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Biomedical subjects

R Cardinal

Publications and source records attributed to R Cardinal.

99 records · Page 6Linked to original sources
PubMed1971

Repression of the overproduction of porphyrin precursors in acute intermittent porphyria by intravenous infusions of hematin.

In a patient with a severe attack of acute intermittent porphyria, hematin given intravenously caused marked diminution of serum delta-aminolevulinic acid and porphobilinogen. The decline of aminolevulinate was more rapid than that of porphobilinoge. After 2 days of hematin administration, about 5 days were required for delta-aminolevulinic acid, and 11 days for porphobilinogen to return to the concentrations that were detected before treatment. Urinary excretion of both compounds also decreased after hematin administration. Considerable amounts of porphobilinogen were also found in the cerebrospinal fluid of the patient.

Adult↗
PubMedDate not supplied

Relationship between an arrhythmogenic action of lidocaine and its effects on excitation patterns in acutely ischemic porcine myocardium.

To investigate the relationship between the effects of lidocaine on excitation patterns and its effects on the incidence of arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine, at a dose of either 2.5, 5.0, or 10.0 mg/kg i.v., in 29 open-chest anesthetized pigs. Sixty-three unipolar electrograms and a surface lead electrocardiogram were continuously recorded during atrial pacing and spontaneous ventricular arrhythmias. Ventricular fibrillation (VF) occurred only in four of a total of 45 control occlusions. VF occurred in two of five pigs following injection of lidocaine 2.5 mg/kg, in 15 or 17 pigs following injection of a 5 mg/kg dose, and in all three preparations following injection of a 10 mg/kg dose. Just prior to VF during occlusions preceded by injections of lidocaine 5 mg/kg, activation time of ischemic myocardium in atrial-paced beats was delayed by only 30 +/- 17 ms beyond preocclusion values, compared with 18 +/- 11 ms at a similar time during control occlusions and 33 +/- 18 ms at the end of control occlusions (mean +/- SD; n = 8). As ventricular tachycardia (VT) developed in the presence of lidocaine, conduction was further slowed or blocked in ischemic areas, and slowed in nonischemic regions; at the transition from VT to VF, excitation patterns displayed circus movement involving nonischemic regions.

Animals↗
PubMedDate not supplied

Spontaneous changes in ventricular tachycardia cycle length and their relation to earliest sites of epicardial activation in a canine model.

BACKGROUND: The purpose of this study was to examine the spontaneous changes in cycle length during episodes of sustained monomorphic (MVT) and polymorphic (PVT) ventricular tachycardias and to relate these changes with the earliest epicardial activation site of the beat. METHODS: Isochronal activation maps were obtained from 127 unipolar electrograms recorded from the surface of both ventricles with a sock electrode array in 24 open chest anesthetized dogs. After atrioventricular block, the left anterior descending coronary artery was occluded for 60 min under ventricular pacing (140/min), followed by reperfusion. In 7 dogs the left stellate ganglion was stimulated 5 min after reperfusion. RESULTS: In 7 MVTs (reperfusion) and 4 PVTs (sympathetic stimulation), cycle length changes showed an initial acceleration, reaching a minimum cycle length and then decelerating before termination. Isochronal maps showed radial spread from earliest activation, without conduction block. Cycle length (481 +/- 80 msec) in MVT had beat to beat variations of 15 +/- 17 msec corresponding to small shifts in sites of the earliest activation, clustered along the border of the ischemic myocardium. In PVTs the cycle length (352 +/- 90 msec, p < 0.01) had a variability of 62 +/- 23 msec, corresponding to wide changes in the sites of earliest activation in right and left ventricles. Linear regression analysis showed a strong and significant correlation between cycle length variability and the number of electrodes with the earliest activation (r = 0.77, p < 0.0001). CONCLUSION: In these models of monomorphic and polymorphic ventricular tachycardias, cycle length variability showed a significant correlation with the number of electrodes with the earliest activation. MVTs showed concentrated origins with regular cycle length, whereas PVTs showed dispersed origins with irregular cycle length. These results suggest that the earliest epicardial activation site of the beat could be a factor in determining the dynamics in the cycle length.

Animals↗
PubMedDate not supplied

Continuous ST segment recording during thrombolysis in acute myocardial infarction: a report on orthogonal ECG monitoring.

BACKGROUND: A noninvasive, real time method is needed to identify failures of thrombolysis and evaluate new treatments in acute myocardial infarction (MI). OBJECTIVE: To study XYZ monitored ST segment evolution during thrombolysis in acute MI and to examine the correlation of ST parameters to outcome. DESIGN: Thirty-five patients receiving tissue plasminogen activator (tPA) (n = 18) or streptokinase (SK) (n = 17) for acute MI were monitored by vector-cardiography during the first 12 h of thrombolytic therapy. Computer constructed ST vector magnitude (ST-VM) trends were analyzed for 0.5 or greater decline from the initial ST amplitude (IA) lasting for 10 mins or longer (ST response) and for ST re-elevation 0.75 IA or more following ST decline. The degree of ST response, time from treatment onset and ST-VM re-elevation were correlated to peak creatine phosphokinase (CPK), left ventricular ejection fraction (EF) and final ST-VM. RESULTS: The presence of an ST response correlated with a lower peak CPK (2691 +/- 1625 versus 4057 +/- 1622 U/L, P = 0.043) and tended to higher EF (0.48 +/- 0.11 versus 0.36 +/- 0.09, P = 0.057). The ST responder group had fewer patients with ST re-elevation than the group of nonresponders (13 of 30 versus five of five patients, P = 0.041). Moreover, ST response before 120 mins was associated with lower peak CPK (2089 +/- 1299 versus 3367 +/- 177 U/L, P = 0.02) and better EF (0.54 +/- 0.06 versus 0.41 +/- 0.12, P = 0.02) compared with later or no ST response. The degree of ST response correlated significantly with a lower ST-VM during the last hour (r = -0.744, P = 0.001). ST trends showed no significant differences between treatment groups (tPA versus SK). The tPA group, however, tended to an overall earlier ST response (117 +/- 75 versus 163 +/- 64 mins, P = 0.13). CONCLUSIONS: Early ST-VM trends are closely associated with electrocardiographic and clinical outcome and may provide a basis for clinical management, therapeutic comparisons and better insight into thrombolysis in MI.

Aged↗