Improvement in exercise haemodynamics by isosorbide dinitrate in patients with severe congestive cardiac failure secondary to ischaemic heart disease.

Stephens, J; Camm, John; Spurrell, R. A. J.

doi:10.1136/hrt.40.8.832

Cited by 30 publications

(3 citation statements)

References 28 publications

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“…isosorbide dinitrate (ISDN).6-8 Although nitrates are predominantly venodilators,3' 9-1" decreases in systemic vascular resistance and increases in cardiac output have been reported.7' [12][13][14][15][16] Nitrates are helpful in many patients with coronary heart disease, although a sudden, sharp decrease in the diastolic arterial pressure may enhance myocardial ischemia, particularly in the acute cases.17 19 The present study was performed to evaluate the hemodynamic effects of i.v. ISDN in 40 patients with acute and chronic pump failure.…”

mentioning

confidence: 99%

Intravenous isosorbide dinitrate in patients with refractory pump failure and acute myocardial infarction.

Rabinowitz¹,

Tamari²,

Elazar³

et al. 1982

Circulation

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confidence: 99%

Intravenous isosorbide dinitrate in patients with refractory pump failure and acute myocardial infarction.

Rabinowitz¹,

Tamari²,

Elazar³

et al. 1982

Circulation

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“…1 2, [8][9][10][11] Therefore, a key question as to the usefulness of vasodilator treatment of chronic heart failure is how cardiovascular transport changes. Transport should be considered in terms of tissue blood flow and of tissue uptake, utilization and removal of metabolites.…”

Section: Discussionmentioning

confidence: 99%

Metabolic assessment of exercise in chronic heart failure patients treated with short-term vasodilators.

Rubin¹,

Chatterjee²,

Parmley³

1980

Circulation

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Short-term vasodilators increase exercise cardiac output without an increase in exercise tolerance when administered to chronic heart failure patients. This study was designed to examine cardiac output, oxygen consumption, and lactate metabolism during exercise in chronic heart failure. Thirteen patients participated in 17 studies during control exercise (C) and during vasodilator exercise after short-term treatment with either hydralazine (H) or prazosin (P). Cardiac output increased during exercise both with hydralazine (C = 5.8 2.3 1/min, H = 6.9 i 2.3 1/min; p < 0.001) and with prazosin (C = 5.9 ± 2.3 1/min, P = 7.6 ± 2.7 1/min; p < 0.005). Oxygen consumption did not change during exercise either with hydralazine (C = 663 249 ml/min, H = 651 ± 200 mI/min; p > 0.10) or with prazosin (C = 696 ± 246 ml/min, P= 734 245 ml/min; p > 0.10). Peak blood lactate did not change either with hydralazine (C = 49.7 i 24.2 mg/dl, H = 44.0 ± 21.4 mg/dl; p > 0.05) or with prazosin (C = 33.8 ± 16.5 mg/dl, P = 32.1 i 12.2 mg/dl; p > 0.10). Vasodilators did not change the rate of lactate disappearance during recovery from exercise. We conclude that short-term administration of vasodilators increased cardiac output during exercise but did not improve nutritional flow to exercising muscle. However, chronic administration of vasodilators with sustained improvement in cardiac output may allow the readjustment of peripheral mechanisms that control the nutritional flow of muscle in order to take advantage of improved cardiac performance caused by vasodilators.

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“…Given as the oral 5-mononitrate form, plasma con centrations of mononitrate are high, due to almost complete bioavailability [2,3]. There are several reports in the literature suggest ing that nitrates are effective in improving left ventricular performance [4,5]. Periph- cral arteriolar vasodilatation, which reduces systemic vascular resistance with agents such as hydralazine, has been shown to be equally effective in increasing cardiac output [6].…”

Section: Introductionmentioning

confidence: 99%

Calcium Channel Blocker and Isosorbide 5-Mononitrate in the Management of Chronic Cardiac Failure

Hutton¹,

McGhie²,

Martin³

et al. 1987

Cardiology

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In the management of the patient with chronic cardiac failure, the combination of an arteriolar vasodilator and venodilator should be beneficial. 8 patients with NYHA grade III-IV chronic cardiac failure were studied following placebo, after 4 weeks’ therapy with the arteriolar vasodilator felodipine, and with the combination of felodipine and oral isosorbide 5-mononitrate. Haemodynamic measurements were made at rest and during dynamic exercise at an individual, fixed, near maximal workload. Ejection fraction (EF) was obtained by gated radionuclide ventriculography. At rest, heart rate was unchanged 73 ± 6 at control, 72 ± 4 with felodipine and 74 ± 4 beats/min with the addition of isosorbide 5-mononitrate. Mean arterial pressure fell from 98 ± 5 to 84 ± 4 (p < 0.02) and 84 ± 3 mm Hg (p < 0.02) with nitrate. Cardiac index increased from 2.2 ± 0.1 to 2.5 ± 0.2 litres/min/m² with felodipine and further to 2.6 ± 0.2 litres/min/m² (p < 0.02) with nitrate. Exercise tachycardia and mean arterial pressure were not significantly affected by therapy. Cardiac index increased on exercise from 4.4 ± 0.3 to 4.8 ± 0.3 litres/min/m² with felodipine and 4.9 ± 0.3 litres/min/m² (p < 0.05) with the addition of nitrate. Stroke volume index increased from 35.4 ± 4 to 40.8 ± 4 beats/min/m² and further to 41.0 ± 4 beats/min/m² (p < 0.05) and EF from 14 ± 3 to 18 ± 3% with nitrate. In conclusion, in patients with chronic cardiac failure, treatment with a calcium channel blocker produced sustained haemodynamic improvement, particularly on exercise, and combination with nitrate produced further benefit.

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Improvement in exercise haemodynamics by isosorbide dinitrate in patients with severe congestive cardiac failure secondary to ischaemic heart disease.

Cited by 30 publications

References 28 publications

Intravenous isosorbide dinitrate in patients with refractory pump failure and acute myocardial infarction.

Intravenous isosorbide dinitrate in patients with refractory pump failure and acute myocardial infarction.

Metabolic assessment of exercise in chronic heart failure patients treated with short-term vasodilators.

Calcium Channel Blocker and Isosorbide 5-Mononitrate in the Management of Chronic Cardiac Failure

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