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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the converting enzyme inhibitor captopril as long term treatment was investigated in 14 patients with severe congestive heart failure in a double blind trial. Captopril reduced plasma concentrations of angiotensin II and noradrenaline, with a converse increase in active renin concentration. Effective renal plasma flow increased and renal vascular resistance fell; glomerular filtration rate did not change. Serum urea and creatinine concentrations rose. Both serum and total body potassium contents increased; there were no long term changes in serum concentration or total body content of sodium. Exercise tolerance was appreciably improved, and dyspnoea and fatigue lessened. Left ventricular end systolic and end diastolic dimensions were reduced. There was an appreciable reduction in complex ventricular ectopic rhythms. Adverse effects were few: weight gain and fluid retention were evident in five patients when captopril was introduced and two patients initially experienced mild postural dizziness; rashes in two patients did not recur when the drug was reintroduced at a lower dose; there was a significant reduction in white cell count overall, but the lowest individual white cell count was 4000 X 10(6)/l. Captopril thus seemed to be of considerable value in the long term treatment of severe cardiac failure.
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PMID:Captopril in heart failure. A double blind controlled trial. 638 12

The cause of exercise intolerance in congestive heart failure is unclear. Hemodynamic and ventilatory responses were measured during symptomatic maximal upright bicycle exercise in 28 patients with chronic severe left ventricular failure who achieved a maximal oxygen uptake of only 12 +/- 4 ml/min/kg (+/- standard deviation). All patients reached anaerobic metabolism as the respiratory exchange ratio rose and arterial pH fell significantly. Pulmonary capillary wedge pressure increased from 20 +/- 10 mm Hg at rest to 38 +/- 9 mm Hg at peak exercise and cardiac index increased from 2.51 +/- 0.73 to 4.54 +/- 1.65 liters/min/m2 (both p less than 0.001). Systemic vascular resistance decreased, but pulmonary vascular resistance did not change during exercise. Despite the marked pulmonary venous hypertension at peak exercise, blood gases were unchanged (PaO2, 96 +/- 15 mm Hg; PaCO2, 35 +/- 7 mm Hg). Systemic arterial oxygen content increased from 16 +/- 2 to 17 +/- 2 vol% (p less than 0.01). Changes in pulmonary capillary wedge pressure did not correlate with changes in arterial oxygen content. Results were similar whether patients were limited by dyspnea or fatigue. Thus, exercise intolerance in patients with severe left ventricular failure is associated with marked elevation of pulmonary capillary wedge pressure and anaerobic metabolism without hypoxemia or altered carbon dioxide tension. These findings suggest that exercise ability in congestive heart failure is more dependent on cardiac output than on ventilatory consequences of pulmonary congestion.
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PMID:Relation between hemodynamic and ventilatory responses in determining exercise capacity in severe congestive heart failure. 641 73

Based on the findings of 50 patients with infective endocarditis, 37 affecting the aortic, six the mitral and seven both the aortic and mitral valves, in addition to analysis of predisposing factors, prominent signs and symptoms distinctive for the clinical entity were assessed (Tables 1 to 3). Preexistent conditions such as aortic valve lesions including bicuspid aortic valve as well as mitral valve lesions including mitral valve prolapse were proven in 66%. Factors which may have compromised host defense mechanisms such as cachexia and chronic alcohol or intravenous drug abuse were present in isolated cases. In 38% of the patients, a diagnostic or therapeutic manipulation, suspected to have given rise to the bacteremia, antedated the onset of endocarditis. Malaise, fatigue and chills were the most frequent symptoms (Table 4). Fever and cardiac murmurs were observed in all patients, anemia and bacteremia in 74% of the patients, respectively (Tables 4 to 6). In blood cultures, the most common microorganisms were found to be hemolytic and nonhemolytic streptococci accounting for 65% of positive findings, followed by enterococci and gram-negative bacteria each with 14% respectively (Table 6). Congestive heart failure predominated among cardiac complications with its occurrence in 84% of the patients. Valvular ring or myocardial abscess, aortic or sinus of Valsalva aneurysm, occasionally with perforation, were found in 24% of our patients. Coronary embolism was documented in 6%; infection-associated pericarditis was observed only rarely (Table 7). Extracardiac complications involved the skin, central nervous system, spleen and kidneys, respectively, in 20 to 30% of the patients. Complications afflicting the eyes, lungs, gastrointestinal tract and the musculo-skeletal system were seen with a lesser frequency of 0 to 12% (Table 8). The diagnosis of infective endocarditis, rendered highly-probable by the constellation of fever, cardiac murmur, bacteremia and anemia, necessitates, however, confirmation through cardiac examinations. In this respect, electrocardiographic and radiologic findings are of limited value, although they may be useful in the detection of cardiac complications. In 6% of the patients, positive criteria for myocardial infarction were indicative of coronary embolism and, i 30%, atrioventricular or fascicular block suggested the presence of abscess formation (Table 9). As radiologic evidence of heart failure, 74% of the patients were found to have pulmonary vascular congestion (Table 10).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Detection and evaluation of infectious endocarditis]. 664 98

Twelve patients with severe chronic congestive heart failure (CHF) received prazosin in a dose of 4 to 20 mg daily for a period of 2 months, in addition to cardiac glycoside and diuretic drugs. After this treatment left ventricular end-diastolic diameter decreased from 5.7 +/- 0.4 to 5.4 +/- 0.4 cm (p less than 0.001), left ventricular end-systolic diameter decreased from 4.3 +/- 0.5 to 4 +/- 0.5 (p less than 0.001), left ventricular stroke excursion increased from 1.03 +/- 0.11 to 1.27 +/- 0.15 cm (p less than 0.01), the ejection fraction increased from 24.9 +/- 2.1 to 32.2 +/- 2.8 (p less than 0.001) and the mean velocity of circumferential fiber shortening increased from 0.68 +/- 0.06 to 0.79 +/- 0.08 circumferences/s (p = 0.06). Prazosin treatment clearly relieved dyspnea and fatigue. Three patients improved from Class IV to Class III, four patients improved from Class IV to Class II and 3 patients from Class III to Class II.
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PMID:The effects of prazosin in severe congestive heart failure. An echocardiographic study. 671 45

The maximal exercise capacity of patients with congestive heart failure (CHF) is frequently reduced, partly because of inadequate skeletal muscle nutritive flow. To investigate whether this altered muscle nutritive flow is a result of inability of the heart to increase cardiac output normally during exercise, the effect of dobutamine on systemic and leg blood flow and metabolism during maximal exercise was examined in 11 patients with CHF. At maximal exercise before dobutamine, all patients were limited by fatigue and had reduced maximal systemic oxygen uptake (11.9 +/- 1.1 ml/min/kg) (+/- standard error of the mean), markedly elevated leg oxygen extraction (85 +/- 2%) and elevated femoral venous lactate (53 +/- 5 mg/dl), consistent with impaired nutritive flow to working muscle. Dobutamine increased the peak cardiac output from (6.5 +/- 0.9 0.74 +/- 0.7 liters/min, p less than 0.01) and peak leg flow (from 1.7 +/- 0.3 to 2.1 +/- 0.3 liters/min, p less than 0.05) during exercise. In contrast, no change occurred in maximal exercise duration (5.5 +/- 0.8 vs 5.8 +/- 0.8 min), peak systemic VO2 (829 +/- 97 vs 869 +/- 77 ml/min), peak arterial lactate (34 +/- 2 vs 35 +/- 4 mg/dl) or peak leg lactate output (248 +/- 39 vs 275 +/- 53 mg/min), whereas peak leg oxygen extraction decreased (85 +/- 2 to 80 +/- 2%, p less than 0.01), suggesting no improvement in muscle nutritive flow. These data suggest that nutritive flow to working skeletal muscle is impaired in patients with CHF and that this impairment is not due simply to an inability of the heart to increase the cardiac output normally during exercise.
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PMID:Impaired skeletal muscle nutritive flow during exercise in patients with congestive heart failure: role of cardiac pump dysfunction as determined by the effect of dobutamine. 671 33

Artificial pacing of the heart has evolved rapidly over the last 20 years; the physician can now implant "physiologic" pacemakers that preserve the natural order of atrial and ventricular systole. The commonly used pacemakers that pace only the ventricle can induce dizziness, fatigue and syncope and increase congestive heart failure. Physiologic pacemakers can eliminate many of these side effects, but they are more expensive, can be less durable and may induce arrhythmias. Physiologic pacing can provide the greatest benefit and cost-effectiveness when the particular functions of the device are matched to the specific needs of the patient.
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PMID:Artificial cardiac stimulation: a current view of physiologic pacemakers. 685 Apr 63

The exact incidence of diaphragmatic paralysis complicating secondary heart procedures is not known. The postoperative period can be complicated by difficulty in weaning from mechanical ventilation and misinterpretation of the clinical signs of respiratory muscle fatigue for congestive heart failure and acute bronchospasm. We present 3 patients, all of whom had right diaphragmatic paralysis and recurrent respiratory failure after a second mitral valve replacement. Long-term management with night-time ventilation in 2 patients resulted in no further episodes of respiratory failure and physical rehabilitation with exercise tolerance significantly greater than the preoperative state.
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PMID:Long-term management of diaphragmatic paralysis complicating prosthetic valve replacement. 685 2

The role of pindolol in treating ventricular arrhythmia was studied in 43 patients with this disorder. Of these patients, 23 had coronary heart disease, 5 had valvular disease, and 15 had no demonstrable heart disease. patients underwent acute drug testing with 20 mg pindolol (phase 1) followed by maintenance therapy (phase 2) for 3 days (20 to 80 mg daily). Efficacy during both phases was evaluated by ambulatory monitoring and treadmill exercise testing. During acute drug testing, 50% of te patients responded. A concordant response between acute drug testing and phase 2 monitoring was seen in 81% (p less than 0.005) of patients and between acute drug testing and phase 2 exercise testing in 88% (p less than 0.005). Arrhythmia was suppressed during the phase 2 exercise test in 53% of patients; these included 80% of the patients without heart disease and 50% of those with coronary heart disease (not significant). During phase 2 monitoring, 60% of patients without heart disease responded vs. 25% with coronary heart disease (not significant). Side effects occurred in 12 patients (28%). These included congestive heart failure (3 patients); fatigue, lightheadedness, and insomnia (2 patients each); nausea, tremor, urinary retention, and bronchospasm (1 patient each); and aggravation of arrhythmia (7 patients). It is concluded that although pindolol alone is marginally effective for treating ventricular arrhythmia in patients with coronary heart disease, it appears to be more valuable in those without heart disease, especially when arrhythmia is provided by exercise. Acute drug testing proved highly predictive of the results with maintenance therapy and is a valuable rapid-screening procedure for identifying potential responders to pindolol.
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PMID:Pindolol for ventricular arrhythmia. 710 35

The cardiocirculatory actions on the oral vasodilator prazosin were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise and symptoms in patients with advanced long-standing congestive heart failure. The administration of oral prazosin (2 to 7 mg) reduced forearm venous tone and forearm vascular resistance. Concomitantly, mean systemic arterial pressure and left ventricular filling pressure decreased, and the cardiac index increased. These effects of a single dose of prazosin on left ventricular function were rapid in onset, maximal at 1 hour and sustained for the entire 6-hour period of observation. After two weeks of outpatient therapy with 2 to 7 mg of prazosin four times daily, echographic end-diastolic dimension decreased, whereas the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of prazosin therapy, and there was an improvement in the New York Heart Association functional class from 3.7 to 2.2. Thus, prazosin possesses sustained nitroprusside-like balanced dilator actions of the systemic arterial and venous beds, which are effectively translated into the beneficial hemodynamic effects of augmenting cardiac output and relieving excessive left ventricular end-diastolic pressure. The delayed vasodilator tolerance that occurs in 30 percent of the patients is prevented by the prior use of aldosterone antagonists and is easily treated when present. Subacute hemodynamic suppression of beneficial prazosin vasodilator actions is transient and does not preclude successful sustained prazosin therapy of severe heart failure.
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PMID:Therapeutic application of prazosin in chronic refractory congestive heart failure. Tolerance and "tachyphylaxis" in perspective. 724 73

The objectives of exercise testing in congestive heart failure (CHF) may be summarized as follows: (a) detect impaired cardiac performance, (b) grade severity of cardiac failure and classify functional capability, and (c) assess effects of interventions. Several different methods are available to make these assessments, and we have to ask ourselves how well exercise testing achieves these objectives. It has to be kept in mind that the power generated by the exercising muscles is dependent on the oxygen delivery to the skeletal muscles. Oxygen uptake is the result of an integrated performance of the lungs, heart, and peripheral circulation. In patients, as well as in normal subjects, oxygen uptake is related to hemodynamic indices such as cardiac output, stroke volume, or exercise duration when a stepwise regulated maximal exercise protocol is used. However, there are major differences in the concept of a true maximum in normal subjects versus heart failure patients. Fit-normal subjects will achieve a real maximal oxygen uptake, whereas patients may stop testing before a maximum is reached because of symptoms such as dyspnea or leg fatigue. Therefore, it is better if the actual oxygen uptake can be measured. "Peak" rather than true maximal oxygen uptake has been suggested for the classification of the severity of heart failure. Peripheral factors modify the cardiac output through such factors as vascular resistance, organ function, and hormonal release. Maximal exercise will stress the cardiovascular system to a point where the weakest chain will impose a limiting effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of exercise testing in heart failure. 751 35


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