Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phrase "heart failure" encompasses many clinical entities. The therapeutic principles determining the treatment of these entities vary according to the etiology of congestive heart failure (CHF), the existing hemodynamics, and the mode of action of different drugs. In acute CHF due to myocardial ischemia, intracellular acidosis and the accumulation of phosphate may be the initial underlying causes of contractile failure while, minutes later, lack of high-energy compounds may be an important contributory factor. The cause of contractile failure in chronic syndromes is less well understood. There is evidence for the desensitization of beta receptors on the cell surface but the precise location of the defect is unclear. The receptors may be down-regulated but, in addition, abnormalities have been reported in several other parts of the contractile pathway including the contractile proteins and the sarcoplasmic reticulum. Deficiency of cyclic adenosine monophosphate has also been suggested as a mechanism of contractile failure. In both acute and chronic CHF, there is a redistribution of blood flow to the body organs. Of particular significance is the reduction of blood flow to the kidneys, and a reversal of this defect is one of the major therapeutic objectives. Positive inotropic drugs, vasodilators and drugs altering relaxation of the heart, have been evaluated in the treatment of CHF. Pure inotropic drugs can cause tachycardia, ischemia and "metabolic exhaustion" of the myocardium. The most advantageous profile for an "inotropic" drug in many patients with CHF would be a drug combining systemic vasodilatation, renal vasodilatation, increased relaxation of the myocardium only a mild positive inotropic effect and no chronotropic effect.
 ...
PMID:Current therapeutic principles in the acute management of severe congestive heart failure. 304 59

Post-infarction angina includes a syndrome of ischemic chest pain occurring either at rest or during minimal activity 24 hours or more following an acute MI. It develops in approximately 10 to 15 per cent of patients and is particularly common in non Q-wave infarcts involving the anterior myocardial wall. Post-infarction angina may result from ischemia either within the infarct zone or at a distance and frequently portends a poor long term prognosis. Platelet aggregation, coronary vasospasm, and thrombus formation at the site of a ruptured atherosclerotic plaque are each involved in its pathogenesis. The initial treatment of post-infarction angina includes identification and correction of factors that increase myocardial demand including congestive heart failure and arrhythmias. beta-Adrenergic blockers, calcium channel blockers, and nitrate preparations constitute the first line of medical therapy. The role of heparin is controversial, yet it continues to be used in clinical practice. Although thrombolytic agents are currently being investigated, early experience suggests that they may accelerate clinical stabilization and allow time for elective revascularization when required. Antiplatelet therapy with aspirin has proven benefit in the long term management of unstable angina. Patients unresponsive to medical therapy should be considered for intra-aortic balloon pump placement and early coronary angiography. Revascularization with either coronary angioplasty or coronary artery bypass grafting may then be performed as dictated by the overall clinical status, available facilities, and coronary anatomy.
 ...
PMID:Management of post-infarction angina. 304 72

Exercise testing has been widely applied for the evaluation of patients with coronary artery disease. The principles underlying its use for this indication make it a useful adjunctive technique, when combined with ambulatory monitoring, to diagnose arrhythmias and monitor antiarrhythmic drug therapy. During exercise, there is a withdrawal of vagal tone and a marked increase in circulating catecholamines and sympathetic inputs to the heart. These changes may directly cause arrhythmias (e.g., catecholamines can enhance automaticity and delayed afterpotentials and can shorten myocardial conduction time and refractory periods). However, they also augment myocardial oxygen demands by increasing myocardial inotropy, heart rate and blood pressure. Such changes may cause ischemia in patients with heart disease, which is a powerful stimulus for arrhythmia, or lead to dysfunction in left ventricular contraction and increased myocardial wall stress, factors that also may precipitate arrhythmia. In approximately 10% of patients with a history of serious arrhythmia, exercise represents the only means for exposing arrhythmia. Importantly, this technique is useful for evaluating the effect of antiarrhythmic drugs. These agents work by reducing membrane automaticity, slowing impulse conduction through the myocardium and prolonging membrane refractoriness. In contrast, catecholamines, which are secreted in response to exercise, have the opposite effect. Thus, exercise may negate the important effects of the antiarrhythmic drugs. Additionally, exercise testing may expose potentially serious toxic drug reactions that may not be obvious at rest. These include conduction abnormalities, negative inotropic effects, congestive heart failure and aggravation of arrhythmia. Although the presence and frequency of arrhythmia with exercise is highly variable in patients with benign arrhythmia, results are more consistent in patients with a history of serious arrhythmia. If arrhythmia is reproducibly provoked with exercise, this technique can be used to judge drug effect. Thus, exercise testing is an important, reliable and helpful technique for exposing arrhythmia, evaluating drug efficacy and identifying potentially serious toxic drug effects.
 ...
PMID:The role of exercise testing in evaluation of arrhythmias. 305 6

Within the past 20 years, our knowledge concerning the epidemiology, natural history, and treatment of VT has expanded greatly. A variety of effective pharmacologic, surgical and electrical therapies for VT are now available to the clinician. Patients who present with ventricular tachyarrhythmias should undergo a comprehensive medical evaluation directed at identifying and treating such factors as ischemia, congestive heart failure, valvular heart disease, sensitivity to cardioactive drugs, and metabolic derangements. Many patients who present with asymptomatic ventricular arrhythmias do not require specific antiarrhythmic drug therapy. However, certain patients who have already suffered a life-threatening arrhythmia or who are at high risk for such arrhythmia should be vigorously treated with specific antiarrhythmic therapy guided for that individual patient. The efficacy of any antiarrhythmic treatment should be assessed by ECG monitoring, exercise testing, and/or electrophysiologic study. In the near future, potentially revolutionary new electrical therapies for ventricular tachyarrhythmias will be evaluated. It is to be hoped that these devices used in combination with pharmacologic and surgical therapies may dramatically reduce the incidence of sudden cardiac death in high-risk patients.
 ...
PMID:Treatment of ventricular arrhythmias. 306 73

Nicardipine hydrochloride is the first intravenous dihydropyridine calcium antagonist to become available in the United States. Its chemical structure makes it unique among its drug class and confers clinically useful properties for the treatment of acute cardiovascular conditions, such as ischemia, hypertension, congestive heart failure, cerebrovascular disease, and related disorders. For patients with coronary artery disease, IV nicardipine reduces myocardial oxygen demand by reducing afterload and increases myocardial oxygen supply through coronary vasodilatation. Preliminary data suggest that nicardipine also has cardioprotective and vascular antispastic effects. Nicardipine has been shown to be effective in the treatment of mild to moderate hypertension both as monotherapy and in combination with other antihypertensive agents. In congestive heart failure, nicardipine enhances left ventricular pumping activity and augments coronary blood flow beyond that required by increased myocardial oxygen consumption. Its lack of major effects on sinoatrial and atrioventricular conduction makes it safe for use in patients with certain types of conduction disturbances. Nicardipine's rapid onset and short duration of action are additional advantages for use in the management of acute cardiovascular disorders.
 ...
PMID:Intravenous nicardipine: cardiovascular effects and clinical relevance. 307 10

While the total ischemic burden on the left ventricle represents the combined effects of both symptomatic and asymptomatic myocardial ischemia, the total vascular burden has many components including an increased systemic peripheral vascular resistance, an increased pulmonary vascular resistance, and an increased coronary vascular resistance. These factors may all influence ventricular function. Hypertension contributes significantly to the vascular burden, especially when combined with left ventricular hypertrophy, which predisposes to ischemia by multiple mechanisms. In patients with hypertension and cardiomegaly, sublingual nifedipine has been shown to increase left ventricular (LV) ejection fraction and the average diastolic filling rate. In the presence of acute myocardial infarction, nifedipine moves the LV function curve onto a better Frank-Starling relationship as pulmonary wedge pressure falls or stays the same and cardiac output rises. However, because of the delicate balance between myocardial perfusion and the benefits of afterload reduction, including improved remodelling, nifedipine should be given only to selected patients. In congestive heart failure, low-dose nifedipine reduces the afterload and has been shown to have beneficial effects in the majority of patients. Two specific adverse outcomes in only two patients have been reported, one with initial hypotension and one given high-dose nifedipine. Combination nifedipine-beta blocker therapy has been shown to be favorable in the treatment of all varieties of angina, hypertension, and hypertrophic cardiomyopathy. Therefore, when administered appropriately, nifedipine reduces the total vascular burden on the heart in a variety of cardiovascular diseases, with consequent improvement in LV function and a diminished threat of potential myocardial ischemia.
 ...
PMID:The total vascular burden, peripheral and coronary: vasodilator effects of nifedipine. 327 10

To determine the prognostic implications of an early peak in plasma MB creatine kinase (MB CK) in patients with acute myocardial infarction who were not treated with an acute intervention, 342 patients with myocardial infarction confirmed by MB CK were retrospectively studied. The patients were classified into those with an early peak MB CK (less than or equal to 15 hours after the onset of symptoms, n = 84) and those with a late peak MB CK (greater than 15 hours after the onset of symptoms, n = 258). Patients with an early peak MB CK were slightly older, were more frequently female and had a higher incidence of prior myocardial infarction, congestive heart failure and arrhythmias compared with patients with a late peak MB CK. Patients with an early peak MB CK more frequently presented with ST segment depression (23 versus 11%, p less than 0.01), with anterior location of ischemia or infarction (71 versus 52%, p less than 0.01) and with a lower mean left ventricular ejection fraction (41.4 versus 47.4%, p less than 0.01). Despite more extensive left ventricular dysfunction at initial presentation, patients with an early peak MB CK had a smaller mean MB CK infarct size index (12.6 versus 18.9 g-Eq/m2, p less than 0.01), with no difference in the incidence of in-hospital complications, including death. The early left ventricular dysfunction improved in the patients with an early peak MB CK, evidenced by a 4.5% increase in ejection fraction from admission to 10 days after infarction, whereas the ejection fraction did not improve in patients with a late peak MB CK. However, the patients with an early peaking MB CK had myocardium in jeopardy as reflected by a higher incidence of ST segment depression and a decrement in the global left ventricular ejection fraction with exercise. The 4 year life table estimate for the rate of recurrent myocardial infarction after hospital discharge was higher in patients with an early peak MB CK (33 versus 22%, p less than 0.05), with an even more striking difference in the 4 year estimate for the rate of fatal recurrent infarction (20 versus 8%, p less than 0.001). The 4 year mortality estimate was markedly higher in hospital survivors with an early peak MB CK than in those with a late peak (47 versus 19%, p less than 0.0001) and, even after adjustment for differences in baseline characteristics, the residual excess mortality in those with an early peak was still significant (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Prognostic implications of an early peak in plasma MB creatine kinase in patients with acute myocardial infarction. 331 68

There is little, if any, good evidence in the literature to indicate a role for cardiovascular PG in congestive heart failure, either in its pathogenesis or as a consequence of and defense against its manifestations. Usually congestive heart failure is considered to develop as a vicious cycle in which impaired cardiac output, increased peripheral resistance, decreased renal blood flow, increased renin release and further increased peripheral resistance and decreased cardiac output are important constituents. Increased sympathetic activity may promote cardiovascular PG formation through the sympathetic neurotransmitter noradrenaline; such an action has, however, not been documented hitherto. Furthermore, increased plasma renin activity may promote PG formation via increased circulating levels of angiotensin; even such an action remains, however, to be demonstrated. If the heart failure leads to local tissue ischemia the hypoxia as such, or the subsequent increase in adenosine production, may also facilitate cardiovascular PG formation. All these mechanisms, if operative, would counteract the increased peripheral resistance, by promoting the formation of vasodilator PG. On the other hand PGI2 stimulates renal formation of renin, which would act to elevate the peripheral resistance. These contradictory effects of endogenously formed PG focus on the need for more careful studies on their involvement in the hemodynamic consequences of congestive heart failure: until more data are available it is impossible to know whether an activated synthesis of PG should be regarded as advantageous and worth therapeutical support, or negative and subject to inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cardiovascular prostaglandins: some comments on their involvement in circulatory physiology and pathophysiology. 352 21

Diastolic perfusion time is an important determinant of coronary blood flow and subendocardial perfusion. It has been proposed that subendocardial ischemia may exacerbate and perpetuate left ventricular dysfunction in congestive heart failure. Diastolic perfusion time in relation to heart rate was analyzed in 29 digitalized (group 1) and 12 nondigitalized patients (group 2) with heart failure and in 58 normal control subjects. In group 1 there was a strong negative exponential correlation (r = -0.85) and in group 2 a strong negative logarithmic correlation (r = -0.95) between heart rate and diastolic time; both regressions differed significantly from normal control. There was a 9% increase of diastolic time at a heart rate of 60 bpm in group 1 and a 7% increase in group 2 (both p less than 0.05) compared with normal subjects. The curves intersected the regression line of normal subjects at a heart rate of 98 bpm in group 1 and 93 bpm in group 2. At 120 bpm there was a 10% decrease in diastolic time for both groups with heart failure (both p less than 0.05). Changes in diastolic perfusion time relative to heart rate are more pronounced in congestive heart failure such that at faster heart rates this relationship may further impede subendocardial blood flow.
 ...
PMID:Diastolic time in congestive heart failure. 367 86

A woman with aneurysms of the right coronary artery and right coronary sinus of Valsalva and a right coronary arterioventricular fistula developed angina during pregnancy. Lumbar epidural anesthesia was utilized during induction of labor and cesarean delivery. The patient had no intrapartum evidence of ischemia or congestive heart failure, and she recovered without an immediate recurrence of angina.
 ...
PMID:Pregnancy in a patient with aneurysms of the right coronary artery and an arterioventricular fistula. A case report. 373 68


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>