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PubMedDate not supplied

Central venous catheter placement using the ECG-guided Cavafix-Certodyn SD catheter.

STUDY OBJECTIVE: To evaluate the clinical use of a new ECG-guided central venous catheter with regard to positioning in the superior vena cava (SVC). DESIGN: Prospective study. SETTING: Operating rooms of a university hospital and a general hospital. PATIENTS: 89 elective and emergency adult surgical patients requiring central venous catheterization perioperatively. INTERVENTIONS: We performed ECG-guided placement of the central venous catheter from several insertion sites. After we observed an intra-atrial p-wave (p-atriale), the catheter was withdrawn 3 cm back into the SVC. Postoperative anterior-posterior chest radiographs were performed for verification of tip localization. MEASUREMENTS AND MAIN RESULTS: In all 81 patients who exhibited a p-atriale that reverted to a normal-size p-wave (p-SVC) after withdrawal of the catheter 3 cm, the tip was located in the SVC or the SVC-right atrial junction on the chest radiograph. In 7 of the 8 cases without a p-atriale, the catheter tip was shown to be located at an incorrect position on the chest radiograph. The size of the p-atriale was always at least twice that of the p-SVC. CONCLUSIONS: Use of this wire-conducted intravascular ECG signal is a reliable tool for positioning the central venous catheter via various insertion sites. The technique proved to be an inexpensive, easy, and clear method. When a p-atriale is seen, uncomplicated insertions do not require radiologic guidance to control catheter tip position.

Adult↗
PubMed2000

Analysis of hemodynamic response with 1/R control on biventricular bypass goat.

A conductance and arterial pressure based method (1/R control) to determine the cardiac output (CO) of a total artificial heart (TAH) was developed to provide a central nervous system with control over the output of TAH. In order to clarify the deference in hemodynamic response between natural heart and 1/R control, biventricular bypass was introduced in the goat. After 2 pneumatically driven sac-type blood pumps were connected to the natural heart, the pulmonary artery was totally clamped to acquire 100% right heart bypass, and the ascending aorta was stenosed to acquire about 60 to 90% left heart bypass; 1/R control was performed substituting the output of the right artificial heart for the CO. The results demonstrated that stable control could be achieved. A discrepancy was often seen between the pulse rate (PR) of the artificial heart and the heart rate (HR) in absolute value. However, the relative changes of PR were quite similar to that of HR for the most part, indicating that the responses of 1/R control were the duplication of natural cardiac responses in normal daily activity.

Animals↗
PubMed1998

Muscle chemoreflex-induced increases in right atrial pressure.

When oxygen delivery to active muscle is too low for the ongoing rate of metabolism, metabolites accumulate and stimulate sensory nerves within the muscle leading to sympathetic activation (muscle chemoreflex). To date, studies on this reflex have focused primarily on its ability to increase arterial pressure or on the activity of the nerves that mediate this response. Clearly, a rise in cardiac output (CO) constitutes an important adjustment, because it increases the total blood flow available to be distributed among organs competing for flow. However, increments in heart rate and contractility provide limited means of raising CO because of the inverse relationship that exists between CO and right atrial pressure (RAP) in the intact circulation. Our goal was to test whether muscle chemoreflex activation, achieved via graded reductions in hindlimb blood flow by partial vascular occlusion, elicits peripheral vascular adjustments that raise RAP. In four conscious dogs exercising on a treadmill at 3.2 km/h 0% grade, RAP was well maintained during reflex activation despite increases in CO and arterial pressure that are expected to reduce RAP. Thus peripheral vascular adjustments elicited by the reflex successfully defend RAP in a setting where it would otherwise fall. To isolate the effects of the reflex on RAP, CO was maintained constant by ventricular pacing in conjunction with beta1-adrenergic blockade with atenolol. When the reflex was activated by reducing hindlimb blood flow from 0.6 to 0.3 l/min, RAP rose from 5.1 +/- 0.8 to 7.4 +/- 0.4 mmHg (P < 0.05) despite continued large (40 mmHg) increases in arterial pressure. During heavier exercise (6.4 km/h 10% grade) in five dogs with normal ventricular function, the reflex raised RAP from 5.7 +/- 0.9 to 6.6 +/- 0.8 mmHg (P < 0.05) despite increases in CO and arterial pressure. We conclude that the muscle chemoreflex is capable of eliciting substantial increases in RAP.

Animals↗
PubMed1994

Myocardial depressant effect of nitrous oxide after valve surgery.

We have studied the cardiovascular effects of 50% nitrous oxide after cardiopulmonary bypass in 14 patients undergoing valve surgery. All patients received morphine as the principal anaesthetic. Nitrous oxide administration for 5 min caused a decrease in mean arterial pressure from 82 +/- 10 to 71 +/- 12.7 mmHg (P < 0.001), cardiac index (2.8 +/- 0.5 to 2.4 +/- 0.5 litres min-1 m-2, P < 0.01), heart rate (104 +/- 17 to 99 +/- 18 beats min-1, P < 0.05), left ventricular stroke work index (29.4 +/- 8.1 to 22 +/- 8.7 gm-m beat-1 mm-1, P < 0.001), stroke volume (45.3 +/- 11.6 to 40 +/- 12.8 ml beat-1, P < 0.05) and an increase in pulmonary vascular resistance from 106.4 +/- 53.9 to 143.9 +/- 81.0 dynes s cm-5 (P < 0.01) and right atrial pressure (1.42 +/- 2.09 to 1.71 +/- 2.21 mmHg, P < 0.05). There was no change in systemic vascular resistance. When nitrous oxide was discontinued all the parameters started to recover within 3 min. Mean arterial pressure returned to control value in 5 min, but cardiac index and pulmonary vascular resistance returned to control value in 10 min. Our results suggest a direct myocardial depression and that the use of nitrous oxide is not recommended immediately after valve surgery and cardiopulmonary bypass.

Adult↗
PubMed2001

Can short-term verapamil therapy reduce the recurrence of atrial fibrillation after successful low energy intracardiac cardioversion?

BACKGROUND: Calcium-lowering drugs seem to be able to reduce the recurrences of atrial fibrillation (AF) after cardioversion by preventing electrical remodeling of atrial cells. The aim of our study was to prospectively evaluate the efficacy of short-term verapamil therapy associated with propafenone or amiodarone in reducing recurrences of AF after low energy intracardiac cardioversion. METHODS: Eighty-two patients with chronic AF (mean duration 6.1 months, range 1-96 months) underwent low energy intracardiac cardioversion. Forty-one patients (Group A) were instructed to suspend antiarrhythmic therapy 48 hours before the procedure (only chronic amiodarone was allowed). The subsequent 41 patients (Group B), in addition to previous prescriptions, had to take verapamil (120 mg twice daily) for 3 days before low energy intracardiac cardioversion and for 7 days after cardioversion. A right atrium-coronary sinus or right atrium-left pulmonary artery electrode configuration was indifferently utilized. Propafenone (450-900 mg daily) or amiodarone (200 mg daily) was prescribed to all patients after cardioversion. RESULTS: Sinus rhythm was acutely restored in 80 patients (97.6%): the mean number of shocks delivered was 2.3 (range 1-5); the mean energy required was 10.5 J (range 7.2-19.8 J). No statistically significant differences were found between the right atrium-coronary sinus vs right atrium-left pulmonary artery electrode configuration regarding the energy required and the number of shocks delivered. Group A and Group B showed the same number of AF recurrences at the first month of follow-up. CONCLUSIONS: In our study, short-term verapamil treatment associated with propafenone or amiodarone seems to be useless for the prevention of recurrent AF after low energy intracardiac cardioversion.

Adult↗
PubMed1992

Increased dispersion of "refractoriness" in patients with idiopathic paroxysmal atrial fibrillation.

The average interval between local depolarizations during atrial fibrillation, the so-called atrial fibrillation interval, was used as an index for local "refractoriness." This was based on the assumption that during fibrillation, cells are reexcited as soon as their refractory period ends. A very good correlation was found between refractory periods determined with the extrastimulus technique at a basic cycle length of 400 ms and atrial fibrillation intervals measured at the same epicardial sites of the right atrium. This new technique was used to assess dispersion in atrial fibrillation intervals in 10 patients with idiopathic paroxysmal atrial fibrillation and in a control group of 6 patients who were undergoing cardiac surgery. After a routine median sternotomy a multiterminal grid with up to 40 electrodes was placed over the right atrium, and atrial fibrillation was induced by premature stimulation. The average fibrillation interval in the test group, recorded at 247 sites, was 152 +/- 3 ms and that in the control group, recorded at 118 sites, was 176 +/- 8.1 ms (p less than 0.05). Dispersion in atrial fibrillation intervals, defined as the variance of the fibrillation intervals at all the recording sites, was three times larger in the group with paroxysmal atrial fibrillation than in the control group. This study suggests that both a shorter refractory period and a larger dispersion in refractoriness are responsible for the recurrence of atrial fibrillation.

Atrial Fibrillation↗
PubMed2005

Selective beta(1)-adrenoreceptor blocking activity of newly synthesized acyl amino-substituted aryloxypropanolamine derivatives, DPJ 955 and DPJ 890, in rats.

The in-vivo beta-adrenoreceptor antagonistic activity of test compounds DPJ 955 and DPJ 890 was assessed against beta-adrenoreceptor agonist (isoprenaline) induced tachycardia in anaesthetized rats. The selectivity to block isoprenaline responses on different &beta-adrenoreceptor subtypes (beta(1), beta(2) and beta(3)) of the test compounds was carried out on isolated rat right atria, isolated rat uterus and isolated rat colon preparations, respectively. Intravenous injection of isoprenaline alone in anaesthetized rats caused hypotension and tachycardia. DPJ 955 or DPJ 890 alone produced a fall in mean arterial pressure and bradycardia in a dose-dependent manner. Administration of isoprenaline to anaesthetized rats pre-treated with test compounds significantly blocked both the tachycardial and hypotensive responses induced by isoprenaline. The test compounds shifted the concentration response curves of isoprenaline towards the right for isolated rat right atrial preparations, rat uterus and rat colon, indicating beta(1), beta(2) and beta(3) adrenoreceptor blockade, respectively. The selectivity ratio for beta(1)/beta-adrenoreceptors to DPJ 955 and DPJ 890 was 64.6 and 83.2, respectively. DPJ 890 was more potent in blocking beta(1)-adrenoreceptors and was more selective towards beta(1) receptors than to other beta-adrenoreceptor subtypes. In conclusion, DPJ 955 and DPJ890 have beta-adrenoreceptor blocking activity with high selectivity for the beta(1)-adrenoreceptor subtype.

Acetamides↗
PubMed1995

Effects of atrioventricular intervals on right atrial monophasic action potential duration during pacing or reciprocating tachycardia.

We evaluated the relationship between changes in the atrioventricular (AV) intervals and right atrial monophasic action potential duration at 90% repolarization (RA-MAPD90) in humans. In 4 patients, RA-MAPD90 was measured during AV reciprocating tachycardia (AVRT, n = 2) or AV node reentrant tachycardia (AVNRT, n = 2) and atrial or ventricular pacing at similar cycle lengths. In 10 patients, RA-MAPD90 was measured during continuous atrioventricular sequential pacing at AV intervals of 0, 50, 100, 150, 200, 250, 300, 350 msec for 90 sec at a cycle length of 333-400 msec. In patients with AVRT, the RA-MAPD90 during tachycardia was shorter than RA-MAPD90 during RA or RV pacing. In patients with AVNRT, RA-MAPD90 during tachycardia was similar or longer than RA-MAPD90 during RA or RV pacing. As the AV interval was increased from 0 msec to 150 msec, the peak right atrial pressure decreased from 8-12 mmHg to 2-3 mmHg. RA-MAPD90 decreased to its minimal value at an AV interval of 150 msec. The maximal difference in the RA-MAPD90 obtained by changing the AV interval was 22.5 +/- 3.0 msec. We conclude that 1) a very short AV or VA interval causes an increase in RA-MAPD90 which correlates with an increase in RA pressure, and 2) RA-MAPD90 during supraventricular tachycardia is different from RA-MAPD90 during atrial or ventricular pacing. Thus, a contraction-excitation feedback mechanism may exist in the human atrium.

Action Potentials↗
PubMed1995

Effects of PEEP on liver arterial and venous blood flows.

Total venous return decreases with positive end-expiratory pressure (PEEP). It is likely that the liver plays an important role in this response, either through the development of an increase in venous resistance or through an increase in the venous backpressure at the outflow end of the liver. In addition, hepatic arterial flow is reported to be selectively decreased by the application of PEEP. Therefore, to clarify the effects of PEEP on liver hemodynamics, we generated pressure-flow (P-Q) relationships in both liver vascular beds of anesthetized, mechanically ventilated pigs at PEEP of 0, 5, 10, and 15 cm H2O to obtain values of backpressure (Pback, mm Hg) from linear extrapolation of the P-Q relationships and resistance (mm Hg/ml/min/kg) from its slope. PEEP decreased portal vein flow (Qpv) and caused an increase in the liver venous resistance (from 0.08 +/- 0.01 to 0.16 +/- 0.02 mm Hg/ml/min/kg; p < 0.05). Ppvback and right atrial pressure (Pra) increased equally (from 5.1 +/- 0.3 to 9.9 +/- 0.4 mm Hg, p < 0.05, and from 4.0 +/- 0.2 to 8.6 +/- 0.5 mm Hg, p < 0.05, respectively, at PEEP 15). The reduction in portal venous flow was related to an increase in the backpressure to flow (as a result of an increase in Pra) and to an increase in liver venous resistances that may cause blood pooling in the splanchnic compartment and decrease venous return through the liver. PEEP increased Phaback (from 11.2 +/- 0.9 to 14.5 +/- 0.7 mm Hg at PEEP 15, p < 0.05) but did not change hepatic arterial resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Low doses of inhaled nitric oxide in heart transplant recipients.

BACKGROUND: The purpose of this study was to assess the hemodynamic effects of low doses of inhaled nitric oxide in patients after orthotopic heart transplantation. METHODS: Two hours after the operation 10 adult patients who were still under anesthetic effects and undergoing mechanical ventilation inhaled, during 60 minutes, a mixture of nitrogen, oxygen, and nitric oxide (20 ppm). A standard profile of hemodynamic data was collected at baseline, at 30 minutes, at 30 more minutes of inhalation, and at the same points after nitric oxide suspension. RESULTS: A significant decrease was found from baseline to 60 minutes, immediately after nitric oxide inhalation in the following: systemic vascular resistance index 1268 +/- 409 to 1090 +/- 354 (p = 0.0161); pulmonary vascular resistance index 252 +/- 124 to 154 +/- 98 (p < 0.05); pulmonary vascular resistance index/systemic vascular resistance index ratio 0.21 +/- 0.09 to 0.14 +/- 0.08 (p = 0.0025); transpulmonary gradient 12 +/- 3 to 9 +/- 3 (p = 0.05). A significant increase was also found in cardiac index from 4.2 +/- 1.1 to 4.9 +/- 1.4 (p = 0.0007). Other parameters such as mean pulmonary, systemic, wedge and right atrial pressures, in addition to intrapulmonary shunting, heart rate, and oxygen extraction ratio, did not present any significant changes. The procedure was well tolerated by all patients, and no undesirable effects such as methemoglobin elevation or worsening of pulmonary hypertension after nitric oxide suspension were observed. CONCLUSIONS: The beneficial effects observed by inhaled nitric oxide in the pulmonary vascular resistance index/systemic vascular resistance index ratio, transpulmonary gradient, and cardiac index suggest that nitric oxide acts mainly in pulmonary territory and could be a possible pulmonary vasodilator agent used to control central hemodynamics after heart transplantation.

Adult↗
PubMed1992

[Experimental study of changes in the right-sided heart hemodynamics and in the reserve force of pulmonary vascular bed after pneumonectomy].

Experimental results are reported of the characteristic impedance in the right-sided heart hemodynamics, and of the reserve force of the pulmonary vascular bed, both in the acute phase and in the chronic phase, following pneumonectomy. To investigate the difference in the reserve force of the pulmonary vascular bed between immediately after left pneumonectomy and 30 days afterward, a total of 15 mongrel dogs were divided into three groups for investigation; Group A--examined immediately after left simple thoracotomy, Group B--immediately after left pneumonectomy, and Group C--examined at 30 days after left pneumonectomy. Immediately after left pneumonectomy (Group B), both the mean pulmonary artery pressure and the total pulmonary resistance index were higher than when after only left simple thoracotomy (Group A). However, by 30 days afterwards (Group C), there was no difference between them. The right-sided heart hemodynamics were investigated by repeated infusions through the right atrium of glass beads (diameter size 100-150 microns, 50 mg/kg). In Group C, the mean pulmonary pressure and total pulmonary resistance index did not increase over that in Group B until the volume of the infusion exceeded that in Group B until the volume of the infusion exceeded that in Group B, suggesting that Group C had a large reserve force of the pulmonary vascular bed than had Group B. Furthermore, Group C revealed a significantly decreased characteristic impedance immediately after the infusion of the glass beads compared to before the infusion, but it increased later.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

The effect of non-depolarizing neuromuscular blocking agents on the release of acetylcholine from the right atrium of the guinea pig.

The effect of various non-depolarizing neuromuscular blocking agents (gallamine, pancuronium, vecuronium, d-tubocurarine, metocurine, atracurium and pipecuronium) on [3H]acetylcholine release in the response to field electrical stimulation was investigated in vitro in preparations of the guinea pig right atrium. In this preparation, atropine enhanced and oxotremorine, a muscarinic agonist, reduced the release of [3H] acetylcholine. Atropine reversed the inhibitory effect of oxotremorine in a concentration dependent manner, indicating that there is negative feedback modulation of acetylcholine release from the vagal nerve. While pancuronium, gallamine and atracurium enhanced the release of [3H]acetylcholine, d-tubocurarine, metocurine, vecuronium and pipecuronium did not affect it. Pancuronium and gallamine also reduced the inhibitory effect of oxotremorine and the Kd value of pancuronium for muscarinic receptors located on cholinergic nerve terminals was 2.31 microM. These findings indicate that pancuronium and gallamine enhanced the release of acetylcholine from the atrial parasympathetic nerve, probably by inhibiting presynaptic muscarinic receptors.

Acetylcholine↗
PubMed1992

Effects of morphine on isolated right atria of the rat.

1. The present study describes the effects of morphine in the absence or presence of naloxone or atropine in the isolated right atria of the rat. 2. Morphine significantly decreased the auricular chronotropism. 3. The maximal effect was 10 +/- 1.0%. 4. Similar results were obtained in reserpinized animals (13 +/- 0.2% maximum). 5. Naloxone (5 x 10(-7) or 5 x 10(-6) M) did not change the inhibitory effects induced by morphine. 6. The maximal effect obtained with morphine in the presence of atropine (5 x 10(-7) M) was 9 +/- 0.1% similar to that obtained with morphine alone. 7. These results suggest that opioid or vagal mechanisms may not be involved in the cardiac inhibitory effects induced by morphine.

Animals↗
PubMed1996

Preoptic recess lesions reduce right atrial pressure responses to volume expansion.

Ablation of the periventricular tissue surrounding the anteroventral portion of the third cerebral ventricle (AV3V-X) abolishes natriuresis and diuresis during volume expansion. Although deficits in several efferent mechanisms have been identified, effects of AV3V-X on afferent input to the volume reflex have not been investigated. Therefore, these experiments measured right atrial pressure (RAP) in conscious AV3V-X and control-operated (CONT) rats before, during, and following acute (60 s) or continuous (60 min) infusion of isotonic saline, or vascular volume expansion with whole blood (15 min). Changes in RAP were significantly smaller in AV3V-X rats than CONT animals during acute isotonic saline infusion and during whole-blood expansion. Treatment with hexamethonium abolished the difference in RAP during acute volume infusion. However, there was no significant difference in RAP between groups during continuous isotonic saline expansion. These data suggest that AV3V-X reduces afferent input from cardiopulmonary stretch receptors during acute volume expansion, which may contribute to diminished natriuresis and diuresis observed in these animals.

Animals↗
PubMed1999

Effects of Saiko-ka-ryukotsu-borei-to, a Japanese Kampo medicine, on tachycardia and central nervous system stimulation induced by theophylline in rats and mice.

Effects of Saiko-ka-ryukotsu-borei-to (SRBT) on theophylline-induced tachycardia in anesthetized rats and theophylline-induced locomotion and convulsions in mice were examined. An intraduodenal administration of SRBT (1 g/kg) prevented theophylline (5 mg/kg, i.v.)-induced tachycardia in rats. SRBT also attenuated an increase in arterial blood pressure with a slow reduction in heart rate of rats treated with theophylline, with no influence on the plasma level of theophylline. However, SRBT did not change the beating rate of right atrium isolated from rats in the absence or presence of theophylline or isoproterenol. The locomotor activity of theophylline in mice was reduced by the treatment with SRBT. Furthermore, the latency of convulsions in mice induced by administration of theophylline at a higher dose (240 mg/kg, i.p.) was prolonged by treatment with SRBT (1 g/kg, p.o.) and seven out of fifteen mice were saved from death due to convulsions. These results suggest that theophylline-induced tachycardia and central nervous stimulation are suppressed by SRBT and that SRBT may reduce the undesirable actions of theophylline on the cardiovascular and central nervous systems.

Anesthesia↗
PubMed2001

Predictors of isotonic exercise in patients with heart failure.

PURPOSE: Study aims were to determine the predictors of isotonic resistance exercise performance in patients with advanced heart failure and to compare the preexercise values of patients who experienced a negative physiologic response to resistance exercise with those who had minimal or no response. METHODS: A correlational design was used. After pharmacologic left ventricular unloading therapy using a pulmonary artery catheter, 34 patients with advanced heart failure performed graduated isotonic weight-lifting exercises. Measurements were made of hemodynamics and rating of perceived exertion after each test. RESULTS: The following variables, measured at baseline, were significantly correlated with the amount of weight patients were able to lift: rating of perceived exertion (RPE; r = -0.42, P = 0.014); diastolic blood pressure (DBP; r = 0.49, P = 0.03); systolic blood pressure (SBP; r = 0.40, P = 0.017); pulmonary capillary wedge pressure (PCWP; r = 0.39, P = 0.026); and right atrial pressure (RAP; r = 0.35, P = 0.041). Multiple regression analysis, using a stepwise procedure, showed that 47% of the variance in exercise performance was explained by DBP, RPE, and PCWP. There were no significant differences in baseline hemodynamics, ejection fraction, or age between the group of patients who had a negative hemodynamic response at peak exercise and the group of patients who had minimal or no response. CONCLUSIONS: Resting PCWP, DBP, and RPE can provide important information to help clinicians predict isotonic resistance exercise performance in patients with advanced heart failure. However, those patients who have a negative response to this type of exercise cannot be distinguished at baseline by clinical characteristics or age.

Adult↗
PubMed1998

Inferior vena cava-tricuspid annulus isthmus is a critical site of unidirectional block during the induction of common atrial flutter.

BACKGROUND: Until recently no clinical studies had reported precise right atrium (RA) mapping when performing induction of atrial flutter (AFl). We studied the mode of tachycardia initiation in 16 patients (pts) referred for radiofrequency (RF) AFl ablation. AFl induction was performed at the beginning of the procedure (n = 10), or after previous AFl termination during RF delivery (n = 6). Detailed analysis of AFl initiation was provided by duodecapolar (Halo) and multipolar catheters positioned in the peritricuspidian region at the lateral right atrial wall (LRA), the inferior vena cavatricuspid annulus (IVC-TA) isthmus and the interatrial septum. Induction was obtained during incremental pacing (IAP) (15 pts) or programmed stimulation (1 pt) from the proximal coronary sinus (PCS). RESULTS: Atrial flutter with counterclockwise (CCW) RA rotation was induced in all pts by PCS pacing. During PCS IAP, at long pacing cycle lengths, impulse propagated in a clockwise (CW) direction through the IVC-TA isthmus and then upward at low (L) LRA. This led to a collision at the mid LRA with another wave front propagating in a CCW direction at the septum. IAP from PCS induced a progressive delay of propagation at the IVC-TA isthmus resulting in a prolongation of the PCS-Mid Isthmus interval from 85 +/- 29 to 151 +/- 42 msec. At same pacing cycle lengths (CL), the PCS-HLRA interval was comparatively less prolonged, from 75 +/- 12 to 105 +/- 18 msec, p = 0.0007. This preferential slowing of conduction between PCS and mid isthmus, during IAP from PCS, was associated with a displacement of the zone of collision to the Low LRA. Finally a CW functional block occurred at the IVC-TA isthmus and CCW AFl was induced through a period of transient concealed entrainment. The paced CL required to initiate flutter ranged from 290 to 180 msec and the mean CL of induced atrial flutter was 254 +/- 27 msec. CONCLUSIONS: The IVC-TA isthmus has decremental properties and exhibits wenckebach phenomenon during incremental PCS pacing. Initiation of a counterclockwise flutter by PCS pacing is associated with appearance of a functional unidirectional block at the IVC-TA isthmus.

Atrial Flutter↗
PubMed1996

Early mortality after surgical repair of postinfarction ventricular septal rupture: importance of rupture location.

BACKGROUND: The aim of this study was to identify factors influencing early outcome after surgical treatment of postinfarction ventricular septal rupture. We investigated the influence of proximal or distal rupture location. METHODS: Between 1980 and 1992 109 patients were treated surgically for ventricular septal rupture using a standardized technique. A division in time periods was made. The rupture was categorized according to its anterior or posterior site and proximal or distal location. RESULTS: The 30-day mortality rate was 27.5%. Multivariate logistic regression analysis identified preoperative shock (p = 0.0007) and right atrial oxygen saturation less than 60% (p = 0.021) as predictors for early death; the risk for early death declined over the time periods from 50% to 12.8% (p = 0.0007). Proximal ventricular septal rupture location (p = 0.0092) and interval between infarction and ventricular septal rupture less then 1 day (p = 0.034) were risk factors for the occurrence of preoperative shock. CONCLUSIONS: Proximal ventricular septal rupture location was the main determinant of preoperative cardiogenic shock, which in turn was the strongest predictor of early mortality. Over the time periods a decrease in early mortality was reached.

Aged↗