Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute hemodynamic effects of the Ca-antagonist Diltiazem were measured in the course of diagnostic cardiac catheter examinations in 10 patients with coronary heart disease. After initial step-wise ergometric stress, Diltiazem (D) was applied intravenously for 5 min at a dose of 0.3 mg/kg. The effects on right and left ventricular performance as well as on arterial pressure and heart rate were registered 1, 3, 5, 10 and 15 min after termination of the infusion. Then, a second period of ergometric exertion under identical stress conditions was performed. The results under resting conditions show that D effects a significant increase in left ventricular filling pressure (p greater than 0.005), which, however, only lasts a few minutes. After D, the systolic and mean arterial pressure decreases significantly (p greater than 0.001); there is no reflex-induced increase in the heart rate, which on the contrary is significantly lower (p greater than 0.005) 15 min after termination of the infusion than the initial value. The stroke volume index increases from 40 to maximally 48 ml/m2 after D. Comparison of the hemodynamic parameters under ergometric stress before and 20 min after D shows that, on termination of stress, the filling pressure of the left ventricle is reduced. This behavior can largely be attributed to the reduction of the systolic pressure after D (maximal value before D 181, after D 167 mm Hg). Also, the stress-induced increase in the heart rate takes a flatter course after D than before it. The results obtained thus provide evidence that, at a dosage of 0.3 mg/kg, D has no significant negative inotropic effect and probably leads to a decrease of the myocardial oxygen consumption reducing the systolic pressure and, to a lesser degree, heart rate.
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PMID:[Effects of diltiazem on rest and stress hemodynamics in coronary disease]. 649 10

The acute effects of intravenous diltiazem on exercise performance were studied in 10 patients with coronary artery disease. Haemodynamic measurements were made at rest and during exercise before and after 0.5 mg kg-1 of diltiazem. Diltiazem prolonged the duration of exercise (+2.85 min, P less than 0.001) and delayed the onset of ischaemic ST depression or angina in all patients. The highest tolerated heart rate and pressure rate product were increased in all but one patient after diltiazem. At rest diltiazem decreased mean arterial pressure (-10.8%, P less than 0.005), systemic vascular resistance (SVR) (-11.8%, P less than 0.05) and left ventricular stroke work index (SWI) (-14.1%, P less than 0.005). During exercise under diltiazem therapy, at the level achieved before the drug, the pulmonary capillary wedge pressure (-30%, P less than 0.005) and the SVR (-13.6%, P less than 0.02) were lowered, the SWI (+13%, P less than 0.01) was increased; at the end of exercise only the SVR (-14%, P less than 0.05) was reduced. Two patients experienced angina on lying down and one had orthostatic hypotension after exercise with diltiazem. This study indicates that intravenous diltiazem is a potentially useful agent for the treatment of angina by reducing myocardial oxygen demand at rest and by improving left ventricular performances on exercise.
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PMID:Haemodynamic effects of intravenous diltiazem at rest and exercise in patients with coronary artery disease. 674 87

The calcium antagonists, diltiazem and nifedipine, are effective in mild-to-moderate chronic essential hypertension. The overall responder rate is 80%. Diastolic blood pressure is lowered by 10-15% at rest and during exercise. Systolic blood pressure is reduced only at rest. Heart rate may be unchanged by nifedipine and lowered by diltiazem. Both drugs lead to a decrease of peripheral resistance by 15-20% at rest and 30% during work. As a consequence of afterload reduction, cardiac output, stroke index, and stroke work index increased by 17, 21, and 7% with nifedipine and 34, 26, and 20% with diltiazem. During exercise, these changes are even more pronounced. However, pulmonary artery pressure and pulmonary vascular resistance are reduced only by nifedipine, not by diltiazem. Presumably due to this combined preload and afterload reduction, nifedipine therapy is associated with a reflex activation of the sympathetic nervous system in all cases, with an increase in norepinephrine plasma concentration and, sometimes, tachycardia. Diltiazem, however, has the advantage of being a potent blood pressure-lowering agent, with afterload reduction and increased stroke index, with less pronounced catecholamine increase, and without tachycardia. Side effects with this drug are rare, and long-term therapy is well tolerated.
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PMID:Role of calcium antagonists in the treatment of essential hypertension. 683 51

The hemodynamic effects of intravenous diltiazem, 0.2 mg/kg, were examined in eight patients with recent myocardial infarction. Diltiazem lowered mean aortic pressure (87.0 +/- 3.3 to 79.9 +/- 3.1 mmHg, P less than 0.01) and systemic vascular resistance (1353.0 +/- 136.2 to 964.9 +/- 101.7 dynes.sec.cm-5, P less than 0.01), and increased cardiac index (3.77 +/- 0.27 to 4.72 +/- 0.41 liters/min/sq m, P less than 0.01) and stroke index (57.5 +/- 4.5 to 69.4 +/- 7.6 ml/beat/sq m, P less than 0.05). No significant changes in the left ventricular end-diastolic, right atrial, and pulmonary arterial pressure, or heart rate were noted after diltiazem. These results suggest that the negative inotropic effects of diltiazem are negligible even in patients with recent myocardial infarction. The electrocardiogram should be observed carefully, however, since the PR interval was further prolonged in one patient who had first-degree atrioventricular block before diltiazem.
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PMID:Hemodynamic effects of intravenous diltiazem in patients with recent myocardial infarction. 706 36

Diltiazem (DT), a potent slow channel blocker, has been found to be clinically useful for treatment of coronary vasospasm, hypertension, and tachyarrhythmias. Nevertheless, only limited data are available on the hemodynamic and electrophysiologic effects of DT. Atrial, His, right ventricular apex, aortic, and Swan-Ganz thermodilution catheters were used in 10 anesthetized dogs, and recordings were made during control period and after each of four infusions of DT (0.01, 0.02, 0.04, and 0.08 mg/kg/min) each lasting 30 minutes. Results showed that heart rate, pulmonary capillary wedge pressure, stroke volume, and HV interval did not change significantly. However, two dogs had second-degree AV block and a third had escape junctional rhythm during DT 0.08 mg/kg/min. Mean aortic pressure (AP), corrected sinus node (SN) recovery time, and systemic vascular resistance (SVR) were significantly reduced, whereas AH interval, AV functional and effective refractory periods were prolonged by DT. AV nodal refractory periods and AH interval were the only parameters significantly affected at DT 0.02 mg/kg/min. SN recovery time was significantly shortened at DT 0.04 mg/kg/min, whereas AP and SVR tell significantly at DT 0.08 mg/kg/min. DT had significant electrophysiologic effects at low doses, whereas hemodynamics were significantly altered only at high doses. Further, major electrophysiologic effects were on the AV node with lesser effects on SN function. Therefore, at a dose when antiarrhythmic effects are evident, the safety of diltiazem is corroborated by lack of adverse hemodynamic effects.
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PMID:Electrophysiologic and hemodynamic actions of diltiazem: disparate temporal effects shown by experimental dose-response studies. 721 68

Effects of diltiazem, a calcium antagonist, on the cardiovascular system in the pentobarbital anesthetized dogs were investigated. Diltiazem (100 micrograms/kg and 300 micrograms/kg, i.v.) decreased blood pressure, heart rate and total peripheral resistance, while cardiac output and stroke volume were markedly increased. The max dp/dt of left ventricular pressure tended to increase with a dose of 100 micrograms/kg. Left ventricular end-diastolic pressure was slightly increased with a dose of 400 micrograms/kg. Rate pressure product was significantly reduced. Diltiazem (30 micrograms/kg and 100 micrograms/kg) increased pulmonary arterial flow together with the increase in both systolic and diastolic pulmonary arterial pressure. Diltiazem (100 micrograms/kg) increased common carotid, femoral and superior mesenteric arterial blood flow by 30 to 40%, whereas vertebral blood flow was increased by over 100%. The dose dependency in the vertebral blood flow was remarkable. Response of the vertebral artery to diltiazem was similar to that reported in the case of the coronary artery. In the His bundle electrogram, diltiazem increased the AH interval by about 10% at 100 micrograms/kg and 25% at 200 micrograms/kg, without changing the HV interval. Diltiazem-induced AH prolongation was completely depressed by epinephrine but only partially so by CaCl2. Thus, the effects of diltiazem on sinus rhythm and AV conduction in the anesthetized dog were more potent than the effects on cardiac contractility, although weaker than the effects of the vasodilating action. The vasodilator effects appear to be the primary action of diltiazem on the cardiovascular system.
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PMID:[Effects of diltiazem on hemodynamics and His bundle electrogram in the anesthetized dog (author's transl)]. 723 61

The effects of intravenous infusion of the calcium antagonist, diltiazem (6, 30, and 150 mg/kg/hr) on cardiac and circulatory hemodynamics and on regional blood flow and cardiac output distribution to the major peripheral circulations were studied in conscious, normal Sprague-Dawley rats in the resting state. Therapy with diltiazem consistently increased cardiac output levels, as well as stroke volume, and decreased mean arterial pressure and systemic vascular resistance in a dose-related fashion. Diltiazem had a substantial effect on increasing coronary blood flow and reducing coronary vascular resistance. Effects of similar direction and magnitude were observed in the cerebral and hepatic arterial circulations. In a second study, rats were subjected to a submaximal treadmill exercise protocol during continuous intravenous infusion of either saline solution or diltiazem (DZ) in order to determine the effects of this agent on cardiac output distribution during exercise. The results indicate that the positive effects of diltiazem on cardiac output are maintained during exercise. The increase in cardiac output with diltiazem appears to be distributed throughout the major regional circulations in proportion to regional demand.
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PMID:Regional distribution of cardiac output in conscious rats at rest and during exercise. Effects of diltiazem. 739 5

Although calcium channel blockers may preserve function in ischemic myocardium, they may also produce myocardial depression and dysfunction in the presence of decreased coronary flow. This study was designed to examine the issue of possible protection afforded by diltiazem against ischemia-induced myocardial dysfunction during propofol anesthesia. In eight anesthetized and ventilated dogs, regional myocardial (ultrasonic crystals in both left anterior descending [LAD] and left circumflex [LC] perfusion areas) and global ventricular function were evaluated during progressively severe degrees of myocardial ischemia (LAD constriction) before and after intravenous diltiazem (150 micrograms/kg). As coronary flow decreased, heart rate increased, and arterial and coronary perfusion pressures, left ventricular dP/dt, and cardiac output decreased. Systemic vascular resistance was unaffected. Diltiazem without coronary constriction increased heart rate, and decreased diastolic arterial pressures, left ventricular (LV) end-diastolic, coronary perfusion pressures, LV dP/dt max, LAD coronary blood flow, stroke volume, and cardiac output. At all levels of coronary constriction following diltiazem, there were decreases in systolic and diastolic arterial pressures, stroke volume, cardiac output, LV dP/dt, and coronary perfusion pressure. Heart rate increased at critical coronary constriction, and then remained constant relative to the prediltiazem state. The regional muscle effects of the reductions in coronary flow in the LAD perfusion territory included decreased systolic shortening and increased postsystolic shortening before and after diltiazem. Diltiazem did not alter the magnitude of the alterations in systolic or postsystolic shortening brought about by coronary constriction. No changes occurred in the LC area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diltiazem and regional left ventricular function during graded coronary constriction and propofol anesthesia in the dog. 830 61

Hypertrophic cardiomyopathy (HC) is characterized by impaired diastolic function, and left ventricular (LV) outflow tract obstruction in about one-fourth of patients. Verapamil improves diastolic properties, but may have dangerous adverse effects. This study investigates the effects of diltiazem on hemodynamics and LV function in 16 patients with HC who were studied with cardiac catheterization and simultaneous radionuclide angiography. Studies were performed during atrial pacing (15 beats above spontaneous rhythm) at baseline and during intravenous diltiazem administration (0.25 mg x kg(-1) over 2 minutes, and 0.014 mg x kg(-1) x min(-1). Diltiazem induced a systemic vasodilation (cardiac index: 3.4 +/- 1.0 to 4.0 +/- 1.0 L x min(-1) x m(-2), p = 0.003; aortic systolic pressure: 116 +/- 16 to 107 +/- 19 mm Hg, p = 0.007; systemic resistance index: 676 +/- 235 to 532 +/- 193 dynes x s x cm(-5) x m(-2), p = 0.006), not associated with changes in the LV outflow tract gradient. The end-systolic pressure/volume ratio decreased (30 +/- 42 to 21 +/- 29 mm Hg x ml(-1) x m(-2); p = 0.044). Pulmonary artery wedge pressure (11 +/- 5 to 15 +/- 6 mm Hg, p = 0.006), and peak filling rate increased (4.1 +/- 1.3 to 6.0 +/- 2.4 stroke counts x s(-1), p = 0.004). The time constant of isovolumetric relaxation tau decreased (74 +/- 40 to 59 +/- 38 ms, p = 0.045). The constant of LV chamber stiffness did not change. Thus, active diastolic function is improved by the acute administration of diltiazem by both direct action and changes in hemodynamics and loading conditions. LV outflow tract gradient does not increase despite systemic vasodilation. In some patients, however, a marked increase in obstruction and a potentially harmful elevation in pulmonary artery wedge pressure do occur. Passive diastolic function is not affected.
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PMID:Effects of diltiazem on left ventricular systolic and diastolic function in hypertrophic cardiomyopathy. 875 92

This prospective study was done to compare the control of heart rate and haemodynamics during coronary artery revascularisation without cardiopulmonary bypass using either esmolol or diltiazem. Sixty adult patients with one or two vessel coronary artery disease, were randomly divided into 2 equal groups. Group A received a 500 micrograms/kg loading dose of esmolol followed by a 100 micrograms/kg/h infusion, for control of heart rate during surgical anastomosis of the coronary vessel. While Group B received 0.15 mg/kg diltiazem as a loading dose followed by a 5 mg/h infusion for heart rate control, during the anastomosis. It was seen that heart rate control was better in Group A, 51.4 (+/- 1.3) beats/min, than in Group B, 69.6 (+/- 3.9) beats/min but the decrease in heart rate was significant in both the groups at peak effect compared to respective predrug values. Group A patients had unchanged systemic resistance and pulmonary artery wedge pressure but mean pulmonary artery pressure and pulmonary vascular resistance were significantly raised. Group B patients had decreased systemic resistance, mean pulmonary artery pressure and pulmonary artery wedge pressure, and reduced right ventricular stroke work index. We concluded that although esmolol provided dramatically slower heart rates, during surgery, the resulting elevations in mean pulmonary artery pressure and pulmonary vascular resistance would require caution if used in patients with underlying right ventricular dysfunction from ischaemia or infarction. Diltiazem by virtue of its effects on systemic vascular resistance, cardiac output, and lowering of mean arterial pressure may be a better choice in hypertensive patients.
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PMID:A comparison of esmolol & diltiazem for heart rate control during coronary revascularisation on beating heart. 1068 Mar 3


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