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Biomedical subjects

S Rogel

Publications and source records attributed to S Rogel.

At least 19 recordsLinked to original sources
PubMed1992

A comparison of the day-long antianginal effectiveness of nitroglycerin patches with that of three-times-daily isosorbide dinitrate: a double-blind study using dose titration.

Eight men with stable angina, a positive treadmill test, and demonstrated responsiveness to chronic oral isosorbide dinitrate (ISDN) were studied after they had been taking effective doses of ISDN t.i.d. for at least 2 weeks. Exercise tests were performed every 1-2 h until 19.00 hours over one day after the 08.00 hours application of nitroglycerin patches in a previously titrated dose; on another day after the administration of ISDN capsules q5h; and on a third day after placebo patches and capsules. The mean necessary effective patch dose was 125 cm2 (60-220 cm2). The mean exercise duration to angina rose from 271 to 480 s 1 h after nitroglycerin patches (P less than 0.001). Nitroglycerin patches were superior to the placebo throughout the day, but in a declining degree--by 94 s at 19.00 hours (P less than 0.05). ISDN q5h provided peaks of increased walking time to angina 1 h after each dose, but after 3 h exercise time was down to placebo levels. Furthermore, the peaks were of diminishing amplitude: 200 s at 09.00 hours, 150 s at 14.00 hours, but only 70 s at 19.00 hours. Thus, neither nitrate regimen provided continuous near-peak benefit throughout the 11 h period, although nitroglycerin patches had a significantly greater (P less than 0.05) overall effect during the day.

Administration, Cutaneous↗
PubMed1991

Effects of nisoldipine on myocardial ischemia during exercise and during daily activity.

The antiischemic properties of nisoldipine, a dihydropyridine calcium antagonist, were assessed in a multicenter, double-blind, placebo-controlled trial by repeated exercise testing and 72-hour ambulatory electrocardiographic monitoring in 82 patients with coronary artery disease. Patients with positive treadmill stress test results and greater than or equal to 2 ischemic episodes per 24 hours were included in this study. Administration of all chronic antiischemic medications except beta blockers were discontinued. During the first week all patients received placebo twice daily. During the second and third weeks, 41 patients received nisoldipine 10 mg and 41 patients received placebo twice daily. In the placebo group there were no changes in exercise parameters or in ambulatory electrocardiographic parameters. In the nisoldipine group, exercise duration increased from 403 to 448 seconds (p = 0.0035), time to 1 mm of ST depression increased from 224 to 298 seconds (p = 0.002), time to pain increased from 241 to 321 seconds (p = 0.01), and maximal ST depression was reduced from 2.6 to 2.3 mm (p = 0.002). Among the ambulatory electrocardiographic parameters in the nisoldipine group, only the number of episodes was reduced, from 14.4 to 11.6 (p = 0.0013) per patient. There was no significant reduction in total ischemic time (132 vs 120 minutes per patient). No significant side effects were observed. This is the largest clinical trial to date on the effects of nisoldipine on myocardial ischemia. The results indicate that nisoldipine was effective in improving all exercise parameters and only partially effective in suppressing ischemia during daily activity.

Activities of Daily Living↗
PubMed1990

Hemodynamic evaluation of common cardiac arrhythmias.

Hemodynamic effects of arrhythmias are considered to be relatively unimportant unless the heart rate is very slow or very rapid. The present study describes a simple method which enables determination of beat-to-beat changes in stroke volume, cardiac output, double product and cardiac efficiency expressed as the interrelationship between the last two parameters. It is obtained by calculating stroke volume from directly measured values of arterial pressure, using a modification of a formula described for irregular rhythms. The calculated parameters are expressed as the percentage of the values of the sinus beat or state occurring with normal cardiac rhythm. The results confirmed that atrial ectopic beats have a less deleterious effect on myocardial function than those from ventricular or nodal origin. The change in stroke volume or cardiac output may be accompanied by either a decreased or increased double product and/or cardiac efficiency. This depends on the type of arrhythmia, the number of ectopic beats per minute and the condition of the patient's heart. The method provides measurement of this parameter in a given patient at a given state as well as at other different frequencies of the same arrhythmia. It demonstrates then which frequency induces hemodynamic changes of sufficient degree to justify antiarrhythmic therapy. The method may be useful in optimising care of patients in units for critical care, or even in outpatient departments.

Arrhythmias, Cardiac↗
PubMed1990

Treatment of hypertension by enalapril and hydrochlorothiazide separately and together: a multicenter study.

The efficacy and safety of enalapril and hydrochlorothiazide was investigated in a multicenter study of 81 patients with mild to moderate essential hypertension. The subjects were randomly assigned to one of three groups and, following a placebo period, given enalapril maleate (20 mg), hydrochlorothiazide (12.5 mg), or a combination of the two drugs (32.5 mg). A significant decrease in blood pressure was observed after only 2 weeks in the enalapril and enalapril-hydrochlorothiazide groups. A double dose was required to achieve a satisfactory response in one-third of the patients in both the enalapril (9 of 27) and the enalapril-hydrochlorothiazide groups (8 of 27). Adverse reactions included cough in one patient and mild hyperkalemia in another, both of whom received enalapril. Two patients on the drug combination developed side effects--symptomatic orthostatic hypotension in one and impotence in the second. Enalapril alone and in combination with hydrochlorothiazide appears to be effective and well tolerated.

Adult↗
PubMed1989

The effect of verapamil in patients with asymptomatic stress-induced ischemia.

In 25 patients with asymptomatic exercise-induced positive stress tests heart rate, blood pressure, double product, exercise duration, and ST-segment changes were studied prior to and 4 weeks after administration of 120 mg of verapamil therapy three times a day. Significant improvement was observed at rest and at peak exercise in heart rate, pressure values, double product, and maximal ST depression with a prolongation of exercise duration. Measurements at the same work load in the post-verapamil test as at the pretreatment peak exercise showed a slower heart rate, lower blood pressure, less double product, and less ST depression as a more pronounced expression of drug efficacy. There was no deterioration in any parameter. In conclusion, improved myocardial performance can be demonstrated in asymptomatic ischemic patients when treated with verapamil, and this effect is particularly evident when data are compared with equal exercise duration in the posttreatment test as with peak exercise prior to therapy.

Adult↗
PubMed1984

The effect of single-dose methyldopa and diuretic on BP and left ventricular mass.

The effect of a single daily dose of 500 mg of methyldopa with 50 mg of hydrochlorothiazide and 5 mg of amiloride hydrochloride was studied in 21 patients with mild to moderate hypertension. It was shown that the average morning BP changed from 182/103 +/- 15/9 mm Hg to 145/83 +/- 16/8 mm Hg following one day of treatment. Similarly, the average of seven hourly measurements (7BP) dropped from 170/99 +/- 11/7 mm Hg to 145/86 +/- 11/8 mm Hg. In 12 patients, the same therapy lowered the morning BP from 186/104 +/- 16/9 mm Hg to 144/83 +/- 15/8 mm Hg and the 7BP from 168/98 +/- 10/6 mm Hg to 142/83 +/- 12/7 mm Hg following three weeks. After eight weeks, normal values were still maintained. Left ventricular mass was elevated in all the patients (330 +/- 67) and dropped by an average of 12% and 17% by three and eight weeks after initiation of therapy. Unchanged left ventricular end diastolic volume and decreased muscle thickness indicate true reduction in hypertrophy in addition to the BP-lowering effect of this combined single-dose therapy described.

Adult↗
PubMed1982

Comparative cardiac effects of three hepatobiliary radiopharmacologicals in the dog: concise communication.

Three hepatobiliary agents with an acetanilide-imidoacetic-acid moiety resembling that in lidocaine were investigated for their possible effects on contractility and conductivity in the heart and on arterial pressure and aortic blood flow. This was done in the light of lidocaine's numerous cardiac side effects. HIDA, BIDA, and DIPA, each with traces of decayed Tc-99m, were injected i.v. into anesthetized dogs with an A-V block, and their effects on the above parameters were followed until control levels were reestablished. Whereas lidocaine raises the diastolic threshold and prolongs the refractory period, the three agents tested do not prolong myocardial conductivity. Both HIDA and BIDA have an effect similar to that of lidocaine, but DIPA has no effect on the latter two parameters. Moreover, whereas lidocaine depressed myocardial contractility, blood pressure, and blood flow, HIDA has a less prominent effect on these parameters, and neither BIDA nor DIPA has any such effect. It is concluded that even though the effect of HIDA on the heart is milder than that of lidocaine, the effects of both BIDA and DIPA are even less pronounced, and they are less likely to cause cardiac side effects when similar doses are administered during nuclear medicine procedures.

Animals↗
PubMed1981

Myocardial conduction time and antiarrhythmic drugs.

Complete a-v block was induced in anesthetized mongrel dogs by direct electrocoagulation of the a-v node. The ventricles were paced by steady stimulation (S1) at a rate of 100/min. and by test stimuli (S2) with varying post S1 delay. Right ventricular myocardial tension was measured from the S2 stimulation site of a specially designed miniature strain gage and from a different site by a Walton-Brodie strain gage. A reproducible time lag between the two sites could be measured by comparing the differences in mechanical response to S2 stimuli. This time difference was called delta IT. delta IT varied markedly (from 10-60 msec) when measured at different sites but no linear relationship between delta IT and the inter-gage distance could be observed. Increasing the S2 current intensity induced shortening of delta IT from 37 +/- 13 msec (mean +/- S.D.) at the threshold current to 16 +/- 10 msec (mean +/- S.D.) with 10 mA. A strength-delta IT curve could be constructed and was found to be remarkably reproducible during the experiment. Quinidine and disopyramide induced upward displacement of the curve, lidocaine did not change it while verapamil lowered the delta IT values. We suggest that delta IT can be used as a reliable indicator of myocardial conduction rate. The possible reasoning for this suggestion has been discussed.

Animals↗
PubMed1979

Electrical and mechanical response in biventricular mechanical alternans.

Mechanical alternans of various degrees is produced by rapid heart rates, slower rates in failing hearts and can be brought about by a single extra systole. It has also been shown that the two ventricles may exhibit different degrees of mechanical alternation. The present study was planned to clarify the possible mechanism inducing this latter phenomenon. For this reason myocardial tension was recorded simultaneously from the two ventricles as well as through a miniature strain gage capable of measuring electrogram and myocardial tension of a small area -- just adjacent to a stimulating electrode. The heart was driven at a steady heart rate through one electrode and very late premature beats were applied at various coupling times at another site through an electrode attached to the miniature strain gage. It was found that the degree of mechanical alternans is markedly different at the sites of measurements in either ventricle. These changes could be related to the time interval elapsed between the application of the electrical stimulus and the occurrence of the mechanical response.

Animals↗
PubMed1978

A new hazard in the use of an external demand pacemaker.

Ventricular pacing by a Medtronic model 5880A external demand pacemaker was shown to be inhibited as long as the metal coverplate of the pacemaker was touched with bare hands. The asystolic periods were induced by a previously undescribed malfunction of the pacemaker, inherent in its structure. This phenomenon occurred when both patient and physician were isolated from any main operated instrument. It could be demonstrated that pacer inhibition was induced by capacitive coupled 50 Hz fields from the environment, activating the sensing mechanism through the metal coverplate. The plastic covered Medtronic model 5840 pacemaker does not have such undesirable characteristics.

Electrocardiography↗
PubMed1978

Transtelephone adjustment of antiarrhythmic therapy in ambulatory patients.

The electrocardiograms of 80 ambulatory patients receiving antiarrhythmic therapy were supervised with the help of a transtelephone monitoring system. The patients used a pocket-size modulator and reported several times daily to the receiving center integrated into the intensive cardiac care unit. The surveillance lasted for 5-28 days during which various drugs in varying dosages were administered to suppress or prevent dysrhythmias. In 94% of the patients, a satisfactory therapeutic achievement was obtained. The transtelephone system provides easy diagnosis, immediate pattern recognition, direct and frequent contact with the ambulatory patient and long periods of follow-up. During this time, the proper antiarrhythmic agent can successfully be defined, its effective dose can safely be determined and unnecessary hospitalization can thus be prevented.

Adult↗
PubMed1977

In vivo atrial excitability and anti-arrhythmic drugs.

The threshold of excitability of the atrial muscle was studied in the in vivo beating canine heart. Unipolar cathodal and anodal strength-interval curves were constructed and found to be dissimilar in shape. It was found that at any interval within the relative refractory period of the atrium, as in the ventricle, there is a wide range of current levels delineated by an upper (TU) and lower (TL) limit of threshold which can stimulate the atrial myocardium. Within these limits the threshold varies spontaneously and can be reduced to TL level by a run of extrasystoles. Such TU and TL curves were repeatedly determined following administration of therapeutic doses of quinidine, procaine amide or lidocaine. It was observed that all three drugs prolonged the refractory period. The TU values increased following each of the drugs, and mostly after quinidine, while the TL curve was less affected by quinidine. It is suggested that the exit block thus produced is the principal mechanism whereby quinidine depresses atrial disrhythmias.

Animals↗
PubMed1977

Humoral factors in shock causing bradycardia and myocardial depression.

Hypovolemic shock was maintained for 6 hours in dogs in which the heart was hemodynamically protected by a biological model described earlier. Blood of these dogs was exchanged with that of healthy dogs in which myocardial tension and heart rate were continuously monitored. It was found that rate and force of decline in the recipient dog in a fashion similar to the drop in the animal in shock. If, however, the pH of the infused blood was raised to normal, the bradycardia in the recipient dog was prevented but the myocardial depression was not abolished. Administration of aprotinin alone did not prevent the bradycardia or depression of contractility, whereas correction of the pH and treatment with aprotinin not only prevented the decline in both but led also to a transient increase in myocardial tension of the recipient animal. The results seem to indicate that 1) in shock myocardial depression and cardiac slowing are induced by humoral factors transferable by blood to a normal animal, 2) acidity caused the bradycardia but not drop of tension, 3) aprotinin prevents the depression of contractility only in a normal pH medium, and 4) aprotinin may prevent the action of a preformed myocardial depressant factor rather than inhibit its formation.

Animals↗