Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the acute hemodynamic effects of pimobendan (2.5 mg), a new drug, was compared with that of captopril (12.5 mg) in the same 8 patients with chronic heart failure (NYHA class II-III); 3 with dilated cardiomyopathy and 5 with regurgitant valvular heart disease. The hemodynamics were serially assessed before and after drug administration for at most 6 hours. Pimobendan reduced mean blood pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, right atrial pressure, total systemic vascular resistance, and total pulmonary vascular resistance but it increased heart rate. By contrast, captopril reduced mean blood pressure and double product. No significant changes were noted in the cardiac index, stroke volume index, AV-O2 difference or the arterial oxygen pressure between the 2 drugs. In conclusion, pimobendan seems to function as a strong arterio-veno-dilator rather than as an inotropic agent in patients with chronic heart failure.
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PMID:[Acute hemodynamic effects of pimobendan and captopril: a comparative study in the same patients with chronic heart failure]. 134 39

In the initial evaluation of cardiac patients, valuable information can be derived from the chest radiograph. In general, acute left-sided heart failure is shown by an erate cardiomegaly, cephalization of the pulmonary vascularity, and a mixed type of pulmonary edema. Gross alveolar pulmonary edema with a normal or minimally enlarged heart. Subacute failure is associated with modcardiomegaly, striking cephalization, and interstitial pulmonary edema are hallmarks of chronic left-sided heart failure. Right-sided heart failure is shown by enlarged systemic veins and right-sided chambers as well as pulmonary oligemia. Pleural effusions in heart failure tend to be bilateral or unilateral on the right side.
Heart Dis Stroke
PMID:Radiographic diagnosis of heart failure. 134 88

The actions of angiotensin II can be described in terms of the three paradigms listed in Table 1. According to the first paradigm (organ physiology), angiotensin II is a pressor, while the second (cell biochemistry) views it as an extracellular messenger that, by promoting Ca2+ release within cells, causes vasoconstriction and a weak positive inotropic response by the heart. However, neither of these paradigms fully explains the remarkable ability of angiotensin converting enzyme inhibitors to improve the prognosis for patients with heart failure. To account for these clinical effects of angiotensin converting enzyme inhibitors, we will probably need to invoke the third paradigm (gene expression), which views angiotensin II as a growth factor that promotes and modifies protein synthesis. Angiotensin II, therefore, should probably not be viewed simply as a vasoconstrictor with a side effect to promote hypertrophy, but instead as a growth factor that, because it utilizes Ca2+ to mediate its effects on gene expression, also increases smooth muscle tone and myocardial contractility. This view of angiotensin II as a growth factor helps us to understand the clinical benefit of angiotensin converting enzyme inhibitors as arising from inhibition of maladaptive changes in the failing heart (gene expression) as well as from the reduced afterload (organ physiology) that results from decreased smooth muscle tone (cell biochemistry).
Heart Dis Stroke
PMID:Is angiotensin II a growth factor masquerading as a vasopressor? 134 1

It is important to determine whether a patient's medical problem is a physiological complication that has resulted from a disease process (such as heart failure that is a complication of calcific aortic valve stenosis) or a structural complication that has resulted from a disease process (such as a stroke due to an embolus from a left atrial thrombus caused by atrial fibrillation in a patient with mitral stenosis). Whereas treatment is available for heart failure and stroke regardless of the cause, the progress of medicine is nullified when treatment is not directed at the etiology of heart failure and stroke. Finally, and most importantly, the identification and treatment of cardiovascular diseases that may cause heart failure and stroke may provide the physician with an opportunity to prevent these serious complications. The New York Heart Association four-part diagnosis (a complete diagnosis) requires the physician to consider all the important aspects of a patient's disease.
Heart Dis Stroke
PMID:Etiology: unknown or ignored? 134 27

Clinical and experimental heart irradiation can cause a variety of sequelae. A single dose of greater than or equal to 15 Gy leads to a reversible exudative pericarditis, occurring in dogs, rabbits or rats at around 100 days. Its time-course is very similar in all species investigated, but there are considerable species and strain differences in severity and incidence. After longer, dose-dependent latency times chronic congestive myocardial failure develops. At histological examination myocardial degeneration and necrosis is observed, which in some species is accompanied by a variable degree of interstitial fibrosis. In rabbits and rats, myocardial degeneration becomes apparent at around 70 days after 20 Gy and is preceded by a marked reduction in capillary density as well as ultrastructural endothelial cell degeneration. Simultaneously to structural capillary damage, a focal loss of the endothelial marker enzyme alkaline phosphatase was observed in rats in areas with subsequent myocardial degeneration. Cell kinetic studies in rabbits and rats revealed a radiation-induced wave of increased endothelial cell proliferation at 30-100 days postirradiation. In the rat it is exclusively seen in conjunction with alteration of endothelial cell marker enzymes. The temporal and spatial pattern of proliferative response exludes endothelial cell death in mitosis as the sole pathogenetic mechanism causing capillary loss and myocardial degeneration. Parallel to development of morphological damage, haemodynamic studies in various rats strains revealed a drop in cardiac output and left ventricular ejection fraction to about 64% of normal values after 20 Gy. In vivo, this slightly reduced cardiac function was then maintained in a steady state for many weeks, probably due to a compensatory up-regulation of cardiac beta-adrenergic receptors. In denervated working heart preparations in vitro, however, these compensatory mechanisms are not effective and stroke volume as well as cardiac contractility show a rapid and steady deterioration. In many respects radiation-induced heart disease conforms to radiobiological concepts of late-responding tissues, showing a chronic progressive time-course and a very pronounced fractionation effect. However, pathogenesis cannot be understood in terms of target cell depletion alone, and experimental evidence indicates the importance of alterations of regulatory mechanisms.
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PMID:Radiation-induced heart disease: review of experimental data on dose response and pathogenesis. 135 1

REASON FOR TREATMENT: In patients with asymptomatic high blood pressure, antihypertensive treatment is initiated for only one reason, to prevent the hypertensive sequelae of myocardial infarction, stroke and heart failure. MORBIDITY, MORTALITY AND SURROGATE ENDPOINTS: Only diuretics and beta-blockers have been shown to benefit hypertensive patients in terms of the hard endpoints morbidity and mortality. beta-Blockers and diuretics are cheaper than newer drugs and thus represent good value for money. It is not acceptable to use drug effects on plasma lipids or insulin resistance as measures of the effects on coronary heart disease, since dihydropyridine calcium antagonists improve these parameters while significantly increasing coronary heart disease events in the acute and chronic ischaemic situation. PATIENT PROFILING: Diuretics. Diuretics appear particularly suited to elderly hypertensives, especially those with isolated systolic hypertension, but they may increase cardiac events in younger and middle-aged diabetic and non-diabetic hypertensives. Angiotensin converting enzyme (ACE) inhibitors. ACE inhibitors are undoubtedly valuable in the presence of left ventricular dysfunction, and possibly in the diabetic in maintaining good renal function. beta-Blockers. beta-Blockers are particularly well suited to younger and middle-aged hypertensives at all blood pressure levels, especially white males; where ischaemia and/or stress is a factor, beta-blockers can significantly reduce the incidence of myocardial infarction and strokes. beta-Blockers benefit elderly hypertensives by preventing strokes and may prevent coronary heart disease if prescribed with a diuretic.
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PMID:The case for beta-blockers as first-line antihypertensive therapy. 135 11

The effects of acute and chronic ibopamine treatment on resting and exercise hemodynamics, exercise capacity and plasma catecholamines were evaluated in 25 patients with chronic heart failure, using a double-blind, parallel, placebo-controlled design. During 2 months of therapy with either placebo or ibopamine (100 mg, 3 times daily), 1 patient was withdrawn from each group for worsening heart failure, New York Heart Association functional class improved in 4 patients on ibopamine and in 1 on placebo, and furosemide dose could be decreased in 4 on ibopamine and in no patient on placebo. Acute ibopamine administration induced, in comparison with placebo, a significant increase of cardiac and stroke volume indexes both at rest and peak exercise, with a reduction of systemic vascular resistance. These hemodynamic changes were maintained also after chronic therapy, with no evidence of tolerance development. Exercise capacity (evaluated as peak exercise duration and oxygen consumption, and ventilatory threshold) did not significantly change. Resting and peak exercise norepinephrine plasma levels were significantly reduced after both acute and chronic ibopamine administration. Thus, the hemodynamic and neurohumoral effects of ibopamine make this drug potentially useful for the chronic treatment of congestive heart failure.
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PMID:Effects of acute and chronic ibopamine administration on resting and exercise hemodynamics, plasma catecholamines and functional capacity of patients with chronic congestive heart failure. 135 38

Atrial fibrillation and atrial flutter are common arrhythmias after coronary artery bypass grafting. Although the consequences of the arrhythmia are generally not life-threatening, it constitutes a major clinical problem often requiring conversion to sinus rhythm. Atrial fibrillation or flutter can result in hypotension, heart failure, pneumonia, and stroke. This article reviews the literature on epidemiology, electrophysiology, risk factors, and preventive trials. The major conclusions are: (1) In patients undergoing coronary artery bypass surgery, the incidence of postoperative atrial fibrillation or flutter is 20-30%, the peak incidence being on the second or third postoperative day. (2) The strongest independent preoperative predictor for atrial fibrillation or flutter is the patients' age. (3) Intra-atrial conduction delay recorded pre and peroperatively may predict development of atrial fibrillation. (4) Peroperative inducibility of atrial fibrillation by pacing the right atrium may identify patients at risk for postoperative atrial fibrillation. (5) Development of postoperative atrial fibrillation or flutter has not been associated with peroperative or postoperative events. (6) The specificity and sensitivity of age and other possible relevant factors for prediction of atrial fibrillation or flutter after coronary artery bypass grafting is low. (7) No effective prophylactic regimen has yet been established.
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PMID:Atrial fibrillation and flutter after coronary artery bypass surgery: epidemiology, risk factors and preventive trials. 135 29

Effects of denopamine with or without diltiazem on the ischemic heart were investigated in anesthetized open-chest dogs. Partial occlusion of the left circumflex coronary artery (LCX) produced significant decreases in LCX flow and regional myocardial segment shortening rate (%SS) in the LCX-perfused area, and a significant increase in left ventricular enddiastolic pressure (LVEDP). Heart rate (HR) and mean aortic pressure (mAoP) were not altered, but aortic flow (AoF), positive first derivative of left ventricular pressure ((+)LVdP/dt), stroke volume (SV), stroke work index (SWI) and double product showed a tendency to decrease. Total peripheral vascular resistance (TPR) tended to increase. During coronary stenosis, saline infusion (vehicle group) did not change any parameter, but diltiazem infusion (diltiazem group) decreased HR, mAoP, TPR and double product and increased SV and SWI. Under these conditions, denopamine infusion produced increases in HR, mAoP, AoF, (+)LVdP/dt and double product and decreases in LVEDP and TPR in both groups. %SS in the left anterior descending coronary artery-perfused area was increased, but %SS in the LCX-perfused area was slightly decreased in both groups. SV and SWI were decreased by denopamine infusion in the vehicle group, while they were increased in the diltiazem group. Differences in changes in SV and SWI between the groups were statistically significant. Results suggest that combined treatment of denopamine and diltiazem may exert an advantage in alleviation of heart failure due to coronary stenosis.
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PMID:Effects of denopamine with or without diltiazem on the ischemic heart of anesthetized dogs. 136 33

A total of 1,431 patients (mean age 63.4 +/- 14.1) with pacemakers (96.2% VVI) primoimplanted between 1967 and 1985 were followed for a mean duration of 78.2 +/- 40 pacing months, with 0.6% loss to follow-up. Cumulative survival for 1, 3, and 10 years was 0.9427, 0.9136, and 0.7536, respectively. There was no significant difference in survival between atrioventricular block (AVB) and sick sinus syndrome (SSS) patients. In addition to age and gender, factors existent prior to implantation that independently affected prognosis included manifest coronary heart disease (CHD), congenital/acquired heart lesions, heart failure, noncardiac internal disease, syncope, and generalized fatigue. After implantation, the most important factor was generalized fatigue, then age, stroke, myocardial infarct (MI), gender (male), heart failure, and syncope. Patients with no underlying disease showed an extremely high cumulative survival (0.9173 at 10 years). Compared to the general population of Yugoslavia, the pacemaker patients showed a similar yearly mortality rate until 1981. After that, elderly males (70+) had a significantly lower yearly mortality than the matched population. Thus, in this large series of pacemaker patients followed into the most recent period with an extremely low loss to follow-up, short- and long-term survival was very high. Pacemaker patients of any age who are otherwise in good health have an excellent prognosis.
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PMID:Survival in 1,431 pacemaker patients: prognostic factors and comparison with the general population. 137 12


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