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

A retrospective study of 100 case notes of patients who died from a recent myocardial infarction (less than one month before death) has established the causes of death: cardiac failure (52), rupture of the heart (40), major pulmonary emboli (3), primary irreversible ventricular fibrillation (2), unexplained death (3). Study of the extent of the necrosis by the technique of segmentation of the ventricular mass has allowed us to clarify the correlation between the "index of extent" ("i"), an the clinico-pathological findings. It has been noted in particular that those infarctions complicated by cardiogenic shock and/or by bilateral bundle branch block were those with the highest value of index of extent (i = 8.91, i = 9.40); also that cardiac failure and ventricular tachycardia were found in the extensive infarctions (i = 7,33, i = 9.52); also that rupture of the outer wall and pulmonary thromboses complicated infarctions of very small extent (i = 4,80, i = 5,67). It would not seem possible to reduce the hospital mortality of infarctions significantly, since it is essentially linked with circulatory failure caused by extensive necrosis, and with ruptures of the heart which are unpredictable and untreatable.
Arch Mal Coeur Vaiss 1977 Dec
PMID:[Cause of death in recent myocardial infarct. Correlation between extent of necrosis and clinical, electrocardiographic and anatomical findings]. 41 79

In a series of 51 clinico-pathological examinations on patients who died during the first 15 days after the onset of clinical symptoms of their first and only transmural myocardial infarction (anterior: 29 cases; posterior: 22 cases) the causes of death were divided into: heart failure -- 26 cases (53 p. 100); rupture of the heart -- 22 cases (43 p. 100); disorders of ventricular rhythm -- 2 cases (4 p. 100). The anatomical basis of fatal cardiac failure is twofold: either a very extensive area of necrosed muscle, of poor quality of the mass of muscle not involved in the infarction. In the anterior infarctions (16 cases, representing 55 p. 100 of deaths in this group) the first factor was foremost, the mean extent of necrosed muscle constituting 42 p. 100 of the total left and septal ventricular mass; stenotic coronary lesions, which were commonly found on the anterior descending artery, were confined to this artery alone in 10 cases 62 (p. 100). In posterior infarctions (11 cases, representing 50 p. 100 of deaths in this group), the mass of muscle destroyed was less (mean 36 p. 100), but the stenotic coronary lesions were diffuse, involving the three main trunks in 9 cases, which also explains the poor quality of the muscle not involved by necrosis. Thus there is a clear difference between anterior and posterior infarctions followed by deaths from cardiac failure: in the first group, the remaining muscular mass is quantitatively insufficient to maintain the haemodynamics, while in the second it is qualitatively insufficient, because of poor blood supply, to maintain an adequate cardiac output.
Arch Mal Coeur Vaiss 1977 Dec
PMID:[Fatal cardiac insufficiency in the course of an initial acute myocardial infarct. Anatomical-clinical data]. 41 80

The influence of left ventricular filling pressure on the atrial contribution filling pressure and atrial contribution was seen in studies done at baseline (PCW (r=-.53, p less than .025), as well as in studies done after PCW was modified by volume expansion and/or nitrates (r=-.53, p less than .005). At baseline, atrial contribution averaged 9.3 +/- 1.3 c.c./M.2 in patients with PCW less than 20 mm. Hg, while it was only 2.4 +/- 1.2 c.c./M.2 in patients with PCW greater than or equal to 20 mm. Hg (p less than .005). Atrial contribution was significantly greater in patients who had no history of heart failure when they were volume loaded to a PCW above 20 mm. Hg than in patients with impaired ventricular function whose baseline PCW was above 20 mm. Hg. Thus, atrial contribution tends to be less effective in augmenting cardiac output when filling pressure is already elevated, particularly in patients with impaired left ventricular function.
Am Heart J 1979 Dec
PMID:The influence of left ventricular filling pressure on atrial contribution to cardiac output. 49 26

Serial treadmill exercise testing (mean 5.5 tests/patient) was used to evaluate the prognosis of 200 males (mean age 53 years) without clinical heart failure or unstable angina pectoris 3 weeks after acute myocardial infarction (MI). Exercise-induced ischemic ST-segment depression greater than or equal to 0.2 mV 3 weeks after MI was significantly more prevalent in patients with subsequent cardiac arrest (100%) or coronary artery bypass graft surgery (64%) than in patients without subsequent events within 2 years of infarction (35%) (p less than 0.05). Exercise-induced ventricular arrhythmia on multiple tests 5-52 weeks after MI was more prevalent in patients with recurrent myocardial infarction (90%) than in patients without subsequent events (47%) (p less than 0.001). By contrast, exercise-induced ventricular arrhythmia on a single test at 3 weeks was a less powerful predictor of subsequent cardiac events. Exercise-induced ischemia 3 weeks after MI predicted early fatal events, while ventricular arrhythmia on serial testing predicted later nonfatal events.
Circulation 1979 Dec
PMID:The prognostic significance of serial exercise testing after myocardial infarction. 49 48

In this paper we discuss two infants and one child who experienced a previously unreported complication after complete correction of a large, unrestrictive ventricular septal defect. Two patients had documented pulmonary hypertensive crises and severe right-heart failure secondary to hypoxia and pulmonary vasoconstriction. These crises were associated with significantly increased right ventricular (RV) peak systolic and end-diastolic pressures and right-to-left shunting via a foramen ovale which, in turn, exaggerated the hypoxis. The crises were treated successfully with tolazoline in the second and third patients. RV pressure returned to normal values and have remained normal up to 12 months postoperatively in the second patient. Although the RV pressures decreased with tolazoline in the third patient, they never reached normal values. Postoperative monitoring of pulmonary artery and RV pressures in infants with large ventricular septal defects is essential when unexplained complications are encountered. Tolazoline proved to be very effective in the treatment of two patients with pulmonary vasoconstriction secondary to hypoxia.
Circulation 1979 Dec
PMID:Diagnosis and management of postoperative pulmonary hypertensive crisis. 49 83

After the acute onset of heart failure and in the absence of acute myocardial infarction, plasma volume may occasionally be depleted to the extent that the patient presents with clinical signs of circulatory shock. In five patients, the acute onset of clinical and radiographic signs of cardiogenic pulmonary edema were associated with reduction in arterial blood pressure and cardiac output. The pulmonary arterial wedge pressure was within normal limits but a reduction in plasma volume was demonstrated, which is best explained by the rapid translocation of plasma water that represented pulmonary (and most likely also peripheral) edema fluid. The infusion of 5 percent albumin solution significantly increased cardiac output, mean arterial pressure and cardiac work, reversed lactic acidosis, enhanced furosemide-induced diuresis and was followed by a decrease in both clinical and radiographic signs of pulmonary edema. These observations confirm that volume expansion may constitute appropriate treatment for some patients with cardiogenic pulmonary edema who may present with hypotension and who are unresponsive to conventional therapy.
Am J Cardiol 1979 Dec
PMID:Hypovolemia and hypotension complicating management of acute cardiogenic pulmonary edema. 50 39

In addition to standard treatment with digitalis and diuretics prazosin (20 mg/d) and placebo were given to 14 patients with chronic therapy-resistant cardiac failure mainly of stage III for periods of 6 weeks each. Cardiac frequency, blood pressure, cardiac volume, pulmonary artery pressures and cardiac minute volume were assessed at rest and during physical exercise. Body weight, congestive changes in the chest radiograph, oedema and complaints were evaluated. During the acute trial using 2 mg of prazosin a significant increase of cardiac minute volume was demonstrable at rest and during exercise (2 P less than 0.05). After administration for 6 weeks cardiac minute volume increased from 3.2 to 4.0 l/min at rest and from 6.9 to 8.0 l/min during exercise (2P less than 0.005; n=12). There was a noticeable decrease of cardiac size from 1440 to 1306 ml/1.73 m2 (2 P less than 0.02). Haemodynamic improvement paralleled the decrease of complaints which was equivalent to an improvement of half to one stage of the New York Heart Association. In severe cardiac failure prazosin has thus an additional therapeutic effect beyond digitalis and diuretics.
Dtsch Med Wochenschr 1979 Dec 14
PMID:[Effect of prazosin in therapy-resistant chronic cardiac failure (author's transl)]. 51 Feb 13

In a female 53 year old patient with severe heart failure in haemochromatosis, not responding to digitalis, treatment with prednisolone (40 mg/da) and phlebotomies eventually led to a permanent remission. She is symptom free 4 years after the event. Phlebotomy every 4--6 weeks is the only actual treatment.
Z Gastroenterol 1979 Dec
PMID:[Successful treatment of cardiac failure in haemochromatosis by prednisolone and phlebotomies (author's transl)]. 53 47

The haemodynamic effects of oral prazosin and hydralazine were evaluated in patients with refractory heart failure and compared with those of intravenous nitroprusside in the same patients. Both oral agents were well tolerated and appeared to have beneficial haemodynamic effects. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin resulted in a more significant decline in left ventricular filling pressure and pulmonary vascular resistance than did hydralazine. Haemodynamic alterations induced by prazosin were similar to those induced by nitroprusside, which suggests a relatively balanced reduction of preload and afterload. With hydralazine, the increase in cardiac output without change in left ventricular filling pressure or pulmonary vascular resistance suggests minimal effect on preload but significant reduction in afterload.
Br Heart J 1979 Dec
PMID:Comparison of haemodynamic effects of oral prazosin, oral hydralazine, and intravenous nitroprusside in same patients with chronic heart failure. 53 83

A 25-year-old man with familial pyruvate kinase (PK) deficiency who have been given only 6 transfusions during his lifetime died of cardiac failure from hemochromatosis (HC). This previously unreported association of PK and HC deficiency does not appear to be fortuitous but to be related to possible early hemolysis and intramedullary destruction, features of ineffective erythropoiesis. The role of splenectomy in the progression of the HC could, as in some thalassemias, be an unfavourable factor. Serum iron levels should therefore be measured during the course of AHPK.
Ann Med Interne (Paris) 1979 Dec
PMID:[Hemochromatosis and puryvate kinase deficiency (author's transl)]. 53 87


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