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Biomedical subjects

J Brinker

Publications and source records attributed to J Brinker.

28 records · Page 2Linked to original sources
PubMed1988

Systolic expansion of the aortic root: an echocardiographic and angiographic sign of aortic composite graft dehiscence.

Precise diagnosis of aortic composite graft dehiscence may be difficult. We present a case illustrating this problem and its resolution. Two-dimensional echocardiography and contrast ventriculography revealed a space adjacent to the aortic valve conduit that demonstrated marked systolic expansion. The dynamic variation of this space was secondary to communication with the left ventricular cavity caused by disruption of the composite graft valve ring. Thus, systolic expansion of the aortic root is a useful echocardiographic and angiographic sign of composite graft dehiscence.

Adult↗
PubMed1988

Increased pacing threshold after an automatic defibrillator shock in dogs: effects of class I and class II antiarrhythmic drugs.

A high energy shock delivered by an automatic defibrillator may interfere with pacemaker function. To provide insight into the changes that occur in the threshold for ventricular pacing after the shock from an automatic defibrillator, we measured the time to capture during asynchronous ventricular pacing in dogs from endocardial or epicardial sites, after a 30 joule shock was delivered via conventional automatic defibrillator (AICD) patch electrodes. After a 30 joule shock, there was a transient loss of ventricular capture. The duration of capture loss was related to current strength. During endocardial pacing at threshold current, the time to capture was 4.9 +/- 1.2 s, whereas at current values twice threshold the time to capture from endocardial pacing was 2.2 +/- 0.9 s. No difference was found between endocardial and epicardial pacing sites in the time to capture. To ascertain the mechanism of capture loss we: (1) examined the effects of converting the pacing catheter to a current sink (transiently shunting to ground); (2) altered excitability by an infusion of flecainide; (3) blocked sympathetic input (propranolol). No change in time to capture was noted by shunting the pacer to ground. After an infusion of flecainide the time to capture from endocardial pacing was significantly prolonged to 14.9 +/- 2.2 s at the threshold value (P less than .01) and 5.6 +/- 2.1 s at twice threshold (P less than .05). Conversely, intravenous propranolol had no effect on the time to capture after shock from endocardial pacing. These data indicate that there is a transient increase in pacing threshold after the shock from an automatic defibrillator.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Automatic implantable cardioverter defibrillator/permanent pacemaker interaction: loss of pacemaker capture following AICD discharge.

A 78-year-old man treated with amiodarone for recurrent ventricular tachycardia, had sequential placement of a bipolar VVI pacemaker and an automatic implantable cardioverter defibrillator (AICD). During defibrillation threshold testing, there was failure to capture of the pacer in the post-shock period. The time of failure to capture appeared energy-related: the greater the energy delivered, the longer the failure to capture. Careful attention will be necessary in constructing combined AICD/pacemaker units.

Aged↗
PubMed1983

Transpulmonary artery correction of anomalous origin of the left coronary artery by saphenous vein graft.

A transpulmonary saphenous vein graft was used to repair an anomalous origin of the Left coronary artery from the pulmonary artery (ALCAPA). Postoperative cardiac catheterization revealed correction of the previous systemic arterial to venous shunt and a patent intrapulmonary artery conduit. The patient has experienced substantial symptomatic and functional improvement from the operation operation despite development of mild pulmonary outflow obstruction. Saphenous vein transpulmonary artery correction for ALCAPA offers an alternative surgical approach and may be the procedure of choice when anatomy or prior surgery preclude the more standard modes of revascularization.

Adult↗
PubMed1982

Determinants and clinical significance of jugular venous valve competence.

We studied the function of right internal jugular vein valves during cardiac catheterization in 32 patients and external jugular vein valves in vitro from 13 dogs. Patients with normal central venous pressure had competent valves during cough-induced transvalvular pressure gradients of 52.4 +/- 8.6 mm Hg. Ten of 15 patients with elevated central venous pressure had either incompetent or absent internal jugular valves, the latter occurring only in patients with long-standing, severe tricuspid regurgitation. During coughing, competent valves were also demonstrated in the left internal jugular and in the right and left subclavian veins. The excised canine valves were competent at a static transvalvular pressure of 81.8 +/- 3.7 mm Hg. Five of six excised valves remained competent during pulsatile transvalvular pressure of 64.8 +/- 1.9 mm Hg. Thus, thoracic inlet venous valves are usually competent during sudden increases in intrathoracic pressure. These valves may play an important role in establishing the extrathoracic arteriovenous pressure gradient necessary for forward blood flow during cardiopulmonary resuscitation and other states with high intrathoracic pressure.

Adult↗
PubMedDate not supplied

A behavioral analysis of chest pain in patients suspected of having coronary artery disease.

A group of 83 men and women who had been referred to Johns Hopkins Hospital for cardiac catheterization for evaluation of chest pain and possible coronary artery bypass surgery were assessed behaviorally for their chest pains. During the approximately 2-week period between clinical evaluation and catheterization, the patients completed self-report forms about their chest pains. Patients completed one form for each episode of chest pain. Referring physicians also completed a form about the patients "typical" chest pain. The data were analyzed in terms of the antecedents, concomitants, and consequences of the chest pain, and patients' reports were compared to physicians' judgments. Major findings were as follows: 1) Antecedents--most episodes occurred while the patient was at home at times when his mood was one of contentment. 2) Concomitants--the average patient reported fewer than one episode per day which persisted for about 4 min and was rated as 36 on a scale of 0 to 100. The most common physical symptoms accompanying the episode were breathlessness and weakness, and the most common pain sensations were reported to be pressing or aching. There was no consistency among patients either in primary location or path of radiation of the pain. Duration of pain did not correlate significantly either with sensation or symptoms; however, severity rating did correlate with symptoms and sensations. 3) Consequences--most episodes were self-treated with nitroglycerin or rest. Patients typically returned to their ongoing activities; however, there were a number of interactions between the likelihood of returning to ones ongoing activity and the antecedents of the episodes. 4) The referring physicians significantly overestimated the frequency and severity of their patients' episodes; furthermore, they were selective in their abilities to identify correctly the antecedents or concomitants associated with their patients' pain--e.g., they were reliable in their judgments about subjects who had sleep-related episodes; however, they were inaccurate in characterizing the typical sensations or symptoms reported by their patients. It is suggested that a behavioral analysis may enable a physician to characterize his patient's chest complaints better, and perhaps also may facilitate the differentiation between chest complaints indicative of coronary artery disease and chest complaints of a noncoronary origin.

Coronary Disease↗
PubMedDate not supplied

The relation of chest pain symptoms to angiographic findings of coronary artery stenosis and neuroticism.

The present article examines the relations among self-reported and physician-estimated chest pain variables to angiographically determined coronary stenosis (CAD) and neuroticism scores. Six of the 48 chest pain variables were significantly related to coronary stenosis, but only one variable, chest pain elicited by walking, was positively related to stenosis. Chest pain during sleep, sighing and dizziness accompanying chest pain, right lower chest pain radiation, and infrequent rest to cope with the chest pain were significantly negatively related to stenosis. Neuroticism scores (N) were not significantly related to CAD but were significantly correlated with 13 of the 48 chest pain variables. In addition to correlating positively with the chest pain variables that were negatively correlated with CAD, N scores were significantly related to higher pain severity ratings, being angry, annoyed, tense, afraid, worried, and upset before the chest pain, breathlessness during the pain episode, and pain sensations described as stabbing. The six chest pain variables significantly correlated with CAD yielded a multiple correlation of 0.58, accounting for 34% of the variance, whereas N scores accounted for only 5% of the variance; however, N contributed less than 1% unique variation to stenosis in combination with the six chest-pain variables. That N influences chest pain reports more than actual stenosis is further confirmed by the results of physicians' ratings of their patients' typical chest pain episodes. Recognition of patients' characteristic levels of distress or neuroticism may aid physicians in evaluating symptoms more accurately and in treating their chest pains more appropriately.

Age Factors↗
PubMedDate not supplied

Prevention of contrast media-induced renal dysfunction with prostaglandin E1: a randomized, double-blind, placebo-controlled study.

Preexisting renal impairment is an all-encompassing risk factor for radiocontrast-associated nephrotoxicity. Renal impairment appears to be associated with the inadequate production of renal prostaglandins at the critical time of radiocontrast administration and for a variable time period afterward. We prospectively studied 130 patients with chronic renal insufficiency (serum creatinine > or =1.5 mg/dL) who were undergoing radiocontrast administration. Using a double-blind, randomized, prospective technique, patients were assigned to either placebo or one of three prostaglandin E1 (PGE1) treatment groups (10, 20, or 40 ng/kg/min). Infusion was started 60 +/- 30 minutes before the administration of radiocontrast and was continued for a total of 6 hours. In the placebo group, radiocontrast administration resulted in a mean increase (+/- SD) in serum creatinine of 0.72 +/- 1.15 mg/dL at 48 hours. This increase was less in each of the PGE1 treatment groups after 48 hours, with a significant difference between placebo and the 20 ng/kg/min PGE1 group (P = 0.01). Using baseline adjusted means, analysis of covariance with baseline serum creatinine as the covariable demonstrated significant differences between the placebo and 20 ng/kg/min PGE1 group (P = 0.03) and between the placebo and 10 ng/kg/min PGE1 group P = 0.047). In a subgroup analysis of the diabetic patients, the increase in serum creatinine was less pronounced in the three PGE1 groups versus the placebo group, and the 20 ng/kg/min PGE1 group had the most favorable outcome. The parenteral administration of PGE1 immediately before radiocontrast exposure and continued for a period of 5 to 5.5 hours significantly reduced the elevation of serum creatinine poststudy. The most effective of the three PGE1 dosing regimens was 20 ng/kg/min.

Aged↗