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Biomedical subjects

H Coto

Publications and source records attributed to H Coto.

12 recordsLinked to original sources

Selective effects of tocainide in canine acute myocardial infarction.

We examined the in vivo electrophysiologic effects of tocainide in canine acute myocardial infarction. We compared the effects of tocainide in infarcted and non-infarcted zones. The left anterior descending coronary artery of 8 dogs was ligated and bipolar ventricular electrograms were recorded from a needle electrode placed transmurally in the infarcted zone and from electrodes in the non-infarcted zone. Conduction intervals were measured from the onset of the limb lead QRS to the major deflection of the recorded electrograms in the infarcted and non-infarcted zones. Effective refractory periods were also determined. Measurements were made before, during and after intravenous infusion of tocainide in therapeutic doses 2 hours after infarct. Tocainide prolonged conduction intervals by 26-31% in the infarcted zone at peak (P less than 0.001), but by only 6% in the non-infarcted zone. Similarly, tocainide prolonged the effective refractory period by 27% (P less than 0.001) on the infarcted, but by 8% the non-infarcted zone. Tocainide had very slight effects on QRS duration. The present study shows that tocainide had selective effects in the infarcted zone on both conduction and effective refractory period. These selective effects may explain its antiarrhythmic effects in acute myocardial infarction.

Animals

Dextrorotatory isomer of sotalol: electrophysiologic effects and interaction with verapamil.

The dextrorotatory isomer of sotalol (d-sotalol) has class III antiarrhythmic properties with known action potential duration (APD) prolonging effects, and is largely devoid of beta-adrenergic blocking activity. We studied its electrophysiologic effects and the mechanism of its APD prolonging effects in sheep Purkinje fibers by means of standard microelectrode techniques. At all concentrations (10(-6) to 10(-4) mol/L), d-sotalol had no effect on Vmax. At 10(-6) mol/L, d-sotalol had no effect on APD. A concentration-dependent effect of 10(-5) to 10(-4) mol/L d-sotalol was found on APD. At peak effect, APD was prolonged by 56% and 49% at 50% (APD50) and 90% (APD90) of repolarization (p less than 0.01). Early afterdepolarizations (EADs) were noted at high concentration of d-sotalol (10(-4) mol/L). These EADs were increased in number by epinephrine. To assess the mechanism of APD prolongation, verapamil (2.0 X 10(-6) mol/L) was added before and after d-sotalol treatment. In the presence of verapamil, no APD prolongation was observed even at the highest d-sotalol concentration (10(-4) mol/L). Next, during APD prolongation at the highest d-sotalol concentration, we added verapamil, noticing a remarkable shortening of APD. In addition, d-sotalol-induced EADs disappeared with addition of verapamil. Thus (1) verapamil blocks d-sotalol-induced APD prolongation and EADs and (2) this may be consistent with a mechanism via slow inward current.

Action Potentials

Late potentials in normal subjects and in patients with ventricular tachycardia unrelated to myocardial infarction.

Fifty normal male and female athletes, or athletically active subjects, were evaluated, and a search for low-amplitude late potentials in the terminal part of ventricular activation was performed. Recordings from 3 normal men met the definition of abnormal late potentials, and were indistinguishable by present analytic techniques from those encountered in patients who have ventricular tachycardia (VT) after myocardial infarction (MI). Of 24 patients studied, 11 had VT, but only 2 had had an MI, which occurred in the remote past. Another patient had 1 narrowed coronary artery on arteriography. Group differences could be demonstrated using amplitudes and durations of late potentials, but late potentials generally did not prove the impressive marker of the patient with VT, which other workers, as well as ourselves, have encountered in patients after MI. Late potentials were an impressive marker in a subset of the VT group in whom cardiomegaly developed. Thus, the absence of late potentials is an effective marker in the normal subject, but the presence of late potentials is not an effective marker in identifying the patient with non-MI-related, nonsustained VT before development of cardiomegaly.

Action Potentials

Adult hypophosphatasia.

We have described a case of hypophosphatasia with a mild progressive course. This condition and its familial propensity may be more prevalent than recognized. Thus, family members of a patient with hypophosphatasia should be screened for this disorder. Enthusiastic pharmacologic, hormonal, and/or dietary supplemental therapy should be avoided.

Adult

Endocarditis caused by Streptococcus morbillorum.

Although patients with nutritionally variant streptococcal endocarditis have been reported in recent years, the specific clinical features of this disease have not been well characterized. We report here the clinical and laboratory features of a particularly unusual case of persistent bacteremia caused by Streptococcus morbillorum , one of the nutritionally variant streptococci. The patient was successfully treated with a combination of penicillin and rifampin after two treatment failures. We also review cases of nutritionally variant streptococcal endocarditis published in the English literature since 1971, in an attempt to understand some difficulties encountered in diagnosing and treating this type of endocarditis.

Drug Therapy, Combination