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Biomedical subjects

R García Civera

Publications and source records attributed to R García Civera.

At least 19 recordsLinked to original sources

[Diagnostic accuracy of a protocol in the evaluation of unexplained syncope].

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.

Clinical Protocols↗

[The tilt-table test: is it essential for adequate treatment of vasovagal syncope? Arguments against].

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.

Humans↗

[Survival in patients with sick sinus syndrome and artificial pacemaker. Determining clinical factors].

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.

Age Factors↗

[Auricular fibrillation and stroke in patients with sick sinus syndromeusing permanent pacemakers].

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.

Actuarial Analysis↗

[An analysis of heart rate variability. Spectrum analysis methods and complex signal demodulation].

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.

Electrocardiography↗

[The incidence and significance of late potentials in patients with aborted sudden death].

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.

Aged↗

[Peripheral vascular reflexes during ventricular overdriving and cardiac ischemia. An experimental study].

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)

Acute Disease↗

[Peripheral vascular reflexes in obstructions of the left ventricular outflow tract. Experimental study].

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.

Animals↗

[50 hz alternating current as a cause of inhibition of monopolar ventricular pacemakers].

It is not well established the importance of 50 Hz alternating current (AC) (that supplies most of house appliances) as a source of inappropriate inhibition of today cardiac pacemakers (PM). This problem has been studied in 58 consecutive patients permanently paced (VVI unipolar) for AV block with 27 different PM models from 11 manufacturers. Under ECG monitoring, 50 Hz AC was applied through a pair of electrodes set at both patient's wrists using a battery powered external source, with voltage ranging between 0 and 45 V. Inappropriate inhibition was considered if PM pauses longer than twice the programmed escape interval of the PM were observed during interference. This happened in 46 patients (79.3%), with PM from all 11 manufacturers, with voltages ranging from 3 to 28 V. In each case, inhibition was seen with a narrow voltage window between no interference detection and interference reversion of the PM. Only 3 patients (5.2%) referred perception of electrical current during the study. Three of the patients studied had complained, prior to the study, about dizziness or presyncope related to touching electrical devices and in all of them inappropriate inhibition was observed during interference. We conclude that: 1) it is possible to demonstrate inappropriate inhibition caused by 50 Hz AC galvanic interference in a high percentage of unipolar PM; 2) This inhibition occurs at current levels that in most cases are not sensed by the cutaneous nerves, and 3) although the problem seems to have little clinical significance it should be investigated in paced patients with symptoms attributable to inappropriate inhibition of their PM.

Aged↗

[Anatomo-functional substrate of high risk arrhythmia after myocardial infarct].

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Syncope: epidemiological characteristics of a hospital series].

Three hundred hospital patients with syncope (193 males and 107 females, mean age 61 +/- 17 years) were prospectively evaluated with a standard protocol. Associated diseases were found in 76.7% of cases. The incidence of heart diseases was 50.8% in males vs 32.7% in females (p less than 0.003). The cause of syncope was diagnosed in 250 patients (84%). The diagnosis was made at initial evaluation in 101 patients (group A); in the remaining patients (group B), no diagnosis was made in 25% (16.6% of the overall series) despite a wide array of investigations. Syncope due to arrhythmia was diagnosed in 57.6% (group A: 91.1% group B: 40.7; p less than 0.0001); cardiac syncope not due to arrhythmia was diagnosed in 4%, and other types of syncope in 21.6% (group A; 6.9%; group B: 29.1%; p less than 0.0001). It is concluded that a) the hospital population of patients with syncope represents a subgroup of advanced age and a high incidence of associated diseases; b) one third of patients were diagnosed at the initial evaluation, whereas in 25% of the remaining ones no diagnosis was obtained, and c) in these patients, arrhythmia is the most likely cause of syncope.

Adult↗