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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In previous studies, the treatment of postoperative hypertension with sodium nitroprusside induced ischemic metabolism without a decrease in coronary sinus blood flow. In contrast, the calcium antagonists diltiazem and nifedipine reduce blood pressure and may improve myocardial metabolism. A prospective randomized trial was performed in 62 patients, in whom hypertension developed (mean arterial pressure greater than 95 mm Hg) after coronary bypass procedures, to compare diltiazem (n = 22), nifedipine (n = 20), and nitroprusside (n = 20). All three agents reduced blood pressure equally (p less than 0.0001, by analysis of variance). Heart rate decreased with diltiazem (p = 0.006) but increased with nifedipine and nitroprusside (p less than 0.05). Left ventricular diastolic function (the relation between left atrial pressure and left ventricular end-diastolic volume) was not changed with the three drugs. Systolic function (the relation between systolic blood pressure and left ventricular end-systolic volume) was depressed with diltiazem (p = 0.05 by analysis of covariance) and nifedipine (p = 0.05) but not with nitroprusside. Myocardial performance (the relation between left ventricular stroke work index and end-diastolic volume) was depressed most by diltiazem (p = 0.001 by analysis of covariance), and to a lesser extent with nifedipine (p = 0.03), but not with nitroprusside. Myocardial lactate flux in response to the stress of atrial pacing decreased with nitroprusside but not with diltiazem or nifedipine (p = 0.03 by analysis of variance). Diltiazem and nifedipine are effective agents for treating postoperative hypertension after coronary artery bypass operations.
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PMID:Postoperative hypertension: a comparison of diltiazem, nifedipine, and nitroprusside. 329 May 85

Diltiazem was evaluated as an adjunct to cold blood potassium cardioplegia in 63 patients undergoing elective coronary artery bypass grafting. The dual-phase study compared incrementally increasing doses (50, 100, and 150 micrograms/kg) of diltiazem using a single-blind, randomized schedule with an equivalent volume of placebo added to each of three infusions of cold (10 degrees C +/- 2 degrees C) blood containing potassium chloride at 25 mEq/L for the initial infusion (400 ml) and at 12 mEq/L for the next two infusions (300 ml each). Observations included a number of operative variables, creatine kinase (CK)-MB curves, two-dimensional echocardiography, and pulsed Doppler sonography before operation and on postoperative days 1 and 5. Pulmonary artery thermistor catheter responses were observed for 16 hours postoperatively, as were left ventricular micromanometer-tipped catheter responses in 7 patients. As the dose of diltiazem was increased, there was increasing time to atrioventricular node refunction (23.6 to 62.0 minutes). Diltiazem at 100 micrograms/kg (D-100) resulted in a significantly lower peak CK-MB activity than its placebo. Peak - dp/dt increased in treated patients and decreased in patients given the placebo. The cardiac index in D-100 patients was greater on the first postoperative day than preoperatively. The stroke index returned to the control level by the fifth postoperative day in D-50 and D-100 patients only, and it remained depressed in placebo patients. Although few benefits were realized from the addition of diltiazem to cold blood potassium cardioplegia, there was dose-related prolongation of the atrioventricular node recovery time, which required cardiac pacing and thus was associated with its attendant risks.
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PMID:Diltiazem as an adjunct to cold blood potassium cardioplegia: a clinical assessment of dose and prospective randomization. 349 75

The central and renal hemodynamic effects and the hormonal response to single doses of 60 mg and 90 mg of diltiazem were evaluated in 10 patients with severe chronic left ventricular (LV) systolic dysfunction (ejection fraction 0.22 +/- 0.08). Diltiazem administration resulted in only mild and mostly statistically insignificant changes. After 60 mg, only heart rate (from 86 +/- 10 beats/min at baseline to 79 +/- 14 beats/min at 4 hours) and pulmonary vascular resistance (from 231 +/- 108 to 165 +/- 74 dynes s cm-5 at 4 hours) changed significantly. Administration of 90 mg of diltiazem resulted in no significant change in any of the measured or calculated central hemodynamic variables. Individual data, however, revealed an increase stroke volume index in 3 patients but a decrease in 1 patient and a persistent increase in mean pulmonary artery wedge pressure in another patient. These hemodynamic changes were not associated with symptomatic deterioration in any of the patients. Both renal blood flow and glomerular filtration rate were impaired at baseline on both days and did not show a significant change 1, 2 and 4 hours after diltiazem administration. Similarly, no significant change was noted after either diltiazem dose in plasma catecholamine levels and renin concentration. In conclusion, administration of 60 to 90 mg of diltiazem in patients with severe chronic LV systolic dysfunction results in only mild and mostly insignificant acute effects on central and renal hemodynamics, plasma hormonal levels and patient clinical status.
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PMID:Central and renal hemodynamic effects and hormonal response to diltiazem in severe congestive heart failure. 355 52

A single blind study between placebo and diltiazem (25 mg i.v. single dose) was carried out on 20 male patients with previous myocardial infarction and without exertional ischaemia. Patients, 50 +/- 6.1 (mean +/- SD) years of age, underwent a right heart catheterization with Seldinger's percutaneous approach and brachial or radial artery percutaneous catheterization. Haemodynamic variables were recorded in the supine position after catheterization in baseline conditions at rest, after a warming-up period of 6 min, before and after a first and second exercise test with stepwise increments of 25 W per 3 min. Before the second exercise test, either placebo or diltiazem (25 mg) was injected intravenously in 3 min. In comparison with placebo, diltiazem significantly reduced resting blood pressure (P less than 0.001) and systemic vascular resistance (P less than 0.001) and increased cardiac index (P less than 0.01); during exercise it also reduced the mean pulmonary arterial pressure (P less than 0.05), pulmonary wedge pressure (P less than 0.05), total pulmonary resistance (P less than 0.02), and increased the stroke volume (P less than 0.05). The present study demonstrated that intravenous diltiazem did not induce a significant rise in cardiac index but reduced the afterload and slightly reduced the preload. Diltiazem also reduced myocardial oxygen consumption and decreased blood pressure, mean right atrial pressure and slightly decreased the heart rate.
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PMID:Haemodynamic effects of diltiazem at rest and during exercise in patients with previous myocardial infarction. 365 22

The effects of the calcium entry blocker diltiazem (iv loading dose 0.4 mg/kg, iv maintenance dose 0.4 mg/min) and subsequent isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right ventricular (RV) and left ventricular (LV) performance (ultrasonic dimension technique), on coronary (electromagnetic flow probes) and systemic hemodynamics, and on electrophysiologic parameters (PR, QRS, QTc intervals) were studied in eight open-chest dogs, anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Diltiazem at a plasma concentration of 282 +/- 33 ng/ml (mean +/- SE) caused significant (P less than 0.05) increases in coronary blood flows, and decreases in coronary and systemic vascular resistances with only little effect on global and regional RV and LV function. However, the PR interval increased by 40%, and three animals developed II degrees atrioventricular block type I. At stable diltiazem plasma levels, administration of isoflurane caused dose-dependent decreases in myocardial segment shortening and stroke volume with unchanged LV or increased RV preload, and little changed RV or reduced LV afterload indicating myocardial depression. Coronary and systemic vascular resistances remained unaffected. At the higher concentration of isoflurane (mean inspired 1.3 +/- 0.2%), seven animals developed intermittent sinus node arrests with pauses up to 12 s followed by intermittent junctional escape or sinus rhythms. Similar interactions might develop in patients on diltiazem receiving isoflurane.
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PMID:Cardiovascular and electrophysiologic interactions between diltiazem and isoflurane in the dog. 381 73

The effectiveness and safety of diltiazem (DIL), a slow channel calcium blocker, added in cold potassium cardioplegic (CP) solution was evaluated in coronary artery bypass graft (CABG) surgery for 2 purposes; (1) protection of ischemic myocardium during cardiac arrest and (2) prevention of perioperative coronary artery spasm (PCS). Diltiazem of 15 mg was added to a liter of CP which was administered 10 ml/kg B.W. initially and 5mg/kg thereafter. The serum concentration of DIL was 570 ng/ml at the time of aortic declamping, 210 ng/ml at cardioversion and 150 ng/ml one hour after surgery. The left ventricular stroke work index was increased significantly (p less than 0.05) in patients treated by DIL-CP, compared with the patients treated by regular CP without DIL. However, CPK-MB values were not significantly different in either group. The incidence of PCS has decreased from 9.1% to 0.8% (p less than 0.01) after the use of DIL-CP. Perioperative myocardial infarction rate has also decreased from 5.5% to 1.6%. No major or long-lasting side-effects were encountered. We consider that DIL-CP is a safe and excellent CP in CABG surgery and we are now utilizing this CP in all patients requiring CABG surgery.
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PMID:[Evaluation of the effectiveness and safety in the use of cold-diltiazem-potassium cardioplegia in coronary artery bypass surgery: a first clinical trial]. 391 Oct 52

Systemic and coronary hemodynamic effects of intravenous diltiazem, administered as a bolus of 250 micrograms/kg followed by an infusion of 1.4 micrograms/kg/min, were examined in 14 patients with effort angina. There was no change in heart rate despite significant decreases in systolic, diastolic and mean systemic pressures (13%, 10% and 11%, respectively, all p less than 0.01). The blood pressure decrease was closely correlated with the initial blood pressure (r = 0.81, p less than 0.05). Neither left ventricular end-diastolic pressure nor peak dP/dt changed significantly, but peripheral vascular resistance decreased 16% (p less than 0.001) and stroke volume index increased 10% (p less than 0.05). The pressure-rate product decreased 15% (p less than 0.005), but coronary blood flow was maintained as coronary resistance decreased 14% (p less than 0.025). Diltiazem increased regional coronary flow in some patients. Thus, intravenous diltiazem dilates coronary and systemic resistance vessels, without an increase in heart rate, favorably altering indexes of myocardial oxygen supply and demand.
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PMID:Systemic, left ventricular and coronary hemodynamic effects of intravenous diltiazem in coronary artery disease. 403 21

To test the effect of verapamil and diltiazem in acute stroke, three groups of mongrel cats of either sex underwent occlusion of the middle cerebral artery (MCA) via a transorbital approach under ketamine anesthesia. The first group served as controls, the second received an intravenous infusion of verapamil (0.1 microgram/kg/min), and the third received an intravenous infusion of diltiazem (0.1 to 1.0 microgram/kg/min). All drug infusions began 2 hours before MCA occlusion and continued for the remainder of the experiment. Before and for up to 24 hours after MCA occlusion, regional cerebral blood flow (rCBF), somatosensory evoked potentials (SSEP's), arterial blood gases, blood pressure, temperature, and hematocrit were measured at least every 2 hours. At the experiment's end, brains were perfused with India ink, removed, sliced, photographed for determination of nonperfused brain area, and weighed, dried, and reweighed for H2O content determination. In these studies, verapamil was associated with worsening of rCBF in ischemic regions and inappropriate increases in rCBF in nonischemic regions, indicating intracerebral steal. Diltiazem increased rCBF in marginally ischemic regions. Changes in SSEP's paralleled blood flow changes, with verapamil decreasing amplitude and conduction velocity while diltiazem slightly improved conduction in the ischemic brain. Verapamil increased the area of nonperfused brain and the content of cerebral H2O. Diltiazem-treated animals had decreased cerebral H2O content, but had a marked increase in the area of nonperfused brain, a finding associated with the high incidence of transtentorial herniation in the diltiazem-treated animals. These findings agree with in vitro studies demonstrating high sensitivity of cerebral blood vessels to calcium channel blockers. These studies further support the notion that calcium channel blockers probably affect several different classes of calcium channels, at different brain sites.
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PMID:Effects of verapamil and diltiazem on acute stroke in cats. 405 6

The hypotensive effect of acute and longterm, intravenous and oral administration of the calcium antagonist, diltiazem, was investigated in 8 normotensive volunteers and 55 patients with essential hypertension. Diltiazem i.v. infusion of 45 mg/h (0.5 mg/min, then 1.0 mg/min, each for 30 min rapidly decreased both blood pressure (BP) from 164 +/- 22/98 +/- 8 to 144 +/- 15/86 +/- 9 mmHg (mean +/- SD) and total peripheral resistance from 32.6 +/- 8.4 to 25.3 +/- 5.4 mmHg/l/min (p less than 0.001), and increased stroke volume from 58.2 +/- 9.5 to 64.2 +/- 8.6 ml/beat (p less than 0.05). It altered neither heart rate nor cardiac output in the hypertensives (n = 10). Oral diltiazem 60 mg rapidly decreased BP from 155 +/- 10/103 +/- 6 to 142 +/- 12/90 +/- 8 mmHg after 3 hours (p less than 0.01/p less than 0.001) in hypertensives (n = 8), but not in normotensives (n = 8). Diltiazem 90 mg p.o. decreased BP from 157 +/- 15/102 +/- 9 to 129 +/- 13/83 +/- 8 mmHg (p less than 0.01) in hypertensives (n = 15), and reduced the heart rate from 71 +/- 8 to 65 +/- 8 beats/min (p less than 0.01). The drug did not change plasma renin activity either in normotensives or hypertensives. The fall in diastolic BP was correlated with the plasma diltiazem concentration (r = 0.910, n = 6, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypotensive effects of diltiazem to normals and essential hypertensives. 636 Jun 93

The acute hemodynamic effects of intravenous diltiazem were studied in 8 patients with coronary artery disease, left ventricular (LV) failure (New York Heart Association functional class III), a rest ejection fraction (EF) less than 40% or a cardiac index less than 2.4 liters/min/m2. Hemodynamic measurements and LV angiograms were performed at rest before and after the administration of diltiazem, 0.5 mg/kg, administered at a speed of 5 mg/min. Diltiazem treatment induced a decrease in heart rate from 68 +/- 12 to 55 +/- 9 beats/min (p less than 0.001). Mean aortic pressure decreased from 94 +/- 14 to 81 +/- 15 mmHg (p less than 0.05). Thus, the pressure-rate product significantly decreased under the influence of the drug, from 8,791 +/- 2,465 to 6,342 +/- 1,808 beats mm Hg/min, (p less than 0.001). Diltiazem induced no significant change of LV end-diastolic pressure, pulmonary wedge pressure, cardiac index and LV stroke work index. Systemic vascular resistance decreased (p less than 0.01), whereas pulmonary vascular resistance showed no change. End-systolic volume diminished (p less than 0.02), which accounts for the increase of stroke volume and ejection fraction (p less than 0.001). Disorders of regional contractility were not aggravated by diltiazem, and even improved in individual cases. Thus, intravenous diltiazem may be used safely in patients with heart failure. However, in view of the marked bradycardic effects seen in some cases, heart rate should be carefully monitored.
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PMID:Hemodynamic effects of intravenous diltiazem with impaired left ventricular function. 648 22


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