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

We evaluated the hemodynamic effects of nifedipine in 10 symptomatic patients with chronic refractory heart failure due to idiopathic cardiomyopathy. Nifedipine significantly increased cardiac index (from 1.80 +/- 0.4 to 3 +/- 0.6 L/min/m2), stroke volume index (from 21 +/- 6 to 33 +/- 8 ml/beat/m2), and stroke work index (from 17.9 +/- 7 to 25.5 +/- 7 g-m/m2). The drugs also produced a significant decrease in left ventricular filling pressure (from 24.6 +/- 3 to 19 +/- 2 mm Hg), mean blood pressure (from 86 +/- 9 to 74 +/- 5 mm Hg), mean pulmonary arterial pressure (from 31.9 +/- 5 to 25.6 +/- 3 mm Hg), total systemic vascular resistance (from 2,104 +/- 329 to 1,088 +/- 249 dyn/s/cm-5), and pulmonary vascular resistance (from 200 +/- 71 to 107 +/- 50 dyn/s/cm-5). Heart rate remained unchanged. In all patients maintained on nifedipine therapy, repeat hemodynamic studies at 2 months revealed sustained effects, and all patients had symptomatic improvement of at least one New York Heart Association (NYHA) functional class. Long-term treatment was well tolerated. Forty-eight hours after discontinuation of nifedipine administration the hemodynamic benefits were lost. We conclude that nifedipine may be of value for long-term ambulatory therapy of severe chronic heart failure.
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PMID:Oral nifedipine in the long-term management of severe chronic heart failure. 618 18

Molsidomine, one of the sydnonimine group of drugs; the object of this study was to evaluate its efforts in refractory cardiac failure. In the first part of the study, the haemodynamic effects of a single oral dose of 2 or 4 mg of molsidomine were compared with placebo controls in 23 patients. This showed molsidomine to be an active venous vasodilator reducing pulmonary artery and right atrial pressures without changing cardiac index or systemic pressures. The peak effect was observed after 1 to 1,5 hours. In the second phase, molsidomine was used in 9 patients aged 32 to 71 years (mean 47 +/- 12 years) over an average period of 19 months (3,5 to 42 months). The maintenance dose varied from 8 to 24 mg/24 hours. These patients had refractory cardiac failure secondary to primary cardiomyopathy with dilatation (6 cases) or ischemic heart disease (3 cases). The 9 patients were in functional classes IV (5 cases) or III (4 cases). Four patients were theoretically good indications for transplantation. Haemodynamic control was performed 1,8 +/- 5 months after a washout period of 8 hours, and after initial right heart catheterisation, the measurements were repeated 1 hour after oral administration of a 4 mg dose of molsidomine. Two patients did not respond initially to molsidomine; one died, the other remained in functional Class III. Another patient who responded initially was improved for over two years but died in cardiac failure after 42 months' treatment. The other six patients have been significantly improved and were in functional Class II at their last control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term clinical and hemodynamic results of the treatment of refractory cardiac failure with molsidomine]. 642 98

The acute effects of captopril on haemodynamics, coronary flow and myocardial metabolism were studied in 12 patients with chronic severe cardiac failure (primary cardiomyopathy: 10 cases; ischaemic: 2 cases) in functional Classes III or IV of the NYHA. All patients were male and their average age was 51.3 +/- 14.1 years (range 27 to 68 years). Measurements were carried out under basal conditions and 90 minutes after a single dose of 50 mg (5 cases) or 100 mg (7 cases) of captopril. Captopril administration leads to an increase in cardiac index from 2.05 +/- 0.32 to 2.34 +/- 0.35 l/min/m2 (p less than 0.05) and a greater increase in systolic index from 23.9 +/- 6.7 to 29.8 +/- 6.9 ml/syst/m2 (p less than 0.01), because the heart rate decreased slightly (p less than 0.05). These changes were the result of a decrease in afterload: mean aortic pressure fell from 85 +/- 11.8 to 68 +/- 19.6 mmHg (p less than 0.01) and systemic arterial resistance fell from 2 886 +/- 745 to 2 010 +/- 610 dynes/cm-5/sec/m-2 (p less than 0.01). Captopril also led to a fall in venous tone, i.e. pre-load: left ventricular end diastolic pressure fell from 26.9 +/- 6.1 to 20.8 +/- 6.6 mmHg: p less than 0.01. There was no change in contractility as shown by the absence of variation of the V.max (0.92 +/- 0.18 under basal conditions, and 0.90 +/- 0.15 after 90 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute hemodynamic and coronary effects of captopril in chronic cardiac failure]. 643 65

ARL 115 has vasodilator and positive inotropic properties which justify its use in heart failure. The effects of this drug were studied in 8 patients with advanced myocardial failure (7 cases of primary cardiomyopathy and 1 case of ischaemic cardiomyopathy) undergoing diagnostic cardiac catheterization, 15 minutes after angiocardiography. The cardiac output pressures were measured and the M mode electrocardiogram was recorded under basal conditions and following an infusion of 1 mg/kg of ARL 115 over 10 minutes. An improvement was observed in 7 cases, with an increase in the cardiac output and a decrease in the left ventricular diastolic pressure (p less than 0.05). There was no significant modification in the heart rate and there were no side effects. In one case, an abrupt fall in the diastolic pressure led to a decrease in the cardiac output. The arterial and venous vasodilator properties were demonstrated in every case, but a positive inotropic action (increase in the dp/dtmax and modification of the end-diastolic pressure: dimension ratio) was demonstrated in only two cases. The absence of positive inotropic action in the 6 other cases could be due to the advanced myocardial deterioration in these patients or to a delay in the positive inotropic effect in relation to the vasodilator effect.
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PMID:[Hemodynamic effects of ARL 115 in left ventricular insufficiency]. 650 98

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.
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PMID:Hypertropic cardiomyopathy and hyperthyroidism in the cat. 654 Feb 56

The pathological findings in nineteen cats with idiopathic cardiomyopathy are reported. The disease is marked by a usually short clinical course, often without the specific symptoms of heart failure. Some cats die suddenly. The heart usually shows dilatation, occasionally accompanied by hypertrophy. Histological findings include various degrees of degeneration, inflammation and fibrosis. Histological changes are absent in some cases. The pathogenesis is discussed. The aetiology has not been elucidated so far.
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PMID:[Pathologic anatomical findings in 19 cats with idiopathic cardiomyopathies]. 670 81

28 patients with primary congestive cardiomyopathy in heart failure identified by cineangiographic criteria (end-diastolic volume greater than 120 ml/m2; parietal thickness less than 11 mm; normal coronary angiography), underwent 131-Cesium and 201-Thallium myocardial scintigraphy in antero-posterior and LAO projections, and 17 also underwent angiocardiography with 99 Technetium labelled albumin. This condition usually gives an appearance of an enlarged heart with diffuse or localised (antero lateral wall) hypofixation, dilatation of the left ventricular, left atrial and right ventricular cavities and a very low ejection fraction with diffusely hypokinetic wall motion. Radio-Isotopic methods may help discriminate primary and ischaemic cardiomyopathy but are not diagnostic. A low ejection fraction and marked diffuse hypofixation are poor prognostic indices. Radio-Isotopic methods are valuable in the classification of primary cardiomyopathy.
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PMID:[Isotopic methods and primary congestive cardiomyopathies]. 677 Jul 86

The prognosis of congestive cardiomyopathy was studied in 132 consecutive patients (110 male, 22 female, average age 45 +/- 11 years) in whom a thorough clinical evaluation had excluded a secondary cause. The patients presented with left ventricular failure, a history of systemic embolism, syncope or radiological cardiomegaly. Right (100 p. 100) and left (81 p. 100) heart catheterisation was performed and left ventricular endiastolic volumes (202 +/- 77 ml/m2) and ejection fractions (31 +/- 12 p. 100) calculated from angiography in the 30 degrees right anterior oblique projection. Regional abnormalities of contraction were observed in 32 patients. The average follow up period was 40,4 +/- 23,8 months. At the end of the study 48 patients (37 p. 100) had died and 2 had been lost to follow up. Survival rates were calculated by actuarial methods. Age, sex, the period they had been symptomatic, alcoholic intoxication and the degree of cardiac dilatation were not significant prognostic factors. Patients in Class IV NYHA had the worst prognosis: 63 p. 100 2 year mortality. Atrioventricular conduction defects were observed in 56 patients and were associated with a significantly increased mortality rate (43 p. 100 compared with 23 p. 100, p < 0.001). Atrial fibrillation (32 patients) was a better prognostic factor than the persistence of sinus rhythm; 2 year mortality 11,1 p. 100 compared to 37,6 p. 100 (p < 0.001). Increased left ventricular end diastolic pressures greater than 20 mmHg were related with a mortality of 51,5 p. 100. Also, the patients with a ejection fraction of 30 p. 100 and a 2 year mortality rate of 44 p. 100 compared to 17,5 p. 100 when the ejection fraction was greater than 30 p. 100 (p < 0,001). In conclusion : 1. Regional abnormalities of left ventricular contraction are not rare in primary cardiomyopathy. 2. The prognosis is directly related to the degree of cardiac failure and the extent of left ventricular dysfunction.
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PMID:[Prognosis of primary non-obstructive cardiomyopathies]. 677 38

Although a variety of vasodilator drugs produce acute hemodynamic improvement in patients with severe chronic heart failure, long-term treatment with these agents may be associated with the development of drug tolerance and loss of initial beneficial effects. Five serial right heart catheterizations in a 78 year old man with severe chronic heart failure due to idiopathic cardiomyopathy documented the development of hemodynamic and clinical tolerance to oral hydralazine and oral captopril after initial responses were observed to both agents. However, sustained hemodynamic and clinical improvement by invasive testing was noted with minoxidil (20 mg orally twice daily) after 4 and 9 weeks of continuous therapy. These observations indicate that pharmacologic tolerance may occur with a variety of vasodilator drugs and may account for the failure of some patients to improve clinically with long-term therapy despite initial favorable hemodynamic effects. However, such tolerance seems to be drug-specific and, hence, its recognition in an individual patient does not prelude responsiveness to other vasodilator agents.
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PMID:Sustained effectiveness of minoxidil in heart failure after development of tolerance to other vasodilator drugs. 679 86

To determine whether cardiomyopathy could be distinguished from coronary artery disease, we used thallium scanning to study 25 patients with severe left ventricular dysfunction and chronic heart failure. Ten patients had normal coronary arteries and idiopathic cardiomyopathy (ejection fraction 20 +/- 5%), and 15 patients had multivessel coronary disease and left ventricular dysfunction (ejection fraction 25 +/- 6%). The exercise time and maximal heart rate were similar in the two groups. Two patients with cardiomyopathy and 11 with coronary artery disease had a positive exercise ECG (p less than 0.05). Thallium scans showed perfusion defects in all 25 patients. The perfusion defects were complete in nine coronary artery disease patients (60%) and in one patient (10%) with cardiomyopathy (p less than 0.05). Extensive defects involving more than 40% of the left ventricular circumference, the number of segments involved, redistribution on the 4-hour scan, lung uptake and ventricular size were similar in the two groups. Perfusion defects on thallium scanning can occur in patients with idiopathic dilated cardiomyopathy and chronic heart failure. Thallium scanning cannot be reliably used in patients with chronic heart failure to distinguish coronary artery disease from cardiomyopathy unless complete defects are present.
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PMID:Comparison of thallium-201 scanning in idiopathic dilated cardiomyopathy and severe coronary artery disease. 688 74


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