Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of glucose-insulin-potassium (GIK) and placebo normal saline (S) infusion on treadmill-walking time to angina, ST depression, heart rate (HR), systolic blood pressure (SBP), rate pressure product (RPP), blood glucose (G), lactate (L) and free fatty acids (FFA) were studied in 14 non diabetic patients with exertional angina. For the whole group, the post-GIK walking time to angina (393 +/- 33 sec, mean +/- SEM) was greater than the values during control GIK (319 +/- 20 sec, p less than 0.02) and post-S infusion (334 +/- sec, p less than 0.05), but circulatory and ST responses were similar in post-GIK and post-S studies. 7 of the 14 patients experienced significantly greater improvement in exercise tolerance following GIK (467 +/- 39 sec) in comparison to control GIK (313 +/- 29 sec, p less than 0.001) and post-S infusion (334 +/- 32 sec, p less than 0.005) and exercised to a higher HR, SBP and RPP after GIK than after S infusion. At the onset of angina these patients had similar ST-segment depression before and after GIK but when ST segments were assessed after GIK at the same exercise duration when angina had occurred during the control and post-S studies, there was significantly less ST depression (p less than 0.01). Of the remaining 7 patients exercise tolerance following GIK deteriorated in 3, remained unchanged in 2 and increased by 12 and 48 sec in 2 patients in comparison to post-S values. Comparison of post-GUK and post-S values for G, L and FFA for the whole group showed significantly lower resting values of FFA and post-exercise values of G following GIK infusion. The differences in clinical and circulatory responses between patients who improved and those who did not improve following GIK were not related to the angiographically determined severity of coronary artery disease or to GIK-induced metabolic changes. Results suggest that some patients with angina pectoris do benefit from GIK infusion but the response in a given patient to this therapeutic modality is unpredictable.
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PMID:Effects of glucose-insulin-potassium infusion on the angina response during treadmill exercise. 38 19

Eighty-six of 452 patients (19%) with chronic bifascicular block were found to have no clinically apparent associated organic heart disease (OHD) and were defined as having primary conduction disease (PCD). Comparison of patients with PCD and OHD revealed a significantly lower incidence of the following clinical variables in the PCD patients (p less than 0.001): exertional angina, dyspnea, congestive heart failure, cardiomegaly, functional class I (all by study design), left bundle branch block and premature ventricular contractions. Both mean AH and HV intervals were significantly shorter in patients with PCD (p less than 0.01). The incidence of HV prolongation was 21% in PCD and 41% in OHD patients (p less than 0.001). All patients were prospectively followed for 21-2998 days with a mean +/- SEM of 1209 +/- 66 days for PCD and 1172 +/- 36 days for OHD. Atrioventricular (AV) block developed in three patients from the PCD group and 26 from the OHD group (NS), with spontaneous block occurring in one (1%) PCD patient and 19 (5%) OHD patients (p less than 0.05). Annual mortality due to sudden death as well as total cardiovascular mortality (including sudden death) for the 5-year follow-up was significantly lower in patients with PCD. Patients with PCD have significantly lower incidence of electrophysiologic abnormalities and subsequent spontaneous AV block as well as cardiovascular and sudden death mortality. The diagnosis of PCD based on clinical criteria probably underestimates the presence of underlying OHD, as suggested by a small but definite risk of cardiovascular mortality.
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PMID:Significance of chronic bifascicular block without apparent organic heart disease. 44 30

The effects of diltiazem, 240 mg/day, were studied in 12 patients with chronic exertional angina and angiographically proven coronary artery disease, who received maintenance therapy with propranolol. Mean age was 60.1 years (range 46 to 67). Patients received propranolol, 60 to 240 mg/day, before and during the study. A double blind, placebo controlled, cross-over design was used to test the effect of added diltiazem, during 8 weeks. Duration of exercise varied from 398 +/- 30 (mean +/- SEM) to 419 +/- 37 (placebo) or 469 +/- 35 sec (diltiazem) (NS). Time to appearance of angina varied from 283 +/- 32 to 313 +/- 34 and 302 +/- 27 sec, respectively (NS). Resting and maximal effort heart rate and blood pressure did not differ among basal, placebo and diltiazem conditions. Segmental wall motion analysis by radioisotopic ventriculogram revealed dyskinetic zones during placebo or diltiazem therapy. Basal ejection fraction did not increase during exercise and this was not modified by diltiazem or placebo. Thus, the addition of diltiazem to propranolol in patients with chronic, exertional angina failed to modify angina threshold, exercise duration or left ventricular performance.
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PMID:[Combined therapy with propranolol and diltiazem in chronic exertional angina]. 215 33

Seventy three patients (63 males and 10 females) aged 41-75 years with established stable exertional angina pectoris were studied in a double-blind fashion to confirm the efficacy of 80 mg propranolol administered three times daily and also to examine its effect on ST-segment changes in the electrocardiogram by ambulatory ST-segment monitoring and exercise testing using on-line computer analysis. During ambulatory monitoring, episodes of ST-segment depression in lead CM5 were significantly reduced from 6.5 +/- 0.7 during placebo to 3.4 +/- 0.6 during propranolol therapy (p less than 0.001). The total duration of ST-segment depression was also significantly reduced and the maximal depth of ST-segment depression improved from 2.6 +/- 0.2 mm during placebo to 1.7 +/- 0.2 mm during propranolol therapy (p less than 0.001). The mean +/- SEM exercise time of 5.5 +/- 0.2 minutes on placebo increased to 8.6 +/- 0.4 minutes on propranolol 240 mg daily (p less than 0.001). The 1 mm ST-segment depression time of 3.5 +/- 0.2 minutes on placebo in lead CM5 was prolonged to 6.2 +/- 0.3 minutes during propranolol therapy (p less than 0.001). Propranolol treatment significantly reduced the resting and maximal heart rates (p less than 0.001). The maximal ST-segment depression during exercise in lead CM5 was reduced from 2.3 +/- 0.1 mm on placebo to 1.9 +/- 0.1 mm with propranolol (p less than 0.01). Similarly, the rate-pressure product at peak exercise of 188 +/- 5 units on placebo was reduced to 144 +/- 3 units with propranolol (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of propranolol on indices of intermittent myocardial ischemia, assessed by exercise testing and ambulatory ST-segment monitoring. 373 66

The anti-anginal effects of KB-944 (Fostedil), a new calcium ion antagonist with a half life of approximately 23-28 hr, were evaluated in 20 patients with exertional angina pectoris in a placebo-controlled single-blind dose titration trial. Ambulatory monitoring and multistage treadmill exercise with computer-assisted electrocardiographic analysis was performed after 2 weeks of placebo therapy and after two 2-weekly periods of KB-944 therapy. The mean (+/- SEM) exercise time to the development of angina on treadmill walking increased from 6.9 +/- 0.4 min on placebo to 9.4 +/- 0.5 min on KB-944 100 mg/day (P less than 0.001) and 9.7 +/- 0.8 min on KB-944 200 mg/day (P less than 0.001 vs placebo and not significant vs KB-944 100 mg/day). The time to the development of 1 mm ST-segment depression of 5.3 +/- 0.4 min on placebo increased to 6.5 +/- 0.5 and 6.6 +/- 0.5 min on KB-944 100 and 200 mg/day, respectively (P less than 0.01 vs placebo). The heart rate at rest of 77 +/- 3 beats/min on placebo was reduced to 68 +/- 3 beats/min on KB-944 100 mg/day (P less than 0.001) and 71 +/- 2 beats/min on KB-944 200 mg/day (P less than 0.01). The maximal heart rate and the rate-pressure product were not altered by KB-944 therapy. One patient developed unstable angina during the treatment phase of KB-944 200 mg/day and was withdrawn. Five patients complained of dyspepsia and one of headache and lethargy during KB-944 200 mg/day. One patient developed ventricular tachycardia during treadmill testing while on KB-944 200 mg/day. The 24-hr ambulatory monitoring data confirmed the findings of exercise testing. KB-944 (Fostedil) in a dose of 100 mg once daily was well tolerated as compared to KB-944 200 mg once daily and both the doses were equally effective. The drug merits further evaluation for the treatment of exertional angina pectoris.
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PMID:Ambulatory monitoring and exercise testing in the evaluation of a new long-acting calcium ion antagonist KB-944 (Fostedil) for the treatment of exertional angina pectoris. 390 75

PY-108-068 (PY) has calcium antagonist and coronary dilatory activity in animals, suggesting that it may be useful for the treatment of angina pectoris. We have studied its effects in 19 patients with stable exertional angina. After a 2-week single-blind placebo run-in phase, patients were randomised double-blind to either 75 mg or 150 mg of the drug (in three divided doses) daily for 2 weeks, crossing over to the alternate dose for a further 2 weeks. Maximal treadmill tests with computer-assisted electrocardiographic analysis were used to evaluate efficacy. The mean +/- SEM exercise time to onset of angina increased from 6.1 +/- 0.5 min on placebo to 9.3 +/- 0.8 min on PY 75 mg (P less than 0.001) and to 9.2 +/- 0.8 min on PY 150 mg (P less than 0.001) vs placebo; NS vs 75 mg). The time to development of 1 mm ST-segment depression in lead CC5 also increased from 5.0 +/- 0.7 min on placebo to 6.4 +/- 0.9 min on PY 75 mg (P less than 0.01) and to 7.0 +/- 0.8 min on PY 150 mg (P less than 0.01 vs placebo; NS vs 75 mg). Unlike other calcium antagonists, treatment with PY-108-068 did not significantly alter the resting or maximal heart rates or the heart rate gain during exercise. Resting blood pressure was reduced at the higher dose level but peak blood pressure during exercise and peak double product were unaltered by PY-108-068 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Objective evaluation of PY-108-068, a new calcium channel inhibitor for the treatment of chronic stable angina pectoris. 405 38

Infusions of DL-carnitine are reported to improve the tolerance to atrial pacing of patients with angina pectoris. In the present study, six patients with angina of effort and triple vessel disease received two placebo and two carnitine infusions administered in a double-blind randomized fashion. Carnitine did not affect either the double product (heart rate X systolic blood pressure) at maximal pacing (ST depression: 2.3 +/- 0.2 mm, +/- SEM) or the tolerated pacing time. Intravenous carnitine, in the dose given, is of no therapeutic benefit in myocardial ischemia precipitated by tachycardia. It could be effective when free fatty acids are elevated as during catecholamine stimulation.
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PMID:Intravenous dl-carnitine fails to increase the double-product during atrial pacing in patients with effort angina. A double-blind randomized study. 666 14