the mitral ring and tip level; the inflow jet cross section is effectively circular.

Adolescent↗
PubMed2004

Intrauterine pulmonary venous flow and restrictive foramen ovale in fetal hypoplastic left heart syndrome.

OBJECTIVES: We sought to determine whether direct foramen ovale (FO) assessment or pulmonary venous (PV) flow patterns in fetal hypoplastic left heart syndrome (HLHS) correlate with clinical markers of postnatal left atrial (LA) hypertension severity associated with restrictive FO. BACKGROUND: Restrictive FO places a newborn with HLHS at high risk of mortality and morbidity. METHODS: We reviewed the prenatal and postnatal echocardiograms and outcomes of 45 fetuses with variants of HLHS diagnosed since May 1999 to determine whether direct FO assessment or PV flow patterns correlate with clinical LA hypertension after birth. RESULTS: Direct FO assessment in utero showed a poor correlation with postnatal FO size, Pao(2), base excess, and the need for atrial septoplasty (p > 0.05). In 40 fetuses with available PV spectra, three PV flow patterns were observed: 1). continuous forward flow with a small a-wave reversal (velocity time integral [VTI] for reverse/forward flow [VTIR/VTIF ratio <0.18]); 2). continuous forward flow with increased a-wave reversal (VTIR/VTIF ratio >or=0.18); and 3). brief to-and-fro flow. Among 19 live-borns, the postnatal FO diameter was smaller in patients with type B than in those with type A flow (1.6 +/- 1.6 mm and 4.5 +/- 2.1 mm, respectively; p = 0.0015), and all patients with type C flow had an intact atrial septum. All three patients with type C flow were critically ill at birth, requiring emergent atrial septoplasty, and two died after heart transplantation, whereas patients with type A or B flow were clinically stable, with only one postoperative death. CONCLUSIONS: Prenatal PV flow patterns in HLHS identify the fetus at risk of severe LA hypertension at birth.

Atrial Function, Left↗
PubMed2000

Pulse dispersion due to atrial fibrillation causes arterial thrombosis in a rabbit experimental model.

Thrombosis associated with atrial fibrillation (AF) is usually caused by a left atrial (LA) thrombus, but it is not always detected. The present study was based on the hypothesis that abnormalities in peripheral artery are responsible for the ischemic stroke associated with AF. Peripheral arterial coagulability was investigated in a rabbit experimental model in which AF was induced by high-frequency stimulation of the right atrium, creating stenosis of the carotid artery together with endothelial damage. The rabbits were classified into 4 groups: (i) sinus rhythm only (group 1), (ii) sinus rhythm after 6 h of pacing (group 2), (iii) short AF (continuous pacing for 5 min; group 3) and (iv) long AF (continuous pacing for 6 h: group 4). The carotid blood flow developed a typical pattern, called cyclic flow reductions (CFRs), the frequency of which (CFRF) was 18.59+/-2.85 in AF (group 3+4) compared with 14.46+/-2.1 in sinus rhythm (group 1+2) (p<0.0005). Among the groups with AF, correlation analysis showed an association between CFRF and pulse dispersion (p<0.02, r=0.58). This study suggests that the distinctive hemodynamic effects with AF, in particular pulse dispersion, substantively influence thrombus formation on injured vascular endothelium.

Animals↗
PubMed1990

Differential influence of various calcium-modulating compounds on ouabain intoxication in isolated rat left atria.

Various calcium-modulating compounds were tested with respect to their protective action against cardiac glycoside toxicity. At the concentrations applied, control force of contraction was reduced by nifedipine and verapamil and slightly attenuated by flunarizine, R 56865, and cimetidine, while it was strongly enhanced by Bay K 8644. The positive inotropic response to ouabain (stimulation rate: 1 Hz) was impaired by nifedipine and verapamil. The increment in contractile force induced by Bay K 8644 was not enhanced by ouabain. The increase in diastolic tension during toxic conditions of ouabain (stimulation rate: 3 Hz) was attenuated by nifedipine, verapamil, bepridil, flunarizine, cimetidine, phenytoin, and R 56865 but not by diltiazem, amiodarone, and amiloride. K loss was prevented by nifedipine, verapamil, diltiazem, bepridil, flunarizine, cimetidine, phenytoin, and R 56865. The increase in cellular Na content was inhibited by R 56865 only. Ca gain was prevented by verapamil, bepridil, flunarizine, R 56865, and cimetidine but not by nifedipine, diltiazem, phenytoin, amiodarone, and amiloride. Ionic deterioration was enhanced by Bay K 8644. These results suggest that pretreatment with various calcium-modulating compounds protects against mechanical and ionic changes during ouabain intoxication induced by Na-Ca overload through different mechanisms.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2004

Left atrial vein pacing: a technique of biatrial pacing for the prevention of atrial fibrillation.

Biatrial pacing is a promising new therapy for drug refractory AF. This article reports two studies. First, an initial 14-patient experience with a novel technique for biatrial pacing. The authors attempted to pace from the LA vein branches of the proximal CS for LA stimulation. LA vein pacing would potentially offer the advantages of greater interatrial synchronization and possibly greater reduction in AF burden and also of lesser far-field R wave sensing and greater lead stability. Second, a postmortem series examining the number, size, and site of LA veins draining into the proximal CS is described. LA vein pacing was successful in 9 of 14 patients. LA vein electrode parameters have been stable during a median follow-up of 580 days. There were three early lead dislodgments but no other complications. In the second study, a postmortem analysis of 43 human hearts was performed. The study found that 38 (88.4%) of 43 hearts had at least one LA vein draining into the proximal 5 cm of the CS. In addition, 81.2% (33/43) had at least one vein greater than 4 Fr caliber. Thus, pacing in a greater proportion of patients might be achieved by the development and use of smaller (3, 4, and 5 Fr) electrodes. Furthermore, these smaller leads would obviously allow deeper advancement into the LA veins with the potential advantages of greater interatrial synchronization and lead stability and lesser far-field R wave sensing.

Aged↗
PubMed1992

Early and late changes in left ventricular filling after acute myocardial infarction and the effect of infarct size.

To characterize the early (1 week) and late (6 weeks) changes in left ventricular (LV) filling pattern associated with acute myocardial infarction (AMI) 45 patients (mean age 65 +/- 2 years) were studied by Doppler echocardiography. Based on clinical criteria, patients were divided into those with large (group L; n = 12) and those with small (group S; n = 33) infarcts and then compared with 16 age-matched control subjects. The following parameters were calculated from the mitral velocity waveform: (1) peak early and peak atrial velocities and their integrals; (2) peak early to atrial velocity ratio and velocity integral ratio; and (3) the pressure half-time of the early wave. One week after AMI, group L showed a decreased atrial and increased early velocity, velocity ratio and integral ratio, whereas the pressure half-time of the early wave was shorter than that in group S and in control subjects. At 6 weeks group L showed a reduction in early velocity, early to atrial velocity ratio and integral ratio, whereas pressure half-time increased. When groups S and L were combined there was a good inverse correlation between pressure half-time and infarct size as measured by peak enzyme release (r = -0.64, p < 0.001). These data suggest that, depending on infarct size, patients exhibit a "restrictive" filling pattern early after the acute event. This is manifested by the greater proportion of filling occurring in early diastole, reflecting an overall increase in chamber stiffness. At 6 weeks, this pattern is less pronounced presumably due to the remodeling process.

Aged↗