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

We evaluated the effects of selective activation of H1 receptors on coronary hemodynamics in 16 patients divided into two groups: group A, 11 patients with atypical angina or valvular heart disease and normal coronary arteries, and group B, five patients with spontaneous angina, four of whom had significant (greater than 70% stenosis) coronary artery disease and one with normal coronaries. Selective H1 receptor stimulation was achieved by infusing 0.5 microgram/kg/min of histamine intravenously for 5 min after pretreatment with cimetidine (25 mg/kg). Heart rate was maintained constant (100 beats/min) by coronary sinus pacing and coronary blood flow (CBF) was measured by thermodilution. In group A, during histamine infusion mean aortic pressure fell from 99 +/- 5 to 77 +/- 4 mm Hg (mean +/- SEM, p less than .001), coronary vascular resistance (CVR) decreased from 1.07 +/- 0.17 to 0.82 +/- 0.14 mm Hg/ml/min (p less than .02), and CBF and myocardial oxygen consumption remained unchanged. None of the patients in this subgroup developed angina during histamine infusion. In group B, while no significant average changes in mean arterial pressure, CVR, or CBF were observed, two of the five patients (40%) developed angina during histamine infusion, accompanied by ST-T elevation, a decrease in CBF, and an increase in CVR. In one of these two patients circumflex coronary arterial spasm was angiographically demonstrated during histamine-induced angina. Our results suggest that stimulation of the H1 receptor induces a reduction of CVR, probably resulting from vasodilation of small coronary resistance vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of activation of the H1 receptor on coronary hemodynamics in man. 369 50

Twenty-one patients, ranging in age between 28 and 59 years, who survived hospitalization for an acute myocardial infarction in association with repetitive attacks of variant angina, were followed prospectively for 59.1 +/- 5.1 (SEM) (range 17-120) months. Four patients died, one of sudden death 17 months after admission, one of congestive heart failure at 33 months, and two of cancer at 43 and 45 months of follow-up. Three patients had four new myocardial infarctions at 22, 32, 33, and 61 months of follow-up. Six patients were readmitted for angina or other cardiac reasons. Twelve patients remained asymptomatic throughout the follow-up and one more patient was asymptomatic before and after his recurrent myocardial infarction. No relapse of variant angina was documented. Thus, the long-term course of patients with variant angina culminating in acute myocardial infarction is relatively benign, despite the highly unstable features of their initial presentation.
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PMID:The long-term outcome of patients who suffered and survived an acute myocardial infarction in the midst of recurrent attacks of variant angina. 372 51

Atrial pacing was performed in 16 patients with angina at rest and significant coronary artery stenosis (greater than 70%) over 2 consecutive days in the morning (10 A.M. to 1 P.M.), in the afternoon (4 to 7 P.M.), and at night (12 midnight to 3 A.M.) to assess possible circadian variations of their ischemic threshold. Overall, the incidence of resting angina was highest at night. All pacing results were positive (greater than or equal to 1.0 mm ST segment shift) and tended to be reproducible in nine patients, whereas some or all were negative in seven. Among all positive results, ischemic thresholds at night were significantly lower than those in the morning and in the afternoon (125 +/- 3 vs 138 +/- 3 and 139 +/- 2 beats/min, mean +/- SEM; p less than .005). In nine patients, 19 pacing tests produced ST segment elevation, of which 13 were performed at night (68%). We conclude that patients with resting angina and severe coronary stenosis often exhibit a nocturnal decline in their ischemic threshold, which seems to facilitate development of transmural ischemia during atrial pacing.
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PMID:Resting angina with fixed coronary artery stenosis: nocturnal decline in ischemic threshold. 377 12

Perhexiline maleate, which causes inhibition of myocardial fatty acid catabolism with a concomitant increase in glucose utilization, is particularly useful in the management of patients with severe angina pectoris. While perhexiline exerts no significant negative inotropic or dromotropic effects, its short- and long-term use has hitherto been restricted because of complex pharmacokinetics and the eventual development, in many patients, of hepatitis and peripheral neuropathy. Correlations between perhexiline dose, plasma drug concentrations, efficacy and development of toxicity were examined prospectively in 3 groups of patients. The first group (n = 29) were patients in whom perhexiline was added to previously prescribed anti-anginal medication for short-term (pre-surgical or post-myocardial infarction) control of angina pectoris. Over a mean treatment period of 18 +/- 2 (SEM) days, 13 patients experienced a marked reduction in frequency and severity of attacks. No adverse effects occurred. A second group of patients (n = 19) were treated chronically with 50-400 mg/day of perhexiline, dosage being adjusted to minimize symptoms. Over a mean treatment period of 8.8 +/- 1.7 months, 5 patients became asymptomatic, while 9 developed evidence of hepatitis or neurotoxicity, with concomitant plasma perhexiline concentrations of 720-2680 ng/ml. Subsequently, a further group of similar patients (n = 22) were treated for 12.4 +/- 2.6 months, perhexiline dosage being adjusted to maintain plasma perhexiline concentrations below 600 ng/ml. Nine patients became asymptomatic, while none developed adverse effects. It is concluded that perhexiline is useful both as a short-term adjunct to anti-anginal therapy and in the long-term management of patients unsuitable for coronary artery bypass grafting. The risk of long-term toxicity can be reduced markedly by maintenance of plasma drug concentrations below 600 ng/ml without significantly compromising anti-anginal efficacy.
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PMID:Perhexiline maleate treatment for severe angina pectoris--correlations with pharmacokinetics. 379 79

The pharmacokinetics and associated pharmacodynamics of nifedipine were studied at steady state in 12 patients with angina pectoris who were receiving nifedipine 10-40 mg tid. After dosing, serum nifedipine concentrations rose rapidly and decayed in a log-linear fashion. The mean (+/- SEM) maximum serum concentration (Cmax) after dose normalization, and the time to Cmax (tmax) were 115 +/- 7 ng/mL and 0.72 +/- 0.13 hr, respectively. The mean area under the plasma concentration-time curve per 10-mg dose was 304 +/- 34 hr-ng/mL. The average elimination rate constant was 0.205 +/- 0.016 hr, and the harmonic mean elimination half-life was 3.4 hr (range, 2.5-4.9 hr). Heart rate increased (5-6 beats/min, P less than .05) from baseline for up to one hour after dose, while mean diastolic blood pressure decreased (6-15 mm Hg, P less than .05) for up to four hours. Cardiac output was increased (1.1-2.8 L/min, P less than .05), and calculated total systemic resistance (3.8-6.3 mm Hg/L/min, P less than .05) was decreased for the entire dosing interval after nifedipine dosing. Hysteresis plots for heart rate and mean diastolic blood pressure showed a time lag between changes in serum nifedipine concentrations and heart rate, but not between serum nifedipine concentrations and blood pressure. Changes in cardiac output did not correlate with serum nifedipine concentrations. The steady-state kinetic and dynamic parameter values in patients with angina pectoris in this study were similar to those found in healthy volunteers or hypertensive patients after acute nifedipine administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacokinetics and pharmacodynamics of nifedipine in patients at steady state. 379 48

Invasive studies in patients with left ventricular dysfunction show that data at rest (e.g. ejection fraction-EF) are poor predictors of the changes in cardiac output (CO) which occur with exercise. This investigation was undertaken to determine whether impedance cardiography could be used in such patients to assess CO response to exercise. The method was compared with the direct Fick method. Over a range of COs between 4 and 18 min-1 there was no systematic error. Reproducibility for CO over one week was highly significant (r = 0.94; P less than 0.001). Impedance cardiography was incorporated into routine exercise testing on a bicycle ergometer for a group of 15 patients (mean age 53.2 +/- 3.0 yrs, SEM) who had sustained a major myocardial infarct 6 to 12 months previously, (EF 38.1 +/- 3.5%, SEM). CO was measured at the end of each 3-min stage. In eight patients (EF 40.0 +/- 3.4%, SEM) CO response was abnormal with either a decrease or a failure to increase with increasing workloads. Conventional end-points i.e. angina, attainment of 85% of predicted maximum heart rate, abnormal blood pressure response or excessive dyspnoea did not indicate consistently a need to terminate the test. It is suggested that impedance cardiography is a useful non-invasive method of evaluating patients with left ventricular dysfunction.
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PMID:Use of impedance cardiography in evaluating the exercise response of patients with left ventricular dysfunction. 383 Jul 7

The antianginal effects of diltiazem 180 mg/day and propranolol 240 mg/day, alone and in combination, were investigated in 15 patients with effort related angina in a double blind placebo controlled crossover trial, with each period of treatment lasting four weeks. Patients performed a symptom limited treadmill exercise test at the end of each period of treatment. Mean (SEM) time to onset of angina was increased from 293(32) s when receiving placebo to 347(38) s when receiving diltiazem alone, to 350(30) s when receiving propranolol alone, and further to 421(34) s when receiving diltiazem and propranolol combined. Similar changes occurred in the duration of exercise testing and time to 1 mm ST segment depression. The sum of ST segment depression at peak exercise was reduced by both diltiazem and propranolol alone compared with placebo, and combination treatment produced a further significant improvement. Rate pressure product was significantly reduced at rest and at peak exercise after propranolol alone and combination treatment. The study clearly showed the superior value of diltiazem and propranolol combined in effort related angina when compared with either drug used alone.
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PMID:Beneficial effects of diltiazem and propranolol, alone and in combination, in patients with stable angina pectoris. 388 Nov 4

A randomized, double-blind, placebo-controlled trial was performed in 12 patients with chronic and stable effort angina to study the antianginal and anti-ischemic actions of a single dose of molsidomine in addition to long-term therapy with a long-acting beta-adrenergic blocker (100 mg of atenolol daily). Efficacy was assessed by means of objective endpoints obtained by computer-assisted exercise testing. The mean exercise time to produce angina improved significantly from 330 +/- 38 seconds (mean +/- SEM) in patients after administration of atenolol and placebo to 420 +/- 36 seconds after administration of atenolol and molsidomine. Similar significant improvements were seen in ST segment changes at an identical exercise duration, in maximal heart rate, and in maximal exercise duration. The increased anginal threshold and the reduced ischemic changes were not explained by changes in the rate-pressure product at submaximal levels. Thus molsidomine showed antianginal and anti-ischemic efficacy in the treatment of stable effort angina additional to the effect of long-term therapy with beta-adrenergic blockers.
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PMID:Double-blind, randomized, placebo-controlled study of molsidomine in patients with stable effort angina receiving beta-blocker therapy with atenolol. 388 35

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

The efficacy of labetalol, an alpha and beta receptor antagonist, was evaluated in 12 normotensive patients with stable angina pectoris in a single blind dose ranging study. After a two week period of placebo treatment, labetalol was given in doses of 100, 150, 200, and 300 mg twice daily, each for two weeks. Frequency of angina attacks decreased from 9.4 (SEM 2.3)/week in the control period to 7.3 (2.8), 5.2 (2.6), 3.8 (1.8), and 3.3 (1.9)/week in the four successive treatment periods. In the same periods the number of glyceryl trinitrate tablets consumed decreased from 7.0 (2.6)/week to 5.8 (3.3), 3.9 (2.9), 2.7 (1.8), and 2.6 (2.1)/week. Maximal symptom limited treadmill exercise tests were performed three and 12 hours after dosage at each dose. Exercise tolerance (expressed as seconds of the Bruce protocol) increased from 266 (44) with placebo to 306 (44), 369 (50), 396 (48), and 413 (51) in the four treatment periods. This improvement was accompanied by a significant blunting of the heart rate and blood pressure responses to exercise. Trough point exercise tolerance did not differ significantly from that at three hours after dosage. Thus labetalol is effective as an antianginal agent at doses of 150-300 mg twice daily and is well tolerated by the normotensive patient with angina.
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PMID:Oral labetalol in the management of stable angina pectoris in normotensive patients. 391 74


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