Nondominant right coronary artery occlusion and ventricular tachyarrythmias.

It is usually considered that occlusion of a nondominant right coronary artery is not associated with significant consequences. We report two cases of nondominant right coronary artery occlusion that presented with sudden cardiac death. Timely intervention resulted in complete resolution of the ventricular arrhythmias. This highlights the need for greater vigilance in the recognition and treatment of these lesions.

Successful use of eptifibatide as an adjunct to coronary stenting in a patient with abciximab-associated acute profound thrombocytopenia.

A 72-year-old male who was given abciximab for unstable angina developed acute profound thrombocytopenia with a platelet count nadir of 6,000/mm3. He was treated with steroids and platelet transfusion. Four days later, he underwent coronary angioplasty after pretreatment with eptifibatide without development of thrombocytopenia. This suggests that the development of thrombocytopenia with abciximab is not necessarily a contraindication to subsequent use of glycoprotein (GP) IIb/IIIa receptor antagonists. Eptifibatide may be an appropriate consideration in high-risk patients who would benefit from a GP IIb/IIIa receptor antagonist, in spite of acute profound thrombocytopenia due to abciximab therapy.

Acute profound thrombocytopenia without bleeding complications after re-administration of abciximab.

Abciximab (c7E3) is the Fab fragment of the chimeric (murine/human) monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor, which is the final common pathway for platelet aggregation. Abciximab has been widely used for patients undergoing angioplasty who are at high risk for ischemic complications. Severe thrombocytopenia (defined as platelet count < 50,000 platelet/mm3) has been observed in both first-time administration and re-administration of abciximab. Platelet transfusion as treatment for the reversal of thrombocytopenia is ubiquitously accepted. Intravenous corticosteroid as an adjunctive therapy is being explored. We previously reported our experience with platelet transfusion combined with corticosteroid treatment for acute thrombocytopenia following first-time abciximab administration. We now report a case of acute profound thrombocytopenia following re-administration of abciximab successfully treated with a combination of platelet transfusion and intravenous corticosteroid.

Combination of abciximab with primary stenting in patients with acute myocardial infarction: a community hospital experience.

Abciximab administration during primary coronary angioplasty in patients with acute myocardial infarction (AMI) reduces death, reinfarction, and the need for urgent target vessel revascularization (TVR). Stenting in AMI reduces the rate of repeat in-hospital TVR. There is limited information on the effectiveness and one-year clinical event rate of combined abciximab and primary stenting in patients with AMI at community hospitals. We evaluated the outcome of 40 consecutive patients treated with both abciximab and primary stenting at our institution. All patients underwent primary stenting of the infarct-related artery. All patients received abciximab, aspirin, ticlopidine, and heparin. TIMI grade 3 flow was established in all 40 patients. No patient required urgent TVR. There was no in-hospital reinfarction or cardiac-related death. All patients were followed for at least one year, and no patient died after hospital discharge. Thallium exercise stress test revealed no evidence of ischemia at 12 months follow-up. We conclude that combined abciximab and primary stenting in this series of patients with AMI was associated with excellent results.

Abciximab readministration: A single-operator community-hospital experience.

Abciximab, a monoclonal antibody to the platelet glycoprotein IIb/IIIa receptor, reduces ischemic complications of coronary interventions after first administration. In this study, We sought to determine whether readministration of abciximab is associated with equal efficacy and safety. We retrospectively reviewed the charts of 35 patients who received two doses of abciximab at separate intervals. We monitored patients clinically for recurrent ischemia, bleeding complications, and thrombocytopenia. We measured hemoglobin and platelet counts before and after readministration of abciximab. There was no cardiac-related death, myocardial infarction, or recurrent ischemia. No obvious bleeding occurred in any of the 35 patients, although 1 patient had a drop of hemoglobin >3 gm/dl. We observed one episode of severe thrombocytopenia without any complication, and this patient improved without requiring platelet transfusion. There was no profound thrombocytopenia. We conclude that readministration of abciximab was well tolerated without any evidence of altered efficacy or safety. Cathet. Cardiovasc. Intervent. 47:294-296, 1999.

Normal electrocardiogram with total occlusion of the left anterior descending coronary artery.

Total occlusion of the left anterior descending coronary artery is usually characterized by ST-segment elevation in the anterior leads of the surface electrocardiogram. We report a case of a patient who had a persistently normal electrocardiogram throughout his hospitalization despite the angiographic findings of total occlusion of the left anterior descending coronary artery and no collateral vessels. Percutaneous transluminal coronary angioplasty with stent placement was performed successfully.

Acute profound thrombocytopenia without bleeding complications after abciximab administration.

Abciximab (c7E3) is the Fab fragment of the chimeric monoclonal antibody directed against glycoprotein IIb/IIIa found on the surface of platelets. It is the first FDA-approved platelet receptor glycoprotein inhibitor. Severe thrombocytopenia (defined as platelet count < 50 x 109/L) on first administration is a rare complication, occurring in only 1.6% of patients in the EPIC (Evaluation of 7E3 for the Prevention of Ischemic Complications) study. Bleeding complications were the rule in these thrombocytopenic patients as reported by EPIC investigators, Kereiakes et al. and Berkowitz et al. Platelet transfusions are required to reverse the bleeding diathesis. Intravenous IgG has not reportedly been helpful in reversing thrombocytopenia, and experience with corticosteroids is not reported in the literature. We report a case of acute profound thrombocytopenia following abciximab administration treated with platelet transfusion augmented by intravenous corticosteroids, in whom there was no bleeding complication.

Cardiomyopathy of limb-girdle muscular dystrophy.

OBJECTIVES: This study sought to find an association between dilated cardiomyopathy and limb-girdle muscular dystrophy. BACKGROUND: Cardiomyopathy has been seen in various neuromuscular disorders, but it has not been recognized to be associated with limb-girdle muscular dystrophy. METHODS: We investigated three sisters with well documented limb-girdle dystrophy and congestive heart failure by the 3rd decade of life. All underwent noninvasive evaluation of left ventricular systolic function by both echocardiography and radionuclide scanning, and one also had cardiac catheterization. Deoxyribonucleic acid (DNA) linkage analysis was performed in these affected subjects and in the unaffected family members, and DNA was extracted from mononuclear cells with primer sequences for three chromosome 13q microsatellite markers. RESULTS: The parents had no evidence of clinical disease, but all three sisters had echocardiographic evidence of dilated cardiomyopathy. The sister with additional evidence of left ventricular dysfunction of cardiac catheterization had no coronary artery disease. The affected subjects had the same paternal allele for three potential markers of limb-girdle muscular dystrophy but different maternal alleles. The very small family size did not permit statistical confirmation or refutation of linkage for chromosome 13q markers. CONCLUSIONS: Demonstrable cardiomyopathy accompanying limb-girdle muscular dystrophy and its probable genetic associations require continued investigation by anticipating the cardiomyopathy in limb-girdle muscular dystrophy.

Pneumocystis carinii pneumonia. Rare cause of hemoptysis.

Pneumocystis carinii pneumonia is a frequent manifestation of the acquired immunodeficiency syndrome (AIDS). It commonly presents with nonproductive cough, fever, and dyspnea. We report this case of P carinii pneumonia presenting with hemoptysis, since to the best of our knowledge, hemoptysis has not been reported to be a presenting manifestation of P carinii pneumonia. Autopsy revealed multiple lung cavities.

Cytomegalovirus necrotizing bronchiolitis with HIV infection.

Cytomegalovirus (CMV) is frequently isolated from respiratory secretions of human immunodeficiency virus (HIV)-infected patients. Even in the presence of histopathologic evidence of CMV cytopathic abnormalities, the true clinical significance of CMV pneumonitis is not well established. Airways disease is increasingly recognized in HIV-infected patients, but its etiology is unclear. We describe an HIV-infected patient who presented with fever, wheeze, and micronodular interstitial infiltrates and developed severe hypercapnic and hypoxemic respiratory failure. Open lung biopsy showed necrotizing bronchiolitis with cytopathic changes characteristic of CMV infection; no other pathogens were isolated. He responded well to treatment with ganciclovir.

The effect of ouabain on hearts of cardiomyopathic hamsters: potentiation by isoproterenol.

The isometric twitch properties of papillary muscles from hearts of 30- to 53-day-old cardiomyopathic hamsters (BIO 14.6) were studied before and after exposure to the cardiac glycoside, ouabain. The diseased tissue was weakly responsive to ouabain (3 to 100 microM), as compared to a more appreciable positive inotropic response in papillary muscle of similarly aged normal hamsters (BIO F1B). These data suggest that the activity of Na+,K+-ATPase is attenuated in the diseased sarcolemma. Pretreatment with the beta-adrenoceptor agonist, isoproterenol (0.1 microM), slightly increased the sensitivity of normal muscle to ouabain, however the response of myopathic muscle was greatly enhanced. These findings may be of significance to the genesis of cellular calcium overload hypothesized to be involved in the necrosis and degeneration of heart cells in this animal model of genetic cardiomyopathy.