Maternal cardiac arrest in early pregnancy.

A primigravid woman suffered a prolonged cardiac arrest at 18 weeks of gestation. Dilated ischemic cardiomyopathy was diagnosed. After recovery, the patient received an implantable cardioverter-defibrillator. At 38 weeks of gestation she had an elective caesarean delivery. Both mother and child had a favourable outcome. The effect of pregnancy on underlying cardiac disease and the management of maternal cardiac arrest with a pre-viable fetus are discussed. The importance of a multidisciplinary approach is emphasized. Continued neurodevelopmental assessment of the newborn is necessary to detect the long-term effects of fetal hypoxia in early pregnancy.

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.).

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.

Continuous 48-h C1-inhibitor treatment, following reperfusion therapy, in patients with acute myocardial infarction.

AIMS: Complement inhibition by C1-inhibitor has been shown to reduce myocardial ischaemia-reperfusion injury in animal models. We therefore studied the effects of intravenous C1-inhibitor, following reperfusion therapy, in patients with acute myocardial infarction. METHODS AND RESULTS: C1-inhibitor therapy was started not earlier than 6h after acute myocardial infarction, in order to prevent interference with thrombolytic therapy. A loading dose of C1-inhibitor was followed by a continuous infusion for 48 h, using three escalating dosage schemes. Efficacy of complement inhibition was estimated from C4 activation fragments. Plasma concentrations of myocardial proteins were compared to values measured in matched control patients. In 22 patients, C1-inhibitor was well tolerated and drug-related adverse events were not observed. Target plasma levels of C1-inhibitor were reached, with values of 48.2 ml.kg(-1) for distribution space and 35.5h for the half-life time of C1-inhibitor. A dose-dependent reduction of C4 fragments was found P=0.005). In 13 patients who received early thrombolytic therapy, release of troponin T and creatine kinase-MB(mass) was reduced by 36% and 57%P =0.001), compared to 18 controls. CONCLUSION: Continuous 48-h treatment with C1-inhibitor provides safe and effective inhibition of complement activation after reperfused acute myocardial infarction and may reduce myocardial injury.

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.

Early referral for intentional rescue PTCA after initiation of thrombolytic therapy in patients admitted to a community hospital because of a large acute myocardial infarction.

BACKGROUND: If no in-house facilities for percutaneous transluminal coronary angioplasty (PTCA) are present, thrombolytic therapy is the treatment of choice for acute myocardial infarction (AMI). A few studies have shown benefit from rescue PTCA in patients directly admitted to centers with PTCA facilities. The obvious question arises whether patients with AMI initially admitted to a community hospital can benefit from early transfer for intentional rescue PTCA. METHODS AND RESULTS: One hundred sixty-five patients were transferred early for intentional rescue PTCA from a community hospital at a distance of 20 miles. On arrival at the angioplasty center, bedside markers were used to determine reperfusion. In case of obvious reperfusion, no invasive procedure was done; otherwise, coronary angiography and rescue PTCA, if necessary, was performed. During transfer, 1 (1%) patient died and 15 (9%) patients had arrhythmic or hemodynamic problems. Median time delay between onset of chest pain and arrival at the community hospital and the PTCA center was 61 minutes (range 0 to 413) and 150 minutes (range 28 to 472), respectively. In 66 (40%) patients, reperfusion was diagnosed by noninvasive reperfusion criteria on arrival at the PTCA center (group 1). Ninety-eight (59%) patients without evident noninvasive criteria of reperfusion underwent angiography 187 median minutes after the onset of chest pain. Forty-one (25%) patients had Thrombolysis In Myocardial Infarction grade 3 flow, and no further intervention was performed (group 2). In the remaining 57 (35%) patients, rescue PTCA was performed, which was successful in 96% (group 3). In-hospital mortality rate was lowest in group 1 compared with the other 2 groups (0% vs 7% vs 11%; P <.05). Reinfarction was highest in group 1 compared with the other groups (17% vs 5% vs 2%; P <.01). No significant differences were found in coronary artery bypass grafting, stroke, or bleeding complications. The 1-year follow-up data showed low revascularization rates; 2 (1%) patients died after discharge from the hospital. CONCLUSIONS: Early transfer of patients with large AMI for intentional rescue PTCA can be done with acceptable safety and is feasible within therapeutically acceptable time limits and results in additional early reperfusion in 33% of patients. A large, randomized, multicenter trial is needed to compare efficacy of intravenous thrombolytic treatment in a community hospital versus early referral for either rescue or primary PTCA.

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.

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.

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.

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.

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.

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.

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)

Thrombolysis in patients with unstable angina improves the angiographic but not the clinical outcome. Results of UNASEM, a multicenter, randomized, placebo-controlled, clinical trial with anistreplase.

BACKGROUND: The value of thrombolytic therapy in unstable angina is unclear. METHODS AND RESULTS: To study this problem, 159 patients were studied in a double-blind, placebo-controlled multicenter trial. Patients without a previous myocardial infarction, with a typical history of unstable angina, and ECG abnormalities indicative of ischemia were included. After baseline angiography, study medication (anistreplase or placebo) was given. Angiography was repeated after 12-28 hours. A significant decrease occurred in diameter stenosis between the first and second angiogram in the anistreplase group compared with the placebo group (11% versus 3%, p = 0.008). This difference was caused by reopening of occluded vessels in the thrombolytic group. However, no beneficial clinical effects of thrombolytic treatment were found. Bleeding complications were significantly higher in patients who received thrombolytic therapy (21 versus seven patients, p = 0.001). CONCLUSIONS: Thus, angiographic but no clinical improvement after thrombolytic treatment with anistreplase was found in patients with unstable angina with an excess of bleeding complications. Therefore, thrombolytic treatment cannot be recommended in patients diagnosed as having unstable angina until proven otherwise.

Sudden arrhythmic death without overt heart disease.

Nine patients (eight males) are reported with one or more episodes of circulatory collapse in the absence of overt heart disease or other known causes of arrhythmias; sudden arrhythmic death occurred in one of these patients. Age at first episode ranged from 16 to 41 (mean, 28) years. In seven patients, ventricular fibrillation was documented at the time of resuscitation. One patient had ventricular flutter. In the remaining patient, documentation of the arrhythmia during the collapse was not available. Four patients had frequent early ventricular premature beats, and in three of these patients, they were accompanied by episodes of rapid nonsustained polymorphic ventricular tachycardia. Failure to suppress this ectopic activity by drug therapy seems to be of prognostic significance. Of the three patients showing persistence of frequent early ventricular premature beats, one died suddenly, and two had recurrences of symptomatic arrhythmic episodes. The value of noninvasive and invasive tests in the management of these patients is not clear, with the exception of exercise testing in patients with exercise-related arrhythmias and long-term electrocardiographic monitoring in patients with frequent spontaneous ventricular ectopic activity. Follow-up varied from 21 to 192 (mean, 84) months. One patient died suddenly 21 months after his first collapse. Selection of antiarrhythmic drug therapy was largely empirical. In view of the relative rarity of sudden arrhythmic death in the absence of heart disease and the many uncertainties about its mechanism(s) and management, a worldwide registry of these patients is suggested.

Improvement of systolic and diastolic left ventricular wall motion by serial echocardiograms in selected patients treated for unstable angina.

The purpose of the study was to evaluate the effect of antiischemic treatment on left ventricular function in selected patients with unstable angina pectoris that was due to severe proximal left anterior descending coronary artery narrowing and to identify subgroups liable to an adverse outcome (mean term 2.7 years). Effect of antiischemic treatment on systolic and diastolic left ventricular wall motion was studied in 35 patients who had unstable angina pectoris and an electrocardiogram that indicated severe proximal left anterior descending coronary artery narrowing. Treatment consisted of either a revascularization procedure (17 patients) or antianginal drug therapy (18 patients). All patients underwent a two-dimensional echocardiographic study within 48 hours (mean 20 hours) of entry into the study. This study semiquantitatively analyzed systolic performance of the ischemia-related segments by calculation of a total wall motion score. In 16 patients this investigation was combined with a continuous detailed recording of only the apical interventricular septal wall motion. This detailed study included measurements for regional function by providing a typification of the pattern of systolic and early diastolic excursion of the endocardial border of the apical interventricular septum. A repeat ultrasonic study was performed at least 1 month (median 2 months, 7 days) after admission. Results of the systolic wall motion analyses of all 35 patients showed, in both treatment groups, a significant improvement in systolic wall motion of the anterior and apical segments (mean total wall motion score at early study vs late study: revascularization, 6.9 vs 2.2 and medical therapy, 4.6 vs 1.0).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery.

One hundred eighty of 1260 patients consecutively admitted to the hospital because of unstable angina pectoris had the typical ST-T segment changes suggestive of a critical stenosis in the proximal LAD. In 108 patients the ECG abnormalities were present at the time of admission. In the remaining 72 patients they developed shortly thereafter. The difference between these two groups was a longer duration of anginal complaints in the former (mean 2.3 days). Results of coronary angiography, performed a mean of 4.6 days after the last attack of chest pain, showed 50% or more narrowing in the proximal LAD in all patients. Thirty-three patients had complete occlusion of the LAD and 75 had collateral circulation to the LAD. Results of left ventricular angiography showed abnormal systolic left ventricular wall motion in 137 patients and normal systolic motion in the remaining 43 patients. The difference between these two groups was a shorter mean time interval between the last attack of chest pain and angiography in the former group (p less than 0.001). Twenty-four patients had only abnormal diastolic wall motion. Twenty-one patients had a small increase in the creatine kinase level at the time of admission. Fifteen patients (nine before and six during early revascularization) had an anterior wall myocardial infarction in the hospital; these patients had a patent but severely narrowed LAD and a low incidence of collateral circulation to the LAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Greater than expected alanine aminotransferase activities in plasma and in hearts of patients with acute myocardial infarction.

Early increases in the activity of alanine aminotransferase (ALT, EC 2.6.1.2) in plasma are observed in about 7% of patients with acute myocardial infarction (AMI), of whom about half die. Some type of liver injury, secondary to AMI, could be responsible for this phenomenon. However, quantitative analysis shows that the release of ALT in most of these patients conforms to the myocardial release pattern. Moreover, extra release of hepatic aspartate aminotransferase (EC 2.6.1.1) is not observed. These findings suggest that the heart may occasionally contain a high ALT activity. This hypothesis was verified by determination of enzyme activities in 10 hearts obtained from patients who died after AMI. The mean ALT activity in these hearts, 21 (SD 12) U per gram wet weight, significantly (P less than 0.01) exceeds the value of 7.7 (SD 4.9) U/g found for seven control hearts and may reflect increased amino acid metabolism in the energy-depleted heart muscle, as described earlier for skeletal muscle.