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The chronic treatment with phenytoin or the acute intoxication by this drug may cause permanent cerebellar injury with atrophy of cerebellum vermis and hemispheres, which can be detected by neuroimaging studies. The aim of the present study was to investigate the correlation between the dosage and duration of treatment with phenytoin and the occurrence of cerebellar atrophy. Sixty-six patients were studied and had their tomographies analyzed for cerebellar atrophy. Of the 66 patients studied, 18 had moderate/severe atrophy, 15 had mild atrophy and 33 were considered to be normal. The patients with moderate/severe atrophy were those with higher exposure to phenytoin (longer duration of treatment and higher total dosage) showing statistically significant difference when compared to patients with mild atrophy or without atrophy (p=0. 02). Further, the patients with moderate/severe atrophy had serum levels of phenytoin statistically higher than those of patients with mild atrophy or without atrophy (p = 0.008). There was no association between other antiepileptic drugs dosage or duration of treatment and degree of cerebellar atrophy. We also found that older patients had cerebellar atrophy more frequently, indicating that age or duration of the seizure disorder may also be important in the determination of cerebellar degeneration in these patients. We conclude that although there is a possibility that repeated seizures contribute to cerebellar damage, long term exposure to phenytoin, particularly in high doses and toxic serum levels, cause cerebellar atrophy.

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Permanent pacemakers capable of noninvasive electrophysiologic testing were used to study and treat 26 patients with spontaneous sustained ventricular tachycardia (VT) or fibrillation (VF). One hundred nine episodes of sustained VT or VF were induced in these patients. In 8 patients spontaneous VT was reverted by noninvasive means. Drug changes based on noninvasive testing were made in 12 patients. In the 1- to 67-month follow-up period, drug therapy based on noninvasive electrophysiologic testing was predictive of outcome in patients with spontaneous arrhythmias. Thus, noninvasive electrophysiologic testing using permanent pacemakers is a useful method for studying and treating patients with recurrent sustained ventricular arrhythmias.

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Accelerated idioventricular rhythm has been used as a marker for coronary reperfusion. The incidence of accelerated idioventricular rhythm and ventricular tachycardia was evaluated in 52 consecutive patients undergoing thrombolysis with intracoronary streptokinase during acute myocardial infarction. Complete 12-hour Holter recordings during and after intracoronary streptokinase were obtained in 39 patients. Reperfusion was documented in 17 patients (44%), no reperfusion in 14 (36%), and subtotal occlusion in eight (20%). Accelerated idioventricular rhythm occurred in 83%, 57%, and 63% of patients by group, respectively (p greater than 0.05). Ventricular tachycardia occurred in 100%, 71%, and 100% of patients by group, respectively (p less than 0.05). These data demonstrate that accelerated idioventricular rhythm is not specific for reperfusion and cannot be used as a marker for this event, and that ventricular tachycardia is more common with reperfusion and subtotal occlusion.

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"Stunned" myocardium prevents the assessment of myocardial salvage after streptokinase. In order to unmask "stunning," we sought to evaluate left ventricular inotropic contractile reserve of patients after streptokinase. Radionuclide ventriculograms were obtained in 75 consecutive patients 2 weeks after myocardial infarction, at rest and during intravenous isoproterenol infusion. Resting and isoproterenol-stressed ejection fractions were compared in the patent and closed-infarct vessel groups. Although there was no difference in the resting ejection fractions between the patent group (0.48 +/- 0.02) and the closed group (0.48 +/- 0.02), isoproterenol increased the ejection fractions in the patent group (increase 0.14 +/- 0.01) significantly more than in the closed group (increase 0.06 +/- 0.01) (p less than 0.0001). Thus, despite identical resting ventricular function, the greater inotropic contractile reserve in the patent infarct vessel group suggests that restoration of blood flow in acute myocardial infarction salvages myocardium.

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Continuous ST-segment Holter recordings were analyzed from 46 patients with acute myocardial infarction (AMI) receiving intracoronary streptokinase (SK) during the first 48 hours of hospitalization. Changes in ST deviation and the time periods of these changes were quantitated and correlated with angiographic evidence of reperfusion. Thirty-six patients had total occlusion of the infarct vessel and 10 had subtotal occlusion. Of the 36 vessels that were totally occluded, 19 were reperfused and 17 were not. In patients in whom reperfusion was successful, an ST steady state was achieved 55 +/- 32 minutes after SK administration. In patients in whom it was not successful, a steady state was achieved in 219 +/- 141 minutes (p less than 0.001). Achievement of steady state within 100 minutes after SK reperfusion indicated successful reperfusion with 89% sensitivity and 82% specificity. All patients with subtotal occlusion achieved an ST steady state before SK infusion. No patient with total occlusion achieved a steady state before SK. Achievement of ST steady state before SK infusion was 100% sensitive and 100% specific for subtotal occlusion at initial angiography. Continuous, quantitative ST-segment analysis is a sensitive and specific noninvasive technique for following coronary artery patency during AMI.

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The role of pacing for arrhythmias will inevitably increase, both temporarily until a patient can be controlled with drug therapy and permanently in those cases in which drug therapy fails. While "ideal" antiarrhythmic drugs will continue to be sought, "ideal" pacing therapies will be developed. Inevitably the average patient with severe arrhythmia will benefit from a synergistic use of both modalities. The methods for capture, techniques to ensure success, standard and advanced pacing sequences, and specific indications will become as much a part of the armamentarium of the front-line clinician controlling the initial potentially lethal episodes as it has for the experienced electrophysiologist.

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Emergency cardiac catheterization and angiography in patients have resulted in an appreciation of the pathogenesis of AMI and the efficacy of thrombolytic therapy. Simple reperfusion of the infarcted myocardium, however, does not necessarily guarantee myocardial salvage, and preliminary studies have been somewhat confusing as to its beneficial effects. Metabolic support of the ventricle during early reperfusion may enhance left ventricular performance. Although the potential effects of thrombolytic therapy are still unclear, the routine administration of these agents has resulted in more frequent performance of early coronary angiography, with the result that appropriate therapeutic decisions can be made immediately regarding medical treatment, coronary angioplasty, or complete myocardial revascularization. In fact, in prolonged chest pain syndromes, emergency angiography may play a very important role in establishing appropriate initial therapy early in the course of hospitalization, potentially lowering mortality, morbidity, and cost. These issues will be answered ultimately only by carefully designed long-term randomized trials.

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Contemporary approaches to the diagnosis and treatment of acute coronary syndromes have revolutionized the role of the nurse in the coronary care unit. No longer solely the agent of the physician's orders, today's coronary care unit nurse intimately works with the physician and other allied health technical personnel to help stabilize patients initially, to guide them through the early phases of therapy, to help them understand their disease, and to educate them as to their medications. In the process, the nurse gauges patient progress, is mindful of recurrent myocardial ischemia and alerts others to its presence, identifies complications of thrombolytic therapy and PTCA, is alert to potentially malignant rhythm disturbances, and finally is the advocate of patient rehabilitation. Thus, the coronary care unit nurse plays a great role in the modern care of the patient with a myocardial infarction and materially contributes to patient recovery.

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A variety of acute supraventricular tachycardias may be encountered. In many instances the therapies for these rhythm disturbances overlap, but a rational approach to individual disturbances should be based on an understanding of the anatomy and physiology involved in the individual dysrhythmia. Numerous investigative approaches are underway at present, especially with regard to interruption of arrhythmia pathways by electroshock therapy or surgical therapy. In addition, pacing overdrive may be very effective, especially in patients with reentrant arrhythmias.

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Each component of a pacemaker system is a potential weak link in the pacing chain. Whether or not pacing failure is caused by battery depletion or by electrode fracture, these malfunctions can be diagnosed with the help of intermittent and regular transtelephonic surveillance. Sufficiently large numbers of patients enrolled in such surveillance systems enable the early identification of faulty pacers and leads and alert the medical community against their use. Indeed, the pacemaker surveillance systems in operation at present form the cornerstone of defense against pacemaker malfunction emergencies.

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The modern coronary care unit now can provide hemodynamic measurements that characterize the determinants of myocardial oxygen consumption and mechanical performance. These determinants of preload, afterload, contractile state, and heart rate can be obtained from measurements with the Swan-Ganz catheter, systemic blood pressure, assessment of ventricular function, and heart rate. With the hemodynamic characterization of the determinants of left ventricular function, drugs can be selected that either decrease or increase the specific determinants in order to optimize left ventricular performance. Thus, a physiologic approach can be taken to the pharmacologic management of patients with acute myocardial infarction based on hemodynamic measurements and appropriate therapeutic strategies.

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Newer programmable DDD pacemakers prevent pacemaker-mediated tachycardia by automatic extension of the atrial refractory period after a detected premature ventricular contraction. We present an example in which the automatic extension of the atrial refractory period resulted in pacemaker inhibition, which should not automatically be assumed to represent pacemaker malfunction. A careful understanding of pacemaker timing intervals may allow for identification and correction of this problem.

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Although thrombolytic therapy can result in lysis of a coronary artery thrombus, salvage of myocardium as measured by enzymatic, electrocardiographic and regional wall motion evaluation has not been clearly documented. Many patients after successful reperfusion continue to experience recurrent chest pain. The presence of recurrent chest pain suggests salvaged myocardium. Controlled reocclusion of the infarct vessel with the use of coronary angioplasty may support evidence for myocardial salvage. Experience in 50 patients who underwent angioplasty was reviewed retrospectively. Sixteen of the 50 patients had electrocardiographic or clinical evidence of ischemia at the time of balloon inflation. Prospectively, all patients who underwent angioplasty after they had received streptokinase were evaluated, and 5 of 5 patients had chest pain and ST-segment elevation during balloon inflation. The development of ischemic changes during balloon catheter inflation suggests the presence of persistently viable, salvaged myocardium after successful thrombolysis.

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To assess the reliability of M-mode echocardiographic patterns of mitral valve prolapse (MVP) (echo MVP) in detection of morphologic evidence of MVP (morphologic MVP), operatively excised mitral valves and corresponding M-mode echocardiograms from 65 patients with chronic, severe, isolated, pure mitral regurgitation (MR) were studied. Of the 65 patients, 45 (69%) had echo MVP (either holosystolic or mid-to-late systolic prolapse patterns on preoperative M-mode echograms) and 42 (93%) of them had morphologic MVP; of the 3 without morphologic MVP, 2 had ruptured chordae tendineae from infective endocarditis and 1 had papillary muscle dysfunction from atherosclerotic coronary heart disease. Of the 20 patients without echo MVP, 14 (70%) had no morphologic MVP (9 had papillary muscle dysfunction from coronary heart disease, 4 had infective endocarditis on previous normal valves and 1 had rheumatic heart disease). Of the 48 patients with morphologic MVP, 42 (88%) had echo MVP and most had considerably dilated mitral anulae; the other 6 had ruptured chordae tendineae with less degrees of anular dilatation. Of the 17 patients without morphologic MVP, 3 had echo MVP (coronary artery disease in 1 and infective endocarditis on a previous normal valve in 2); of the 14 with neither echo nor morphologic MVP, 9 had papillary muscle dysfunction from coronary artery disease, 4 had infective endocarditis on previously normal valves and 1 had rheumatic heart disease. The patients with very dilated mitral anuli and leaflet areas generally had holosystolic (hammocking) patterns on echo; the patients with small anuli and leaflet areas usually had mid-to-late systolic (buckling) prolapse patterns.

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