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Biomedical subjects

L M Rodriguez

Publications and source records attributed to L M Rodriguez.

69 records · Page 4Linked to original sources
PubMed1992

Clinical characteristics and electrophysiologic properties of atrioventricular accessory pathways: importance of the accessory pathway location.

OBJECTIVES: This study was designed to assess the influence of accessory atrioventricular (AV) pathway location on the clinical and electrophysiologic characteristics of 384 consecutive symptomatic patients having a single accessory pathway. METHODS: Four locations were studied: left free wall (n = 270), posteroseptal (n = 52), anteroseptal (n = 29) and right free wall (n = 33). Ten clinical variables and 12 electrophysiologic variables were analyzed, including the effective refractory period of the accessory pathway and the different clinically occurring and inducible arrhythmias. RESULTS: Only two clinical findings were associated with accessory pathway location: 1) later age at onset of symptoms in the left free wall versus other accessory pathway locations (24 +/- 12 vs. 20 +/- 11 years, p = 0.02), and 2) later age at the time of electrophysiologic study in the left free wall accessory pathway location (36 +/- 13 vs. 32 +/- 11 years, p = 0.01). Six electrophysiologic variables showed a correlation with the accessory pathway location: 1) retrograde conduction only was found less frequently in right free wall (9%) and anteroseptal (10%) than in left free wall (26%) and posteroseptal (29%) accessory pathway locations (p = 0.05); 2) the retrograde effective refractory period of the accessory pathway was shorter in anteroseptal (253 +/- 52 ms) and left free wall (270 +/- 72 ms) as compared with right free wall (296 +/- 101 ms) and posteroseptal (301 +/- 76 ms) locations (p = 0.05); 3) retrograde decremental conduction over the accessory pathway was present in the posteroseptal (17%) and left free wall (3%) but absent in the other locations (p less than 0.001); 4) anterograde decremental conduction was only seen in the right free wall location (12%) (p less than 0.001); 5) orthodromic reentrant tachycardia was induced less frequently in the right free wall than in other locations (70% vs. 93%, p less than 0.001); and 6) inducibility of atrial fibrillation was greater in anteroseptal (62%) than in right free wall (21%), left free wall (44%) and posteroseptal (36%) locations (p = 0.01). CONCLUSIONS: The location of the accessory AV pathway is associated with specific electrophysiologic characteristics.

Adolescent↗
PubMed1990

Time course and prognostic significance of serial signal-averaged electrocardiograms after a first acute myocardial infarction.

The prognostic significance of serial signal-averaged electrocardiograms recorded during the first 3 days (period 1), in the second week (period 2) after a first acute myocardial infarction (AMI) and 6 months later (period 3) was prospectively assessed in 190 patients. No patients were treated with thrombolytic therapy. Patients with conduction disturbances were excluded. Mean age of the 190 patients was 57 years (range 34 to 74) and mean left ventricular ejection fraction was 40 + 6% (range 12 to 70). Eighty-four patients had an anterior wall AMI and the remaining 106 patients an inferior wall AMI. After a mean follow-up of 24 months, 16 patients developed sustained symptomatic monomorphic ventricular tachycardia, 7 patients were resuscitated from an episode of ventricular fibrillation, and 10 patients died suddenly. Multivariate regression analysis using continuous variables showed that the strongest predictor of sustained ventricular tachycardia and ventricular fibrillation was the left ventricular ejection fraction (p less than 0.0001) followed by the duration of QRS complex on the signal-averaged electrocardiogram recorded during the first 3 days of AMI (p less than 0.0005). Sudden death was only predicted by left ventricular ejection fraction (p less than 0.02).

Death, Sudden↗
PubMed1990

Maternal weight gain in low-income black and Hispanic women: evaluation by use of weight-for-height near term.

This study determined the prevalence of low maternal weight gain among a target group of low-income black and Hispanic women and compared weight-for-height near term with total weight gain during pregnancy as an index of birth-weight classification. One-third (30.8%) of 325 women had weights near term less than 120% of their standard pregravid weight-for-height; there was little variation by ethnic group. After adjusting for gestational age as a covariate of birth weight (P = 0.0001), maternal weight-for-height near term (P = 0.0010), ethnicity (P " 0.0068), and parity (P = 0.0083) significantly influenced birth weight. Women with near-term weights greater than or equal to 120% of their standard pregravid weight-for-height delivered infants with higher birth weights (P = 0.001). Comparison of weight-for-height near term with total weight gain as an index of birth-weight classification (less than or greater than or equal to 3000 g) revealed that the two methods differ in terms of sensitivity and specificity with variation in pregravid weight.

Adolescent↗
PubMed1990

Exercise-induced sustained symptomatic ventricular tachycardia: incidence, clinical, angiographic and electrophysiologic characteristics.

Among 112 patients with sustained ventricular tachycardia, 15 were found to have exercise-induced symptomatic ventricular tachycardia. This population was divided into two subgroups: group 1A included five patients with coronary artery disease and group 1B consisted of 10 patients with no structural heart disease. All patients underwent clinical examination, exercise electrocardiography, left ventriculography, coronary angiography (n = 14) and electrophysiologic study. In group 1B, right ventriculography (n = 7), M mode and two-dimensional echocardiography were also obtained. Group 1A patients were compared with a population of 27 patients with coronary artery disease and chronic sustained ventricular tachycardia not related to exercise (group 2). There were no statistically significant differences between group 1A and group 2 in terms of age, sex, incidence of prior myocardial infarction, NYHA functional class, angina pectoris, symptoms during arrhythmia, severity and extent of coronary arterial lesions, ventricular dysfunction and wall motion abnormalities. In group 1B, coronary angiography and right and left ventricular function were normal. During electrophysiologic study, ventricular tachycardia was initiated in four group 1A patients. In group 1B, ventricular tachycardia was initiated in eight patients. In four of these patients ventricular pacing had to be combined with isoproterenol administration. In group 2, ventricular tachycardia was induced in 26/27 patients. From this study we conclude that in patients with coronary artery disease the electrophysiologic substrate of exercise-related sustained ventricular tachycardia does not differ from the substrate of non-exercise-related ventricular tachycardia. Re-entry is the most likely electrophysiologic mechanism. In patients without structural heart disease, the mechanism of the arrhythmia remains speculative.

Angiography↗
PubMed1989

Mechanisms of termination of supraventricular tachycardias by intravenous class III antiarrhythmic agents. A comparison of amiodarone and sotalol.

The effects of amiodarone and sotalol were studied with programmed electrical stimulation of the heart in 19 patients with inducible tachycardia (AV nodal tachycardia: 10 cases, circus movement tachycardia: 9 cases). Amiodarone was administered intravenously at a dose of 300 mg over 2 min and sotalol at a dose of 1.5 mg kg-1 over 10 min. Both i.v. amiodarone and sotalol lengthened the transnodal conduction time, the effective refractory period of the AV node and the AV nodal Wenckebach cycle length. Only sotalol significantly lengthened the effective refractory periods of the right atrium and the right ventricle. Infused intravenously during tachycardia, amiodarone interrupted arrhythmia in five of six patients and sotalol in seven of ten cases. Tachycardia was stopped by blockade of the impulse into the AV node in three amiodarone patients and in five sotalol patients. In the remaining four cases, the weak link of the circuit was the accessory pathway. Thus i.v. sotalol exhibits electrophysiologic effects consistent with both class II and III activity, whereas the effects of i.v. amiodarone are the result of different activities throughout all areas of the cardiac tissue.

Adolescent↗
PubMed1989

Antegrade conduction over a concealed accessory pathway after His bundle catheter ablation.

The existence of unidirectional retrograde preexcitation or concealed bypass fibers and their role in paroxysmal supraventricular tachycardia have been known for a long time. However, the exact anatomic and physiological nature of this retrograde limb remains unclear. We report here on a patient who had a concealed accessory pathway (AP) with circus movement tachycardia. After His bundle catheter ablation the AP had the property to conduct in the antegrade direction. The absence of antegrade conduction over the AP before ablation is likely due to its decremental properties of conduction and to repetitive retrograde concealed conduction from the normal pathway.

Adult↗
PubMed1987

Effects of intravascular volume expansion on lung fluid balance in a canine model of septic shock.

We tested the early effects of endotoxin on both the permeability of capillary membranes and microvascular pressure. One group of dogs (n = 8) were fluid loaded (30 ml/kg dextran-40) after having been subjected to a 2-h Escherichia coli endotoxin infusion (0.25 micrograms/kg X min). A second control group of animals (n = 6) was submitted to a similar (25 ml/kg) volume loading over an equivalent 30-min period. We estimated extravascular lung water (EVLW), calculated the effective pulmonary capillary pressure, and determined the alveolar-capillary filtration coefficient (Kf) after volume loading. Only the septic animals consistently showed elevated EVLW values consistent with pulmonary edema. The results showed, however, that the Kf calculated for the dogs that received endotoxin was no different from that of control group (Kf = 0.005 ml/kg X min X mm Hg). Instead, endotoxin constricted the pulmonary veins which led to a considerable rise in microvascular hydrostatic pressure above the level at which the lungs could not resist edema formation. We conclude that acute pulmonary edema that follows endotoxin insult and subsequent therapeutic volume replacement is due to an increased filtration force instead of an alteration in the microvascular permeability.

Animals↗
PubMed1987

A comparison of Escherichia coli endotoxin single bolus injection with low-dose endotoxin infusion on pulmonary and systemic vascular changes.

The purpose of this study was to compare effects of single bolus endotoxin injection with sustained low-dose endotoxin infusion on systemic and pulmonary hemodynamics in anesthetized dogs. When administered as a bolus (.01 mg/kg), endotoxin induced systemic vascular changes whose evolution could be divided into two consecutive phases. In the early phase, marked hepatic venoconstriction caused a rise in portal pressure followed by abrupt decreases in both cardiac output and blood pressure. Mean pulmonary artery pressure remained unchanged. Because of lowered blood flow, both peripheral and pulmonary resistances increased. The rise in the latter was due to a prominent vasoconstriction of pulmonary arteries. Following a partial spontaneous recovery from shock, the late phase was characterized by a low-output state combined with high systemic vascular resistances. In contrast, when endotoxin was given at a slow infusion rate (250 ng/kg/min) over a 2-hour period of time, cardiovascular effects were basically different from the preceding ones, and they were measurable only after a certain period of time had elapsed from the start of endotoxin insult. First, blood pressure decreased gradually, while cardiac output remained almost unchanged. Therefore, peripheral resistance was decreased. Second, in the pulmonary circulation, the site of vasoconstriction was shifted from arteries to veins. We conclude that there is a fundamental difference in the response of the dog's systemic and pulmonary circulation as a function of endotoxin administration as either a bolus or slow infusion. This difference might be due to sudden elevated portal pressure responsible for an abrupt cardiovascular collapse in dogs subjected to bolus injection.

Animals↗
PubMed1987

Pulmonary hydrostatic microvascular pressure changes and lung fluid balance during histamine infusion in intact dogs.

The effects of histamine on systemic and pulmonary hemodynamics of dogs were studied in six intact animals. Histamine infusion resulted in an almost immediate, precipitous fall in blood pressure (BP), pulmonary capillary wedge pressure (PCWP), and right atrial pressure (RA) as well as an increase in heart rate. Partial recovery occurred about 5 minutes after infusion was stopped. Cardiac output did not change significantly. Consequently, the calculated peripheral resistance decreased afterwards. Hepatic portal pressure rose significantly after 2 minutes of histamine infusion with partial recovery in about 5 minutes. Suprahepatic venous pressure did not change significantly. Although pulmonary arterial pressure did not necessarily rise, total pulmonary vascular resistance increased in every dog. If the absolute level in pulmonary arterial resistance remained greater (Ra 105 mm Hg/liter-1 min X kg-1) than the level of venous resistance (Rv 70 mm Hg/liter-1 min X kg-1), the relative increase in venous resistance (100%) was higher than the increase in Ra (35%). On the other hand, effective capillary pulmonary pressure remained unchanged. Central blood volume and extravascular lung water increased upon histamine infusion and returned rapidly to baseline when histamine infusion was stopped. No significant changes occurred in either effective pulmonary compliance and arterial blood gas values. Our data lead us to conclude that histamine's major action occurs in the venous pulmonary segments; pulmonary and splanchnic blood pooling is responsible for a fall in cardiac preload; and an increase in extravascular lung water and central blood volume with unchanged effective pulmonary pressure might be explained by an increase in microvascular surface area.

Animals↗
PubMed1986

Effects of Escherichia coli endotoxin on pulmonary vascular resistance in intact dogs.

The effects of endotoxin on pulmonary hemodynamics were studied in seven intact dogs. The distribution of pulmonary vascular resistance was estimated by the effective pulmonary capillary pressure, which was derived from the pressure transient recorded while the pulmonary artery catheter was rapidly wedged. After the injection of endotoxin, cardiac output and aortic pressure consistently fell. Pulmonary artery occlusion (wedge) pressure also decreased, but not significantly. Although pulmonary artery pressure did not necessarily rise, total pulmonary vascular resistance increased in every dog. The absolute increase in pulmonary artery resistance was greater (142 mm Hg/L X min/kg); than in venous resistance (111 mm Hg/L X min/kg); however, the relative increase in venous resistance was higher (410% for venous resistance vs. 220% for pulmonary artery resistance). As a result of venoconstriction, there was a consistent increase in effective pulmonary capillary pressure (from 2.5 to 6.3 mm Hg). Our data indicate that the pulmonary vascular response to endotoxin injection is characterized by constriction of both pulmonary arteries and pulmonary veins. The capillary wedge pressure did not reflect the pulmonary microvascular pressure, since it varied in the opposite direction to the effective capillary pressure.

Animals↗
PubMedDate not supplied

Idiopathic ventricular tachycardia--characterisation and radiofrequency ablation.

Forty patients (14 women and 26 men; mean age 40 +/- 13 years, range 7 to 60) diagnosed to have idiopathic ventricular tachycardia (right ventricular 28, left ventricular 12) underwent electrophysiologic study and radiofrequency catheter ablation. Echocardiography, signal averaging, magnetic resonance imaging and cardiac catheterisation with angiography were used as indicated to rule out identifiable underlying etiologies. Gross localisation of the area of origin of the ventricular tachycardia from the surface electrocardiogram could be made in all cases. Accurate localisation of the site of origin was done by activation mapping and pace mapping. Radiofrequency application was successful in achieving a cure in 34 (85%) patients, with a mean of 8.3 +/- 4.7 energy applications and a fluoroscopy time of 38 +/- 19 minutes. Unsuccessful cases were characterised by wide and slurred QRS complexes during ventricular tachycardia, possibly indicating a deeper intramyocardial or epicardial site of origin of the tachycardia. Radiofrequency ablation appears to be the treatment of choice for symptomatic idiopathic ventricular tachycardia, having a high success and safety rate.

Adult↗