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

We studied a group of 30 patients to determine the effect of captopril on the exercise training response after a period of training in patients with ischemic heart disease but without cardiac failure. The study was a double-blind placebo-controlled comparison of captopril and placebo. The patients studied were 28 men and 2 women, mean age 53.6 +/- 6.9 years. All were 8 to 12 weeks postmyocardial infarction or coronary artery bypass surgery. These patients underwent an organized exercise training program consisting of exercise training sessions 3 times weekly for a period of 8 weeks. On commencement and completion of the program patients were assessed for exercise tolerance using submaximal exercise stress testing. Patients were assessed in the untreated state. Both groups showed a statistically significant training effect with increased exercise duration, decreased heart rate for equal workload, increased energy expenditure, and reduced functional aerobic impairment. There was no statistically significant change in systolic blood pressure, but the captopril group alone showed a significant reduction in diastolic blood pressure (p less than 0.001). The change in heart rate at rest over the 8-week period was not significant in both groups. In summary, this study shows that treatment with captopril does not affect the exercise training response in patients with ischemic heart disease undergoing an organized exercise training program.
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PMID:The effects of captopril on training in patients with ischemic heart disease. 162 53

The clinical usefulness of cardiac imaging modalities that rely upon the detection of perfusion defects and wall motion disturbances requires conditions that provoke a heterogeneity of coronary flow and a myocardial oxygen imbalance, respectively. Traditionally, this has been achieved by exercise stress testing. Many patients cannot perform dynamic exercise sufficiently for various reasons. Pharmacologic stress has been proven to be an attractive alternative for physical exercise. Currently, several stressing agents are used in conjunction with thallium-201 scintigraphy, 2-D echocardiography and, recently, MRI. The most employed agents include vasodilators, such as dipyridamole and adenosine, and catecholamines, such as dobutamine (Table VI). The predominant rationale of thallium-201 perfusion scintigraphy is based on the creation of a flow maldistribution between territories supplied by normal arteries and those supplied by stenotic arteries that does not necessarily require ischemia. Dipyridamole and adenosine, as rather selective coronary vasodilators, are well suited to provoke such a condition and may be classified as the ideal markers of myocardial perfusion. 2-D echocardiography and MRI have the potential to provide noninvasively derived information of cardiac dynamics and regional myocardial function. To assess the functional significance of coronary artery disease, detection of wall motion abnormalities and alterations in ejection fraction require the presence of myocardial ischemia. Dobutamine, as a widely applied inotropic agent in the management of severely depressed left ventricular contractile function, seems to be an appropriate pharmacologic stressor when heart failure is absent. By increasing contractility, heart rate, and systolic arterial pressure, it is capable of inducing an imbalance between myocardial oxygen demand and supply, leading to ischemia in patients with coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New developments in pharmacologic stress imaging. 163 90

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
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PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

The aim of the study was to analyze changes in myocardial angiotensinogen gene expression and myocardial angiotensin converting enzyme activity in slowly progressing low-output failure. In adult, male Wistar rats, acute ventricular tachypacing by 610 to 620 impulses per minute lowered end-diastolic external diameter of the left ventricle by 2.6% (p less than 0.01), but did not lower cardiac output or abolish coronary reserve, since left-ventricular subendocardial blood flow of paced rats increased under dipyridamole (2 mg/kg i.v.) by 56% (p less than 0.01). Systemic neuroendocrine activation and ventricular dilation without enlargement of ventricular mass developed subsequent to chronic tachypacing, but left-ventricular diameter during pacing never exceeded the value of sham rats on sinus rhythm. After 2 weeks, cardiac output was lowered by 14% (p less than 0.001), cardiopulmonary blood volume was elevated by 30% (p less than 0.001), and angiotensinogen mRNA and angiotensin converting enzyme activity in ventricular myocardium were doubled. We conclude that conditions for an enhanced intracardiac angiotensin II-formation developed in tachypacing-induced heart failure, but that enhanced systolic wall stress or myocardial ischemia are not required for this activation of the local cardiac renin-angiotensin system.
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PMID:Enhanced cardiac angiotensinogen gene expression and angiotensin converting enzyme activity in tachypacing-induced heart failure in rats. 165 3

Previous studies on isolated blood vessels indicate that acute withdrawal of extracellular magnesium ions ([Mg2+]o) induces calcium-dependent contractile responses, including coronary blood vessels. The present study, using isolated perfused rat hearts, was designed to assess whether low [Mg2+]o could result in cardiac failure and to gain some insight into the mechanism of action. The results show that both the myocardial oxygen consumption (by 29-38%) and oxygen tension in the coronary effluent decreased (by 18-26%) as the [Mg2+]o was decreased stepwise from 1.2 to 0.6, 0.3 and 0.0 mM. Linear-regression analysis of a plot of coronary flow versus the rate of oxygen consumption shows that there is a tendency for a rightward shift of this relationship in low [Mg2+]o and a leftward shift of the curve in elevated [Mg2+]o (4.8 mM). The experiments also show that with low [Mg2+]o, coronary flow declines 20-37%, and cardiac output and stroke volume fall 24-50% accompanied by 3- to 4-fold elevations in lactate production and eventual, irreversible cardiac failure. An interesting finding, of this study, is that the alpha-adrenoceptor constrictor agonist, phenylephrine (1-5 microM), was found to have effects very similar to low [Mg2+]o. This latter finding is consonant with our hypothesis that progressive lowering of extracellular, ionized magnesium initiates progressive coronary vasoconstriction, decreased tissue oxygenation and myocardial ischemia, which given time, in situ, in the intact host can lead to cardiac failure.
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PMID:Low extracellular magnesium results in cardiac failure in isolated perfused rat hearts. 166 20

Catecholamines mediate their effects in the heart through beta 1- and beta 2-receptors. Beta 1-receptors mediate the effects of sympathetic nerve stimulation. Alpha-receptors may have a role but, unlike the beta-receptor mediated responses, act without producing any increase in cyclic AMP. Prolonged receptor stimulation results in a reduction in beta-receptor sensitivity. In contrast blockade with a non-agonist agent is associated with an increase in catecholamine sensitivity which may be responsible for the withdrawal reactions that can occur when beta-blocking drugs are rapidly withdrawn in patients with ischaemic heart disease. Experimentally, prolonged noradrenaline infusions result in ventricular hypertrophy. Catecholamines have been implicated in several pathologies. High and rising catecholamine levels are associated with worsening of prognosis in patients with heart failure. These patients show a decreased beta-receptor number and cellular concentration of catecholamines. On the other hand cardiomyopathy is associated with an increased sensitivity to catecholamines. Catecholamines aggravate cardiac damage in ischaemia. Excessively high catecholamine loads cause myocardial damage in otherwise normal hearts, for example in patients with a phaeochromocytoma and those with various forms of cerebral damage such as subarachnoid haemorrhage, cerebrovascular accidents, and head injury.
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PMID:Heart and catecholamines. 168 38

Beta-blockers were initially given to patients with chronic heart failure due to ischemic heart disease and resting tachycardia. The prompt effect on severe backward heart failure was directly associated with an immediate fall in heart rate. This observation led to long-term administration to patients with idiopathic dilated cardiomyopathy and, later, to patients with ischemic cardiomyopathy and secondary cardiomyopathies as well. Due to marked down-regulation of beta receptors, patients with heart failure are extremely sensitive to beta blockade. A test dose of metoprolol 5 mg b.i.d. for 2 days is recommended to select patients for long-term beta-blockade, followed by careful titration with increment in dose over 6 weeks. One important effect of beta-blockade in the early phase of treatment is a reduction in the myocardial energy demand early after the onset of long-term treatment. After 1 month of treatment with beta-blockers, marked improvement of diastolic function is observed. This effect might be attributed to inhibition of calcium overload. After 3 months of treatment, an increase in ejection fraction can be observed, which might be attributed to upregulation of beta receptors. The withdrawal of long-term treatment was followed by a deterioration of heart function in 61% of patients and improvement was seen after reinstitution of beta-blockade. There was an increase in cardiac index and stroke work index at rest as well as during supine exercise. A marked fall in left ventricular filling pressure at rest and unchanged filling pressure during supine exercise was noted, while exercise capacity increased by 25%. A similar pattern was seen in patients with ischemic cardiomyopathies and other secondary cardiomyopathies. However, the increase in ejection fraction in the ischemic cardiomyopathy group was lower (0.06) compared to the groups with dilated cardiomyopathy and other secondary cardiomyopathies (0.18).
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PMID:Beta-adrenergic blockade in dilated cardiomyopathy, ischemic cardiomyopathy, and other secondary cardiomyopathies. 168 23

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

Recent studies have shown that beta-blockers may be effective in the management of heart failure. However, negative inotropic effects of these agents may offset the beneficial properties of up-regulation of the beta-receptors and reduction in myocardial oxygen demand. Carvedilol is a new drug which possesses a balanced combination of vasodilatation and beta-blockade. Previous studies have shown that carvedilol may have beneficial effects on left ventricular function in patients with ischemic heart disease. We have performed a preliminary study to address the safety and acute effects of intravenous carvedilol in 17 patients with chronic congestive heart failure secondary to ischemic heart disease. Acute hemodynamic changes were monitored by right heart catheterization and arterial cannulation. Ejection fraction was also monitored by radionuclide ventriculography. Significant reductions in heart rate (79 +/- 14 to 72 +/- 12 beats/min, p less than 0.001) systolic and diastolic blood pressure (137 +/- 20/72 +/- 8 to 119 +/- 19/66 +/- 8 mm Hg, p less than 0.001 and p less than 0.01), systemic vascular resistance (1766 +/- 367 to 1518 +/- 377 dynes/s/cm-5/m2, p less than 0.001) and pulmonary artery wedge pressure (20 +/- 8 to 15 +/- 7 mm Hg, p less than 0.001) were observed. Ejection fraction increased significantly from 24 to 28% (p less than 0.001) but there was little change in cardiac index or stroke volume index. The peak changes occurred at 10 min and the effect on pulmonary wedge pressure was maintained up to 30 min. No adverse effects were noted. The improvements in left ventricular filling pressure and systolic function, and the reduction in sympathetic activity may combine to produce an important therapeutic advantage in congestive heart failure. Further studies with this interesting agent are recommended.
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PMID:The effects of intravenous carvedilol, a new multiple action vasodilatory beta-blocker, in congestive heart failure. 172 73

The recognition and management of heart failure is based on the knowledge of the underlying disease and precipitating factors. The underlying causes are all cardiovascular whereas precipitating factors comprise both cardiac and a variety of noncardiac factors. The influence of hypertension on the development of heart failure is complex. Increased ventricular systolic pressure raises myocardial oxygen demand, resulting in ischemic heart syndromes and arrhythmias. Also, systemic hypertension leads to hypertrophy, resulting in systolic and diastolic function abnormalities. Generally, heart failure is controlled by treating the underlying cause, by removal of precipitating factors, and by treatment of failure itself. Heart failure therapy involves general measures, and pharmacological and surgical therapy. The pharmacological treatment involves the use of diuretics, vasodilators, and positive inotropic agents. In patients with heart failure and hypertension, arterial and mixed type vasodilators are the drugs of choice. Positive inotropic agents have to be used with care because of the potential induction or aggravation of myocardial ischemia. Interest in beta-adrenergic-blocking agents, especially those with ancillary properties similar to vasodilators, has recently surged and will continue to provoke more and more clinical research in an attempt to unravel the complexities of these cardiovascular diseases and their therapies.
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PMID:Congestive heart failure: pathophysiology and management with special reference to systemic hypertension. 172 86


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