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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite the total-body consequences of congestive heart failure, little information is available on the distribution of cardiac output and regional-organ hemodynamics in this condition in humans. Technical and methodologic limitations probably account for the paucity of data in this area. Available data indicate that blood flow to the regions or organs studied, namely, the kidneys, hepatosplanchnic region, and upper limbs, decreases in proportion to the reduction in cardiac output. However, renal blood flow appears to be protected in human heart failure by a form of "autoregulation" during marked depression of cardiac output (less than 2.0 L/min/m2). Results of preliminary studies suggest that the regulation of regional-organ hemodynamics is disturbed in this human condition. Cardioactive drugs profoundly affect regional-organ hemodynamics independent of changes in central hemodynamics and cardiac output. The determination of regional blood flow responses in human heart failure will become more important as we expand our knowledge base of the pathophysiology of heart failure, learn more about local vascular control mechanisms, and pursue the potential therapeutic objective of selectively augmenting regional-organ hemodynamics and function.
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PMID:Regional blood flow in human congestive heart failure. 151 1

Over the past decade we have seen a shift in the strategy for the treatment of hypertension, from stepped therapy--involving a highly structured, unvarying series of steps--to recommendations for more individualized treatment. How shall we accomplish that goal? Severe hypertension provides a clear indication to bypass earlier recommendations. Demographic data such as age, gender, and race, often cited, have proved less helpful. Concomitant medical problems, which are found in greater than 50% of hypertensive patients, are most often the crucial determinants in the selection of antihypertensive therapy. Concurrent coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, chronic obstructive pulmonary disease, borderline cognitive dysfunction, anxiety, and depression are all common. Each has implications for antihypertensive therapy. Moreover, blood pressure reduction is a surrogate for our real goal, which is reduction of cardiovascular risk. Thus, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, hyperlipidemia, and insulin resistance as additional risk factors in hypertension. Consideration of all of these factors makes it possible to individualize antihypertensive therapy in most patients.
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PMID:Evolution of the treatment of hypertension: what really matters in the 1990s? 151 35

During the acute phase of myocardial infarction, the generation of thrombin is reflected in the sudden rise of fibrinopeptide A (FPA) and the thrombin-antithrombin III (TAT) complex in blood. We have systematically determined the FPA and TAT plasma concentrations over a period of 14 days after acute myocardial infarction in 100 patients. Mean levels of both thrombin markers were the highest on admission, remained elevated over the following few days, and then gradually declined after day 5. Still, by the end of the first week two thirds of the patients had distinctly elevated TAT and FPA levels, and by the end of the second week such an abnormality was present in half of them. Continuous intravenous heparin infusion at a dose of 20,000 units/day, administered for 1 week to patients who had either received (n = 21) or not received (n = 17) streptokinase, led to a significant depression (p less than 0.05) of thrombin markers over the first 48 hours, an effect that did not persist over the subsequent days of treatment. In patients not assigned to heparin treatment, those in heart failure had significantly (p less than 0.05) higher mean TAT and FPA values on days 3, 5, and 7 compared with patients in whom heart failure was absent. Infarct extension, pulmonary embolism, and death were also associated with a rise in one or both thrombin markers, often preceding the onset of clinical symptoms. Thrombinogenesis was not accompanied by changes in mean plasma concentrations of prothrombin, antithrombin III, or alpha 2-macroglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent generation of thrombin after acute myocardial infarction. 157 16

Although evaluation of the treatment of congestive heart failure is usually based on objective clinical outcomes, patient self-assessment is increasingly recognized as an important component of evaluation. A study was designed to measure the quality of life of 134 patients with symptoms of advanced heart failure who were being evaluated for possible heart transplantation. The patients' quality of life was assessed using a mix of subjective and objective measures, including functional status, physical symptoms, emotional state, and psychosocial adaptation. There was no significant relationship between patients' cardiac ejection fraction and any quality-of-life measures; however, the results of a 6-minute walking test, New York Heart Association classification, and self-reported functional status were all significantly correlated with psychosocial adjustment. Self-reported functional status, depression, and hostility accounted for 43% of the variance in total psychosocial adjustment to illness. These findings support the inclusion of quality of life as an outcome measure in any evaluation of treatment efficacy and suggest that interventions to improve the quality of life of patients with advanced heart failure need to be targeted at reducing depression and hostility and increasing daily activity levels.
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PMID:Quality of life in patients with advanced heart failure. 157 33

To determine whether heart failure is a consequence of alterations in cardiac cellular performance, myocytes were isolated from Fischer 344 rats at 4, 12, 20, and 29 mo of age and studied mechanically and morphometrically. Left ventricular myocyte length increased by 14.5, 14.4, and 24.0% at 12, 20, and 29 mo when compared with 4-mo-old animals. An 11.4 and 14.2% increase in length was seen for right ventricular myocytes from 4 to 12 mo and from 20 to 29 mo, respectively. Although no change in cell width was seen in either ventricle as a function of age, myocardial cells were more irregular in shape and consistently longer in the left ventricle at 20 and 29 mo. Left myocytes at 29 mo revealed diminished velocities of shortening (31.7%) and relengthening (59.5%). Contraction duration increased due to a 28.9% prolongation of time to peak shortening and a 26.5% increase in time to relengthening, resulting in a 25.8% decrease in myocyte shortening at 29 mo. Similar changes were observed in right ventricular myocytes, but they occurred later in life. Thus the alterations in myocyte geometry and depression in contractile performance seen here are major contributors to the eccentric dilated ventricular chamber and diminished pump function previously documented in the age-related transition from normal cardiac dynamics to left ventricular dysfunction and failure.
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PMID:Cellular mechanisms of ventricular failure: myocyte kinetics and geometry with age. 162 35

We have previously demonstrated that in furazolidone-induced congestive heart failure in turkeys the specific Ca(2+)-ATPase activity of myocardial sarcoplasmic reticulum (SR) is 60% increased in compensation for a 50% depression in net Ca(2+)-sequestration activity. This study tested the hypothesis that SR Ca(2+)-uptake and Ca(2+)-ATPase activities were uncoupled in this cardiomyopathy because of increased Ca(2+)-release channel activity. A novel microassay was used to monitor Ca2+ transport by myocardial homogenates using the fluorescent Ca2+ dye indo 1 to indicate extravesicular ionized Ca2+. The method is applied to cyropreserved biopsy specimens of myocardium and requires only 50 mg tissue. Both SR Ca(2+)-pump and SR Ca(2+)-channel activity were estimated using the channel-inhibitor ruthenium red (RR) and the mitochondrial inhibitor sodium azide. The specificity of the RR inhibition was confirmed using ryanodine. Cardiomyopathy was induced in 2-week-old turkey poults by the addition of 0.07% furazolidone to their feed for 4 weeks. Compared with controls, myocardial maximal Ca(2+)-channel activity relative to maximal Ca(2+)-pump activity was 22% greater and duration of Ca(2+)-channel activity was 100% increased. However, the heart failure birds had 43 and 53% decreases in absolute maximal Ca(2+)-pumping and Ca(2+)-channel activities, respectively. The abnormal Ca(2+)-channel activity resulted in 200% greater time before initiation of net Ca2+ sequestration and 700% greater final myocardial Ca2+ concentrations. For all birds, the Ca(2+)-accumulating activity was highly correlated with Ca(2+)-release activity (all p less than 0.05). These data indicate that in this animal model of congestive heart failure there is defective SR Ca(2+)-channel function resulting in abnormal Ca2+ homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial calcium cycling defect in furazolidone cardiomyopathy. 166 32

Although alcohol has long been known to induce cardiac depression and cardiomyopathy, it is not known whether drug therapy or pharmacologic manipulation can be used to prevent or reverse these toxicities. With this in mind, high levels (15 mM) of magnesium (Mg) were investigated for their potential antialcohol effects on perfused rat hearts. A high concentration of ethanol (135 mM) was used to induce rapid cardiac failure as assessed by hemodynamic and metabolic parameters. During ethanol perfusion in normal 1.2 mM [Mg2+]o physiologic salt solution, coronary flow decreased immediately, and all of the hemodynamic parameters studied (except for heart rate) were depressed significantly. After 10 min of 135 mM ethanol perfusion, only 60% of the hearts kept beating; at 15 min, only 42% of the hearts continued to beat. Myocardial metabolism under such conditions as assessed by examination of coronary effluent concentrations of lactic acid (LA), lactic acid dehydrogenase (LDH) and creatine phosphokinase (CPK) was rapidly and severely compromised. Although 15 mM MgSO4 alone did not alter coronary flow and systolic pressure under the conditions studied, it did decrease cardiac output, heart rate and total pressure developed. However, when 15 mM MgSO4 was given 10 min before ethanol, and continued during ethanol perfusion, the usual depression in all assessed cardiac hemodynamic parameters (except heart rate) caused by ethanol was not observed. During 15 min of high [Mg2+]o perfusion, coronary flow recovered from 19.1 +/- 6.8% (ethanol alone) to 68.1 +/- 9.9% of control values (p < 0.01); cardiac output recovered from 10.4 +/- 4.6% (ethanol alone) to 43.6 +/- 7.5% of control (p < 0.01); stroke volume went from 12.9 +/- 5.8% (ethanol alone) to 97.1 +/- 14.5% of control (p < 0.01); systolic pressure from 55.3 +/- 3.6% (ethanol alone) to 88.8 +/- 4.0% of control (p < 0.01), and total pressure developed from 23.9 +/- 7.8% (ethanol alone) to 35.0 +/- 4.5% of control (p < 0.05). Assessment of the metabolic biochemical parameters supported these changes in hemodynamic improvement. For example, LA, LDH and CPK all went from elevated values towards normal levels. There were similar hemodynamic and metabolic responses to high [Mg2+]o given during ethanol perfusion to that given before ethanol perfusion. The hemodynamic and metabolic beneficial effects between groups pretreated or treated with high [Mg2+]o exhibited no significant differences. These results suggest that high [Mg2+]o (15 mM) given either before or during ethanol-induced cardiotoxicity is effective in attenuating both functional and metabolic damage caused by high ethanol perfusion in the rat heart.
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PMID:Beneficial effects of high magnesium on alcohol-induced cardiac failure. 166 23

The cardiovascular effects of the phenyldihydropyridine derivative elgodipine (0.3, 1, 3, 10, and 30 microgram/kg/min) were studied in normal conscious pigs and in pigs with chronic left ventricular dysfunction (LVD, caused by coronary artery occlusion) without and after beta-adrenoceptor blockade with propranolol (0.5 mg/kg + 0.5 mg/kg/h). In normal pigs, elgodipine increased cardiac output from 2.57 +/- 0.09 to 5.21 +/- 0.24 L/min (p less than 0.05) as a result of a doubling of the heart rate. Mean arterial blood pressure decreased from 94 +/- 2 to 76 +/- 3 mm Hg (p less than 0.05) as a result of a decrease in systemic vascular resistance. Left ventricular (LV) dP/dtmax increased (by up to 78 +/- 9%), but left ventricular end-diastolic pressure (LVEDP) remained unchanged. After propranolol administration elgodipine did not increase LV dP/dtmax, and the increase in heart rate was attenuated, resulting in a smaller increase in cardiac output (from 2.11 +/- 0.13 to 3.09 +/- 0.23 L/min, p less than 0.05), but an unchanged vasodilator response. In pigs with LVD, elgodipine increased cardiac output and LV dP/dtmax less than in normal animals, but the vasodilator response was not affected. LVEDP decreased from 14.6 +/- 1.6 to 11.7 +/- 2.5 mm Hg (p less than 0.05). In animals with LVD, propranolol caused a more severe depression of systemic hemodynamics, but did not modify the cardiovascular responses to elgodipine. Its cardiovascular profile suggests that elgodipine may not only be useful in the treatment of cardiovascular disorders for which other dihydropyridines are already in use, but also in mild chronic heart failure.
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PMID:Cardiovascular effects of elgodipine in conscious pigs with a normal coronary circulation and in conscious pigs with a healed myocardial infarction. 171 24

Patients with left ventricular hypertrophy (LVH) often exhibit manifestations of myocardial ischemia. In 17 hypertensive patients (group 1, mean age of 56 +/- 4 years, 10 females, 7 males) with ST-segment depression during the exercise electrocardiogram (ECG) and effort angina and normal coronary arteriograms, the left ventricular function at rest and during exercise was studied by heart catheterization. The results were compared with 17 hypertensive patients (group 2, mean age of 56 +/- 6 years, 6 females, 11 males) with coronary artery disease (CAD). The normal pulmonary wedge pressure at rest (group 1, 8.9 +/- 3 mm Hg; group 2, 8.9 +/- 3 mm Hg) was pathologically increased (p less than 0.001) in both groups (group 1, 27.1 +/- 5 mm Hg; group 2, 28.8 +/- 7 mm Hg) even at a work load of 50 W with a further increase at 75 W to 31 +/- 4 and 29.7 +/- 4 mm Hg, respectively. Cardiac output was normal. There was no significant correlation between ST-segment depression, pulmonary wedge pressure, LVH, and Holter ECG. Hypertensive patients without CAD may reveal a disturbed pump function due to ischemia even at low work loads, which does not differ significantly from patients with CAD. This may provoke subendocardial fibrosis and thereby contribute to the development of heart failure.
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PMID:Impaired left ventricular function during exercise in hypertensive patients with normal coronary arteriograms. 171 61

Holter monitoring was performed on days 1-2, 6-9 of the disease and on days 30-60 before their discharge from hospital in 54 patients with acute gross myocardial infarction. The presence of cardiac rhythm and conduction disturbances and ischemic ST-segment depression or elevation was evaluated. The patients having frequent and prolonged (more than 3 hours during a 2-day follow-up) showed a complicated course of the disease: recurrent pain syndrome, signs of heart failure, prolonged cardiac arrhythmias, and fatal outcomes. The patients with uncomplicated acute myocardial infarction had no long-term episodes of ischemic ST-segment depression or elevation, as recorded by Holter monitoring in the first 2 days of the disease. On days 6-9 no cardiac rhythm and conduction disturbances that had been observed in them were recorded. The patients in whom the episodes of silent myocardial infarction remained on their discharge exhibited a high (35%) incidence of myocardial infarction recurrence within a year.
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PMID:[Study of the dynamics of cardiac rhythm and the ST segment in patients with acute myocardial infarction based on the data of Holter ECG monitoring]. 171 34


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