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

Seven patients with severe chronic congestive cardiac failure secondary to ischaemic heart disease performed submaximal supine exercise before and after 5 mg sublingual isosorbide dinitrate at the time of cardiac catheterisation. Exercise before isosorbide dinitrate produced a poor response in left ventricular performance. After isosorbide dinitrate this response was significantly improved. Compared with the control exercise period, cardiac index increased from mean 2.6 to 3.1 1/min per m2 (P less than 0.0025), stroke volume index from mean 22 to 27 ml/m2 (P less than 0.0025), and left ventricular stroke work index from mean 21 to 30 g m/m2 (P less than 0.01). Mean left ventricular filling pressure fell from 37 to 26 mmHg (P less than 0.01). Although isosorbide dinitrate reduced left ventricular filling pressure at rest from mean 26 to 17 mmHg (P less than 0.005), there was no significant change in mean cardiac index or stroke volume index, while left ventricular stroke work index decreased from mean 29 to 22 g m/m2 (P less than 0.05). Isosorbide dinitrate effectively reduces left ventricular filling pressure in the resting patient with congestive cardiac failure but produces a more comprehensive improvement in left ventricular performance during exercise.
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PMID:Improvement in exercise haemodynamics by isosorbide dinitrate in patients with severe congestive cardiac failure secondary to ischaemic heart disease. 68 84

Haemodynamic investigations were performed before and after oral ingestion of nitroglycerine and isosorbide dinitrate, both in depot form, in eleven and nine patients, respectively, with coronary heart disease. Nitroglycerine (5 mg) led to a significant decrease in arterial and pulmonary artery mid-pressure over one to two hours. Heart rate and mean pulmonary capillary pressure as well as cardiac output and stroke volume hardly changed. After ingestion of isosorbide dinitrate (20 mg) there was a continuous and significant fall in mean arterial, pulmonary artery, and pulmonary capillary pressure already demonstrable during the first hour. Cardiac output and left ventricular work decreased accordingly for up to four hours. At the same time the cardiac output remained constantly lowered over four hours despite the significant increase in frequency. Isosorbide dinitrate has thus a more complete and longer lasting protective haemodynamic effect than nitroglycerine.
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PMID:[Long-term action of nitrites in coronary heart disease (author's transl)]. 80 39

Hemodynamic and electrocardiographic analysis during rapid right atrial stimulation was performed before and one, two, and four hours after oral application of longacting nitroglycerin (5 mg) and isosorbide dinitrate (20 mg) in 11 and 9 patients, respectively with coronary heart disease. Atrial stimulation without nitrate induced significant ischemic ST segment depression. Cardiac output showed a small decrease and the mean arterial, pulmonary artery, and pulmonary wedge pressure increased. Isosorbide dinitrate reduced the ischemic reaction by 40% from the first to the fourth hour after application. Cardiac output, stroke volume, aterial, pulmonary artery, and pulmonary wedge pressure also decreased continuously. Nitroglycerin caused a similar reduction of ischemic ST segment depression for two hours. Systolic, diastolic, and mean arterial pressure decreased significantly. Cardiac output, stroke volume, and pulmonary artery pressure remained unchanged. It was concluded that the applied dose of isosorbide dinitrate showed a more extensive longacting effect.
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PMID:[Hemodynamic and electrocardiographic prolonged nitrate effect during frequency load in coronary disease]. 82 Jan 4

The results of the present investigation indicate that ISDN infusion following experimental coronary occlusion in anesthetized dogs (1) lowers systemic, cardiac, and pulmonary blood pressures; (2) decreases systemic resistance; (3) has no significant effect on cardiac output, heart rate, and stroke volume; (4) decreases serum CPK levels; and (5) has little effect on blood biochemical parameters. These results suggest that ISDN may have a minimal effect on the ischemic heart by means of a slight decrease in peripheral vascular resistance and systemic blood pressure.
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PMID:The effect of isosorbide dinitrate following experimental coronary occlusion. 94 33

Comparative hemodynamic effects of placebo and 10 mg of oral isosorbide dinitrate were studied in patients with significant coronary artery disease (larger than or equal to 75 per cent lumen narrowing) proved angiographically. Isosorbide dinitrate or placebo was given to eight and 10 patients, respectively, in a double-blind fashion. Cardiac performance at rest and during supine leg exercise was evaluated before and 60 minutes after drug administration. In the resting state, isosorbide dinitrate compared to placebo significantly reduced the left ventricualr (systolic and diastolic), mean pulmonary artery and mean aortic pressures, cardiac index, stroke index, left ventricular work index, stroke work index, and mean systolic ejection rate. Isosorbide dinitrate also significantly reduced left ventricular (systolic and diastolic and mean pulmonary artery pressures during exercise. This study indicates that 10 mg of isosorbide dinitrate has a significant influence on ischemic left ventricular dysfunction 60 minutes after its oral administration.
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PMID:Comparative hemodynamic effects of placebo and oral isosorbide dinitrate in patients with significant coronary artery disease. 109 19

The link between arterial caliber and distensibility has been studied extensively, with conflicting results. As have other researchers, we previously showed evidence of an increase in arterial diameter and a decrease in arterial stiffness with use of nitrates at the site of the brachial artery (BA) and the aorta. Whether these results would apply to other large superficial arteries remained to be established. In the present study, by means of an original pulsed ultrasound echo-tracking system based on Doppler shift, we measured internal diastolic diameter and stroke change in diameter of the common carotid artery (CCA), the femoral artery, and the BA in patients with essential hypertension and determined the acute effects of administration of isosorbide dinitrate (ISDN 20 mg). Twenty untreated hypertensive patients entered this randomized, placebo-controlled, double-blind, parallel study. No significant change occurred during placebo. During ISDN therapy, blood pressure (BP) decreased significantly; cross-sectional compliance increased at the site of the CCA, the BA, and the common femoral artery (CFA). The increase in cross-sectional compliance was mainly due to an increase in internal diameter for CCA and to an increase in distensibility coefficient (DC) for BA. The pattern of cross-sectional compliance was intermediate for CFA. During ISDN therapy, the augmentation index of the CCA distension waveform was significantly reduced, whereas no change occurred during placebo, suggesting a reduction in wave reflection by nitrates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of nitrate-induced improvement on arterial compliance depends on vascular territory. 138 Jun 9

The following hemodynamic parameters were measured at rest and 1, 2, 4, 6, 8, 12 and 24 hours after 100 mg of ISDNSR p.o. in 10 patients with dilated cardiomyopathy (NYHA class III-IV): mean pulmonary artery, pulmonary capillary wedge (PCW) and arterial pressures (AP), and cardiac output (thermodilution). Plasma levels of ISDN were determined by capillary gas chromatography at the same intervals and correlated with the hemodynamic changes. PCW fell from 24 +/- 1.5 (SE) to 18 +/- 1.8 mm Hg after 1 hour (p less than 0.05) and after 2 hours to 16.9 +/- 1.6 mm Hg. This change was sustained for 8 hours. At 12 hours PCW had increased again to 21 +/- 1.5 mm Hg and at 24 hours to 22 mm Hg. AP dropped from 89 +/- 5 to 81 +/- 4 mm Hg at 1 hour (p less than 0.2) and remained 80-84 mm Hg for 8 hours. It returned to baseline levels at 12 hours. Heart rate, cardiac index, systemic vascular resistance, stroke index and left ventricular work index did not change significantly during the observation period. Plasma levels of ISDN remained between 3 and 12 ng/ml for 16 hours. Thus, ISDNSR is an effective long-acting nitrate preparation which reduces preload for 8-12 hours. After this interval, nitrate tolerance starts to develop.
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PMID:[Hemodynamic effects of a new long-acting isosorbide dinitrate]. 408 1

We undertook a randomised between-group comparison of the haemodynamic effects of arteriolar dilatation and venodilatation in 20 males, following acute myocardial infarction, with persisting left ventricular failure after pretreatment with intravenous frusemide. All had radiographic pulmonary oedema and a pulmonary artery occluded pressure (PAOP) exceeding 15 mm Hg. The average cardiothoracic ratio was 52% (range 48-65%). Following control haemodynamic measurements, 10 patients received intravenous hydralazine (0.15 mg/kg) and 10 received intravenous isosorbide dinitrate infusion (50-200 micrograms/kg/h). Subsequent measurements were made at 30, 60, and 90 min. Isosorbide dinitrate reduced the PAOP by 3 mm Hg (p less than 0.01) and the mean systemic arterial pressure by 9 mm Hg (p less than 0.05) without significant change in the heart rate, cardiac output, or systemic vascular resistance. In contrast, hydralazine reduced the PAOP and systemic arterial pressure by a similar amount, but this was accompanied by a reduction in the systemic vascular resistance (p less than 0.01) and an increase in the cardiac output (p less than 0.01), heart rate (p less than 0.01), and stroke volume (p less than 0.01). This randomised study defines the contrasting haemodynamic results of arteriolar dilatation and venodilation in patients with resistant left ventricular failure following acute myocardial infarction. The different pharmacodynamic effects of these two methods of circulatory manipulation suggest that they are not mutually exclusive and together may offer therapeutic advantages.
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PMID:Arteriolar or venous dilatation in left ventricular failure following acute myocardial infarction: a haemodynamic trial of hydralazine and isosorbide dinitrate. 619 53

A randomised between-group study of the immediate haemodynamic effects of venodilatation by intravenous isosorbide dinitrate infusion (50-200 micrograms/kg/h) and arteriolar dilatation by intravenous hydralazine bolus (0.15 mg/kg) given either in random sequence (Groups 1 and 2; n = 12) or simultaneously (Group 3; n = 6) was undertaken in 18 men with radiographic and haemodynamic evidence (left ventricular [LV] filling pressure greater than 20 mm Hg) of LV failure 6-19 h following acute myocardial infarction. Control measurements (1 h) preceded either two consecutive 90-min treatment periods (Groups 1 and 2) or a single 90-min period (Group 3). Given independently, both drugs reduced systemic arterial pressure and vascular resistance, whereas only isosorbide dinitrate reduced LV filling pressure and only hydralazine increased cardiac output and stroke volume. Isosorbide dinitrate/hydralazine in combination significantly reduced LV filling pressure, systolic and diastolic arterial pressure, and total systemic vascular resistance. Cardiac output, stroke volume, and heart rate were increased. In conclusion, combined arteriolar dilatation and venodilatation appears to be of greater haemodynamic benefit than either alone, if the fall in mean systemic pressure does not compromise peripheral perfusion.
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PMID:A randomised study of the haemodynamic changes induced by venodilatation and arteriolar dilatation singly and together in left ventricular failure complicating acute myocardial infarction. 620 Jul 24

The hemodynamic effect of venous dilatation (intravenous isosorbide dinitrate [ISDN]) and arteriolar dilatation (intravenous hydralazine), both as firstline treatment and then combined with intravenous furosemide, were evaluated in a randomized, between-group comparison in 20 men with severe acute left-sided cardiac failure after myocardial infarction (MI). Both ISDN (50 to 200 micrograms/kg/hour) (Group 1) and hydralazine (0.15 mg/kg) (Group 2) reduced systemic arterial pressure (p less than 0.05) and vascular resistance (p less than 0.05). Pulmonary artery occluded pressure was reduced (p less than 0.01) only by ISDN, whereas heart rate (p less than 0.01), cardiac output (p less than 0.01) and stroke volume (p less than 0.05) were increased only after hydralazine. After ISDN, furosemide (1 mg/kg) decreased left-sided cardiac filling pressure by 1 mm Hg (p greater than 0.05), whereas after hydralazine, furosemide in a similar dose reduced pulmonary artery occluded pressure by 5 mm Hg (p less than 0.01). In both groups of patients, furosemide transiently increased systemic arterial pressure (p less than 0.05). Cardiac output was reduced (p less than 0.05) and systemic vascular resistance increased (p less than 0.05) in Group 1 patients after furosemide. Similar changes in both variables in Group 2 patients did not attain statistical significance. In conclusion, ISDN-induced venous dilatation is preferable to primary arteriolar dilatation by hydralazine as first-line treatment in acute left-sided cardiac failure. However, hydralazine and furosemide in combination were equally effective in reducing pulmonary artery occluded pressure and increasing cardiac output. The influences of each regimen on prognosis await further investigation.
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PMID:Hemodynamic comparison of primary venous or arteriolar dilatation and the subsequent effect of furosemide in left ventricular failure after acute myocardial infarction. 663 19


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