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

The effects of intravenous trinitrin on myocardial function have been studied in 40 patients with heart failure (26 cases of coronary artery disease and 14 of apparently primary cardiomyopathy). Each patient had measurements made of left ventricular pressure, of cardiac output by the dye dilution method, of volume, of the left ventricular ejection fraction, and of the segmental parietal kinetics by means of left side ventriculography both before and after trinitrin. The following results were obtained after injection of trinitrin:--no change in rhythm and cardiac index;--an almost constant decrease in left ventricular end diastolic pressure (38 cases out of 40);--a decrease in arterial pressure and ventricular volume in about two thirds of cases;--improvement of the ejection fraction (25 cases out of 40), and of segmental parietal kinetics (26 cases out of 40) in the left ventricle. These findings were equally true in the patients with coronary artery disease and in the cardiomyopathies. In the light of these results, it appears that when used in left ventricular failure, trinitrin almost always decreases the load, but improves ventricular kinetics only in two thirds of cases, while it has no influence on cardiac output. In addition, given the difficulties in establishing a standard dose of trinitrin, the authors discuss the methods of establishing the optimal dose.
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PMID:[Effects of intravenous trinitrine on myocardial function in left ventricular insufficiency]. 10 Nov 68

One hundred consecutive cases of valve replacement for aortic regurgitation performed between 1967--1971 were analyzed to identify and quantitate factors related to a favorable result. Of 83 perioperative survivors, 78% (n = 65) became asymptomatic and 58% (n = 48) were alive 5--9 years postoperatively. The cause of aortic regurgitation affected both the speed of progression of symptoms and the postoperative result. Death due to myocardial failure may be prevented by optimal timing of operation. Accordingly, we identified variables that discriminated between patients who had an excellent postoperative result and those who died of myocardial failure. The most important discriminators were the severity (p = 0.03) and duration (p = 0.04) of dyspnea, the extent of therapy for heart failure (p = 0.001), physical findings of left ventricular failure (p = 0.002), the cardiothoracic ratio (p = 0.007), the resting pulmonary capillary wedge pressure (p = 0.01), and a cardiac index less than 2.2 1/min/m2 (p = 0.03). The data suggest that evidence of left ventricular failure, even of mild degree, is an indication for operation in patients with severe aortic regurgitation.
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PMID:Valve replacement for aortic regurgitation: long-term follow-up with factors influencing the results. 11 Apr 91

In acute and chronic left heart failure peripheral resistance is elevated due to increased sympathetic tone. This should compensate the decrease in stroke volume. In the diseased left ventricle however the augmentation of afterload leads to further reduction of stroke volume and to increase of heart size and myocardial oxygen consumption. This vitious cycle may be interrupted by vasodilators. Drugs like nitroglycerin, mainly acting on the venous system, reduce preload and thereby relieve symptoms of pulmonary congestion (backward failure). Phentholamin on the other hand primarily reduces afterload by an action on the resistance vessels and thereby increases cardiac output (forward failure). Nitroprusside has effects on both, the capacity and resistance vessels. So nigroglycerin is the remedy of choice in acute pulmonary edema. Nitroprusside in leftf heart failure in acute myocardial infarction and Phentolamin in acute left ventricular failure due to critical rise in blood pressure. For long term treatment of chronic left heart failure (coronary heart disease, cardiomyopathy, rheumatic heart disease) hydralazin or prazosin may be used as well as long acting nitrates.
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PMID:[Progress in the therapy of acute and chronic cardiac insufficiency by means of systemic vasodilators. Studies with prazosin and nitroglycerin]. 12 80

The purpose of the present study was to investigate the effect of the dose of nitroglycerin (NTG) on myocardial ischemic injury. In 20 closed chest dogs the anterior descending branch of the left coronary artery was occluded by inflating a balloon in its lumen. Compared with the untreated control group the sigma ST elevation was significantly lower when NTG was applied at a rate of 0.02 mg/min, but significantly higher when NTG was administered at a rate of 0.10 mg/min. In 12 patients with acute myocardial infarction NTG was infused at a rate of 3 mg in the first hour (0.05 mg/min) and 6 mg in the second hour (0.1 mg/min). Sigma ST elevation and sigma ST depression decreased during the lower infusion rate (p less than 0.001). When the rate of NTG infusion was raised to 6 mg/hr, the improvement in ST segment deviation was partially reversed. This effect, particularly evident in patients not in heart failure, was associated with a significant rise in heart rate (p less than 0.05) and a fall in diastolic arterial pressure (p less than 0.025). Patients with left ventricular failure were less sensitive to higher doses of NTG than those without failure. Thus, the effect of NTG on myocardial ischemic injury depends on the NTG dose and on the functional state of the injured left ventricle.
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PMID:Nitroglycerin in acute myocardial infarction. X. Effect of small and large doses of nitroglycerin on sigma ST segment deviation -- experimental and clinical results. 12 66

In cardiac failure unresponsive to digoxin and diuretics, afterload reduction brings about a dramatic increase in cardiac output, renal perfusion and responsiveness to diuretics; furthermore, the decrease in venous pressure relieves the dyspnoea. Intravenous vasodilators should only be used when sophisticated haemodynamic monitoring equipment and experienced physicians are at hand. Indications for the use of these agents are severe cardiac failure, acute myocardial infarction complicated by left ventricular failure, persistent ischaemic pain and limitation of infarct size. A wide variety of oral vasodilator agents is available, all having different sites of action; the choice of vasodilator agents should be tailored to the needs of the patient. Treatment with these agents is indicated in patients in whom cardiac failure becomes refractory to conventional therapy with digoxin and diuretics. The utmost care must be taken to avoid further impairment of cardiac output by excessive reduction of the left ventricular end-diastolic pressure (LVEDP) and hypotension, which will jeopardize myocardial, renal and cerebral perfusion.
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PMID:The use of vasodilator agents in the treatment of heart failure. 15 2

Left ventricular function was studied at rest and during post-extrasystolic potentiation in 18 patients with chronic obstructive lung disease. The contractility indices used were obtained from pressures recorded in the isovolumetric period (left ventricular end-diastolic pressure, Vmax., VECmax., dP/dtmax.) and from volume variations during ejection (end-diastolic volume, ejection fraction, VCF). Left ventricular diastolic compliance was also evaluated. All patients were hypoxic (PaO2 = 58 +/- 7 torr); six of them had cor pulmonale (group B); the remaining 12 patients constituted group A. Left ventricular function of groups A and B was similar; we conclude that right cardiac failure, in cor pulmonale, is not secondary to left ventricular failure. However, left ventricular dysfunction exists; the left ventricle is hypertrophied (probably resulting from chronic hypoxia). Pump function is altered (abnormal ventricular function points are found), but left ventricular kinetics is normal or exaggerated (ejection fraction and VCF are increased). Isovolumetric phase contractility indices are diminished; however, they may increase normally during post-extrasystolic potentiation. Left ventricular compliance is abnormal due to left and right ventricular hypertrophy and to paradoxical movement of the interventricular septum which impedes diastolic expansion of the left ventricle. These changes are responsible for decreased left ventricular output. There seems to exist an impairment of left ventricular function related to both intrinsic (secondary to hypoxia, hypercapnia, left ventricular hypertrophy) and extrinsic factors (right ventricula hypertrophy deviating interventricular septum, lowering of left ventricular preload).
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PMID:[Left ventricular function in chronic obstructive lung disease (author's transl)]. 15 43

In 15 patients with acute gastrointestinal bleeding, central hemodynamics were monitored by means of a flow directed thermodilution catheter. Also, the systemic blood pressure, heart rate, blood volume and oxygen saturation in arterial and mixed venous blood were measured. In patients without cardiac insufficiency, the pulmonary artery mean pressure was found to be the hemodynamic parameter giving the most clear and constant evidence of hypovolemia. In patients with left ventricular failure and hypovolemia, the pulmonary artery pressures revealed cardiac insufficiency, and the central venous pressure indicated the degree of hypovolemia. The method has proved useful in observing patients with acute gastrointestinal hemorrhage complicated by cardiac disease, cirrhosis of the liver or the frailty of old age.
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PMID:Central hemodynamics in acute gastrointestinal bleeding. 30 94

The left ventricle in left heart failure can be elliptical, spherical or funnel shaped. There is no firm correlation between the different shapes and the hemodynamics. Left ventricular failure results in dilatation, deformation and loss of funnel function of the left atrium. In more advanced stages of left ventricular failure the pulmonary veins become coiled, dilated and narrow stepwise instead of the normal harmonic narrowing to the periphery. The pulmonary parenchyma exhibits fibrosis and septal siderosis at that stage. Heart failure cells can be observed frequently. In later stages, when pulmonary arteries and the right ventricle is involved, secondary global heart failure develops. Right ventricular failure may lead to necrosis of liver cells with jaundice and elevated levels of liver specific enzyms. Primary global failure has no hemodynamic consequences on the pulmonary circulation, as long as left and right ventricular failure are of equal severity. If one form prevails, the clinical picture will be that of left or right ventricular failure respectively.
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PMID:[Morphologic consideration of heart failure (author's transl)]. 36 77

The widespread use of cardiac ventriculography has focused interest on the frequency with which asynergy accompanies coronary heart disease as well as on its clinical and prognostic implications and dynamic nature. Recently, "intervention ventriculography" using nitroglycerin or postextrasystolic potentiation has indicated that asynergic zones may be more accurately classified as reversible (implying viable myocardium) or irreversible (nonviable or scarred myocardium), and thus the ventriculographic definition of aneurysm must reflect not only the severity of asynergy but its contractile reserve. Surface electrocardiogram Q waves, the severity of asynergy, and degree of coronary occlusion all adversely affect the potential for reversibility, whereas coronary collaterals enhance it. Important clinical applications include assessment of the potential utility of coronary bypass surgery in improving asynergy and of vasodilators in the treatment of patients with left ventricular failure. With refractory sequelae of aneurysms (heart failure, ventricular tachyarrhythmias, and systemic emboli) and a discrete aneurysm, surgical resection has been increasingly used with generally good results.
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PMID:Asynergy in coronary heart disease. Evolving clinical and pathophysiologic concepts. 41 Mar 36

Patients with severe left ventricular failure generally have both reduced cardiac output and increased pulmonary and systemic venous pressures. A study was therefore made of the use of combined vasodilator therapy with nonparenterally administered nitrates, which act primarily on venous capacitance vessels and thus reduce preload, and orally administered hydralazine, which acts on arteriolar resistance vessels and thus reduces afterload. Twelve patients with chronic refractory heart failure were given these drugs individually and in combination during continuous hemodynamic monitoring. Heart rate and arterial pressure did not change significantly. Nitrates significantly reduced filling pressures of both ventricles without affecting cardiac index. Hydralazine did not alter filling pressures but dramatically increased cardiac index. The hemodynamic effects of each drug were additive during combined therapy, resulting in a 36 percent (28 to 18 mm Hg) mean decrease in left ventricular filling pressure and a 58 percent (2.1 to 3.3 liters/min per m(2)) mean increase in cardiac index. The seven patients who have continued to receive combined therapy for 3 to 10 months have shown sustained clinical improvement.
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PMID:Hemodynamic advantage of combined administration of hydralazine orally and nitrates nonparenterally in the vasodilator therapy of chronic heart failure. 41 64


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