Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of long-term treatment with diltiazem on the heart in normotensive (WKY) and spontaneously hypertensive rats (SHR) were studied. Diltiazem was added to the drinking fluid (900 mg/liter) and given ad libitum from 19 to 26 weeks of age, whereas tap water was given to the control animals. Although diltiazem did not decrease blood pressure in SHR, it decelerated the increase in their left ventricular weight (p less than 0.01). Hearts were removed and perfused by the working heart technique for 15 min, and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The extent of recovery of coronary flow after reperfusion, following 30 min of ischemia in the diltiazem-treated SHR, was higher than that in the control SHR (p less than 0.01). The levels of adenosine triphosphate (ATP), creatine phosphate (CrP), and energy charge potential in the SHR heart reperfused after 30 min of ischemia were lower than those in the reperfused WKY heart (p less than 0.01, respectively). Diltiazem improved the restoration of ATP and CrP and prevented the decrease in energy charge potential in SHR after reperfusion following 30 min of ischemia (p less than 0.01, respectively). In conclusion, long-term treatment of SHR with diltiazem may protect the myocardium when myocardial ischemia occurs.
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PMID:Response of isolated perfused heart to ischemia after long-term treatment of spontaneously hypertensive rats with diltiazem. 213 6

Diltiazem is a commonly prescribed calcium-channel antagonist for hypertension and ischemic heart disease. The incidence of rash associated with diltiazem therapy is reported to be 1.3 percent. We describe two patients who developed erythematous, macular skin eruptions, approximately two weeks following institution of diltiazem. The skin eruptions resolved after symptomatic treatment and the patients received further therapy with another calcium-channel antagonist. Diltiazem-associated skin eruptions are a rare adverse effect; however, the incidence of rash may occur more frequently than reported in postmarketing surveillance studies.
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PMID:Reports of erythematous macular skin eruptions associated with diltiazem therapy. 214 57

Diltiazem is a calcium antagonist effective in the treatment of stable, variant and unstable angina pectoris and mild to moderate systemic hypertension, with a generally favourable adverse effect profile. It is also effective in terminating supraventricular tachycardia and in controlling the ventricular response to atrial fibrillation/flutter. Atrioventricular block, the risk of which may be exacerbated by concomitant beta-adrenoceptor antagonist therapy, occurs rarely as an adverse effect of diltiazem treatment. Diltiazem appears to exert complex cardioprotective effects which have been of benefit after intracoronary administration to patients undergoing coronary angiography and bypass procedures. In addition, long term diltiazem treatment has produced a significant reduction in subsequent cardiac events in patients with non-Q wave myocardial infarction. Thus, diltiazem is an effective and well-tolerated first-line or alternative treatment of patients with ischaemic heart disease, systemic hypertension, and supraventricular arrhythmias, with possible potential in limiting ischaemia-induced myocardial damage.
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PMID:Diltiazem. A reappraisal of its pharmacological properties and therapeutic use. 219 51

Diltiazem and nifedipine improve coronary blood flow and reduce peripheral determinants of myocardial oxygen demand through activation of similar but distinct cellular mechanisms. To identify differences during myocardial ischemia, systemic and coronary hemodynamics were measured continuously before and during brief periods of left anterior descending coronary balloon occlusion in 23 patients undergoing single-vessel angioplasty. Data were compared for two matched ischemic periods, one control and one "drug" period. In 13 patients, diltiazem, 10 mg (intravenous bolus with continuous 500 mg/min infusion), was given; in 10 patients, nifedipine, 10 mg sublingual, was given and after 15 minutes, ischemia was reinduced. Both drugs significantly reduced systolic and mean arterial pressure (for diltiazem, 108 +/- 15 to 93 +/- 10 mm Hg; and for nifedipine, 117 +/- 20 to 96 +/- 8 mm Hg, both p less than 0.01). Diltiazem significantly reduced heart rate-pressure product (with heart rate unchanged), while both drugs maintained the resting great vein blood flow (for diltiazem, 97 +/- 25 to 91 +/- 34 ml/min; for nifedipine, 115 +/- 49 to 98 +/- 58 ml/min, p = ns) with reduced arterial pressure. Coronary flow during occlusion was unchanged (for control versus diltiazem, 63 +/- 21 versus 59 +/- 14 ml/min; for nifedipine, 66 +/- 33 versus 73 +/- 38 ml/min, both p = ns). Neither drug improved collateral hemodynamics or resistance index during ischemia. Both diltiazem and nifedipine prolonged the time to ischemic ST segment alteration (for diltiazem, 27 +/- 10 to 40 +/- 16 seconds, p less than 0.05; for nifedipine, 24 +/- 14 to 38 +/- 14 seconds, p = ns) during transient coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of diltiazem and nifedipine on systemic and coronary hemodynamics and ischemic responses during transient coronary artery occlusion in patients. 229 73

Diltiazem, a calcium-channel blocking agent, has been shown to be a potent coronary vasodilator used in the treatment of ischaemic heart disease. The present study was conducted to compare the bioavailability of regular 60 mg tablets administered every 6 h with sustained release capsules of 120 mg administered every 12 h. High-performance liquid chromatographic analysis was carried out for determination of diltiazem and one of its metabolites desacetyldiltiazem in six male patients. The relative bioavailability of this sustained-release pharmaceutical form did not show any significant difference with that of tablets.
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PMID:Bioequivalence of two pharmaceutical forms of diltiazem. 232 38

The effects of diltiazem during transient myocardial ischemia were studied in 17 patients (age 58 +/- 11 years, 12 men, 5 women) undergoing 1-vessel left anterior descending percutaneous transluminal coronary angioplasty (PTCA). After hemodynamic, echocardiographic and electrocardiographic data were obtained during the control ischemic periods, diltiazem (10 mg intravenous bolus with 500 micrograms/min infusion) was given and 15 minutes later ischemia reinduced. Diltiazem reduced mean arterial pressure (113 +/- 16 to 95 +/- 15 mm Hg, p less than 0.05) and heart rate-pressure product (p less than 0.05) with no change in heart rate, pulmonary pressures or coronary (sinus, thermodilution technique) blood flow at rest. After diltiazem, times to ischemia-induced 1.0 mm ST-segment elevation (28 +/- 10 to 42 +/- 17 seconds, p less than 0.05) and new left ventricular wall motion abnormalities (by 2-dimensional echocardiography, 24 +/- 8 to 36 +/- 12 seconds, p less than 0.001) were prolonged without significant augmentation of great cardiac vein flow during coronary occlusion. Left ventricular (LV) ejection fraction decreased from 51 +/- 7 to 41 +/- 12% (p less than 0.05) during control ischemia, but declined less after diltiazem (54 +/- 12 to 47 +/- 14%, difference not significant; 47 +/- 14 vs 41 +/- 12%, p less than 0.01). Diltiazem can attenuate, but not abolish, some of the effects of myocardial ischemia on LV function during transient coronary artery occlusion. These data support the use of diltiazem as a beneficial adjunct that may be used acutely and safely during routine PTCA.
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PMID:Hemodynamic and echocardiographic assessment of the effects of diltiazem during transient occlusion of the left anterior descending coronary artery during percutaneous transluminal coronary angioplasty. 267 30

After examining the properties of the 3 most widely used calcium antagonists, the paper assesses the efficacy of Diltiazem in reducing blood pressure rises after exercise in a group of 7 patients with chronic atrial fibrillation. The blood pressure response to a standard load (50 W x 3 m2) on the exercise cycle was monitored in a group of patients under chronic digitalis treatment (phase I) after which the same patients' response to varying doses of Diltiazem (180-240 mg/day) was assessed (phase II) and finally (phase III) their response to treatment with Diltiazem alone but no digitalis. A significantly greater reduction in the systolic pressure and heart rate after exercise was noted in patients given Diltiazem with or without Digoxin than in those given digitalis alone. It is therefore concluded that Diltiazem may be useful in controlled blood pressure and heart rate increases after exercise, especially in patients with ischaemic heart disease.
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PMID:[Efficacy of diltiazem in blood pressure increase caused by exertion]. 274 39

The effects of orally administered diltiazem combined with maximally tolerated doses of beta-blockers and nitrates were assessed in 12 patients, who during stress testing exhibited persistent effort angina and continued objective evidence for inducible myocardial ischemia. Patients performed multistage semisupine exercise on a bicycle ergometer during equilibrium-gated radionuclide angiography after consecutive 2 week treatment periods of placebo or diltiazem 90 mg qid (mean dose 340 mg/day) combined with maximally tolerated propranolol (mean dose 178 mg/day) and isosorbide dinitrate (mean dose 137 mg/day). All medications (including diltiazem or placebo) were administered four times daily for the duration of the study. Diltiazem or placebo was administered according to a double-blind design, with randomized cross-over at the end of each 2 week treatment period. The average number of angina attacks decreased during the double-blind cross-over phase of the trial (7 +/- 7 episodes/week at baseline vs 4 +/- 3 on placebo vs 2 +/- 2 on diltiazem; p = .08). Angina pectoris was abolished during peak exercise in eight of 12 patients on diltiazem (p less than .05 vs placebo). Diltiazem increased total exercise duration from 276 +/- 92 to 310 +/- 78 sec (p less than .005 vs baseline). Diltiazem likewise increased the time to onset of angina from 231 +/- 84 sec at baseline to 305 +/- 77 sec (p less than .005), as well as the time to the onset of 1 mm ischemic ST segment depression (p = .01). Diltiazem decreased heart rate at rest, during submaximal workload, and at peak exercise (p less than .05), and decreased systolic blood pressure at peak exercise only (p less than .05). A significant decline in rate-pressure product at submaximal and peak exercise was noted (p less than .05). At any given workload there was significantly less ST segment depression during submaximal (p = .05) and peak exercise (p less than .025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effects of high-dose diltiazem in patients with persistent effort angina on beta-blockers and nitrates: a randomized, double-blind, placebo-controlled cross-over study. 285 31

The safety and efficiency of the administration of diltiazem was evaluated in 10 patients with class II-III chronic stable angina. All the patients had ischemic heart disease documented by coronary angiography and/or an abnormal exercise test. A dose related improvement in both frequency of angina and exercise capacity were obtained by diltiazem administered in increased doses using a single blind protocol. The weekly frequency of angina was reduced from 7.5 +/- 9.8 with placebo to 3.8 +/- 5.5, 1.1 +/- (p less than 0.05) and 0.7 +/- 0.9 (p less than 0.01) with doses of 120, 240 and 360 mg/day respectively. The exercise duration on treadmill was significantly increased from 8.5 +/- 3.6 to 10.6 +/- 3.7 min (p less than 0.05) with the 360 mg/day dose. The mean exercise time required to develop 1 mm ST depression was 6.1 +/- 3 min on placebo and was significantly delayed to 9.0 +/- 3.8 min (p less than 0.05) with the 240 mg/day dose and to 10.7 +/- 4.0 min with 360 mg (p less than 0.01). In a double blind randomized crossover phase, the time to the onset of ischemia during exercise was increased from 8.5 +/- 3.8 min with placebo to 11.05 +/- 2.8 min with 360 mg/day of diltiazem (p less than 0.01). Diltiazem in doses ranging from 120 to 360 mg/day is an effective antianginal agent with no significant adverse effects.
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PMID:[Diltiazem in chronic stable angina]. 294 27

This study evaluated left ventricular (LV) and coronary hemodynamic effects of intravenous nitroglycerin (NTG) in the presence of an intravenous infusion of diltiazem in 15 patients with severe coronary disease. Diltiazem (250 microgram/kg bolus followed by 1.4 micrograms/kg/min infusion) alone decreased mean systemic blood pressure (mean 6%) without changing heart rate or LV end-diastolic pressure. The rate of rise in LV pressure declined slightly (4%), and peripheral resistance decreased (19%). Coronary sinus (CS) and great cardiac vein (GCV) flows were preserved. Addition of NTG (average, 68 micrograms/min) decreased systemic pressure further (7%) as LV end-diastolic pressure declined (5 mm Hg). These pressure changes were accompanied by a 10% increase in heart rate (compared with the heart rate found with diltiazem alone). Peripheral resistance was similar to values after diltiazem alone. The CS and GCV flows did not decrease. The sequence of intravenous drug administration was reversed in three other patients with combination therapy, producing similar effects, regardless of which drug was administered first. Hemodynamic effects of intravenous diltiazem alone and its combination with intravenous NTG seemed potentially favorable for patients with ischemic heart disease.
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PMID:Systemic and coronary hemodynamic effects of combined intravenous diltiazem and nitroglycerin administration. 310 25


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