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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Optimal therapy for congestive cardiac failure requires identification of correctable factors that aggravate it as well as an understanding of its etiology. Increased sympathetic nervous system activity, reduced renal blood flow, and cardiac hypertrophy and dilation are the main compensatory processes that occur in response to cardiac failure. Although they may be of initial benefit in supporting a reduced stroke volume, they may ultimately prove self-defeating. New drugs for the treatment of severe congestive heart failure include dopamine, which has a selective nonadrenergic dilator effect on the renal vascular bed, and dobutamine, which has potent inotropic effects, lowers the left ventricular filling pressure and does not increase the heart rate or the systemic vascular resistance. By reducing both the resistance to left ventricular ejection and the venous return to the right heart, vasodilators result in improved peripheral perfusion and reduced pulmonary congestion. Optimal therapy for refractory cardiac failure can be rationally determined by characterizing the hemodynamic profile through measurement of the mean arterial pressure, the left ventricular filling pressure, the cardiac output and the systemic vascular resistance. The specific therapy can then be effectively and safely delivered by a careful analysis of the dose-response relation as identified by hemodynamic monitoring.
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PMID:Contributions of hemodynamic monitoring to the treatment of chronic congestive heart failure. 49 82

The comparative haemodynamic effects of oral prazosin hydrochloride and hydralazine were evaluated in 11 patients with chronic congestive heart failure. The maximum total dose of prazosin received by an individual varied up to 25 mg. Ten patients received a maximum of 75 mg and one received 50 mg of hydralazine at six-hour intervals. There was no significant change in heart rate with either drug. Decrease in mean arterial and left ventricular filling pressures were modest and similar with both agents. With prazosin, the average cardiac index increased 20 per cent and systemic vascular resistance decreased 20 per cent. By contrast, hydralazine increased cardiac index by 58 per cent and decreased systemic vascular resistance by 40 per cent. The increase in stroke work and stroke volume indices was significantly greater with hydralazine than with prazosin. These findings suggest that in some patients with severe chronic congestive heart failure, improvement in left ventricular performance may be greater with hydralazine than with prazosin.
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PMID:Comparison of haemodynamic effects of oral hydralazine and prazosin hydrochloride in patients with chronic congestive heart failure. 53 82

A patient with intractable congestive cardiac failure secondary to renovascular hypertension and severe coronary artery disease was infused with the competitive antagonist of angiotensin II, saralasin acetate. The infusion produced an impressive increase in cardiac output and left ventricular stroke work index in parallel with a striking decrease in the systemic and pulmonary vascular resistance, the coronary resistance, and the myocardial oxygen consumption. It is suggested that angiotensin inhibition may present advantages over other forms of treatment of congestive cardiac failure in selected cases.
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PMID:Angiotensin II inhibition. Treatment of congestive cardiac failure in a high-renin hypertension. 57 78

Patients in congestive heart failure are known to have altered autonomic responses to circulatory stress. In this study, two different age groups of male coronary heart disease (CHD) patients, not in failure, as well as normal male subjects, underwent standard 20-min 70 degrees head-up tilt and Valsalva tests. Responses were monitored by noninvasive methods and cardiac output was estamated with a transthoracic impedance method. During tilt, the CHD patients and control subjects had similar heart rate and diastolic pressure responses. However, the CHD patients had a greater decline in pulse pressure during tilt, mainly due to a decrease in systolic pressure. CHD patients had lesser declines in stroke volume and cardiac index and lesser increases in total vascular resistance than did control subjects. In the Valsalva, the heart rate phase increments (and decrements) from control and rate increments (and decrements) between successive phases were less in the coronary patients. The results indicate that coronary patients, not in failure, have diminished circulatory responses to the tilt and Valsalva maneuver and suggest that these tests may be useful functional indices of cardiovascular capability in coronary disease.
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PMID:Alterations of postural and Valsalva responses in coronary heart disease. 59 67

We compared cardiocirculatory actions of nitroprusside (NP) to prazosin (PZ) in eleven chronic coronary patients with refractory congestive heart failure. Each drug equally lowered systemic arterial pressures mildly while heart rate was unaltered. NP decline (P less than .001) in left ventricular filling pressure (28 to 17 mm Hg) and rise (P less than .005) in cardiac index (2.20 to 2.96 L/min/m2) were similar to PZ (30 to 17) and (2.08 to 3.00). PZ and NP equally enhanced cardiac efficiency of stroke work and myocardial oxygen consumption index. Total systemic vascular resistance declined (P less than .001) the same with NP and PZ. Forearm vascular resistance (FVR) and venous tone (FVT) diminished equally with NP and PZ. Similar FVR/FVT percent changes of 0.88 and 0.64 with NP and PZ indicated relatively balanced systemic arteriovenous relaxation. Sinze PZ effects persisted six hours with symptomatic improvement, oral PZ is the best vasodilator for long-term use, extending in-hospital NP-like actions to ambulatory heart failure therapy.
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PMID:Comparison of effects of nitroprusside and prazosin on left ventricular function and the peripheral circulation in chronic refractory congestive heart failure. 61 83

A population of 199 patients from Rochester, MN, was followed from the time of their first carotid or vertebral-basilar transient ischemic attack (TIA). Patients treated with anticoagulants had no significant difference in survival from untreated patients. Among patients with carotid TIA who received anticoagulants, the net probability of stroke was slightly but not significantly lower than in untreated patients. The difference favoring treated patients with vertebral-basilar TIA was significant starting at three months. The rate of intracranial hemorrhage was higher higher among all patients receiving anticoagulant treatment than among untreated patients and was significantly higher among those 55 to 74 years old. Almost all the hemorrhages occurred after a year or more of anticoagulant treatment and in patients more than 65 years old. Patients with high diastolic blood pressure had a significantly higher net probability of stroke than did patients with lower blood pressure and those receiving antihypertensive drugs. By implication, treatment of hypertension was effective in preventing stroke in patients with TIA. Linear discriminant analysis and actuarial analysis indicated that diastolic blood pressure and anticoagulant therapy were the only factors that influenced stroke occurrence. There was no suggestion that previous myocardial infarction, angina pectoris, valvular heart disease, cardiac arrhythmia, or congestive heart failure--individually or in combination--influenced the occurrence of stroke or survival.
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PMID:Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence--a population study. 65 61

Theories on the nature of cancer may be classified into two categories. One regards cancer strictly as a local phenomenon while the second looks at cancer as a local manifestation of a systemic process or disease. Although the first dominates current medical thought, the theories of immunological surveillance and of protovirus-oncogene implicitly assume cancer to represent a local manifestation of a systemic process or disease. This is supported also by epidemiological data forwarded in the present paper. In order to clarify the exact meaning of a systemic disease, cancer and its manifestation are compared with arteriosclerosis and its sequelae. Arteriosclerosis could be regarded as a prototype of a systemic disease. It presents itself clinically solely by its local manifestations, like myocardial infarction or stroke. These local manifestations may be followed by secondary systemic sequelae like congestive heart failure. In the same context, it is proposed to regard cancer as one systemic disease which presents itself clinically by local phenomena like carcinoma, lymphoma and sarcoma. These local manifestations may lead further to secondary systemic sequelae like metastasis.
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PMID:Cancer as a systemic disease. 67 9

Seven patients with severe chronic congestive cardiac failure secondary to ischaemic heart disease performed submaximal supine exercise before and after 5 mg sublingual isosorbide dinitrate at the time of cardiac catheterisation. Exercise before isosorbide dinitrate produced a poor response in left ventricular performance. After isosorbide dinitrate this response was significantly improved. Compared with the control exercise period, cardiac index increased from mean 2.6 to 3.1 1/min per m2 (P less than 0.0025), stroke volume index from mean 22 to 27 ml/m2 (P less than 0.0025), and left ventricular stroke work index from mean 21 to 30 g m/m2 (P less than 0.01). Mean left ventricular filling pressure fell from 37 to 26 mmHg (P less than 0.01). Although isosorbide dinitrate reduced left ventricular filling pressure at rest from mean 26 to 17 mmHg (P less than 0.005), there was no significant change in mean cardiac index or stroke volume index, while left ventricular stroke work index decreased from mean 29 to 22 g m/m2 (P less than 0.05). Isosorbide dinitrate effectively reduces left ventricular filling pressure in the resting patient with congestive cardiac failure but produces a more comprehensive improvement in left ventricular performance during exercise.
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PMID:Improvement in exercise haemodynamics by isosorbide dinitrate in patients with severe congestive cardiac failure secondary to ischaemic heart disease. 68 84

Cardiovascular risk factors in 566 patients with peripheral arterial disease undergoing major vascular operations were analyzed by chi-square analysis. There were 37 postoperative deaths, for a mortality rate of 8.5%. Cardiovascular complications were responsible for 23 deaths (62%). Five risk factors--congestive heart failure, prior myocardial infarction, prior stroke, arrhythmia, and abnormal electrocardiogram--showed significant individual associations with postoperative cardiovascular complications. A multivariate analysis of these five risk factors and angina led to the development of an equation which predicts the probability of a postoperative cardiovascular complication. The number of complications observed corresponded closely to that predicted by the equation. There was a significantly higher incidence of complications in patients predicted to be at high risk than in those at low risk.
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PMID:Cardiovascular risk factors in patients with peripheral vascular disease. 69 38

The role of the renin angiotensin system was evaluated in 18 normotensive patients with chronic congestive heart failure and in 5 controls. No correlation was observed between plasma renin activity and cardiac index. There was a significant inverse correlation between renin and pulmonary capillary wedge pressure (r = -0.61, P less than 0.01). Renin values of the patients appeared to be increased when compared with controls with similar left ventricular filling pressure. Specific angiotensin II inhibition by saralasin decreased arterial pressure in 8 out of 14 patients: their renin was significantly higher than that of the remaining 6 patients (P less than 0.01). The 2 patients with the lowest renin levels responded to saralasin with a blood pressure increase. Left ventricular filling pressure decreased in all but these latter 2 patients with either little change or an increase in stroke volume. Thus, renin levels appear to be increased in normotensive patients with congestive heart failure when related to left ventricular filling pressure. Renin via angiotensin II plays a role in the blood pressure control of many patients with congestive heart failure. In some patients angiotensin II blockade appears to improve cardiac function by unloading the left ventricle.
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PMID:Congestive heart failure in normotensive man. Haemodynamics, renin, and angiotensin II blockade. 70 15


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