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Biomedical subjects

A Castellanos

Publications and source records attributed to A Castellanos.

At least 19 recordsLinked to original sources
PubMed1992

Mechanisms and dynamics of episodes of progression of 2:1 atrioventricular block in patients with documented two-level conduction disturbances.

Twenty episodes of progression of 2:1 atrioventricular (AV) block were identified during incremental atrial stimulation in 7 patients with documented (2-level) block in the AV node and His-Purkinje system. All occurred at cycle lengths shorter than those at which stable 2:1 HV block had been detected. Thirteen episodes were typical since 2:1 increased to 3:1 AV block when an atrio-His (AH) Wenckebach period was completed with an atrial impulse that otherwise would have been conducted. These episodes occurred with dynamic A(M): V(N) ratios similar to those seen at the AV node. Seven atypical episodes were identified (while AH Wenckebach periods were occurring): (1) 2:1 increasing to 3:1 AV block and then to 4:1 AV block resulting from prolonged refractoriness in the His-Purkinje system subsequently followed by concealed conduction in the latter structure; (2) conversion of 3:2 directly into 3:1 AV block due to block of the next-to-last atrial impulse in the His-Purkinje system with completion of AH Wenckebach period with the following atrial impulse; and (3) 4:2 AV block presumably due to supernormal conduction in a transversely dissociated His-Purkinje system. These episodes occurred with A(M): V(N) ratios, which in other structures would have been indicative of different degrees of AV block. In conclusion, progression of 2:1 AV block during documented 2 level conduction disturbances (1) can be explained by mechanisms different than those currently known, and (2) has rich, but different dynamics from those observed exclusively in the AV node and exclusively in the His-Purkinje system.

Bundle of His↗
PubMed1992

Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm.

BACKGROUND: Silent myocardial ischemia in patients with coronary atherosclerosis is associated with an increased risk of adverse cardiac events, including sudden death. The relation between silent ischemia and the initiation of potentially fatal ventricular arrhythmias has not been defined, however. METHODS: As part of a long-term study of sudden cardiac death, data on arrhythmias, coronary anatomy, and responses to ergonovine testing to provoke coronary-artery spasm were collected prospectively among survivors of out-of-hospital cardiac arrest who had no flow-limiting coronary-artery lesions, prior myocardial infarctions, or other structural causes of cardiac arrest and no angina pectoris. Associations between silent myocardial ischemia due to coronary-artery spasm and the occurrence and characteristics of life-threatening ventricular arrhythmias were studied by both invasive and noninvasive techniques. RESULTS: Silent ischemic events were associated with the initiation of life-threatening ventricular arrhythmias in five patients with induced or spontaneous focal coronary-artery spasm (or both). These patients were identified among a group of 356 survivors of out-of-hospital cardiac arrest who were evaluated between 1980 and 1991. In two of the five patients reperfusion, rather than ischemia itself, correlated with the onset of the ventricular arrhythmia. Only one of the five had an inducible arrhythmia during electrophysiologic testing. Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested. CONCLUSIONS: Silent myocardial ischemia due to coronary-artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting structural coronary-artery lesions. The role of silent ischemia, reperfusion, or both in the initiation of fatal arrhythmias in larger groups of patients with advanced coronary-artery lesions remains to be defined.

Adult↗
PubMed1992

[Allergic conjunctivitis].

The eye reacts to foreign substances through a variety of specific and non-specific defense mechanisms. Constantly exposed to a great variety of microorganisms, the eye is capable of protecting itself without altering its own structure and function. Its resistance relies upon anatomic and physiological properties of its external components (eyelids, tears, conjunctiva and cornea). Most of the times, the conjunctiva becomes affected, resulting in a clinical picture of conjunctivitis where allergy predominates, expressed as allergic rhinoconjunctivitis, allergic conjunctivitis, vernal keratoconjunctivitis, giant papillary conjunctivitis and flictenular conjunctivitis. The physiopathology is considered to be of type I reaction (IgE mediated). Frequent complains often associated with other allergic diseases are: pruritus, tearing, photofobia and ocular redness. The diagnosis of allergic conjunctivitis in done by means of a throughout clinical history, conjunctival citology and evaluation of specific IgE with immediate skin tests. Treatment is symptomatic (antihistamines, antibiotics and/or topic steroids), but prevention (environmental control and sodium cromoglycate) and specific immunotherapy must be considered.

Conjunctivitis, Allergic↗
PubMed1992

Sudden cardiac death. Structure, function, and time-dependence of risk.

Sudden cardiac death (SCD) remains a major unresolved clinical and public health problem, accounting for more than 300,000 of the deaths in the United States annually. The ability to identify potential SCD victims is limited by the large size of the population subgroups that contain the majority of SCD victims and by the apparent time dependence of risk of sudden death. The latter refers to the tendency for SCD to follow other cardiovascular events within a high-risk period of 6-18 months after a primary cardiovascular event, with risk decreasing thereafter. The combination of time dependence and denominator pool size provides a basis for future studies to identify the higher risk individuals. Pathophysiologically, SCD can be viewed as an interaction between structural abnormalities of the heart, transient functional disturbances, and the specific electrophysiological events responsible for fatal arrhythmias. Structural abnormalities provide the anatomic substrate for chronic risk and include the myocardial consequences of coronary artery disease, left ventricular hypertrophy, myopathic ventricles, and specific electrophysiological anatomic abnormalities such as bypass tracts. The functional factors responsible for destabilizing a chronic electrophysiological abnormality include transient ischemia and reperfusion, systemic factors (e.g., electrolyte disturbances, acidosis, and hemodynamic dysfunction), autonomic fluctuations (both systemic and at a tissue level), and myocardial toxic influences such as proarrhythmic effects of various drugs. Each of these changes is able to destabilize myocardial membrane integrity, some regionally and some globally, making the heart susceptible to an electrical triggering event for ventricular tachycardia or fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1991

Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias.

Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61%) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (+/- SD) plasma procainamide level was 7.2 +/- 2.8 micrograms/ml after intravenous dosing and 7.9 +/- 2.5 micrograms/ml after oral dosing (p = 0.09). In 15 (65%) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 +/- 2.1 micrograms/ml, oral = 7.5 +/- 2.1 micrograms/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 +/- 3.3 micrograms/ml) and oral (8.8 +/- 3.1 micrograms/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47%) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 +/- 2.7 micrograms/ml) after failure of intravenous procainamide (mean plasma level 10.3 +/- 2.3 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Myocarditis simulating acute transmural myocardial infarction.

A patient with cardiogenic shock had typical electrocardiographic findings of acute anterior transmural myocardial infarction. Cardiac catheterization revealed normal coronary arteries and severe biventricular failure. Postmortem examination confirmed normal coronary arteries; acute myocarditis, but no evidence for infarction, was found. Electrocardiographic changes of myocarditis may be indistinguishable from acute transmural infarction. In suspected cases, cardiac catheterization should be considered prior to thrombolytic therapy.

Acute Disease↗
PubMed1990

Interrelationship of variable coupling, multiformity and repetitive forms: implications for classification of ventricular arrhythmias.

One hundred 24-hour ambulatory electrocardiograms were prospectively examined to determine the relationship of variable coupling and multiformity of single premature ventricular complexes to repetitive forms. Premature ventricular complexes were present in 86 patients and were categorized by a three-tier decision-making tree using (1) multiformity confirmed in two channels, (2) variable coupling of greater than 80 msec of premature ventricular complexes of similar QRS morphologies, and (3) repetitive forms of greater than or equal to 2 premature ventricular complexes. Variable coupling was present in 51 patients, among whom 35 (69%) had repetitive forms; multiformity was present in 46 patients, among whom 37 (80%) had repetitive forms; repetitive forms were present in 41 patients, among whom only one patient (2%) did not demonstrate multiformity or variable coupling. Variable coupling, multiformity, or either were significantly associated with the occurrence of repetitive forms (chi square = 34, 15, 29, respectively, each p less than 0.005). There was a bimodal distribution between patients with uniform, fixed coupled premature ventricular complexes who had rare repetitive forms (1 of 26) and patients with multiformity and variable coupling of premature ventricular complexes who had significantly more repetitive forms (30 of 37; p less than 0.001). The frequency distribution of repetitive form length suggested a natural break point between five and six consecutive complexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1989

Efficacy of intravenous propranolol for suppression of inducibility of ventricular tachyarrhythmias with different electrophysiologic characteristics in coronary artery disease.

The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed greater than or equal to 1 membrane-active antiarrhythmic drug (mean 2.2 +/- 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had greater than or equal to 1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29%) became noninducible (responders) and 17 patients (71%) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 +/- 14 vs 86 +/- 11 beats/min, p less than 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 +/- 14 to 80 +/- 9 beats/min, p less than 0.001) than in nonresponders (from 86 +/- 11 to 74 +/- 9 beats/min, p less than 0.01) (p less than 0.05 between the groups), despite equal plasma propranolol concentrations (84 +/- 50 vs 88 +/- 43 ng/ml, difference not significant). Seven of 11 patients (64%) who had greater than or equal to 1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after beta blockade (p less than 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 +/- 38 vs 302 +/- 66 ms, p less than 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.

Aged↗
PubMed1989

Changes in spontaneous sinus node rate as an estimate of cardiac autonomic tone during stable and unstable ventricular tachycardia.

Changes in sinus node rate were measured as an estimate of reflex control of cardiac autonomic tone during 32 episodes of stable ventricular tachycardia (without loss of consciousness) and 21 episodes of unstable ventricular tachycardia (loss of consciousness requiring electrical cardioversion) in 32 patients without retrograde ventriculoatrial conduction. Sinus node rate was measured before induction of ventricular tachycardia (at 5 s intervals during tachycardia) and 5 s after termination of ventricular tachycardia. It increased from 85 +/- 12 beats/min to a maximum of 109 +/- 25 beats/min during stable ventricular tachycardia (p less than 0.001) and from 82 +/- 15 beats/min to a maximum of 105 +/- 34 beats/min during unstable ventricular tachycardia (p less than 0.001). During unstable ventricular tachycardia, the increase in sinus rate was more abrupt and was followed by a sharp decrease beginning before termination of the tachycardia and resulting in a slower rate after termination (56 +/- 15 beats/min) than before tachycardia (p less than 0.001). Stable ventricular tachycardia resulted in a continuous increase of sinus node rate, which remained higher after termination (102 +/- 15 beats/min) than before tachycardia (p less than 0.001). Autonomic mechanisms responsible for changes in sinus rate were evaluated by reinducing the ventricular tachycardia after beta-adrenergic blockade by propranolol in 10 patients. Intravenous propranolol (mean dose 11 +/- 4 mg) had no effect on the magnitude of increase in sinus rate (+18 +/- 6 beats/min before and +17 +/- 7 beats/min after propranolol).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗