Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the mechanism of relief of angina pectoris by diltiazem administration, 14 patients with effort angina were studied using a protocol to control heart rate. Coronary, systemic and left ventricular (LV) hemodynamic function was assessed at rest and during tachycardia stress (atrial pacing)-induced angina before and during diltiazem infusion. Angina occurred in all patients during tachycardia stress before diltiazem administration. During tachycardia stress at the heart rate that produced angina after diltiazem infusion, pressure-rate product, coronary sinus flow and resistance and ST-segment depression were all similar to findings before diltiazem. Although at the onset of angina, systolic pressure was usually slightly lower after diltiazem infusion (138 +/- 11 vs 128 +/- 11 mm Hg, p less than 0.05), the pacing rate at onset of angina was higher in only 3 patients and the pressure-rate product was higher in only 1 patient. After diltiazem, left ventricular end-diastolic pressure increased less frequently after interruption of pacing. The results suggest that diltiazem favorably alters the relation between myocardial oxygen demand and supply at rest, but during tachycardia, anginal threshold and coronary reserve do not change. Diltiazem's potent antianginal action, shown in previous investigations using exercise-induced angina, is not prominent when heart rate is controlled. The major benefit of diltiazem in patients with stress-induced angina is related to reduction of myocardial oxygen demand rather than improved myocardial oxygen delivery.
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PMID:Effects of diltiazem during tachycardia-induced angina pectoris. 394 50

Diltiazem and propranolol alone and in combination as antianginal agents were compared with placebo in 12 patients with stable exertional angina at Stanford University Medical Center. The patients performed symptom-limited, multi-stage upright bicycle ergometric exercise while undergoing radionuclide angiographic studies every two weeks while being treated with 90 mg of diltiazem four times daily, 60 mg of propranolol four times daily, a combination of 90 mg of diltiazem and 60 mg of propranolol four times daily, and placebo. Diltiazem, propranolol and a combination all significantly increased exercise duration compared to placebo (526 +/- 149, 525 +/- 115, and 549 +/- 129 vs 430 +/- 132 sec.). Although rate pressure product and heart rate decreased with diltiazem therapy at submaximal workloads, these values were unchanged at peak exercise in contrast to propranolol or the combination of propranolol or diltiazem. Diltiazem decreased the sub-maximal and maximal degree of exercise-induced ST segment depression by over 50% compared to placebo (P less than 0.01 vs placebo). Diltiazem resulted in a higher exercise left ventricular ejection fraction compared to placebo, propranolol or the combination of diltiazem or propranolol (all less than P less than 0.05). Sinus bradycardia or orthostatic hypertension occurred in four patients on the high-dose combination therapy and required dose reduction. We concluded that high-dose diltiazem, appeared to be even more effective than moderate-dose propranolol or the combination of diltiazem and propranolol in improving exercise tolerance, electrocardiographic evidence of myocardial ischaemia and left ventricular function in patients with stable effort angina due to occlusive coronary artery disease.
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PMID:Diltiazem and propranolol, alone and in combination, on exercise performance and left ventricular function in patients with stable effort angina: a double-blind, randomized, and placebo-controlled study. 406 Nov 5

The effect of Diltiazem, a calcium antagonist drug, were compared with those of placebo on exercise performance. Twenty four patients with exercise-inducible chronic stable angina pectoris were studied over a double-blind period of 8 weeks. The active product was generally well tolerated. Diltiazem was effective in increasing the anginal threshold, in decreasing the ST-segment depression at an identical submaximal workload and in increasing the time to termination of exercise. These results are in accordance with those of others but the mechanisms whereby these effects occur are unclear; the observed results suggest that peripheral effects are not primarily responsible for the drugs' efficacy.
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PMID:Double-blind comparison of Diltiazem and placebo in the treatment of exercise-inducible chronic stable angina pectoris. 621 14

Few studies have been devoted to the role of calcium blockers in stable angina of effort. For this reason, we undertook, a double-blind, randomized study with placebo, to compare the effects of diltiazem (D) and nifedipine (N) on the ergometric parameters of 20 patients with angina of effort and with mono- or multivessel disease. The study protocol extended over 3 weeks and included a reference stress test, 8 days of placebo followed by a repeat yesy, an then 15 days during which each patient received 180 mg of D and/or 30 mg of N in cross-over. A stress test was performed at the end of each week. The calcium blockers appeared to improve the effort tolerance, the duration of the ergometric test and the amplitude of the maximal ST segment depression. Diltiazem showed itself to be superior to nifedipine by the absence of side effects and by an improved cardiac performance on effort.
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PMID:[Value of calcium inhibitors in stable effort angina. Diltiazem versus nifedipine]. 635 43

Calcium channel blockers suppress early ischemic arrhythmias, possibly by diminishing intracellular calcium overload and its effect on the ventricular action potential. To explore this, we compared the effects of diltiazem on ischemic "injury" potentials and ventricular fibrillation during serial coronary artery occlusions in dogs. Injury potentials and ventricular fibrillation were elicited every 15-25 minutes by simultaneous occlusion of the left anterior descending and circumflex arteries during rapid atrial pacing. DC epicardial electrograms were recorded differentially between the ischemic region and a small nonischemic region supplied by a proximal branch of the left anterior descending artery. Injury potentials developed with a uniform time course during five control occlusions, but were reduced by diltiazem infusion (0.5 mg/kg over 25 minutes) in each of eight dogs. The mean diastolic injury potential (T-Q depression) at 150 seconds of ischemia was 9.1 +/- 2.7 mV before diltiazem and 6.1 +/- 1.6 mV afterward (P less than 0.001). Diltiazem increased the mean time between coronary occlusion and ventricular fibrillation from 186 to 366 seconds (P less than 10(-5), but did not change the magnitude of the diastolic injury potential at onset of ventricular fibrillation. Diltiazem also delayed ischemia-induced conduction impairment to the same extent that it delayed injury potential development. In five dogs, the effect of diltiazem on regional blood flow near the epicardial electrodes was measured by infusion of radionuclide-labeled microspheres. Coronary occlusion reduced flow to the ischemic zone from 0.86 to 0.05 ml/min per g (P = 0.001). Diltiazem increased preocclusion flow by 11% (P = 0.03), but did not significantly alter flow during occlusion. Hemodynamic measurements show that diltiazem did not diminish cardiac work. Diltiazem therefore produced a flow-independent reduction of cellular depolarization during ischemia, which may be due to relief of calcium overload, and which may explain the antifibrillatory effect.
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PMID:Reduction of ischemic depolarization by the calcium channel blocker diltiazem. Correlation with improvement of ventricular conduction and early arrhythmias in the dog. 669 97

The efficacy of therapy with diltiazem, 360 mg/day, was studied in 11 men with chronic, stable angina pectoris. An initial dose-titration schedule in which diltiazem was increased weekly from placebo to 120, 240 and 360 mg/day (Period I) was followed by a randomized, double-blind, 1-month crossover trial of placebo vs diltiazem at 360 mg/day (Period II). A computer-assisted treadmill exercise test was performed at the end of each dose and each 2-week crossover period. Diltiazem at 360 mg/day, compared with placebo (Period II), significantly improved exercise performance. Exercise duration to onset of chest pain increased 40% from 5.3 +/- 2.1 to 7.4 +/- 2.7 minutes (p less than 0.01). Time to reach 1 mm of ST-segment depression increased 33%, from 5.1 +/- 2.0 to 6.8 +/- 1.8 minutes (p less than 0.01). Total exercise duration increased 16%, from 7.5 +/- 2.0 to 8.7 +/- 2.0 minutes (p less than 0.005). A computer-derived quantitative treadmill exercise score improved 27%, from -13.1 +/- 9.4 to -9.5 +/- 7.6 units (p less than 0.005), and the ST-segment depression at peak exercise improved from -1.9 +/- 1.1 to -1.6 +/- 1.2 mm (p less than 0.05). Progressive improvement in these variables was seen during the single-blind dose-titration period between 120 and 240 mg/day and between 240 and 360 mg/day (Period I). Baseline heart rate (HR) and diastolic blood pressure (BP) in the supine and upright position were significantly lower with diltiazem than with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved efficacy of high-dose versus medium- and low-dose diltiazem therapy for chronic stable angina pectoris. 670 13

The clinical applications of calcium channel blockers are rapidly growing; as barbiturates interfere with intracellular calcium movements, the possibility of drug interaction at this level must be considered. We have studied the haemodynamic interaction of Thiopentone and Diltiazem in pigs. A loading dose of Diltiazem (0.15 mg X kg-1) was injected followed by a continuous administration of 0.07 mg X kg-1 X hour. From the fifth to the tenth minute, the reduced afterload was associated with a moderate depression of the contractility of the left ventricle. These values returned to the initial level within 30 minutes. Heart rate and cardiac output were not modified. The stability of these two parameters is thought to result from the complex interaction of both drugs on the sympathetic nervous system and the ventricular function.
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PMID:[Hemodynamic interferences between diltiazem and thiopental--experimental study in the pig]. 670 81

The acute effects of intravenous diltiazem on exercise performance were studied in 10 patients with coronary artery disease. Haemodynamic measurements were made at rest and during exercise before and after 0.5 mg kg-1 of diltiazem. Diltiazem prolonged the duration of exercise (+2.85 min, P less than 0.001) and delayed the onset of ischaemic ST depression or angina in all patients. The highest tolerated heart rate and pressure rate product were increased in all but one patient after diltiazem. At rest diltiazem decreased mean arterial pressure (-10.8%, P less than 0.005), systemic vascular resistance (SVR) (-11.8%, P less than 0.05) and left ventricular stroke work index (SWI) (-14.1%, P less than 0.005). During exercise under diltiazem therapy, at the level achieved before the drug, the pulmonary capillary wedge pressure (-30%, P less than 0.005) and the SVR (-13.6%, P less than 0.02) were lowered, the SWI (+13%, P less than 0.01) was increased; at the end of exercise only the SVR (-14%, P less than 0.05) was reduced. Two patients experienced angina on lying down and one had orthostatic hypotension after exercise with diltiazem. This study indicates that intravenous diltiazem is a potentially useful agent for the treatment of angina by reducing myocardial oxygen demand at rest and by improving left ventricular performances on exercise.
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PMID:Haemodynamic effects of intravenous diltiazem at rest and exercise in patients with coronary artery disease. 674 87

Effects of diltiazem, a recently introduced calcium antagonist, on exercise performance were studied in nine coronary disease patients with effort angina. The duration of exercise before the onset of angina and the time to the onset of ischemic ST depression 2 hours after 90 mg of oral diltiazem were compared with those 2 hours after oral placebo and a few minutes after 0.3 mg of sublingual nitroglycerin. Diltiazem prolonged the duration of exercise in all nine patients (average 2.5 minutes, p less than 0.001) and delayed the onset of ischemic ST depression (average 2.4 minutes, p less than 0.001). The increment of the duration of exercise and the time to the onset of ischemic ST depression following 90 mg of oral diltiazem were almost equivalent to that following sublingual nitroglycerin. These results in fixed coronary atherosclerosis indicate the clinical antianginal efficacy of diltiazem which persists for at least 2 hours after oral administration.
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PMID:Increased exercise tolerance after oral diltiazem, a calcium antagonist, in angina pectoris. 678 21

The cause of recurrent resting angina one year after aorto-coronary bypass is presented. A 65 year old female with effort and resting angina with syncope had an isolated narrowing of the proximal portion of the left anterior descending artery on coronary angiography. Saphenous vein aorto-coronary bypass and cardiac plexectomy were performed on the 18 . 12 . 78, and an excellent result was obtained in the first postoperative year. Nocturnal angina with syncope recurred on the 31 . 12 . 79 and anterior subendo-cardial ischaemic changes were noted on the post critical electrocardiogramme. On control angiography 10 days later, the bypass graft was shown to be patent. A provocative test with methylergometrine showed spasm of the whole of the revascularised artery without any changes in the other vessels. Attacks of spontaneous angina with ST depression on Holter monitoring continued despite treatment with Nifedipine (6 capsules/day). The substitution of Diltiazem (3 capsules/day) prevented further recurrence with a follow-up of three months. The authors conclude that spontaneous angina after aorto-coronary bypass is not synonymous with graft dysfunction, and suggest that the effects of cardiac denervation in vasospastic angina, where Nifedipine and Diltiazem seem to have different modes of action, need further confirmation.
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PMID:[False failure of an aortocoronary bypass. Spasm of an artery revascularized by 2 saphenous vein graft]. 678 80


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