Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the pathogenesis of angina pectoris in 101 patients with one-vessel disease except those with 99% to 100% occlusion. The attacks could not be induced or could not be reproducibly induced by maximal treadmill exercise at the same hour of different days within a week period in 54 (53.5%) of the patients. In the 47 patients whose attacks were reproducibly induced by the exercise, propranolol, 80 mg orally, did not suppress the attacks in 41 (87.2%) of the patients. Diltiazem, 90 mg, and nifedipine, 20 mg given orally, suppressed the attacks completely in 39 (83.0%) of the 47 patients and in 36 (81.8%) of the 44 patients, respectively. Coronary arteriography showed that dynamic obstruction of the artery supplying the area of myocardium represented by ST segment deviation appeared during the attacks and disappeared with subsidence of the attacks in all 55 patients in whom coronary arteriography was done during the attack. We conclude that angina pectoris is usually caused not by increased myocardial oxygen demand but by dynamic coronary obstruction or by a combination of both in most patients with one-vessel disease.
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PMID:Pathogenesis of angina pectoris in patients with one-vessel disease: possible role of dynamic coronary obstruction. 373 79

The short-term effects of intravenously administered diltiazem on pulmonary and systemic hemodynamics were evaluated in patients with hypoxic pulmonary hypertension. Twelve patients were randomly assigned to two groups in a double-blind fashion. One group (eight patients) received diltiazem, and the other group (four patients) received a placebo. Three increasing doses of diltiazem (0.2, 0.3, and 0.4 mg/kg of body weight) were injected into each patient, followed each time by an infusion (2 micrograms/kg/min, 3 micrograms/kg/min, and 4 micrograms/kg/min). The effects of the drug were also compared with those of oxygen, and the combined effect of high oxygen and diltiazem was tested. The mean plasma concentrations of diltiazem were, successively, 64 +/- 4, 158 +/- 19, and 267 +/- 40 ng/ml with the three increasing doses. There was no significant effect of diltiazem on the pulmonary vascular resistance even when given with oxygen. Diltiazem was well tolerated even at high doses. The arterial oxygen pressure, systemic oxygen supply, and oxygen consumption were unchanged. We conclude that diltiazem does not seem to decrease acutely hypoxic pulmonary vasoconstriction in patients with chronic hypoxia; however, diltiazem may be given safely to these patients for other indications, such as angina pectoris.
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PMID:Hemodynamic effects of intravenous diltiazem in hypoxic pulmonary hypertension. 380 28

Using Holter monitoring the Authors compared the effectiveness of diltiazem 120 mg every 8 hours for three consecutive days with the results of a placebo administered with the same regimen, following a double-blind completely balanced cross-over trial in 20 patients with angina at rest. During treatment with diltiazem the total number of recorded ischemic episodes was 100, during treatment with placebo the total number was 357 (Tab. I); P less than 0.01 at analysis of variance (Tab. II). Ischemic episodes during treatment with diltiazem had a shorter duration (3.9 versus 5.1 min.), less marked ST segment shifts (1.3 versus 2 mm), and were less symptomatic (20% versus 29%) than ischemic episodes during placebo (Tab. III). No significant differences at a paired t test were noted. Diltiazem was more effective in the morning (12 p.m. - 12 a.m.: from 187 to 34 ischemic episodes) than in the evening (12 a.m. - 12 p.m.: from 170 to 66 ischemic episodes) (Fig. 1); P less than 0.01 at the chi-square test (Tab. IV). Diltiazem reduced the number of ischemic episodes with ST segment elevation, peaking of T waves and negative T wave inversion (from 188 to 39) more than the number of episodes with ST segment depression (from 169 to 61) (Tab. V); P less than 0.05 at the chi-square test. In conclusion, in patients with angina at rest, diltiazem reduces the incidence and seems to reduce the severity of ischemic episodes, too.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diltiazem in spontaneous angina: double-blind cross-over study with Holter monitoring]. 383 Jul 64

Since their introduction in the United States about 4 years ago, the calcium antagonists have achieved an important place in the medical therapy of several cardiovascular disease entities. These pharmacologic agents differ markedly in their clinical utility. Verapamil is extremely effective in patients with supraventricular tachyarrhythmias, hypertrophic cardiomyopathy, and the various anginal syndromes, but it appears to be ineffective or possibly even deleterious in those with pulmonary hypertension, congestive heart failure of any cause, and Raynaud's phenomenon or disease. Nifedipine exerts a powerful vasodilatory effect and, as a result, is efficacious in individuals with systemic or pulmonary hypertension, congestive heart failure, and Raynaud's phenomenon or disease. It is also beneficial in patients with various kinds of angina, especially when it is administered concomitantly with a beta-adrenergic blocker. It is totally ineffective as an antiarrhythmic agent. Diltiazem is an effective antianginal agent and may be beneficial as an antiarrhythmic agent, but it is largely untested in patients with systemic or pulmonary hypertension, Raynaud's disease, and hypertrophic cardiomyopathy. A thorough understanding of each drug's hemodynamic and electrophysiologic effects allows the practicing physician to prescribe them skillfully and safely.
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PMID:Calcium antagonists in patients with cardiovascular disease. Current perspectives. 388 Aug 54

In order to assess the long-term efficacy of diltiazem for the treatment of angina pectoris, eight patients with chronic stable exertional angina who were previously entered into a 4-month randomized, double-blind placebo controlled study, were studied for an additional 12-months. The patients continued to take diltiazem, 360 mg/day, and underwent treadmill exercise testing after 10 and 16 months of therapy. A single-blind placebo week was introduced after 16 months and a treadmill test was performed at the end of this week. Diltiazem therapy continued to augment exercise duration until 0.1 mV of ECG ST depression at 10 and 16 months as compared to the final placebo period: 573 +/- 133 (SD) seconds at 10 months; 565 +/- 148 seconds at 16 months; vs 431 +/- 151 seconds at final placebo (both p less than 0.001). Also, the time to angina pectoris was prolonged on diltiazem by 181 seconds at 16 months (p less than 0.01) and the total duration of exercise was increased by 101 seconds (p less than 0.001) as compared to placebo. In addition, angina frequency decreased from 17 +/- 11 attacks/week on placebo to 0.6 +/- 0.6 attacks/week during diltiazem therapy at 16 months. Two of the eight patients noted mild pedal edema, but no other adverse effects were experienced. Thus diltiazem, 360 mg/day, can be an effective single agent for the long-term treatment of chronic stable angina pectoris.
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PMID:Long-term efficacy of high-dose diltiazem for chronic stable angina pectoris: 16-month serial studies with placebo controls. 388 Sep 93

Diltiazem is an orally and intravenously active calcium channel blocking agent shown to be an effective and well-tolerated treatment for stable angina and angina due to coronary artery spasm. Its efficacy in these diseases has generally been similar to that of nifedipine or verapamil - alternative calcium channel blockers with which diltiazem has many electrophysiological, haemodynamic, and antiarrhythmic similarities. The antianginal mechanism of diltiazem cannot be precisely described; however, it appears to increase myocardial oxygen supply and decrease myocardial oxygen demand, mainly by coronary artery dilatation and/or via both direct and indirect haemodynamic alterations. Diltiazem has also shown substantial efficacy in the treatment of unstable angina, hypertension, and supraventricular tachyarrhythmias, but further study is necessary before its place in the treatment of these diseases may be clearly established. Although headache due to peripheral vasodilatation and depression of atrioventricular nodal conduction may be troublesome, side effects occur in only 2 to 10% of patients receiving diltiazem and are generally minor in nature. Thus, diltiazem offers a worthwhile alternative to other agents currently available for the treatment of angina pectoris. Although the infrequency of serious side effects may offer an advantage, its relative place in therapy compared with that of other calcium channel blockers remains to be clarified.
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PMID:Diltiazem. A review of its pharmacological properties and therapeutic efficacy. 389 2

Diltiazem, as well as other calcium entry blockers, is widely prescribed for the treatment of various types of angina. This review summarizes the current state of knowledge of the pharmacokinetics of diltiazem and of two other calcium entry blockers: verapamil and nifedipine. Although unrelated in their chemical structure, these three drugs have common features. They are highly lipophilic and have a large volume of distribution, are mainly cleared by metabolism and undergo an extensive first-pass extraction. On the other hand, as expected from their quite dissimilar structures, they have their own particular kinetic characteristics. For example, metabolism of diltiazem and verapamil gives rise to active metabolites; repeated administration influences the kinetic profile of verapamil but not those of diltiazem and nifedipine. Absorption, distribution and elimination of these three drugs are differently affected by age and pathological conditions. The possible drug interactions involving diltiazem and the other calcium entry blockers are discussed, particularly that with digoxin. Due to its large therapeutic index, there is no need for treatment monitoring of diltiazem. Nevertheless, this procedure may provide useful information for optimizing the dosage regimen of each patient as the pathological condition and drug therapy may be quite complex.
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PMID:Pharmacokinetics of diltiazem and other calcium entry blockers. 390 30

In a randomized, double-blind, placebo-controlled crossover trial, diltiazem and nifedipine were compared in 10 patients with stable angina pectoris and mild to moderate hypertension (supine diastolic blood pressure greater than or equal to 90 mm Hg). Patients received placebo for 2 weeks, then increasing doses of diltiazem (90 to 360 mg/day) or nifedipine (30 to 120 mg/day) in 3 daily divided doses over 2 weeks, followed by 1 week of therapy at the maximal dose, a 1-week placebo "washout," then crossover to the other drug. Heart rate and blood pressure at rest and during exercise, anginal frequency, nitroglycerin consumption and treadmill exercise tolerance were assessed. Compared with placebo, anginal frequency and nitroglycerin consumption were reduced with both diltiazem and nifedipine (p less than 0.01) and exercise tolerance was increased with both drugs (p less than 0.01). Standing blood pressure at rest was reduced by diltiazem and nifedipine (146.6 +/- 11.4/97.7 +/- 5.3 mm Hg at placebo, baseline reduced to 129.6 +/- 15.2/79.5 +/- 13.7 mm Hg with diltiazem, and to 122.2 +/- 9.9/82.0 +/- 7.1 with nifedipine, p less than 0.01 for both). Compared with placebo, diltiazem and nifedipine also reduced exercise diastolic blood pressure (p less than 0.01), but not systolic blood pressure. Diltiazem lowered the heart rate at rest from 88.5 +/- 14.4 beats/min at placebo baseline to 79.7 +/- 17.9 beats/min (p less than 0.01); the heart rate with diltiazem was 11 beats/min lower than that with nifedipine (p less than 0.05). Both diltiazem and nifedipine had similar effects on the heart rate-blood pressure product at rest and during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of diltiazem and nifedipine for both angina pectoris and systemic hypertension. 393 48

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

To determine the systemic and coronary hemodynamic effects of diltiazem at rest and during pacing, 14 patients with stable angina pectoris undergoing coronary angiography were studied before and after 0.165 mg/kg (n = 7) and 0.25 mg/kg (n = 7) of intravenously administered diltiazem. Hemodynamic variables, metabolic measurements and left ventricular (LV) ejection fraction (EF) were obtained at rest and during coronary sinus (CS) pacing before and during diltiazem administration. Lactate production during control pacing turned into extraction after diltiazem (p less than 0.05). At rest, systemic resistance was reduced by 21% (p greater than 0.01) and mean arterial pressure by 12% (p less than 0.01); cardiac index increased from 2.4 +/- 0.4 to 2.6 +/- 0.4 liters/min/m2 (p less than 0.01), with no significant change in heart rate. The mean pulmonary artery pressure increased from 17 +/- 2 to 19 +/- 3 mm Hg (p less than 0.01), but other hemodynamic variables were not affected. Diltiazem given during pacing reduced the mean aortic pressure (from 112 +/- 15 to 104 +/- 15 mm Hg, p less than 0.05), but other hemodynamic variables were not affected significantly. LVEF decreased 16%, from 0.63 +/- 0.9 to 0.53 +/- 0.8 with CS pacing (p less than 0.01); when the pacing was performed after diltiazem administration the 8% decrease in LVEF from 0.64 +/- 0.09 to 0.59 +/- 13 was less marked (p less than 0.01). Diltiazem had no significant effect on LVEF at rest. The overall data suggest that the ischemic manifestations of CS pacing are attenuated by diltiazem in doses of the drug that exert no significant depressant effect on LV function in patients with coronary artery disease.
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PMID:Hemodynamic and metabolic effects of diltiazem during coronary sinus pacing with particular reference to left ventricular ejection fraction. 396 63


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