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

Coronary artery disease is a common and particularly severe complication of cardiac transplantation because it may cause progressive destruction of the graft by acute or chronic ischemia. The ischemia is usually silent because of cardiac denervation. Cardiac failure related to graft dysfunction, asymptomatic infarction on the ECG, or sudden death, are sometimes the only signs of severe coronary disease. The prevalence of coronary lesions has been evaluated by coronary angiography at nearly 25% at 2 years and 50% at 5 years. The distribution and morphology of the lesions are characteristic: diffuse concentric, irregular and occlusive, predominantly distal stenoses, without a distal and usually without a collateral circulation. The histological features are variable: the association of medial necrosis, severe endothelial lesions and intense parietal inflammation are suggestive of acute arteriolitis, often present during acute rejection, may be related to a common pathological process. Diffuse obliterative arteriolar lesions with concentric proliferation of medial smooth muscle are the usual appearances in transplant patients who have died or been retransplanted. There is no non-invasive diagnostic method sufficiently sensitive of specific which justifies the practice of many groups of systematic annual coronary angiography in transplanted patients. The pathogenesis is poorly understood and probably multifactorial: disorders of lipid metabolism, immunological factors, the atherogenic role of Cytomegalovirus infection. The absence of an identifiable risk factor makes preventive measures difficult. The evolutive risk justifies retransplantation in selected patients, the results of which are less satisfactory but which reduces the risk of acute coronary events and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary disease in patient following heart transplantation]. 185 May 86

The clinical characteristics and long-term survival of 284 patients from the Coronary Artery Surgery Study (CASS) registry data base who had moderate to severe congestive heart failure symptoms and a left ventricular ejection fraction greater than or equal to 0.45 were studied. A control group consisting of registry patients with an ejection fraction greater than or equal to 0.45 who did not have heart failure was used for comparison. Patients who had heart failure were older and more likely to be female and to have a higher incidence of hypertension, diabetes and chronic lung disease than registry patients who did not have heart failure. As a group, patients with heart failure had more severe angina and were more likely to have had a prior myocardial infarction than were registry patients without heart failure. At 6 year follow-up, 82% of patients in the heart failure group survived compared with 91% of patients in the control group (p less than 0.0001). Multivariate analysis using the Cox proportional hazards model identified the following independent predictors of mortality: regional ventricular systolic dysfunction, number of diseased coronary arteries, advanced age, hypertension, lung disease, diabetes, increased left ventricular end-diastolic pressure and heart failure symptoms. Among patients with heart failure, the 6-year survival rate of those who had three-vessel coronary artery disease was 68% compared with 92% for the group without coronary artery disease. However, the 6-year survival rate for patients with heart failure who underwent surgical revascularization of diseased coronary arteries was not significantly improved compared with that of patients treated medically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Congestive heart failure symptoms in patients with preserved left ventricular systolic function: analysis of the CASS registry. 185 5

Exacerbation of heart failure may increase susceptibility to arrhythmias. Therefore tests to assess the risk of arrhythmia, performed after hemodynamic improvement, may be of limited value. To determine whether hemodynamic improvement alters ventricular late potentials detected by signal-averaged ECG, we studied 27 consecutive patients with dilated heart failure (left ventricular ejection fraction 0.20 +/- 0.06, 15 with coronary artery disease) before and 3 +/- 2 days after tailored vasodilator and diuretic therapy reduced ventricular filling pressures. QRS duration, terminal QRS amplitude (root mean square [RMS]), and low-amplitude (less than 40 microV) signal (LAS) duration were determined by an automated algorithm from the vector magnitude of the QRS high-pass filtered at 25 Hz and at 40 Hz. Despite marked decreases in pulmonary capillary wedge (27 +/- 7 to 16 +/- 5 mm Hg, p less than 0.001) and right atrial (13 +/- 7 to 7 +/- 4 mm Hg, p less than 0.001) pressures and a 20% increase in cardiac output, there was not a significant change in QRS duration, RMS, or LAS. Before and after therapy late potentials, defined as abnormal QRS duration RMS, or LAS, were present in 14 (52%) patients with filtering at 25 Hz and in 22 (81%) patients with filtering at 40 Hz. The signal-averaged ECG after hemodynamic improvement predicted the results during exacerbation of heart failure in all patients. Thus in patients with advanced heart failure the signal-averaged ECG obtained after hemodynamic improvement reflects the findings during exacerbation of heart failure.
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PMID:Late potentials are unaltered by ventricular filling pressure reduction in heart failure. 185 28

The relation between left ventricular (LV) shape and functional mitral regurgitation (MR) was evaluated in 39 patients with congestive heart failure. Heart failure was due to coronary artery disease in 23 patients (group I) and to idiopathic dilated cardiomyopathy in 16 (group II). LV shape was quantitated based on the ratio of LV major-to-minor axis and LV sphericity index calculated at end-systole and end-diastole. In group I, 9 patients had angiographic evidence of MR and 14 did not. In group II, 10 patients had MR and 6 did not. Within each group, there were no differences between patients with and without MR with regard to LV chamber volume and regional segmental wall motion abnormalities. In both groups, however, a significant difference was observed between patients with and without MR with respect to end-systolic and end-diastolic LV shape indexes. In group I, the end-systolic major-to-minor axis ratio was lower in patients with (1.42 +/- 0.04) than without (1.72 +/- 0.05) MR (p less than 0.001). Similar differences were observed in group II (1.41 +/- 0.06 vs 1.69 +/- 0.04) (p less than 0.01). In group I, the end-systolic sphericity index was also greater in patients with (0.32 +/- 0.02) than without (0.25 +/- 0.01) MR (p less than 0.02). Similar differences were observed in group II (0.37 +/- 0.03 vs 0.26 +/- 0.01) (p less than 0.02). These data indicate that in patients with severe heart failure, functional MR is present in those who manifest a more spherical LV cavity.
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PMID:Left ventricular shape as a determinant of functional mitral regurgitation in patients with severe heart failure secondary to either coronary artery disease or idiopathic dilated cardiomyopathy. 185 76

Ischemic cardiomyopathy refers to a significant impairment of left ventricular function, a condition resulting from atherosclerotic coronary artery disease. The left ventricular ejection fraction is usually 35% or less, and electron microscopy shows an increased deposition of collagen in the space between the capillaries and the myocytes. The present study shows the alteration in collagen concentration and phenotypes in ischemic cardiomyopathy, and the effect captopril treatment has on these parameters. In patients with ischemic cardiomyopathy, collagen concentration estimated from hydroxyproline increased from 7.96 +/- 1.24 mg/g to 13.9 +/- 1.30 mg/g, P less than 0.05. Ischemic cardiomyopathic patients given captopril therapy had a significantly lower collagen concentration of 10.03 +/- 1.46 mg/g, P less than 0.05. The collagen type I:III ratio decreased from 1.93 +/- 0.52 to 1.23 +/- 0.27 in patients with ischemic cardiomyopathy. Of these patients, those receiving captopril had a collagen type I:III ratio of 1.49 +/- 0.38, which did not differ significantly from the ratio of individuals with normal myocardium. There was no significant difference in type I collagen concentration in the myocardium of normal individuals, patients with ischemic cardiomyopathy, and patients with ischemic cardiomyopathy receiving captopril therapy. The type III collagen concentration increased significantly from 2.56 +/- 0.21 mg/g in normal myocardium to 6.10 +/- 0.58 mg/g in ischemic cardiomyopathic myocardium. Patients receiving captopril had a myocardial collagen type III concentration of 4.87 +/- 0.64 mg/g, which was significantly lower than that found in patients with ischemic cardiomyopathy. An increased deposition of type III collagen may be partly responsible for altering the compliance of the myocardium, resulting in dilatation of the heart and possibly leading to eventual heart failure.
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PMID:Alteration of collagen phenotypes in ischemic cardiomyopathy. 191 69

The relationship between myocardial ischemia and biochemical changes has been well documented. For example, hyperlipidemia is one of the largest risk factors for the development of coronary artery disease. Decreased coronary blood flow produces various changes in cardiac metabolism, which cause severe cardiac function abnormalities, including heart failure and arrhythmias. Many biochemical markers have been used for both diagnosis and evaluation of the severity of myocardial infarction. In this symposium the speakers have discussed: 1) the relationship between the changes in the ionic environments in the intra- and extra-cellular spaces and the genesis of cardiac arrhythmias, with special reference to the role of increased intracellular resistance in conduction delay during ischemia (Dr. Takao Fujino), 2) metabolic basis of ECG abnormalities in ischemic heart disease and the role of intra-coronary ECG recordings in the evaluation of cardiac ischemia (Dr. Tetsunori Saikawa), and 3) biochemical changes associated with exercise and other stresses, with special reference to the roles of increased catecholamines and decreased blood fluidity in the genesis of cardiac abnormalities (Dr. Takehiko Fujino). Prof. Takeshi Kanno gave a special lecture entitled "Approaches from clinical laboratory to hereditary variants". He showed an excellent model of approach from clinical laboratory medicine to detect important biochemical abnormalities which may be overlooked by routine daily analyses in the clinical laboratory.
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PMID:[Cardiac function abnormalities and biochemical changes in myocardial ischemia]. 192 Aug 72

Positive inotropy requires a rise in myocardial oxygen consumption (MVO2); as far as PDE-III-inhibitors' beneficial hemodynamic effects, increases in contractility are controversial, in part probably because accurate proving is rather tedious. The clinician, however, requires a clear concept of whether or not enoximone (EN), for example, carries the risk of myocardial ischemia when used in patients with coronary artery disease. Using the analysis of pressure-volume relations, we recently established contractility-increasing as a partial effect of EN. There are indications suggesting that the inotropy-induced added increase in MVO2 of the PDE-III-inhibitor drugs could be compensated for by the simultaneous vasodilation and changes in compliance, so that as a net effect an unchanged MVO2 might result. Since, on the other hand, PDE-III-inhibitor drugs have been said to generate antiischemic properties, further clinical investigations with EN clearly seemed indicated and they are the subject of the present report: In five patient groups with stabile angina (AP) studied the following parameters and methods, respectively, were used for the evaluation of EN-induced changes of the anginal threshold: exercise, using pacing and ergometry; PA- and PC-pressure measurements; MVO2, indirectly assessed; hemodynamic profile and regional wall motion as assessed in the immediate post pacing phase; ST- T-segment evaluation; thalium-201 perfusion scintigraphy; myocardial perfusion, indirectly assessed. Lack of EN-induced AP (ischemia) and an increased AP threshold indicated that the drug can be used safety in patients with heart failure, including that due to coronary artery disease.
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PMID:[Effects of the phosphodiesterase III inhibitor in ischemic heart disease]. 192 97

Xamoterol is a beta-1 selective partial adrenoceptor agonist. Thirty patients (one female, 29 male, mean age 56 +/- 8 years) with coronary artery disease and mild to moderate heart failure, according to NYHA classes II and III, were studied before and 15 min after intravenous administration of 0.2 mg/kg xamoterol, at rest and during standard, supine bicycle exercise. At rest, the pulmonary capillary wedge pressure fell by 39% (p = 0.0001) and the cardiac index increased by 7% (p = 0.0084); heart rate increased only slightly. With exercise, cardiac index did not change and the pulmonary capillary wedge pressure decreased by 11% (p = 0.0003). In addition, the heart rate dropped from 115 to 105 bt/min (p = 0.0001) which resulted in a decrease of the rate pressure product by 9% (p = 0.0041). Arterial blood pressure remained unchanged. Norepinephrine plasma levels did not change at rest or during exercise, whereas at rest plasma renin activity dropped by 18% (p less than 0.05) and by 20% (p less than 0.05) during exercise. No untoward side effects were observed and the drug was well tolerated. In conclusion, xamoterol, given acutely to patients with heart failure NYHA classes II or III exerted advantageous hemodynamic effects at rest and during exercise.
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PMID:[Hemodynamic and humoral changes following intravenous administration of xamoterol in patients with heart failure and coronary heart disease]. 196 85

The beta-blocker carvedilol has been shown to induce vasodilation in patients with coronary artery disease. In a double-blind, randomized, placebo-controlled cross-over study, we looked for the acute vasodilating effect after i.v. administration in patients with heart failure. In 10 patients with coronary artery disease and six patients with dilated cardiomyopathy, all with an ejection fraction lower than 40%, the rate-pressure-product during supine ergometry and Swan-Ganz-catheterization rose to a significantly smaller extent after 5 mg carvedilol i.v. compared to placebo. This was mainly due to a lower heart rate at rest and during exercise, while blood pressure was not changed compared to placebo. Calculated total peripheral resistance during exercise after carvedilol was higher--significantly so in the CAD-group--than after placebo. These results show that in patients with heart failure, an acute vasodilating effect of i.v. carvedilol is not detectable.
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PMID:[Acute hemodynamic effects of the vasodilator beta blocker carvedilol in heart failure]. 197

Postoperative use of as-needed intramuscular narcotics is potentially hazardous in frail elderly patients. Patient-controlled analgesia (PCA) allows patients to self-administer small boluses of narcotic, allowing better dose titration, enhanced responsiveness to variability in narcotic requirements, and reduction in serum narcotic level fluctuation. Although theoretically useful, this method has not bee well studied in the elderly or medically ill. A prospective controlled trial among 83 higher-risk elderly men after major elective surgery compared PCA containing morphine sulfate with intramuscular morphine injections as needed (mean [+/- SD] age, 67.4 +/- 5.6 vs 67.0 +/- 6.3 years). Subjects had a variety of medical illnesses, including chronic lung disease (57%), coronary artery disease (43%), heart failure (13%), and liver disease (12%). Preoperative and postoperative assessments included chest roentgenograms; daily mental status and pulmonary function testing; twice-daily serum morphine levels; and oxygen saturation values, linear analogue pain and sedation scores, and vital signs every 2 hours. Care was taken to optimize narcotic administration in control subjects as well as PCA subjects. Analgesia was significantly improved by PCA (3-day mean pain score, 40.5 +/- 18.0 vs 32.5 +/- 15.0), without an increase in sedation. Significant postoperative confusion (18% vs 2.3%) and severe pulmonary complications (10% vs 0%) occurred significantly more frequently in intramuscular-treated controls. Patient-controlled analgesia was quickly mastered by most patients; no major problems referable to its use occurred. Patients who had previously received intramuscular injections reported that PCA was easier to use and provided better analgesia. Serum morphine levels showed significantly less variability on postoperative day 1 with PCA, compared with intramuscular injections. We conclude that PCA is an improved method of postoperative analgesia in high-risk elderly men with normal mental status, compared with as-needed intramuscular injections.
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PMID:Randomized trial of postoperative patient-controlled analgesia vs intramuscular narcotics in frail elderly men. 197 90


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