Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathologic substrate for sudden death in the middle-aged or elderly adult is usually ischemic heart disease. In contrast, few data are available regarding the pathology of sudden death in teenagers. This report describes three teenagers without clinically suspected heart disease dying suddenly. Patient 1 (age 15, male) was known to have right ventricular premature ventricular beats. Postmortem examination revealed marked premature aging, sclerosis of the cardiac skeleton extending to the right side of the summit with fibrosis of the left and right bundle branches. Patient 2 (age 17, male) was a trained athlete who died during football scrimmage. Autopsy revealed moderate mitral valve prolapse and marked premature aging, sclerosis of the left side of the cardiac skeleton, which extended to the right ventricular side, and secondary involvement of the trifascicular conduction system with mononuclear cell infiltration. Patient 3 (age 19, female) died suddenly at home. Autopsy revealed mitral valve prolapse, thrombosis of the sinoatrial (SA) node artery, and premature aging, sclerosis of the left side of the cardiac skeleton, with involvement of the ventricular septum more on the right ventricular side and involvement of the atrioventricular bundle and trifascicular conduction system. In conclusion, unexpected deaths in three teenagers occurred with demonstrable pathologic findings in the heart. Two of the three patients had mitral valve prolapse, one of whom also had thrombosis or embolism of the sinoatrial node artery. All three had sclerosis of not only the left side but also the right side of the ventricular septum with involvement of the conduction system. The anatomic substrate demonstrated in these three patients could relate to lethal bradyarrhythmia or tachyarrhythmia, or both.
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PMID:Sudden death in three teenagers: conduction system studies. 682 76

Forty-four cases with myocardial rupture (33 with free wall rupture, 9 with interventricular septal perforation and 2 with papillary muscle rupture), all of which were ascertained by autopsy and/or at surgery, were analyzed. When the following 7 risk factors were actively managed in the acute stage of myocardial infarction, the incidence of myocardial rupture was significantly reduced: a) high blood pressure on admission, b) physical and emotional instability, c) recurrent chest pain, d) aged females, e) no history of angina or myocardial infarction, f) large myocardial infarction on ECG and g) the first 10 days after the attack of myocardial infarction. If cardiogenic shock occurs, surgery should be performed as soon as possible; if not, it should be delayed 3 weeks. The natural history of ischemic heart disease was analyzed in 400 medically-treated patients with significant coronary artery disease. They had been followed up continuously and periodically for more than one year. The prognosis of the patients with 3-vessel disease or left main trunk disease, those with poor left ventricular function (EF less than 30%) and of old age (greater than or equal to 60) and those who had a history of ischemic heart disease was poor. Follow-up study was done in 30 patients with variant angina. They often had life-threatening arrhythmias during attacks (8 ventricular tachycardia or ventricular fibrillation, 8 serious bradyarrhythmia). All patients with variant angina should be treated medically at first, and only patients with organic coronary artery disease and chest pain on effort in spite of the medical treatment should be considered as candidates for AC bypass surgery.
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PMID:Natural history and prognosis of ischemic heart disease. 688 95

In recent years, several laboratories have suggested that serum levels of antioxidant activity and redox balance are reduced in patients with chronic renal failure. Some clinical reports have also proposed that defective serum antioxidative enzymes may contribute to a certain uremic toxicity through peroxidative cell damage. A 48-year-old woman was referred to us from the surgical department of our hospital because of consciousness disturbance, pancytopenia and acute acceleration of chronic azotemia after postoperative radiation therapy. We diagnosed acute acceleration of chronic renal failure with severe acidemia and started hemodialysis therapy immediately. Two days after admission to our department, she developed upper abdominal sharp pain and bradyarrhythmia. Serum amylase activity was elevated markedly and the ECG finding showed myocardial ischemia. On the 24th hospital day these complications were treated successfully with conservative therapy and hemodialysis. We considered that radiation therapy in this patient with chronic renal failure evoked marked oxidative stress and that deficiency of transferrin played an important role in peroxidative cell damage.
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PMID:[A case of multiple organ failure induced by postoperative radiation therapy probably evoking oxidative stress]. 769 60

Use of non-selective beta-blockers: Non-selective beta-blockers reduce blood pressure by reducing cardiac output. They have a proven record of efficacy, alone or in combination with other drug classes, in the treatment of hypertension, ischemic heart disease and some tachyarrhythmias. They have also proved effective in the primary and secondary prevention of myocardial infarction. However, adverse effects include increased peripheral resistance, limitation of exercise tolerance, and bradyarrhythmia, cold extremities and bronchoconstriction in susceptible patients. Effects of beta 1-selective blockers: beta 1-Selective antagonists cause less vasoconstriction and less bronchoconstriction than non-selective beta-blockers, but the reduction in cardiac output may still activate a sympathetically mediated increase in peripheral resistance. beta 1-blockers with beta 2 agonist activity are vasodilatory because they activate postsynaptic beta 2 receptors on vascular smooth muscle cell membranes, via the formation of cyclic AMP. Non-selective beta-blockers with alpha 2-adrenoceptor blocking activity: Non-selective beta-adrenoceptor blockers with alpha 1-adrenoceptor blocking activity, such as carvedilol, labetalol, medroxalol and bucindolol, combine the advantages of beta- and alpha 1-blockade, including peripheral vasodilation. As an example of this class of agent, carvedilol has been shown to be effective in the treatment of hypertension by reducing peripheral resistance. There are some indications, still to be confirmed, that it improves left ventricular diastolic function and causes regression of left ventricular hypertrophy, and that it may be useful in the treatment of some patients with congestive heart failure or arrhythmia. In animal models of myocardial ischemia, carvedilol has proved to be cardioprotective.
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PMID:Beta-blocking agents with vasodilator activity. 810 40

Bradyarrhythmias arising in the setting of myocardial infarction occur in a significant minority of patients with AMI. In the majority of cases, these abnormalities are owing to myocardial ischemia or infarction with necrosis of the cardiac pacemaker sites and/or conduction system. Other factors responsible for these bradyarrhythmias include altered autonomic influence, systemic hypoxia, electrolyte disturbances, acid-based disorders, and complications of various medical therapies. This article will focus on not only the diagnosis and management of these rhythm disturbances, but also on the pathophysiology of the arrhythmias.
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PMID:Diagnosis and management of bradycardia and atrioventricular block associated with acute coronary ischemia. 1137 84

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

Eighty-three patients with acute ischemic stroke (56 men and 27 women, mean age 90.1 +/- 10.8 years) were examined in order to elucidate the significance of paroxysmal heart rhythm disorders and silent myocardial ischemia and determine the pattern of hemorheological changes. Traditional clinical instrumental examinations were supplemented by Holter monitoring and measurements of a wide spectrum of hemostatic and hemorheological values. Cardiogenic ischemic strokes were pathogenetically heterogeneous. Holter monitoring helped detect the significance of paroxysmal atrial fibrillation in the pathogenesis of embolic cardiogenic stroke. One of the key factors in development of hemodynamic cardiogenic stroke was transitory bradyarrhythmia and deterioration of left-ventricular contractility. Cardiogenic strokes are associated with hemostatic activation with predominant changes in the plasma hemostasis, which dictates purposeful hemocorrection.
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PMID:[Cardiogenic ischemic strokes: pathogenetic aspects]. 1151 Jan 77

In patients with heart failure, sudden death is very common, particularly in subjects in NYHA functional class II and III (respectively 50-80% and 30-50% of all deaths). The mechanisms at the root of sudden death depend on whether heart failure is secondary to an ischemic or non-ischemic heart disease. In ischemic heart disease, sudden death is mainly arrhythmic (ventricular tachycardia/ventricular fibrillation caused by the reentry circuits in the infarct area or by acute ischemic episodes or bradyarrhythmia). In non-ischemic heart disease, the percentage of arrhythmic sudden deaths seems to be lower. Furthermore, a percentage of sudden death cases with heart failure can be linked to electromechanical dissociation and to pulmonary or systemic embolism. Moreover the risk stratification level differs depending on whether heart failure is caused by an ischemic or a non-ischemic heart disease. The various non-invasive studies mainly employed in patients with ischemic heart disease cannot be reliably used to study patients with non-ischemic heart disease. Even the programmed ventricular stimulation demonstrated prognostic reliability only in cases involving ischemic heart disease. The therapeutic approach may also be conditioned by the heart disease responsible for heart failure. To date, for example, all the studies published on primary prevention of sudden death with an implantable defibrillator have been carried out in patients with ischemic heart disease.
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PMID:[Arrhythmia risk stratification based on etiological and anatomo-structural factors]. 1183 46

Symptomatic bradycardia in the emergency department may have several causes (excessive vagal tone, drug toxicity, acute myocardial ischemia, sick sinus syndrome, heart block, and electrolyte imbalance); among these, hyperkalemia may develop as a complication of chronic medical treatment with angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers, and must be considered in the early approach to the bradyarrhythmic patient with possible electrocardiographic signs of hyperkalemia. We report a case of an 87-year-old woman with a clinical history of chronic angiotensin-receptor blocker consumption that led her to dangerous bradyarrhythmia, cardiogenic syncope, and risk of sudden cardiac death.
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PMID:Syncope caused by iatrogenic hyperkalemia. 1970 28

Arrhythmia aggravation by antiarrhythmic drugs (proarrhythmia) can be caused by worsening or a change of a preexisting arrhythmia, development of a new arrhythmia, or development of a bradyarrhythmia. Aggravation of arrhythmia usually occurs within several days of beginning an antiarrhythmic drug or increasing the dose of the drug. The time of occurrence is based on the particular drug and its pharmacokinetic properties. Although there are no ways to predict the patient at risk for developing arrhythmia aggravation with any specific agents, risk factors include QT interval prolongation, elevated serum levels of the drug, electrolyte abnormalities, presence of heart failure, a history of a sustained ventricular tachyarrhythmia, and underlying myocardial ischemia.
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PMID:Aggravation of Arrhythmia by Antiarrhythmic Drugs (Proarrhythmia). 2877 Aug 3


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