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

Diltiazem (DTZ), a calcium slow channel blocker, is estimated to be highly effective for myocardial protection and the prevention of perioperative coronary spasms (PCS). However, the use of high doses of DTZ sometimes results in difficulty in coming off cardiopulmonary bypass due to negative chronotropic activity. Nicorandil (NCD) has remarkable coronary vasodilating effect but possesses little negative chronotropic activity. The purpose of this study was to compare NCD with DTZ with respect to effect on myocardial protection during coronary artery bypass grafting (CABG). As parameters, excess lactate (delta XL), redox potential (delta Eh), left and right ventricular stroke work indices (LVSWI, RVSWI), cardiac index (C.I.), systemic vascular resistance index (SVRI.), myocardial isoenzymes (CK-MB, LDH1), number of PCS and recovery time of chronotropic action were used. delta XL, delta Eh, LVSWI, RVSWI, C.I., SVRI, CK-MB, LDH1 were measured at 0, 1, 3, 6, 9, 18 and 24 hours after the removal of aortic cross clamping. The degree of chronotropic action was evaluated by the length of the recovery time to self beat or normal sinus rhythm after the removal of aortic cross clamping. Forty patients who underwent CABG with retrograde cold blood cardioplegia between Dec. 1989 and May 1991 were divided into the NCD group (n = 20), in which 1.1 micrograms/kg/min NCD was continuously administered from the beginning of the operation and the DTZ group (n = 20), in which the initial St. Thomas cardioplegia containing 5 mg/L and subsequent cold blood cardioplegia solution contained DTZ 3.5 mg/L, for a total DTZ dose of less than 10 mg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Efficacy of nicorandil on myocardial protection during coronary artery bypass grafting--a comparison with diltiazem]. 140 65

The anti-ischemic efficacy of diltiazem may improve with increments in dosage and with additional beta-blocking therapy. However, the combined administration could lead to adverse effects through amplification of negative inotropic and chronotropic properties. To evaluate hemodynamic tolerability and safety of high-dose intravenous diltiazem in patients with coronary artery disease receiving long-term metoprolol treatment, 9 such patients were studied for 30 minutes after onset of intravenous diltiazem administration (0.5 mg/kg for 5 minutes, followed by 15 mg/hour). Diltiazem plasma levels peaked at 5 minutes (641 +/- 74 micrograms/liter), decreasing to 177 micrograms/liter at 30 minutes. Average metoprolol levels (43 +/- 12 micrograms/liter) did not change. Diltiazem immediately decreased systemic vascular resistance, left ventricular systolic and mean aortic pressures (29, 21 and 20%, respectively, at 5 minutes), and they remained significantly reduced at 30 minutes. Heart rate initially increased by 11% during the bolus infusion (p < 0.05). Concomitantly, contractility indexes Vmax and Vce40, measured at fixed heart rates, also increased significantly by 11%. Both heart rate and contractility indexes returned to baseline levels thereafter. Cardiac output increased by 10% (p = not significant), stroke index remained unchanged, but stroke work decreased significantly by 20%. Also, the tension-time index was significantly reduced (23%). Diltiazem induced moderate negative lusitropic effects, the first derivative of negative left ventricular pressure decline decreased by 12% and Tau 2 lengthened by 13%. Concomitantly, left ventricular filling pressure increased from 19 +/- 2 to 23 +/- 3 mm Hg, but only at 5 and 15 minutes. PQ, QRS and QTc intervals were not affected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute hemodynamic and electrophysiologic effects and safety of high-dose intravenous diltiazem in patients receiving metoprolol. 141 18

The effect of fish oil on potassium efflux and basal tension in aortas from stroke prone spontaneously hypertensive rats (SHRSP) was evaluated. Four-week-old male Wistar-Kyoto rats (WKY) and SHRSP were divided into two groups: one received a 5% corn oil diet; the other a 5% menhaden oil diet. After 15 weeks, mean systolic blood pressure (mm Hg) was reduced in SHRSP-fish (202 +/- 5) compared to SHRSP-corn (227 +/- 4). Systolic pressure of WKY-fish (146 +/- 3) was not different from WKY-corn (151 +/- 4). Potassium efflux was evaluated with the isotope 86Rb. Basal 86Rb efflux from aorta of SHRSP-corn was evaluated compared to WKY-corn. Diltiazem or sodium nitroprusside decreased 86Rb efflux and basal tension in SHRSP. Basal 86Rb efflux, tension, and the magnitude of this diltiazem- or nitroprusside-induced inhibition were decreased in SHRSP-fish. At maximal diltiazem or nitroprusside concentration, 86Rb efflux from both SHRSP dietary groups was similar but still greater than control aorta. The IC50 values for diltiazem or nitroprusside effects on 86Rb efflux and tension were not altered by diet in SHRSP. Qualitatively similar changes in basal 86Rb efflux and tension were noted in WKY-fish compared to WKY-corn. These experiments demonstrate that dietary fish oil supplementation decreased calcium-sensitive 86Rb efflux and basal tension in vascular smooth muscle and suggest that these changes may contribute to the concomitant antihypertensive effect of dietary fish oil in SHRSP.
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PMID:Effects of dietary fish oil on Rb+ efflux from aorta of stroke prone spontaneously hypertensive rats. 163 20

In 80 patients with moderate hypertension the effects of nisoldipine 10 mg b.i.d., nifedipine 10 mg and 20 mg t.i.d., diltiazem 60 mg and 120 mg t.i.d., and verapamil 40 mg q.i.d. (all after single dose and 14 days' treatment) on blood pressure; hemodynamic parameters (cardiac output, stroke volume, left ventricular ejection fraction, and total peripheral resistance); and red blood cell and platelet functional state parameters (platelet aggregation, erythrocytal mechanical resistance, and free hemoglobin and ADP levels in plasma) were studied. All of the drugs studied in doses mentioned produced statistically significant hypotensive effects. Nifedipine 20 mg and nisoldipine 10 mg produced the most peripheral vasodilatator activity after a single dose and chronic treatment. Diltiazem had the same effect only in doses of 120 mg and after chronic treatment. However, all the drugs significantly normalized the red blood cell and platelet functional state disturbances in 70-80% of patients with moderate hypertension, even 2 h after a single dose. Disaggregation effect was parallel to clinical improvement. These data make it possible to predict the individual response of most patients to antihypertensive drugs on the basis of acute pharmacological tests, with determination of disaggregation effect.
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PMID:The effects of nisoldipine, diltiazem, nifedipine, and verapamil on hemodynamic parameters and red blood cells-platelet interactions in patients with arterial hypertension. 172 40

The short-term effects of oral diltiazem on hemodynamics and distribution of cardiac output at rest and during semiupright bicycle exercise were evaluated in eight patients with stable effort angina on long-term beta 1-adrenergic blockade. Cardiac output and iliofemoral blood flow were measured using thermodilution. The patients were exercised to the same work load on a bicycle before and 2 h after oral diltiazem (60 mg in two patients and 120 mg in six). At maximal exercise, diltiazem reduced heart rate from 94 +/- 5 to 88 +/- 6 beats/min (p less than 0.01), mean arterial pressure from 139 +/- 5 to 127 +/- 4 mm Hg (p less than 0.01) and systemic vascular resistance from 9.7 +/- 0.7 to 8.4 +/- 0.4 x 10(2) dynes.s.cm-5 (p less than 0.05) compared with control. During exercise, cardiac output, iliofemoral blood flow, mean pulmonary wedge pressure and mean right atrial pressure were not altered, but stroke volume increased from 119 +/- 11 to 131 +/- 10 ml (p less than 0.05). Maximal ST segment depression during exercise was decreased and angina was less. Diltiazem does not alter the distribution of the cardiac output during exercise but improves ischemia.
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PMID:Effects of diltiazem and long-term beta 1-adrenergic blockade on hemodynamics and blood flow during exercise in patients with stable angina pectoris. 196 60

Twenty-four patients were randomized to a double-blind, triple placebo controlled, latin square protocol to examine the relative efficacy of propranolol or diltiazem given as monotherapy or in combination with isosorbide dinitrate. Treatment phases were preceded and followed by placebo control periods. At the end of each phase, symptom-limited treadmill exercise stress tests were performed, as well as rest and exercise radionuclide ventriculography. Both forms of monotherapy were effective in reducing episodes of angina and nitroglycerin use, and in improving exercise tolerance. Diltiazem monotherapy was associated with slightly higher treadmill times (509.9 +/- 123 s) compared to propranolol (462.7 +/- 131 s, P less than 0.05). The addition of isosorbide dinitrate to either form of monotherapy allowed no further improvement in any of the measured clinical responses. Radionuclide ventriculography showed no significant difference in resting left ventricular function. The addition of isosorbide dinitrate to propranolol showed a reduction in end diastolic volume in keeping with a reduction in preload. In response to exercise, stress-induced left ventricular dysfunction was equal in all groups except for the diltiazem-nitrate combination, which was associated with a higher ejection fraction (56.2 +/- 8.6%) compared to monotherapy (52.6 +/- 10.9%, P less than 0.01). A higher cardiac output could be achieved in the groups treated with diltiazem; this was related to increased heart rate and maintenance of stroke volume. It was concluded that diltiazem is equally effective as propranolol for the treatment of chronic stable angina and, in terms of exercise capacity and cardiac output, superior to beta-blockade. The addition of isosorbide dinitrate appears to impart no overt benefits, but some evidence suggests a reduction in left ventricular decompensation in the face of stress.
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PMID:Clinical response and effects on left ventricular function of isosorbide dinitrate added to propranolol or diltiazem monotherapy in patients with chronic stable angina. 204 86

The responses to a supine rest, norepinephrine (NE) and angiotensin II (Ang II) were investigated in the absence and presence of calcium antagonist nifedipine or diltiazem in essential (genetic, arterial) hypertension and normotension in humans. A supine rest significantly decreased blood pressure (BP), heart rate (HR), stroke volume index (SI), and cardiac output index (CI). On the contrary, the rest increased total peripheral vascular resistance index (TPRI) in both normotensives and hypertensives. The decrease in BP was significantly greater in hypertensives than in normotensives. NE significantly increased BP and TPRI, whereas it decreased HR, SI, and CI. The increase in BP was greater in hypertensives than in normotensives. Nifedipine and diltiazem inhibited the NE-induced increases in BP and TPRI. Ang II increased BP and TPRI, but it decreased HR, SI, and CI. Diltiazem did not inhibit the Ang-II-induced increases in both BP and TPRI. The increased responses to a rest and NE were observed in the early stage of essential hypertension. The increased responses may contribute to both the increase in BP and the induction of high blood pressure in essential hypertension. The calcium antagonists inhibited the NE-induced increases in BP and TPR. The results suggest that the antagonists inhibit the NE-dependent calcium influx and calcium release in the arterial smooth muscle. The observed responses to Ang II suggest that the antagonists may not inhibit Ang-II-dependent calcium-channel activity in the smooth muscle.
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PMID:Increased cardiovascular responses to norepinephrine and calcium antagonists in essential hypertension compared with normotension in humans. 241 85

We studied 14 patients to determine whether sustained-release diltiazem is a satisfactory long-term substitute for the combination of propranolol plus hydrochlorothiazide (HCTZ), control phase, in the treatment of systemic hypertension with coexisting chronic stable angina pectoris. All patients had either one- or two-vessel coronary disease and normal left ventricular systolic function. Measurements were made during the control phase and 4 and 8 weeks after substitution of sustained-release diltiazem. Only the sitting blood pressure was available before the control phase (pretreatment). Blood pressure and heart rate were measured with patients supine, sitting, and 5 minutes after standing. Cardiac output was measured in the supine position using a computerized Doppler system, and stroke volume, mean arterial pressure, and total systemic resistance were calculated. Symptom-limited modified Bruce protocol treadmill tests were performed to determine time to onset of 1 mm ST segment depression, time to termination of exercise, reason for cessation of exercise, and maximum rate-pressure product. The patients were initially receiving 160-240 mg/day of propranolol (40-60 mg q.i.d.) plus 25-50 mg/day of HCTZ and, subsequently, 12 of 14 had substitution with 240 mg/day (120 mg b.i.d.) of sustained-release diltiazem, and two received 360 mg/day with one of these patients also receiving 50 mg/day of HCTZ. These patients are a subset of a larger group of patients in whom the response of blood pressure alone has been previously reported. Diltiazem resulted in reduction of blood pressure equivalent to that with the propranolol plus HCTZ combination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of blood pressure, cardiac output, peripheral resistance, and exercise performance to substitution of calcium blocker for beta-blocker plus thiazide diuretic therapy in patients with both systemic hypertension and mild stable angina. 257 40

Diltiazem is a calcium channel blocker whose effects lie between those of the two other important calcium antagonists nifedipine and verapamil. In addition to vasodilation, it has a negative dromotropic effect with prolongation of the A-V interval. In animal experiments and human investigations, diltiazem improves the function of ischemic myocardium due to a direct dilating effect on coronary vessels. The purpose of the present study was to investigate the hemodynamic effects of diltiazem in patients before and during coronary revascularization. METHODS. The study included 60 consenting male patients with coronary heart disease. Twenty premedicated patients randomly received 0.3 mg/kg diltiazem or placebo within 3 min before induction of anesthesia. Hemodynamic measurements (arterial pressure, heart rate, mean pulmonary arterial pressure, pulmonary capillary pressure, right atrial pressure and cardiac output) were taken during the following 21 min. Before cannulation of the great vessels for institution of extracorporeal circulation (ECC), 20 other patients received 0.014 mg diltiazem or placebo/kg per min over 20 min. In addition to the above mentioned hemodynamic measurements, left ventricular parameters (LVP, LVEDP, dp/dt) were directly registered, and 5 min after the end of ECC the measurements were repeated with the same preload as before the ECC. Twenty additional patients received 0.014 mg diltiazem or placebo/kg per min within 21 min during ECC observing arterial perfusion pressure and oxygenator volume. RESULTS. Pre- and intraoperatively diltiazem caused a decrease in mean arterial pressure; cardiac index increased only during the preoperative investigation period (Tables 1, 2), whereas stroke volume index increased pre- and intraoperatively; heart rate decreased in all patients as well as dp/dt (Fig. 1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experiences with parenteral administration of diltiazem in coronary surgery patients]. 304 82

Diltiazem given 48 hours before experimental subarachnoid hemorrhage protects the cerebral vasculature of monkeys against the widespread cerebrovascular spasm seen on angiography after 5-6 days and against associated neurologic defects. In vitro examination of the cerebral arteries from treated monkeys shows that compared with untreated animals, the functional changes in the vascular smooth muscle cells, the increase in arterial wall stiffness, and the decrease in contractility, all of which were prominent in untreated monkeys, were relatively small. Other changes such as abnormal spontaneous myogenic tone, decreased responsiveness to constrictor and dilator nerve activation, and other indexes of neuronal function were little influenced by the drug. We suggest that chronic cerebrovasospasm may be initiated by the combined action of exceptionally high concentrations of a number of putative spasmogens causing injury to the larger cerebral arteries. However, the later development of intractable spasm is related to the location of blood clot and to the involvement of the vascular wall in an inflammatory process. The combined insult results in pathologic changes in the artery wall resulting in increased thickness and stiffness. Diltiazem acts on cerebrovascular smooth muscle in lower concentrations than on smooth muscle in other vascular beds, interfering with calcium entry through receptor-operated and potential-sensitive channels, and may protect against calcium-induced cell death through these and additional actions. Protection against early events presumably prevents the genesis of the subsequent chronic state.
Stroke 1988 Jan
PMID:Diltiazem protects against functional changes in chronic cerebrovasospasm in monkeys. 312 76


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