Disease relevance of diltiazem

• Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested [1].
• We conclude that diltiazem was effective in preventing early reinfarction and severe angina after non-Q-wave infarction and that it was also safe and generally well tolerated [2].
• Diltiazem and subacute cutaneous lupus erythematosus-like lesions [3].
• Diltiazem prophylaxis in refractory migraine [4].
• We report that D-cis-diltiazem, a calcium-channel blocker that also acts at light-sensitive cGMP-gated channels, rescued photoreceptors and preserved visual function in the retinal degeneration mouse [5].

Psychiatry related information on diltiazem

• Diltiazem and akathisia [6].
• When given alone by the intraperitoneal route, diltiazem decreased spontaneous locomotor activity and lowered body temperature [7].
• The effects of diltiazem on hemodynamics and seizure duration during electroconvulsive therapy [8].
• This new extended-release formulation of diltiazem should significantly facilitate blood pressure control because of better patient compliance with a once daily regimen [9].
• OBJECTIVE: To examine the efficacy of a slow-release formulation of diltiazem as adjunctive therapy in patients with treatment-resistant bipolar disorder [10].

High impact information on diltiazem

• Diltiazem therapy had the highest rate of success: 59 percent of the treated patients had reached the blood-pressure goal at the end of the titration phase and had a diastolic blood pressure of less than 95 mm Hg at one year [11].
• Because calcium-channel blockers can suppress diet-induced atherosclerosis in laboratory animals, we assessed the efficacy of diltiazem in preventing coronary artery disease in transplanted hearts [12].
• Enrollment in the study after the publication of the Multicenter Diltiazem Postinfarction Trial independently predicted the use of calcium antagonists after myocardial infarction (odds ratio, 0.47; 95 percent confidence interval, 0.39 to 0.57) [13].
• Excretion of diltiazem in human milk [14].
• The long record of diltiazem prescription in cardiology should facilitate the design of clinical trials for some forms of retinitis pigmentosa [5].

Chemical compound and disease context of diltiazem

• An assessment of diltiazem and hydrochlorothiazide in hypertension. Application of factorial trial design to a multicenter clinical trial of combination therapy [15].
• To find out the effect of the non-dihydropyridine-like calcium-channel blocker diltiazem, a randomised, double-blind trial was conducted comparing diltiazem with glyceryl trinitrate, both given intravenously, in 129 patients with unstable angina [16].
• Effects of diltiazem or lisinopril on massive proteinuria associated with diabetes mellitus [17].
• Sustained-release diltiazem (D-SR) and sustained-release verapamil (V-SR) when given twice a day have been successfully used to treat both essential hypertension and angina pectoris [18].
• The efficacy of a single oral dose combination of 120 mg diltiazem and 160 mg propranolol in terminating paroxysmal supraventricular tachycardia (PSVT) was evaluated in 15 patients [19].

Biological context of diltiazem

• Association of diltiazem therapy with increased insulin resistance in a patient with type I diabetes mellitus [20].
• Exposure to diltiazem, a Ca channel antagonist, for 18-24 h had no effect on number of DHP binding sites [21].
• To determine if ischemic injury alters vascular contractility by increasing smooth muscle cell calcium or calcium influx, the renal blood flow (RBF) response to reductions in RPP within the autoregulatory range and to RNS were tested before and after a 90-min intrarenal infusion of verapamil or diltiazem in 7-d ischemic ARF rats [22].
• Heart-rate pressure product was reduced significantly only by diltiazem (p < 0.05) [16].
• First, the pharmacokinetics of diltiazem in patients with atrial fibrillation or atrial flutter is nonlinear with an apparent dose-dependent decrease in systemic clearance with increasing infusion rate [23].

Anatomical context of diltiazem

• Diltiazem in the prevention of coronary artery disease in heart-transplant recipients [24].
• Diltiazem and internal anal sphincter [25].
• LN-induced neurite growth, like that induced by N-cadherin, is insensitive to diltiazem and conotoxin, but is highly sensitive to Ni2+ inhibition [26].
• K+ depolarization experiments suggest that voltage-dependent Ca2+ influx pathways in CG neurons (cell bodies and growth cones) are largely blocked by the combination of diltiazem and Ni2+ [26].
• The increase in LVSR during administration of diltiazem did not appear to be mediated by changes in contractility or regional myocardial blood flow, but were probably mediated in part by afterload reduction and possibly by a reduction in calcium entry into ischemic myocardium [27].

Associations of diltiazem with other chemical compounds

• INTERVENTION: Diltiazem (mean dose, 392 +/- 27 mg/d) or nifedipine (mean dose, 83 +/- 9 mg/d) was used to decrease blood pressure to less than 140/90 mm Hg [28].
• Ca(2+) channel blockers such as 1,4-dihydropyridines, phenylalkylamines, diltiazem and mibefradil exert their anti-arrhythmic and anti-hypertensive action by restricting Ca(2+) entry into myocardial cells and smooth muscle cells [29].
• Treadmill exercise tests were done according to a randomized double-blind protocol 90 minutes after administration of placebo, 80 mg propranolol, or 120 mg diltiazem, each at both -8 degrees and 20 degrees C. Eight of the patients were classified by history as cold-sensitive before the study [30].
• Change in luminal area after acute administration of a calcium antagonist (diltiazem or nicardipine), during exercise, and after sublingual nitroglycerin (percent change compared with rest = 100%) was assessed by biplane quantitative coronary arteriography [31].
• Cardiovascular responses to handgrip, diltiazem, their combination, and nitroglycerin were assessed by hemodynamic and electrocardiographic measurements and by computer-assisted measurements of normal and diseased segments of epicardial coronary arteries [32].

Gene context of diltiazem

• In contrast to these findings, the IL-6 plasma concentrations were comparable in both groups, whereas the serum concentration of soluble IL-2 receptors was decreased in patients treated with diltiazem [33].
• Both, CsA and high doses of diltiazem caused an increase of IL-6 mRNA [33].
• Role of CYP3A4 in human hepatic diltiazem N-demethylation: inhibition of CYP3A4 activity by oxidized diltiazem metabolites [34].
• AIMS: To determine the effect of diltiazem on intestinal CYP3A activity and protein and mRNA expression in vivo in healthy subjects [35].
• It has earlier been shown that the isoenzymes CYP2D6 and CYP3A4 are involved in O- and N-demethylation of diltiazem (DTZ), respectively [36].

Analytical, diagnostic and therapeutic context of diltiazem

• Measured by a conventional sphygmomanometer, systolic and diastolic blood pressures fell significantly in patients who received diltiazem, whereas no consistent changes occurred in those who received placebo [37].
• BACKGROUND: Diltiazem reduces non-fatal reinfarction and refractory ischaemia after non-Q-wave myocardial infarction, an acute coronary syndrome similar to the incomplete infarction that occurs after successful reperfusion [38].
• Patients in the diltiazem group had better (p < 0.05) event-free survival while taking the drugs [16].
• The oral administration of 90 mg of diltiazem, a calcium antagonistic drug, two hours before, completely suppressed the attack induced by the procedure in all of the five patients who received this drug [39].
• Short- and long-term efficacy of high-dose oral diltiazem for angina due to coronary artery disease: a placebo-controlled, randomized, double-blind crossover study [40].

References