Biomedical subjects

R Nadeau

Publications and source records attributed to R Nadeau.

At least 73 records · Page 4Linked to original sources

PubMed1994

QRS alterations in body surface potential distributions during percutaneous transluminal coronary angioplasty in single-vessel disease.

Body surface QRS potentials were recorded with 63 chest leads in 20 patients with proximal single-vessel disease located on either the left anterior descending coronary artery (n = 10), the right coronary artery (n = 6), or the left circumflex coronary artery (n = 4) before, during, and after percutaneous transluminal coronary angioplasty. In each case, three consecutive inflations of relatively short duration (37 +/- 14 seconds) were carried out. Electrical activity was displayed as unipolar electrograms and body surface potential maps. The total QRS complex duration decreased in 14 of the 20 patients. Focal conduction disturbances were observed in six cases; all six had left anterior descending coronary artery occlusion and two were also accompanied by a clear shortening of the right epicardial breakthrough time. In these two cases, an initial activation loss seemed to be characteristic, whereas in the other four cases, a rather diffuse slowing of intraventricular conduction, especially during the terminal portion of the QRS, could be observed. Individual and group mean isointegral difference body surface potential maps (during-minus-before dilation) were considered valuable for the interpretation of localized changes in intraventricular conduction during percutaneous transluminal coronary angioplasty, and their individual variations could, at least partly, be explained by the presence or absence of collateral circulation. Two different hypotheses are suggested to account for the QRS complex shortening observed during short-term myocardial ischemic injury: (1) coronary artery occlusion delayed activation of the portion of the septal region that is normally activated early during the QRS, and/or (2) coronary artery occlusion increased the speed of propagation within the ventricles. Both of these hypotheses are discussed in light of earlier clinical and experimental results.

Angioplasty, Balloon, Coronary↗

PubMed1994

Oxygen-free radicals and myocardial nerve fibers endings.

Previous data from our laboratory have shown that electrolysis-induced oxygen free radicals (OFR) and ischemia/reperfusion (I/R) injury both produced a significant decrease of myocardial noradrenaline (NA) stocks in the isolated perfused rat heart. Therefore, we carried out the present study by immuno- and fluorescence histochemistry techniques to demonstrate the possibility that fibers nerve endings of the heart may be injured and to evaluate the subsequent damages. Isolated rat hearts were perfused according to the Langendorff technique and subdivided into i) control; ii) electrolyzed (two platinum electrodes, DC current, 10 mA, 1 min); iii) xanthine and xanthine oxidase (X-XO) perfusion for 30 min, and iv) 30 min global ischemia followed by 5 min reperfusion. Results indicate that in the last three groups myocardial fibers were altered. However, in electrolyzed hearts and those submitted to X-XO perfusion, but not in the I/R model, a disruption of many of the nerve fibers could be noted. Thus, NA leakage may be due to a neural injury when OFR are generated exogenously, whereas in the I/R model NA overflow may be explained by a metabolic dysfunction such as the inversion of the uptake I carrier. The major conclusion of this study is that OFR as generated exogenously (by electrolysis or by X-XO) cannot be considered to closely mimic the conditions of I/R injury, at least as concerns neural injury.

Animals↗

PubMed1994

Prolongation by captopril of action potential duration in the normal and hypertrophied rat ventricle: direct action or inhibition of the local angiotensin converting enzyme?

OBJECTIVE: The aims were: (1) to study the acute effects of captopril on the action potential characteristics of ventricular fibres from the normal rat, (2) to compare the effects of captopril with those of perindoprilat, a non-thiol angiotensin I converting enzyme (ACE) inhibitor, (3) to determine the electrophysiological properties of the peptide substrates of converting enzyme, bradykinin and angiotensin I, and (4) to investigate whether the effects of captopril occurring in the healthy heart also occur in two models of ventricular hypertrophy. METHODS: Action potentials were recorded with the standard glass microelectrode technique in right ventricular preparations excised from rat hearts and superfused under baseline conditions and with drug containing or peptide containing Tyrode solution. Ventricular hypertrophy was induced in response to hypertension (unilaterally nephrectomised, DOCA-salt model) or 4 week old left ventricular infarction. RESULTS: In preparations from normal rat hearts, captopril increased action potential duration in a concentration dependent fashion [EC50 = 3.5 x 10(-8) M; maximum effect = 44(SEM 5.1)% prolongation at 10(-5) M for action potential duration at 90% repolarisation, APD90]. Perindoprilat similarly caused a dose dependent increase in action potential duration, but with 100 times greater potency [EC50 = 3.1 x 10(-10) M; maximum effect = 71(11)% prolongation at 10(-5) M for APD90]. SQ 14,534, a stereoisomer of captopril with one hundredth the ACE inhibitor potency, had no significant effect on action potential duration at 10(-5) M. Angiotensin I and bradykinin caused concentration dependent prolongation of action potential, but angiotensin II (10(-6) M) had no effect. Captopril (10(-5) M) had no significant effect in the hypertrophied right ventricle from DOCA-salt hypertensive rats, but significantly increased APD90 [39(4.9)%] in right ventricular preparations from rats with 4 week old anterior left ventricular infarction. CONCLUSIONS: In the rat, captopril prolongs action potential duration, an effect possibly due to local accumulation of bradykinin and angiotensin I.

Action Potentials↗

PubMed1994

Forward and inverse problems of electrocardiography: modeling and recovery of epicardial potentials in humans.

To assess the accuracy of solutions to the inverse problem of electrocardiography in man, epicardial potentials computed from thoracic potential distributions were compared to potentials measured directly over the surface of the heart during arrhythmia surgery. Three-dimensional finite element models of the thorax with different mesh resolutions and conductivity inhomogeneities were constructed from serial computerized tomography scans of a patient. These torso models were used to compute transfer matrices relating the epicardial potentials to the thoracic potentials. Potential distributions over the torso and the ventricles were measured with 63 leads in the same patient whose anatomical data was used to construct the torso models. To solve the inverse problem, different methods based on Tykhonov regularization or regularization- truncation were applied. The recovered epicardial potential distributions closely resembled the epicardial potential distributions measured early during ventricular preexcitation, but not the more complex distributions measured later during the QRS complex. Several problems encountered as the validation process is applied in man are also discussed.

Electrocardiography↗

PubMed1994

Intracoronary infusion of bradykinin: effects on noradrenaline overflow following reperfusion of ischemic myocardium in the anesthetized dog.

OBJECTIVE: The aim of this study was to investigate the effects of intracoronary bradykinin (BK) infusion on noradrenaline release and ventricular arrhythmias induced by coronary occlusion and reperfusion in the anesthetized dog. METHODS: 14 anesthetized adult mongrel dogs of either sex underwent a 60 min occlusion of the left anterior descending coronary artery (LAD) followed by a 30-min reperfusion period. BK (1 ng.kg-1.min-1, n = 7), or its vehicle (Lactate Ringer, n = 7), infusions just distal to the left coronary ostium started 15 min before the LAD occlusion and were maintained throughout the experimental period. An epicardial vein, running parallel to the LAD was cannulated to enable the biochemical determinations. The effects of BK on ventricular arrhythmias, cardiac noradrenaline and lactate releases and creatine kinase activity were assessed. RESULTS: BK significantly reduced the amount of noradrenaline released at reperfusion by ischemic myocardium (from 82.1 +/- 31.7 to 11.9 +/- 9.6 ng.min-1), as well as plasma creatine kinase activity at 30 min of reperfusion. This is accompanied by a significant reduction in the incidence of reperfusion-induced sustained ventricular tachycardia. CONCLUSION: This suggests that the protective effect of bradykinin against reperfusion-induced sustained ventricular tachycardia could be associated with a reduction in cardiac noradrenaline release.

Animals↗

PubMed1994

Radiofrequency catheter ablation of an accessory pathway in a young man with dextroversion.

We report an observation of a radiofrequency catheter ablation of an accessory pathway (AP) in a patient with Wolff-Parkinson-White syndrome (WPW) and dextroversion. Atrioventricular rings were mapped by the ablation catheter to locate the shortest local atrioventricular conduction time in sinus rhythm and ventriculoatrial conduction time during orthodromic tachycardia or ventricular pacing. Successful ablation confirmed a right posteroseptal AP localization. Thus, the electrocardiographic modifications due to an AP in this location in the presence of dextroversion were defined.

Adult↗

PubMed1994

Atrial natriuretic peptide release from the ventricles in response to exercise in dogs with atrioventricular block.

The purpose of this study was to examine atrial natriuretic peptide (ANP) secretion at rest and in response to moderate treadmill exercise (10 min, 4 km/h, 26% slope) in control dogs (n = 17) and in dogs (n = 14) with complete atrioventricular block produced by electrocauterization of the His bundle. Atrial rates were similar in both groups (103 +/- 13 vs. 102 +/- 9 beats/min at rest and 162 +/- 10 vs. 160 +/- 17 beats/min at exercise in control dogs and in dogs with atrioventricular block, respectively; mean +/- SE), but ventricular rate was markedly lower in dogs with atrioventricular block (47 +/- 9 and 61 +/- 10 beats/min at rest and exercise, respectively). The lower ventricular rate was associated with an increased cardiac preload, as evidenced by the higher right atrial pressure in dogs with atrioventricular block at rest (2.2 +/- 1.4 vs. 1.1 +/- 0.9 mmHg; p < 0.05) and exercise (7.6 +/- 3.1 vs. 4.2 +/- 1.7 mmHg; p < 0.05). Arterial plasma ANP concentrations were markedly higher at rest (151 +/- 21 vs. 36 +/- 10 pg/mL; p < 0.05) and exercise (353 +/- 31 vs. 72 +/- 17 pg/mL; p < 0.05) in dogs with atrioventricular block. This observation supports the hypothesis that atrial wall stretching is a major stimulus for ANP release at rest and exercise. Ventricular release of ANP could also contribute to the higher plasma ANP concentrations observed both at rest and during exercise in dogs with complete atrioventricular block. Indeed, a large ANP concentration gradient was measured between the aorta and the distal part of the coronary sinus in these dogs at rest (227 +/- 55 pg/mL) and exercise (240 +/- 57 pg/mL) but not in control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Norepinephrine and dihydroxyphenylglycol effluxes from sympathetic nerve endings during hypoxia and reoxygenation in the isolated rat heart.

The present experiments were carried out in isolated rat hearts perfused according to the Langendorff method at a constant pressure of 10 kPa. The aim was to measure norepinephrine (NE) overflow and its deaminated metabolite dihydroxyphenylglycol (DOPEG) by changing the composition of the buffer perfusing the heart to simulate hypoxia. When aerobic and glycolytic pathways were simultaneously reduced, NE and DOPEG overflow increased 711 and 145%, respectively, after 30 min, compared with control values of 0.45 +/- 0.06 and 0.66 +/- 0.7 ng.min-1.g-1 of heart (n = 8, p < 0.05). Whereas NE leakage decreased sharply after reoxygenation and glucose addition, DOPEG continued to increase up to 260% after 5 min of normal reperfusion. This mechanism was calcium independent and inhibited by 80% with desipramine (1 microM), confirming the role of the uptake I carrier, which reversed its normal transport direction. Neuropeptide Y, a marker of exocytotic release, did not increase in the perfusate with the progression of hypoxia, which supports the hypothesis of a nonexocytotic release. Tyramine (1 microM) significantly enhanced NE outflow by displacing the amine from its storage vesicles through a calcium-independent mechanism, indicating that a pool of NE was still available. In the presence of 1 microM clorgyline (a monoamine oxidase A inhibitor) but not deprenyl (a monoamine oxidase B inhibitor), NE outflow increased 934% and DOPEG only 40% at 30 min (n = 6, p < 0.05 versus control hearts).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effect of changes in myocardial epinephrine stores on plasma norepinephrine gradient across the dog heart.

Plasma norepinephrine (NE) concentration ([NE]) gradient across the heart was measured under electrical stimulation of the left stellate ganglion (LSG; 4 Hz, 4 V, 2 ms pulse width, 1 min) in control (Ctrl) and in adrenalectomized (Adrx) dogs, without and with a 10-min epinephrine (Epi) infusion (92 ng.kg-1.min-1), which partly restored myocardial Epi stores in Adrx dogs (2.9 +/- 0.7 ng/g vs. 6.4 +/- 0.7 ng/g in Ctrl dogs) and slightly increased tissue Epi stores in Ctrl dogs (10.5 +/- 1.3 pg/g). Compared with Ctrl dogs (1,069 +/- 172 pg/ml), the [NE] gradient across the heart under stimulation of the LSG was not modified 1 wk after bilateral adrenalectomy (1,190 +/- 122 pg/ml) or after Epi infusion in Ctrl (1,134 +/- 276 pg/ml) and Adrx (1,259 +/- 279 pg/ml) dogs. The beta 2-antagonist ICI-118,551 significantly reduced the stimulation-induced [NE] gradient across the heart in Ctrl dogs (621 +/- 190 and 603 +/- 86 pg/ml without and with a 10-min Epi infusion, respectively) but not in Adrx dogs deprived of tissue Epi (1,345 +/- 345 pg/ml). Partial repletion of myocardial Epi stores in Adrx dogs restored the effect of ICI-118,551 on the stimulation-induced [NE] gradient (776 +/- 121 pg/ml). These results provide direct support of the hypothesis that tissue Epi, which originates from the adrenal medulla and which is released locally along with NE, is the endogenous agonist for presynaptic beta 2-receptors and potentiates NE release.

Adrenalectomy↗

PubMed1994

Altered cardiorespiratory transfer in hypertension.

The effect of continuously slowing respiration (from 0.46 to 0.05 Hz, eg, from 30 to 3 breaths per minute) on cardiovascular variables was studied in 14 hypertensive patients and 16 normotensive subjects. Beat-to-beat time-frequency (Wigner) distributions were used for dynamic analysis of RR interval and systolic and diastolic pressures. Dominant breathing frequency at rest did not differ in hypertensive patients from the control group (0.21 versus 0.19 Hz). However, in the hypertensive group it was disturbed 34.4% of the time by slow breathing and apneas, which evoked transient blood pressure instability and increased spectral powers at low frequencies (range, 0.01 to 0.1 Hz). The nonrespiratory fluctuations (NONRFs) and respiratory fluctuations (RFs) in RR interval and NONRFs in systolic pressure were smaller in hypertensive patients (P < .001). In both groups, slowing of respiratory frequency from 0.46 to 0.05 Hz entrained RFs in the RR interval and systolic and diastolic pressures. RFs in the RR interval remained diminished in hypertensive patients (P < .001), but RFs in systolic pressure increased higher at maximum, corresponding to breathing frequencies from 0.07 to 0.09 Hz (P < .001). A dynamic cardiorespiratory index (ratio of RFs in RR interval and systolic pressure) was smaller (P < .01) in hypertensive patients than in normotensive subjects. Irregular breathing at rest was found in hypertensive patients. The transfer from respiration into RR interval was diminished, suggesting an impaired parasympathetic responsiveness in mild hypertension.

Adult↗

PubMed1993

Body surface potential mapping of ST-segment shift in patients undergoing percutaneous transluminal coronary angioplasty. Correlations with the ECG and vectorcardiogram.

The purpose of this study was to investigate the thoracic patterns of ST-segment shift induced by the occlusion of different coronary arteries during percutaneous transluminal coronary angioplasty. Body surface potential maps were recorded with 63 leads during sinus rhythm before, during, and after balloon inflation in 20 patients. Two patients underwent dilatation of both the right and circumflex coronary arteries. A 12-lead scalar electrocardiogram and a Frank vectorcardiogram with orthogonal leads X, Y, and Z were obtained with the body surface potential maps. The body surface potential maps at 40 ms during the ST-segment showed patterns that were specific to the dilated vessel. The left anterior descending coronary artery (n = 10) was associated with the largest ST-segment shifts with a precordial maximum and negative potentials over the back; for the right coronary artery (n = 7), negative potentials covered the upper left torso with a left mid-axillary minimum and positive potentials over the rest of the torso; for the left circumflex coronary artery (n = 5), negative potentials covered the anterior torso with a precordial minimum and positive potentials over the back. These changes dissipated rapidly after balloon deflation. ST levels measured on orthogonal leads showed values greater than standard electrocardiographic leads for circumflex and right coronary arteries. In conclusion, body surface potential mapping provides a comprehensive approach for the evaluation of electrocardiographic changes and the development of optimal leads for the detection of acute occlusion of a coronary artery.

Adult↗

PubMed1993

Protective effects of bradykinin on the ischaemic heart: implication of the B1 receptor.

1. We studied the role of bradykinin (BK) and its active metabolite Des-Arg9-BK on noradrenaline release in association with the incidence of ventricular arrhythmias at reperfusion of the ischaemic myocardium. 2. Experiments were performed in Langendorff perfused isolated hearts of rats subjected to 30 min no flow followed by 5 min reperfusion. The electrocardiogram was monitored continuously and noradrenaline was measured in the effluent as well as in the myocardial tissue. 3. In untreated hearts, cumulative noradrenaline overflow following global ischaemia reached 226 +/- 35 pmol g-1 of heart (n = 8, P < 0.05) during the 5 min of reperfusion along with ventricular tachycardia and/or fibrillation. A decrease in myocardial noradrenaline (-31%) was also observed. 4. Bradykinin perfused at concentrations between 0.01 and 1 microM, 10 min before flow was stopped and at reperfusion, inhibited noradrenaline overflow in a concentration-dependent manner. At a concentration of 1 microM, bradykinin completely abolished noradrenaline overflow. For the same concentration of bradykinin, myocardial noradrenaline contents were significantly higher (n = 5-8, P < 0.05). Ventricular fibrillation but not ventricular tachycardia was also prevented. 5. Des-Arg9-BK (0.1 microM) in the same experimental conditions had similar effects. While Hoe 140, a selective antagonist at B2 receptors, did not abolish the effects of bradykinin, Lys [Leu8] Des-Arg9-BK, an antagonist at B1 receptors, abolished the effects of both Des-Arg9-BK and bradykinin. 6. These results suggest that the cardioprotective action of bradykinin in the preparation may be mediated partially by an inhibitory effect on noradrenaline liberation which could be mediated by the activation of B1 receptors.

Animals↗

PubMed1993

Mediation by B1 and B2 receptors of vasodepressor responses to intravenously administered kinins in anaesthetized dogs.

1. Vasodepressor responses to intravenous (i.v.) injection of bradykinin (BK) and des-Arg9-BK, a selective B1 kinin receptor agonist, were characterized following i.v. pretreatment with selective B1 ([Leu8]-des-Arg9-BK) and B2 (Hoe 140) kinin receptor antagonists in anaesthetized dogs. 2. Des-Arg9-BK (0.05-3.3 nmol kg-1) produced dose-dependent decreases in mean arterial blood pressure with a ED50 0.4 nmol kg-1. The vasodepressor effects evoked by des-Arg9-BK (0.6 nmol kg-1) and BK (0.2 nmol kg-1) were greater after i.v. and i.a. injections, respectively. 3. The vasodepressor response to BK (0.6 nmol kg-1) but not to des-Arg9-BK (0.6 nmol kg-1) was significantly (P < 0.001) blocked by pretreatment with the B2 receptor antagonist, Hoe 140. 4. The vasodepressor response to des-Arg9-BK (0.6 nmol kg-1) but not to BK (0.6 nmol kg-1) was significantly (P < 0.001) reduced by pretreatment with the selective B1 receptor antagonist, [Leu8]-des-Arg9-BK. Although both B1 and B2 receptor antagonists caused a transient fall in blood pressure, their inhibitory action was unlikely to be related to a desensitization mechanism. 5. Inhibition of prostaglandin synthesis with indomethacin prevented the vasodepressor response induced by arachidonic acid (1 mg kg-1, i.v.) but not that to BK or des-Arg9-BK (0.6 nmol kg-1). 6. These results suggest, firstly, that the vasodepressor responses to i.v. BK and des-Arg9-BK are mediated by the activation of B2 and B1 receptors, respectively; secondly, that prostaglandins are not involved in the vasodepressor responses to kinins.These findings provide pharmacological evidence for the existence of functionally active B1 receptors in canine cardiovascular homeostasis.

Anesthesia↗

PubMed1993

Bipolar transseptal radiofrequency ablation of AV node: an alternative to high energy shocks?

Atrioventricular (AV) node ablation to control ventricular response was attempted in two patients with recurrent drug refractory atrial flutter. Standard radiofrequency (RF) procedure, which delivers energy through the 4-mm tip electrode of an ablation catheter positioned at the right AV junction and a large back plate (unipolar mode), failed in both patients. As an accepted second step, high energy direct current (DC) ablation under general anesthesia was then performed in patient one. After two shocks of 200 J, complete AV block occurred, but complete recovery was noted 3 hours later. In a third session for patient 1 and in the first session for patient 2 (after 15 unsuccessful unipolar right-sided RF applications), a second ablation catheter was introduced via the femoral artery on the left side of the His bundle area under the aortic valves. Energy was then delivered in a bipolar fashion between the tip electrodes of the right-sided and the left-sided catheter. Complete and permanent AV block (follow-up: 3 and 1 months) was created within 4 and 1.5 seconds, respectively, in each patient. No complication was encountered and echocardiograms and blood levels of cardiac enzymes were all normal after the procedures. This new approach, after further evaluation, may represent a useful additional step in the strategy of AV node ablation and could be applied before high energy DC shock when the standard RF procedure is unsuccessful.

Adult↗

PubMed1993

Presynaptic effects of epinephrine on norepinephrine release from cardiac sympathetic nerves in dogs.

The possible functional role of tissue epinephrine in the modulation of norepinephrine release from cardiac sympathetic nerve endings in anesthetized dog was investigated. Observations were carried out under control conditions and after a short- (10 min) and long-term (180 min) epinephrine infusion (92 ng.kg-1.min-1). An increase in the stimulation-induced release of norepinephrine after intravenous administration of a selective beta 2-agonist (fenoterol, 0.5 micrograms/kg) indicated the presence of the beta 2-facilitatory mechanism. Furthermore, the facilitatory effect of fenoterol was inhibited by intravenous administration of a selective beta 2-antagonist (ICI 118551, 1 mg/kg). Short-term epinephrine infusion did not facilitate the stimulation-induced release of norepinephrine, when tissue epinephrine content in the left ventricle was increased 1.5-fold, without, as well as with, alpha 2-blockade (yohimbine, 0.3 mg/kg). However, stimulation-induced release of norepinephrine from the myocardium was significantly potentiated in animals in which tissue epinephrine in the left ventricle was greatly increased (5.6-fold) by a prolonged infusion of epinephrine (180 min). It is concluded that a facilitatory mechanism mediated by presynaptic beta 2-adrenoceptors is present in cardiac sympathetic nerve endings of the dog. Some of our observations support the hypothesis that this mechanism may be influenced by locally released epinephrine and, thus, by tissue epinephrine content.

Animals↗

PubMed1993

In vivo B2-receptor-mediated negative chronotropic effect of bradykinin in canine sinus node.

The chronotropic response to bradykinin (BK) injected into the sinus node artery was evaluated in anesthetized dogs. The animals (n = 14) were vagotomized and pretreated with propranolol (1 mg/kg i.v.) to prevent baroreceptor-mediated effects. Dose-dependent decreases in heart rate (from 2.4 +/- 1.3% for 1 microgram of BK to 13.1 +/- 3.7% for 10 micrograms of BK), as well as a significant fall in systemic systolic and diastolic blood pressures, were observed. Captopril (2 mg/kg i.v.) caused significant decreases in systolic (from 117 +/- 11 to 77 +/- 12 mmHg, P < 0.001) and diastolic (from 87 +/- 8 to 52 +/- 8 mmHg, P < 0.001) blood pressures but had no effect on heart rate. Converting-enzyme inhibition potentiated the BK-induced bradycardia. The new potent B2-receptor antagonist, HOE 140 (100 micrograms), significantly blocked the BK-induced chronotropic effect, whereas desArg9-BK, a B1-receptor agonist, was without effect. Prostaglandin involvement was excluded, since pretreatment with indomethacin did not prevent the bradycardia. In conclusion, in vivo BK induces a direct negative chronotropic effect, which is potentiated by converting-enzyme inhibition and is mediated by the B2-receptors independently of the prostaglandins.

Adrenergic beta-Antagonists↗

PubMed1993

Influence of respiration on heart rate and blood pressure fluctuations.

The dynamics of the respiratory and cardiovascular systems were studied by continuously slowing respiration from 0.46 to 0.05 Hz. The time-frequency distribution and global spectral analysis were used to assess the R-R interval (R-R) and the systolic and diastolic blood pressure fluctuations in 16 healthy subjects. During rest, the nonrespiratory-to-respiratory frequency ratios were not affected by occasional slow breathing, whereas the low- (0.01-0.15 Hz) to high- (0.15-0.3 Hz) frequency indexes for blood pressure were increased (P < 0.05). The respiratory fluctuations in R-R and the systolic and diastolic pressures were paced over the 0.46- to 0.05-Hz range. As respiration slowed to 0.07-0.09 Hz, the frequency content of the respiration and cardiovascular variables increased sharply and nonlinearly to a maximum that exceeded values at higher frequencies (P < 0.001). The nonrespiratory frequency content remained stable in the 0.01- to 0.05-Hz range and did not significantly differ from that at rest. In contrast, the nonstable 0.05- to 0.1-Hz component was suppressed. A slow 0.012- to 0.017-Hz rhythm modulated respiration and hemodynamic fluctuations at both respiratory and nonrespiratory frequencies. The study indicated that respiration input should be considered in the interpretation of global spectra. Furthermore the time-frequency distributions demonstrated that a close nonlinear coupling exists between the respiratory and cardiovascular systems.

Adult↗

PubMed1993

Pace mapping using body surface potential maps to guide catheter ablation of accessory pathways in patients with Wolff-Parkinson-White syndrome.

BACKGROUND. A pace mapping technique using body surface potential maps (BSPMs) was developed to guide the positioning of an ablation catheter at the ventricular insertion point of accessory pathways (AP) in patients with the Wolff-Parkinson-White syndrome (WPW). METHODS AND RESULTS. The study was performed on 30 WPW patients. BSPMs were recorded with 63 leads distributed over the entire torso surface. The catheter used for radiofrequency ablation was first placed in the vicinity of the ventricular preexcitation site predicted by BSPMs recorded during the delta wave. BSPMs were then recorded during pacing with this catheter, the comparison between the preexcited and paced BSPMs indicated whether the pacing site was too anterior or posterior with respect to the preexcitation site, and the catheter was moved accordingly. This process was repeated until the preexcited and paced BSPMs were highly correlated (r > or = 0.8), and ablation then was attempted. It was possible to successfully ablate the AP in 28 patients after an investigation that lasted 54 +/- 44 minutes between the recording of the first paced BSPM and that of the BSPM paced at the successful ablation site. Patients with left free wall pathways needed less investigation time compared with patients with pathways of other locations (46 +/- 9 versus 100 +/- 25 minutes, p = 0.031). The sensitivity of BSPM pace mapping was assessed using pacing with a multipolar catheter, and significant changes were observed on the BSPMs for beats with pacing sites that were only 5 mm apart. CONCLUSIONS, BSPM pace mapping allowed us to achieve a 93% success rate with short investigation durations, provides significant information that cannot be obtained with the standard 12-lead ECG, is a self-correcting procedure that reduces the importance of BSPM alterations due to individual differences in the shape of the torso or heart, and is applicable only to patients with AP showing antegrade conduction.

Adolescent↗