Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that hydralazine is beneficial in chronic heart failure by virtue of its afterload reducing effect. Nitroglycerin paste results in venodilation and fall in left ventricular filling pressure (LVFP). Thirteen patients with chronic heart failure were given a combination of oral hydralazine and nitroglycerin paste. With oral hydralazine (75 to 100 mg every 8 h), left ventricular stroke work increased and LVFP slightly fell. Following addition of 2% nitroglycerin paste, an additional decline in mean pulmonary artery and LVFP was observed without significant changes in heart rate and arterial pressure. There were no untoward side effects from either therapy. Eight patients followed for three to eight months (mean five months) reported subjective improvement in shortness of breath and other symptoms related to ventricular dysfunction. This study shows that in certain patients with chronic heart failure, hydralazine and nitroglycerin paste combination produces salutary clinical effects on long term probably through afterload and preload reduction, respectively.
 ...
PMID:Non-parenteral combined afterload and preload reduction therapy in congestive heart failure. 11 91

Of 88 consecutive patients aged 20 to 77 years with severe symptomatic aortic valve disease requiring surgery, 51 patients had angina pectoris; of these 51, 41 had predominant aortic stenosis and 10 had severe aortic regurgitation. All patients with angina pectoris underwent coronary angiography; significant coronary arterial disease was encounted in 24 per cent of those with aortic stenosis and 20 per cent of those with aortic regurgitation. By contrast, of 37 patients without angina pectoris 19 underwent coronary arteriography; none showed significant coronary artery disease (P smaller than 0.05). Among patients with angina pectoris, 17 per cent of those with aortic stenosis experienced prolonged, rest or nocturnal pain, compared to 70 per cent of those with aortic regurgitation (P smaller than 0.005). At the time of onset of angina pectoris, there were features of heart failure in 34 per cent of those with aortic stenosis, and in 90 per cent of those with aortic regurgitation (P smaller than 0.005). Nitroglycerin promptly relieved angina pectoris in 56 percent of patients with aortic stenosis and in 50 per cent of those with aortic regurgitation (P smaller than 0.05). Neither the pattern of angina pectoris nor the response to nitroglycerin was dependent upon the coexistence of significant coronary artery disease. In patients with aortic stenosis, there was not significant difference between those with angina pectoris, and those without angina with regard to left ventricular end-diastolic volume, end-diastolic pressure, ejection fraction, peak systolic pressure, wall thickness, cardiac index, or the product of these factors. In patients with aortic regurgitation, cardiac index was significantly lower (P smaller than 0.05), left ventricular end-diastolic volume tended to be larger, and ejection fraction tended to be lower in patients with angina pectoris as opposed to those without angina pectoris.
 ...
PMID:Clinical, haemodynamic, and coronary angiographic correlates of angina pectoris in patients with severe aortic valve disease. 80 13

Nitroglycerin reduces ischemic injury during acute myocardial infarction (AMI) in dogs--an effect that is potentiated when drug-induced hypotension and tachycardia are prevented with phenylephrine. To determine the effectiveness of nitroglycerin, alone or with phenylephrine, during AMI in man, 12 patients (five or whom had left heart failure) were evaluated by summing ST-segment abnormalities (sigmaST) from 35 precordial electrodes. The seven patients without heart failure did not benefit consistently from nitroglycerin alone; however, addition of phenylephrine to abolish nitroglycerin-induced arterial pressure reduction uniformly diminished sigmaST (4.9 to 3.2 mv; P less than 0.05). In patients with heart failure, nitroglycerin alone consistently reduced ischemia (5.8 to 4.4 mv, P less than 0.05); addition of phenylephrine often partially reversed this effect. Thus, administration of nitroglycerin, alone or with phenylephrine, can reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends on the presence or absence of left ventricular failure before treatment.
 ...
PMID:Reduction in myocardial ischemia with nitroglycerin or nitroglycerin plus phenylephrine administered during acute myocardial infarction. 80 12

The authors investigated the effect of intravenous nitroglycerin and trimepranol on the haemodynamics of patients with acute myocardial infarction. They found that nitroglycerin has a favourable effect on haemodynamics as it leads to a reduction of the pressure in the wedged pulmonary artery and to a reduction of oxygen requirement of the cardiac muscle, while the changes of the minute volume and pulse rate are insignificant. Trimepranol leads to a rise of pressure in the wedged pulmonary artery, sometimes to critical values, and to a decline of the cardiac minute output. The authors conclude that trimepranol is suitable for a selected group of patients with sinus tachycardia and without signs of cardiac failure while the pulmonary pressure is carefully monitored. Nitroglycerin can be administered to the majority of patients with acute myocardial infarction. To ensure safe administration it is sufficient to monitor the heart rate and in particular the systemic pressure. It is best to administer it to patients with extensive myocardial infarctions with a high filling pressure of the left ventricle.
 ...
PMID:[Hemodynamic effects of nitroglycerin and trimepranol in acute myocardial infarct]. 135 22

Nitroglycerin, isosorbide dinitrate and sodium nitroprusside, like nifedipine, were found to inhibit the receptor-provoked increase of cytosolic free calcium concentration in human platelets loaded with 2-[(2-amino-5-methylphenoxy)methyl]-6-methoxy-8-aminoquinoline-N,N,N',N' - tetraacetate. Sodium nitroprusside and nitroglycerin induced elevation of cyclic guanosine 3',5'-monophosphate content in platelets which correlated with their calcium-blocking activity. Methylene blue and epinephrine decreased the calcium-blocking effect and the influence of nitroglycerin on cyclic guanosine 3'-5'-monophosphate content, but failed to suppress the inhibitory effect of sodium nitroprusside. Ascorbic acid increased the calcium blocking effect of sodium nitroprusside and its influence on cyclic guanosine 3'-5'-monophosphate content, but did not alter the inhibitory effect of nitroglycerin. In order to evaluate the relationship between the mode of action of nitrates at cellular level and their vasodilatory effectiveness, we studied the circulatory response of the forearm to isosorbide dinitrate and the influence of nitroglycerin on free calcium concentration in the platelets in 10 patients with chronic heart failure. We established a significant positive correlation between the basal values for venous tone and its peak decrease after administration of the 10-mg dose of isosorbide dinitrate. A correlation was also found between the deviation of maximal decrease of venous tone by this dose of isosorbide dinitrate from the regression line (the relationship between the basal venous tone and its lowering by the drug) and mean inhibitory concentration values for nitroglycerin in blocking that proportion of the rise of calcium ion concentration in platelets due to blocking of the platelet-activating factor. Thus, nitrates, like calcium antagonists, inhibit the receptor-provoked calcium supply to the contractile system of the cells so neutralizing the effects of increased concentrations of vasoconstrictors. This suggests that the effectiveness of nitrates appears to be positively related to the contribution of receptor-induced increase of cytosolic free calcium concentration in vasoconstriction together with their capacity to raise cyclic guanosine 3',5'-monophosphate.
 ...
PMID:Relationship between the inhibition of receptor-induced increase in cytosolic free calcium concentration and the vasodilator effects of nitrates in patients with congestive heart failure. 210 12

During exercise in subjects with congestive heart failure and mitral regurgitation the rise in systemic arterial pressure is usually accompanied by increase in systemic vascular resistance. That could cause decrease of cardiac output not only because of a lack of myocardial reserve, but also because of an increase of mitral regurgitant volume. In such situation decrease in left ventricular preload could further increase the regurgitant volume and cardiac output. Whether changes in pre-or afterload can cause significant changes in mitral regurgitation, nitroglycerin and phentolamine was assessed in that group of patients. 22 patients with significant mitral regurgitation (3+,4+) was randomly divided into two groups. The first one received short intravenous infusion of nitroglycerin at a rate of 170 micrograms/min. The second one received phentolamine intravenously 1-1,5 mg/min. Patients underwent right heart catheterization with Swan-Ganz thermodilution catheter. Mean pulmonary, pulmonary capillary wedge, and right atrial pressure were monitored and recorded. Cardiac output was determined by thermodilution technique using iced 5% dextrose. If there were no contraindications (PWP greater than 30 mm Hg) an effort test was performed (cycloergometer, supine position). The same protocol was repeated during administration of nitroglycerin and phentolamine. Nitroglycerin significantly decreased right atrial and capillary wedge pressure (from 22.9 to 15.6 mm Hg). There were no significant differences in cardiac output, pulmonary and systemic vascular resistance. Pulmonary artery pressure decreased after nitroglycerin but the difference was not significant. All above effects of nitroglycerin persisted during effort. Phentolamine decreased significantly right atrial, pulmonary and capillary wedge pressure with simultaneous increase of cardiac output (30%) and decrease of pulmonary and systemic vascular resistance. In summary, nitroglycerin decreases only symptoms and theoretically could worsen forward flow in patients with mitral regurgitation and heart failure, especially in subjects with a significant increase of systemic vascular resistance during effort.
 ...
PMID:[Effect of intravenous administration of nitroglycerin and regitine on hemodynamics in mitral valve insufficiency]. 212 94

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.
 ...
PMID:Haemodynamic comparison of different routes of nitrate administration in postmyocardial infarction left ventricular failure. 251 87

Nitroglycerin and its derivatives have become widely used agents in the treatment of severe forms of heart failure. Their beneficial effects in this disease results from their ability to reduce preload and afterload of the heart muscle leading to an increase of cardiac index, a decrease in mean pulmonary artery and wedge pressures as well as pulmonary and peripheral vascular resistances. This is associated with reducing the patients' complaints. Intravenous nitrates are used in the treatment of myocardial infarction complicated by an increased left ventricular filling pressure as well as in various forms of acute and worsening left ventricular failure, mainly in pulmonary edema. Oral and transdermal nitrates are administered in chronic congestive heart failure NYHA class III and IV.
 ...
PMID:[Use of nitroglycerin in the treatment of congestive heart failure]. 251 63

Nitroglycerin has long been a mainstay of the treatment of ischemic cardiac pain. The introduction of transdermal formulations and in particular the development of controlled methods of delivery have been responsible for the renaissance of clinical interest in this simple and effective treatment. The pathophysiologic abnormality accompanying myocardial ischemia affords a natural theater for the exhibition of the therapeutic utility of these preparations and methods. The means whereby nitrates induce relaxation of vascular smooth muscle are not entirely clear, but their pharmacodynamic activities are perfectly plain. In the doses used in clinical practice, nitrates exert their predominant hemodynamic effects and therapeutic benefits through their peripheral vasodilator activities. This is particularly marked in veins, although in higher doses nitrates also dilate the larger systemic and coronary arteries. Criticisms of the efficacy of transdermal formulations of nitrates in the treatment of angina pectoris have arisen largely from uncritical acceptance of a small number of studies of questionable methodologic validity. Large-scale general practice studies have invariably found that transdermal nitrate delivery systems improve the quality of life in ambulant patients: anginal attacks are reduced with a minimum of side effects. The widespread acceptance of this novel form of drug delivery has stimulated its application in other therapeutic avenues. The efficacy of transdermal nitroglycerin in the suppression of silent ischemic attacks has been demonstrated. The maintenance of benefit initiated by intravenous nitroglycerin in patients with unstable angina also broadens the use of this method of nitrate delivery. In patients with acute myocardial infarction, whether complicated by left ventricular failure or not, the nitrates, and transdermal nitroglycerin in particular, appear to hold considerable promise. Improvement of hemodynamic abnormalities may cause reduction in infarct size and fewer life-threatening arrhythmias. Even survival may be extended. The utility of transdermal nitrates in the treatment of severe chronic heart failure is less certain. But the use of higher doses and an interval regimen of administration may hold promise for such patients. Naturally, more information is required before the overall therapeutic profile of this new method of controlled nitroglycerin delivery across the whole spectrum of coronary heart disease can be fully described. Fortunately, the high level of efficacy and safety of transdermal nitroglycerin demonstrated in the majority of reported studies encourages the pursuit of such an important therapeutic target.
 ...
PMID:The role of transdermal nitroglycerin in the treatment of coronary heart disease. 308 57

Nitroglycerin delivered by transdermal patch technology has been used in angina pectoris patients as well as in heart failure. In angina pectoris patients the plasma concentrations are low over the 24 hours. Effects can be found especially during the first 12 hours after application of the drug even during steady state conditions. The effect of the drug wanes after 24 hours and some studies suggest reduced effect when the patches have been applied for seven to 14 days. The attenuated effects have been claimed to be due to tolerance. Tolerance is, however, never absolute and in other studies this phenomenon is not shown. Furthermore, rebound phenomena may develop when nitroglycerin therapy is withdrawn. The optimal doses and schemes for nitroglycerin administration thus remain to be clarified.
 ...
PMID:Tolerance development during transdermal administration of nitroglycerin in angina pectoris. 309 45


1 2 3 4 Next >>