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

Vasodilator and inotropic drugs work through independent mechanisms in augmenting left ventricular pump function in patients with heart failure. The selection between these two classes of pharmacologic agents for an individual patient may be based on the control blood pressure as well as the underlying disease. Although vasodilator drugs are easiest and safest to employ in patients with normal or high arterial presure levels, even in relatively hypotensive subjects (systolic arterial pressure less than 105 mm Hg), a salutary hemodynamic effect can be achieved without an undue decrease in pressure. Inotropic drugs may be safest to administer to patients without coronary artery disease, but the oxygen-consuming effect of these drugs need not necessarily have an adverse effect on patients with ischemic heart disease. Combined vasodilator and inotropic drug therapy is the most potent pharmacologic means of restoring pump function in patients with severe heart failure. The long-term use of vasodilator and inotropic drugs in the treatment of heart failure is dependent on the availability of agents that will produce a sustained hemodynamic effect. Hydralazine, nitrates and prazosin have been employed alone or in combination and provide a promising approach to vasodilator treatment of heart failure. Better and more selective oral inotropic agents are needed to allow this therapeutic modality to be employed optimally.
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PMID:Selection of vasodilator, inotropic or combined therapy for the management of heart failure. 68 92

The effect of permanent pacing on chronic complete atrioventricular block complicated by cardiac failure was studied in 6 patients by measurement of indirect left atrial pressure 15 minutes after institution of pacing and again 3 to 12 months later. In addition, 21 patients with complete heart block and clinical plus radiological evidence of cardiac failure at the time of pacing 3 to 6 years earlier were also reviewed. Only 1 of 6 patients studied haemodynamically improved and 1 died in cardiac failure. Of 21 patients assessed clinically, 10 had improved and 8 had died after a mean follow-up of 53 months. In the absence of syncope, pacing was of little symptomatic benefit but still may be justified to prolong survival. Both studies indicated a particularly poor prognosis for patients known to have coronary artery disease. No reliable means were found of determining the prognosis in the individual patient with cardiac failure before pacing.
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PMID:Value of pacing in cardiac failure associated with chronic atrioventricular block. 68 87

The cardiovascular system of aging people exhibits a number of morphological, functional and clinical special features. Alterations in shape, size and weight of the heart, alterations of coronary arteries, valves and aorta are accompanied by typical changes in several hemodynamics variables. The result is a diminution of the adaptation capacity to physical exertion and increased incidence of failure. However, heart failure cannot be regarded as a physiological process; it is caused by a coincidence of an increasing polypathy of the aging heart (coronary artery disease, arteriosclerosis, hypertrophy, valve-changes,disseminated degenerative changes) and the polypathy or multimorbidity of the whole aging organism. In advanced age the various forms of ischaemic heart disease (angina pectoris, infarction, failure, arrhythmias) show increasingly atypical courses, complications and a higher degree of mortality. Modern therapeutic measures like demand pacemakers or bypass operations are principally applicable. Our study of now 326 patients of very high age shows that the good state of their cardiovascular system (probably genetically determined) is mainly responsible for reaching high age.
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PMID:[The so-called aging heart in 50- to 100-year-old subjects]. 79

Of 88 consecutive patients aged 20 to 77 years with severe symptomatic aortic valve disease requiring surgery, 51 patients had angina pectoris; of these 51, 41 had predominant aortic stenosis and 10 had severe aortic regurgitation. All patients with angina pectoris underwent coronary angiography; significant coronary arterial disease was encounted in 24 per cent of those with aortic stenosis and 20 per cent of those with aortic regurgitation. By contrast, of 37 patients without angina pectoris 19 underwent coronary arteriography; none showed significant coronary artery disease (P smaller than 0.05). Among patients with angina pectoris, 17 per cent of those with aortic stenosis experienced prolonged, rest or nocturnal pain, compared to 70 per cent of those with aortic regurgitation (P smaller than 0.005). At the time of onset of angina pectoris, there were features of heart failure in 34 per cent of those with aortic stenosis, and in 90 per cent of those with aortic regurgitation (P smaller than 0.005). Nitroglycerin promptly relieved angina pectoris in 56 percent of patients with aortic stenosis and in 50 per cent of those with aortic regurgitation (P smaller than 0.05). Neither the pattern of angina pectoris nor the response to nitroglycerin was dependent upon the coexistence of significant coronary artery disease. In patients with aortic stenosis, there was not significant difference between those with angina pectoris, and those without angina with regard to left ventricular end-diastolic volume, end-diastolic pressure, ejection fraction, peak systolic pressure, wall thickness, cardiac index, or the product of these factors. In patients with aortic regurgitation, cardiac index was significantly lower (P smaller than 0.05), left ventricular end-diastolic volume tended to be larger, and ejection fraction tended to be lower in patients with angina pectoris as opposed to those without angina pectoris.
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PMID:Clinical, haemodynamic, and coronary angiographic correlates of angina pectoris in patients with severe aortic valve disease. 80 13

1. Study of a group of 50 patients suspected to have coronary artery disease. This is a complement to a previous study concerning "definite" coronary patients. 2. The method followed consisted in cross-examination of the files by three observers in order to separate the subjects who seemed really affected by coronary artery disease. This treble examination led to a rather restrictive selection. To facilitate the study, the patients were subdivided into 4 groups: patients with arterial hypertension, with diabetes mellitus, with cardiac failure, with a heart disease and miscellaneous patients. 3. The study of the 20 files which were discarded was peculiarly interesting as it provided the opportunity to underline the differential diagnosis either with common diseases (left ventricular overload, heart block, brain vascular accident), or with more specific diseases for Black Africa (endomyocardial fibrosis, aneurysm of the left ventricle, cardiomyopathy). In that respect, it is underlined that, in the absence of any anatomical or functional disease, the electrocardiogram of the healthy Black is identical to that of the White. 4. Study of the 30 patients considered as coronary made it possible to underline aetiological and epidemiological factors, although some are still lacking. However the facts observed could be compared with those reported in a previous work concerning 45 "definite" coronary patients. The overall documents thus gathered in 75 patients suggest that the African candidate to coronary artery diseases resembles his Occidental homologue, but that he might have kept a traditional diet.
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PMID:[Coronary diseases in the black African. Apropos of a 2d group of 50 patients. Diagnostic and epidemiological aspects]. 80 91

Acute changes in the diastolic pressure-volume relationship of the left ventricle. Europ. J. Cardiol., 4/Suppl., 105-120. The present study was designed to investigate acute changes in the passive length-tension relations of isolated heart muscle and acute alterations of the left ventricular diastolic pressure-volume relationship of patients. In isolated heart muscle a constant lengthening and shortening technique with computer curve fitting was used to characterize the entire passive length-tension relation. There was no change in passive elastivity following an increase in stimulation frequency or an increase in muscle stretching rate. During the transition from stimulated to nonstimulated contractions, there was a shift to the left in the passive length-tension relation, with a shorter muscle length at the same resting force. In 10 patients undergoing revascularization for preinfarction angina, 7 patients showed a significantly reduced left ventricular enddiastolic pressure at the same enddiastolic volume, together with an improvement in postoperative ejection fraction. In 6 patients who experienced a perioperative myocardial infarction, variable changes in the pressure volume relationship occurred. These presumably reflected the opposite effects of stiffening of infarcted muscle and cardiac dilatation secondary to heart failure. 26 patients with chronic coronary artery disease had ventriculograms before and after 0.4 mg sublingual nitroglycerin. 9 patients showed a significant shift downwards in their pressure-volume relation, with a decreased enddiastolic pressure at the same volume. 2 showed a shift upwards, while the remaining patients showed no measurable change. It is proposed that this latter shift in pressure-volume relationships is due to hemodynamic factors rather than to intrinsic changes in muscle stiffness. Theoretical calculations utilizing A SIMPLIFIED SPHERICAL MODEL of the ventricle suggest that the magnitude of the changes observed cannot be explained by stiffening of the muscle alone and is therefore probably due to hemodynamic factors.
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PMID:Acute changes in the diastolic pressure-volume relationship of the left ventricle. 81 75

Congestive heart failure is a frequent and important manifestation of cardiovascular disease, but no uniform clinical criteria are available for use in epidemiologic studies. To develop diagnostic criteria, we related pertinent clinical findings to physiologic measures of left ventricular function in patients with coronary artery disease. When left ventricular end diastolic pressure or arteriovenous oxygen difference was used as the physiologic criterion, the following variables contributed significant (P less than 0.01) information: heart volume, ventricular gallop, heart rate, and blood pressure. The most reliable and valid set of descriptors determined in one group was tested in a second group of 1306 patients who had been followed for 6 to 36 months after initial evaluation. The validity of the descriptors was confirmed, and patients identified as having heart failure by these criteria experienced a worse survival rate (P less than 0.001). These criteria characterize patients likely to have impaired left ventricular function and a greater risk of death.
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PMID:Chronic congestive heart failure in coronary artery disease: clinical criteria. 83 34

In 1164 cases clinical and electrocardiographical findings were correlated with serum digoxin concentrations (SDC). The diagnosis of digitalis intoxication was based on rhythm disturbances which disappeared on withdrawel of the drug. The mean SDC for patients with digitalis-induced arrhythmias was 3.07 ng/ml compared to 1.02 ng/ml for patients with normal Ecg's and 1.01 ng/ml for patients with rhythm disturbances of other origin. Taking 2.0 ng/ml as the lower limit of digitalis intoxication a more than 85% coincidence was found between the diagnosis based on serial Ecg's and on SDC levels. No signs of cardiac toxicity were found in patients with SDC's less than 1.6 ng/ml, some patients, however, showed normal Ecg's despite SDC's up to 4.5 ng/ml. Patients with SDC's greater than 1.9 ng/ml and normal Ecg's were significantly younger than patients with digitalis-induced arrhythmias at comparable SDC's. Although no definite diagnosis of cardiac toxicity could be established in 327 cases, the clinical data of patients with SDC's of 2.0 ng/ml and greater resemble closely those with digitalis-induced arrhythmias while patients with SDC's less than 2.0 ng/ml showed close resemblance to patients with no cardiac evidence of toxicity with regard to: mean age, kidney function, mean digoxin dosage and mean body weight. Patients with elevated SDC's showed a 45% incidence of severely impaired kidney function in contrast to 28% of the patients with SDC's less than 2.0 ng/ml. Even in patients with normal kidney function the correlation between the orally administered digoxin dosage and SDC levels was poor. The correlation was significantly better when dogoxin was administered intravenously. Therefore knowing the amount of digoxin taken (according to the patient's statement) seems of little benefit in the evaluation of digitalis toxicity. In patients with digitalis-induced arrhythmias mean age and mean body weight were significantly lower, mean creatinine concentration and the incidence of severe cardiac insufficency and of typical ST-T-changes were significantly higher. There was no significant difference in mean potassium concentration and incidence of coronary artery disease compared to nontoxic patients. Compared to patients with cardiac arrhythmias of other origin there were no significant differences in mean age, mean potassium and creatinine concentrations and cardiac insufficiency while the incidence of coronary artery disease was significantly higher among patients with rhythm disturbances of other origin. Every type of rhythm disturbance can be digitalis-induced. Among our patients the incidence of digitalis-induced second-degree atrioventricular block (Wenckebach), ventricular bigeminy, nonparoxysmal nodal tachycardia and PAT with block was significantly higher while patients with rhythm disturbances of other origin showed an equally high incidence of PVB's and prolongation of PQ interval...
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PMID:[Digitalis intoxication: specifity and significance of cardiac and extracardiac symptoms. part I: Patients with digitalis-induced arrhythmias (author's transl)]. 85 52

Data are presented on 282 patients who began taking prazosin before March, 1975, and whose progress was followed until March, 1976. The following conclusions can be drawn. (i) Prazosin is an effective and useful antihypertensive agent, best used with a diuretic and a beta-blocker. (ii) For patients with suspected or definite coronary artery disease, prazosin should not be used without a beta-blocker. (iii) In patients suspected of having incipient heart failure, prazosin should not be used without a diuretic, and the latter should be given first. (iv) many patients have little or no rise in heart rate with prazosin. However, patients with sinus tachycardia or a history of arrhythmias should preferably not be treated with prazosin. (v) The initial dose should be kept small (0-25 to 0-5 mg). Subsequent increments should also be small, not more than 2 mg/day. (vi) If prazosin is added to a regimen containing an adrenergic neurone-blocking drug, the dose of the latter should first be reduced. (vii) Prazosin should not, in the meantime, be used concomitantly with a phenothiazine, as the combination appears to be capable of causing agitation and confusion. (viii) There seems to be no long-term toxicity.
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PMID:Initial experience with prazosin in New Zealand. A multicentre report. New Zealand Hypertension Study Group. 91 29

The possible relationship between the cardiac volume, as determined radiologically in the supine position in 119 patients with angiographically proven coronary artery disease, and the results of ergometry and balloon catheterization was investigated. There was no relationship between the heart size on the one side and the maximum exercise tolerance and the maximum cardiac output on the other, except for the fact, that these parameters tended to decrease with increasing heart size. This was especially true in patients with angina. The maximum cardiac output of patients with angina was always below the value of patients without angina but comparable heart size. Reduced cardiac output under exercise (exertional cardiac insufficiency) was present in 50% of patients with enlarged hearts but already in 22% of patients with heart volumes in the lower range of normal. The diastolic pulmonary artery pressure, determined under exercise, was the only parameter with a significant relationship to the heart size: The larger the heart size, the higher the diastolic pulmonary artery pressure. On the other hand: the diastolic pulmonary artery pressure at rest was abnormal with significant frequency only, when the heart was enlarged. Our data suggest, that the hemodynamics are determined by 2 factors: Myocardial scarring secondary to infarction and coronary insufficiency (ischemia). Of these two factors only the former influences cardiac size. Therefore, determination of the heart volume helps evaluating the respective role of these two factors in individual cases.
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PMID:[Heart size and left ventricular function in coronary artery disease: I. Heart size, exercise tolerance, cardiac output and filling pressures (author's transl)]. 92 89


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