Mechanism of syncope in patients with bundle branch block and negative electrophysiological test.

BACKGROUND: In patients with syncope and bundle branch block (BBB), syncope is suspected to be attributable to a paroxysmal atrioventricular (AV) block, but little is known of its mechanism when electrophysiological study is negative. METHODS AND RESULTS: We applied an implantable loop recorder in 52 patients with BBB and negative conventional workup. During a follow-up of 3 to 15 months, syncope recurred in 22 patients (42%), the event being documented in 19 patients after a median of 48 days. The most frequent finding, recorded in 17 patients, was one or more prolonged asystolic pause mainly attributable to AV block; the remaining 2 patients had normal sinus rhythm or sinus tachycardia. The onset of the bradycardic episodes was always sudden but was sometimes preceded by ventricular premature beats. The median duration of the arrhythmic event was 47 seconds. An additional 3 patients developed nonsyncopal persistent III-degree AV block, and 2 patients had presyncope attributable to AV block with asystole. No patients suffered injury attributable to syncopal relapse. CONCLUSIONS: In patients with BBB and negative electrophysiological study, most syncopal recurrences have a homogeneous mechanism that is characterized by prolonged asystolic pauses, mainly attributable to sudden-onset paroxysmal AV block.

Mechanism of syncope in patients with isolated syncope and in patients with tilt-positive syncope.

BACKGROUND: Because of its episodic behavior, the correlation of spontaneous syncope with an abnormal finding can be considered a reference standard. METHODS AND RESULTS: We inserted an implantable loop recorder in 111 patients with syncope, absence of significant structural heart disease, and a normal ECG; tilt-testing was negative in 82 (isolated syncope) and positive in 29 (tilt-positive). The patients had had >/=3 episodes of syncope in the previous 2 years and were followed up for 3 to 15 months. Results were similar in the isolated syncope group and the tilt-positive group: syncope recurred in 28 (34%) and 10 patients (34%), respectively, and electrocardiographic correlation was found in 24 (23%) and 8 (28%) patients, respectively. The most frequent finding, which was recorded in 46% and 62% of patients, respectively, was one or more prolonged asystolic pauses, mainly due to sinus arrest, preceded for a few minutes by progressive bradycardia or progressive tachycardia-bradycardia. Bradycardia without pauses was observed in 8% and 12% of cases, respectively. The remaining patients had normal sinus rhythm or sinus tachycardia, except for one, who had ectopic atrial tachycardia. In the tilt-positive group, an asystolic syncope was also recorded when the type of response to tilt-testing was vasodepressor or mixed. Presyncopal episodes were never characterized by asystolic pauses; normal sinus rhythm was the most frequent finding. CONCLUSIONS: Homogeneous findings were observed during syncope. In most patients, the likely cause was neurally-mediated, and the most frequent mechanism was a bradycardic reflex. In the other cases, a normal sinus rhythm was frequently recorded. Presyncope was not an accurate surrogate for syncope in establishing a diagnosis.

[Diagnostic accuracy of a protocol in the evaluation of unexplained syncope]. / Rendimiento diagnóstico de un protocolo de estudio del síncope de causa no aparente.

INTRODUCTION AND OBJECTIVES: To assess the diagnostic capacity of a protocol to study syncope of unknown cause in which electrophysiological studies and tilting table tests are selectively used. PATIENTS AND METHODS: The study was performed in 137 consecutive patients (94 men and 43 women, with a mean age of 57.6+/-18.3 years) with syncope of unknown cause after the initial clinical evaluation, who were divided into two groups. Group A consisted of 77 patients meeting any of the following criteria: a) presence of structural heart disease; b) abnormal ECG; c) presence of significant non-symptomatic arrhythmia in the Holter recording, and d) presence of paroxysmal palpitations. These patients initially underwent an electrophysiological study. Group B consisted of 60 patients not meeting any of the above criteria, who were initially submitted to tilting table tests.Results. In group A, the electrophysiological study was positive in 43 patients (55%). In group B, the tilting test was positive in 41 patients (68%). Among patients in group A with a negative study, 20 (59%) were submitted to the tilting table test, with positive results in 7 cases (35%). Five patients from group B with a negative tilting test underwent the electrophysiological study, which was negative in all of them. Overall, a positive diagnosis was achieved in 91 of 137 patients (66%). CONCLUSIONS: In patients with syncope of a non-apparent cause in the initial assessment, selective use of electrophysiological studies or tilting table tests, guided by clinical criteria, allows for a positive diagnosis in over 60% of the cases. Our results suggest that the tilting table test should be performed in cases of group A with a negative electrophysiological study.

Relationships between heart rate variability, functional capacity, and left ventricular function following myocardial infarction: an evaluation after one week and six months.

BACKGROUND: Relationships between heart rate (HR) variability and different prognostic markers such as ejection fraction, functional capacity, and patency of the infarct-related artery, as well as the comparison of their time courses are not fully elucidated. HYPOTHESIS: The aim of study was to assess prospectively the early postinfarction changes in HR variability and its evolution over a period of 6 months: the relationships between HR variability and functional capacity in exercise testing; left ventricular function in cardiac catheterization: status of the infarct-related artery; and the comparison of their time courses. METHODS: In 42 patients with anterior myocardial infarction, a study was made of the early changes in HR variability analyzed by the complex demodulation method, its evolution over a period of 6 months. and the relationships between HR variability and (1) functional capacity in exercise testing, (2) left ventricular function in cardiac catheterization, and (3) status of the infarct-related artery. RESULTS: At 1 week HR variability parameters correlated directly with functional capacity indicators such as METS, percent change in HR from rest to peak exercise (%deltaHR), difference between initial and peak HR (HR range), percent peak theoretical HR (% peak HR), left ventricular ejection fraction (EF), and, inversely, with end-systolic volume (ESV). Stepwise multiple regression analysis to establish HR variability parameters (recorded at 1 week) as related to functional capacity and left ventricular function at 1 week and 6 months postinfarction established the following variables: (1) At 1 week: standard deviation (SD) of the RR cycles in relation to %deltaHR (r = 0.60, p <0.0001), HR range (r = 0.43, p < 0.01), and EF (r = 0.79, p < 0.0001). (2) At 6 months, the sole accepted HR variability parameter was the SD in relation to %deltaHR (r = 0.38, p < 0.05) and HR range (r = 0.45, p < 0.01). No variability parameter was accepted in relation to METS, % peak HR, or ESV. Relationship between EF or ESV and HR variability parameters was not significant when both were evaluated at 6 months. At that time, there was a significant increase in all HR variability parameters among all surviving patients (n = 39), with the exception of the LF/HF ratio and mean RR cycle. The percent increase in HR variability between the first week and 6 months was greater among those patients with the lowest basal EF. No relation was established between HR variability and patency of the infarct-related artery. CONCLUSION: The decrease in HR variability observed following myocardial infarction is associated with a diminished functional capacity and an increased alteration of the EF. This does not affect the recovery of HR variability, which was observed in all surviving patients.

Acute effects of radiofrequency ablation upon atrial conduction in proximity to the lesion site.

The electrophysiological effects of RF ablation upon the areas in proximity to the lesioned zones have not yet been well characterized. An experimental model is used to investigate atrial conduction in the boundaries of RF damaged zones. In 11 isolated and perfused rabbit hearts, endocardial atrial electrograms were recorded using an 80-lead multiple electrode positioned in the left atrium. Both before and after the RF application (5 W, 8 s, 1-mm diameter unipolar epicardial electrode) in the mid-portion of the free left atrial wall, measurements were made of conduction time from the pacing zone (posterior wall of the left atrium) to three points between 7.5 and 7.9 mm distal to the damaged zone. Conduction velocity and the direction of the activation propagation vector were determined in ten groups of four electrodes positioned around the damaged zone, and at the left atrial appendage. The mean diameter (+/- SEM) of the transmural lesions produced by RF ablation and defined by macroscopic examination was 4.2 +/- 0.2 mm. The conduction times to the three points distal to the lesion site were significantly prolonged as a result of RF ablation; 7.6 +/- 0.4, 7.4 +/- 0.5, and 6.9 +/- 1.0 ms (control); and 11.3 +/- 1.0 (P < or = 0.01), 11.1 +/- 1.3 (P < 0.01), 10.6 +/- 1.4 ms (P < 0.05) (post-RF). The differences between the conduction velocities determined in the areas surrounding the lesion, before and after RF application, failed to reach statistical significance: 86.2 +/- 6.5 cm/s (control) versus 75.5 +/- 5.7 cm/s (post-RF) (NS). After RF, significant variations were only observed in the direction of impulse propagation in the proximal-inferior quadrant adjacent to the lesion site, the difference being -61 degrees +/- 18 degrees (P < 0.02). In 2 of 4 experiments in which the lesion size was increased by a second RF application (5 W, 16 s), tachycardias with activation sequence around the lesion could be induced, with cycle lengths of 56 and 50 ms, respectively. In the atrial wall, the conduction times to the regions distal to the RF lesion are significantly prolonged. No significant changes are observed in conduction velocity in the areas in proximity to the lesion. Prolonged conduction to the areas distal to the ablation site is due to the lengthened pathway traveled by the impulses in reaching these areas. Tachycardias with activation patterns that suggest reentry around the RF damaged zone may be induced.

Are double potentials markers of a specific zone of the atrioventricular junction in the isolated rabbit heart?

A study is made of the characteristics of the atrial potentials recorded in the Koch triangle and its proximity, their variations on modifying the site of cardiac pacing, and their usefulness as markers of a distinct zone of the AV junction. In 12 isolated and perfused rabbit heart preparations an analysis was made of the endocardial atrial electrograms recorded with a multiple electrode positioned in the AV junction. The electrograms were obtained during spontaneous rhythm and on pacing at the crista terminalis (CT), interatrial septum (IAS), left atrium, and right ventricle. Double potentials were frequently obtained. On pacing at the CT, high-low double potentials (DP [H-L]) were more frequent (P < 0.05) in the low CT (11% +/- 4% of the electrodes) and posterior zone of the Koch triangle (6% +/- 5%), than in the IAS (1% +/- 2%) and anterior zone of the Koch triangle (2% +/- 3%). A similar tendency was observed either on pacing at the left atrium or during spontaneous rhythm. During pacing at the IAS the percentages of low-high double potentials (DP (L-H]) were significantly higher (P < 0.05) in the low CT (7% +/- 6%). DP (H-L) were of low sensitivity in indicating a given zone; maximum sensitivity was 61% in the low CT when pacing at the CT. DP (L-H) proved even less sensitive in indicating a given zone, though their specificity was greater in the low CT (91%) during pacing at the IAS. The specific zones in which the highest percentages of DP (H-L) or DP (L-H) are obtained depend on the site of cardiac pacing. On pacing at the IAS, DP (L-H) are more specific of the low CT. During pacing at both the CT and at the IAS, DP (H-L) sensitivity in indicating a given zone is low.

[The tilt-table test: is it essential for adequate treatment of vasovagal syncope? Arguments against]. / Test de mesa basculante: es imprescindible para el tratamiento adecuado del síncope vasovagal? Argumentos en contra.

The knowledge about vasovagal syncope has hugely grown since its initial description by Lewis in 1932. Nevertheless some critical gaps remain, affecting specially to the patient management. There are not enough data about the natural history of the process and, because of that, no useful markers are known to identify patients who need or would benefit from a specific treatment. A diagnostic test with a sensibility/specificity relationship good enough to be a diagnostic gold standard is lacking. Although tilt-table test can be helpful in diagnosis, its sensitivity is, nowadays, unknown. Available data about reproducibility of tilt test are scarce and sometimes contradictory, specially with positive tilt test results. Should the lack of reproducibility of positive results found by some authors be confirmed, the usefulness of serial tilt tests in selecting treatment would be seriously affected. No evidence about the existence of an effective treatment for vasovagal syncope has been published yet, not either about the advantage of an specific strategy in selecting it. Therefore, tilt test has not been proved to be a more useful tool in selecting therapy for patients with vasovagal syncope.

[Auricular fibrillation and stroke in patients with sick sinus syndromeusing permanent pacemakers]. / Fibrilación auricular y accidente vascular encefálico en pacientes con enfermedad del nodo sinusal portadores de marcapasos definitivos.

INTRODUCTION AND OBJECTIVES: Since physiological pacing systems have become available, a debate has raged about the merits of atrial versus ventricular pacing in the sick sinus syndrome. The goal of this retrospective report was to study the long term incidence and the independent predictors for atrial fibrillation and stroke in 153 paced patients with sick sinus syndrome, adjusting for differences in baseline clinical variables with multivariate analysis. METHOD AND RESULTS: From 1980 to 1994, we implanted 32 dualchamber, 33 atrial, and 88 ventricular pacemakers to treat patients with sick sinus syndrome. After a maximum follow-up of 177 months (median 30 months for paroxismal atrial fibrillation, 45 months for chronic atrial fibrillation and 43,5 months for stroke) the actuarial incidence of paroximal atrial fibrillation was 7.8% at 1 year, 29% at 5 years and 42% at 10 years. The actuarial incidence of chronic atrial fibrillation was 1.3% at 1 year, 9.8% at 5 years and 22% at 10 years. Independent predictors for paroxismal AF from Cox's model was history of atrial tachyarrhythmias (p < 0.0001), chronic obstructive pulmonary disease (p = 0,006) and age (> 70 years-old) (p = 0.035). Only a history of atrial tachyarrhythmias before pacemaker implant was an independent predictor for chronic atrial fibrillation (p < 0.0001). The odd ratio for paroxismal atrial fibrillation in patients with previous atrial tachyarrhythmias and chronic atrial fibrillation were 6 (2.8-12) and 4 (1.6-9.7) (95% confiance limits). Actuarial incidence of stroke was 3% at 1 year, 10% at 5 years and 14% at 10 years. Independent predictors for stroke were history of peripheral vascular disease (p = 0.033) and hypertensive cardiomyopathy (p = 0.015). Development of paroxysmal and chronic atrial fibrillation during the follow-up were higher in patients with stroke (p < 0.001 and p < 0.05). CONCLUSIONS: Development of atrial fibrillation and stroke in paced patients with sick sinus syndrome are strongly determined by clinical variables. Preimplant paroxysmal atrial tachyarrhythmias is the most important predictor for atrial fibrillation in the follow-up.

[Survival in patients with sick sinus syndrome and artificial pacemaker. Determining clinical factors]. / Supervivencia en pacientes con enfermedad del nodo sinusal portadores de marcapasos. Factores clínicos determinantes.

INTRODUCTION AND OBJECTIVE: The hypothesis that ventricular pacing is the most important factor in the survival of patients with Sick Sinus Syndrome remains controversial. The aim of this report was to determine independent clinical variables to predict survival in paced SSS patients. METHODS: Retrospective, nonrandomized study of 153 patients with a mean age of 69 +/- 11 years, who received an initial pacemaker for Sick Sinus Syndrome between 1980 and 1994: 65 physiologic pacing (32 dual chamber, 33 atrial) and 88 ventricular pacing mode. After a maximum follow up of 177 months (median 57 months) the end point was total mortality. RESULTS: Total mortality was 21%. Using univariate analysis, single chamber ventricular pacing, age > or = 70 years and NYHA > or = 2, was associated with a higher risk for total mortality (4 times increased risk for ventricular pacing compared to other pacing modalities). Independent predictors using multivariate analysis were: 1) NYHA > or = 2 (p < 0.05). 2) Coronary artery disease (p < 0.01). 3) Chronic obstructive pulmonary disease (p < 0.05) and 4) Gender (p < 0.05). CONCLUSIONS: Mortality in patients with the Sick Sinus Syndrome is strongly predicted by preimplant baseline clinical variables. Our data indicate that the role of ventricular pacing mode remains inconclusive. A large, randomized study is necessary to confirm these results.

[An analysis of heart rate variability. Spectrum analysis methods and complex signal demodulation]. / Análisis de la variabilidad de la frecuencia cardíaca. Métodos espectrales y demodulación compleja de la señal.

The analysis of heart rate variability provides valuable information in the noninvasive study of neurovegetative activity and its modifications induced by drugs, physiological maneuvers or disease processes, and in the evaluation of prognosis and risk stratification in different cardiovascular diseases. A review is made of the different methods used to study heart rate variability, and an account is given of the information provided by spectral methods and the new procedures based on the complex demodulation of the time series composed of consecutive cardiac cycles. The limitations of the spectral methods are deal with, particularly in defining the time-dependent changes in variability and their relation to clinical events. Likewise, a description is given of the ability of complex demodulation to define the time course of the oscillations into which the analyzed time series is decomposed. Complex demodulation based on the fast Fourier transform and its inverse is able to establish the instantaneous amplitude and frequency of each of the oscillations contained in the time series, separated by specific filters in the previously selected frequency bands (high: 0.15-0.40 Hz, low: 0.04-0.15 Hz, or very low: < 0.04 Hz), and from which the original signal may be reconstructed. The evaluation of the different methodological approaches, and the analysis of the causal relations between the variability modifications and clinical events will further extend the clinical relevance of the study of heart rate variability.

Continuous heart rate variability monitoring through complex demodulation implemented with the fast Fourier transform and its inverse.

UNLABELLED: A new method for the analysis of 24-hour heart rate variability (HRV) using complex demodulation (CDM) implemented with the fast Fourier transform (FFT) and its inverse is described. In a control group with palpitations and dizzy spells (n = 30, 47.2 +/- 16.7 years) the relationship between HRV parameters and subject age was investigated. CDM was used to obtain the amplitude and frequency of the low frequency (LF) and high frequency (HF) oscillations for 8 diurnal hours and 4 nocturnal hours. Differences between the two periods were seen in the LF/HF ratio (2.2 +/- 0.6 vs 1.5 +/- 0.6; P < 0.0001), HF amplitudes (12 +/- 6 vs 17 +/- 7 normalized units, P < 0.05), and in the mean frequency of the LF oscillations (0.078 +/- 0.008 vs 0.073 +/- 0.007 Hz, P < 0.01). During the daytime, age was inversely correlated to HF amplitude (r = -0.60), directly correlated to HF mean central frequency (r = 0.40), inversely correlated to LF amplitude (r = -0.55), and likewise inversely correlated to LF mean central frequency (r = -0.74, P < 0.001). At night, age was only inversely correlated to HF amplitude and to LF mean central frequency. CONCLUSIONS: Continuous HRV monitoring through CDM implemented with the FFT and its inverse differentiates the periods of diurnal activity and nocturnal rest as an expression of two different activity states of the autonomic nervous system. It allows nonstationary analysis, and separately provides mean and instantaneous oscillation amplitude and frequency. Subject age is not equally related to mean amplitude and frequency of a given oscillation.

Kent bundle visualized in situ at operation after unsuccessful radiofrequency ablation.

Kent bundles are seldom visualized at operation, but, in the patient described, the pathway was subepicardial, running superficial to the right coronary artery. This was probably why radiofrequency ablation failed. When this unusual pathway course is encountered, the epicardial approach should be used at operation.

[The incidence and significance of late potentials in patients with aborted sudden death]. / Incidencia y significado de los potenciales tardíos en pacientes con muerte súbita abortada.

BACKGROUND: Reentrant ventricular tachycardia and fibrillation probably have different electrophysiological bases. Regional conduction delay during sinus rhythm seems to be greatest in patients with spontaneous sustained ventricular tachycardia than in patients with spontaneous sustained ventricular fibrillation. We investigated the prevalence and significance of late potentials in patients with documented VT or VF in the setting of coronary diseases and other organic heart diseases. PATIENTS AND METHODS: Nineteen patients with a history of spontaneous sustained ventricular tachycardia (11 patients) or fibrillation (8 patients) were studied with signal-averaged ECG. All patients had been resuscitated of sudden cardiac death. All recordings were made in sinus rhythm in an antiarrhythmic free state following the recommendations of the Committee of the European Society of Cardiology for data acquisition and analysis of ventricular late potentials using Signal Averaged Electrocardiography. The relationship between this late potentials and tachyarrhythmia inducibility during electrophysiologic study were established. RESULTS: Abnormal late potentials were found in 79% of patients with sudden cardiac death. Patients with spontaneous ventricular tachycardia had a longer ventricular activation time in sinus rhythm than did patients with spontaneous ventricular fibrillation, but this difference did not reach statistic significance. The only analysis of late potentials could not discern the mechanism of sudden cardiac death. However when sudden cardiac death was caused by a spontaneous ventricular tachycardia, a good correlation between abnormal late potentials and induced ventricular tachycardia by programmed stimulation was found. Quantitative indices of late potentials did not correlate with ventricular tachycardia cycle length. CONCLUSIONS: 1) We have found and elevated incidence of abnormal late potentials in patients with sudden cardiac death, and 2) only when the mechanism of sudden cardiac death was a spontaneous VT, we were able to correlate abnormal late potential with provoked ventricular tachycardia during electrophysiologic study.

[Peripheral vascular reflexes during ventricular overdriving and cardiac ischemia. An experimental study]. / Reflejos vasculares periféricos durante sobreestimulación ventricular e isquemia cardíaca. Estudio experimental.

The aim of this paper is to analyze the behaviour of the muscular arteries during ventricular tachycardia in normal and in ischemic hearts. In 19/30 anaesthetized dogs in which a resistance vessel (gracilis muscle artery) was isolated (while innervation and venous backflow remained intact), we performed transient (20 min) coronary artery occlusions and ventricular overdriving (30 sec). A systolic left ventricular pressure decrease (144.2 +/- 18.2 mmHg vs 114 +/- 16.1) (p < 0.001) was produced with the coronary circumflex obstruction. Changes in the end-diastolic left ventricular pressure and muscular artery pressure were not significant. A new systolic left ventricular pressure decrease (114 +/- 16.1 mmHg vs 64.8 +/- 27) (p < 0.001) was induced when the ventricular overdriving (272.2 +/- 46.1 bpm) was added to the coronary circumflex obstruction. The end-diastolic left ventricular pressure increased (6.8 +/- 10.1 mmHg vs 18.3 +/- 4.8) (p < 0.001) and the muscular artery pressure increased (121 +/- 27.3 mmHg vs 158.1 +/- 21.3) (p < 0.01) in these circumstances. When the ventricular overdriving (275 +/- 70.7 bpm) was added to the left descendent anterior coronary occlusion a significative decrease of left systolic ventricular pressure (141 +/- 23 mmHg vs 84.4 +/- 28.4) (p < 0.01) and an increase of the muscular artery pressure (124.3 +/- 25 mmHg vs 149 +/- 25.1) (p < 0.01) was produced. Ventricular overdriving-induced hypotension produced an isolated muscular artery response with clear vasoconstrictor predominance, which indicates that there is a natural compensatory capacity with predominance of efferent sympathetic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

[Peripheral vascular reflexes in obstructions of the left ventricular outflow tract. Experimental study]. / Reflejos vasculares periféricos en las obstrucciones del tracto de salida del ventrículo izquierdo. Estudio experimental.

UNLABELLED: The aim of this work is to analyze the vascular tone behaviour of the muscular arteries in relation to the reflexes generated during aortic root obstruction when spontaneous heart rate is permitted and also with induced tachycardia. An experimental model used involved anaesthetized and intubated dogs in which a resistance vessel (gracilis muscle artery) was isolated, while innervation and venous backflow remained intact. Moderate (54.4 +/- 23.2 mmHg of mean increase in left ventricular pressure) and severe (240.1 +/- 92.5 mmHg) aortic obstructions for 30 s were provoked during spontaneous heart rate (n = 15) and during ventricular overdriving (n = 13) at 200, 250 and 300 bpm for 30 s. Ventricular overdriving at 200, 250, 300 and 400 bpm for 30 s without aortic root obstruction was induced in 20 dogs. Ventricular overdriving in intact hearts produced an initial decrease in the isolated muscular artery pressure of 12.0 +/- 7.2 mmHg (p < 0.01), 9.5 +/- 5.7 mmHg (p < 0.001), 13.6 +/- 8.6 mmHg (p < 0.001) and 14.3 +/- 8.7 mmHg (p < 0.01) at 200, 250, 300 and 400 bpm respectively followed by a recovery, so that at the end of overdriving (30 s), exceeded basal values in 11.9 +/- 10.0 mmHg (p < 0.05), 21.1 +/- 12.4 mmHg (p < 0.001), 21.9 +/- 10.4 mmHg (p < 0.001) and 36.1 +/- 21.3 mmHg (p < 0.001) for each overdriving rate respectively. Aortic obstruction during spontaneous heart rate produced and initial decrease in the isolated muscular artery pressure of 12.0 +/- 7.3 mmHg (p < 0.01), when the aortic obstruction were moderate, and 31.4 +/- 15.7 mmHg (p < 0.01) when the obstructions were severe, followed by a recovery of its basal values at the end of the obstruction time. Ventricular overdriving with aortic root obstruction did not produced significant changes in the isolated muscular artery pressure except in the highest rates of overdriving, that produced an increase of isolated muscular artery pressure of 23.9 +/- 16.2 mmHg (p < 0.01). IN CONCLUSION: ventricular overdriving-induced hypotension in intact hearts produces an isolated muscular artery response with clear vasoconstrictor predominance. Aortic obstruction-induced hypotension does not produce a vasoconstrictor response in the isolated muscular artery but rather an initial vasodilation response which does not revert to vasoconstriction at any point during the hypotensive process. Overdriving was not capable of inducing a peripheral vasoconstriction in presence of aortic root obstruction except in the highest rates of overdriving.