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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of vasodilators represents a new approach to the treatment of cardiac insufficiency, either chronic or acute. Their field of action is venous, arterial or mixed. Decreasing the pre-load, the "venous" vasodilators lighten the congestive symptoms of cardiac insufficiency. By decreasing the post-load, the "arterial" vasodilation increases the cardiac output. Some vasodilators, venously administered, imply a continuous hemodynamic checking (Sodium Nitroprussiate, Phentolamine, injectable Trinitrine). Others are active orally (Trinitrine, Isosorbide Dinitrate, Hydralazine, etc.). Vasodilating treatment is recommended for acute cardiac insufficiency, particularly during myocardium infarct and some acute valvular insufficiencies. It is also successfully used in acute lung edema. Finally it takes an increasing importance in the treatment of chronic cardiac insufficiency.
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PMID:[Vasodilators in the treatment of cardiac insufficiency (author's transl)]. 53 77

In treating heart failure, the physician must remain cognizant of pathophysiology as he prescribes and monitors therapy. In addition to seeking underlying and precipitating causes of the patient's heart failure, he must treat the congestive state by enhancing myocardial contractility, controlling excessive fluid retention, and reducing afterload. Figure 7 summarizes the theoretical shifts on a patient's left ventricular function curves that might occur with therapy. Left ventricular function might move from point A to point B with diuretic therapy, but overdiuresis could aggravate symptoms of low cardiac output, including postural hypotension. Digitalis would effect a shift from A to C. Isosorbide dinitrate would produce a shift from A to D in a patient not on digitalis and from C to D in a patient already receiving digitalis. Isosorbide dinitrate, in conjunction with more usual therapeutic measures, has proved clinically beneficial in the treatment of heart failure.
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PMID:Treatment of congestive heart failure. 82 68

Isosorbide dinitrate (ISD) was administered before, during and after 178 operations performed on 127 patients with arterial occlusive disease. Its influence on postoperative myocardial infarction, heart failure and mortality was tested by comparison with 188 operations performed on 140 patients with hypertension and/or old myocardial infarction receiving no ISD prophylaxis. Risk of cardiac complications was similar in both groups. Mortality in the ISD-treated group was significantly lowered as compared with the control group and was about half of the overall mortality in patients with arterial occlusive disease operated on at our hospital over the past 10 years. This difference depended partly on the influence of ISD on cardiac complications. Post-operative myocardial infarction during ISD prophylaxis occurred in 0.6% of cases as compared with 3.7% in the control group (p less than 0.05), whilst the respective values for postoperative heart failure were 5.7% and 18.2% (p less than 0.001). Both complications are related to absolute or relative hypoxia during the post-operative stress period. ISD is effective by lowering cardiac preload and afterload and thereby diminishing myocardial oxygen demand. ISD is the drug of choice for surgical patients since it provides a steady and long-lasting effect after sublingual absorption. ISD prophylaxis during the perioperative period is indicated in cases with coronary artery disease and with increased cardiac preload or afterload.
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PMID:[Prophylactic effect of isosorbide dinitrate on postoperative cardiac complications (author's transl)]. 99 28

To compare the benefit of angiotensin-converting enzyme inhibition and direct vasodilation on the prognosis of advanced heart failure, 117 patients evaluated for cardiac transplantation who had severe symptoms and abnormal hemodynamic status at rest were randomized to treatment with either captopril or hydralazine plus isosorbide dinitrate (Hy-C Trial). Comparable hemodynamic effects of the two regimens were sought by titrating vasodilator doses to match the hemodynamic status achieved with nitroprusside and diuretic agents, attempting to achieve a pulmonary capillary wedge pressure of 15 mm Hg and a systemic vascular resistance of 1,200 dynes.s.cm-5. Treatment with the alternate vasodilator was started because of poor hemodynamic response or side effects (40% of patients in the captopril group and 22% in the hydralazine group). Adequate hemodynamic response in patients with a serum sodium level less than 135 mg/dl was more likely with hydralazine than with captopril (71% vs. 33%, p = 0.04). Isosorbide dinitrate was prescribed in 88% of the hydralazine-treated patients and 84% of the captopril-treated patients. The hemodynamic improvements from each regimen were equivalent. After 8 +/- 7 months of follow-up, the actuarial 1-year survival rate was 81% in the captopril-treated patients and 51% in the hydralazine-treated patients (p = 0.05). The improved survival with captopril resulted from a lower rate of sudden death, which occurred in only 3 of 44 captopril-treated patients compared with 17 of 60 hydralazine-treated patients (p = 0.01). In the subset of patients who continued treatment with the initial vasodilator, results were similar to those for the entire treatment group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of direct vasodilation with hydralazine versus angiotensin-converting enzyme inhibition with captopril on mortality in advanced heart failure: the Hy-C trial. 154 80

The effect of 2-month treatment with isosorbide dinitrate (120 mg day-1), nifedipine (2 x 20 mg day-1) and their combination has been assessed in 16 patients with mild to moderate chronic cardiac failure. Isosorbide dinitrate decreased right atrial (-23%), pulmonary wedge (-20%) and pulmonary arterial (-17%) pressures but did not significantly change either cardiac output or systemic and pulmonary vascular resistance. Nifedipine increased cardiac output (+13%) and decreased systemic and pulmonary vascular resistance (both -17%) with no change of pressures. Combined therapy with both drugs decreased ventricular filling pressures (-8% and -15%), systemic (-20%) and pulmonary (-13%) arterial pressures, increased cardiac output (+26%) and decreased both systemic (-29%) and pulmonary (-29%) vascular resistances. Changes during exercise were almost the same as at rest. The effect of both drugs was more pronounced in patients with more severely pathological haemodynamic measurements before treatment. We conclude that combined treatment with both preload- and afterload-reducing agents can preserve or even potentiate a favourable haemodynamic effect of individual drugs.
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PMID:Long-term effect of isosorbide dinitrate and nifedipine, singly and in association, in patients with chronic heart failure. 229 52

An open randomised parallel group comparison of the haemodynamic effectiveness of three different routes of nitrate administration was undertaken in 36 male patients aged 40-69 years who had developed acute left ventricular failure within 18 h of the onset of myocardial infarction. All patients had electrocardiographic and serum cardiac enzyme changes compatible with transmural myocardial infarction and all had both radiographic and haemodynamic evidence of left ventricular failure. None were hypotensive, all were in sinus rhythm and none were receiving other cardioactive drugs. Control haemodynamic measurements were made over a period of one h, following which patients were randomised to receive either intravenous isosorbide dinitrate (mean dose 12.9 mg; range 7.7-14.9), buccal nitroglycerine (5 mg) or transdermal nitroglycerin (nitro TTS 10). The raised left heart filling pressure was reduced by all nitrate preparations but none significantly changed the heart rate or cardiac output. Systemic arterial pressure and vascular resistance were reduced by i.v. ISDN and buccal NTG but not by a transdermal NTG. The only adverse circulatory reaction was hypotension in the three patients following buccal NTG. Nitroglycerin by the transdermal route appears to be equally effective in reducing the raised left heart filling pressure in patients with postinfarction heart failure without the practical disadvantages of monitoring its intravenous administration or the potential hazard of hypotension with buccal NTG.
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PMID:Haemodynamic comparison of different routes of nitrate administration in postmyocardial infarction left ventricular failure. 251 87

Isosorbide dinitrate (ISDN) improves the clinical and hemodynamic state of patients with heart failure, but may cause dizziness and syncope. To characterize patients in whom cardiac output falls with high-dose nitrate therapy and to examine further the pathophysiology of the fall in cardiac output in these patients, we studies the effect of sublingual ISDN on forward cardiac output in 14 patients with severe cardiac failure (New York Heart Association grades 3-4). We examined systolic and diastolic left ventricular (LV) function from pressure and volume analyses of LV function. After administration of 15 mg ISDN, cardiac output was either unaltered or increased in 7 patients (Group 1) (11 +/- 12%, mean +/- SD), and decreased in 7 (Group 2) (-13 +/- 10%) (Group 1 vs. 2, p less than 0.002). Initial systemic arterial pressure, LV ejection fraction, wedge and LV transmural filling pressures were similar in both groups, but Group 2 patients had a lower systemic vascular resistance (p = 0.07) and tended to have a larger initial LV end-diastolic volume and increased end-diastolic compliance; following ISDN the decrease in LV filling pressure and end-diastolic volume was larger and the product of the changes greater (p less than 0.02). Thus ISDN decreases filling pressure and improves forward cardiac output in some patients with congestive heart failure, but large doses may decrease cardiac output in a subset of patients who have a lower systemic vascular resistance and a larger more compliant ventricle, maintaining forward blood flow predominantly by a preload reserve mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of isosorbide dinitrate on cardiac output in severe cardiac failure: relation to initial hemodynamics, ventricular volume, and the preload reserve mechanism. 279 73

The results of prolonged infusion treatment with Trinitrosan and Isoket of 29 patients with acute myocardial infarction and unstable angina pectoris are reported. The drug action on the anginal syndrome, accompanying cardiac failure, heart rate and arterial tension is analysed. The action on the dynamic of enzyme activity and of the electrocardiograms during the treatment is compared with a control group of healthy persons. The results show full therapeutic efficacy in relation to the anginal syndrome and cardiac failure without any other medication in 1/2 of the patients; a partial antianginal effect is found in 1/4 of the patients treated. The examinations did not show any favourable action of the drugs on the enzymes and ECGs followed up in dynamics. The nitrites in the doses applied show no negative action on the heart rate and arterial tension and no special hemodynamics control is required.
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PMID:[Infusion treatment with nitrites of patients with acute myocardial infarct and unstable angina pectoris]. 311 74

In several studies the nitrate effects on central hemodynamics during less than 24 hours have been evaluated in heart failure. Higher doses than in angina have been used. A pronounced response is seen acutely. An attenuation has been reported after 12-24 hours. A relation to continuous (intravenous, transdermal) administration of nitroglycerin has been proposed, but it is not clear. During chronic treatment with ISDN a tolerance is not obvious within 12 weeks. The heart failure patient has a different neurohumoral situation compared to angina patients. This could be one reason for differences in tolerance development during nitrate therapy.
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PMID:Development of tolerance to nitrate therapy in chronic congestive heart failure. 353 80

Congestive heart failure is accompanied by a number of compensatory mechanisms that may overshoot the mark. Among these are excessive arteriolar and venous constriction. Nitrates are effective in producing venodilation, redistributing blood from the chest to the periphery, and lowering right and left atrial pressures. Although oral isosorbide dinitrate is effective in producing acute beneficial hemodynamic effects, it usually does not increase exercise tolerance in the short term. Prolonged administration, however, does increase exercise tolerance and improve clinical class. Isosorbide dinitrate can be effectively combined with an arteriolar dilator such as hydralazine, which increases cardiac output. Such vasodilator therapy is symptomatically effective in patients with heart failure, although there is no evidence to date to suggest a prolongation of life.
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PMID:Role of isosorbide dinitrate in management of chronic congestive heart failure. 389 81


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