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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-four patients with sick sinue syndrome (SSS) who had been treated with a permanent pacemaker were followed for an average period of 39 months. Fifteen patients had bradyarrhythmia alone (group 1) and 29 had bradycardia-tachycardia syndrome (group 2). Eight patients, all from group 2, died within a short period following pacemaker implantation. They all had ischemic heart disease, congestive heart failure and a short history of the symptomatic dysrhythmia. Eleven patients developed stable chronic atrial fibrillation, which terminated the clinical syndrome. In the remaining 25 patients, all without evidence of ischemic heart disease, the dysrhythmia persisted although symptoms were successfully controlled following pacemaker therapy. Based on these observations and data obtained from other surveys, we delineated three courses of SSS: 1) a subacute course, characterized by a short-term survival; 2) a transient, self-limited course in which conversion to stable atrial fibrillation occurs; and 3) a chronic course, in which the dysrhythmia persists and permanent pacemaker therapy is indicated.
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PMID:Natural history of sick sinus syndrome following permanent pacemaker implantation. 52 72

Under observation were kept 80 patients with signs pointing to the sick sinus syndrome. Most of them suffered from ischemic heart disease, from atherosclerotic cardiosclerosis and acute myocardial infarction. Persistent sinus bradycardia with active and passive heterotopic arrhythmias were recorded in 42 patients. Sino-auricular block of the II and III degrees or asystolia of the atria with ectopic arrhythmias were observed in 37 cases. A number of patients displayed fibrillary bradyarrhythmia, extrasystole with post-extrasystolic depression of the rhythm and other disturbances. The so-called tachycardia-bradycardia syndrome characterized by the presence of tachycardiac arrhythmias occurring against the background of a marked bradycardia was registered in 25 persons. Fifteen patients demonstrated attackes of the Morgagni-Adams-Stokes syndrome, usually associated with lengthy periods of cardiac asystole. The treatment of ectopic arrhythmias in patients with the sick sinus syndrome presents considerable difficulties, but in many of them these disorders could be successfully eliminated by a careful and rigidly controlled application of antiarrhythmic agents (isoptin, ajmalin, pulsnorma, rhythmodan, beta-adrenergical blocking agents). For some patients exhibiting a tendency toward asystole electric stimulation of the heart is indicated.
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PMID:[Syndrome of sino-atrial node asthenia]. 79 80

Transesophageal atrial stimulation was performed in 168 patients, 95 males and 73 males, 20 to 81 years of age. The indication for atrial stimulation was the study of some bradyarrhythmia in 109 and ischemic heart disease in 59. An esophageal catheter was introduced through the nose and placed at a spot where a bimodal P wave was obtained. Stimulation was performed using a baby Medtronic stimulator coupled to a Vygon amplifier delivering an output of 30 volt. Sinus node recovery time was measured after 2 to 3 min of stimulation at different rates. Wenckebach and 2:1 A-V block as well as ST deviation were determined. Sick sinus syndrome was diagnosed in 41 cases through altered sinus node recovery time and/or secondary pauses; 35 patients showed Wenckebach rhythm at a stimulation rate over 120 per min; 2: 1 A-V block appeared in 22. Ischemic ST-T changes were produced in 20 subjects. No complications were observed, confirming this approach as a simple and effective way to achieve atrial stimulation for diagnostic purposes.
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PMID:[Transesophageal atrial stimulation in 168 patients]. 134 May 67

Although both asymptomatic ventricular arrhythmias and sudden death are common in patients with chronic heart failure, there is little evidence that patients who have frequent or complex ventricular arrhythmias are at increased risk of sudden death. Two hypotheses may explain the lack of an arrhythmia-sudden death relation in this disorder. First, complex ventricular arrhythmias may be a nonspecific manifestation of a dying left ventricle rather than an indication of a specific arrhythmogenic substrate. In fact, during long-term follow-up, patients with mild heart failure who have nonsustained ventricular tachycardia are more likely to develop clinical progression of the disease rather than sudden death. Second, sudden death may be related to events other than a malignant ventricular arrhythmia. The most common myocardial ischemia, whereas the terminal event in patients with an idiopathic dilated cardiomyopathy is commonly a severe bradyarrhythmia or electromechanical dissociation. Neither outcome can be predicted by a prior history of ventricular arrhythmias on ambulatory electrocardiographic monitoring. If asymptomatic ventricular arrhythmias do not lead to sudden death, then there would appear to be little reason to expect that antiarrhythmic drugs could prevent cardiac arrest in patients with chronic heart failure. This may explain why drugs that suppress ambulatory arrhythmias do not prevent sudden death in these patients, whereas interventions may reduce the risk of unexpected circulatory collapse in this disorder without suppressing ventricular ectopic activity. To make matters more complicated, the desirable actions of antiarrhythmic drugs are attenuated and their negative inotropic and proarrhythmic actions are enhanced in patients with severe cardiac dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of relation between ventricular arrhythmias and sudden death in patients with chronic heart failure. 172 5

In order to reduce the high mortality from ischemic heart disease, a mobile coronary care unit manned by a cardiologist has been operating in Florence since 1979. From 1980 to 1989 there were 13,029 interventions, 8,718 (66.9%) of which were cardiac emergencies. 1,718 (19.7%) patients showed acute myocardial infarction while in 2,274 angina was diagnosed (26.1%). Acute pulmonary edema and paroxysmal supraventricular tachyarrhythmias accounted, respectively, for 6.2% and 18.3% of total cardiac emergencies; moreover there were 753 (5.8%) attempted resuscitations in sudden cardiorespiratory arrest from cardiac causes. In acute myocardial infarction, the median time between the onset of symptoms and mobile coronary care unit arrival was 85 minutes, and 69.9% of patients were reached within 3 hours from the onset of symptoms. Ventricular fibrillation, ventricular tachycardia and asystole were observed respectively in 80 (4.6%), 42 (2.4%) and 50 (2.9%) patients. Success rate of emergency treatment was 81.3% for ventricular fibrillation, 88.1% for ventricular tachycardia and 18% for asystole. Prehospital mortality was 4.06%. The ECG picture of the 753 patients found in cardiac arrest showed sustained ventricular tachycardia in 12 (1.6%), ventricular fibrillation in 198 (26.3%), bradyarrhythmia in 28 (3.7%), and asystole in 431 (57.2%). Cardiopulmonary resuscitation was successfully performed in 230 patients (30.5%). Finally, more than 50% of the patients with angina, 20% of the patients with acute pulmonary edema, and 70% of the patients with paroxysmal supraventricular tachyarrhythmia were adequately treated at home and needed no hospitalization. The ten years experience of Florence Mobile Coronary Care Unit suggests that a community wide emergency cardiac care system can significantly reduce the pre-hospital mortality and the time delays preceding thrombolysis and intensive care in acute myocardial infarction. Moreover, the cardiac "sudden death" can often be successfully treated. Most other cardiac emergencies may be adequately treated at home and unnecessary hospitalizations can be avoided.
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PMID:[The mobile coronary unit of Florence: an evaluation of 10 years of prehospital cardiac care]. 186 89

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

Clinical experience with the calcium channel-blocking agents has established their efficacy in the therapy of painful and silent myocardial ischemia. Questions have arisen, however, about side-effect characteristics of these medications as clinical practice has led to utilization of higher doses of individual drugs than employed in large numbers of patients in early clinical trials as well as combinations with other antianginal agents including beta-blockers. A study was undertaken to examine the published literature regarding side effects associated with high-dose versus low-dose therapy with nifedipine and diltiazem and the use of these agents in combination with beta-blockers. This investigation demonstrated that utilization of high-dose diltiazem (more than 240 mg per day) as opposed to low-dose diltiazem (no more than 240 mg per day) was associated with an increased incidence of atrioventricular block, and increased peripheral vasodilatory effects. In contrast, the use of high-dose nifedipine (more than 60 mg per day) was not associated with atrioventricular block. At clinically high dosage levels, the incidence of peripheral edema was comparable for both nifedipine and diltiazem, although low-dose nifedipine resulted in a significantly greater incidence of edema compared with low-dose diltiazem. This analysis also demonstrated that bradyarrhythmia is associated with the combination of a beta-blocking agent and either low- or high-dose diltiazem, but not with nifedipine-beta-blocker combinations. Clinical experience suggests caution in the combined use of diltiazem and a beta-blocking agent because of the demonstrated additional adverse negative chronotropic and dromotropic effects. No additional adverse electrophysiologic effects have been noted for nifedipine-beta-blocker combinations. The literature analysis supports and mirrors widespread clinical experience obtained since nifedipine and diltiazem were introduced. It should be noted, though, that combination therapy with calcium channel blockers and beta-blockers should be done with caution, since there have been occasional reports of congestive heart failure or exacerbation of angina with this combination.
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PMID:High-dose monotherapy and combination therapy with calcium channel blockers for angina. A comprehensive review of the literature. 256 36

Patients with ischemic heart disease who present for surgery are frequently managed with a "high dose" narcotic technique utilizing fentanyl or sufentanil in combination with neuromuscular blockade. Narcotic anesthetic induction has been associated with perioperative cardiac conduction disturbances, particularly in patients previously treated with calcium channel and/or beta-adrenergic antagonists. The purpose of the present investigation was to examine in chronically instrumented dogs the effects on systemic and coronary hemodynamics and regional contractile function of sufentanil alone or in combination with the nondepolarizing neuromuscular blocking agent vecuronium, with and without pretreatment with the calcium channel blocking agent diltiazem, and/or the beta-adrenergic antagonist propranolol. Thirty-six experiments were conducted in four groups of 19 chronically instrumented dogs. Administration of sufentanil (25 and 50 micrograms/kg of normal body weight IV) resulted in a significant sinus or junctional bradyarrhythmia without alteration in systemic and coronary hemodynamics. Pretreatment with propranolol (1 mg/kg IV) decreased left ventricular +dP/dt without other hemodynamic alterations. After propranolol pretreatment, sufentanil (25 and 50 micrograms/kg IV) produced statistically significant dose-dependent decreases in heart rate and +dP/dt, while increasing mean and diastolic coronary vascular resistances. After pretreatment with diltiazem (0.3 mg/kg IV) and propranolol (1.0 mg/kg IV), sufentanil (25 micrograms/kg IV) produced significantly greater bradycardia (38 +/- 4 beats/min) than it did in non-pretreated or propranolol-pretreatment dogs. Similarly, administration of sufentanil (25 micrograms/kg IV) in combination with vecuronium (0.1 mg/kg IV) after propranolol and diltiazem pretreatment resulted in the appearance of bradyarrhythmias (32 +/- 2 beats/min) and two episodes of asystole, responsive to atropine sulfate (0.4 mg). In spite of severe bradycardia, arterial pressure was well maintained in all groups. In all groups, administration of naloxone (0.2 mg/kg IV and 0.2 mg/kg IM) after sufentanil produced significant increases in arterial pressure, left ventricular +dP/dt, and diastolic coronary blood flow velocity. Therefore, the combination of sufentanil and vecuronium in chronically instrumented dogs may result in the appearance of cardiac conduction disturbances. This action is more likely to occur after pretreatment with diltiazem and propranolol. Although systemic hemodynamics were well maintained in dogs in the present study during the episodes of bradyarrhythmias, potentially significant cardiovascular deficits may occur in pa
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PMID:Negative chronotropic actions of sufentanil and vecuronium in chronically instrumented dogs pretreated with propranolol and/or diltiazem. 256 3

The present work is divided into two parts: clinical observations and experimental investigations. The endogenic formation of nicotinic acid was decreased in all patients with ischaemic heart disease, and we have found an increased accumulation of kynurenine in blood serum after tryptophan loading in many cases - a clear indication of pyridoxal-5-phosphate (P-5-P) deficiency in the organism. The results of experimental investigations showed that L-kynurenine sulphate initiates cardiac dysrhythmias as well as dystrophic changes in cardiomyocytes. Both the clinical observations and experimental investigations point out a previously unknown pathogenetic mechanism for the ischaemic heart disease, and for bradyarrhythmia as well as myocardial cell failure, caused by P-5-P deficiency in the organism.
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PMID:[Peculiarities of nicotinic acid formation in coronary heart disease with special reference to heart arrhythmias]. 336 17

Electrocardiographic abnormalities associated with intracranial diseases, especially subarachnoid hemorrhage, are well known, while there is hardly mention of cardiac arrhythmias in the neurological and cardiological literature. In order to assess the incidence of arrhythmias 52 consecutive patients with subarachnoid hemorrhage secondary to ruptured aneurysm were investigated with 24-hour Holter recordings. Bradyarrhythmias and tachyarrhythmias were found in 46 patients (88%); premature ventricular beats in 25 pts (12 of these in 3rd-5th Lown classes), ventricular tachycardia in 2, premature supraventricular beats in 14, paroxysmal atrial fibrillation in 1, sinoatrial blocks and arrests in 18, atrioventricular dissociation in 2 and idioventricular rythm in 2. Moreover in 5 pts ST segment changes were found, suggestive of transitory acute myocardial ischemia. The presence and severity of arrhythmias were correlated with the time elapsed from the episode of bleeding, with the QT interval, and with the hemorrhage extent. Our results indicate an high incidence of arrhythmias in subarachnoid hemorrhage, sometimes serious mainly in early stage. Continuous electrocardiographic monitoring is therefore extremely useful and provides data for therapeutic consideration.
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PMID:[Cardiac arrhythmias associated with subarachnoid hemorrhage. Prospective study with dynamic electrocardiography]. 646 12


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