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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.
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PMID:Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease. 192 Dec 30

The antiarrhythmic and antifibrillatory actions of dilevalol, the R,R-isomer of labetalol, were evaluated in conscious dogs 4 to 6 days after anterior myocardial infarction. The administration of dilevalol in a lower dose of 0.3 mg/kg i.v. q 8 hr or a higher dose of 3.0 mg/kg i.v. q 8 hr over a period of 24 hr failed to alter electrophysiologic parameters or significantly suppress the induction of ventricular tachycardia by programmed ventricular stimulation (incidence of ventricular tachycardia suppression: 4 of 25 [16%] dilevalol vs. 1 of 14 [7%] vehicle). Pretreatment with dilevalol failed to reduce arrhythmic death in response to the subsequent development of ischemia at a site distant to the area of previous infarction (mortality: 8 of 10 [80%] dilevalol vs. 14 of 14 [100%] vehicle), but did alter the nature of the lethal ischemic arrhythmia from ventricular fibrillation (incidence of ventricular fibrillation: 14 of 14 [100%] vehicle vs. 2 of 8 [25%] dilevalol, P less than .05) to bradyarrhythmia with eventual sinoatrial arrest (6 of 8 [75%] dilevalol). The administration of methylscopolamine, 0.01 mg/kg both i.v. and i.m., to postinfarction animals pretreated with dilevalol, 3.0 mg/kg i.v. q 8 hr for 24 hr, reduced significantly mortality in response to subsequent posterolateral ischemia (mortality: 4 of 10 [40%] dilevalol plus methylscopolamine vs. 14 of 14 [100%] vehicle, P less than .05). However, methylscopolamine alone failed to suppress the development of ischemic ventricular fibrillation in 5 of 6 (83%) postinfarction dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antifibrillatory efficacy of concomitant beta adrenergic receptor blockade with dilevalol, the R,R-isomer of labetalol, and muscarinic receptor blockade with methylscopolamine. 288 7

Bradyarrhythmias, with or without hypotension, may be associated with acute myocardial infarction, especially inferior. The early use of atropine in the management of sinus bradycardia, with associated hypotension, spurred a continuing controversy that has found only partial solution in animal models. Experimentally there is increased sensory and autonomic motor activity with acute coronary occlusion. For example, in the cat, increased cholinergic activity was evidenced by the absence of bradycardia with atropinization and vagotomy, although these pretreatments accelerated the onset of significant ventricular arrhythmias. Atropine in experimentally infarcted dogs increased ischemia, while elevated heart rates reduced the threshold for ventricular fibrillation (VF) and vagal stimulation increased the threshold for VF, largely independent of heart rate. Specific clinical studies failed to support much of the animal data, although reports of tachyarrhythmias and VF resulting from the administration of atropine extended the controversy. The animal models, in the main, failed to mimic the clinical situation, for: 1) pentobarbital, with its propensity to alter some autonomic reflexes, dominated earlier work; 2) relatively large doses of atropine were employed; 3) the animals were presumed to be free of coronary and cardiac disease, factors known to influence autonomic reflexes; and 4) vagotomy and atropinization commonly preceded the acute occlusion.
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PMID:Atropine: animal models. 647 48

Right ventricular (RV) ischemia occurs in 50% of patients with acute inferior myocardial infarction, and may result in severe hemodynamic compromise associated with poor clinical outcome. Acute right coronary artery (RCA) occlusion proximal to the RV branches results in right ventricular free wall (RVFW) dysfunction. The ischemic, dyskinetic RVFW exerts mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function leads to a decrease in transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally-mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling, thereby resulting in further depression of RV performance and more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with right ventricular infarction and hemodynamic compromise often respond to volume resuscitation and restoration of a physiological rhythm. Vasodilators and diuretics should generally be avoided. In some, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover even after prolonged occlusion. Therefore, the term RV infarction appears to be somewhat of a misnomer, for in most patients a substantial proportion of acute RV dysfunction represents ischemic but viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances the recovery of RV performance and improves the clinical course and survival of patients with ischemic RV dysfunction.
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PMID:Right heart ischemia: pathophysiology, natural history, and clinical management. 944 58

Right ventricular (RV) ischemia occurs in 50% of patients with acute inferior myocardial infarction, and may result in severe hemodynamic compromise associated with poor clinical outcome. Right coronary artery occlusion proximal to the RV branches results in RV systolic dysfunction, which decreases transpulmonary delivery of left ventricular (LV) preload and diminishes cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction. Under these conditions, RV pressure generation and output depend on LV-septal contractile contributions. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling and performance, leading to more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with RV ischemia and hemodynamic compromise often respond to volume resuscitation and restoration of a physiologic rhythm. In some patients, parenteral inotropic stimulation may be required. The ischemic right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover. The term RV infarction appears to be a misnomer, as RV performance improves spontaneously even in the absence of reperfusion. Reperfusion, however, enhances the recovery of RV performance and improves the clinical course.
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PMID:Pathophysiology and clinical management of right heart ischemia. 1044 14

Atropine has also been suggested to potentially worsen the ischemic situation in patients who are in the midst of acute coronary ischemia. We report the case of a female patient with ischemic chest pain and third degree atrioventricular block who developed acute myocardial infarction (AMI) immediately after atropine administration. The use of atropine in this instance remains a reasonable option and should be strongly considered-despite this apparent complication. Undoubtedly in some cases, acute ischemia is intensified by hypoperfusion attributable to vagally mediated bradyarrhythmia; atropine is the antidote for such situations. An awareness of this potential adverse reaction coupled with a prudent selection of candidates for atropine therapy will show the risk/benefit ratio in each individual patient and, therefore, guide the clinician.
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PMID:Administration of atropine in the setting of acute myocardial infarction: potentiation of the ischemic process? 1114 27

Ligation of the posterior interventricular branch of the right coronary artery in rats induced bradyarrhythmia similar by its pathophysiological mechanisms to bradyarrhythmias developed in humans during acute ischemia of the posterior cardiac wall. The type and severity of arrhythmia and conduction disturbances, their latency and duration, and correlation with the volume of damaged myocardial tissue were determined. The efficacy and safety of the use of methylxanthines during acute myocardial ischemia was proved.
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PMID:Acute bradyarrhythmia induced by occlusion of the posterior interventricular branch of the right coronary artery. 1142 2

Increased inducible nitric oxide synthase (iNOS) expression is a component of the immune response and has been demonstrated in cardiomyocytes in septic shock, myocarditis, transplant rejection, ischemia, and dilated cardiomyopathy. To explore whether the consequences of such expression are adaptive or pathogenic, we have generated a transgenic mouse model conditionally targeting the expression of a human iNOS cDNA to myocardium. Chronic cardiac-specific upregulation of iNOS in transgenic mice led to increased production of peroxynitrite. This was associated with a mild inflammatory cell infiltrate, cardiac fibrosis, hypertrophy, and dilatation. While iNOS-overexpressing mice infrequently developed overt heart failure, they displayed a high incidence of sudden cardiac death due to bradyarrhythmia. This dramatic cardiac phenotype was rescued by specific attenuation of transgene activity. These data implicate cardiomyocyte iNOS overexpression as sufficient to cause cardiomyopathy, bradyarrhythmia, and sudden cardiac death.
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PMID:Cardiomyocyte overexpression of iNOS in mice results in peroxynitrite generation, heart block, and sudden death. 1190 Nov 82

Nineteen patients with major depression were alternately given intravenous atropine or saline immediately prior to anesthesia for electroconvulsive therapy (ECT). Atropine increased the heart rate, reduced the number of dropped beats, and reduced the number of premature atrial beats. These features may be advantageous in patients with cardiac hypodynamic states presenting for ECT, that is, with bradycardia, bradyarrhythmia, or hypotension. However, as atropine also increased the cardiac work, we recommend that it not be given to patients with hypertension, tachycardia, or who are at risk for cardiac ischemia.
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PMID:Atropine in Electroconvulsive Therapy. 1194 Sep 94

Modern cancer therapy employs a combination of chemotherapy, antibody-based therapy, radiotherapy, and surgery to prolong life and provide cure. However, many of the chemotherapy agents and antibodies, either singly or in combination, can affect the cardiovascular system. Common cardiovascular manifestations of these therapies include heart failure, ischemia, hypotension, hypertension, edema, QT prolongation, bradyarrhythmia, and thromboembolism. The patient's age, underlying cardiovascular status, and genetic background, as well as the route of drug administration and dosage, can all contribute to the development of cardiotoxicity. Strategies to monitor for and to manage these effects are discussed in this review.
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PMID:Cardiotoxicity induced by chemotherapy and antibody therapy. 1640 62


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