The ictal bradycardia syndrome.

The ictal bradycardia syndrome is an uncommon diagnosis in which bradycardia is accompanied by simultaneous epileptic discharges in the EEG. We describe a patient who was referred to the emergency ward because of syncope. Ictal semeiology and EEG-EG findings are discussed and compared with those published in the literature. Therapeutic options are discussed in relation with those published in the literature. The ictal bradycardia syndrome is probably underdiagnosed, while its recognition is of utmost importance because of potential life threatening complications such as asystole. Up to now, its aetiology is poorly understood, its ictal semeiology is often described insufficiently and its therapy is still discussed.

Primary monophasic mediastinal, cardiac and pericardial synovial sarcoma: a young man in distress.

A 19-year-old male was admitted because of exertional dyspnoea. The imaging studies revealed epicardial, pericardial and mediastinal masses. The tumours could not be resected through a minor thoracotomy, only biopsies could be taken. Analyses led to the final diagnosis of a monophasic synovial sarcoma. The patient preferred a conservative and palliative approach. Three months later he died at home. Autopsy demonstrated dramatic extension of the tumour masses. We conclude this report with a discussion on primary cardiac tumours. (Neth Heart J 2007;15:226-8.).

Left ventricular aneurysm subsequent to cleavage of myocardial bridging of a coronary artery.

In two patients, an aneurysm of the left anterior wall developed at the site of periarterial muscle resection of a myocardial bridge over the proximal portion of the left anterior descending coronary artery. One patient had a severe atherosclerotic stenosis proximal to the bridge. He also received a bypass graft to the left anterior descending coronary artery distal to the bridge. In the other patient without signs of atherosclerotic disease, only cleavage of the myocardial bridge was performed. Observations in these two cases suggest the need to reevaluate the risks of surgical treatment in symptomatic patients with myocardial bridging.

Right and left ventricular ejection fraction in acute inferior wall infarction with or without ST segment elevation in lead V4R.

To detect right ventricular involvement, lead V4R was recorded within 10 hours of the onset of chest pain in 42 consecutive patients admitted with acute inferior wall myocardial infarction. One week after the acute infarction, multigated equilibrium radionuclide ventriculography was performed to assess right and left ventricular ejection fraction. Two weeks after the acute infarction, coronary angiography was performed to determine the site and location of the obstruction leading to the infarction. Seventeen patients had an obstruction in the right coronary artery proximal to the first branch to the right ventricular free wall (group 1); all of these had ST segment elevation in lead V4R. Fourteen patients had an obstruction in the right coronary artery distal to the first branch to the right ventricular free wall (group 2); only two of these patients had ST segment elevation in lead V4R. In 11 patients, the obstruction was located in the circumflex coronary artery (group 3); none of these had ST segment elevation in lead V4R. Nineteen patients had ST segment elevation of 1 mm or greater in lead V4R (group 4). Left ventricular ejection fraction was not different among the four groups of patients, although the right ventricular ejection fraction was significantly lower in group 1 and group 4 patients. It is concluded that ST segment elevation in lead V4R reliably identifies the group of patients with inferior wall myocardial infarction with depressed right ventricular function. This phenomenon persists for at least 1 week after infarction.

Coronary angiographic findings do not predict clinical outcome in patients with unstable angina.

OBJECTIVES: The presence of thrombus formation and type of coronary artery lesion were determined in patients with unstable angina and correlated with the angiographic findings and clinical outcome. BACKGROUND: Some previous studies have suggested that thrombus formation and lesions are predictive of the angiographic and clinical findings. This was evaluated in a retrospective analysis of 159 patients participating in the placebo-controlled Unstable Angina Study Using Eminase (UNASEM) trial on the effect of thrombolysis in unstable angina. METHODS: Patients without a previous myocardial infarction who presented with a typical history of unstable angina in the presence of abnormal findings on the electrocardiogram indicative of ischemia were included in the study. After baseline angiography, study medication (anistreplase or placebo) was given to 126 to 159 patients. Thirty-three patients did not receive medication because of significant main stem disease or normal coronary arteries or for other reasons. Angiography was repeated after 12 to 28 h. RESULTS: Quantitative angiography showed a significant decrease in diameter stenosis in the anistreplase-treated group compared with the placebo-treated group (decrease 11% vs. 3%, p = 0.008). No differences in clinical outcome were found when thrombolytic treatment was compared with placebo (p = 0.98). Neither the presence nor absence of thrombus formation (p = 0.98) nor the type of lesion (p = 0.96) was related to the changes in diameter stenosis or to clinical outcome (p = 0.90 and p = 0.77, respectively). The power of these analyses to detect a 20% difference varied between 56% and 74%. CONCLUSIONS: In this selected group of patients with unstable angina, type of coronary artery lesion and the presence or absence of thrombus formation does not predict clinical outcome.

Effects of thrombolytic therapy in unstable angina: clinical and angiographic results.

The incidence of intracoronary thrombus and the effects of thrombolytic therapy were studied in 41 patients with unstable angina. All patients underwent coronary angiography 2 to 69 h (mean 19) after their last attack of chest pain. Immediately after angiography, 21 patients received intracoronary streptokinase (250,000 IU in 45 min) and were retrospectively analyzed. Twenty patients received intravenous recombinant tissue-type plasminogen activator (rt-PA) (100 mg in 3 h) and were involved in a prospective study. Eleven of the 21 patients from the streptokinase group and 11 of the 20 patients from the rt-PA group showed a decrease in the severity of the coronary stenosis on repeat angiography 1 day later. A decrease in coronary obstruction was primarily observed in 10 of 13 patients with a complete stenosis and in 6 of 9 patients with a subtotal stenosis and markedly diminished coronary flow. Improvement in coronary anatomy was not determined by the clinical characteristics of the patients. Twenty-eight of the 41 patients had angiographic evidence of intracoronary thrombus formation before and 16 had such evidence after thrombolytic treatment. Nine patients developed a small increase in serum cardiac enzymes before or during treatment. Ischemic symptoms and the incidence of surgical or angioplastic intervention were not different in patients with or without a reduction in coronary artery stenosis after fibrinolytic therapy. These observations suggest a high incidence of coronary thrombosis in patients with unstable angina. The data do not permit assessment of the clinical therapeutic efficacy of thrombolytic therapy. Better risk stratification and placebo-controlled prospective studies are required to obtain information on the risk/benefit ratio of such therapy in unstable angina.

Effects of early reperfusion in acute myocardial infarction on arrhythmias induced by programmed stimulation: a prospective, randomized study.

This study compares inducibility of ventricular tachyarrhythmias by programmed electrical stimulation of the heart in patients with myocardial infarction with and without reperfusion after streptokinase therapy. Sixty-two consecutive patients admitted with an acute myocardial infarction were randomized to either combined intravenous and intracoronary streptokinase (streptokinase group) or to standard coronary care unit treatment (control group). Thirty-six of the 62 patients (21 patients from the streptokinase and 15 from the control group) with a first myocardial infarction were studied by programmed ventricular stimulation after a mean of 26 +/- 14 days. No patient had a history of antiarrhythmic drug use or documentation of a ventricular arrhythmia before the initial admission. A sustained ventricular arrhythmia was induced in 10 (48%) of the 21 patients randomized to streptokinase therapy and in all 15 (100%) control patients (p less than 0.001). Sustained monomorphic ventricular tachycardia was induced in 6 (29%) and 10 (67%) patients, respectively (p less than 0.05). To terminate an induced arrhythmia, direct current countershock was required in 33% of patients in the streptokinase group and 73% of patients in the control group (p less than 0.02). Seventeen of the 21 patients treated with streptokinase and no control patient had evidence of early reperfusion 200 +/- 70 minutes after the onset of pain. In comparison with patients without early reperfusion, patients in the reperfused group had a lower maximal serum creatine kinase value (p less than 0.01), a shorter time to peak creatine kinase value (p less than 0.001) and a higher angiographic left ventricular ejection fraction (62 versus 45%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Early thrombolysis in acute myocardial infarction: limitation of infarct size and improved survival.

The effect of thrombolysis in acute myocardial infarction on infarct size, left ventricular function, clinical course and patient survival was studied in a randomized trial comparing thrombolysis (269 patients) with conventional treatment (264 control patients). All 533 patients were admitted to the coronary care unit within 4 hours after the onset of symptoms related to the infarction. Baseline characteristics were similar in both groups. Informed consent was requested only of patients allocated to thrombolysis; no angiography was performed in 35. The infarct-related artery was patent in 65 patients and occluded in 169. Recanalization was achieved in 133 patients. The median time to angiographic documentation of vessel patency was 200 minutes after the onset of symptoms. The clinical course in the coronary care unit was more favorable after thrombolysis. Infarct size, estimated from myocardial enzyme release, was 30% lower after thrombolysis. In patients admitted within 1 hour after the onset of symptoms the reduction of infarct size was 51%, in those admitted between 1 and 2 hours it was 31% and in those admitted later than 2 hours it was 13%. Left ventricular function measured by radionuclide angiography before hospital discharge was better after thrombolysis (ejection fraction 48 +/- 15%) than in control patients (44 +/- 15%). Similar improvement was observed in patients with a first infarct only (thrombolysis 50 +/- 14%, control subjects 46 +/- 15%), in patients with anterior infarction (thrombolysis 44 +/- 16%, control subjects 35 +/- 14%) and in those with inferior infarction (thrombolysis 52 +/- 12%, control subjects 49 +/- 12%). Similar results were obtained by contrast angiography. Mortality was lower after thrombolysis. After 28 days 16 patients allocated to thrombolysis and 31 control patients had died. One year survival rates were 91 and 84%, respectively. On the other hand, nonfatal reinfarction occurred more frequently after thrombolysis (36 patients) than in control subjects (16 patients). Early thrombolysis by intracoronary streptokinase leads to a smaller infarct size estimated by enzyme release, preserves left ventricular function at the second week and leads to improved 1 year survival.

Effects of intracoronary thrombolysis on global left ventricular function assessed by an automated edge detection technique.

Three hundred and two patients with acute myocardial infarction were enrolled in a randomized multicenter trial to compare conventional treatment with attempted recanalization by intracoronary streptokinase. In a subgroup of patients, the effects of thrombolysis on left ventricular function were evaluated within 48 hr, at 2 wk, and at 3 mo after admission. Global left ventricular ejection fraction (LVEF) was obtained by radionuclide angiography and analyzed with an automatic detection program. Paired data were determined in 160 patients (control 78, thrombolysis 82) within 48 hr and at 2 wk, and in 143 patients (control 71, thrombolysis 72) at 48 hr, 2 wk, and 3 mo. It was shown that LVEF significantly improved in the thrombolysis group as compared with controls both at 2 wk (delta LVEF thrombolysis 3.9 +/- 7.9%, p less than 0.001 compared with delta LVEF control 0.6 +/- 9.7%, p = N.S.) and at 3 mo (delta LVEF thrombolysis 3.1 +/- 12.4%, p less than 0.05 compared with delta LVEF control 2.1 +/- 12.2%, p = N.S.). When patients were divided according to infarct site, however, significant improvement at 3 mo was only observed in the patients with anterior infarction (delta LVEF thrombolysis 5.5 +/- 13.1%, p less than 0.05 compared with delta LVEF control 3.3 +/- 10.4%, p = N.S.). It was shown that acute intervention with intracoronary streptokinase has a potentially favorable and lasting effect on left ventricular function in patients with anterior myocardial infarction. This improvement might be related to the rather rapid administration of thrombolytic therapy with a median time of approximately 4 hr after onset of symptoms.

Treatment with a GPIIb/IIIa antagonist inhibits thrombin generation in platelet rich plasma from patients.

Infusion of the GPIIb/IIIa-inhibitor MK383 inhibits thrombin generation in platelet rich plasma by interfering with the production of platelet procoagulant phospholipid exposure. The effect is similar to that of 0.2 U/ml of heparin. Heparin infusion, well known to inhibit thrombin generation by fostering antithrombin activity, inhibits the formation of platelet-derived procoagulant microparticles, probably by decreasing the formation of free thrombin, which, under our circumstances, is the main platelet activator.

Value of left ventricular ejection fraction in extensive anterior infarction to predict development of ventricular tachycardia.

In 33 patients admitted with an extensive acute anterior myocardial infarction (MI), left ventricular ejection fraction (LVEF) was determined within 1 week after MI using radionuclide angiography. In 15 patients, sustained ventricular tachycardia (VT) developed in the second and third week after MI. Thirteen of the 15 patients had an LVEF less than 40%. Only 3 of 18 patients who did not develop late VT had an LVEF less than 40%. Of the 15 patients who developed VT, 8 had right bundle branch block within 48 hours after the onset of chest pain. Right bundle branch block was seen in only 3 of the 18 patients who did not develop VT. We conclude that in patients with extensive anterior MI, a radionuclide LVEF of less than 40% identifies a group at high risk of developing VT within a few weeks after MI.

Value of the electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest angina pectoris.

The aim of this study was to assess the value of the electrocardiogram recorded during chest pain for identifying high-risk patients with 3-vessel or left main stem coronary artery disease (CAD). Therefore, the number of leads with abnormal ST segments, the amount of ST-segment deviation, and specific combinations of leads with abnormal ST segments were correlated with the number of coronary arteries with proximal narrowing of > 70%. Electrocardiograms recorded during chest pain were compared with one from a symptom-free episode. In this retrospective analysis, 113 consecutive patients were included. One-vessel CAD was present in 47 patients, 2-vessel CAD in 22, 3-vessel CAD in 24 and left main CAD in 20. Stratification was performed according to the presence of an old myocardial infarction. The number of leads with ST-segment deviations, and the amount of ST-segment deviation in the electrocardiogram obtained during chest pain at rest showed a positive correlation with the number of diseased coronary arteries. These findings were more marked when the absolute shifts from baseline were considered, because ST-segment abnormalities could be present also in the electrocardiogram obtained during the symptom-free episode. Left main and 3-vessel CAD showed a frequent combination of leads with abnormal ST segments: ST-segment depression in leads I, II and V4-V6, and ST-segment elevation in lead aVR. The negative predictive and positive accuracy of this pattern were 78 and 62%, respectively. When the total amount of ST-segment changes was > 12 mm, the positive predictive accuracy for 3-vessel or left main stem CAD increased to 86%.(ABSTRACT TRUNCATED AT 250 WORDS)

Value of admission electrocardiogram in predicting outcome of thrombolytic therapy in acute myocardial infarction. A randomized trial conducted by The Netherlands Interuniversity Cardiology Institute.

To determine the value of the admission 12-lead electrocardiogram to predict infarct size limitation by thrombolytic therapy, data were analyzed in 488 of 533 patients with acute myocardial infarction (AMI) from a randomized multicenter study. All patients had typical electrocardiographic changes diagnostic for an AMI and were admitted within 4 hours after the onset of chest pain; 245 patients were allocated to thrombolytic treatment and 243 to conventional treatment. Cumulative 72-hour release into plasma of myocardial alpha-hydroxybutyrate dehydrogenase (HBDH) was used as a measure of infarct size. In general, the amount of infarct limitation due to thrombolytic therapy was proportional to the size of the area at risk. Patients with new Q waves, high QRS score and high ST-segment elevation or depression had the largest enzymatic infarct size in both treatment groups, irrespective of location of the AMI. Compared with conventionally treated patients, patients with anterior AMI treated with streptokinase had significant infarct size limitation (480 U/liter HBDH, 37%), and limitation was most prominent in those with Q waves (820 U/liter HBDH) or high ST elevation (750 U/liter HBDH). Infarct size limitation in inferior AMI was less impressive (330 U/liter HBDH, 33%) and patients with high ST-segment elevation (460 U/liter HBDH) or marked contralateral ST-segment depression (430 U/liter HBDH) had the most notable infarct limitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute coronary thrombolysis with recombinant human tissue-type plasminogen activator: initial patency and influence of maintained infusion on reocclusion rate.

An intravenous infusion of 40 mg of recombinant tissue-type plasminogen activator (rt-PA) was given intravenously over 90 minutes to 123 patients with acute myocardial infarction (AMI) of less than 4 hours' duration. A coronary angiogram was recorded at the end of the infusion in 119 patients. Central assessment of the angiograms revealed a patent infarct-related artery in 78 patients (patency rate 66%, 95% confidence limits 57 to 74%). Patients with a patent infarct-related artery at the first angiogram were randomized in a double-blind manner to receive a subsequent 6-hour infusion of either 30 mg of rt-PA or placebo. All patients had received an initial bolus of 5,000 IU of heparin and then 1,000 IU/hour until a second angiogram was recorded 6 to 24 hours after the start of the second perfusion. At central assessment of the second coronary angiogram the reocclusion rate was 2 of 36 patients who received rt-PA at the second infusion and 3 of 37 patients not receiving this drug (or the 2 groups combined 7%, 95% confidence limits 2 to 15%). Three of 60 patients (5%, 95% confidence limits 1 to 14%) with patent arteries on both previous angiograms had a later occlusion as judged on the angiogram recorded at hospital discharge. No difference in late reocclusion rates between the 2 treatment groups was observed.

Unstable angina: are we able to recognize high-risk patients?

It is difficult to identify characteristics of patients with unstable angina that are predictive of a high likelihood of developing clinical events. However, several features have been recognized. Patients with a clinical history of previous stable exertional angina symptoms who began to experience rest pain appear to be at risk and tend to have more extensively underlying coronary disease. When the ischemic episodes are accompanied by rates, a new or worsening mitral regurgitation murmur, or hypotension, there is a high likelihood of significant coronary artery disease and one should triage these patients to early cardiac catheterization and prompt revascularization. An angiographic feature that carries a high risk is a lesion in the proximal left anterior descending or in the left main coronary artery. Certain typical ECG patterns are very suggestive for a critical narrowing in these coronary arteries. If chest pain and ST-segment changes recur on vigorous medical management, early invasive evaluation should be strongly considered. Even so, the left ventricular function is very important prognostically. According to serologic tests, the level of C-reactive protein and serum amyloid A protein suggesting that there may be active inflammation predicts an early poor outcome. However, these serologic abnormalities do not have much clinical value. An increased platelet activation and a reduced fibrinolytic capacity play a role in the pathogenesis of unstable angina, but thrombolytic therapy does not improve the prognosis in patients with unstable angina.

Changes in wall motion in patients treated for unstable angina. A suggestion of the stunned and hibernating myocardium in humans. UNASEM Collaborative Study Group. Unstable Angina Study Using Eminase.

BACKGROUND: A double-blind, placebo-controlled study using anistreplase was performed in 159 patients with unstable angina. All patients had a history of unstable angina combined with typical ECG changes and without evidence of a previous, recent, or ongoing myocardial infarction. The purpose of the present study was to analyze the relationship between the patency of the culprit artery and the behavior of the ischemia-related regional left ventricular (LV) wall motion. METHODS AND RESULTS: On entry to the study, all patients received conventional drug therapy: i.v. nitroglycerin therapy, an oral beta-blocking agent, and a calcium antagonist. Baseline angiography was carried out within 3 h after randomization, a mean of 4.2 +/- 3.0 h (range, 1 to 17 h) after the last attack of chest pain. Treatment with trial medication was withheld in 33 cases. Sixty-five patients with coronary artery disease received anistreplase (30 U/5 min)/heparin and 61 patients heparin-only therapy. Angiography was repeated 20.6 +/- 4.6 h (mean +/- SD; range, 12 to 39 h) after the baseline angiographic study. To assess changes in regional myocardial wall motion, the LV wall was divided into seven segments. The ischemia-related coronary artery stenosis was calculated quantitatively and related to the quantitatively assessed mean regional left ventricular ejection fraction (RLVEF) of the ischemia-related segments. In 118 of 126 patients who received trial medication, we found that anistreplase/heparin therapy leads to a significantly (p < 0.01) greater reduction in coronary artery diameter stenosis than heparin-only therapy (n = 63, mean +/- SD, 11 +/- 22, vs n = 55, mean +/- SD, 3 +/- 11%). Anistreplase/heparin therapy was related to a larger significant improvement of the ischemia-related RLVEF than heparin-only therapy, although the latter association was not statistically significant (n = 63, mean +/- SD, 7 +/- 15, vs n = 55, mean +/- SD, 5 +/- 14%). The effects of change of coronary artery stenosis on regional LV wall motion were also determined. A paradoxical finding was that a persistently occluded vessel or a vessel showing an increase in coronary artery stenosis was associated with a greater improvement of the ischemia-related RLVEF than a reopened vessel or a vessel with a reduction in coronary artery stenosis (n = 15, mean +/- SD, 7 +/- 11, vs n = 41, mean +/- SD, 8 +/- 13, vs n = 15, mean +/- SD, 1 +/- 12, vs n = 47, mean +/- SD, 5 +/- 16%, NS). One day after the last attack of chest pain, the regional LV wall motion was still abnormal in about 20% of patients. CONCLUSION: In these patients with unstable angina, the LV wall motion improved both in the treated and the control group at follow-up angiography 1 day later. Improved coronary arterial anatomy was associated with a lesser improvement of the LV contractile function than when worsening of the coronary angiographic appearance occurred. There is no rational explanation of these results. This is a beginning of an effort to elucidate the clinical significance of the stunned and hibernating myocardium in humans.

Rescue PTCA Following Failed Thrombolysis and Primary PTCA: A Retrospective Study of Angiographic and Clinical Outcome.

Evidence is increasing that a patent culprit artery improves the prognosis of patients with acute myocardial infarction (AMI). Primary percutaneous transluminal coronary angioplasty (PTCA) has shown to be more effective than thrombolytic therapy alone. How effective is rescue PTCA after failed thrombolytic treatment? In a retrospective analysis, 176 consecutive patients with AMI and TIMI 0 or 1 perfusion grade were included. Patients had either rescue PTCA after failed thrombolysis (100 patients) or primary PTCA (76 patients). Angiographic data and in-hospital and 1-year outcome were analyzed. Comparison of baseline data of the two groups showed a higher proportion of long-standing angina and use of nitrates and aspirin in the primary PTCA group. Also, the delay between the onset of pain and PTCA was not significantly different, with a mean of 222 minutes for rescue PTCA and 245 minutes for primary PTCA (p = 0.52). The angiographic outcomes in the rescue PTCA group and the primary PTCA group were identical: The intervention was successful (TIMI 3 flow and residual stenosis <50%) in 86.0% and 85.5%, respectively. Complication rates of the procedure were also similar, except for bleeding complications. Blood transfusion was only needed after rescue PTCA in 3.0% versus 0.0% in primary PTCA patients. Clinical outcomes during hospital stay in terms of death rate (4.0% and 6.6%), reinfarction (6.0% and 3.9%), recurrent angina (16.0% and 11.8%), and repeat interventions were comparable, as was the first-year outcome. Failed PTCA was the most important predictor of a poor 1-year outcome; 28.0% died after failed PTCA versus 4.6% after successful PTCA (p < 0.001). In this retrospective analysis of 176 AMI patients, angiographic and clinical outcome, including a 1-year follow-up in patients who had rescue PTCA after failed thrombolysis, were of the same magnitude of patients in whom primary PTCA was performed. These findings suggest that in this subset the outcome of patients with rescue PTCA because of failed thrombolysis is good and is comparable with patients who underwent primary PTCA.

Explaining cost variations in DRGs 'Acute Myocardial Infarction' by severity of illness.

The empirical relationship is analyzed between the severity of illness and costs of medical care for 464 patients classified into DRGs 121-123, Acute Myocardial Infarction (AMI), in the University Hospital, Maastricht. Severity of cardiac and cardiovascular disorders characteristic of acute myocardial infarction is defined and operationalized in a sense that closely resembles the clinical practice of cardiologists. The effect of the severity of illness on DRG cost variations is studied separately for the costs of acute care (such as thrombolytic therapy, cardiac catheterization and percutaneous transluminal coronary angioplasty (PTCA)), length of hospital stay, costs of intensive nursing care at the coronary care unit (CCU) and the costs of ECGs, laboratory tests, echocardiography, exercise tests and drugs. For AMI patients, severity of illness measured by specific clinical criteria is found to give better predictions (higher R2) for costs of medical care than the DRG classification.

Mechanisms of cell death in acute myocardial infarction: pathophysiological implications for treatment.

The purpose of this review is to draw attention to the growing list of pathophysiological phenomena occurring in blood, the vessel wall and cardiac tissue during myocardial infarction. A further aim is to point to the complexity of factors, contributing to cardiac dysfunction and the implications for therapy, aimed at limiting myocardial cell death. Not all pathophysiological mechanisms have been elucidated yet, indicating the necessity for further research in this area. In addition we describe interventions which have shown promise in animal studies, those which may show promise in humans, and those which are accepted as therapies of choice.