Impending paradoxical embolism presenting as a pulmonary embolism, transient ischemic attack, and myocardial infarction.

A 25-year-old man presented with complaints of nonpleuritic, substernal chest pain, dyspnea, and decreasing exercise tolerance. His vital signs were normal, with the exception of an oxygen saturation level of 93% while breathing room air. During his assessment, he developed transient left facial droop, left arm and leg weakness, and an ataxic gait, which lasted 15 min then resolved spontaneously. Cardiac enzyme levels were elevated, and an ECG revealed T-wave inversion in leads III, aVF, V1, and V2 with evolving ST-segment elevation in leads V3 through V5. The findings of a CT scan and MRI of the head were negative; a Doppler ultrasound of the right lower extremity revealed a thrombus extending from the common femoral vein to the popliteal vein. Cardiac catheterization revealed no evidence of epicardial coronary artery disease. CT pulmonary angiography revealed bilateral pulmonary emboli. Transesophageal echocardiography (TEE) showed a 4-cm, dumbbell-shaped mass lodged in a patent foramen ovale, confirming the diagnosis of an impending paradoxical embolism. The patient was started on therapy with unfractionated heparin, and his thrombus resolved spontaneously by hospital day 5. An impending paradoxical embolism is rare but should be suspected in anyone presenting with evidence of both venous and arterial emboli. The therapeutic options include anticoagulation, thrombolysis, and surgical embolectomy. We would propose that initial treatment with anticoagulation therapy and following with serial TEEs may be appropriate therapy in an otherwise stable patient, with surgical embolectomy or thrombolysis reserved for the treatment of thrombi that do not resolve with anticoagulation therapy or for patients with clinical deterioration.

Use of beta-blockers and aspirin after myocardial infarction by patient renal function in the Department of Defense health care system.

BACKGROUND: Whether the previously reported underutilization of standard-of-care medications in the management of patients with acute myocardial infarction (AMI) persists in more recent years or differs by ward of admission has not been reported. METHODS: We performed a retrospective cross-sectional study of patients hospitalized with a discharge diagnosis of incident AMI to a Department of Defense hospital (Walter Reed Army Medical Center, Washington, DC) from 2001 through 2004. Use of beta-blockers and aspirin at the time of discharge after AMI was assessed according to Modification of Diet in Renal Disease (MDRD) estimated glomerular filtration rate (eGFR) in milliliters per minute per 1.73 m2, stratified by admission to the coronary care unit (CCU) versus other wards. Adjusted odds ratios for discharge beta-blocker and aspirin therapy were calculated by using logistic regression. RESULTS: Among 431 patients, overall discharge use of beta-blockers was 86.8%, and aspirin, 86.8%, both significantly greater after CCU admission than admission to other wards (93%, aspirin use; 91.7%, beta-blocker use; P < 0.001 and P < 0.001). In logistic regression, CCU admission was the only independent factor associated with either beta-blocker or aspirin use; MDRD eGFR was not associated significantly with beta-blocker and aspirin use regardless of admission to the CCU or non-CCU. CONCLUSION: Future studies of disparities in use of standard-of-care medications after AMI according to renal function should account for the primary site of admission, particularly CCU versus others. In addition, legitimate contraindications to the use of beta-blockers and aspirin may be subtle, including appropriate end-of-life decisions.

The role of exercise in modulating the impact of an ultralow-fat diet on serum lipids and apolipoproteins in patients with or at risk for coronary artery disease.

BACKGROUND: Ultralow-fat diets are known to reduce high-density lipoprotein cholesterol (HDL-C) levels. In the setting of a multicomponent lifestyle intervention program, relationships between exercise variables and HDL-C levels were examined to determine whether exercise moderates this dietary effect on serum lipids and apolipoproteins. METHODS: We performed a 3-month, prospective, nonrandomized lifestyle intervention study (< or = 10% dietary fat; aerobic exercise [180 min/wk], group support, and yoga [60 min/day]) in 120 subjects with or at risk for coronary artery disease. RESULTS: After 3 months, dietary fat intake was reduced to 8.7% +/- 2.6% of total intake and the median weekly exercise time was 194 minutes. High-density lipoprotein cholesterol levels decreased by 8.3 +/- 11.3 mg/dL (P < .001), and triglyceride levels increased by 17.6 +/- 102.7 mg/dL (P = .026). A small dense low-density lipoprotein cholesterol (LDL-C) phenotype emerged indicated by a 13.8% LDL-C reduction accompanied by only a 2.3% reduction in apolipoprotein B levels (P = .064). Among subjects with exercise amounts less than those of the group median, HDL-C reductions were greater in those with more than (-13.5 +/- 16.0 mg/dL) versus less than (-2.5 +/- 7.5 mg/dL) the median reductions in fat intake (P = .026). Even among subjects who exercised > 194 min/wk, HDL-C was reduced compared with baseline (-7.4 +/- 7.9 mg/dL, P < .001). CONCLUSIONS: An ultralow-fat diet as a component of a comprehensive lifestyle intervention induces reductions in HDL-C and the emergence of a dyslipidemic lipid profile. Aerobic exercise only partially mitigates this effect.