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

The effects of intravenous dopamine were evaluated in 10 patients with severe but stable coronary artery disease, 17 consecutive patients with primary cardiogenic shock and 3 with severe congestive heart failure and oliguria. Dopamine infusion at 10 mug/kg.min in the 10 patients increased cardiac output by 35%, left ventricular peak dP/dt by 38%, left ventricular minute work index by 44% and mean systolic ejection rate by 7% (P < 0.01); heart rate, aortic pressure, left ventricular end-diastolic pressure and tension-time index were unchanged. For oxygen, potassium and lactate, arterial and coronary sinus values, coronary arteriovenous oxygen differences and myocardial extraction were unchanged. Hemodynamically 13 of the 17 patients in shock responded favourably to dopamine infusion (0.5 to 15 mug/kg.min), with decrease in heart rate, increase in systolic arterial pressure from 75 to 100 mm Hg (P <0.001), decrease in ventricular filling pressure from 20 to 16 mm Hg (P < 0.01) and increase in urine output from 10 to 100 ml/h (P < 0.01). Eleven of those patients survived the shock episode. A close relation was observed between the hemodynamic response to dopamine, survival from the shock episode and the time between onset of shock and initiation of therapy. Low rates of dopamine infusion induced diuresis in the three patients with severe cardiac failure.Dopamine thus seems to improve the mechanical efficiency of the heart in coronary artery disease. Cardiac output is selectively increased and myocardial ischemia does not appear to be induced; those beneficial effects as well as presumably specific action on renal flow and natriuresis, improve immediate survival from cardiogenic shock and severe heart failure.
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PMID:Hemodynamic and therapeutic effects of intravenous dopamine. 60 65

In 21 patients with ischaemic heart disease, the values of the anginal threshold were investigated during cardiac pacing and an exercise test. It was found that in the pacing test, ischemia could be expected to appear at a heart rate by 30% faster than that in ischaemia induced by exercise. If ischaemia was successfully induced in both tests, the threshold values of the time-tension indexes were equal, whereas the value of the pressure-time per minute index was 20% higher in exercise-induced ischaemia. In patients with hypokinetic circulation, during pacing the pressure-time per minute index first increased and then paradoxically decreased; this reaction can help find out patients with haemodynamic signs of heart failure.
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PMID:A comparison between cardiac pacing and exercise tests in patients with angina pectoris. 61 Sep 93

Nineteen patients with chronic low output cardiac failure were studied before, during and after infusion of phentolamine in doses of 10, 20, 30 and 40 microgram/kg/min. Significant reduction of left- and right-sided pressures and increases in cardiac index and heart rate (HR) were present within 15 minutes of starting phentolamine at the 10 microgram/kg/min dose. Minimal additional effect was observed at 30 minutes. Increased dose from 10 to 20 mu/kg/min resulted in small but significant (P less than 0.05) additional reduction in pressures and increases in HR. No additional significant changes occurred at doses of 30 or 40 microgram/kg/min. Significant hemodynamic changes persisted for at least an hour (53 +/- 3 min) after the phentolamine infusion was discontinued. Near maximal ;emodynamic effects occur within 15 minutes of starting phentolamine infusion and can be achieved at doses of 10 to 20 microgram/kg/min. Increased HR during phentolamine infusion may limit its usefulness in patients with ischemic heart disease.
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PMID:Hemodynamic effects of intravenous phentolamine in low output cardiac failu;e. Dose-response relationships. 64 80

Selection of therapy for subjects with acute congestive dardiac failure usually involves a choice among a diuretic, a vasodilator and an inotropic agent. Three principal questions are involved in the decision: (1) Is cardiac out normal or depressed? (2) Is blood pressure normal or depressed? (3) is regional myocardial ischemia present? Diuretics are safe and easy to administer, but they do not increase cardiac output or relieve hypoperfusion. Inotropic agents increase cardiac output but differ widely in their effects on blood pressure: selection of specific agents is influenced by their blood pressure effect. All inotropic agents, however, potentially aggravate regional myocardial ischemia. In ischemic heart failure, therefore, vasodilators which also increase cardiac output, may be chosen. Vasodilator administration is in turn limited by the decrease in arterial pressure which accompanies increasing infusion rate. When these three questions are considered in combination, an effective therapeutic regimen can be identified. Thus, congestion without hypoperfusion requires a diuretic if blood pressure is normal; and a vasodilator when blood pressure is increased. In the presence of congestion with hypoperfusion, a vasodilator is employed if blood pressure is normal; and a positive inotropic drug when blood pressure is depressed.
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PMID:Hospital treatment of congestive heart failure. Management according to hemodynamic profile. 68 90

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

Both vasodilator and inotropic agents improve cardiac function in ischemic heart failure. However, since vasodilators may reduce coronary perfusion pressure and inotropic interventions may increase myocardial oxygen consumption (MVO2), both may increase myocardial ischemia. Accordingly, we determined myocardial blood flow and MVO2 in a canine model of failure induced by propranolol and volume load combined with acute coronary ligation. Both nitroprusside and digitalis reduced ventricular diastolic pressure (LVDP) and increased myocardial blood flow in the ischemic subendocardium. Decreased systolic wall tension also caused a significant reduction MVO2. The benefit of nitroprusside in failing hearts was obtained even with the addition of critical obstruction of the main left coronary artery (LCA). The role of preload reduction is emphasized by the contrasting results with nitroprusside in hearts with low LVDP: (1) decreased myocardial blood flow in ischemic subendocardium, and (2) left ventricular decompensation in animals with critical LCA obstruction. Thus, reduction of LVDP, which decreases subendocardial ischemia, is essential for the beneficial effects of vasodilators and inotropic interventions in ischemic heart failure. Decreased MVO2 caused by reduced heart size may also have a salutary role.
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PMID:Mechanisms of beneficial effects of vasodilators and inotropic stimulation in the experimental failing ischemic heart. 68 93

Eight patients in whom cardiac dysfunction developed within four weeks of receiving their first or second course of daunorubicin or doxorubicin are described. Four patients presented with pericarditis; three of these four had evidence of myocardial dysfunction. Histopathologic analysis of these patients was consistent with an acute myocyte damage and secondary inflammatory process. An additional group of four patients presented with symptoms and signs of heart failure. These patients were either elderly or had evidence of previous cardiac disease. One of these patients suffered a myocardial infarction 24 hours after receiving 60 mg/m2 of daunorubicin; earlier doses in the same course had been associated with evidence of myocardial ischemia. We conclude that anthracycline antibiotics may manifest clinically significant cardiotoxicity at total cumulative doses much less than have been associated with chronic cardiomyopathy.
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PMID:Early anthracycline cardiotoxicity. 70 41

1329 patients were discharged alive after acute myocardial infarction initially treated in a CCU. In a five-year follow-up, 537 (40%) of the patients died. Routine data registered uniformly during the CCU period showed that, apart from age, the most important factors regarding long-term prognosis in general were previous ischaemic heart disease and direct or indirect signs of heart failure registered in the CCU. The possibilities to predict sudden death (130 patients died within 2 hours of onset of final symptoms during the follow-up period) were small, although a definite dominance of this mode of death was noted in patients below 60 years of age. The clinical profile of the majority of the 134 patients who died during the first half-year was distinguished by a history of prior myocardial infarction and signs of left heart failure during the CCU stay. However, in a significant number of patients dying early after discharge, none of the ordinary unfavourable prognostic signs had been registered.
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PMID:Early and sudden deaths after myocardial infarction. A report from the Swedish CCU study. 76 Apr 5

The circulatory effects of anileridine, a derivative of pethidine, have been little studied. Therefore we compared the haemodynamic effects of equianalgesic doses of pethidine (1 mg/kg i.v.) and anileridine (0.25 mg/kg) in matched patients requiring myocardial revascularization. Cardiac output was significantly increased 5 min after the administration of pethidine, mainly due to an increase in heart rate. A transient rise in the systolic pulmonary-arterial pressure was found after anileridine. No remarkable changes were found in systemic arterial pressures, central venous pressure, balloon-occluded pulmonary-arterial pressure, stoke volume, systemic or pulmonary vascular resistances and derived oxygen consumption. Further, 20 min after drug administration, there were no significant differences in any circulatory parameters between the two groups. One patient developed acute cardiac failure after anileridine, though as he had very severe coronary heart disease it remains an open question whether this was spontaneous or drug-induced. Since the rate-pressure product tended to increase after pethidine, this drug may not be considered an ideal analgesic for patients with ischaemic heart disease. Anileridine had less influence on this variable. Since the circulatory effects of pethidine seem to depend on the haemodynamic status of the patient, the haemodynamic properties of anileridine may also deserve further investigation.
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PMID:Comparison of haemodynamic effects of pethidine and anileridine in patients with coronary-artery disease. 77 91

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


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